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RF_DIS_L_PART_1_SUDHA
■
I
ted in
ogical,
Indian J Med Res 72, August 1980, pp 153-158
■
Epidemiology and prevention of measles in rural
south India
xpects.
T <only
ut has
where
oduced
ing.
T. Jacob John, Abraham Joseph, T.I. George, Janaki Radhakrishnan,
Rajdayal P.D. Singh and Kuryan George
Departments of Community Health and Virology, Christian Medical College
and Hospital, Vellore
1
Received September 24, 1979; revised article received January 28. 1980
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The epidemiology of measles was investigated in a village without any health care
supervision, 3 villages with health care supervision but without measles immuniza
tion and in 2 villages covered with measles vaccine as part of health care, near
Vellore in south India. There was an epidemic of measles in and around Vellore during
the last quarter of 1977 and the first of quarter of 1978. In the first village, the
attack rate among preschool children was 26 per cent and the overall case-fatality
rate 14 per cent. In the second group of villages, the attack rate was 20 per cent
and case-fatality 3'7 per cent. In the vaccinated villages, the attack rate was 4 per
cent with no death; measles was confined to the unvaccinated children in these tillages.
No measles occurred among 121 vaccinated children. Complications of measles
were predominantly gastrointestinal (35 to 52 per cent) and respiratory (37 to 58
per cent). In the light of the results these and other studies, the inclusion of measles
vaccine is strongly recommended in the routine immunization of preschool children
in India.
In the planning of health care in
India, measles immunization has yet to
find a place. Measles vaccine is not
included in the current recommendations
for routine immunization of infants and
children in India, either by the Health
ervice Agencies or by the Indian Acade
my of Paediatrics. This situation appears
be due to a general lack of understand°f measles and its adverse effects on
e child-population, inadequate knowledge
a out the efficacy of the vaccine and the
1 datively high cost of the vaccine.
mortality in India1”4. Three of them were
in rural or low-income urban commu
nities2”4. Two of these reports described
measles as an important public health
problem2,3. One of the authors described
it as a mild disease without serious com
plications and with low rate of mortality
confined m children with kwashiorkor4.
Experience with measles vaccine is
also limited in India. The World Health
Organization (WHO) conducted a vacci
nation-trial in 408 children in India with
93 per cent seroconversion5. The feasibi
^aVC keen only ^011r commulity of mass vaccination was demonstrated6
, aseci studies of measles and its epidin Vellore and surrounding area in 1967.
biology,
severity, complications and
The efficacy of the vaccine in protecting
153
iii
IIP'
Epidemiology and prevention of measles
‘•I
complications and counted as mortality
children against measles has also been
due to measles.
Ji
Jat dly demonstrated1’2. Over 90 per
As many exanthematous diseases are
Pt antibody response was reported2
tooetlier call J ‘annnat' by the commu£ vaccinated children in New Delhi. Thus
X it was assumed that accurate
the need, feasibility, effectiveness and
information on a past history of measks ■ s
Jnnce
of measles vaccination
would be difficult to obtain. 1her
e
Ze been repeatedly pointed out m
no
attempt
was
made
m
the
fcs
MUa.e
India1.1.6'8 In ’uPPort of these’ wc alSO
Xt our roeeru observations and expento classify children according to . the past
r ^PA.les In the remaining
ence of measles and its prevenuon tn
history of measles.
_
qtt9rk of
villages history of previous attack of
rural populations.
Measles was elicited by detailed puesi'ons . ,
154
■
Hi".
I
•;<
addressed to the parents.
Material and Methods
••3 measured in
Measles antibody was
The studies were conducted in a
previously1
sera
as described
c----villagc about 5 km west of Vellore town
.
and'’in 5 villages about 10 km south of
Results
Vellore. The first village had no health
care supervision by any agency.
ie
,hc
: The ag’-’1™ "
remaining live villages were among those
poputeuon, fhe
'
under the health care supervision ot the
Community Health Department. In late
and early 1977, measles vaccine
(Attenuvax, Merck Sharp and Dohmc)
to all preschool 26 per cent (57 cases).
wqs made available 1
...............
" '
DMn or dysenw 8im™ J® '
children of village No. 2 and’the
Harijan
area of village No. 3.
During the last quarter of 1977 and
the first quarter of 1978, an epidemic of
measles was prevalent m and around
Vellore. Information on measles mor iZ complications and mortality was
i
1W i.
collected during-repeated visits to every
house in the 6 villages until the epidemic
was over. The diagnosis of measles was
made on the basis of history and/or chmca
features, vic. coryza, cough, sore eyes
maculopapular rash
and a generalised
■ r after 3 or more days of high
appearing
Desquamation of the skin was
fever.
characteristic during convalescence.
or mediately after "1»81's. “™": and
34 ebildrea (52 P=r o”1)le4 1
prolonged respiratory d.sease va^
in 38 children (58 per centbO^j
4
with discharge of pud
sVith.
children. Antons the 65
;
measles 9 died,
Qn:ratorY diseas^'X
dysentery and 3 with re.p
<
XT the case-fatality rate,
U» ;
cent (Table I).
Measles in the five villages :
Reliability of; a past history
lustory- of
of
check
the
reliability
f^
aS.
In order to check the re ia ^blood
V®
^hhistory of measles; in
m children, W
h
cohected from 8 children
with
and
39
ol
ihildren with and 3
1 and
out such lustory, between
Death within a month of the onset
Of measles was attributed to measles or its
i
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John et al.
155
pll
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a.
Table I. Age specific measles morbidity and mortality in village No. 1
A Age
(yr)
1I1W ■ 21
-i-
Ifc-
- >
Measles
case
Attack
rate/100
Deaths
Case-fatality
rate
23
9
14
8
39
2
22
45
22
3
21
13
31
37
43
32
48
J
23
10
9
6
>10
214
166
901
56
9
0
28
13
26
5
0
Total
1,281
65
5
1
i1
S2
0
9
0
0
9
;
Br
w
■up
■jB-i
10
22
0
#
16
0
0
■ {■
14
■
■"i
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Population
■
-•■
•
It- ■
age. Among the 8 children with previous
e history of measles, 6 had measles antiBSS body indicating about 75 per cent
ii ; accuracy of the history. Two children had
|y ;
presumably some other exanthematous
illness. However, among the 39 children
without history of measles, 12 (31 per
cent) were also seropositive, indicating
;
previous
sub-clinical infection with measles
i®
^^JjVirus .......
as has been postulated previously11.
w
^^yleasles morbidity in immunized children :
I ■ In village No. 2 and in
the Harijan area
^^^village
village No. 3, there were 180
^Hfe?1001 children> of "hom 30 had
|
\previous
previous attack of measles, 121 were
and
refused to get
However, there was not a
^p^-ase of measles
___ j among
among the
the 121
121
^^fenated children during the epidemic,
per cent) among the 29 unvaccichildren contracted the disease
ftbl.II).
®f!
^mMbidity and mortality in unIn rhe remaining
Were aIt°Sether 775 preof whom
85 had
a
'■.history of measles. Among the
lnmg 690 ‘susceptible’ children, 136
.
/J
■
iifep
■
■ ■
developed measles during the epidemic,
for an attack rate of 20 per cent (Table II).
’■■ is
; $
Prolonged diarrhoea or dysentery
occurred among 56 children (35 per cent),
bronchopneumonia in 43 (37 per cent) and
suppurative otitis media in 16 (10 per
cent). Among the 136 children with meas
les 5 died, for a case-fatalit\ rate of 3*7
per cent.
:-k
i
Discussion
Morbidity, complications and mortality
due to measles : In the first village with
no previous health care supervision,
the rate of complications following
measles and the case-fatality rate were
quite high. In the four villages which
were provided with health education
and care over several years, the rate
of complications and mortality were
considerably less. In an earlier study
83 children with measles in a well
nounshed group on a university campus,
serious complications
were virtually
absent and there was no death1. In
a village under nutrition supplementa
tion programme, the case-fatality rate
was 3*6 per cent, almost identical to
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156
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Epidemiology and prevention of measles
I
according to the availability
/ and mortality in pre-school children a<
Table U. Measles morbidity
and measles vaccination
of health care facilities
1----Case-fatality
No.
Attack
No- with
No. of
rate
died
Health care
Vaccination
rate,%
Village
measles
children
facilities
no.
16
9
26
56
214
Nil
Not available
1
2, 3
3-6
Available
Available
Measles vaccination was
P Offered and
| taken
121
0
0
| Offered not
taken
29
6
21
0
690
136
20
5
Nil
offered in village No. 2 and Harijan area
|
3’7
■
of village No. 3
s
■
Thus proxection was clearly relaxed to ,3a
immunization.
In an earlier report of an epidemic
in a village, 82 (67 2 pci cent) among
122 immunized children and only 2 ./•
among 72 immunized
;
(2-8 per cent).) among
children had cdeveloped measles2. Thus,
* l due to immuthe degree of protection
of the
nization was c.
. order of 96 per centa
is
In another report i of measles on
20
only
1
among
university campus,
* r immunized
children developed
previously
i---measles, whereas 22 ^among 39 un- Ir
Protective efficacy of measles immuniza
immunized children of
c_ comparable age
tion • The protective efficacy of measles
developed the disease, with an attack
this
immunization was confirmed in
In both these groups, |
rate of 56 per cent.
study, since no immunized child develope
f measles vaccine,
Schwarz strain of the disease.
The vacane had been
—t checked locally n
nearing expiry date, not
administered only to children above
had been given to infants
for potency, --one yr of age and without a past histo y
and children aged 9 months and above ;
of measles. While a majority of he
ine-failure •
Thus the few instances of vaccine-fail
children in the second village and the
nnght have been to interference
interference^.^ |
Harijan area of the third village had
account
immune response on account of
o res:
accepted immunization, the parens of
vaccine
maternal antibody, or vaccme co
29 children had refused it. The attack
potency. In the present study, Atti
rate (20 per cent) among them was
strain of vaccine was given to ch
similar to that in the villages where
above one yr and its potency had
the vaccine was not offered (21 per cent).
the 3'7 per cent rate in the four villages
referred to above2. In the first village
with no health care supervision the
case-fatality rate was 14 percent Thus
mortality due to measles is largely
preventable by improving the nutrition
and health care of a community, n
rural communities, such improved living
conditions may take a long time to e
achieved. Without waiting long tor it
to happen, measles mortality, can
prevented at once by immunization.
fe8P‘
* J
John et al.
■ checked and found to be adequate, thus
. ^voiding the two problems identified earlier.
had evidence
infection12.
157
of previous sub-clinical
■
.
5
■ Reliability of past history of measles :
It is important to ascertain the reliability
of the past history, since immunization
/ is not necessary in children who have
had measles. In addition to the sero
logical data presented earlier, the total
absence of measles in 115 children who
gave a past history of measles, in the
five villages, confirms the high degree
. of reliability of a positive history. In
eliciting such history, we have used the
precise term used for measles in the local
community9 and also checked if sore
yes, running nose, cough* fever and
rash were present.
On the other hand, serological
evidence of previou' infection was
obtained in over 30 per cent of children
in whom a history of measles was denied.
In earlier (unpublished) studies, we had
tested sera from 31 children in New
8 . Delhi and 45 children in Ferozporc,
r
between 1 and 5 yr of age, without a
8
previous history of measles. In the
former group 19 per cent and in the
8,8. latter 44 per cent had measurable
measles antibody, indicating earlier in
fection. Such consistent results cannot
k
be ignored I as unreliable history; rather,
||||
__
bey indicate
subclinical infection or
I’very mild Unrecognisable illness. HowF
eVCr’ a rePort on fbe sero-epidemiology
measles in Bombay, Mehta and
>
co-workers12 could find no evidence
Of
subclinical infection.
On close
scrutiny Of this report, it was found,
•8
5children between 1 and
8' . n
demonstrable measles virus
’
antibody, only 29 (62 per
cIn^t)' had
" ’ a Previ°us history of measles,
T
.w*
°ther words, 38 per cent of children
I
i
"
Thus, evidence
previous subclinical or unrecognised infection with
measles virus in approximately 20 to
40 per cent of preschool children seems
to be a real phenomenon in different
parts of India—both urban and rural.
As postulated earlier, this may be
related to exposure to infection while
the infant still has residual antibody transferred from the mother which is
sufficient for protection from disease
but not enough to prevent infection13.
The priority for measles immunization :
Should measles be included in the expa tided programme of immunization in
India?
Sinha4 had suggested that
measles immunization is of low priority
in India because of the mild nature of
the disease, lack of serious complications
and low mortality.
In his experience
in a village in West Bengal, measles
occurred mainly from May to August,
and the prevalence rates were fairly
uniform in 1971, 1972 and 1973. These
features are very different from what
we have observed in southern Indian
villages, where it is a disease of the
first and last quarters of the year and
occurs in a cyclic pattern with epidemics
once in 3 to 5 yr. In Punjab, measles
is a frequent cause of death among
infants and preschool children14, The
reported picture of measles in rural
West Bengal is quite different from
that in any other part of India from
where reports are available.
As documented in this and other
reports2 A14 measles and its compli
cations are a major cause of morbidity
and mortality among rural Indian children.
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2)15
J. Com. Dis., 22 (3): 165-172, 1990
il
11
Sero-Epidemiology of Measles-A Three Years Prospective
Study in a Rural Population of Rajasthan
D. C. JAIN*, H. S. MEENA*, B. S. YADAV*, K. C. MEENA*
SHASHI KHARE** AND K. K. DATTA**
■■
{Received for publication : 20 November 1989}
ABSTRACT
to ^C8O8mrnUnR7m5eh pr^peCtivef8tu^ on measle8
undertaken during 1986
to 1988 in Ramgarh village of Alwar district (Rajasthan) to elucidate
epidemiological features of measles. The initial population of the viUaue
Snd?eTlnh1988eD(i14
ThiCh rOS£ ‘O ‘OtaI P°Pulatlon °f ’92! with 2200
children In 1988. During the entire period of study, all the children (0-14 years)
ere covered regularly through monthly domlcilliarv visits hv
paramedical personnel under direct supervision of Medical Officers A t«al of 208
rhndrZnTo3ei4WCre ^teCted Wh‘Ch
aD °Vera11 lncidence
o^eTroupl^^
of 31.5 per 1000
Kolmogrov-smlrnov statistical method validated the seasonal character of the
disease (Vo - 5.36, p < 0.01). Asignlflcant (P< 0,005) rise in seronnsMvin ,5
inj^eagein^ge was observed ^THM^TK^onih^^^
~“«^£5_5fldm^slesjmmunization during their life time^UHgher rate
than TOnVCbrS O" WaS Observcd ,n chlldrcn vaccinated after 10-months of age
than those before. No significant relationship of seroconversion following
sTatus (p°> 0 10)
Wlth a8C °f Vacc,natlon (? >
8=x and nutrition J
INTRODUCTION
Measles is a highly communicable disease among children in develooim?
aCXtbrS’tChOmribUtin8 t07he high degree Of morbidir>' and mortality. From reports
000 ’ t?ean"UaI incidence
measles in India has been estimated to be 19 per
1000 population2. During 1987 a total, of 2,28,166 measles cases with 639 deaths
were reported from different parts of the country^ Although meaiies is a mdd
alwsTairchdd11'1^ StUd‘eSi
th3t il iS 3 mai°r Public health Problem as
almost
imost all children get measles by the time they attain school going age and its
Xe oTdeTth
high' 11 has been found that ” the thifd leading
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I
I
£Pf death among pre-school children after respirator)- infections and diarrhoea*.
cOmXSPtitalS bn‘y 566 thC Proverbial tjP °f the iceberg and that also when
on the natural hT
COmmunity which Provides the best information
i
conduced in d f
1
measles
V
ser°ePidemiological studies5’8 have been
,tO d”w the attention to the magnitude of
‘Field Practice Unit, NICD, Alwar-301001 (Rajasthan).
National Institute of Communicable Diseases, Delhi-54.
165
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D. C. Jain ci al.
166
Rajasthan. Therefore, a prospective study was undertaken in Ramgarh V! lage of
Alwar district (Rajasthan) from January, 1986 to December, 1988 to elucidate
epidemiological features of measles. The present paper deals with the findings of
this study.
MATERIAL AND METHODS
1. The study village had a population of 5258 comprising of 723 families with
2018 children (0-14 years) in the year 1986 which rose to total population of 5923
with 2200 children (0-14 years). The increase was mostly due to growth of
population through births minus deaths.
2. The village was a typical Indian village and the community belonged to the
lower socio-economic group.
3. From Jan., 1987 to Dec., 1988 all the children (0-14 years) were covered
regularly through monthly domiciliary visits by trained paramedical personnel under
direct supervision of the Medical Officer.
4. The paramedical personnel enquired about the occurrence of cases of fever
with rash and at least one of the symptoms like fever, coryza, and redness of eyes. All
the cases of fever were verified by the Medical Officers for the confirmation of the
diagnosis.
5. The cases detected were recorded in the prescribed pretested proforma
designed for the purpose and followed up till recovcw or death and to observe
complication, if any, during the study period of three years.
6. Blood samples were collected from children who did not give any history of
measles during their life time to know the measles antibody status. Tlie blood
samples were collected in filter paper strips. After collection of blood samples the
children were immunized with one dose of measles vaccine. A second sample of
blood from the same child was collected after 1 month of immunization to knov* the
sero-conversion following use of measles vaccine. The filter paper strips were tested
for measles antibody by HI test in the laboratory of the National Institute of
Communicable Diseases, Delhi.
An Hl titre of 1 : 8 or more was considered as sero positive.
RESULTS
A total of 2200 children (0-14 years) were observed in Ramgarh village during
the period of three years from January, 1986 to December, 1988. A total of 208 cases
of measles were detected (Table 1) which gave an overall incidence rate of 31-5 per
1000 children per year. Incidence rate was found to be high in 2-3 years and in 4-5
years age groups. The lowest (4.6 per 1000) incidence vas recorded in 10-14 "years
of age group. Infants had an incidence rate of 26.5 per 1000. Tlie relationship o
measles with age was found to be highly significant (p <C 0.001). Incidence rate v>as
found almost to be similar in both the sexes (p > 0.101.
Table 2 shows the seasonal variation in respect of occurence of measles during
the vear 1986 to 1988. It reveals that the disease occurred in all the months (except
...
Wa
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.
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Prospective study on measles in Rajasthan
167
Table 1—Age & sexwise distribution of cases of measles in Ramgarh village
Male
Age group
(Years)
Number No. of
examined cases
Female
■
Total
Attack Number No. of
rate per examined cases
1000.
per year
Attack Number No. of
rate per examined
1000
per year
0-1
2-3
4-5
6-7
8-9
10
254
325
147
138
112
270
23
48
26
11
3
3
30.2
49.2
59.0
26.6
8.9
3-7
173
275
125
113
108
160
11
44
22
10
4
3
21.2
53.3
58.7
29.5
Total:
1246
114
30.5
954
94
34
92
48
21
26.5
51.1
58.8
2^.9
10.6
6.3
427
600
272
251
220
430
6
4.6
328
2200
208
31.5
12.-1
I
.Attack
rate per
1000
per year
Table 2 —Seasonal variation with respect to measles incidence in Ramgarh village
during 1986-1988
Month
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Frequency
January
February
March
/\pril
May
June
July
August
September
October
November
December
28
28
16
6
5
5
3
3
6
Cumulative
frccjueiH y
bn
I-
28
o.i s
0 OStO
61
0.2-
0 lulu
KO
0 -12“-
1 It)
i(H
180
0.55—
0.2-106
0 3288
OTs-'
0.8i)A.
0.4 13'’
0.4959
18o
0.89-t2
191
1%
0.9-12?
0.942?
0.9x"
0.5808
O-ObS”
199
202
208
0.9" N.
i.ooo:
0.”4’9
0.8329
0.915!
1.0000
■
■
-
0.1813
0.22.8'
0 3~i8
0 3o95
0.3134
0.2~ixj
0.1944
0.1238
O.OSoO
0.0000
Vn = 5.40, p<0.01, Highly significant
August and November 1988) during the entire period of three years. 86.5 per cent of
i measles cases occured in the first half of the year and the month of May recorded
the highest number of cases (23.1 per cent). Very7 few cases were observed in the
months from July^to December (Fig. 1).
I
.
H j.
Among 333 children of the age group of 6-36 months with no history of measles
and measles vaccination, 154 (46.2 per cent) were seropositive while 179 (53.8 per
cent) were seronegative (Table 3). A gradual rise in seropositivity was observed with
advance in age. The association of seropositivity’ with age was found to be
statistically significant (p < 0.005).
Table 4 reflects the seroconversion rates according to age at vaccination. A
higher rate of seroconversion could be observed in children vaccinated after 10
months of age than those vaccinated before 10 months of age (Table 4). The
relationship of seroconversion with age at vaccination was not found statistically
significant (p>0.50).
t
I
S
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D. C. Jain el al.
168
----- I9B6
\/
13
32'
3<r
2B26-
22’
26-
IBMJ
16-
c
■
u
nlo-
96-
2c
t—r
N
0
-MONTH---------------- —
Fig. 1. Seasonal pattern of measles
Table 5 reveals that no significant (p > 0.10) association could be obvserved
between sex and seroconversion following measles vaccination.
Although the well nourished children had higher seroconversions rate (67.1 per
cent) as compared to that of undernourished children (56.6 per cent) following
found to be statistically not
measles vaccination (Table 6), but this difference was L
significant (p>0.10).
Prospective study on measles in Rajasthan
169
■
Table 3—Measles serology status indicating sero positive (HI titre of 1:8 or >) and
seronegative (HI titre of < 1 : 8) children 6-36 months without any history of measles and
measles vaccination during their life time.
1I
t.
a ■
Age in
months
Sera
tested
Positive
0 1:8)
Negative
« 1 : 8)
6-10
11-15
16-20
21-25
26-30
>31
61
46
71
30
52
73
22 (36.1)
21 (45.6)
24 (33.8)
11 (36.7)
31 (59.6)
45 (61.6)
39 (63.9)
25 (54.4)
47 (66.2)
19 (63.3)
21 (40.4)
28 (38.4)
Total:
333
154 (46.2)
179 (53.8)
)
J
(Figures in parenthesis indicate percentages)
■
Table 4—Sero conversion .rates according to age at Measles vaccination
Age in
months
Number
vaccinated
Seroconversion
0 1:8)
No sero conversion
« 1 : 8)
6-10
11 15
16 20
21 25
26 30
> 31
39
25
19
21
28
21 (53.8)
16 (6-i.O)
31 (66.0)
11 (5"’.9)
13 (61.9)
17 (6O.~)
18 (46.2)
9 (360)
16 (3-1.0)
8 (41.1)
8 (38.1 )
11 (39.3)
total;
r9
109 ( 60.9)
"O (39.1)
1 ■
(Figures in parenthesis indicate percentages)
Table 5 —Sero conversion and sex of Measles vaccinated children
Sex
...* ••.
Number vaccinated
Sero conversion
No sero conversion
Male
Female
101
78
65 (64.4)
44 ( 56.4)
36 (35.6)
34 (43.6)
Total:
179
109 ( 60.9)
70 (39.1)
(Figures in parenthesis indicate percentages)
Table 6—Sero conversion and nutritional status at the time of Measles vaccination
Number
vaccinated
Sero conversion
01:8)
No. sero conversion
« 1 : 8)
Well nourished
Under nourshed
73
106
49 (67.1)
60 (56.6)
24 (32.9)
46 (43.4)
Total:
179
109 (60.9)
70 (39.1)
Nutritional
Status
(Figures in parenthesis indicate percentages).
■
.............. —....... ...................... .. ........... ’
-
■
■
KB
I
•
)
ill
s
170
M
■I
,.u;
v <
D. C. Jain et al.
DISCUSSION
The present study which was carried out in a rural population (0-14 years) of
Alwar district (Rajasthan) showed an overall incidence rate of measles as 31.5 per
1000 children (0-14 years) per year. Approximately similar rates were noted
°
in their studies. Phool Chand et aP observed higher rate (44.7 per 1000
workers8’10
a similar study in a village Nirmanpur, Varanasi conducted for a period
children) in a
of 13 years ((1974-1986). Swami et aP in a study by monthly home visit in M
Rajasthan found annual incidence rate of measles to bel3.8 per thousand children
(0-14 years), being much lower than that of present study. The difference in
incidence rates in various studies is probably due to cyclic trend or nature and
design of different studies or both.
In this study the incidence rate was recorded highest (58.8 per 1000 children)
in 4-5 years of age group and lowest (4.6 per 1000 children) in 10-14 years of age
group (Table 1). Infants had an attack rate of 31.6 per thousand. The relationship o
fhe disease with age was found to be highly significant (p < 0.001). No significant
(p > 0.10) difference could be observed in attack rates of two sexes. Other authors
12 also had similar observations.
There has been a definite seasonal variation in the occurence of measles (Fig1). .Although disease was present through out the year but 86.5 per cent ot the cases
occured in the first six months of the year (Table 2). The maximum was in month o
May (23.1 per cent). It may be due to a small outbreak which occured in May, 1987.
The seasonal variation was put to statistical test with the help of Kolmogorov
Smirnow Method13 which validated the seasonal character of the diseases (\ n = 5.36,
p < 0.01). Labo et aP in Ballabhgarh and Morley14 in West Africa has described t re
same type of seasonal variations. Other authors'1’12’ 15 also reported the maximum
incidence between January and April. The reason for the seasonal variation could be
due to the fact that during winter months the communities remain inside and stay
closer enhancing the chances of transmission of the disease. This has a great bearing
in planning of immunization programme. It is also pointed out that the transmission
and spread of disease can occur in any season depending upon the mobility' and
susceptibility status of the community.
Seropositivity (HI titre >1:8) rate in children (6-36 months) who gave no
history of measles and measles vaccination in our study was higher (46.2 per cent,
in comparision to 36.1 per cent and 32.3 per cent recorded by Sehgal et aF and
Bhardwaj et al’6 respectively in their studies. In contrast to our findings, higher rates
were reported in other studies7'17’18. A significant (p < 0.005) rise in seropositivity
with advance in age was observed in the study. The variation in the seropositivity
rates as reported in different studies may be due to geographical difference an
peculiar climatic and social conditions prevailing in the study areas. In addition to
these, the prevalence of measles infection might have also contributed.
The present study had shown an overall seroconversion in 60.9 per cent
children (6-36 months) one month after measles vaccination which is in accordance
to the findings of other workers19’21. A high rate (83.3 per cent) of seroconversion
was reported by Bhardwaj et al16 in their study as compared to the rate of our study.
-
IHbhhhhhh
Prospective study on measles in Rajasthan
171
reported a positive correlation between seroconversion
f uerestingly, Swami et aF'
but
no
increasing age
n: such correlation could be obserx'ed by us.
i showed no significant
Seroconversion following measles immunization
_ —reported
by b ,ni et aP1. No
p>0.10) difference between two sexes asjwas
i
■"
! c
observed
in the seroconversion rate of
Significant (p>0.10)■ difference
----well nourished children. Our findings support the results
undernourished and
”
;
2
1
'
22
in their studies.
^served by workers'
■
references
Morley, D. C. (1962). Measles in Nigeria, Amer. J. Dis. Child. 103 ; 230.
^■HO (19-8) Expanded programme of Immunization Reported and working Papers of the Technical
2
Discussion. 22-28. August. SEARO. New Delhi.
A
Central Bureau of Health Intelligence (1988). Health Information
India. DGHS, Ministry of Health.
Govt, of India, New Delhi.
Indian Pediatr
on causes of death Model registration
Sinclair, S. (1974) Viral Statistics Report
11 : 69.
, M. v. ( nr2 i Sc-ro hp-.de-'.iologv of measles m
S Mehta N A.. NanaW.r. A N D . Ihala. M. and bant
Bombay. md,ar. I Med Res 60 txrl hdO.
sero epidemiological
Broor. S. Pal. S >< Banerjee. A K. Chitkara. N. L and Ciraudhrr.
and around Chandigarh. Indian J Med Ke. 64
study of measles virus in ;
/pidcmiol'.ig’' of measles in Dclb.i
Kumari, S. and Basu. R- N. (198 )Khare, S., Duita, A..
-'ll 'IS
Implications tor age of vaccination Indian J. Paediir 54
. Sebestcin, M. and Arora. R R- UdS’ Scro epidemiological
8. Sehgal, S.. Sharma. R. S., Mehta. P K.
survey of measles. ,/. Com. Dis 15 : 1 ’.
of measlv> in rura: area of Punjab.
9. Lakhanpal, U. and Rathore , M. S. (1986). Epidemiology
Dis. 18 : 185-188.
. S K and Nath. L M. (W). Epidemtolop' of measles in a rural
10. Lobo, J.. Reddaiah. V. P.. Kapoor
- ”communitv. Inci.an J. Paediatr. 54 ■ 261-265.
, Ph„, Chand * K. N- Cha.da, V-. T.ipa.hh K. L -d Dana. K M
Ep,da atopy d<
11. tnooi cnauu,
- =n a village (Under publication).
A thirteen years prospective study in
Chandra Shiv (198-). Epidemiology of measles in western Rajasthan.Com. D,s
12. Swami, S. S. and
19 : 370-372.
”
j use of Kolmogorov-Smirnov type statistics in testing hypothesis about
13. Freedman, L S. (19"9). The
seasonal variation. J. Epid Com Hlth. 33 • —3—8.
i
U. htorty. D. < 1575>. O,.™« o< p.«»»
“ to
» "" ■1"to!”n8
Tr"''‘ R“r“
Soc. Trap. Med. Hyg. 69 : 22-23.
15. Garni. R. and Chakmborty, A. K. (1980). Measles in rural community. Indian J. Phi Hid, 2^ . 1-0.
,,
c
• H M
16 ^iXtoototoS™;
Gunta B P Saha, S. M., Ahlusvalia, S. K. and Vaidya, N. K. (1988).
xx. io.
or
j c». ®-
316-320.
17 John T J. Joseph. A. and George. T. T. (1980). Epidemiology and prevention of measles in rural
sourth India. Indian J. Med. Res. 72 : 153-158.
■
st
T
■
1^. 3
■
MEASLES OUTBREAK IN A
| TRIBAL POPULATION OF
I THANE DISTRICT,
Kt
MAHARASHTRA
*.
K';.
A.R. Risbud
S.R- Prasad
V
S.M. Mehendale
Sy- N. Mawar
K N. Shaikh
U.B. Umrani
S.S. Bedekar
j i K. Banerjee
K
I O':V-
r
ABSTRACT
In March 1992, an outbreak ofmeasles, in the
tribalpopulation of Vavar village, Mokhada Taluk,
Thane district, Maharashtra, was investigated. Two
hamlets of Vavar village namely Sagpanipada
(epidemic in October, November 1991) and
Behedpada (epidemic in January, February 1992)
fet
affected. In both hamlets, measles cases were
confitted to children below 10 yrs and 96% of the
cases occurred in children below 6 yrs. Attack
rates were 527% and 51.4% and case fatality
^tt 31.2% and 15.6% at Sagpanipada and
Behedpada, respectively.
St **
convalescent patients’ sera possessed
; IgM antibodies against measles. A clear drop in
^gM and a rise in IgG antibodies against measles
observed in 35 paired samples from convas lescent Patients. Fifty four per cent of sera from
i controls, possessed IgM antibodies.
■
Migrating population appeared to have imP°fted measles which flared up in an epidemic
the susceptibles. Priority immunization of
children of remote isolated populations may
rgt Pf^cnt such epidemics.
bywords Measles outbreak. Tribals.
Measles is endemic in urban parts of
India. Epidemics of measles have occurred
in rural areas and in isolated remote pop
ulations^^). In March 1992, an outbreak
of measles occurred in the tribal population
of Vavar village, Mokhada Taluk, Thane
district, Maharashtra. We investigated this
outbreak on being requested by the De
partment of Health, Government of Maha
rashtra. This report presents our observa
tions on the epidemic, which has occurred
during the present era, when world wide
efforts are being made to overpower mea
sles to the point of eradication(5).
Material and Methods
Vavar village, situated at the south
western end of the north Sahyadri moun
tain ranges is in the Mokhada taluka of
Thane district, Maharashtra (Fig. 1). The
village is comprised of 9 hamlets, locally
called ‘padas’, separated from each other
by a distance of 3-5 km. The hamlets arc
isolated, lack electricity and medical faci
lities. One had to walk 8 km to avail the
nearest bus facility, travel 9 km to visit the
nearest market at Ozar and transport a
patient 20 km to the nearest Primary Health
Centre (PHC) at Sakharshct to seek
medical help.
The present outbreak of measles oc
curred in two hamlets of the Vavar village:
Sagpanipada, situated on the top of the hill
and Behedpada, situated 3 km away at the
foot of the hill. Both these hamlets were
From the National Institute of Virolgy, 20-A, Dr
Ambedkar Road, Pune 411 001.
Reprint requests: DrA.R. Risbud, National Institute
of Virolgy, 20-A, Dr Ambedkar Road, Pune
400 001.
Received forpublication: July 22, 1993;
Accepted: December 27, 1993
risbudetal
measles OLTBREAK IN THANE
mamvushtra
•)Lvavar village I
SAICXAR0
SXT
O
OMOKHADA
JAWHAN
)
thane District
thane )
Fig. 1. Location of Vavar village, where measles
outbreak occurred.
inhabited by intermingling tribal popula
tion.
'
Enquiries made at PHC Sakharshct
revealed that one vaccinator from the PHC
used to visit these hamlets for immunizing
children with polio, triple and measles
vaccines. The vaccinator had to carry the
vaccine on foot to these hamlets as no
transport facility was available. At the PHC
no records of immunization at these ham
lets were available.
Locally no qualified medical practitio
ner was available. However, there was one
person locally, who used to treat some
ailments with herbs and roots. The villagers
preferred him to a Doctor as he did not
take any remuneration in cash, instead
accepted food/dnnk or even fowl which was
easier for the villagers to pay. He did not
treat patients too long and often referred
them to PHC.
544
The team visited all the households in
both the hamlets, enumerated the popula
tion, examined the patients and noted the
details about their illIness. In addition, the
available children at 1Behedpada were
weighed
and their height
.
~ andI mid arm I
circumferences were noted to assess their
nutritional status.
To serologically confirm the epidemic,
*
8 single convalescent sera from
f
patients of
Sagpanipada, 35 paired convalescent and 8
single convalescent samples from patienfc
There^was
of Behedpada were collected. There
was an
interval of 2 months between the paired
convalescent samples.
To serve as controls, 7 single serum
samples from normal subjects at Sagpani
pada and 6 paired sera and 20 single scrum
samples from normal subjects at Behedpa
da were collected. These normal subjects
belonged to similar age groups and had not
suffered an attack of measles during the
epidemic.
I
1
All scrum samples were tested for the
presence of IgM and IgG antibodies to
measles virus by indirect ELISA(6,7). Briefly
the serum samples were diluted 1:100 (in
phosphate buffered saline pH 7.2 supple
mented with 1% bovine serum albumin).
Then the samples were added to Nunc
polystyrene plates, coated with purified
measles antigen. After appropriate washing O
steps, goat antihuman IgM (Sigma Chemi- ||
cal Co., 1:1000 dil.) was added for detection
of IgM antibodies and goat antihuman IgG
(Sigma Chemical Co., 1:1000 dil.) was added
for detection of IgG antibodies. This was
followed by washing steps and addition of
substrate (H2Op and the Chromogen (orthophenylene diamine in phosphate citrate |
buffer pH 5). After the development of the |
color, the reaction was stopped with 4N |
PEDIATRICS
H SO4 and the wells were read in a
pynatech ELISA reader at 492 nm. Appro
priate strong positive, weak positive and
negative controls for measles IgM and IgG
antibodies were run in each test. Measles
IgM and IgG ELISA carried out by us,
were standardized by using a commercial
jnt (Pharmacia) and second international
standard antimeasles serum obtained from
Staten Serum Institute, Copcnhagan, respec
tively.
A serum giving an optical density (OD)
of 0.7 or more in the antimeaslcs IgM
ELISA corresponding to a titre of 1:50 was
onsidered positive for IgM antibodies to
ineasles(8) and a serum giving an OD of
0.6 or more in the IgG ELISA correspond
ing to a titre of 1:100 was considered posi
tive for IgG antibodies to mcaslcs(9).
<
Chi-square test was used for making
comparisons between the males and fc•
.
1 _ * _ C*
male's,
and between the
two thamlets
Sag-a
panipada and Behcdpada. Student t test
was used for comparisons of anthropolo
gical measurements.
I
I1-
fe... . Results
Epidemiological Features
K>-'- B:
ft’?.
I
1B#.'-
II
:•
I
1 IV
[
.
By mid March 1992, when we actually
carried out investigations, the outbreak of
measles in the two hamlets of Vavar village
had waned. The records at PHC, Sakharshet, showed that the outbreak at Behcdpada
had commenced in the last week of January
1992, reached a peak in the third week of
February and ended abruptly in the last
week of February. No such information was
available for the outbreak at Sagpanipada.
Sagpanipada had 44 households with a
population of 270; 176 (65%) were adults
and 94‘ ‘(35%)) were children. A total of 48
measles cases occurred and 15 died. In 103
VOLUME 31—may 1994
w
household of Behcdpada, 593 people resi
ded, comprising 325 (55%) adults and 268
(45%) children. Among them 128 cases of
measles occurred and 20 died.
The age specific measles morbidity at
Sagpanipada and Behcdpada is presented
in Table I. In both the hamlets the measles
cases were confined to children below 10
years and 96% of the cases occurred in
children below 6 years. The overall attack
rate of measles for children was 52.7% at
Sagpanipada and 51.4% at Behcdpada.
Infants 9 months and younger had lower
attack rate at both the hamlets.
: • h'-;
I
I
o
;A
1
The age specific measles mortality at
both the hamlets is presented in Table II.
The overall case fatality rate was 31.2% at
Sagpanipada which differed significantly
from 15.6% at Behcdpada, (p<0.05,
X2 = 4.414, df=l). Three infants from each
of the two hamlets, below nine months,
contracted measles and one child expired
at each place. At Sagpanipada the high
case fatality rate (25-50%) was noticed in
all age groups below 5 yrs (60 months),
whereas at Behcdpada the high case fatality
rate of 30% and above was confined to
children 2 yrs (24 months) and younger.
However, in both the hamlets, majority of
deaths occurred in children below 4 years.
The attack rates and case fatality rates
for male children did not differ significantly
from those for female children in both the
hamlets (p>0.05).
The precise cause of death in fatal cases
could not be ascertained; however, based
on the history given by the parents of the
survivors, 63% among them had suffered
from diarrhea, and or dysentery and 60%
from respiratory complications.
Anthropometric measurements of chil545
‘
■
• .^4
I
I
I
,T
*
fi
. ill
i!
MEASLES OUTBREAK IN THANE
RISBUDETAL.
TABLE \~Age Specific Measles Morbidity at Sagpanipada and Behedpada
I
i
0-9
10-12
13-24
25-36
I
=4K?
37-48
49-60
61-72
73-120
re
>1
Population Cases (AR)*
10
10
21
21
3 (30.0)
5a (50.0)
11
11
3
4
11
13
8
4
2
2
91
48 (52.7)
(523)
(61.9)
(72.7)
(36.4)
(66.7)
(50.0)
s
Behedpada
Sagpanipada
Age
(mo)
.I
Cumulative
percentage
Population
Cases (AR)
Cumulative
percentage
62
16
24
37
35
3 (18.7)
IS6 (75.0)
30 (81.1)
27 (77.1)
23
16.4
31
33
19
54
23
12
10
5
249
128 (51.4)
16.7
39.6
66.7
833
91.7
95.8
100.0
(74.2)
(36.4)
(52.6)
(093)
f3
39.8
60.9
78.9
883
I
96.1
100.0
i!
AR*
a
b
Attack rate.
2 cases 10 months old and 3 cases 12 months old.
2 cases 10 months old, 1 case 11 months old and 15 cases 12 months old.
I
TABLE ll-Age Specific Measles Mortality at Sagpanipada and Behedpada
Age
(mo)
§
t
Ii
Cases
3
5
0-9
10-12
13-24
25-36
37-48
49-60
11
13
8
4
61-72
73-120
2
2
48
CFR*
a
b
546
Cumulative
percentage
i
1
Behedpada
Sagpanipada
Deaths (CFR)*. Cumulative
percentage
Cases
Deaths (CFR)
(333)
(40.0)
(36.4)
(30.8)
6.7
20.0
46.7
733
3
18
30
27
1
6b
9
1
(333)
(333)
(30.0)
(03.7)
5.0
35.0
2 (25.0)
2 (50.0)
86.7
100.0
23
12
2 (08.7)
0
95.0
95.0
0
0
10
5
1 (10.0)
0
100.0
15 (31.2)
128
20 (15.6)
1
2a
4
4
= Case totality rate.
= Both deaths in 12 months old.
= 1 death in 11 months old and 5 deaths in 12 months old.
80.0
85.0
VOLUME 31“MAY 1994
INDIAN PEDIATRICS
ren (1-5 yrs of age) of Behcdpada were
compared with the standards from the
population of Bombay (ICMR Technical
Report Series 26, Studies on pre-school
children: 1986). The weights of the children
in different age groups did not differ sig
nificantly than those for the children in the
respective age groups of the standard pop
ulation. However, arm circumference mea
surements of the 3-5 yrs old children in the
study group were significantly lower than
those for the children of the standard
population.
II
F
urological Findings
Serological results of the IgM tests and
IgG on the single and paired sera from
convalescing patients and from the control
children arc presented in Table III. All the
single convalescent samples from both the
hamlets were positive for IgM antibodies
against measles. Among the 35 paired
convalescent scrum samples of the patients
from Behcdpada, fifst samples of all the
pairs, obtained in the month of March 1992
possessed IgM antibodies at significant OD
values. In the second samples collected after
an interval of 2 months, IgM antibody levels
showed a clear cut drop and in 16 patients
TD values had become insignificant (Fig
2) whereas in the first samples of all the 35
paired sera the IgG antibody titres were
low and in 16 patients it was below the cut
off values. All the second samples of 35
pairs showed an impressive rise in IgG
antibody (Fig 3).
i
- -- - - -- -
I
»
B
E
«■
E
2.
-
2
fa
I;
L
k
-
-
-------—
As is seen from Table III, many of the
samples from the control children also were
positive for IgM antibody and most of them
were positive for IgG antibody. Five out of
six paired samples showed significant IgM
levels in the first samples and a fall in the
second samples. Both the samples of these
,7;.
. i
pairs from the controls were positive for
IgG antibody against measles.
J
; ■' II
mH
Discussion
In the outbreak of measles described
here, all the cases were confined to children
below 10 years of age and 96% of the cases
occurred in children below 6 years. The
overall attack rate was 52.7% at Sagpanipada and 51.4% at Behcdpada. These fea
tures arc common to the measles outbreaks
described from the other parts of the country(l,2). However, in an outbreak in a re
mote isolated population, residing at the
Himalayan foot hill, more than 50% of the
cases were encountered in children between
5 and 14 years of age(3). The occurrence
of this outbreak in the dry season also cor
related with some of the rural epidemics
described earlier from India and Bangladesh(l,5,10) although outbreaks have been
described even in the rainy season by
olhers(2,3,l 1).
■' f
'■ ’■ J:
- W||■
■i
I
■' ■! i
The overall case fatality rale (CFR) seen
in the present outbreak was 31.2% at Sagpanipada, situated at the top of the hill and
15.6% at Behcdpada, situated at the foot
of the hill. The CFR at Behcdpada was
comparable with that described in a village
of Tamilnadu where health care facility was
not available(l).
The CFR seen at Sagpanipada appeared
to be the highest for the epidemics reported
so far from India. Thus, though the deter
minants of infection, as reflected by the
attack rates appear to be similar, the de
terminants of mortality seem to differ in
the two hamlets. The population pattern,
socio-economic status, literacy, health seek
ing behavior were similar in both the ham
lets. Both the hamlets suffered equally from
lack of medical facility close by. In the light
of this, it is difficult to comment as to why
547
1
■
:-: 13
i
•"^4
'i • •
|
j- a
“r' ■ 4
! 7 I
■ ■ ■ ■
i
I
'7W
■7.*
i
' J
i
y
' Mi
; -fl
i
■
■;7g
MEASLES OUTBREAK IN THANE
RISBUDETAL.
TABLE W-Results of ELISA to Detect IgM and IgG Antibodies to Measles
Behedpada
Sagpanipada
:t ■
IgM
IgG
IgM
IgG
Patients
i
8/8
4/8
8.8e
Single convalescent
samples
Paired convalescent
samples
I sample
II sample
(2 months later)
5/8
35/35
19/35
19/35
35/35
10/20
19/20
5/6
4/6
6/6
6/6
I
■
‘W
-i
Controls
■
2/7
Single samples
7/7
Paired samples
I sample
II sample
(2 months later)
'I
I
I
' a
-I
Num « Number positive.
Den - Total number of sera tested.
'1
w ■
2
1.9 1.8 _
1.7 _
1.6 _
1.5 _
o
o •
o
o
S
>
d
6
■a
1.3
1.2
1.1
1 _
0.9
0.8
0.7
0.6
0.5
0.4
0.3
O.2 _
0.1
0
o
c
0
0
0
o o
0
0
0
•*
I
I
.9
1
■ Si
0
o
0 0
0
0
0
0
0
o
s•C
0
ODD
n n
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Fig. 2. ELISA OD values for IgM antibodies to measles virus in paired convalescent samples from
patients at Behedpada.
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INDIAN PEDIATRICS
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VOLUME 31—MAY 1994
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Fig. 3. ELJSA OD values for IgG antibodies to measles virus in paired convalescent samples from
patients at Behedpada.
there was higher mortality al Sagpanipada.
The outbreak at Sagpanipada occurred
earlier (Octobcr/Novcmbcr 1991) whereas
at Behedpada it occurred in February 1992
after a gap of three months. It is possible
that during this period a lot of publicity was
generated which resulted in active efforts of
Health Services persdnncl to control the
outbre which might have resulted in better
treatment of very sick children at Behed
pada preventing the mortality to some
extent.
.jb?;-
? .It has been postulated that malnutri
tion, lack of easy access to medical facility,
2»a , hygiene, poor management of measles
Patients at home and local beliefs contri
assess the nutritional status of children at
Sagpanipada. The post epidemic anthro
pological studies carried out by us on the
survivors at Behedpada did not suggest
severe malnutrition in children as most of
the values did not differ significantly from
those described for normal Indian children
of similar age groups. However, no com
ment can be made on the nutritional status
of the deceased children. It is quite possible
that poor nutrition, dehydration and inter
current respiratory and gastrointestinal in
fections might have played a role.
faclors m’ght have been responJ e lor the high mortality rates observed
J^the present epidemic.
All the convalescent sera tested both
from Sagpanipada and Behedpada showed
the presence of IgM class of antibodies.
The paired convalescent sera tested show
ed a drop in IgM titres. Both these fea
tures were suggestive of a recent measles
infection.
MUe to non cooperation, we could not
The indirect ELISA test performed to
ve to high mortality due to measles(l,2).
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II
MEASLES OUTBREAK IN TIIANE
RISBUD ET AL.
detect IgG class of antibodies to measles
virus in 35 paired sera clearly showed a rise
in antibody titres in all the patients. This
observation confirms the earlier report by
Lievens ct al. on the suitability of indirect
ELISA test for the diagnosis of measles
infection using paired sera(12).
I
!
Fifty four per cent of the control child
ren studied by us showed IgM class of
antibodies in addition to good titres of IgG
antibodies. These findings suggest a possi
bility of subclinical measles infections among
the controls. Earlier studies using HI test
have estimated the subclinical infections to
the tune of 30%(l).
a
f
F
Discussions with the local population
revealed that many families of Vavar village
migrate to adjoining urban areas for work
during winter and return home around the
month of October for Diwali celebrations.
This is the time when the outbreak occurred
at Sagpanipada. It is possible that this
migrating population imported measles from
the urban area, which flared up into an
epidemic among the susceptible young
children in the village. Spread of measles
from urban to rural areas has been des
cribed earlier from India and Africa(4,13).
Measles epidemics do not occur in
vaccinated villages(l,2). It is unfortunate that
the epidemic such as the one described here
should have occurred even after seven years
of inclusion of measles vaccination in the
EPI programme. It seems to reflect the
lacunae in the strategy and implementation
of our measles control programme.
We feel that for the success of measles
control, the population living in isolated
villages, far away from the medical facility
should receive priority and all the children
under five years of age of such population
should receive vaccination.
i
550
REFERENCES
1. John TJ, Joseph A, George TI,
Radhakrishnan Singh RPD, George, K.
Epidemiology and Prevention of Measles
in rural South India. Indian J Med Res
1980, 72: 153-158.
•i
•i
2. Pereira SM, Benjamin V. Measles in a
South Indian community. Trop Geogr Med
1972, 24: 124-129.
I
3.
Narain JP, Khare S, Rana SRS, Banerjee
KB. Epidemic measles in an isolated
unvaccinatcd population in India. Int J
Epidemiol 1989, 18: 952-958.
4.
Salunkc SR, Natu M. Epidemiological
investigations of measles: An outbreak in
Ajiwali. Indian Pcdiatr, 1977, 14. 519-521.
5.
Mitchell CD, Balfour HH. Measles con
trol: So near and yet so far. Prog Med
Virol 1985, 31: 1-42.
6.
Tuokko H, Salmi A. Dcteaion of IgM
antibodies to measles virus by Enzyme
immunoassay. Medical Microbiol Immu
nol 1983, 171: 187-198.
7. Christenson
c.nrisicnsuii B,
d, Bottigcr M. Method for :
screening the naturally acquired and vac
cine induced immunity to the measles
virus. Biologicals 1990, 18: 207-211.
Chen RT, Markowitz LE, Albrecht P,
Stewart JA, Mofcnson LM, Preblud SR,
Orenstein WA. Measles antibody: Reevaluation of protective titres. J Infect Dis
1990, 162: 1036-1042.
9. Salonen J. Vainionpaa R, Halonen PAssay of measles virus IgM and IgG class
of antibodies by use of peroxidase labelled
viral antigens. Arch Virol 91: 93-106.
10. Fauveau V, Chakraborty J, Sarde AMN J
Khan MA, Koenig MA. Measles among |
under-9-months-olds in rural Bangladesfcg
Its significance for age at immunization. |
Bull WHO 1991, 69: 67-72.
?|
8.
11. Sinha DP. Measles and malnutrition M |
West Bengal village. Trop Geogr M j
1977, 29: 125-134.
K* •
INDIAN PEDIATRICS
12. Lievens AW, Brunnell PA. Specific im
munoglobulin M enzyme linked immu
nosorbent assay for confirming the diag
nosis of measles. J Clin Microbiol 1986,
24: 391-394.
VOLUME 31—MAY 1994
13.
Guyer B, McBean AM. The epidemio
logy and control of measles in Yaounde,
Cameroun, 1968-1975. Int J Epidemiol
1981, 10: 263-269.
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A
OTES AND NEWS
■
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V CONGRESS OF ASIAN PEDIATRC NEPHROLOGY ASSOCIATION
1
The V Congress of the Asian Pediatric Nephrology Association will be held at New
Delhi, India on December 1 to 3, 1994. This will be followed by an Update on Pediatric
Nephrology on T
December 4, 1994. The scientific programme of the Congress and the
Update should be very useful to pediatricians.
8
|j
Forfurther information please write to:
I
I
I
"
I
]
I
Prof. ILN. Srivastava,
Congress President,
17 Asian Pediatric Nephrology Congress,
eParfnient of Pediatrics,
AIIMS, New Delhi 110 029.
India.
■
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Phones : 661123; 6864851 Ext. 3472
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551
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Oration
Neurology India, 46, 1-4, 1998
Global Campaign Against Epilepsy
Agenda for IEA / IES**
K.S. Mani
Consultant Neurologist,
Neurological Clinic,
No.1, Old Veterinary Hospital Road,
Basavanagudi, Banglore-560 004, India.
Introduction
epileptics - i.e., one neurologist for 13,500 epileptics
which is indeed a skewed distribution ! Epilepsy is an
eminently controllable problem in a vast majority of
cases, especially of the tonic-clonic seizure variety
which poses a potential danger to life or limb. Hence
in a developing country with poor infrastructure primary
health care should be targeted to achieve epilepsy
control, through primary care physician.
“What disease affects 40 million people worldwide, yet
three quarters are untreated ? Paradoxically, the same
disease, with early diagnosis and treatment, can be
controlled in about three-quarters of those affected. The
disease is epilepsy, the commonest serious brain disorder
in every country in the world” (Editorial, 1997).
Approximately 75% of the 40 million patients with
epilepsy worldwide are from developing countries. The
population of India is 980 million. If the prevalence of
active epilepsy in the country is accepted as around 5.5
/ 1000, the number of patients with active epilepsy in
India would amount to 5.4 million - which is one-eighth
of the worldwide estimate. 70% of the Indian population
is rural and thus around 3.8 million epileptics will be
in rural areas. Community based studies on epilepsy in
Yelandur in Mysore district, Karnataka state have
shown that there is a large treatment gap of 78% in
rural areas - i.e., they have not had treatment with anti
epileptic drugs (AEDs) except perhaps in a perfunctory
manner (Mani and Rangan 1997). This is not only due
to poor socio-economic status but due to lack of
awareness of therapeutic potential of AEDs and the need
for long term medication. The core of the problem is
failure to educate the primary care physician and also
the general public.
Training of Primary Care Physicians
The medical curriculum for undergraduate students with
reference to neurological disorders including epilepsy
requires revision. The quantum and quality of teaching
in epilepsy leaves much to be desired. The emphasis
should be on practical epileptology - an opinion shared
in UK (Mason et al 1990) and in USA (Devinsky et al
1993). This should include basics of applied
neuroanatomy, neurophysiology clinical neuro
pharmacology; recognition of - common seizure types
and epileptic syndromes and how to make a quick
neurological assessment. Emphasis also should be on
the choice of appropriate AED, primarily as
monotherapy - very often inexpensive phenobarbitone
(PB) or phenytoin (PHT) in minimum effective dose,
importance of a seizure calendar, basics of treatment,
drug compliance, life style compliance and health
education of the patient /relatives regarding their life
style. There should be guidelines on when and how to
change the dose of drugs; duration of drug treatment,
when to reduce / stop the AEDs and the chances of
relapse.
Global campaign against epilepsy in our country can
be discussed under three main headings 1. Training of primary care physicians
2. Public education / health education
3. Dialogue with the Government
A primary care physician should know when to refer a
case to secondary/tertiary centre. This is of practical
relevance in the present day situation in the country
than theoretical expertise on EEG, imaging studies or
serum levels of AEDs which are anyway either not
available or frightfully expensive for the rural
population. However they are very important at a post
graduate level. This curriculum on practical
epileptology for medical undergraduates is a prime task
70% of the Indian population is rural, but 70% of the
medical manpower is urban. 100% of neurologists/
neurosurgeons practice in urban areas, especially in
large metropolitan cities because of infrastructural
facilities. We have 400 neurologists for 5.4 million
Presidential address during EPICON-5 of Indian Epilepsy
Association held in Jaipur on December 10,1997.
1
Oration
Neurology India, 46, 1-4, 1998
for the members of Indian Epilepsy Society (IBS),
almost all of them members of the Neurological Society
distribute the monthly quota of drugs at nodal points in
each village to the palients/carers. These visits can be
of India (NSI) and/or Indian Academy of Neurology
(IAN). These medical societies are made up of
professionals dealing with epilepsy and include
neurologists and neurosurgeons, many of them holding
high academic positions in various universities. This
utilized to enquire about drug/life style compliance,
response to drug therapy, side effects and advice to visit
the monthly medical clinic for reassessment/
clarification, if required. The all important health
education must be emphasized at these monthly visits
view is submitted before them for their consideration
with adequate regard for socio-cultural ethos.
and discussion. Recommendation should be made to
University Board of Studies and to the Medical Council
Is this only an utopian dream, or a practical reality?
The experience obtained during the IEA Bangalore
chapter / Karuna Trust, Yelandur Rural Epilepsy
Control Project From April 1, 1990 to January 1997 is
of India.
Rural Epilepsy Control
worth a perusal (Mani 1997). The team was made up
of specialists - 3 neurologists teamed up with an
established local NGO having 2 medical members, 6
PMWs and a transport to go round the villages. The
specialists gave their time oralis and met their own
travel expenses to Yelandur 150 Km (4 hours drive)
away from Bangalore. The PMWs trained in
epidemiology and practical epileptology by the writer
made a door-to-door survey of a population of 64, 963
in 13,562 families, identified the suspects and brought
them to the Yelandur clinic once a fortnight for
In India, if epilepsy has to be controlled early, the
treatment facilities should reach the villages and not
the other way around, as is the case at present. (Mani
and Rangan 1997). Out of 365,000 registered allopaths,
only 89% are MBBS degree holders. Non-allopathic
doctors account for an additional 510,000. Besides,
there are over 4,000 non-governmental organizations
(NGOs) committed to rural health care. These could
be part of a supervised team for organized primary
health care, including epilepsy. There is a vast pool of
unemployed local graduates who can be enrolled as
paramedical workers (PMWs) to be trained in simplified
and practical epileptology. Fool proof arrangements for
assessment, diagnosis, drug treatment and follow-up.
The specialists visited the Yelandur clinic as 2 teams once a fortnight during the first year, once a month
during second year, once in 3 months lor the next two
years and once in 6 months thereafter. The 3
neurologists also camped twice in the villages for 2
nights and 3 days each during this 6 year period - visited
the homes of all the epilepsy patients in all the 40
villages to personally check the follow-up data at the
end of 3 and 5 years. Additional 2 other visits were
made to gather information on inactive cases who
understandably would not Visit the medical centre and
for a random resample survey to assess the false
a 100% unbroken drug chain from manufacturer to
patient is a must and the PMWs can be trained to make
home delivery of AEDs once a month to ensure better
drug compliance. This can be combined with leprosy,
tuberculosis and mental health (especially depression)
control programs to make it cost effective.
There are over 160 medical colleges in the country.
Their departments of medicine should actively train
and utilize the services of medical undergraduates in
the peripheral decentralized management of epilepsy,
negatives - i.e., cases missed by the PMWs - the last to
arrive at figures for a maximum prevalence rate. This
tuberculosis, leprosy and depression. The target
population could be those in I or 2 taluks with in
leaving it for the local medical manpower to continue
the work. The trained PMWs should interact with the
was a 100% clinical study only and the drugs used were
PB or PHT essentially as monotherapy. Thanks to the
monthly visits of the PMWs, follow-up was available
practically in 100% of patients and included data on
those who accepted treatment, refused treatment, natural
history ol untreated epilepsy, follow-up data on febrile
local community, identify the suspects - be of epilepsy,
seizures, mortality in epilepsy and the all important
leprosy, tuberculosis or depression - and persuade them
to attend the primary care clinic where the doctors will
Knowledge Attitude Practice (KAP) study.
examine them, explain about the illness and prescribe
Analysis of data of treated cases at the 3 year follow-up
drug treatment. They must maintain basic health records
and the entire operation must be supervised by a general
physician or a neurologist. The emphasis should be on
free or subsidized inexpensive AEDs - PB or PHT supplied in an unbroken drug chain from governmental
sources, voluntary NGOs, donations from service
organizations like Rotary,-Lions etc. Once seizure
control has been achieved, the PMWs can be trained to
period in 203 patients, showed that complete remission
of over 3 years was noted in 40% and 2-3 years in an
additional 9%. Improved category (no seizures fqr I 2 years or reduction by more than 50%) accounted lor
32%; 15% were unchanged and 4% worse. Thus
worthwhile improvement was achieved in (49 + 32)
8I% of patients with epilepsy using only inexpensive
service training of the local primary care physicians.
After a period of 3 - 5 years the college team can shift
to another taluk - something like a shifting cultivation
PB / PHT, with the help of PMWs and without recourse
2
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Oration
Neurology India, 46, 1-4, 1998
to investigatory procedures. Side effects interfering with
the medical aspects of epilepsy in simple laymens
language, therapeutic potential in epilepsy, drugs and
quality of life were minimal - gingival hyperplasis in
7%, somnolence in 1% and no hyperkinesia. This type
life style compliance, positive aspects of life in epilepsy,
of beneficial experience with PB in primary rural
psychosocial problems and the role of individualization
epilepsy control in developing countries is nothing new
or group discussions as in self-help groups, the ultimate
and has been noted before by Watts (1989) in Malawi,
aim being improvement in quality of life. In the
Feksi et al (1991) in Kenya and Placencia et al (1993)
Yelandur study, there was a van equipped with TV,
video, screen and diesel generator. This would cover
in Ecuador, h is to be noted that Pal et al (1998) found
)
that PB used for rural epilepsy control in children in
all the 40 villages by turns in the evenings for screening
West Bengal, did not produce behavioural side effects
as assessed by a standard questionnaire or parental
reports. It is also gratifying that there was not even a
educational slides and video programs. This was found
to be very popular amongst the village folk and included
health educational programs not only on epilepsy but
single death from status epileptics in those on regular
)
treatment and without any overt brain damage. The
also other common problems like leprosy, tuberculosis,
family planning, environmental and individual
n
6
total amount spent by IEA for the project over 6 years
sanitation and universal
was of Rs. 130,()()() (US
be stressed that in a rural area one well
c
computerization of demographic data and cost of PB /
patient is the best advertisement for management of
n
PHT.
To these must be added the cost of the salary of
')
n
PMWs from Karima Trust - the local NGO - while travel
epilepsy rather than a propaganda barrage, which ought
to be resorted to judiciously.
a
■3
$3,250)
mainly
for
proved (hat with commitment and proper planning,
rural epilepsy control is well
Dialogue with the Government
within the realms of a
practical proposition. Collaboration with a willing/
u
committed partner is very important.
This has lo be carried out as a joint endeavour by both
the 1ES and IEA with support from ILAE, IBE and
P-
WHO - the latter 3 being the originators of the global
Prevention of Epilepsy
campaign against epilepsy. The Government of India
ih
3
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-40
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cost for the specialists was from their own pockets. This
al
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immunization. But it must
must be persuaded to include epilepsy in its National
Improved maternal and child welfare programs starting
Health
Program
(NHP)
along
with
malaria,
care through delivery lo childhood
tuberculosis, leprosy etc. We ought to emphasize that
immunization and improved nutrition are likely to
85% of the patients with epilepsy are absolutely normal
in between their seizures like anyone else and all quite
capable of contributing their mite to society. Control of
disease under NHP is a priority item with greater
allocation of funds from both the Union and State
Governments. This would also enable AEDs to be
from antenatal
reduce the prevalence of epilepsy. To this must be added
measures for improved public hygiene resulting in
protected water supply and established methods of
sanitation and sewage disposal - eminently attainable
goals if we invest wisely and adequately. Is it not a
shame that we should still talk of expensive CT vs.
included under the category of life saving drugs with
MRI, role of immunology, and whether to start or
resultant waiver of import (customs) duty and excise
withhold albendazole for a small single contrast
duty. The IEA Bangalore chapter had successfully
enhancing lesion (SSCEL) when cysticercosis ought to
persuaded
have been eradicated as in the developed countries ?
Then we have the preventable scourge of modern times
- cranio-ccrebral trauma. How lo convince the powers
that be and the public about the protective value ofcrash
helmets and seat belts ?
exempt AEDs from sales tax. This was nearly a decade
ago. Other chapters of the IEA/NS1 and other State
Governments should follow suit? Epilepsy should be
included in Health Insurance Schemes and we should
do away with barbaric laws linking epilepsy with
insanity and divorce. The present over-liberalized
driving license regulations with regard to epilepsy for
heavy duty vehicle drivers need to be tightened keeping
in mind individual liberty and aspirations on one hand
and public safety on the other.
Public Education
Till recent times the IEA had to involve itself not only
in education of the general public but also in that of the
primary care physician. Now that the professional body
the State Government of Karnataka to
Conclusion
-IBS - has been formed, chapters of IEA ought to give
greater attention to public education. These depend on
the population to be addressed, their local language and
socio-cultural mores. By and large they ought to be in
the form of attractive flip charts, posters, pamphlets,
booklets, newsletters, TV/radio programs, articles in
Ramamurthi (1997) has cautioned neurologists and
neurosurgeons to shed their “super speciality status”,
come down to terra firma and involve themselves in
primary health care. Can’t we make a start with epilepsy,
an eminently controllable and most common
the lay press, dramas and skits. These should highlight
3
neurological problem ? In the global campaign against
epilepsy, it is suggested that the role of IBS and IEA
along with NS1 and /or IAN are well defined and needs
active encouragement and support from the 1LAE, IBE
and WHO. This is a challenge which must be faced
and can be overcome if there is a sense of commitment,
unity of purpose, and a dogged pursuit towards the
objective of total welfare of patients with epilepsy. Try
we should, try we ought to and try we must.
Acknowledgement
The time effort and commitment - all with a smile - from Drs
Geeta Rangan, HV Srinivas, S Kalyanasundaram,
Samanthakamani Narendran and AK Reddy are gratefully
acknowledged. Drs. H Sudarshan and VS Sridhar from VGKK,
BR Hills and Karuna Trust Yelandur, along with their team of
paramedical workers carried out the basic ground work for which
a special thanks is necessary. The IEA Bangalore chapter provided
the drugs which deserves a special mention.
References
Devinsky O. Lowenstein D. Bromfield E, Duchowny M.
Smith DB : Epilepsy education in medical schools :
Report of the American Epilepsy Society Committee on
medical student education. Epilepsia, 34,809-811. 1993.
Editorial. In the shadow of epilepsy. Lancet, W), 1851, 1997.
p
Neurology India, 46, 1-4, 1998
Oration
FcksiAT, Kaamugisha.1, Sander JW. Gatili S, Shorvon SD
Comprehensive primary health care - antiepileptic drug
treatment programme in rural and semiurhan Kenya.
Lancet, 337. 406-409, 1991.
Mani KS : Essentials of diagnosis and management of epilepsy
for a primary care physician in a developing country.
Antiseptic. 89. 462-465, 1992.
Mani KS : The Yclandur story : A practical approach to
epilepsy control in developing countries. EPICAL)EC
NewsV^a.*), 13-14. 1997.
Mani KS. Gccta Rangan : Delivery of Health Care and socio
economic issues - India in Epilepsy - A comprehensive
Textbook Ed. Engel J. Jr.. Pedley TA. Lippincott-Raven
Philadelphia. 1997 III Vol. Ch 216, 2835-2840.
Mason C. Feri ton GW. Jamieson M : Teaching medical
students about epilepsy. Epilepsia, 31, 95-100, 1990.
Pal DK and Tulika Das : Randomised controlled trial to
assess acceptability of phenobarbital for childhood epi
lepsy in rural India. Lancet, 357, 19-23, 1998
Placencia M. Sander JW, Shorvon SD. Roman M, Alarcon F.
Bimos C, Carcante S : Antiepileptic drug treatment in a
community health care setting in northern Ecuador A
prospective 12 month assessment. Epilepsy Research,
14, 237-244. 1993.
Ramamurlhi B : Neurology - a Public Health Problem.
Neurology India. 45, 284-285, 1997.
Theodore WH, Porter R.l : Epilepsy : 100 Elementary
Principles. Saundcrs/Prism. London/Bangalorc. Ill Ed.
1996,74-76.
Walls AE : A model for managing epilepsy in a rural
community. British Medical Journal. 298, 805-807,
1989.
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Neurology India, 46, 15-17, 1998
Views and Reviews
Antiepileptic Pharmacotherapy :
Prevalence of Polytherapy and its Implications
K. Radhakrishnan, S. Dinesh Nayak
Comprehensive Epilepsy Program,
Sree Chitra Tirunal Institute for Medical Sciences and Technology,
Trivandrum, Kerala, India
Introduction
Since epilepsy is a common condition affecting 0.5
to 1.5% of the population (Hauser and Hesdorfer,
1990), antiepileptic drugs (AEDs) are frequently
used in clinical practice (Masland, 1978; Beghi and
Perucca 1995). More than 90% of the burden of
epilepsy is carried by the developing countries
(Pedley and Kale, 1996).
I
j
The approach to pharmacological treatment of epi
lepsy has changed substantially in the past two dec
ades. This change has resulted from improved knowl
edge of the efficacy and tolerability of available
standard AEDs such as phenobarbitone (PB),
diphenyl hydantoin (DPH), carbamazepine (CBZ)
and valproate (VPA) (Mattson et al, 1985; Heller et
al, 1995), acquisition of new information through
observational studies and clinical trials (Beghi and
Perruca, 1995), introduction of new AEDs (Marson
et al, 1996) and availability of surgical treatment
for refractory partial epilepsy. (Engel, 1996;
Radhakrishnan, 1997). Recent trends in the man
agement of patients with epilepsy focus on
monotherapy in preference to poly therapy all over
the world (Reynolds and Shorvon, 198 I; Pellock,
1994; Chadwick, 1994).
d
r.
•n
J.
Ph
he
al
ol
lduil-
BV
and
)96.
ixia
ini'.
ions
'lure
j
Very little information regarding the current epilepsy
pharmacotherapy practices and its economics are
available from developing countries, including India.
Considering the greater economic constraints, there
is a need for the widespread use of monotherapy with
less expensive AEDs in developing countries.
AED usage profile and cost
We recently compared the AED usage profile at en
try and at last follow-up of 972 patients seen during
(Radhakrishnan et al, 1997). SCTIMST is a tertiary
referral center which receives patients from all over
Kerala and from neighbouring states. The patients
referred to our comprehensive epilepsy program
came from general practitioners, and primary and
secondary care facilities. A majority of them had had
multiple consultations prior to seeing us. Hence, we
concluded that the AED usage profile at entry to
SCTIMST is likely to represent the pharmacotherapeutic pattern in the general epilepsy care in this
geographical region.
Our patient sample comprised 570 male and 402
female subjects. The mean age was 22.8 ± 14.5 years,
range, (0.7 - 86 years). 33.7% of patients were
younger than 15 years of age. Idiopathic generalized
epilepsy was diagnosed in 39.6% patients, while
49.2% had cryptogenic or symptomatic partial
epilepsies. Among the patients with idiopathic
generalized epilepsy, 14.8% had juvenile myoclonic
epilepsy and 2.9% had childhood absence epilepsy.
Among patients with partial epilepsies, 67.6% had
temporal lobe epilepsy. Thus, the distribution of the
age and epilepsy syndrome in our sample of patients
is remarkably similar to other recently reported
studies from the West. (Loiseau et al I99I;
Osservatorio Regionale per L’ Epilessia, 1996).
The distribution of our patients according to AED
usage at entry and at last follow-up in SCTIMST is
depicted in Table 1. At entry 58% of patients were
receiving multiple AEDs. We attempted to change
them over to monotherapy. At the last follow-up, 76%
of patients were on monotherapy. CBZ was the most
frequently used AED, followed by DPH, VPA and
PB. The absolute percentage increase in the preva
lence of monotherapy through our comprehensive
epilepsy program was 34%.
1993 through 1995 in the Comprehensive Epilepsy
Care Program of SCTIMST, Trivandrum, Kerala
We calculated the absolute daily cost of therapy with
AEDs from their local price and daily dosage. The
relative annual cost of AED therapy was calculated
as a percentage of the gross national produce (GNP)
per inhabitant. Thus, a patient who is being treated
Reprint request to : Dr. K. Radhakrishnan, Professor
and Head, Department of Neurology, Sree Chitra Tirunal
Institute for Medical Sciences and Technology,
Trivandrum - 695 011.
15
____________ Neurology India, 46, 15-17, 1998
. Views and Reviews
Table I
Distribution of 972 patients according to antiepileptic drug
(AED) usage at entry and at last follow-up at SCTMST
At last follow-up
At entry
n
409
Monotherapy
43
Phenobarbitone*
131
Phenytoin (DPH)
169
Carbamazepine**
63
Valproate (VPA)
3
Other AEDs
562
Polytherapy
327
2 AEDs
164
3 AEDs
71
>4 AEDs
Specific combinations
58
PB+DPH
65
PB+CBZ
66
DPH+CBZ
26
DPH+CBZ
59
VPA+CBZ
53
Other duotherapy
1
No AED
%
%
n
42.1
4.4
13.5
17.4
6.5
0.3
58.0
33.6
16.9
7.3
743
57
189
329
159
9
223
194
27
2
76.4
5.9
19.4
33.8
16.4
0.9
22.9
20.0
2.7
0.2
6.0
6.7
6.8
2.7
6.1
5.5
0.1
29
19
40
5
62
39
6
3.0
2.0
4.1
0.5
6.4
4.0
0.6
*PB, “CBZ
with PB will spent 4% of GNP for AED therapy,
while those on DPH, CBZ and VPA monotherapy
will spent 5%, 27% and 30%, respectively, for AED
therapy. These figures may be compared with cor
responding figures from France for PB, DPH, CBZ
and VPA monotherapy of 0.2, 0.3, 1.2 and 1.5%,
respectively. Among our patients with poly therapy,
the cost increased enormously: PB + DPH 9% GNP
to VPA + CBZ 57% GNP. Through our change over
to monotherapy from 42% at entry to 76% at last
follow-up, the money saved per patient per year was
Rs.816 (7.5% of GNP).
Our study shows that better availability of AEDs in
recent years in this geographical region has not been
supplemented adequately by education of the primaly
and secondary care physicians about the cun ent
trends in the pharmacotherapy of epilepsy. Although
the results obtained through our study from a rela
tively affluent society of Kerala with a literate and
health conscious population cannot be extrapolated
to rest of India, we presume that the data from else
where will not be vastly different. More studies on
the epidemiology and econonics of epilepsy treat
ment from our country are warranted.
Monotherapy versus Polytherapy
There was a long tradition of using several AEDs
simultaneously for the treatment of epilepsy. It is
now generally accepted that monotherapy is the best
therapeutic option when a diagnosis of epilepsy has
been established (Reynolds and Shorvon. 1981;
Pellock, 1994; Chadwick, 1994). Reynolds and
Shovon (1981) showed that 70-80% of patients can
be controlled of their epilepsy with monotherapy.
Among patients entering the Medical Research
Council AED Withdrawal Study (1991) in the United
Kindoin, 83% of the patients were treated with
monotherapy. The percentage of patients on
monotherapy was almost 80% in a community dwell
ing Dutch epilepsy population. (Lammers et al 1996).
Even with most effective AEDs, the proportion of
patients who become seizure-free after adding a
second or third AED is very small (Mattson I994;
Beghi and Perucca 1995). In a prospective study of
the reduction in the number of AEDs among 44
institutionalized patients with multiple handicaps,
who were receiving 4 or 5 AEDs, Mirza et al (1993)
achieved monotherapy in 64% and duotherapy in (he
remaining 36^> with significantly improved seizure
control. Although newer AEDs. such as gabapentin,
vigabatrin, lamotrigine, tiagabine and topiramate are
becoming available, most patients do not become
seizure free with add-on therapy with these new
AEDs (Marson et al, 1996; Walker and Sander 1996).
In many patients, a 50% seizure reduction may have
little effect on the quality of life, especially when
such an improvement is achieved at the expense ol
added AED toxicity and several fold increase in the
cost of pharmacotherapy.
Choice of AEDS
Althogh several factors influence the choice ol AEDs,
the best AED is the one that control seizures (ie ef
ficacy) without causing unacceptable side effects (ie
tolerability). VPA or ethosuximide is the drug of
choice for absence seizures. In contrast, no evidence
convincingly indicates that substantial differences
exist among the primary AEDs in their ability to
control partial seizures (the most common type of
seizure) and secondarily generalized seizures,
although PB is significantly less well" tolerated than
DPH, CBZ and VPA (Mattson et al, 1985; Heller et
al, 1995).
There are wide regional differences in the prescrib
ing patterns of AEDs. Multiple factors such as effi
cacy, tolerability, recommendation from peers, past
experience with epilepsy treatment and the system
of health care prevailing in an area influence the
selection and acceptance of AEDs by physicians and
patients. The availability of AEDs and its cost are
additional important factors relevant especially for
developing countries like India.
We observed that in Kerala, CBZ is the commonest
AED used either alone or in combination, followed
by DPH. VPA and PB which is similar to the prac
tice in most European nations (Reynolds, 1994;
Lammers et al, 1996). In the United States. DPH
continues to be most commonly used AED (Pellock,
1994). VPA appears to be the most prescribed AED
in France (Genton et al I992), while PB is more
16
li
I
(
A
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11
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K
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P
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th
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th
er
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Bi
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Views and Reviews
98
ch
ed
uh
on
■II6).
Neurology India, 46, 15-17, 1998
frequently used in Italy (Collaborative Group for
Genlon
Remy
C,
Vespignani
II :
Monotherapie et
antiepileptiquc : enqucle prospective multiccntrique de
Conclusions
la ligue francaise centre 1’epilepsie, avec suivi a 6 mois
el a 1 an. Epilepsies, 4, 75-81, 1992.
Hauser WA, Hcsdorffcr DC : Epilepsy : Frequency, Causes
A majority of patients with epilepsy in developing
countries are treated by clinicians without specific
of
’
P,
polytherapie lovs de la miso cn route d’un traitement
Epidemiology of Epilepsy, 1988).
and consequences. Demos : New York, 1990.
Heller A.I, Chesleman P, Elwcs RDC, Crawford P, Chadwick
training and expertise in this disorder. There is only
a
>4;
of
one qualified neurologist per one million population
D. Johnson AL, Reynolds EH : Phenobarbitone, pheny
of Kerala; this ratio will be far worse elsewhere in
toin, carbamazepine, or sodium valproate for newly
our country.
44
Kerala, we conclude the following:
ps,
B)
the
me
diagnosed adult epilepsy: a randomized comparative
Based on the result of our study in
monotherapy trial. Journal of Neurology, Neurosurgery
polytherapy is
and Psychiatry, 58, 44-50, 1995.
still quite prevalent in this part of India,
less ex
pensive AEDs such as PB and DPH
remain
WO, Herings RMC : Use of antiepileptic drugs in a
underutilized in this geographical region, and
community dwelling Dutch population. Neurology, 46,
Lammers MW, Hekstcr YA, Keyser A, Meinardi H. Renier
polytherapy and the use of expensive drugs such as
im.
are
Loiscau P, Duche B, Loiseau J : Classification of epilepsies
Our observations need to be confirmed by
and epileptic syndromes in two different samples of
therapy.
me
62-67, 1996.
CBZ and VPA have escalated the cost of AED
patients. Epilepsia, 32, 303-309,1991.
more studies on the epidemiology and economics of
ew
Marson AG. KadirZA, Chadwick DW : New antiepileptic
epilepsy in other regions of India.
drugs : a systematic review of their efficacy and toler
)6).
avc
ability. lirilish Medical Journal, 313, 1169-1174, 1996.
There is ample evidence to illustrate that more than
hen
Masland RL : Commission for the control of epilepsy.
70% of patients with epilepsy can be controlled by
• of
the
Neurology, 28, 861-863. 1978.
the primary AEDs. Even in
Mattson RH : Current challenges in the treatment of epilepsy.
the small group of patients in whom polytherapy im
proves seizure control, it often does so at the ex
Neurology, 44 (suppl 5). S4-S9, 1994.
Mattson RH. Cramer J A. Collins JI7, cl al : Comparison of
pense of undesirable side effects, unaffordable cost
carbamazepine, phenobarbital, phenytoin, and primidone
treatment with one of
and disturbed quality of life. Alternate modes of
in partial and secondarily generalized tonic-clonic
Ds.
therapy such as epilepsy surgery should be consid
seizures. New England Journal of Medicine, 313, 145-
cl
ered early in patients with medically difficult to con
151, 1985.
Medical Research Council Antiepileptic Drug Withdrawal
> (ic
trol partial epilepsies. The mean duration ol epilepsy
: of
among 55 patients who underwent anterior tempo
nice
ral lobectomy in SCTIMST for intractable complex
ices
partial epilepsy was 16.6 years (Radhakrishnan et
Mirza WV, Credcur LJ and Pcnry JK : Results of antiepileptic
y to
al, 1997), which reflects the late referral for epilepsy
drug reduction in patients with multiple handicaps and
e of
surgery prevailing in this region. Surgical treatment
epilepsy. Drugs Investigation 5. 320-326, 1993.
res.
of epilepsy should not be considered as a last resort
Osservatorio Regionalc per L’Epilcssia (OREp), Lombardy.
than
after all combinations of AEDs (including the newer
ILAE classification of epilepsies: its applicability and
?r el
AEDs) have been tried. As neurologists, we should
Study Group.
1180, 1991.
practical value of different diagnostic categories.
Epilepsia, 37. 1051-1059, 1996.
Pedley T, Kale R. Epilepsy information for the developing
educate the primary and secondary care providers
about these recent trends in the management of
:rib-
world. Epilepsia Digest, 1,1. 1996.
epilepsy.
Pellock JM : Standard approach to antiepileptic drug treatment
in the United Stales. Epilepsia, 35 (suppl 4), 511-518,
effipast
■
Randomized study of antiepileptic drug
withdrawal in patients in remission. Lancet, 337, 1175-
References
1994.
stem
Radhakrishnan K, Nayak SD, Kumar SP, Sanna PS : Profile
• the
Beghi E, Perucca E: The management of epilepsy in the 1990s.
. and
Acquisitions, uncertainities and priorities for future
center in South India : a pharmacovigilence and
research. Drugs, 49, 680-94, 1995.
Britton J W, So EL. Selection of antiepileptic drugs: a practical
pharmacoeconomic study. Epilepsia (in press).
Radhakrishnan K : Medically intractable partial epilepsy.
approach. Mayo Clinic Proceedings,! 778-786, 1996.
Chadwick D : Standard approach to antiepileptic drug
treatment in the United Kingdom. Epilepsia, 35, (suppl
4), S3-S10, 1994.
Neurology India, 45, 1-3, 1997.
Reynolds EH, Shorvon SD : Monotherapy or polylherapy for
epilepsy? Epilepsia, 22. 1-10, 1981.
Walker MC, Sander JWAS : The impact of new antiepileptic
t arc
v for
most
> wed
nac994;
DPH
lock,
AED
i
of antiepileptic pharmacotherapy
in a tertiary referral
Collaborative group for Epidemiology of Epilepsy : Adverse
drugs on the prognosis of epilepsy:
reactions to antiepileptic drugs : a follow up study of 355
patients with chronic antiepileptic drug treatment.
Epilepsia, 29, 787-793, 1988
Engel J, Jr. Surgery for seizures. New England Journal of
Medicine, 334, 647-652, 1996.
should be the ultimate goal. Neurology, 46, 912-914,
1996.
Accepted for publication : I Olli February, 1998
more
17
seizure freedom
ARTICLES
Randomised controlled trial to assess acceptability of phenobarbital
for childhood epilepsy in rural India
^.3
Deb K Pal, Tulika Das, Gautam Chaudhury, Anthony L Johnson, Brian G R Neville
Summary
Background The use of phenobarbital for childhood epilepsy
Is controversial because of reported behavioural side-effects;
however, whether this research can validly be extrapolated
to developing countries is not clear. We undertook a
randomised comparison of phenobarbital and phenytoin to
assess the acceptability and efficacy of phenobarbital as
monotherapy for childhood epilepsy in rural India.
Methods Between August, 1995, and February, 1996, 109
unselected children aged 2-18 years with partial and
generalised tonic-clonic epilepsy were identified by
population screening. 15 families declined to take part. 94
children
were
randomly
allocated treatment with
phenobarbital (1-5 mg/kg daily for 2 weeks; maintenance
dose 3-0 mg/kg daily; n=47) or phenytoin (2-5 mg/kg daily
then 5-0 mg/kg daily; n=47). Children were followed up for
12 months. The primary outcome measure was the frequency
of behavioural side-effects; behaviour was assessed by the
Conners parent rating scale for children aged 6 years and
older, and by the preschool behaviour screening
questionnaire (BSQ) for those aged 2-5 years, at 12 months
or at withdrawal from treatment. Analysis was by intention to
treat.
Findings The mean log-transformed scores on the behaviour
rating scales did not differ significantly between the
phenobarbital and phenytoin groups (Conners 2-64 [SD 0-71]
vs 2-65 [0-89], p=0-97; n=32 in each group: BSQ 2-12
[1-31] vs 2-18 [1-02], p=0-94; n=4 vs 3). The odds ratio for
behavioural problems (phenobarbital vs phenytoin) was 0-51
(95% Cl 0-16-1-59). There was no excess in parental reports
of side-effects for phenobarbital. We found no difference in
efficacy between the study drugs (adjusted hazard ratio for
time to first seizure from randomisation 0-97 [0-28-3-30]).
Interpretation This evidence supports the acceptability of
phenobarbital as a first-line drug for childhood epilepsy in
rural settings in developing countries.
Lancet 1998; 351:19-23
Neurosciences Unit, Institute of Child Health, University College
London, London, UK (D K Pal mrcp, Prof B G R Neville frcp);
SANCHAR-AROD, Pallan, West Bengal, India (D K Pal, T Das ma,
G Chaudhury); MRC Blostatlstlcs Unit, Institute of Public Health,
University Forvle Site, Cambridge, UK (A L Johnson pkd); and
Chlld-ln-Need Institute, Daulutpur, West Bengal, India (D K Pal)
Correspondence to: Dr Deb K Pal, Neurosciences Unit, Institute of
Child Health, University College London, Wolfson Centre, London
WC1N 2AP, UK
(e-mail: d.pal@ucl.ac.uk)
THE LANCET • Vol 351 • January 3, 1998
Introduction
Phenobarbital is recommended by the WHO as the firstline drug for the treatment of partial and generalised tonicclonic epilepsies in developing countries? Widespread use
of phenobarbital, one of the oldest antiepileptic drugs, has
been encouraged because its efficacy for a wide range of
seizure types and its low cost make it suitable for use in
primary health care in developing countries.2 However,
studies from the USA and Europe raised concerns about
the suitability of phenobarbital as an antiepileptic drug for
children, and use of the drug in developing countries has
become controversial,’"’ especially as newer, more
expensive alternatives, such as carbamazepine and sodium
valproate, became available. In India, phenobarbital is the
cheapest antiepileptic drug, with a cost of about USS20-30
for a year’s treatment.6 Phenytoin costs slightly more,
whereas carbamazepine and sodium valproate cost 15-30
times more, and imported drugs such as lamotrigine and
vigabatrin are not available outside specialist centres.
Several clinical trials have recorded higher frequencies of
behavioural problems associated with phenobarbital than
with other drugs or no treatment;7"9 another study found a
significantly reduced Stanford-Binet test score after 2 years
of phenobarbital treatment, which persisted for 6 months
after withdrawal of the drug, although there were no
differences in behavioural problems after 2 years.10 In three
other trials, no excess of adverse effects was found when
phenobarbital was compared with other active drugs."’1’
The strength and generalisability of evidence of serious
behavioural and cognitive effects of phenobarbital in
recurrent childhood afebrile seizures is controversial, largely
because of methodological problems of published trials.
Establishment of the acceptability of phenobarbital in
appropriate context is of enormous importance in
developing countries?4 Several other considerations also
have to be taken into account before available research can
be validly applied to such populations. These include the
ecological factors influencing the labelling and social
significance of mental disorders,” cultural perceptions of
epilepsy, physiological differences (such as age at diagnosis,
number of seizures before treatment, and aetiology),16 and
the feasibility, sustainability, and cost-effectiveness of
alternative interventions within an existing framework of
local and national needs and health priorities.
Our aim was to assess through a randomised trial the
acceptability and efficacy of phenobarbital as monotherapy
for childhood epilepsy in a rural Indian setting. The
primary hypotheses were that children treated with
phenobarbital would have a 25% greater frequency of
behavioural problems than those treated with phenytoin,
and that there would be equivalence of seizure control to
within 15%. We also aimed to assess the feasibility of
conducting a randomised controlled trial where such a
design had not been used before.
Methods
The study took place in 24 Parganas(S), a rural district of West
Bengal, India, south of Calcutta, of area 213 km2. Income is
seasonal, from farming and local trades. The median monthly
income of USS30 and the infant mortality of 65 per 1000 livebirths
19
' -,.
ARTICLES
109 patients eligible
-------±____
* 15 declined treatment
94 randomised
_____________
______________
47 assigned phenytoin
47 assigned phenobarbital
I
I
Followed up:
31 for 12 month seizure outcomes
43 for behavioural outcomes
Followed up:
31 for 12 month seizure outcomes
39 for behavioural outcomes
16 withdrawn
2 excessive seizures
4 access difficulties
5 refused to continue
3 remission
1 died
1 lost to follow-up
4
31 completed trial
16 withdrawn
1 excessive seizures
3 access difficulties
5 refused to continue
*
3 remission
1 side-effects
3 lost to follow-up
31 completed trial
Figure 1: Trial profile
are fairly typical of the rest of India. Families are mostly nuclear in
terms of living arrangements, but retain strong intergenerational
ties. SANCHAR-AROD is a non-govemmental organisation that
has been working in community-based rehabilitation for children
and their families in this area since 1988. An epilepsy service was
offered for the first time, jointly by SANCHAR-AROD and
another long-standing NGO providing mother and child health
services in the area (Child-in-Need Institute).
The study took place between August, 1995, and February,
1997. Children identified by population ascertainment (to be
published elsewhere) through house-to-house survey or key
informants were invited to attend the clinic. Operational definitions
for epileptic seizures were used.17 After clinical assessment and
counselling, parents were asked for verbal consent for their child to
take part in the trial, provided that they satisfied the entry criteria.
Eligible children were aged 2-18 years, were resident in the field
area of either organisation, had had two or more unprovoked
seizures within the previous 12 months, and had not been treated
during the previous 3 months. Children with myoclonic, absence,
or multiple seizure types were treated but not enrolled in the study.
Children with febrile convulsions alone were excluded. Any child
with clinical evidence of a progressive neurological disorder was
referred to the metropolitan neurology centre. Ethical approval for
the study was obtained from the local research ethics committee
and from the Institute of Child Health, London.
Participants were randomly assigned treatment with
phenobarbital or phenytoin in clinic immediately after the diagnosis
had been confirmed and parental consent obtained. The first ten
children were assigned treatment by means of a pre-prepared,
balanced random number list. Thereafter, randomisation was by
the technique of minimisation with stratification by age-group and
presence of cerebral impairment (severe mental retardation or
cerebral palsy). Five separate index cards were used to maintain
lists of participants in five categories: aged 2-12 years, aged 13-18
years, with cerebral impairment, without impairment, and overall
treatment allocation. All randomisation was carried out by a
research assistant who kept the cards in a locked cabinet and took
no part in management of patients.
For practical and ethical reasons, the treating physician, child,
and parents were aware of the treatment assigned. Outcome was
assessed by an investigator unaware of the treatment assignment.
Treatment started with a small, weight-related dose, and was
20
increased after 2 weeks to a maintenance dose consistent with
WHO recommendations.' Phenobarbital was started at 1-5 mg/kg
daily; the maintenance dose was 3-0 mg/kg daily, and one
increment was allowed to 5-0 mg/kg daily if seizures were not
controlled. Phenytoin was started at 2-5 mg/kg daily; the
maintenance dose was 5 0 mg/kg daily, and one increment was
allowed to 7-0 mg/kg daily. Any child who had intolerable adverse
effects was withdrawn from the trial if necessary. If the seizures
were not controlled despite full-dose monotherapy, treatment was
changed to the other study drug.
Participants were medically reviewed every month. Occasionally,
the interval between reviews was longer if the child was stable and if
access to the clinic was difficult. Blood concentrations of drugs
were not monitored because of expense. Fieldworkers visited
families at home to check on the child’s health, to count tablets, to
educate the family about first aid, and to encourage the
rehabilitation of the child. Children who withdrew from the
treatment programme were visited by a senior disability worker and
DKP. Thus, possible data loss was kept to a minimum.
Participants were followed up for 21 months after
randomisation. Antiepileptic efficacy was measured as time to first
seizure after randomisation and the actuarial proportion of each
treatment group free of seizures in each treatment quarter.
Behavioural side-effects were measured by means of a Bengali
adaptation of the Conners parent rating scale (CPRS-48) for
children aged 6 years or over,'" and by the preschool behaviour
screening questionnaire for 2-5-year-olds."’ Assessments were
made at 12 months or at the time of withdrawal from treatment.
Total and cut-off scores were compared between treatment
groups. A checklist of side-effects was used for systematic
collection of parental reports of side-effects at clinic visits.
We expected that there would be an important excess of side
effects with phenobarbital and consequently the frequency of side
effects was chosen as the primary outcome. 3 o demonstrate a
difference of 25% in side-effects, with an assumed incidence of
side-effects with phenytoin of 15%, 80% power, and a one-sided
significance level of p=0 05, 39 children were required in each
treatment group. We were aware that the trial would have limited
power to establish equivalence of the two drugs for late seizure
control (between 9 and 12 months after randomisation). On the
assumption that 40% of patients in each treatment group are
seizure-free during this period, to demonstrate equivalence of
THE LANCET ’ Vol 351 • January 3, 1998
ARTICLES
Phenytoin
(n=47)
6(5-7)
Occupation of head of household
Waged labourer
Business
Skilled trade
Salaried
Not recorded
23(49%)
6(13%)
7(15%)
7(15%)
4(9%)
18(38%)
6(13%)
9(19%)
7(15%)
7(15%)
Maternal literacy
Illiterate
Intermediate
Proficient
Not recorded
19(40%)
10(21%)
14(30%)
4(9%)
23(49%)
9(19%)
9(19%)
6(13%)
CD
<b
Household type
Nuclear
Joint
Not recorded
36(77%)
7(15%)
4(9%)
34(72%)
7(15%)
6(13%)
Religion
Hindu
Muslim
Christian
28(60%)
19(40%)
0
27(57%)
19(40%)
1(2%)
1000(675-1500)
1000(700-1500)
6-12
13-18
8(17%)
18(38%)
21(45%)
6(13%)
21(45%)
20(43%)
Sex
Male
Female
25(53%)
22(47%)
24(51%)
23(49%)
Cerebral Impairment
Absent
Present
35(75%)
12(25%)
35(75%)
12(25%)
Median (IQR) age at onset (years)
6-75 (3-75-10)
8(5-12)
Median (IQR) monthly Income (Rs)
Age-group (years)
2-5
Mean (SD) body-mass Index (kg/m’)
13-3 (5-5)
14-8(3-3)
Aetiology
Idiopathic
Symptomatic
34(72%)
13(28%)
38(81%)
9(19%)
Seizure type
Partial only
Secondary generalised
Primary generalised
16(34%)
19(40%)
12(26%)
7(15%)
18(38%)
22(47%)
Median (IQR) number of seizures
Lifetime
3 months before study
61(6-1002)
12 (4-5—93)
51(5-200)
9(4-27)
Febrile convulsions
Negative history
Positive history
Not recorded
24(51%)
5(11%)
18(38%)
26(55%)
5(11%)
16(34%)
Family history of seizures
Absent
Present
Not recorded
26(55%)
3(6%)
18(38%)
29(62%)
2(4%)
16(34%)
Previous exposure to antiepileptic drugs
Negative
Positive
22(47%)
25(53%)
29(62%)
18(38%)
Data are number of participants (% of group) unless otherwise stated. *Rs30
approximately $1: Rs50 approximately £1.
Table 1: Baseline characteristics of treatment groups
effect to within 15% at a two-sided significance level p=01 with
50% power, 58 children were required in each group (88 for 65%
power). We aimed to recruit 70 children to each group. The design
did not allow for early stopping or interim analysis.
Analysis was by intention to treat. Treatment effects, adjusted
for design (age and cerebral impairments) and prognostic variables
(total number of seizures, interval between first seizure and
seizures
<D
6(5-8)
Median (IQR) family size
randomisation,
100 n
Phenobarbital
(n=47)
in
3
months before randomisation,
previous antiepileptic treatment, sex, seizure type, symptomatic
epilepsy) were estimated by means of the Cox proportional hazards
model. Log-transformed total behaviour rating scores were
compared by Student’s t test at a significance level of p=0 05. A
dichotomous variable was created from cut-off scores for
behaviour. The effects of age-group, sex, cerebral impairment,
THE LANCET • Vol 351 - January 3, 1998
so
co
75Phenobarbital
50Phenytoin
25 o
o
CL
0 J r
0
300
50
100 150 200 250
Time to first seizure (days)
Number at risk
Phenobarbital
47
31
24
19
17
Phenytoin
47
25
17
14
11
Figure 2: Kaplan-Meier curves of seizure-free Interval by
treatment group
antiepileptic drug, and first-order interactions between these
variables, were tested in a multiple logistic regression model,
summarised as odds ratios with 95% CI, by means of STATA
(version 5 0) for Macintosh software.
Results
Between August, 1995, and February, 1996, 109 eligible
children were identified by population screening; 15
families declined any treatment (figure 1). 94 children were
randomly assigned one of the trial drugs. 62 (66%)
remained on treatment and were followed up for 12
months. In the phenytoin group, 31 children completed 12
months of follow-up; 16 withdrew (four during the first
quarter, six during the second, four during the third, and
two during the fourth). One child in the phenytoin group
drowned in a pond; this death may have been seizure
related, but it was unwitnessed. In the phenobarbital group,
31 children completed 12 months of follow-up; 16
withdrew (six during the first quarter, seven during the
second, and three during the fourth). 82 (87%) had
behavioural outcomes recorded at 12 months or at the time
of withdrawal from treatment. In all, 61 (65%) children
had complete follow-up data, with similar proportions of
missing data between treatment groups.
Most of the participating families were nuclear, with a
median size of six (table 1). 59% of families were Hindu,
the rest predominantly Muslim. 50% of households were
headed by a daily-waged labourer. 45% of mothers were
unable to read, write, or tell the time. Reported monthly
income varied from Rs300 to Rs6000 (median Rs 1000).
The typical house was made of mud with a thatch or tile
roof, two rooms, no latrine, no other land, and no
electricity. Families had to travel for up to 3 h to reach the
clinic, often with substantial hardship, by bus, foot, and
Side-effects reported
Phenytoin group
Phenobarbital group
Number of
participants
Number who
did not
complete trial*
Number of
participants
Number who
did not
complete trial*
No side-effects
33
13
34
12
Single side-effect
Behavioural
Sleep disturbance
Anorexia/nausea
Dizziness
6
2
1
1
it
2
6
2
3
5
1
16
47
16
Several side-effects
4
Total
47
♦For any reason. fDied.
Table 2: Side-effects reported at clinic and numbers of children
who did not complete the trial for any reason
21
ARTICLES
Phenytoin
group
Phenobarbital
group
P
2-65 (0-89)
2 18(102)
3 03(0-38)
2-64(0-71)
2- 12(1-31)
3- 51 (0-33)
0-97
0-94
0-07
Number with behavioural problems/total In group
Male
6/22(27%)
Female
7/21(33%)
Aged 2-5 years
3/7(43%)
Aged 6-12 years
5/17(29%)
Aged 13-18 years
5/19(26%)
Cerebral Impairment
4/11(36%)
No cerebral Impairment
9/32(28%)
Total
13/43(31%)
3/20(15%)
4/18(22%)
3/6(50%)
3/16(19%)
1/16(6%)
4/11 (36%)
3/27(11%)
7/38(18%)
Mean (SD) log total score*
Conners
BSQ
BSQ (adapted)
•Conners parent rating scale for 32 children in each group aged >6 years; preschool
behaviour screening questionnaire (BSQ) for children aged 2-5 years (4 phenytoin, 3
phenobarbital): adapted BSQ for children with cerebral Impairment (7 phenytoin, 4
phenobarbital). Information was not available for 4 children In phenytoin group and 9
In phenobarbital group.
Table 3: Distribution of behavioural problems at outcome
cart, at the expense of housework and agriculture, and with
significant costs (eg, to buy meals and pay bus fares for
themselves and accompanying relatives).
There was balanced distribution by age-group, cerebral
impairment, and treatment (table 1). The median age was
12 years, with a median age at seizure onset of 8 years and
a median of 50 seizures before randomisation. 64% of
children had partial seizures, the remainder primary
generalised seizures. A history of febrile convulsions was
recorded in 11%. 43 (46%) children had been treated with
antiepileptic drugs previously; nine had received
phenobarbital and eight carbamazepine, for a median of 18
months (IQR 0-5-60). Homoeopathic treatments had been
tried by ten families, and expensive “brain tonics” and
vitamins were commonly prescribed concurrently with
allopathic drugs (n=12).
Compared with the phenobarbital group, children in the
phenytoin group were slightly younger, smaller, and
younger at onset of epilepsy and they had a higher
cumulative number of seizures, both lifetime and within the
3 months before the trial; higher proportions had a remote
symptomatic cause, partial seizure semiology, a first-degree
family history of seizure disorder, and previous exposure to
antiepileptic drugs. Overall, therefore, children in the
phenytoin group had a worse outlook.
Compliance was estimated by tablet counting in the
home by fieldworkers. In each treatment group, there was
an 8% excess of tablets at the end of the trial, which
suggests reasonable compliance for both drugs. In the
phenytoin group, two children required increases in dose to
7 mg/kg daily and three required dual therapy (after cross
over) for seizure control. In the phenobarbital group, six
Variable
Odds ratio (95% Cl) for behavioural problems
Unadjusted (95% Cl)
Adjusted (95% Cl)*
Single variables
Phenobarbital vs phenytoin
Male vs female
Cerebral impairment, present vs
absent
0-52 (018-1-48)
1- 44 (0-52-3-97)
2- 24 (0-76-6-56)
0-51 (0-16-1-59)
0-44 (0-11-1-75)
0-35 (0-04-3-29)
Age 13-18 vs 2-12 years
0-47 (0-16-1-39)
0-42 (0-13-1-39)
Sex xcerebral Impairment Interaction
Male, no impairment
Male, impairment
Female, no impairment
Female, impairment
10
0-33 (0 04-3 06)
0-52(0-14-1-97)
24-2 (1-60-363-6)
1-0
0-35 (0 04-3-29)
0-44 (0-11-1-75)
25-1 (1-57-402-0)
•For antiepileptic drug. sex. cerebral impairment, age-group. and sexxcerebral
Impairment interaction.
Table 4: Multiple logistic regression model for behavioural
problems at outcome
22
children required increases in dose to 5 mg/kg daily, but
none needed to switch to the other study drug.
At the beginning of each successive quarter the
proportion of participants entering that quarter who were
seizure free was 42%, 49%, 48%, and 56% in the
phenytoin group and 56%, 64%, 67%, and 73% in the
phenobarbital group. Seizure recurrence occurred earlier
in the phenytoin group than in the phenobarbital group
(figure 2: log-rank test, p=0-046). After adjustment for
design factors (age and cerebral impairment) by the Cox
proportional hazards model, the difference between
treatments remained (hazard ratio 0-57 [95% CI
0-32-1 00]). However, once all prognostic variables (log
lifetime seizures, log pretrial seizures, time between first
seizure and randomisation, seizure type, and previous
exposure to antiepileptic drugs) had been entered into the
model, there was no evidence of a significant difference in
efficacy between the drugs, although the hazard ratio of
0-97 had wide 95% CI (0-28-3-30).
27 parents or children reported symptoms that they
ascribed to treatment (table 2). The frequency of side
effects was similar in the phenytoin and phenobarbital
groups (14 [30%] vs 13 [30%], p=0-77). Two families in
the phenytoin group who reported sleep disturbance
withdrew the child from treatment. Three families in the
phenobarbital group who reported behavioural problems
(hyperactivity) left the study; two migrated and were lost to
follow-up and one withdrew.
There were no significant differences between the
treatment groups in behaviour rating scores (table 3). 20
children were rated as having behavioural problems on the
basis of cut-off scores—13 in the phenytoin group and
seven in the phenobarbital group. Behavioural problems
were more common among children with cerebral
impairments, those under 5 years old, and girls. All these
patterns were stronger in children treated with phenytoin
than in those who received phenobarbital.
There was no evidence of association between
behavioural problems and age, sex, cerebral impairment, or
antiepileptic drug by multiple logistic regression (table 4).
We looked for first-order interaction between combinations
of these variables but found evidence of interaction only for
sex and cerebral impairment—girls with cerebral
impairment were significantly more likely to have
behavioural problems than boys without cerebral
impairment (p=0-02). There was, therefore, no evidence of
an excess of behavioural problems in the phenobarbital
group. The adjusted odds ratio even suggested fewer
behaviour problems with phenobarbital (0-51 [95% CI
016-1-59]).
Discussion
We aimed to recruit 70 children to each group but could
not achieve this target in the time available. In this trial in
India, we achieved 67% of the target sample size, which is
similar to rates achieved in clinical trials in Europe and
the USA. Despite substantial logistical difficulties in
mounting the study, we achieved a follow-up rate similar
to that in clinical trials in western countries.8 Poverty,
difficulties with travel, the seasonal pattern of work, the
monsoon, and the wide choice of other health
practitioners were all obstacles to regular clinical follow
up. This service could not have been offered, and this
study could not have been undertaken, without regular
home visits by disability workers within the setting of
community-based rehabilitation.
THE LANCET • Vol 351 • January 3, 1998
ARTICLES
Among this representative sample of children with
epilepsy in rural India, the overall age distribution was
wider than in some previously reported trials.8,11 The age at
onset of epilepsy was similar to that in the UK
monotherapy study.9 Compared with that study, our
participants had poorer prognostic features: 25% had
cerebral impairments, and they had had many seizures
before randomisation, a pattern typical of unselected
patients in developing countries.21 A high proportion (46%)
had received drugs in the past, compared with 6-26% in
other developing countries.16,21 Many of these families had
consulted a doctor in Calcutta at the onset of their child’s
epilepsy and could not afford to continue treatment with
carbamazepine or expensive, concurrent “brain tonics”.
This trial did not show a difference in efficacy between
phenobarbital and phenytoin when design and prognostic
factors were taken into account, although we lacked the
sample size to demonstrate equivalence of efficacy to our
desired level of precision. This equivalence of effect is
consistent with other studies of monotherapy in
childhood,8*10 and does not allow any conclusion about
absolute efficacy to be drawn. Overall, 65% of children
were seizure free in the final quarter, a success rate similar
to that obtained in community-based studies in Kenya and
Ecuador.15,20 These results therefore confirm the usefulness
of first-line antiepileptic drugs for the primary-care
treatment of partial and generalised tonic-clonic childhood
epilepsy in developing countries.
We found no difference in the incidence of serious
behavioural
side-effects
between
phenytoin
and
phenobarbital, using both objective, masked assessments
and parental reports. We were seeking a difference of 25%
and had the intended statistical power, and our instruments
were validated in a standard manner. Behavioural
problems, on our adapted rating scales, were as common as
reported in western population studies.19,22 The finding of
no excess of serious behavioural problems with
phenobarbital accords with results of other clinical trials
that used objective, masked outcome assessment89,25 and
suggests that previous reports of intolerable adverse effects
may have been influenced by observer bias.7,10 Another
explanation is that the context of the study influenced the
outcomes we measured, and that the threshold at which
childhood hyperactivity becomes intolerable is higher in
this setting, which would explain the low rate of withdrawal
due to adverse effects. However, this factor would not
explain the lack of a difference in side-effects between the
two drugs. In view of the equivalence of effect, frequency of
other side-effects, and careful tablet counting, we do not
believe that differential non-compliance could explain these
findings. Although our results do not support an excess of
behavioural effects with phenobarbital in the preschool agegroup or in children with cerebral impairments, we cannot
rule out this possibility. A separate study would be
necessary to answer this question and examine long-term
effects on cognitive functioning.
This study was carried out within a primary-health-care
service structure, at low cost, and using a model integrated
within community-based rehabilitation. Access was an
important issue in follow-up, and emphasised the lack of
choice in terms of drug cost and availability. International
trade agreements will further restrict the transfer of new
pharmaceutical technology to developing countries24 and
make replacement of phenobarbital as a first-line drug in
developing countries impossible in the near future.
Therefore, the main conclusion of this study, that
THE LANCET • Vol 351 • January 3, 1998
phenobarbital is an effective and acceptable antiepileptic
drug for rural Indian children, has great relevance for
WHO strategy and epilepsy-control programmes in
developing countries.
Contributors
All five investigators contributed to the design of the study. Deb Pal took the
baseline measurements and with Gautam Chaudhury and Tulika Das
adapted the outcome measures, which were undertaken by Tulika Das. Data
handling and statistical analysis were done by Deb Pal with assistance from
Anthony Johnson, who also gave advice about practical issues during the
trial. Deb Pal wrote the first draft of the paper, and all the investigators
contributed to the final version.
Acknowledgments
Deb Pal was supported by a Wellcome Trust Research Training Fellowship.
Additional support was received from the International League Against
Epilepsy. We thank Samaresh Bhattacharya, medical officer at the Child-inNeed Institute, for medical follow-up; Debolina Roy Chaudhuri, research
assistant, for randomisation and record keeping; Suryanil Sengupta for
helping with the behaviour ratings; and the SANCHAR field workers.
References
WHO. Initiative of support to people with epilepsy. Geneva: WHO,
1990.
2 Gastaut H, Osontokun BO. Proposals on antiepileptic pharmacotherapy
for use in developing countries. Epilepsia 1976; 17: 355-60.
3 Dekker N. Community approach in epilepsy treatment: the KAWE
experience. Trap Geograph Med 1993; 45: 248-52.
4 Senanayake N. Community project in epilepsy control in Kandy, Sri
Lanka. Trap Geograph Med 1994; 46: 6-8.
5 Shorvon SD. Drugs in developing countries. BMJ 1986; 292: 1666-67.
6 Kshirsagar NA, Shah PU. Management of epilepsy in developing
countries. In: Pedley T, Meldrum B, eds. Recent advances in epilepsy.
Edinburgh: Churchill Livingstone, 1992: 159-76.
7 Wolf SM, Forsythe A. Behaviour distance, phenobarbital, and febrile
seizures. Pediatrics 1978; 61: 728-31.
8 Vining PG, Mellits ED, Dorsen MM, et al. Psychologic and behavioural
effects of antiepileptic drugs in children: a double-blind comparison
between phenobarbital and valproic acid. Pediatrics 1987; 80: 165-74.
9 de Silva M, Macardle B, McGowan M, et al. Randomised comparative
monotherapy trial of phenobarbitone, phenytoin, carbamazepine, or
sodium valproate for newly diagnosed childhood epilepsy. Lancet 1996;
347: 709-13.
10 Farwell JR, Lee YJ, Hirtz DG, Sulzbacher SI, Ellenberg JH, Nelson KB.
Phenobarbital for febrile seizures—effects on intelligence and on seizure
recurrence. N Engl J Med 1990; 322: 364-69.
II Mitchell WG, Chavez JM. Carbamazepine versus phenobarbital for
partial onset seizures in children. Epilepsia 1987; 28: 56-60.
12 Garcia FO, Campos-Castello J, Maldonado JC. Fenobarbital oral
continuado o diazepam rectal intermitente para la prevencion de las
crisis febriles. Anole Espanol Pediatr 1984; 20: 763-69.
13 Placencia M, Sander JWAS, Shorvon SD, et al. Antiepileptic drug
treatment in a community health care setting in northern Ecuador: a
prospective 12 month assessment. Epilepsy Res 1993; 14: 237-44.
14 Varmus H, Satcher D. Ethical complexities of conducting research in
developing countries. N Engl J Med 1997; 337: 1003-05.
15 Anderson JC. Is childhood hyperactivity the product of western culture?
Lancet 1996; 348: 73-74.
16 Shorvon SD, Farmer PJ. Epilepsy in developing countries: a review of
epidemiological, sociocultural and treatment aspects. Epilepsia 1988; 29
(suppl 1): 36-54.
17 Placencia M, Suarez J, Crespo F, et al. A large-scale study of epilepsy in
Ecuador: methodological aspects. Neuroepidemiology 1992; 11: 74-84.
18 Goyette CH, Conners CK, Ulrich RF. Normative data on Revised
Conners Parent and Teacher Rating Scales. J Abnormal Child Psychol
1978; 6: 221-36.
19 Richman N, Graham P, Stevenson J. Pre-school to school: a behavioural
study. New York: Academic Press, 1982.
20 Feksi AT, Kaamugisha J, Sander JWAS, Gatiti S, Shorvon SD.
Comprehensive primary health care antiepileptic drug treatment
programme in rural and semi-urban Kenya. Lancet 1991; 337: 406-09.
21 Feksi AT, Kaamugisha J, Gatati S, Sander JWAS, Shorvon SD. A
comprehensive community epilepsy programme: the Nakuru project.
Epilepsy Res 1991; 8: 252-59.
22 Rutter M, Graham P, Yule WA. A neuropsychiatric study in childhood.
Philadelphia: JB Lippincott, 1970.
23 Camfield PF, Camfield CS, Shapiro SH, Cummings C. The first febrile
seizure-antipyretic instruction plus either phenobarbital or placebo to
prevent recurrence. J Pediatr 1980; 97: 16-21.
24 Pillai AM. Impact of GATT Agreement on drug prices. J Indian Med
Assoc 1995; 93: 113-20.
I
23
ARTICLES
Effect of diagnosis on survival benefit of lung transplantation for
end-stage lung disease
Jeffrey D Hosenpud, Leah E Bennett, Berkley M Keck, Erick B Edwards, Richard J Novick
Summary
Background Although certain forms of end-stage lung
disease are debilitating, whether the associated mortality
rate exceeds that of transplantation is unclear. We
undertook analysis to clarify the survival benefit of lung
transplantation for various types of end-stage lung
disease.
Methods We analysed data for all patients listed for
transplantation in the USA for emphysema, cystic fibrosis,
or interstitial pulmonary fibrosis in the years 1992-94.
The numbers of patients entered on the waiting list, post
transplantation, died waiting, and currently waiting were:
emphysema group 1274, 843, 143, and 165; cystic
fibrosis group 664, 318, 193, and 59; interstitial
pulmonary fibrosis group 481, 230, 160, and 48. A time
dependent non-proportional hazard analysis was used to
assess the risk of mortality after transplantation relative
to that for patients on the waiting list.
Findings
The clearest survival benefit from lung
transplantation occurred in the cystic fibrosis group. The
relative risks of transplantation compared with waiting
were 0-87, 0-61, and 0-61 at 1 month, 6 months, and
1 year (p=0-008), respectively. For interstitial pulmonary
fibrosis, the corresponding relative risks were 2-09, 0-71,
and 0-67 (p=0-09). No survival benefit was apparent in
the emphysema group. The risks of transplantation
relative to waiting were 2-76, 112, and 1-10 at 1 month,
6 months, and 1 year, respectively, and the relative risk
did not decrease to below 1-0 during 2 years of follow-up.
Interpretation
These findings suggest that lung
transplantation does not confer a survival benefit in
patients with end-stage emphysema by 2 years of follow
up. Other benefits not accounted for in this analysis such
as improved quality of life, however, may justify lung
transplantation for these patients.
Lancet 1998; 351: 24-27
See Commentary page 4
Introduction
Although lung transplantation has become an invaluable
approach for the treatment of end-stage respiratory
disease, rates of successful outcomes are not yet as good
as those for other transplanted organs. Based on data
from the Joint United Network for Organ Sharing
(UNOS)/International Society for Heart and Lung
Transplantation (ISHLT) Thoracic Registry, 1-year
mortality is more than 25% and 5-year mortality is
greater than 50%.' In addition, obliterative bronchiolitis
affects more than 50% of patients late after
transplantation2 and accounts for 57% of the deaths after
1 year.1
The most common indication for lung transplantation
is emphysema.1 Although emphysema is debilitating,
mortality from this disorder may not be as high as that
from other forms of end-stage lung disease, especially in
patients younger than 60 years.’6 Moreover, for some
patients with emphysema, volume-reduction surgery7 9
may be an alternative. To clarify the actual survival
benefit of lung transplantation for the more common
causes of end-stage lung disease,, including emphysema,
we undertook an analysis of data from the Joint
UNOS/ISHLT Thoracic Registry.
Methods
The cohort for this study included all patients listed for
transplantation with UNOS (listed for transplantation in the
USA) between Jan 1, 1992, and Dec 31, 1994. The cohort
included patients with the three most common indications—
emphysema, cystic fibrosis, and interstitial pulmonary fibrosis.
Cystic
fibrosis
Interstitial
pulmonary
fibrosis
Emphysema
664
481
1274
193
318
94
160
230
43
143
843
123
59
68
48
55
165
142
398(18)
304(17)
361(23)
250(14)
560(16)
260(17)
354(19)
327(21)
391(12)
Mean (SD) total follow-up (days)
All patients
Transplant patients only
512(15)
658(21)
454(17)
577(24)
616(10)
651(12)
Mean (range) age In years*
25-8
(10-49-3)
49-6
(16-1-71-4)
53-5
(17-8-68-4)
Total cohort
Outcome at time of analysis
Died on waiting list
Underwent transplantation
Removed from waiting list and
censored for other reasons
Still on waiting list
Died after transplantation
Mean (SD) days on waiting list
Non-transplant patients
Transplant patients
Mean (SD) post-transplant
follow-up days
Joint United Network for Organ Sharlng/lnternatlonal Society for
Heart and Lung Transplantation Thoracic Registry, Richmond, VA,
USA (J D Hosenpud md, L E Bennett Pho, B M Keck mph,
E B Edwards pud, R J Novick md)
Sex
M
F
357(54%)
307(46%)
293(61%)
188(39%)
567(45%)
757(55%)
White patients
616(93%)
382(79%)
1187(93%)
Correspondence to: Dr Jeffrey D Hosenpud, Division of
Cardiovascular Medicine, Medical College of Wisconsin,
9200 West Wisconsin Avenue, Milwaukee, Wl 53226, USA
*At time of analysis.
24
Table 1: Characteristics of patients, outcomes, and time spent
In each clinical stage
THE LANCET • Vol 351 • January 3, 1998
s-
I ,F VIRUS ENCEPHALITIS:
Jiffis
JS EPIDEMIC AT
at
ftSgSAKHPUR
goiUKHPUR________
!
i
K.P* Kushwaha
S_ YJ). Singh
1 ■ J-Singh
>
jLSirohi
B
R.K. Singh
Japanese encephalitis (JE) has become
an important health problem in India,
more so in children, who bear the major
brunt of the disease. The disease was first
reported in India in 1954 by Khan(l) from
Jamshedpur. This was followed by several
reports of occurrence of JE epidemics
from other parts of the country(2).
Gorakhpur and surrounding districts of
eastern Uttar Pradesh first experienced an
epidemic of JE in 1978 and then in 1980,
1985 and 1986(3). A severe epidemic of JE
seen in Gorakhpur area in the late rainy
season of 1988 is reported in the present
U.K. Singh
r
communication.
Material and Methods
I
-ft
M .
4-:
B
I
W/
W
abstract
‘
> Gorakhpur region experienced the most
serious outbreak of Japanese encephalitis (JE) in
1988 in which 875 children were admitted in the
Depa/tment of Pediatrics, BRD Medical College.
Gorakhpur. Children between 7JO years age
gvup constituted half (49Jr< ) of these cases,
convulsions (83.8%), altered sensonum
(7&2%), headache (68.8%) and hypertonia
(77.0°7o) were the main presenting features. IgM
^rinst JE virus was demonstrated in 18/25 CSJ
Ond 27/53 sera collected from these children.
^ff^ificant titres of III antibodies against JE were
present in 498/670 patients.
r^a^e,ds were managed symptomatically,
.^^^tethasone and dopamine were given to
137 (15.7%) children admitted with shock
circulatory failure.
^Almost a third (31.8%) of the patients
W . •
51.4% recovered completely and 10.7%
ft> ..; ^0vere<l partially. Corticosteroids did not
1
the outcome.
■^Twenty four patients had recurrence of symp_ excellent recovery from acute attack of
Qf
fl^r
t»o died and 5 developed neurological
W’*' "-*>? Words: Japan ese
virus
encephalitis,
Epidemic, Neurological dificits,
- Recunvnce.
9;
-
Patients clinically diagnosed as en
cephalitis and admitted to the pediatric
wards of Nehru Hospital, BRD Medical
College, Gorakhpur from September to
November, 1988 constituted the case
c*
rial for the present study. Laboratory
estigalions done included hemoglobin, total
and differential leucocyte counts and com
plete cytochemical examination of cerebro
spinal fluid (CSF). On admission blood
samples were taken for demonstrating
anti-JE virus antibodies (IgM and IgG)
with repeat sampling after 15 days to sec
the rise in IgG antibody titre. Sera sepa
rated wore stored in sterile containers at
-20°C till tested. CSF samples obtained at
the time of admission were examined for
IgM antibodies to JE virus. Needle biopsy
of brain was also done in 4 children imme
diately after death for isolation of virus.
From the Department of Pediatrics, Biochemistry
and Microbiology, B.R.D. Medical College,
Gorakhpur.
Reprint requests: Dr. A.K. Ralhi, Lecturer in Pe
diatrics, B.R.D. Medical College, Gorakhpur.
Received for publication: March 22, 1989;
Accepted: November 27, 1992
325
JAPANESE ENCEPHALITIS
RATHI ET AL.
Patients were largely managc^
symptomatically and supportively. Airway
kept clean, fever brought down with
antipyretics
and
cold /Pongm^
Phenobarbitone, phenytoin and d.azepam
were used for seizures. Brain edema was
reduced by mannitol, glycerine and in
selected cases by dexamethasone. Most
patients were on intravenous fluids for 4-5
;.n v
days keeping »
considered
considered positive.
positive. A titre <80 without
subsequent rise was taken as negative.
Results
___
A total of 875 children (3 months to 15
Years) with clinical features of encephahtis
were admitted to the Pediatric wards of
Nehru Hospital during a period of 3 g
writhe /"V75 456 and 44 children m
September, October and November 1988,
respectively). Of them, 431 (42.3%) were
hormone. Dopamine was used to maintain
blood pressure in patients with pcrip
circulatory failure (PCF). Dc^hasone
was used only in children with PCF and
Ze with central cardiorespiratory
Zlvement and other features of brain
edema, not responding adequat y
mannitol and glycerine. Oral predmsolonc
(1 mg/kg/day) was admmistcrcd to
selected patients not showing recovery in 3
weeks to see its possible effect on the
a a
outcome.
.
After the initial discharge from the
hospital, patients were followed up every
fortnight. Cases with neurological deficits
sensory/motor and behavioral problems
were managed symptomatically with
I
C
V
i! i
judicious use of physiotherapy.
The isolation of the virus was one
employing infant mice model and was
carried out at the Departmen of
Microbiology, KG Medical College
Lucknow. The estimation of IgM agai
jE by MAC ELISA mcthod(4) using 1.5
dilution of scrum or CSF was earned out
at the National Institute of Virology, Pune.
Hemagglutination inhibition (HI test for
IgG aSibodies(5,6) was earned out m
Department of Microbiology, BRD
Medical College, Gorakhpur. HI antibody
titre >80 in single sample and minimu
of four fold rise in titre in sccon
sample taken after 10-15 days was
326
between 7-10 years of age and boys
outnumbered girls (Table 7). Fever
headache, convulsions and altered
sensorium were the mam presenting
features (Table IT).
TABLE 1-/1^ and
D^thbution ofJE Cases
Age group
Male
Female
Total
3 mo-3 yrs
18
(72.0)
7
(28.0)
25
(2.9)
3-6 yrs
174
(68.8)
79
(31.2)
253
(28.9)
7-10 yrs
305
(70.8)
126
(29.2)
(493)
11-15 yrs
119
(71.7)
47
(28.3)
166
(19.0)
Total
616
(70.4)
259
(29.6)
875
(100)
431
_
;nthcscs indicate percentages.
Figures in pare!
and,
The total duration of signs
cases
symptoms and the outcome of these
third
is shown in Table II & HIpatients
- Jchildren (31.8%) died. Most of the p
.
of :
who expired did so w.thin firs 3
included,
admission. The causes of death
PCF;
cardiac failure, respiratory fadu ,
and gas}r°';
associated with toxemia a-.- .
intestinal bleeding. .Neurological
9
PEDIATRICS
TABLE H-Pnesenting Features ard Outcome in JE
i:,; I
features
1i
3H
1
-^1
■
I
3^
a
t
Outcome of illness
Partial
recovery’
Death
LAMA*
®!r
I
Fever
865(98.9)
467(54.0)
94(10.0)
269(31.1)
35(4.1)
Convulsions
733(83.8)
356(48.6)
87(11.9)
259(35.5)
31(4.2)
Altered
sensori um
684(78.2)
322(47.1)
99(14.5)
231(33.8)
32(4.7)
Headache
558(63.8)
330(59.1)
65(11.7)
138(24.7)
25(4.5)
Vomiting
476(54.4)
201(42.3)
54(11.3)
178(37.4)
43(9.0)
Constipation
346(39.5)
169(48.8)
25(7.2)
145(41.9)
7(2.0)
Neck rigidity
223(25.5)
107(48.0)
33(10.3)
91(40.8)
2(0.9)
;‘•^11Il
I
Ei.
Gastric
bleeding
115(13.1)
Central respiration
irregularities
113(12.9)
15(13.3)
27(23.9)
70(61.9)
1(0.9)
Positive Kernig’s
69(7.7)
30(43.5)
11(15.9)
26(37.7)
2(2.9)
Diarrhea
32(3.4)
21(65.6)
1(3.1)
10(31.3)
21(18.3)
14(12.2)
i t
1
80(69.5)
i
E it
1
Other
S
- s g.
(n = 875)
Recovery'
B—;
volume 3()-march 1993
-PCF
59(6.7)
8(13.5)
5(11.8)
45(77.6)
1(1-6)
-Pneumonia
26(3.0)
13(50.0)
9(34.7)
2(7.6)
2(7.6)
Figures in parentheses denote percentages.
■;5
1
i.r
ii
A
Left agaisnt medical advice; outcome not known.
’
-----------------------------------------------
behavioral problems were seen in 94
Bt'-
r
r
I
|;
V • %) children comprising mainly of
Rental retardation, aphasia, paresis,
and seizurcs (Tablc IV)-
°pamine and corticosteroids were
adminiSte.red to 137 (15.7%) cases
m,ttcd in the acute stage with PCF and
ju
shock. Of the 35 children who were
administered prednisolone at 3 weeks of
illness, 20 (57.1%) recovered completely,
10 (28.6%) partially and 3 expired (Table
J7). When compared with non-stcroid
group (56 children) findings were not
statistically significant.
J
I
327
I
i
I I
I®
■/IL.
JAPANESE ENCEPHALITIS Al
RATHI ETAL.
TABLE \ll-Duration of Signs and Symptoms in Patients who Survived
Presenting
features
■3 5
-1
Duration in days
(n = 597)
3
3-7
7-10
10
----------------------------------- ■'
Fever
531
185
(34.8)
239
(45.0)
76
(14.3)
31
(5-8)
Convulsions
542
178
(32.8)
291
(53.6)
47
(8.6)
26
Altered scnsorium
378
172
(45.5)
153
(40.4)
29
(7.6)
Headache
317
317
(WO)
Vomiting
223
223
(100)
24
9
(6-3)
?
'I
■
Constipation
162
126
(77.7)
36
(22.2)
Neck rigidity
177
21
(11.8)
119
(67.2)
Gastric bleeding
34
23
(67.6)
11
(32.3)
Central respiratory
irregularities
59
34
(57.6)
16
(27.1)
9
(15.2)
-
54
9
(16-6)
33
(61.1)
12
(22.2)
-
Positive Kcrnig’s
Diarrhea
32
14
(43.7)
8
(25-0)
I
!
■
J
37
(20.9)
J
_ -SI
f
Figures in parentheses indicate percentages.
(
/
Ak.
\
V
Out of the 278 children who were
discharged after complete recovery in one
week, 24 had recurrence of symptoms and
were readmitted. Two of these children
expired and rest showed variable recovery
(Fig. L Table VT).
n
The laboratory investigations showeO
moderate leucocytosis in 661 (80.3%)
(Table VIT) with neutrophil P>^on11"*
in 60%. Rise in CSF protein level was
Jr
in 70.8% cases of whom 20% showe
CSF
above 100 mg/dl or more whereas
W
328
ii
'?•’1
11! «■ ’ i ■
pediatrics
RLE IV- Neurological and Behavioral
Problems in Patients Showing
Recoven-
-i®
^'Sequelae
1
■;{ I
volume 30-marci i 1993
Number
Percentage
38
34
40.3
rBwental retardation
b"-'
Hemipares*5
K
sI
IIF
1
at
■
i
Dystonia
Seizures
Incontinence of bladder
anal canal
Hiw**-Involuntary movement
I
Cranial nerve palsy
Monoparesis
Irrelevant behaviour
-
ir
I
■■
Irrelevant talk
Insomnia
Tongue protrusion
|
/
I
I
Weeping
Excitement
Irritability
&
34
36.2
33
26
35.1
27.7
19
20.2
19
20.2
6.4
6
5
11
10
10
I■g—
8
7
8.5
7.5
64
, •a-'y-X’* • ■
•W
.Jfcr ■
Ml PAL
a
''C
^>2abaD
'-■wB:
aZamgaRh
,.
E*
BALIA
S-1. Geographical distribution of cases of JE
• (1988-89).
1
........-T~
I
Fig. 2. Geographical distribution of cases of JE
(198T8S).
The 1988 epidemic of encephalitis in
Gorakhpur region was one of the most se
rious epidemics in India so far with 875
children admitted to Nehru Hospital alone
in a period of 3 months. Most of the cases
from Gorakhpur and Deoria districts and
some were from Basti and Azamgarh dis
tricts and bordering towns of Nepal (Fig.
2). As in past epidemics (1978, 1980, 1985,
1986)(3,7) the present epidemic loo oc
curred at the end of rainy season. Occur
rence of these epidemics at the end of rainy
season has also been reported from West
Bcngal(8).
Encephalitis affected all age groups but
the brunt of the disease fell on children
■
e
'
BALIA
Discussion
10.6
2
■J'
tv
/ p1
FAJZA6AD
2.1
10
-
P
1
2.1
10.6
10.6
sJ'.r
JhI- ®
s‘
sugar levels were not much altered. Major
ity of CSF samples had cell count upto 50
x 10f,/U in 17r? samples count was still
higher. The virological investigations
showed evidence ol IgM antibodies in
18/25 CSF and 27/53 sera. Ill antibodies
(IgC) to J EV in significant litres were seen
in 498/670 sera tested (Table \T1).
lour
fold or more rise in Hl antibodies was seen
in sera of 13/14 patients tested out of 24
children readmitted with recurrence ol
symptoms.
5.3
11.7
6
Assaultive behavior
!wIII
Kw,_
36.2
Inappropriate laughing
i g-fr'
I
2•
it
:r
B
ps
'11
-ip
-u
W
o
•s
i? f
UB
329
■
■
■'
r’
■'
'
JAPANESE ENCEPHALITIS
RATHI ETAL.
I
TABLE V-EJ]ect of Steroids in Chronic Phase
Groups
Cases
Complete
recovery
Partial
recovery
Expired
Steroid
35
(4.0)
20
(57.1)
10
(28.6)
3
(8.6)
---------------LAMa*
---3 11
'
(5 7)
|
56
(6.4)
Non-steroid
14
(25.0)
38
(67.9)
-A’
X22df = 1.448; p>0.05.
Figures in parentheses indicate percentages.
■a
* Left against medical advice.
I
TABLE VI-Profile of Patients Admitted with Recunence
--------------
Expired
(n = 24)
Complete
recovery
Partial
recovery
13
(54.2)
10
(76.9)
2
(15.4)
Altered
sensorium
3
(12.5)
1
1
(33.3)
(33.3)
Involuntary
movements
6
(25.0)
4
(66.7)
(33.3)
Convulsions
14
(58.3)
11
(78.6)
(14.3)
1
(7.1)
24
(100.0)
16
(66.7)
5
(20.8)
2
(8-3)
Presenting
features
Fever
Total
—I
1
1
(7.7) I
1
(33.3)
2
2
LAMAJt
11
1 5
(4.2) I
Figures in parentheses indicate percentages.
between 7-10 years of age. Males were
often affected in all age groups and is in
line with the earlier reports(9, 10).
Clinical features of JE epidemic were
similar to these reported earlicr(ll,12), as
were the findings in CSF(10,11,13) and
blood showing marked polymorphonuclear
leucocytosis(ll,13). The early and high
mortality and the causes of death are also
330
similar to previous reports(14,15).
patients came in the acute stage and inor^3
than half of them showed complete reC^S
ery in 7-10 days. Significant number of ch
dren died in acute phase, mainly wit
first three days of admission, a third
of children went into a chronic phase,
of them developing neurological ^cJCI J
and behavioral problems. A fourth\ course
J® fit •
PEDIATRICS
INDIANi
^|bI __
-;t 1|||
VOLUME 30—MARCH 1993
TABLE VW-Labointoiy Findings in JE
Feature
Investigation
Hemoglobin
(g/dl)
>12
10-12
<10
Leucocyte
counts
(xl09/L)
TLC
(n=823)
»
1
243 (29.5)
418(50.8)
162(19.7)
Neutrophils (109/L)
>10
5-10
<5
486(59.1)
309 (33.5)
28 (7.4)
Proteins
(mg/dl)
^40
>40
242 (70.6)
226(29.4)
Pleocytosis
50
5^50
131 (17.1)
434(56.5)
K'"
■
1
CSF
(n=768)
(xioyt)
J
Virology
(n=745)
JlEEF
.<T
W
101(123)
268 (32.6)
454 (55.1)
18
12-18
4-11
■ B' .
I
I
Result
Blood
Virus isolation
from brain
IgM - CSF
Scrum
IgG Scrum
-------- -FiSures in parentheses indicate percentages.
2/4 (50.0)
18/25 (72.0)
27/53 (51.0)
498/670 (74.3)
.. . "
1B
R j ■
HE?; I50 Came t0
'n the present epidemic.
?
Twenty four children who had shown comt
*n Car*.y P^asc
epidemic
aft WerC -SCnl homc in 7 days came back
Bf
Vaidable period with recurrence
‘ ' Ifi/Td1^01115
On readmission,
2 diei^d.completely, 5/24 partially
Such a course of JE has not
ken repOrtcd
1 ; J,
J so far. It has been suggested
.imnnrt
1 hostt defence mechanisms play an
I
I
L
t
enCCP“s’ domife *cove™ l Ch by thc Xdrus in carIy P°st
K
cjy phase from first attack led
He ^ntrollrdT"
control.. . Ul
01 Illncss
1IIncss wh,ch
which asain was
to thc
ue to further stimulation of the
immunological apparatus chiefly cell medi
ated immune response. It is as best a
speculation as investigations were not car
ried out to see thc behavior of immune
mechanisms in these children. Role of
auto-antibodies in recurrence too can
be possiblc(16). It has been shown that JE
virus persists in body in lymphocytes par
ticularly in thymus and spleen for many
months and can be reactivated at a later
dale (Mathur A, personal communication).
In our cases this may be the source of
relapse.
Mental retardation, hemiparesis,
aphasia and seizures were the chief
331
1
..3
I
JAPANESE ENCEPIIALITIS
RATI II ET AL.
neurological deficits noted in the present
epidemic. Behavioral problems occurred
during phase of recovery in chronic cases.
Neurological deficits and bchaviora
__
r^Hnw’incr
rnccohalitis
are well
problems
following
encephalitis
known(17,19).
acute
phase, use of
In the
corticosteroids was restricted to very sick
children, generally with dopamine in PCF
and in patients with raised intracranial
tension refractory to other measures
When used in children with prolonged
illness 5/35 patients showed remarkable
recovery. However, the difference in
steroid and non-steroid groups was not
statistically significant suggesting that
steroids do not hold the key to
management in chronic cases.
Poor availability of medical care facili
ties to the masses was also exposed during
this epidemic. All Stale Hospitals and Pri
vate Nursing Homes in Gorakhpur were
overflowing?This led to shortage of essen
tial drugs and medical and paramedical
personnel. Nursing staff being short even
at other times, adequate nursing care could
not be provided. Advanced medical facili
ties to maintain respiration, circulation and
temperature were also not available.
Probably, the outcome of epidemic would
have been much better, had these facilities
been available to us.
Acknowledgement
The authors are thankful to the upgraded Department of Microbiology, KG
Medical College, Lucknow and the Na
tional Institute of Virology, Pune for ren
dering help in investigating the epidemic.
REFERENCES
1. Khan N. Jamshedpur fever. Indian J Med
Sc 1954. 8: 597-609.
2. Mcdappe N. Japanese encephalitis in
India. Bull ICMR 1980,10: 29-38.
332
- Kumar
_• R, Mishra PK. Japanese X
3.
encephalitis’in India. Indian Pcdiatr 1988, W
25:354-355.
4 Godhai DA, Shaikh BH. IgM antibodyM
capture ELISA in diagnosis of JE, WN®
and Dengue virus. Indian J Med Res 1984, .®|
80:613-619.
5 Clark DH, Cassel J. Techniques of
hemagglutination and hemagglutination ||
inhibition with arthropod borne viruses.
Am J Trop Med Hyg 1958, 7: 561-573.
6 Sever JL. Application of microtechniques
to a viral serological investigation. J
Immunol 1962, 98: 320-323.
7. Maihur A, Chaturvcdi DC, Tandon HO, et fl
nl
IE epidemic
al. JE
epidemic in
in Uttar Pradesh, India
during 1978. Indian J Med Res 1982, 75:®
161-169.
Banerjee
K. |
rXK,
8. Chaterjce
studies
on
the
||
Epidemiological
encephalitis epidemic in
i Bankura. Indian J|g
Med Res 1975. 63: 1164-1179.
9 Grossman RA. Edelman R, Chcowanich |
' P Sirwan C. Study of Japanese:^
encephalitis virus in Chiang Mat
Thailand. 11: Human Clinical Infection^
Amer J Epid 1973,98: 121-132.
10 Webb JKG. Pereira S. Clinical diagnosisj|
arthropod borne type of virus encef^J
in children of North Arcot distnet, Ma* State, India. Indian J Med Set 195 ,
573-581.
11. Dickerson RB, Newton JR, ^anS^ ofJ|
Diagnosis and immediate
^Ji
Japanese B encephalitis. Ame
1952,12:277-288.
12. Li Hsiang Jung, Ch’ens
Ch’un. A clinical analysis of 319
Japanese B encephalitis. Zhong
1965, 51: 423-425.
13. Sen Gupta SN, Sen MK,
Bhattacharya DP, Rath BB.
® f' Japancs<!|
profile of the epidemic
■
1
2
11I ^lAN PEDIATRICS
11
■m
Hi ■ .^
r .'fB
I
F
■
W!
VOLUME 30—MARCH 1993
‘ encephalitis. Indian J Med Res 1976, 54:
; 1393-1407.
14 Simpson TW, Mciklcjohn G. Sequelae of
I Japanese B encephalitis. Amer J Trop
® Med 1947, 27: 727-731.
'15 Tigertt WD, Hammon WM. Japanese B
I Encephalitis. A complete review of
| expericnce on Okinawa 1945-1949. Amer J
? Trop Med 1950, 30: 689-722.
16 Cherry JD- Encephalitis. In: Nelson’s Text
I i» .
•
Book of Pediatrics, 13th edn. Eds. Nelson
WE, Bchrman RE,
Vaughan VC.
Philadelphia, WB Saunders Co, 1987, pp
556-560.
17. Goto A. A stud\- of long term sequelae of
Japanese encephalitis. J Psychiat Neurol
1957,59: 147-149.
18. Piper SJL, Kulan LT. Sequelae of
Japanese B and mumps encephalitis. Amer
J Trop Med Hyg 1958. 7: 481-487.
-2“
___
■■
NOTES AND NEWS
:T.'
THIRD COMMONWEALTH CONFERENCE ON DIARRHEA AND
MALNUTRITION
|y;.
i'A/, ’
i The Third Commonwealth Conference on Diarrhea and Malnutrition is to be held
in Shatin, New Territories, Hong Kong from November llth-l'lth, 1991. This
conference is organized jointly by the Department of Pediatrics, The Chinese
University of Hong Kong and the Hong Kong Pediatric Society. Participation by over
300 delegates from throughout the Commonwealth is anticipated and, in this special
meeting, we will be joined by colleagues from China.
L
|
IgBfe.•
Further details are available from:
if
■
—
Secretary,
B BL^ Paganizing
pr. Peter B. Sullivan,
Department of Pediatrics,
Prince of Wales Hospital,
uatin> N-T”
1
®!
rfK
I*' Hong K°ng-
Wi|
s
‘ B
Jel: (852J-636-2854
tax: [852]-636-0020
I
J
I
31 ■
■ ■
;
•
/
; ■si
H
1|Ki
333
j||8n ~
^W-.- y-:-,:-. ■.-
:’lw
•
? -t’.vsy'KP. ;■ >,r‘HW3S»WW*®'3K'«'.» -~ ■
,-'
.
■
■
■
■
STUDIES ON THE MOSQUITO VECTORS OF JAPANESE
ENCEPHALITIS VIRUS IN MANDYA DISTRICT, karnatak^I
INDIA
•s
G Geevarghese, AC Mishra, P George Jacob and HR Bhat
J
i
I
■'
National Institute of Virology, 20-A, Dr Ambedkar Road, Pune-411 i001, India
'f-
u
Abstract. Entomological investigations were carried out in areas affected by Japanese encephalitis (JP) 8
tn Mandya District, Karnataka, India, from 1983 to 1988, to determine species composition and the ’
density of mosquito vectors, in relation to the incidence of JE cases. JE cases occurred in two spells in a
year, one during April-June (summer epidemic) and another during October-December (winter epidemic)
There was very high incidence of JE cases in extensively irrigated areas and a low incidence in some of the T
taluks with less or no irrigation systems. Among culicines. Culex Iruaeniorhymhus was the most predomi- S
nant species (20.54%), followed by Cx. fuscocephalu (16.94), Cx tishnui (16.48%), Cx. gelidus (10.70%)
and other^species. The overall mosquito population showed two peaks in a year, one during the March- ■
April, and another during September, usually preceding the human epidemics. Relative abundance of
certain species varied in diflerent years.
.. .......-I
INTRODUCTION
Among Japanese encephalitis (JE) endemic
areas in India, Mandya District in Karnataka
state is unique in having two seasons of epidemics,
one during April to June and other during Octo
ber to December (Mishra ct al. 1984; Geevarghese
cl al, 1991). Outbreaks of JE of varying intensity
have been occurring in Mandya District since 1979
with a major outbreak in 1983. Entomological
studies were carried out in Mandya District from
April, 1983 to December. 1988 to study the vector
density and seasonal prevalence in relation to JE
epidemics. The results of preliminary studies car
ried out during the initial 4 months, ic. April-July
1983, has been already reported earlier (Mishra et
al, 1984). The present paper reports the results of
the studies carried out during the entire period
from 1983 to 1988.
MATERIALS AND METHODS
Description of the area
Mandya has a total area of about 4,961 km2
with a population of about 14.14 lakhs with an
average density of about 285 personsTcm2. It is
divided into two sub-divisions : Mandya subdivi
sion comprising Mandya, Maddur and Malavalli
taluks; and Pandavapura sub-division compri-
378
e •
W
smg Snrangapatna, Nagamangala. Pandavapua-
and Krishnarajpet taluks. The Mandya subdivision
is mostly irrigated by Vishweshwaraiah canal sy*
terns, from Krishnarajasagar reservoir on theffl®
ven river. Pandavapura sub-division was compara
tively dry during the initial stage of the study but—
was brought under irrigation recently via theeast=
bank canal from Hemavathi dam in Hassan Districts
Karnataka State. The average rainfall in the distrW"
is 691.2 mm. South-west (June to September)and=
north-east monsoons (October to December)™
share 37.9‘zo and 35.6% of the annual rainfal
respectively. The showers during the interventi^S
periods contribute 26.5% of the total rainfall. Ri#
and sugarcane are the major crops. Usually ?_
crops of paddy are cultivated, the first cropf^;_._
March to June and the second from AugustS
January. One of the largest wetland bird sanctuary
in the country is located at Ranganathittu in
rangapatna taluk. In addition, breeding placeSM
ardeid and other wetland birds are found in n1^
localities in the district.
-
Mosquito collections
Four villages under Mandya sub-divisioM|g
Hemmige, Madarahalli, Peehalli and
were selected for periodic mosquito coll#^jg|B
These localities had records of JE cases in
outbreaks. Regular fortnightly mosquito
!
were carried out around animal sheds an
Vol 25 No. 2 Jun«
I
MOSQUITO VECTORS OF J EV IN INDIA
5
j in the open during dusk hours with mouth
,ctheretors and with the help of torch lights. This
. ^’^r^nllection is considered superior quantitatvpeoi coi
.. .. , „
, .
well as qualitatively for monitoring the
( dvtly as vMion (Mitchel and Chen, 1973; Mahadev et
’ n0Pu^
1
et al, 1984). A total of 4 man
j \ 1978; Mishra
| Jur collections were made from each locality
*
/
I
j
...
C
T
D
4.^1
Fig I—Mosquito populations and JE cases.
RESULTS
I
in all 200,295 specimens representing 45 species
I
e obtained by 1,120 man hour collections, with
I aInan hour density (MPH) of 178.83. 98.29% of
I the K4''1 collection were represented by thirteen
I enPTK 4S follows: 1. Culex tritaeniorhynchus
I (20.54%); 2. Cx. fuscocephala (16.94%); 3. C.\
vishnui (16.48%); 4. Cx. gelidus (10.7(y/o); 5. Am^phelespediiaeniatus (10.51%); 6. Mansonui uniforms
(9.63%); 7. An. subpictus (4.33%.); 8. An vagus
I (3.92%); 9. Cx. pseudovishnui (2.53%); 10. Cx
quinquefasciatus (0.73%.); 11. An culicifacies
I (0.72%); 12. An. nigerrimus (0.64%.); 13. Aedes
II
2-------------
F eveiyf°rtnlght?
J
1
IX'1
1
1
I
tx-'f
V\
f
•
-
■
i ig 2
Seasonal prevalancc of some culicincs
fl
i
[ vexans (0.62%»).
r
•
Other species which constituted less than 0.5%
ofthe catch were: 1. An. barbirostris. 2. An. lessel[ latus, 3. An. aconitus, 4. An. pallidus, 5. An annulaf ris,6.An.fluviatilis, 7. An. minimus. 8. An varuna.
M 9. An. jamsii, 10. An. karwari, 11. An. stephensi.
I 12. Ae. linneaiopennis, 13. Ae. pseudomcdiofasciatus.
I 14. Ae. pipersalatus, 15. Ae. jamesi, 16. Ae. villaI
17 Ae. albopictus, 18. Ac. unilineatus. 19. Cx.
i
I
-0. Cx. whitmorei, 21. Cx. bitaeniorhynchus.
I 22. Cx. minutissimus, 23. Cx. malayi, 24. Cx. fus| fanus, 25. Cx. univittatus, 26. Cx. sitiens. 27. CoI WHlettidae crassipes, 28. Mimomyia luzonensis,
hybrida, 30. Armigeres subalbatus. 31. Ma.
f annubfera, 32. Uranotaenia recondita.
..
[ Seasonal prevalence
c
A
F4
r
«
'W
J
Fig 3—Seasonal prevalance of some anophelines.
(Fig 2). Similar pattern was also observed in certain
anophelines such as An. subpictus. An. culicifacies
and An. vagus (Fig 3). However, An. pediiaeniatus
and An. nigerrimus showed peaks later in May
and October. Ma. uniformis which breeds mainly
in puddles and ponds with aquatic vegetation was
found having a stable population throughout the
year with a peak in September month. The highest
prevalence of Cx. gelidus was observed in July.
■I
■
'■’W
'A
i F
mosclu^0 population in general showed
I
F^aks of density in a year, one durins Marchg: APnI and
and ianother during September, preceding
t
epidemic
(Fig 1). The same seasonal trend was
| ^rvedin
the mosquito catches of all the years
g ^Ptin 1983 during which the second peak was
I °kerved
in November instead of September. CuliBl
suc
h as
duun
as Cx.
^x- tritaeniorhynchus,
trnaeniornyncnus, Cx.
cx.
.i
*
Cx.
psuedovishnui
and Cx. fuscocephala
f>*edth<
above pattern in their seasonal activity
iI-V-
i^25N(°- 2 June 1994
Mosquito species occurring in peak densities
preceding the summer and winter epidemics were
different. Cx. vishnui (38.63%), Cx. tritaeniorhynchus (15.14%), Cx. fuscocephala (10.46%) and An.
subpictus (10.24%) occurred in peak densities dur
ing March whereas Cx. fuscocephala (38.38%),
Cx. tritaeniorhynchus (13.46%), Cx. vishnui
(13.85%) and An. subpictus (11.63%) occurred in
peak densities in September. Peak density of Cx.
379
I
-
-.7
-1 i
SOI THE AST ASIAN J TROP MID PUBLIC HEALTH
DISCUSSION
vishnui was in March, preceding by a month that
of Cx. triiaeniorhynchus.
The whole Mandya District was considered
be a dry area before the introduction of VishveJt
waraiah canal system in the early 1930s,
gave an irrigation coverage of approximately
of the total irrigated area in the district (Ra
1981). The network of canals has provided assured
irrigation resulting in large scale cultivation 1=
paddy and sugarcane. This has created vast expaiS
of water bodies for the breeding of mosquitos nf
the form of paddy-fields, tanks, seepage swam|n
numerous ground water pools, etc uhich appeaij
to have resulted in the increased incidence of
quito-borne diseases. Rao (1981) had already im
ported an increase in the incidence of malaria cases
in Mandya District when the canal system wS
Encephalitis cases in humans
A total of 539 cases were reported during the
period, the largest number of cases (233) were
recorded in 1983. Maddur (266 cases) was the
worst affected taluk followed by Mandya (177
cases) and Malavalli (65 cases) taluks. Nagamangala
(15 cases), Srirangapatna (5 cases), Pandavapura
(2 cases) and KR Pet (1 case) taluks reported
fewer cases (table 2). The incidence of JE cases
showed two peaks in a year, one during AprilJune and another during October-December, the
former having more cases. Each peak was generally
preceded by a spurt in the vector population (Fig
I
1).
Table 1
*
Frequency (%) of some predominant mosquito species in different years.
Species
Cx. triiaeniorhynchus
Cx. vishnui
Cx. pscudovishnui
Cx. fuscocephala
An. pcdilaeniatus
An. subpictus
Cx. gelidus
Total
1983
1984
1985
1986
1987
1988 j
15.65
16.09
3.66
10.59
' 14.94
8.43
22.29
14.31
2.72
16.7
12.48
3.20
8.75
24.14
13.81
23.96
15.66
19.32
1.49 j
19.06 j
8.36 |
15.72
21.62
16.15
2.98
18.84
11.69
2.35
5.36
40,494
41,994
40,742
21.60
6.43
21.93
1.68
18.54
4.93
2.85
13.68
10.98
10-95-i
29,835
24.646
22,581
1.59
4.95
3-"J
Table 2
I
Taluk-wise incidence of JE cases in Mandya District from 1983 to 1988.
Taluk
1983
1984
1985
1986
1987
1988
Total "21
Mandya
Maddur
86
117
22
5
1
5
10
5
3
1
37
67
20
32
18
266 J
14
16
11
27
1
2
2
3
Malavalli
< Ji
Nagamangala
Srirangapatna
Krishna raj Pet
Pandavapura
Other
Total
2
233
24
13
7
2
1
3
1
2
1
2
125
75
42
1771
65J
15
5J
1 s
8
40
539,
Vol 25No. 2-,une:1
380
mosqi no vi
< >1
JI \
IN INDIA
spells of JE epidemic coinciding with two peak
I
„ introduced. During the present study
I
-tn population showed two density peaks in
I
one during March-April and another durI ”ef’ntember preceding the JE epidemics and
I
with the seroconversions against JE virus
I ^sentinel pigs, reported earlier (Gecvarghese
I i111; 1091). An earlier entomological study earned
I
f re the JE activities were recorded in SnI
tna taluk in 1970-71 had also shown high
^Lce of mosquitos twice in a year, correswith two paddy crops (Soman. 1984).
isolations of JE virus were obtained during
^present study from five species, wz. C.r. mthe Lhync/ius Cx vishnui. Cx. gelidus. Cx. fuscopeditaema^ (Mourya e, al. 1989).
S ise speae's except An. peddaemarus have
i
i
L incriminated as the vectors of JE m other
JL
(Rosen. 1986). Cx. vishnui and Cx inmniorhynchus were collected in good numbers
throughout the epidemic seasons. Preponderance
■ of these two species during the course of the epiI demies has been found to be charactensuc of the JE
I affected areas in many countries mcludmg ndu
I (Rosen, 1986; NIV; 1980). Isolation of JE Horn
I Cx fuscocephala and Cx. gelidus which appear m
| | large numbers preceding and epidemic incriminates
I them as the vectors. These spcu.es may be playing
I an important role in the enzootic cycle which
I usually precedes the epidemic because the peak
I densities of these mosquitos precede the epidemic
I Krishnaraj Peth, Pandavapura, Srirangapalna and
I Nagamangala taluks showed a low incidence of
I JE cases. These taluks arc comparatively dry with
I none or partial irrigation systems and limite
paddv cultivation. It is obvious that the irriga
tion tern plays an important role in increasing
■ the mosquitogenic conditions and the resultant
increase in mosquito-borne diseases in the stud)
• ^as. The situations prevailing in the study area
| are comparable to that reported in Sri Lanka.
Queensland and Brazil, where increased activities
;
arboviruses and malaria were observed subse[ Quently to the introduction of irrigation systems,
i ftamasamy et al, 1992; Smith, 1970; Degalher ei
1989; Kay et al, 1990).
5
I
I
Entomological studies carried out in other JE
I affected areas in India such as North Arcot and
I- Madurai in Tamil Nadu, Bankura in West Bengal
| M Kolar in Karnataka, have shown only one
I
mosquito activity preceding the epidemic
f ^1V> 1980; Mani et al, 1991; NIV unpublished
|
Mandya is therefore unique in having tv»o
I
25 N,
Io. 2 June 1994
densities of the vector population.
z
■>
acknowledgements
ii
i
'1-^' |
The authors wish to thank Dr KM Pavri (tonner
Director) and Dr K Banerjee, Director, for their
encouragement during the study. The assistance
rendered bv the field staff of NIV field units at
Kolar is also gratefully acknowledged.
references
a
Degallier N. Travassos da Rosa APA. Herve JP. el al.
• * » in TucuModifications of arbovirus-ep^emiology
.
—
related
rui, Para. Brazilian Amazonia, rc-t" to
'■ the con*
a hydroelectric dam. Arbovirus Restruclion of
Austraha. Proc 5lh Symposium 1989:
search in /.
124 35.
(ieev trghese Ci. Shaikh. UH. George Jacob P. Bhat HR
Xnonng of Japanese encep^bt.sv.ruv acu^
uslllg demesne sentmel p.gs m Mandya d.stnut Un
dla) huhan J MeJ Res 1991.93: 140 .
Nanonal Hismutc of V.rology, Pune Japanese^eneephabus m India. Informat.on document. 1980
Kav BH. Barker-Hudson P. P.per RG. Stallman Nil
' Arbovirus disease and surveillance methodology
related to water resource development in Austraha.
»
Resour Deeel I9W; 6 : 95 103.
Mahadev PVM. Dhanda V. Gecvarghese G. el al Studies
"lhe mosquitoes of Bankura.Distncl
^a!.
!
I
i
I'1
fl
■
Adult populations. Indian J Med Res 1978. 68 .
248-63.
Mani TR. Mohan Rao CVR. Rajendran R DevcPu‘ra
M. Prasanna Y, Hanumaiah A. Surveillance o
panese encephalitis in v.llages near Madurau Tam.l
Nadu. India. Trans R Soc Trap Med Hy? 1991. 85 .
287-91.
Mishra AC George Jacob P. Ramanujam S. Bhat HR.
Pavri KM. Mosquito vectors of Japanese en«p > litis epidemic in Mandya district (India) C1983).
dian J Med Res 1984; 80 : 377-89.
Mitchel CJ. Chen PS. Entomological stud.es; on the vec■phalitfs. Bull WHO 1973; 49 :
tors of Japanese encej
247.
a DT Ilkal MA. Mishra AC, el al. Isolation of
Mourya
Japanese encephalitis virus from mosquitoes cob
lected in Karnataka State. India from>1985 to
■
Trans R Soc Trap Med Hyg 1989; 83 .: 550-2.
The Anophelines of India.
ICMR. New Delhi. 1981:
381
•
I
•U-fl
..-’.ft
■41
•■‘.1
' r? *
4
vjnmunity-based study of subclinical
Acoii
'Plic ^Civirus infections in children in an area of
te*5 fi
a tl
Voui
llinil Nadu, India, where Japanese encephalitis
wlendemic
if- iGajanana ,1 V. Thenmozhi,2 P. Philip Samuel,3 & R. Reuben4
W Ttfaracteristic feature of the epidemiology of Japanese encephalitis (JE) is the occurrence of a large
> ■
ciihclinical infections. The reporting of only overt cases underestim
of subclinical
underestimates the total level of virus
^^ission, a knowledge of which is essential for the evolution of control strategies. We carried out a
prospective serological study between 1989 and 1991 in a primary health centre in Tamil Nadu
JE IS endemic. Each year paired specimens, taken before and after the transmission season
1 cohort of schoolchildren aged 5-9 years, were tested for haemagglutination inhibition (HI) antiM titres in order to study seroconversion.
Ejte seroconversion rates in the successive years were 37.5, 42.1 and 25 percentage points, and in
of such seroconversions it was possible to establish a specific diagnosis. Seroconversion was
'Mutable predominantly to JE virus and minimally to West Nile virus. Relatively high dengue virus
miff occurred only in 1991. There were statistically significant differences in seroconversion rates
feiwn villages and this was related to variations in the ratio cattle:humans:pigs. Very high seroconJ-rwn rates occurred among children who were negative for HI antibodies before the transmission
iWon. HI antibodies declined to undetectable levels 6-8 months later in half the children who had
'^converted. The average net annual increase of 16.2 percentage points in seropositivity was nevermuch higher than values reported from other areas of endemicity. The overall incidence of
leases was 15 per 10 000 children aged 5-9 years, and the estimated ratio overt:inapparent infec> IT’*as
1 1:270.
fl
I
I ■’
t&duction
s
encephalitis (JE) is an important public
lem in ,south“east Asia, and its transmisto be increasing in several countries (/).
diSease was flrsl rePorted in 1955 (2).
^Uendy many epidemics have occurred in
the country. JE virus infects a large
ov SUSCePtible individuals but only a few
°f the disease. DifferRkbackc>VlrU jnce v^rus stains, host susceptiimmunity, and several other facSe variations in the incidence of the
^esearch in Medical Entomology, Post Box
Saroi'ni-1 treet, Chinna Chokkikulam, Madurai-
*SIiStant-
disease without affecting the total infection rates.
Therefore the current system of reporting only cases
of encephalitis does not reflect the total level of
transmission, measurement of which is an essential
prerequisite for planning control strategies.
Inapparent infection, resulting in the develop
ment of measurable antibodies to JE virus, can be
used to quantify seroconversion rates among suscep
tible groups during the transmission season. In India,
serological surveys have provided valuable data on
the point prevalence of antibodies against JE virus
and other flaviviruses.3 but information on inappar
ent infection rates and the ratio of inapparent to
apparent infections is inadequate. We therefore car
ried out a 3-year prospective serological study of a
cohon of primary-school children in an area in Tamil
Nadu where JE is endemic. At the same time we
monitored the JE virus infection status of sentinel
pigs in the study area.
Sprints should be sent to this author.
a Japanese encephalitis in India. Pune. National Institute of
Virology. 1980 (information document).
r9an'>a''on. 1995, 73 (2): 237-244
ۥ Work: Health Organization 1995
237
A. Gajanana et al.
were conducted before and after the JE transn|«
season as follows: in August and DecembefM
Aueust 1990 and January 1991. and AugusfoB
Materials and methods
and February 1992.
Blood specimens were transported on icejH
field laboratory for separation ot plasma, whiijM
then shipped on ice to Madura! and stored attjM
Study site
In 1981 an extensive eP£C™^
children was reported in the So . h A
of JE
Tamil Nadu, in which a ser0’";'C
(5). Subwas made for 61% of t e pa w
have been
sequently, many cases
October and Novcmreported each year, mamly >.Octolx at
her. coinciding with the P^M of £
monsoon. Nallur Primary Health G t
Aj
pending examination.
Serological tests
B
Tire haemagglutination inhibition (HI) test (IB
nerformed on microtitration plates on acetone^
ted. goose-erythrocyte-absorbed plasma. EachfB
men"was tested against JE. West Nile
den-me (DEN-2) virus antigens. Paired sped
were tested simultaneously and known positi<«
negative controls were included in each day’jW
The diagnostic criteria used were as follows:«
<1:10 Hl titre for all three vfi|
S2£SU?- n* P“M“ H“‘"h Scrv‘“Mosquito blood meal identification
sci ih inversion, pretransimssion season spec, J
negative and post-transnussmn season
positive, or both specimens positive withdP
fold or greater rise in litre in the post-tjf
piL meals have been desenbed previously U).
sion season specimen.
_ scroreversion. post-transmission1 seasonfl
prvtransmissiottil
men positive and next |
specimen negative;
wecifie virus infeetion.. monospecific re«
|4oadly react.ng. with Hl t.tres to
were al least four times greater than W
Seroconversion in sentinel pigs
Ten locally procured piglets bom during
nmv
transmission season ( anua .
Blood
others: and
unclassified, less than fourfold differ® J
bodies, if present, disappeared.
titres for more than one \irus.
Human infections
1
we Carr,Cj
««
villages in Angus, and So>en.he. W
u
the informed
Virus-specific IgM antibodies uere
leM-capture enzyme-linked tmmu
(ELISA) (6) using kits PrS2ld^
Institute of Virology. Pune. The
virus antigens supplied in the kits
each sample.
Statistical analysis
X <*«•
,h0,e in which ».«>one easeo
occurred since 1986. In all me .
laces, primary-school children, mai
Vi
kjs S
iln I
i.j.
x
P
vi|
, 5_7
SE2SH=
sfsegs
The precision level tor the serc^on'oftware f
determined using the £pi into
g
(Centers for Disease Control. Atlant
WHO, Geneva. Switzerland).
Results
Seroconversion in se ntinel pi9s
■ 95 176-6%a-v«
Of 124 animals examined
season. In indlV |j
during the transmission
l letinUl
V.'HO BU>
238
I
Subclinical flavivirus infections in Tamil Nadu, India
-^version rates were as folloxvs: 60-100%
|»seroconve,Q0^‘ in 1990 and 58_66c? in 1991.
75-100%
^1989, /<lus occurred in all the months when
tooconVerrSLried out. i.e., June-December, the peak
8*November (Fig- D- Of the 95 animals that
111 24 (25%) had HI antibodies to JE
42 (44%) had HI antibody titres
IE virus that were at least four times greater
titres against WN/DEN-2. JE virus infection
F
fore confirmed in 69% of the animals that
\erted; the remaining 29 animals (31% ) were
Etesified.
Fig. 2. Age distribution of human cases of encephalitis
recorded at Nallur Primary Health Centre, 1986-90.
r
30 p
100
25 k
-80
!S 20r'
No of cases
Cumuiat ve %
o15r
" J®
■
-60§
■5
,40E
| °
210-
* 'B
-20
5-
^tn cases of encephalitis
Ljn 1981 and 1990. a total of 229 patients with
Eohalitis were reported at the primarx health
Mt the numbers corresponding to the successixe
1^1 be’’"” as follows: 24. 5. 18, 11. 15. 49. 39. o.
J)ata for 1991 were inadequate and were
Before not included in the analysis. As shown in
about 99% of patients were under the age
MJ years and there was a distinct peak in the inci
See among 4-5-year-okls. The male:icmalc ratio
1:0.8, and 80% of cases occurred in Octobci
B November.
bwn seroepidemiology
|» exploratory study, blood specimens trom 79 '
[wen aged 3-14 years were examined lor Hi annMft to flaviviruses. and 271 (34.2% ) proved posiPgainst one or more antigens. Of these seroposipMildren, 221 (81.5%?) were positive for JE. 131
iplfor WN, and 112 (41.3% ) for DEN-2, alone
|iCombination. The age-specific prevalence of HI
F00108 showed a significant linear regression of
positivity on age (^v = 1.25 + 4.72v: r =
Bp?!
Monthly
• Cumulati’
!
1 C:
1
Sep
Oct
Months
Nov
Dec
•234 5 6 7 8 9 10 11 12 13 14 15 -15
■
Age (years)
WHO 94867
0.9159. P <0.005). 'I he value ol the regression coelI ic lent suggested that the annual increment in seroposili\H\ was about 5f». and on this basis it was
considered that a sample size ol 450 children would
be icquiied toi a precision ol ±2'7 in estimating this
inclement We therelore recruited about 1000 chil
dien loi the prospective study, in the expectation that
about 50'/ would drop out during the 3-year stud)
pci lod.
Oui assumption that the rale ol increase m
cohort positi\itx was about < per year proved to be
incorrect. T he precision lex els achieved, as calculat
ed from actual sample sizes and rates of increase,
varied from 2.9'r in the first year to 4% in the third,
when blood samples were obtained in onl) nine ol
the original 15 villages because of lack of coopera
tion (Table 1).
Among children from whom paired blood specimens
were taken in 1989. 15.8% possessed antibodies to
flaviviruses before and 53.3% after the transmission
season, an increase of 37.5 percentage points (Table
1). In 1990. 33.7T of children were positive before
and 75.8% after the transmission season, an increase
of 42.1 percentage points. Before the 1991 transmis
sion season. 48.2% of children were positive; after
this season. 73.2% were positive, an increase of 25
percentage points. Table 1 shows that in the non
transmission season, i.e.. the period between the
post-transmission survey and the following year's
pretransmission survey, there was a considerable
decline in seropositivity. (19.6 and 27.6 percentage
points, in 1990 and 1991. respectively). Thus, the net
annual increases in cohort positivity to Hl antibo
dies. as determined by comparison of pretransmis239
■ n
□
f wI
••
0
Prospective cohort study
—
"Onye^ions
in sentinel pigs in the area
y* by Nallur Primary Health Centre, by month.
S' *
0J
7 t
KOT;
;.■?lg;
■w
wH
m
■
I
"^I1mb
■'
■.
fa
NH
■ii
•W
fl
•, z;Sb
.;4|
' S"
J
ai
■
.SB
A. Gajanana et al.
Table V. Haemagglutination
children, 198^-91
1989
Preseason
Postseason
inhibition antibody against
flaviviruses among the study
___
No. examined
No. positive
1 102
1 102
174 (15.8)b
587 (53.3)
650
650
219 (33.7)
493 (75.8)
440
212 (48.2)
322 (73.2)
Increase
(percentage points)
Precision
level (%)a
37.5
2.9
IB
Net annual increase
in positivity
(percentage points)
17.9
1990
Preseason
Postseason
42.1
-
3.8
14.5
1991
Preseason
Postseason
440
25.0
I
4.0
a 95% confidence interval.
are percentages.
f Figures in parentheses
I
nHi-.l IF virus antibody titres at the end^H
X^mteason. Tabie 3^0^^
sion samples in
ilTpercJntage points in
tape pointsjn 1
or JR virus anll.
1990-91. The geometric
titrated in the post-transmission
bodies of all the sera
reveal differences between age
seasons did not
successive years, varying from
groups or between
1989 from I O.K to 14.5 m
12.3 to 17.1 in December 10.6 to 12.2 »n February
January' 1991. and from
1992.
rates were studied on pre- and
Seroconversion
samples. The rates among
post-transmission season
the transmission
children who were negative before
’460% "IblbX and 71.W. respectively,
h). The rates among
2
the transmission
children who were positive before
ro
-Wr ^7 8cc. and 7.4%.. respectively,
season were 32.//c.
.. , during
.
studied
the nontransSeroreversion rates were s.-■ ’ ce children. 49.7% seromission Period. Among positiv
7989-90: find 50.5% in 1990-91. The
reverted in I —
was inversely related to
probability of seroreversion
;C
li :■
'T
$
children "f,lh t1”
those with an initilllH
JJY w difference .as s.gnificant (M.
28.92./ <(> (15).
nerCeni i0e point increase>-----
and 3b m
However, statisBM
1W1; z; test, not signitic.ini) H -e^
from 23 to
m «
villages were fol**^
(f<().()5). In 1W1 only nmc
■df^
up; in five of 'bent seroposmsny .fn^^™
4-60 percentage pomtsf.
);
marginal increase (1 percent a I 4^
villages there was ai‘’ccreas'e U
q{^
villages, data on the blood-feechn
were available. In Erappavur. * here
J
cohort of scl:hOOl-
L/''
Table 2 Seroconversion and seroreversion
:
■
Year
I l
i.
n
V
Preseason Hlb antibody status:
Positive3
Negative8
No. seroconverting
n
No. seroconverting
i
240
158
51 (32.7)
1989
928
27 (27.8)
1990
330 (76.6)
97
431
164 (71.9)
10 (7.4)
228
135
1991
See text tor definitions.
» H7emaggrut.nat.on
inhibition.
Haemagglutmation i..h:t
c Figures in parentheses are percentages.
I
------ ---------
429 (46.2)c
|L
I
X
children covered by hwNallur
Seroconversion:8
/
Seroreversion^^. -1^;
No. serorevertM > jH
n
493
--- 1
245 (49.7)
141 (50-5)
279
|
I■
ran
WHO Bu»e'ir,0MJ
Subclinical flavivirus infections in Tamil Nadu, India
Seroreverston rate in relation to Japanese
□Jhaemagglutination inhibition anti-
it* virurthe study children
1989-91
^titre^gL
No. examined
g ^Hltitre^____
IttO
ltS0
’
OrMO____ ____
3^?7japanese
No. serorevemng
1991
1990
Total
142(29.6)* 134(37.5) 41(23.6)
317(31.4)
19(1.9)
163
(58.0)?
90
48
(53.3)
WN
18(3.8)
1(0.28)
0
27(15.5)
27(2.7)
38
DEN
0
94
(38.3)
0
75
21
(28.0)
222 (62.2) 106 (60.9)
648 (64)
32
572"
10
27?
(31.3)
(48.6)
* JE = Japanese encephalitis virus: WN = West Nile virus: and
371
211
(56.9)
DEN = dengue virus.
c Figures in parentheses are percentages.
201
67
(33.3)
Unclassified
.7
H
4 JI
1989
281
320 (66.7)
Total_________ 480
357
\74 Z12LL_Z
A
ill
-It
encephalitis virus-haemagglutmation mhi-
L,. was high relative to that of humans, the perSrfJpc
vectors feeding on cattle was greater
Ke Conversion rate was lower than tn two
EL villages where the cattle:humans ratio and the
racentage of feeding on cattle were relativelx lou
ra|e4). The humans:pigs ratio and the correspondtLfeeding rates were approximately the same in all
[ifK villages.
I Among those children who seroconverted. \ inis
pKificity was established in about a third, while the
ittremained unclassified (Table 5). JI-.-viriis-sjKi.il
»leroconversions occurred in 29.6f<. 37.5f<. and
OM over successive years; the corresponding \alTBforWN virus were 3.8%. 0.3%, and 0. DEN-24: Seroconversion rates, animal and human popuratios, and blood-feeding rates of Japanese
|j^*phalltls vectors in three villages covered by Nallur
Health Centre
II 4
Village:
Erappavur
Sepakkam Kodikkalam
26.5
32.5
48.5
1:12:25
1:4:20
1:4:29
'ersion in
^^eniorhynchus
on;
92.3
1.6
1.6
85.8
3.8
5.9
85.2
5.9
5.4
93.5
2.4
0.6
86.3
5.1
11.5
83.3
11.5
7.9
on:
’ **>989
Seroconversion
to:a
JE
S flares in parentheses are percentages.
s
j
Table 5. Virus-specific seroconvcrsions among school
children covered by Nallur Primary Health Centre,
and logo.
Vo173 1995
virus-specific seroconversions were seen only in
1991. when the\ accounted for 15.5r/r of seroconverters.
'■ ", ’were demonJE-virus-specific IgM antibodies
iron) chilstrated in 10 of 134 postseason sattniples
.
1989,
bin
in
none
oi the
dren v.ho seroconverted in
m
1990.
No
WNor
DEN
60 similar samples tested
detected
in
cither
year.
2-virus-specilic IgM was
-
T ~I
4' f
I
Apparent:inapparent infection ratio
In the first 2 years of the stud), seroconvcrsions
were mainly due to JE virus, and il was therefore
assumed for the purposes ol calculation that the post
transmission rise m positivity was due to Jl; virus
infections. On this basis we estimated the number
of cases of mapparent infection among the 10 4(X)
children aged 5-^ years who were covered by the
primary health centre and compared this with the
number of clinically diagnosed cases of encephalitis
in this age group, also presumably due mainly to
JE virus (Table 6): the ratio was 1:282 in 1989 and
1:257 in 1990. with an average of 14.9 cases per
10 000 population. No calculations were attempted for
1991. since DEN-2 virus was also active and data on
encephalitis cases were inadequate.
t.:
I
I
- I
Lb me
■i
ill
,4'
7 j
Discussion
The present study followed the temporal changes in
transmission rates over 3 years in an area where JE
was endemic, unlike previous investigations that
have covered only one transmission season (7-9).
Schoolchildren aged 5-9 years were selected so that
there would be an adequate number of susceptible
individuals and sufficient participation. Of the
10 400 children aged 5-9 years covered by the pnmarv health centre, the study sample size ranged
from 10% in 1989 to 4.2% in 1991. The Hl test has
several advantages making it particularly appropriate
241
is
hi
1
11ill
A. Gajanana et al.
w
Table 6: Apparent:inapparent Infection ratios for children aged 5-9 years in the area covered M
by Nallur Primary Health Centre (population 10 400), 1989-90
■3
1989
1990
w
O' '
Proportion
seroconverted
Estimated number of
inapparent
infections
Observed number
of cases
of encephalitis
Apparentinapparei
!nt
infection
ratio
0.38
0.42
3 952
4 368
14
17
1:282
1:257
w
"
'■
■
ib -
J--;
ij'-Xi-
■?
L
\
1^*.
for following the same cohort through more than one
transmission season. It is a sensitive and accurate
indicator of subclinical infection with JE virus in the
early postinfection phase (10). needing only a small
quantity of serum or plasma, easily obtainable from
fingerprick blood specimens. HI antibodies develop
faster than neutralizing antibodies and previously
infected persons may show measurable HI antibody
responses (7. //).
There was intense flavivirus activity in all 3
years, and the annual seasonal increase in HI sero
positivity ranged from 42.1 to 25 percentage points.
This was considered to be caused predominantly by
JE virus activity in 1989 and 1990, when the major
ity of the seroconversions diagnosed serologically
were attributable to this virus. The fact that only JEvirus-specific IgM antibodies were identified in a
sample of children provided supporting evidence;
furthermore, 69^ of the sentinel pigs in the area, all
primary responders, exhibited mainly monospecific
JE virus seroconversions during the season. WN
virus activity was either absent (in 1991) or present
al a low level (in 1989 and 1990), whereas in a post
epidemic survey in South Arcol District in 1982 the
prevalence of WN neutralizing antibodies was signif
icantly higher than that of JE (12). This indicates
shifting patterns of virus activity in the area. Thus
DEN-2 virus, which was not active in 1989 and
1990. exhibited relatively high activity in 1991.
when 16% of seroconversions in children were due
to it.
Previous studies in southern India have shown
that, among cases of serologically confirmed JE. HI
antibody titres began to fall about 3-4 months after
onset (13). In the present study, for about half the
children who suffered inapparent infections during
the transmission season HI antibody titres had
declined to undetectable levels 6-8 months later,
before the start of the next transmission season; also,
there was an inverse relationship between seroreversion rates and initial antibody titres. Similarly, in
Chiangmai Valley. Thailand. 21% of people who had
monospecific JE virus litres of 1:20 as a result of
subclinical infection had reverted to <1:20 within 12
months, while none of those with titres of >1:40
reverted (11). The high seroreversion rate in the
present study arose at least partly because only small
242
children were investigated. It is interestim
only other record of high seroreversion (fgS
among American servicemen in Korea, all om
were nonimmune before the transmission W
who lost detectable HI antibodies in 7 q 9
(/0).
‘
Notwithstanding the high seroreversion®
the net annual increases in Hl positivity (on
16.2 percentage points, were much higher thai?
reported for populations in other areas of endpajj
although the data ace not strictly comparable3
of differences in the study designs and t£^
groups observed. Among Japanese schoolci
aged (>-12 years, annual rates of increase of1
and 9— 10C7 (8) have been reported. In the Chid
Valle), annual increments were in thS
2.5-1 IT; in individual villages, while amonf
schoolchildren the increment was 4.3% (77) j*
undcr-40-ycar-olds in Sarawak the overall 3
was 6fr (/•/). However. 50% of a group ofi
tible American servicemen al an airbase ffl
developed antibodies in a single season (75).J
\ erv high seroconversion rates wereobsiffl
children who did not possess Hl antibodies!
the transmission season (46.2%. 76.6% and^
successive years). Each seroconversion was®
ably the result of al least one infective mosquti
The minimum probability of a child receSI
infective bite during the transmission seasoul
the range 0.47-0.77. Studies are in progress tol
virus in wild-caught vectors in order to3
whether such intense transmission can takej
Presumably the children who were already®
live at the beginning of the season received uW
number of infective bites, but they did not awi
a detectable response. In successive
increasing acquisition of immunity, the seiw
sion rate in the group of positive children det®
Statistically
significant
difference^
obserx ed between seroconversion rates in
villages. Al least, in part, these differences
sibly caused by variations in cattle popul^SM
a low seroconversion rate in children was ygS
with a high cattle:humans ratio. Vector
was approximately the same in these villag SI
for Research in Medical Entomology’’^
unpublished data).
CT
PS
WHO Bulletin
4o
■
Subclinical flavivirus infections in Tamil Nadu, India
|
overall incidence of JE cases in the Nallur
I ^Health Centre was 6.0 per 10 000 popula&*^heage gr0UP 1_1^ years, higher than in ChiW*0. yailey (Thailand) where ii was 3.8 per
for the same group (16). However, in Nallur
■I* ^cidence among 1-9-year-olds was strikingly
g^(94per 10 000) than that among 10-19-yearr(23Per l000°)’ whereas in Chiangmai Valley
incidence for the younger age group was lower
that for the older (3.1 and 4.6 per 10 000.
ELtively)- Th*s suggests that immunity develops
encephalites declarees. La notitication des seuls
cas declares sous-estime done le niveau general
de transmission du virus, dont la determination
quantitative est indispensable pour (’elaboration
de strategies de lutte. Nous avons realise une
enquete seroiogique prospective sur la penode
1989—1991, sur une cohorte de 1102 ecoliers
ages de 5 a 9 ans. selectionnes dans 15 villages
couverts par le centre de sante primaire de
Nallur. au Tamil Nadu, ou fencephalite japonaise
est endemique. Pour chaque enfant, on a determi
rFfo Nallur as a result of repeated exposure to
ne les titres d anticorps par inhibition de I’hemaFL, transmission. The ratio of overt:inapparent
glutmation (HI), a regard du virus de fencephalite
Sections (1:270) for children aged 5-9 years in
japonaise (JE). du virus West Nile (WN), et du
£ present study was similar to the ratios observed
virus de la dengue type 2 (DEN-2), avant et apres
|Chiangmai Valley (1:300) (11). Sarawak and
la saison de transmission. On a egalement etudie.
^(Province of Taiwan) (1:250-500) (11). Japan
paralieiement. les seroconversions chez des pores
KJo)(#), and West Bengal (1:400) (17).
sentmelles.
sent study has revealed that young chilChez fenfant. faugmentation post-saisonmere
hiniu. area of endemicity in southern India are
du pourcentage de positivite en HI etait. pour les
■vely at risk of developing JE during the transinistrois annees successives. de 37,5, 42,1 et 25
jiseason because of the high probability of recei\
points Chez environ un tiers des enfants ayant
|in infective mosquito bile. However, only about
opere une seroconversion, un diagnostic viral spe1270 will develop the disease and others will sulcifique a ete e:abli. La seroconversion etait due
lllatent infection resulting in high Hl seroconver
au virus JE chez 29,6%. 37,5% et 23,6% des
fa rates, followed by high rates ol seroreversion
enfants pour cnacune des trois annees. alors que
fang the nontransmission season, further studies
pour le virus WN les valeurs correspondantes
^required to elucidate the implications of these
etaient de 3.8% 0.3% et 0. Une activite du virus
Ifings for the development of protective immunit\
DEN 2 n a ete coservee qu’en 1991. au cours de
te population.
laquelle 15,5% des enfants etaient attemts. La
predominance du virus JE dans la region a ete
Stknowledgements
prouvee par la mise en evidence d'lgM anti-virus
JE
chez 7.5% oes enfants ayant opere une sero
very grateful to all the children who donated blood
conversion. alors qu’il n’a pas ete detecte d anti
the'r teachers as weH as the doctors
^^waftn workers of the Tamil Nadu Public Health
corps dinges contre les virus WN et DEN-2 Le
f°r their invaluab|e help. Dr P.S.S. Sundar
taux de seroconversion chez les pores etait de
and Head’ Department of Biostatistics.
76.7%.
dont 69.9% du fait du virus JE. Chez pres
KJ?1 Mescal College, Vellore. Tamil Nadu, is thanked
hek designing the study. The excellent technical
de la moitie des enfants ayant fait une serocon
version. les titres d'anticorps avaient baisse
BltaFni '
Sta^ °f
Centre for Research in
Eg* entomology, Madurai, and its field station at Vridjusqu a n etre plus decelables lors de nouvelles
hpIS grateful acknowledged. The study would
analyses effectuees 6 a 8 mois apres la saison de
Ktorus antfn poss*^,e without the generous donation of
transmission. II y avait. par consequent, une aug
■fcfythe Nat?08’.P.08'*'76 and negative sera, and ELISA
mentation annuelle nette moyenne du pourcenta
^fatwas in°n^ nstitute of Virology, Pune. Mr R. Ilange de seropositivite de 16,2 points dans la cohor
te. Les taux de seroconversion variaient de fagon
statistiquement significative d'un village a I'autre.
et dans trois d'entre eux, ces variations etaient
—------------------------------------------liees a des differences au niveau du rapport
bovin:homme:porc.
Waclinfl18 ,a cornmunaute des infections
Chez les enfants negatifs pour les anticorps
une^8flavivirus chez , enfant
en HI avant la sa son de transmission, des taux de
3^phali^9-°n du Tami1 Nadu (Inde) ou
seroconversion tres eleves ont ete observes
6 JaP°na*se est endemique
(46.5% a 76.6co). .montrant fexistence dune
intense transmission du virus dans la region.
iaponl^11'0^065 Par le virus de I'enceL’incidence des cas de JE diagnostiques d’apres
_
(JE) depassent de tres loin les
fexamen clinique etait de 14,9 pour 10 000 chez
® ss* s,u°' “ “ c-n“
I^fc'V0l73l995
243
-41
.%1|
a
iI
li
IJ
.-W
IF
SI
I
II
B
A. Gajanana et al.
les enfants de 5 a 9 ans. En supposant que la
plus grande partie de la seroconversion observee
au cours des deux premieres annees de 1’etude
etait due au virus JE, nous avons estime que le
rapport entre I’infection declaree et I’infection inapparente etait de 1:270.
II est necessaire de determiner plus avant la
signification des forts taux de seroconversion, qui
peuvent etre attribues a des taux eleves d’inocula
tion par les moustiques, en ce qui concerne I’acquisition d’une immunite protectrice.
References
1. Umenai T et al. Japanese encephalitis: current
world status. Bulletin of the World Health Organiza
tion, 1985, 63: 625-631.
2. Work TH, Shah KV. Serological diagnosis of Japa
nese B type encephalitis in North Arcot District of
Madras State, India, with epidemiological notes.
Indian journal of medical research, 1956, 10:
582-592.
3. Mohan Rao CVR et al. The 1981 epidemic of Tamil
Nadu and Pondicherry Indian journal of medical
research, 1988. 87: 417-526.
4 Reuben R et al. Mosquito blood feeding patterns as
a factor in the epidemiology of Japanese encephal
itis m southern India. American journal of tropical
medicine and hygiene. 1992. 46: 654-663.
5. Clarke DH, Casals J. Techniques for haemagglutination and haemagglutination-inhibition with arthro
pod-borne viruses. American journal of tropical med
icine and hygiene. 1958. 7: 561-573.
6. Burke DS, Nisalak A. Antibody capture immunoas
say detection of Japanese encephalitis virus immu
noglobulin M and G antibodies in cerebrospinal fluid.
Journal of clinical microbiology, 1982. 16: 1034-1042.
7. Scherer WF et al. Ecologic studies of Japanese
encephalitis virus in Japan. America
tropical medicine and hygiene, 195g T71 &
8. Southam CM. Serological studies of n W
Japan. II. Inapparent infections
encephalitis virus. Journal of infectin g
1956, 99: 163-168.
4O
9. Soe T et al. Study of vector, amplified
infection with Japanese encephalitis virJr ’
goon community. American journal of
1988, 128: 1376-1382.
10. Halstead SB, Russ B. Subclinicaj
encephalitis. II. Antibody responses of An3!
single exposure to JE virus. Americans
hygiene, 1962, 75: 202-211.
''
11. Grossman RA et al. Study of Japanese^
litis in Chiangmai Valley, Thailand. III.
epidemiology and inapparent infectioi^
journal of epidemiology, 1973, 98:133-1^
12. Rishbudh AR et al. Post-epidemic serO
vey of Japanese encephalitis virus anjS
South Arcot District, Tamil Nadu. Indiana
medical research, 1991, 93: 1-5.
13. Carey DE, Myers RM. Japanese encephafe
ies in Vellore, South India. Part III. Neil
activity of human survey sera. Indiana
medical research, 1968 , 56: 1330-1339.J
14 Simpson DIH et al. Japanese encepM
Sarawak. Virus isolation and serology h j
Dyak village. Transactions of the RoyalSi
Tropical Medicine and Hygiene, 1970,64:50
15. Halstead SB, Grosz CR. Subclinical
encephalitis. I. Infection of Americas
residence in Korea. American journal olM
1962, 75:190-201.
16. Grossman RA et al. Study of Japanese M
litis virus in Chiangmai Valley, Thailand.
mary and conclusions. American journaTgi
ology. 1974. 100: 69-76.
J
17. Bhattacharya KK. JE in West Bengal.
ings of the Workshop on Japanese eg
18-22 January 1988. Delhi, National Jg
Communicable Diseases, 1988 : 85-92. |||
I'
WHO BuHet'f1
244
I
I
s*
I
I-
£>15 )l
1
pew area ol work. In addition, representatives of fund,jjers and non-fundholders will need to cooperate and
?ve access to specialist advice.
'fhe Nottingham group may be succeeding because
?st of these criteria have been fulfilled, but even when
;se conditions are achieved some groups will find themives in difficulty. Clear agreement on the exact status of
group, its scope for action, and the limitations of its
wer are essential. In contrast with fundholding practices
d the newly emerging “multifunds,” non-fundholding
japs are only advisory to purchasing agencies. Clarity
>out the nature of this relation should help sustain
isory groups and prevent breakdown in the more
dcult debates about resources. Doctors will need to
erience early positive results from their work; suspicion
: consultation is purely cosmetic will produce early
’.lusionment. Anecdote and some reports suggest that
h disillusionment is not unusual.7
>uch groups face other problems. The Nottingham
up rightly recognises the difference between purchasing
planning, and ways must be found of restoring to evety
1th authority and health board a coherent planning
ction, involving not only non-fundholding groups but
fundholding practices and multifunds where they
iroups will be motivated by aspirations to guarantee
ity of access, but defining and proving inequity’ has
ed difficult. To ensure equity requires rigorous con:ing and, better, more accessible information than
n seems available to non-fundholders at present,
■.hermore, although the debate about inequity has
sed on the impact of fundholders’ purchasing de
ns, unpublished reports suggest that some non-fund-
s.
The climate ot continuing change > not conducive to the
establishment of satisfactory working practices and good
relations, and commissioning groups need a period of sta
bility. The function of a group may be undermined if the
agency is simultaneously exploring alternative arrange
ments to secure advice for general practitioners.
Finally, the leaders of general practitioner advisory’
groups will need to maintain the validity of their mandate,
and therefore of their advice, by frequently rechecking that
the arrangements they are negotiating are indeed in line
with colleagues’ views.
The internal market seems with us for the foreseeable
future,0 and some have argued that general practitioners
need to get involved or risk isolation.11 A period of rigorous
evaluation of all systems of purchasing remains essential,
but the Nottingham non-fundholders have described a
model that may merit wider application.
ROGER CHAPMAN
Chairman, Commissioning of Care Task Group,
Royal College of General Practitioners
The Surgery,
Leighton Buzzard LU7 TAR
1 Department of Health. Stansncs/or general medical praainc'V't tn England and Wales. London:
DoH. l«O4.
2 Keeler D The fundholding debate: should practices reconuder the decision not to fundhold?
BM7
3306:097-8.
3 General Medical Services Committee. Commissioning ca^c .'pn.'ru for GP>. London: BMA,
1002
4 Royal College of (icneral Practitioners. Council miniitei ref\-^ uie Commitnoning of Care Task
Cronf London: RCGP. 1904 (paper C./140 ;
5 Black DG. Hirchall AD. Tnmblc IMG N'on-fundholdir.g in Nottingham, a vision of the
future HMJ l‘»o.|.409:»30-2
() Birchall A National association ot non-fundholding groups :s needed. H.Mf I9O430S:47b.
7 Grafts JP. Williams) Purchasing tor all. an alternative to tundnoldmg H.MJ Ibo-I.IOH: VH-I
8 Modes V Empowering GPs us purchasers. HM1 lioj.ioa 1J2-4
*• luibour Pans Healsh
Th. health and Health of the
tn the 21 st century lamdon
laibour Pans'. 1004
10 Maxsscll R. tialekeepers and goalkeepers: general practise bJs-kc to purchasers Hr 7 Gen 1‘ract
1902.42:450-1.
ague in India
sons for public health everywhere
’ecades with no confirmed human plague in India,
authorities there are simultaneously responding to
"eaks of bubonic and pneumonic plague in rural and
n populations of the south central and southwestern
of Maharashtra and Gujurat. A major concern is the
•ld of disease by travellers from these epidemic foci.1
!dwide, public health authorities have been trying
event the introduction of pneumonic plague within
borders, requiring national disease surveillance and
ntine offices to operate on emergency schedules
g with a situation with which almost none has any first
experience.2
olic fascination, confusion, and incredulity have been
oy press reports. A mass exodus including hospital
nts and even staff themselves has occurred from the
ar e
outbreak of pneumonic plague despite
e ?rOnounceinents by the medical community that
readily treated with antibiotics. Assurances of
veness of public health measures have seemed
,riti
g*Ven tbe explosive spread of disease, which
^ubl’8 LVe ^een sl°w t0 con^rrn and explain. Doctors
lc ealth workers have quickly tried to educate
vOLUME 309
8 OCTOBER 1 094
themselves about a disease they had long considered in the
past tense. And everyone asks, “How could this happen?”
Plague is caused by infection with Yersinia pestis, a bac
terium carried by rodents and transmitted by fleas in parts of
Asia, Africa, and the Americas.2 India was one of the coun
tries most affected by the pandemic of plague that began in
the latter half of the 19th century, experiencing an estimated
12-5 million deaths during 1889-1950.4 In recent decades
plague in India and elsewhere has retreated to rural, natural
foci of infection involving mostly wild rodents and their
fleas, with occasional spill over to commensal hosts and
humans in villages and towns. Although a number of coun
tries regularly experience endemic plague, its pattern of
occurrence is mostly sporadic but with occasional limited
outbreaks. In the 1990s outbreaks of both bubonic and
pneumonic plague have occurred in Myanmar, Vietnam,
Tanzania, Zaire, Peru, and Madagascar.5 In 1992, 1758
cases with 198 deaths were reported to the World Health
Organisation.5 None of these outbreaks has aroused much
attention outside the country of occurrence. What is so
different about the current situation in India?
Most human plague is the bubonic form, which results
803
I
•J
r
A
\ i/'
T
from the bites of infected fleas; plague can also be transmit
ted direct to humans if they handle infected animals or
inhale infectious respiratory droplets from people with pneu
monic plague or aerosols from laboratory accidents. The
incubation period for plague ranges from one to seven- days,
and manifestations of the illness include rapid onset of fever,
chills, headache, malaise, myalgias, and prostration, often
with nausea and abdominal discomfort. In particular,
bubonic plague is characterised by painful swelling of lymph
nodes (buboes) in the inguinal, axillary, or cervical regions;
pneumonic plague is characterised by cough, dyspnoea, and
tenacious blood tinged sputum; and septicaemic plague may
result in fulminant Gram negative shock in the absence of
localised signs of infection.6
New cases of bubonic plague were recognised six weeks
ago by Indian health authorities in Beed district,
Maharashtra state, about 300 km east of Bombay. In a
chronolog}’ provided by WHO’s regional office for South
East Asia these cases followed reports of a flea nuisance and
large numbers of dead rats (rat falls) in affected
villages; the diagnosis was supported by positive results of
serum testing in the cases. By 26 September 80 suspected
cases had been reponed by 15 villages. Routine control mea
sures were instituted. On 22 September repons of cases of
suspected pneumonic plague were received from Surat, a
port city with a population of more than a million people,
many of them migrant workers, in Gujurat state, about 200
km north of Bombay. Significantly, no rat falls and no cases
of bubonic plague were reported.
This suggests a spillover from an epizootic cycle of plague
in wild rodents to commensal rodents in Maharashtra state,
resulting in primary cases of bubonic plague and secondary
cases of pneumonic plague and the subsequent importation
by travellers of pneumonic plague from the primary focus
into Surat. The course of the epidemic in India over the next
weeks is unclear; aggressive application of proved methods
of actively detecting and of containing cases, contact tracing,
and treatment as well as improved hygiene and environmen
tal sanitation are necessary to bring about its early control.
Quarantine
Plague is one of the three remaining diseases for which
people can be put in quarantine internationally.’ The
response of countries has ranged from complete termination
of air transport to and from India and the requirement of
proof of recent vaccination against plague for admittance of
anyone travelling from India to the institution of various
systems of heightened surveillance based on international
regulations/
In Britain recommendations were issued to all doctors,
describing the level of risk to travellers and measures to be
taken by those who travel to Gujurat state/ Britain, Canada,
and the United States instituted heightened disease sur
veillance by flight crews, notification of quarantine officers
by pilots of any suspect case before a plane lands, medical
examination of the suspect case before the disembarkation
of passengers and crew, surveillance of those passengers
potentially exposed to the suspect contagious person, pro
viding information to all passengers arriving on direct flights
from India advising that their risk of infection is likely to be
low, and notifying them to report to a doctor immediately
should they develop an illness with fever during the ensuing
week. People suspected of having plague have been
identified in aircraft landing in North America and Europe,
although no cases of plague have been confirmed in .
travellers at the time of writing.
Travellers to India and other countries in which plague
is endemic are considered to be at low risk of infection with
S<)4
Y pestis. To reduce risk,' travellers should avoid areas with
recently reported cases in humans. People who must tra i
to these areas should avoid rat infested areas, especial!
areas where dead rats have been observed; apply
repellants to ankles and legs and apply repellents and i/^'
ticides to clothing and outer bedding as directed bv^/
manufacturer; avoid handling dead or sick animals- and -f
the risk of exposure is high, take prophylactic antibiori “
For adults the preferred antibiotic for prophylaxis
tetracycline or doxycycline; for chUdren aged 8 or less it i *S
sulphonamide. Because desired antibody -responses 7
plague vaccine may require the administration of multinh
doses over several months these vaccines are not rec
mended for immediate protection during outbreaks
Doctors should be alert for evidence of plague
,
who have travelled to areas where plague is endemic and
who develop a febrile illness within seven days of leaving th
area. All patients suspected of having plague should be
placed in hospital in isolation, specimens should be obtained
from patients for laboratory diagnosis, chest roentgeno
graphy should be performed, and antibiotic treatment
should be started promptly. Streptomycin is the preferred
drug for treating plague, but gentamicin, tetracyclines, and
chloramphenicol are also effective?10 Prompt treatment can
reduce overall mortality from plague from 60%-100% to less
than 15%. Prophylactic antibiotic treatment should be given
to all people who have been close enough to a patient with
pneumonic plague to allow the transmission of infective
respiratory' droplets.
The unexpected and dramatic events that are playing
themselves out in India, and the public health responses
around the world to these events, highlight the continuing
threat of emerging and re-emerging infectious diseases
and the ill preparedness of the health community to meet
these threats.1114 The Centers for Disease Control and
Prevention in the United States is currently evaluating what
strategies will be most useful to meet these challenges; one
possibility’ is for doctors to participate in a sentinel network
for the surveillance of emerging infections.14
Outbreaks of plague in India remind us once again of the
need to maintain a core of skill in infectious diseases and the
public health infrastructure to detect, monitor, and combat
a wide range of disease agents, some new, some revisiting.
Plague may have retreated over the past decades, but it has
not gone awav.
D T DENNIS
Chief
Bacterial Zoonoses Branch Division of Vector-Borne Infectious
Diseases,
National Center for Infectious Diseases,
Centers for Disease Control and Prevention,
Fort Collins,
Colorado 80522,United States
1 Nandan G. Plague spreads in India but is “under control.” BMJ
„
2 Court C. Plague threatens prompt worldwide action. BMJ 1994;309.
’ 3tes in: Edwards
3 Bames AM. Surveillance and control of bubonic plague in the
Academy ?****’
MA, McDonnell U, eds. AmmaJ disease in re/anon w conservation. New
1982:237-70.
..
4 World Health Organisation. VTHO consultatwn on piaguc (New Deinh
1989). Genes-a: WHO, 1990.(WHO/MIM?PLA 90.1.)
jpp^S-lO.67
5 World Health Organisation. Human plague in 1992. WTdy Bpidem
(addendum).
.
«[nfta Dii 1987;1S .
6 Hull HF, Montes JM, Mann JM. Septicemic plague in New M
ll3-8,.0zo> Third annotated edsnon.
7 World Health Organisation. Internationa/ health regulations (1
•
‘
Geneva, WHO. 1983.
ad-4f39):lU
8 Plague in India. CDR Weekly Communicable Disease Report 19 <
diseases. Grand RaP
9 Poland JD. Plague. In: Hoepnch PD, Jordan MC, eds- Infe
Michigan: JD Lippincott, 1‘>89:1296-306.
Medical Economics D*
10 Physicians' desk reference. 48th cd. Montvale, New Jerse
t, ■ tbt
Production, 1004:1610-1.
. microbial threats to health "
11 l^derberg J, Shope RE, Oaks SC Jr, eds. Emerging
| Academy Press;
United States. Institute of Medicine, Washington, DG; diseases: who are we kidding12 Berkelman Rl_ Hughes JM. The conquest of infectious
Intern Med 1903;119:426-8.
1994;170:265-7
1 3 Hughes JM. La Montagne JR. Emerging infectious
.
r^. Infectious disc
14 Berkelman RI, Bryan RT, Osterholm MT, LcDuc J«, og
veillance: a crumbling foundation. Science 1994:264:368-
BMJ
VOLUME 309
V2r.
Mj
8 OCTOBER
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.M. 2>3 I
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119
1
INDIAN JOURNAL OF
PUBLIC HEALTH
i ■
Vol.XXXVIll, No.4
October - December 1994
PLAGUE
From 23rd September 1994 reports
began to appear in the news papers that
‘pneumonic plague’ in epidemic form had
hit the city of Surat. Gujarat state, India,
claiming several lives. A large number of
sople,
constituting one third of
population, also left the city. The rumour
and panic spread widely throughout the
country. According to a report, up to mid
October, throughout India (specially
Gujarat. Maharashtra. Rajasthan. West
Bengal. Delhi. Madhya Pradesh, Uttar
Pradesh. Bihar, Orissa, etc.) 6700 people
were admitted in the hospitals for the fear
of plague and 337 of them were supposedly
positive for the plague bacilli. In Surat
alone, about 1000 people were admitted
with 56 deaths presumably due to plague.
By that time many foreign countries
cancelled flights to India and examination
of travellers became compulsory, quaranle was imposed and plague-free certifi
cates were demanded during foreign
travels. The rumour and panic shattered
the prestige of the country throughout the
world. Even mother Teressa, the Nobel
prize winner had to wait at aero-plane in
Rome for several hours for examination.
West Bengal was also in the grip of the
panic. Spurious reports of at least three
deaths due to plague were published in the
news papers on 28.9.94.
The whole condition of the state of West
Bengal was examined by a team of experts
at a small delay and on solid scientific
ground it was pronounced clearly that no
plague bacilli were detected from any
patient died or admitted in the hospitals
with suspected diagnosis of plague. This
wFas done in the first week of October. Then
reports began to come from many states
that plague bacilli were also not found by
them. The panic and rumour which came
suddenly, also vanished within a very
short time.
The episode which started in Surat
raised many questions. Were they all
cases of plague? Some of the cases were
examined by the serological test. No rising
titre could be examined. No culture of
bacilli was possible. The features typical of
plague were not observed. The pattern did
not show actually the pattern of plague
infection, either bunonic or pneumonic.
No definite history of rat fall was there in
Surat. Who knows these might be the
cases of dengue haemorrhagic fever or
malaria or pneumonia?
Were proper
investigations carried out keeping all these
differential diagnosis in mind? How
definitely the concerned authorities
diagnosed those cases as the cases of
plague? Which methods were actually
followed? Different scientists expressed
different: opinions.
These should be
classified before finally saying it plague.
So a highpower committee should
immediately be
constituted taking
1
I
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i
Indian Journal of Public Health Vol.XXXVIII, No.4, October - December, 1994
120
knowledgeable personalities and experts
fr^ . the states who were involved in
investigation of the 'epidemic' and
thorough investigation must be carried
out to state clearly (1) Whether actually
plague occurred or not (2) How the
diagnosis of plague was done (3) in how
many cases and (4) from how many states
the cases occurred. Nature and extent of
plague should also be given in details.
(5) Who were the responsible persons for
raising the panic? In this regard role of
media and concerned doctors should be
analysed thoroughly. (6) Was there any
vested interest behind it? Needless to
mention that certain campaines did a lot of
business with certain antibiotics (7) was
there any deep rooted conspiracy to lower
down the prestige of our country?
Plague or no plague, it is sure that these
unhappy happenings dealt a severe blow
to the reliability and authenticity of the
existing health structure of our country.
A. K. Hati
c
i:
r.
A
ii
From :
Dr. A. S. Bose [PGT In MD(PSM)|
131/55. N.S. Ch. Bose Road
Calcutta • 700 040
To
The Editor
Indian Journal of Public Health
Calcutta
Re :
LETTERS TO THE EDITOR
12th Sept.. 1994.
The lUthors of the above paper have stated In their methods section that out of 76 pair-matched
control families. 29 fam Hies were re-classUled as case families and the data analysed In a case control fash
lTnbk’ "it is inappropriate to change the status of a control family to a case famUy and thus change the pairmatched study design. A bias will be Introduced as shown in the following hypothetical example
Let us say there were 20 case families and 20 control families. Let us a so assume that
famUles
matched case-control series Is to maintain the pairing In the
In case ol
controls (child developing diarrhoea) both the case
are the very palrf which will tend to show a spurious association on reclassification and the unllk. p
and ■V^ens. of 'rstu' table), which are used to measure the relative risk and presence of association
rmtrhed mlr analvsls. will tend to conceal any true association on reclassification.
1.
Mac Mahon B. Pugh T.F. Epidemiology principles and methods. Boston : Little Brown, an
company. 1970 : 275-77.
b
c
p
ii
Ghosh S. Sengupta PG et al. Maternal behaviour and feeding practices
as determinants of childhood diarrhoea : some observations among
rural Bcgalee mothers. Ind. J of Pub. Health 1994 ; 38 (2) : 77-80.
Sir.
where none exists.
A
o
o
Thanking you.
Yours truly.
Sd/- A.S. Bose
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A MONTHLY PUBLICATION
Volume 93, Number 1, January, 1995
Calcutta
99®.
EDITOR-INDRAJIT RAY, MD
■
—
!
r' editorial
iral I
•of I
Return of Plague
cal
India has a ‘natural foci’ and plague season which starts
from September and persists till May because in hot
summer wild rodents undergo aestivation and Eve in
closed burrows with stored food.
That the present epidemic has started in Maharashtra
where a devastating earthquake took place a year ago
and the observation of rat flea in those areas together
with bubonic plague there, in the month of September
does support the epidemiological clues of the present
outbreak. Further, there, man has no natural immunity
against plague and vaccine produced immunity lasts only
for 6 months. The fact that there have been more bubonic
plague cases in Maharashtra some of whom have gone
to Surat not being treated, causing pneumonic plague
reflects more evidences to support the hypothesis. But
surely the epidemic could have been prevented had there
been awareness of the disease among public and profes
sionals that the disease can never be eradicated and can
come back any day and also had there been regular sur
veillance and monitoring programme by the State and
Municipal health departments so as to alert the public
in time and to take appropriate preventive measures.
Human plague has been prevented as observed from
1967 onwards and is preventable if proper surveillance
is routinely done. This includes testing plague antibody
in sera of rats (100 trapping of rats) and measuring flea
index in domestic rats. If there is slight indication of
positivity in these measurements, preventive action like
destruction of commensal rats, extermination of Reas
ICC
' The recent outbreak of human plague after 28 years
f in India does prove the epidemiological features of the
’n-l disease known by the public health professionals for
ral| years. The conquest of plague so long echoed by some
int | has been only limited to control of human plague. Plague
ty. I in wild rodents has never been eliminated and the same
ro-1 holds true for future. It is therefore to be said that the
nd I disease was never eradicated from the country like
ra-
icr | smallpox.
The so called plague cycle is maintained in wild na
>n.
ture through rodent-rat flea-rodent. The wild rodent is
tai
py the reservoir of infection and rat flea is the insect or
iis vector responsible for transmission of the disease. There
be is always* a possibility that infected rat fleas may be
its forced to dwell on the domestic rats thereby infecting
them and subsequently infected fleas may bite human
nid ; being for alternate source of blood meal causing human
plague. Human plague is almost always preceded by
nt
domestic rat plague.
The epidemiology of an outbreak indicates that there
ti
nt I must be a reservoir of infection, an effective vector and
| a non-immunc population. The present outbreak of
ic K plague vividly supports the view and as long as such
re i situation persists there is always a chance of outbreak
I of the disease. Such chances are expected more where
e | there is ‘natural foci’ of plague, a plague season and
it
the area has witnessed a recent natural calamity specially
| like earthquake when domestic rodents are easily ini- I fccted from displaced wild rodents through rat Reas.
i
I
2
J INDIAN MED ASSOC, VOL 93, NO 1, JANUARY, 1995
through insecticides and sanitation at home and public
premises, if adopted, human plague may be prevented.
Even with stringent preventive measures, if cases with
plague occur, it can be arrested with available very ef
fective antibiotics namely, tetracyclines and the disease
can be controlled with prophylactic antibiotics to all the
contacts. In the present outbreak those who died was
due to not taking the treatment in time whether for
pneumonic or bubonic plague and no one should die if
treatment is instituted in time. The available statistics
indicate that there were only 56 deaths among 336
laboratory positive cases giving rise to mortality rate of
17% (some of the deaths were without treatment or not
timely treated) which is1 in sharp contrast with previous
epidemics where 50% deaths were observed in untreated
cases of bubonic and 100% in untreated cases of
.1
i
pneumonic plague.
The lesson learnt from the present outbreak is It
people and professionals were not aware of the fact H
plague has not been eradicated and may come backf
human population. It may also be understood now &
weaknesses of the surveillance and the moniton
programme of the health authorities. Health workers a
professionals need to be more vigilant and monitor li
plague status in rats regularly and make sure to contii
rat and fleas so that people can live in the States
safety and health.
Ex-Dean and Director-Professor and
S P MUKHOPADHYA
Head of the Department of Preventive and
Social Medicine and In-charge,
Disaster Management Centre,
All India Institute of Hygiene and Public
Health, Calcutta 700073.
'Continued from page 22]
agricultural work entails prolonged exposure to sun and rail
In tropical a>untries the climatological thermal load is consii
erable along with metabolic heal load due to strenuous agried
tural operations. When the air temperature exceeds the bod
temperature, it would increase the heat through connective het
gain and thus heat-induced disorders are found amongst th'
agricultural child labourers. Moreover, the children an
employed to operate modern powered agricultural machinert
and they become vulnerable to mechanical injuries. Children
are also employed in spreading fertilisers, pesticides and hei
vicides either by hand or with the help of indigenous equipmeis
without wearing personal protective devices and the children
Table 1 — Showing Health Effects in Different Working Places
become susceptible to the systemic toxic effects of such chemi
cals
causing skin diseases like dermatitis and neurological com
«
Health effects
Working place
plications through skin absorption such as local irritation ani
Nicotine poisoning causes nausea, headache, stimulation of the central nervous system resulting in hyper,
Bidi industry
■■ blackouts and muscle fatigue, loss of eye sight excitability, tremor and convulsion7. Parasitic infestations, spe
Acid bums and tuberculosis
Brass industry
Eye diseases, postural deformities and spinal cially intestinal helminthiasis are endemic in the tropics an(
Zori industry
may be contracted in the course of agricultural operations. Bite$
problems
Pdisoning from colouring agents, lung diseases of poisonous insects, snakes and injuries sustained while aij
Carpel indusiry
from fibre dust
lending farm animals, are the important causes of mortyidily
Household or shops Overwork, physical and sexual abuse, drug ad and mortality of the agricultural child workers.
for domestic workers diction, dependence often develops
CONCLUSION :
or shop boys
Thus health hazards are obviously of varying kinds and
the degree of hazards varies. In some instances, the hazard is
Agricultural child workers are also vulnerable to various
obvious and in others it is insidious. Though Article 24 of the’
types of injuries to their health. In general, higher susceptibility
Indian Constitution states clearly that children below 14 yean1
to ill-health arises because children are generally deputed to
will not be allowed in any hazardous employment, we are, ini
undertake adult jobs and their immatured vulnerable body and
reality, a long way from exercising the law to its fullest extent;
mind become more stressful than those of adult workers. Most
5Naidu US, Kapoor KR, eds — Child Labour and Health. Series 54.
*Pinto GJ — Child Labour, New Delhi : UNICEF, 1989 : 2-8.
Bombay : Tata Institute of Social Sciences, 1985 : 174-6.
^Banerjee SR — Child labour. J Indian Med Assoc 1991; 89 : 281-3.
6Burra N — Seminar on Child Labour. New Delhi : Malabika Singh,1.
JWorld Employment Programme Research Working Paper No 25.
1988 : 24-8.
Geneva : ILO publication, 1988 : 2-3.
^Banerjee SR — Agricultural child labour in West Bengal. Indian]
4Rama Rao R —• Child labour - a demographic perspective. Social
. Pediatr 1993; 30 : 1425-8.
i
Welfare 1986; 33 : 4-9.
aedded in the lung abd cause fibrosis of the tissue. This reduces
the vital Capacity of the lung. A patient of byssinosis is highly
susceptible to bronchitis and tuberculosis.
In the agate cutting and polishing industries, the children
are engaged in various operations like chipping, grinding and
drilling the agate stones. They are exposed to agate dust which
contains elements like iron, calcium, aluminium, copper, nickel,
chromium and silica. These cause lung diseases like tuber
culosis, pneumoconiosis, bronchitis and bronchial asthma.
Table i summatises the health effects of children in other
occupations.
‘
I
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THE LANCET
Plague in India
A
ti
I.'
s.
J'
Sir—The laudable sentiments of your Oct 15 editorial on
plague notwithstanding, your statement that “In a measles
epidemic year more children probably die in a month in
India than have died of plague during the past two
centuries” cannot be true. White1 recorded 10-5 million
deaths from plague in India in the 20 years from 1898 to
1918 alone. According to Clifford Gill,2 the highest plague
mortality was among children aged 10-15. Gill also reponed
that in the plague year of 1924, infant morality in many
parts of India more than doubled over the already enormous
baseline.
Nigel Paneth
Program in Epidemiology, Michigan State University, College of Human Medicine.
East Lansing, Ml 48824, USA
1
2
White FN. Twenty years of plague in India, with special reference to
the outbreak of 1917-1918. hid J Med Sci 1918; 6: 1.
Gill CA. The genesis of epidemics. London: Balliere, Tindall, Cox,
1928.
Editor's reply
Paneth makes a good point. We probably went too far in the
comparison between measles and plague deaths, although
we stand by the underlying point that, both in the present
context and in the past, measles is a far more important
cause of mortality. As the recent outbreak in India has
shown only too clearly, statistics about plague tend to be
highly unreliable. We question, therefore, the figure cited by
Paneth for plague deaths over 20 years towards the start of
this century, but there is certainly now no way of knowing
for sure.
In this unpromising situation it is more realistic to
consider true plague to have formed only a jpart of the high
mortality and to have perhaps been confined
Urable
:d ts,
to iavu
favourabh
urban habitats during hot summers. The acceptance of this
supposition would remove the difficulty of devising
unrealistic scenarios to equate plague with bubonic plague
and make a historical necessity out of a biological
improbability. Even in the city true plague was probably only
one contributor to high mortality. In my study of epidemic
years in London between 1540 and 1665, at least three
major patterns of deaths with time are evident3—only one of
which resembles plague or anotKer single disease causing a
steady incremental increase of deaths. Another has the
characteristics of enteric disease, a not unreasonable
proposition in view of the water supply, general hygiene, and
sewage disposal methods. Closely neighbouring parishes
showed considerable autonomy in not only mortality
patterns but also the timing of epidemics, and the data
suggest not a unity of disease (plague) but a complex pattern
of different diseases across the city—a view’ supported by the
extensive nature of plague “diagnosticks” that encompassed
buboes and most other causes of death as well.
That plague and bubonic plague might not have been the
same thing receives support from an early eighteenth century
source. Writing in 1721 Dr George Pye argued that plague
“differs from an epidemic disease, but in degree of violence
only; and consequently any epidemic sickness that rages with
more than ordinary violence and which occasions an
extraordinary mortality amongst mankind, may be and is
properly termed a pestilence, or the plague”.4
Graham Twigg
Biology Department. Royal Holloway and Bedford College. Egham.
Surrey TW20 OEX. UK
Gatacre WE. Report on the bubonic plague in Bombay. Bombay:
Tinies of India 1897: 52.
2 Twigg G. The Black Death: a biological reappraisal. London: Batsford,
1984: 75-112.
3 Twigg G. Plague in London: spatial and temporal aspects of mortality.
In: Champion JAI, ed. Epidemic disease in London. Centre for
.Metropolitan History, working papers series, no 1. University of
London: Institute of Historical Research, 1993: 1-17.
4 Pye G. A discourse of the plague; wherein Dr .Mead’s notions are
consider’d and refuted. London: J Darby, 1721: 3-4.
1
\n
/
k
it
Sir—Despite modern diagnostic techniques for identifying
plague, your correspondents (Nov 12, p 1359, and Dec 3,
p 1574) cast doubt on the diagnosis in 5559 suspected cases
in India during late 1994. Jacob John (Nov 12) compounds
the situation by questioning whether there was one coherent
clinical epidemic in Surat or whether the higher mortality
was caused by more than one disease.
This problem is not new. In 1897 in Bombay it was
recognised that in its early stages plague might be mistaken
for ague, remittent fever, syphilis, pneumonia, epilepsy,
cerebral apoplexy, uraemic coma, ulcer with inflammation of
lymph glands, diarrhoea, debility, marasmus, and phthisis.1
If, then, modem plague is so difficult to diagnose, it can
scarcely be expected that the retrospective diagnosis of
plague 600 years ago will be any easier, yet no such doubts
are entertained by most of those writing about either the
founeenth century’ Black Death or the numerous
occurrences of so-called plague that dominated the English
epidemic scene until the mid-seventeenth century. In the
absence of any data for case mortality, serology’, organism
culture, the rodent epizootic, fleas, and most other indices, a
retrospective diagnosis is confidently presented and as
stoutly defended.
This was a very cold epoch in northern Europe yet despite
the habitat restrictions imposed by climate, the two warmadapted vectors, the black rat and the rat flea, are supposed
to have been widely present even though their modem
distribution has been severely restricted.2 The Black Death
was active at all times of the year, in settlements of all sizes,
and in locations from coast to upland, and spread at rates far
exceeding those of known plague. In addition, overall
mortality rates were extraordinarily high—far greater than
any seen in modem plague.
258
Sir—We appreciate Bharadwaj and colleagues’ timely report
of melioidosis in Pune in Maharashtra state during October,
1994. We report melioidosis in a boy of 9 years who was a
resident of Trichur town in Kerala state.
He had longlasting fever, cervical lymphadenitis, and
hepatosplenomegaly with multiple ultrasound hypoechoic
lesions in spleen and liver. The illness had started in August,
1994, and gradually progressed until November when a
specific diagnosis was made and correct treatment started.
The boy had insulin-dependent diabetes mellitus. He had
always lived in the town of Trichur and had no particular
contact with rice fields or swampy soil. Bone-marrow and
lymph-node
biopsy
specimens
showed
epithelioid
granulomatous lesions, suggestive of tuberculosis, but
without acid-fast bacilli. However, the disease had
progressed during anti-tuberculosis therapy. We obtained a
non-fermenting gram-negative bacillus (NFGNB) from
aspirated material from one liver lesion. On the assumption
that this was a contaminant, an open-liver biopsy specimen
was taken, from which also a similar NFGNB was isolated.
Both organisms proved to be Pseudomonas pseudomallei. On
intravenous ceftazidime and oral co-trimoxazole therapies,
the boy recovered and went home.
The importance of this case history is that melioidosis has
been identified in Kerala for the first time. Melioidosis can
Vol 345 • Januan- 28. 1995
I
I
w
-Iw.
-^^=-11
T3)|s3
jilL NAiluNAL 5- i’i’-
4 P.n<Uv CS. TSc economic l^ot U.C
“
1
MJrrn O1,ort Ol,ord bn,verM,>
5
1995:12-21.
c. S. PANDAV
H. VISWANATHAN
D. P. HAXTON
International Council for Control of Iodine Defictency Disorder^
■
i
Plague
g-.-
I
diT^<’Si. since 1». tn. » re-ensesgenoe ...es
28 vears conforms to the cyclic nature of this disease—a pattern which has
I
"^X^S“Xee and npda.ing o< inm.s.^nse, Man,
little thev knew of plague’s epidemiology; clinicians had virtually deleteo it
*
for plague surveillance at the National Institute of Commumcable D.sease
i -teM
■
■
^"‘iten^SSuSn’S^aii,, in .be seeen, ou.Pseab was
restricted to 54 cases though several rather controversial statements have been
■••Artr• • •
a;
s c.
There have been three pandemics of plague and India was affected in all o
Since then plague in India has been essentially limited to its
.
■
'^“In^X^inSt— 'quaranifned Some countries slopped all
PiX. io andtomTndi. and u.bers insis.ed on evidence of v.ccn.l.on ag.ms.
plague A few stopped anyone from India entering their countries?
17026
1: ■
52
»
1HE N/XTIONAI. Ml.DICAl. JOURNAL OF INDIA
VOL. 8, NO. 2, 1995
According to the WHO, a case is labelled as ‘suspected plague’ if one of
the following conditions is met:
)-
1. Clinical symptoms are similar.
2. If a Gram-negative bipolar coccobacillus is identified.
A case is labelled as ‘presumptive plague’ if one or both of the following
conditions are met:
1. If the organism is immunofluorescence stain positive for the presence of
the Y. pestis Fl antigen, or if it is both immunofluorescence and Wayson/
Wright-Giemsa stain positive.
2. If a single serum sample is detected to have antibodies against the Fl
fraction of Y. pestis.
?-
fa
A case is ‘confirmed’ to be plague if one or both of the following conditions
are fulfilled:
1. In addition to Wayson/Wright-Giemsa and immunofluorescence positivity
the organism is grown in culture and is positive by both bacteriophage and
biochemical reactions.
2. Two serum samples, taken at appropriate times, demonstrate a fourfold
difference in end point titres of plague specific antibodies.
Human plague was first diagnosed in the Deed District of Maharashtra on
6 September 1994 on the basis of clinical, epidemiological and laboratory
evidence. Facilities for immunofluorescence staining for plague were not
available in India at the time of onset of the outbreak. So the NICD was able
to provide presumptive diagnoses on the basis of serological investigations.
While action to contain the disease in Beed was in progress, pneumonic
plague emerged in Surat, Gujarat on 10 September 1994, the population
panicked and an estimated 0.3-0.5 million left the city and fled to other parts
of the country. The entire health machinery of India and the rest of the world
started aggressive preventive and control measures.
In a serious disease such as pneumonic plague even with the presumptive
diagnosis alone institution of control measures assumes primary importance.
It would have been improper to wait for laboratory confirmation. Thus we
mobilized material resources and personnel for human case surveillance, active
case detection, case containment and treatment and contact tracing as well
as prophylaxis. This paid rich dividends and large scale mortality and morbidity
was avoided.
The increased flea density, rat fall, positive serology in rodents and the
nature of the human cases left little doubt about the occurrence of plague in
Beed. This was confirmed by the WHO international team who also carried
out serological studies. In Surat as well as in Delhi, a fourfold rise of antibodies
in paired serum samples of antibodies specific to the Fl antigen of Y. pestis
was observed in many samples. The WHO international team visited Delhi,
Surat and Beed and endorsed the evidence of recent plague infection in man
and animals in Beed and Surat. They and the WHO Director General also
complimented the Government of India for mobilizing resources to effectively
counter the outbreak.6
During an outbreak of pneumonic plague if half a million potential carriers
of the disease run away to different parts of the country, priorities have to
be set and precious resources as well as manpower have to be reorganized
effectively and deployed to prevent further spread. After the primary objective
of control was achieved efforts were made to purify and characterize the
culture isolates.
Apart from purely scientific issues, two more facets of the plague outbreak
have been fiercely debated. One of them is the role of the press in exaggerating
the facts and thus resulting in huge economic losses. The nation’s vernacular
and English newspapers as well as the international press and mass media
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THE NATIONAL MEDICAL JOURNAL OF INDIA
VOL. 8, NO. 2, 1995
53
exaggerated the extent of the outbreak. Though it may be justified to demand
that the press takes a rational and prudent view of such happenings, it must
also be kept in mind that whatever appears in the media is a reflection of the
thinking of the people. Panic was generated so effectively, because the very
word ‘plague’ seems to be associated with hundreds of deaths and because
both the public and medical profession were unaware of the changing
epidemiology of the disease. Safe and potent antimicrobial agents are now
available which have made plague easily treated.
Although a great deal of noise has been made about the tremendous
economic loss suffered because of the outbreak of plague, very few have
appreciated the role of health authorities in quickly and effectively containing
the disease, without which the loss might have been much greater. What is
more important is that the recent outbreak has exposed the major failings of
our public health system. We need better sanitation, a more effective disease
surveillance system and the institution of early warning mechanisms.
REFERENCES
1 Report. World Health Organization Weekly Epidemiological Record No. 2, 1994.
2 Court C. Plague threatens worldwide action. BMJ 1994;309:897.
3 Wu Lien-Teh, Chun JW II, Pollitzer R, Wu CY. Plague: A manual for medical public health workers.
Shanghai:National Quarantine Service, 1936.
4 World Health Organisations International Health Regulations. Third annotated edition. Geneva: World Health
Organization, 1983.
5 Dennis DT. Plague in India, BMJ 1994;309:893-4.
6 World Health Organization Press Release. SE/PR/1240. New Delhi: SEARO, WHO. 25 October 1994.
K. K. DATTA
National Institute of Communicable Diseases
New Delhi
l3-b
k‘n
‘on
for
nes
nd
Ss
'e$
;,y
itgd.
plague in India: A New Warning from an Old Nemesis
&
The main outstanding problem of the Black Death,
or indeed of the plague in any era, is ... what it is
r which provokes an epidemic of the air-borne pneumo
nic variant of the disease (1).
S
recent Institute of Medicine report, “Emerging Infcctions: Microbial Threats to Health in the United States"
(2), called attention to the complacency that has devel
oped regarding infectious diseases, highlighted the risk for
importation of diseases that develop in remote parts of
the world, and stressed the need to strengthen national
and international infectious disease surveillance. The re-rt cites the introduction of plague from other conti.. nts into Europe in the 14th century' and into North
America in the late 19th century. The recent epidemic of
plague in India highlights the concerns expressed in this
report.
In August 1994, an outbreak of bubonic plague was
reported from the Heed district, a known plague-enzootic
region (3) in Maharashtra Slate in western India. In laic
September, news came of an explosive epidemic of sus
pected primary pneumonic plague in the city of Surat in
neighboring Gujarat State (4). Hundreds of suspected
cases and more than 50 deaths were reported from Surat.
Press accounts described a mass exodus of hundreds of
thousands of persons from this industrialized port city of
nearly 2 million inhabitants (5). By early October, more
than 6300 suspected cases of plague had been reported
from 12 Indian states, including Delhi, but only a few
were considered laboratory' confirmed, primarily by un
validated serologic techniques (6).
Preliminary results of subsequent studies, done by the
,ndian government and an independent World Health
ganization team, provided presumptive evidence of bu
bonic plague cases and enzootic plague activity in Maha
rashtra State (Gage KL. Chu MC, Centers for Disease
Control and Prevention [CDCJ. Personal communication).
In Surat, reviews of clinical records and results of epide
miologic studies confirmed the reports of an outbreak
there of acute respirator}' illness characterized by fever,
COugh, hemoptysis, pulmonary infiltrates on radiographs,
and a high fatality rate in the early course of the outbreak
(Dennis DT, Orloski-Snider KA, CDC. Personal commu
nication). Although some patients studied had antibodies
to the plague bacillus, plague could not be established as
tbe cause of this outbreak in the absence of the confirmed
,solation of the causative agent. Although large numbers
of suspected cases of plague were reported from New
e*hi, Bombay, and Calcutta, no convincing evidence sugRested transmission in any city but Surat. As of 25 Octor 1994, 693 suspected cases of plague with unvalidated
erologic evidence of infection had been identified in six
’an states, and no new cases were being reported (7).
V V o c
x J R.1 C
15 January 1995
y
The initial reports of the outbreak caused considerable
international concern about the risk for exportation of
pneumonic plague from India. Official responses in vari
ous countries ranged from the enhancement of surveil
lance for ill travelers arriving at airports to the closure of
borders, the embargo of flights to and from India, and the
restriction of imports of Indian goods. Commerce be
tween the United Stales and India, however, remained
unrestricted during the epidemic. By enhancing surveil
lance at airports (8). providing written information about
plague to all air travelers arriving from abroad, and
promptly disseminating information on plague to clini
cians and health department personnel, health officials in
this country identified and evaluated for plague 13 trav
elers who had recently arrived from India with febrile
illnesses and other conditions (CDC. Unpublished data)
(7. 9. 10). Two persons were found to have malaria, one
had both dengue and malaria, and one had Salmonella
bacteremia. No tourists in India arc known to have con
tracted plague, and no patients with plague arc known to
have departed India during the crisis. The economic costs
of emergency response systems implemented internation
ally during this crisis undoubtedly were substantial, and
the resulting losses to the Indian tourism industry and
other industries are expected to be staggering (5).
Plague is caused by infection with Yersinia pcslis, a
gram-negative bacillus carried b\ rodents and their fleas
in parts of Asia. Africa, and the Americas (11. 12). Most
human plague is the bubonic form, transmitted by the
bites of infected fleas: however, persons can also acquire
plague by handling infected animals or by exposure to
respiratory droplets from persons or animals with pneu
monic plague. The incubation period for plague is 1 to 7
days (usually 2 to 4 days in primary pneumonic disease).
Manifestations of the illness include acute onset of fever,
chills, malaise, myalgias, and prostration, often with nau
sea. In particular, bubonic plague is characterized by
painfully swollen regional lymph nodes (buboes) draining
from the cutaneous inoculation site (11, 12). Pneumonic
plague is characterized by a productive cough, often with
hemoptysis, and pulmonary infiltrates. Septicemic plague
may result in endotoxic shock and disseminated intravas
cular coagulation without localized signs of infection.
Plague meningitis is a less common presentation, and
overlapping clinical presentations can occur.
Laboratory diagnosis of plague depends on cultural iso
lation of Y. pestis from tissues or body fluids, direct de
tection of antigens in tissues or fluids by fluorescent an
tibody staining, or detection of serum antibodies by
passive hemagglutination assays (11. 12). Visualization of
characteristic bipolar bacilli in Giemsa- or Waysonstained smears supports a diagnosis of suspected plague.
The organism grows slowly on bacteriologic agar media
• Annals of Internal Medicine • Volume 122 • Number 2
151
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and is infective for laboratory mice. Tests for plague are
highly reliable when done by laboratory staff experienced
with Y. pestis, but such expertise is usually limited to
selected reference laboratories. All patients with sus
pected plague should be hospitalized and isolated, with
precautions taken against transmission by respiratory
droplets until pneumonia is ruled out or until specific
antibiotic agents have been administered for at least 48
hours (12). Specimens should be obtained promptly for
laboratory diagnosis, chest roentgenograms should be
done, and specific antibiotic therapy should be promptly
initiated. Appropriate diagnostic specimens include spu
tum samples or tracheal aspirates for suspected cases of
pneumonic plague; bubo aspirates for bubonic cases; and
cerebrospinal fluid for meningitis cases. All specimens,
including blood, should be smeared and examined with a
Wayson or Giemsa stain, and all should be cultured.
Acute- and convalescent-phase serum specimens should
be obtained for antibody testing. Close communication
between clinicians and the diagnostic laboratory is essen
tial when a diagnosis of plague is being considered.
Streptomycin is the drug of choice for treating plague.
Tetracycline is also highly effective, and gentamicin can be
used when streptomycin is not readily available. Chloram
phenicol is the preferred treatment for plague meningitis
(11-14). Prompt treatment can reduce overall plague
mortality from 6()r/f to 1(K)G to less than 15%. Antibiotic
prophylaxis is indicated for persons who have had faceto-face contact or who have occupied a closed space with
a patient who has pneumonic plague. Recommended pro
phylactic drugs include tetracycline in adults and older
children and sulfonamides in children 8 years of age and
younger: chloramphenicol is also effective (14). Prophy
lactic therapy should be continued for the duration of the
potential exposure plus an additional 5 to 7 days. Routine
travel to plague-endemic countries presents a low risk for
infection with Y pestis-. therefore, antibiotic prophylaxis
for plague is rarely indicated for travelers to these coun
tries. Inactivated plague vaccine is apparently ineffective
against primary pneumonic plague (15), and direct evi
dence for its effectiveness against bubonic plague in hu
mans is unavailable (16). It is potentially useful for per
sons who anticipate a visit to an enzootic plague focus
(for example, field biologists studying plague), but it is not
recommended for immediate protection during epidemics
because a maximal antibody response requires the admin
istration of multiple doses over several months (11, 12).
In 1992 (the most recent year for which complete data
are available), human plague was reported in nine coun
tries (Brazil, China, Madagascar, Mongolia, Myanmar,
Peru, the United States, Vietnam, and Zaire) (17). In
addition, cases of bubonic plague have been recently re
ported in Malawi, Mozambique, and Zimbabwe. In India,
large plague epidemics occurred during the first half of
this century and resulted in millions of deaths; however,
until the recent epidemic, the last laboratory-confirmed
cases of human plague in India were reported in 1966
(17-19). Sporadic cases of human plague occur annually
in the western United States, particularly in rural and
suburban regions of New Mexico, Arizona, and Colorado
(20). after exposure to the infected fleas of wild rodents,
contact with infected animal carcasses, or (rarely) droplet
transmission from domestic cats with pneumonic plague.
152
15 January 1995
W~ i'i
The extensive yet focal geographic distribution of T.
is a reminder that when patients are evaluated for infec.
tious diseases, the importance of a detailed travel history
cannot be overemphasized.
The extreme measures taken by some persons and gov.
ernments in response to the initial recent reports from
India can largely be attributed to the widespread impres.
sion that pneumonic plague is not only deadly but also
highly contagious in all circumstances. The latter impres.
sion, however, is not supported by the evidence. Personto-person transmission of Y. pestis occurs by exposure to
respiratory' droplets from a patient with pneumonic
plague who is coughing at close range (probably within 2
meters) (12). Reported rates of secondary transmission of
pneumonic disease have varied widely in different plague
epidemics (15). In epidemics with reportedly high second
ary' transmission rates. ■ poverty and overcrowding in
households was the rule. In contrast, in the plague-en
demic areas of the western United States, no seconuary
plague cases resulting from person-to-person spread have
been reported since 1925 (12), despite the occurrence of
at least 37 pneumonic plague cases in the interim (includ
ing at least six primary pneumonic cases) (CDC. Unpub
lished data) (20). In many of these cases, diagnosis and
treatment were delayed, resulting in many potentially ex
posed persons with close contact and hundreds of persons
with casual contact who received delayed or no prophy
laxis. Thus, the risk for secondary' plague transmission in
the United Stales appears to be low. Clearly, the conta
giousness of pneumonic plague deserves further study
that includes a consideration of sociobehavioral. climatologic, and host-specific factors.
Important lessons can be learned from recent events in
India. When an outbreak of uncertain cause occurs, ap
propriate specimen collection and diagnostic testing for
potential causative agents is of paramount importance.
With several effective antibiotics widely available with
which to treat and prevent clinical plague, draconian mea
sures in response to repons of plague outbreaks arc un
necessary. Instead, a measured response based initially on
a rapid but thorough assessment by a multidisciplinary
team of experts (including clinicians, epidemiologists, en
tomologists. mammalogists. and microbiologists) is needed.
The capacity for such a response depends directly on the
quality of the public health infrastructure, including effec
tive surveillance and laboratory systems, epidemiologic
response capability', and vector and vertebrate host con
trol programs (21). Clinicians play an increasingly impor
tant role in recognizing illnesses and syndromes that re
quire a public health response and alerting health
departments to the need for prompt investigation (22).
Rational responses to future international public health
crises depend on improving linkages between clinicians
and public health professionals in all countries.
Although plague is of obvious historic importance (1)
and continues to be a global threat, little research is
currently being done on the subject. In many countries,
including the United States, few clinicians, scientists, or
laboratory or public health personnel are plague experts.
In all plague-endemic countries, cost-efficient animalbased serosurveillance programs are needed to define and
track the geographic distribution of Y. pestis, and exten
sive ecologic studies are needed to define and control
• Annals of Internal Medicine • Volume 122 • Number 2
..
. ^.JLUS
L-<V-3
otic and epizootic transmission cycles that put huenZ° atZrisk (23). The pathogenesis of plague and deternts of the virulence of Y. peslis should be studied
using the most up-to-date laboratory methods. The
aIie ntja| for the emergence of resistant strains of T pcstis
^l^ted to widespread antibiotic use during pneumonic
ri oue epidemics should be studied. Simpler and faster
? Moratory tests for plague are needed, and these should
h made available for use by local or regional laboratories
^developine countries in which plague is enzootic.
111 Largely because of the efficiency’ of modern air travel,
irrobiai pathogens have shown an ever-increasing disre^ect for international borders (24). With the current
decrease in political and trade barriers worldwide, this
trend will certainly continue. Thus, it is imperative that
the United States maintain multidisciplinary expertise in.
and that clinicians remain alert for. “exotic intectious
diseases, including tropical diseases. The recent events in
India underscore the need for expanding expertise and
opportunities for training in arthropod-borne intectious
diseases in this country and internationally (25) and lor
strengthening clinical, scientific, laboratory, and public
expertise in microbial diseases that arc rarely reche"
J in the United States. The CDC has developed a
0g‘
plan to address these critical emerging infectious disease
issues in collaboration with partners in state and local
health departments, academia, clinical medicine, clinical
laboratories, and international organizations (2(0. 1 he re
cent platzuc experience in India provides a clear example
of the hiuh price of ignoring global microbial threats (_7).
Grant L. Campbell, Ml). PhD
Centers for Disease Control and Prevention
Fort Collins. CO 80522
References
I Ziegler P. The Black Death. New York: Harper
Row; 1969:28.
■' Lederberg J. Shope RE. Oaks SC. Emerging Infections: Microbia
Threats to Health in the United States. Washington. D.C.: National
Academv Press; 1992.
-mu
3 Sant MV. Nimbkar YS. Renapurkar DM. Is plague lurkingMaha
rashtra" A survey in Bhir district. Indian J Med Sa. 19/.;26:480-4.
f„.- Disease Control and Prevention. Human plague---- India.
4. Centers for
1994. MMWR Morb Mortal Wkly Rep. 1994;43:689-91.
5 Fries* K. Mahurka L’. Rattanani L, Kattyar A, Rai S. The plague
peril. .Are vou at risk? India Today. 15 October 1994.
6. World Health Organization, Regional Office for Europe. Plague in
India. Communicable Disease Report (CD News). Issue 5; 11 October
I
1994.
7 Centers for Disease Control and Prevention. Update: human plague
India. 1994. MMWR Morb Mortal Wkly Rep. 1994;43:761-2.
8. World Health Organization. International Health Reguhuons (1969).
3rd annotated ed. Geneva: World Health Organization; 1983:26-9
9 Centers for Disease Control and Prevention. Update: human plague
India. 1994. MMWR Morb Mortal Wkly Rep. 1994:43:7^2-3.
10 Centers for Disease Control and Prevention. Detection of notifiable
diseases through surveillance for imported plague-New York Sep
tember-October 1994. MMWR Morb Mortal Wkly Rep• 1^4*43:805-7II Butler T. Yersinia species (including plague). In: Mandell GL. Douglas
RG. Bennett JE. eds. Principles and Practice of Infectious Diseases.
Neu York: Churchill Livingstone; 1995:2070-8.
12 Craven RB. Plague. In. Hoeprich PD. Jordan MC. Ronald AR eds.
Infectious Diseases. A Treatise of Infectious Processes. 3th ed. Phil
adelphia: J.B. Lippincott Company; 1994:1302-12.
13. Crook LI). Tempest B. Plague. A clinical review of 27 cases. Arch
14.
*' r ,
b. V I
A
f•
4'
Intern Med. 1992;152:1253-6.
.
Tancik CA. Palmer DL. Plague: Bubonic plague, the Black Death In.
( onr. RB. ed. Current Diagnosis. Philadelphia: W.B. Saunders,
llv
IS Burmmter RW, Tigertt WD, Overholt EL. Laboratory-acquired pneumonu plague. Report of a case and review of previous cases. Ann
Inter” Xted 19(>2;56:7K9-K(M).
K, Cavanaugh DC . Elislierg BU Llewellyn CH. Marshall JD Jr Rust JH
Jr et al Plague immunization. V. Indirect evidence lor the efficacy of
place, saccme. J Infect Dis. 1974;129(Suppl):S37-4U
World Health Organization. Human plague in 1W- Wkly Epidemiol
17
Rec l‘M4;2:8-l()
.. Epidemiology and incidence of plague in the world. 195KIS. Akio AK.
Health Organ. 1982;60:165-9.
7V. Bull World
V
I') World Health Organization. WHO C onsultation on plague New
Dclh; India. II to 15 Septcmlvr 1989. Geneva World Health Orga-
f I
11
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n,/'Uh’n '<m7J ML Quan TJ. Barnes AM. Reported
2(1 Craven RB, Maupin (JO. Beard
human plague infections m the United States. 1970-IWl. J
case' ot I
Med Entomol. |993:3(I;758-6I.
21. Bcrkelman RU Bryan RT. Ostcrholm MT. LeDuc ^. Hughes JMIntectious disease surveillance: a crumbling foundation. Science.
James M. Hughes. MD
Centers for Disease Control and Prevention
Atlanta. GA 30333
Requests for Reprints: Grant L. Campbell. MD. PhD. Div.s.on of V ectorBorne Infectious Diseases. Centers for Disease Control and Prevention.
P.O. Box 2087. Fort Collins. CO 80522-2087.
Current Author Addresses: Dr. Campbell: Centers for Disease C ontrol and
Pr- ntion, P.O. Box 2087. Fort Collins. CO 80522-2087.
I
jghes: Centers for Disease Control and Prevention. Mailstop ClAtlanta, GA 30333.
I
• Wa
22. Berkelman RL- Emerging infectious diseases in the United States.
23 BamJ AM^Su^eillance -nJcontrol of bubonic plague in the Unhed
State'. In: Edwards MA. McDonnell U. eds. •An,ni^D,S^.^7R70
iauon to Animal Conservation. New York: Academic Press W8-- —
24. Berketman RL. Hughes JM. The conquest of ‘nfecuous d.seases.
are we kidding [Editorial]? Ann Intern Med.
. ,,
25 Institute of Medicine. The U.S. Capacity to Address Tropica! Infec
tious Disease Problems. Washington. D.C.: National Academy Press.
2b. Centers for Disease Control and Prevention. Adding emerging
infectious disease threats: a prevention strategy for the Unites States.
Atlanta- Centers for Disease Control and Prevention; 1994.
27. dX dT Plague in India. Lessons for public health everywhere.
BMJ. 1994;309:893-4.
^nn Intern Med. 1995;122:151-153.
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• Annals of Internal Medicine . Volume 122 • Number?
153
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PC-SPIRS 3.30
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(R>
1/95-8/95
MEDLINE (R) 1/95-8/95 usage IE subject to the terms and conditions of the
Subscription and License Aqreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by Internationa1 Convention.
1 of 16
TI: Field trial of an ecological approach for the control of Phlebotomus
arqentipes using mud & lime plaster.
AU: Kumar-V; Kesari-SK: Sinha-NK; Palit-A; Ranjan-A; Kishore-K; Saran-R; Kar-SK
AD: Rajendra Memorial Research Institute of Medical Sciences, Patna.
SO: Indian-J-Med-Res. 1995 Apr; 101: 154-6
AB: A pilot study for the control of Ph. arqentipes, a known vector of
ka1a-azar m India, was carried out using an ecological approach. Of the 15
houses selected for the study 10, including the cattle sheds and latrines, were
plastered with a mixture of mud and lime, up to a height of 1 . z.2 ni taking care
to seal all cracks and crevices. The remaining five houses were left
»
’nplastered and were considered as control areas. The pre^trj^tj^^^ and
/Ost—treatment resting densities of the sandfly were monitored both in trE*ated
and untreated houses. A sudden drop in the sandfly density was noticed in the
treated houses, whereas there was no significant reduction in the check houses,
suggesting an effective control.
2 of 16
TI: Endemic kala-azar in eastern Sudan: post-kala-azar dermal 1eishmaniasis.
AU: Zijlstra-EE; el-Hassan-AM: Ismael-A
AD: Department of Infectious Diseases, Tropical Medicine and AIDS. Aoadornio
Medical Center, University of Amsterdam <• The? Netherlands,
SO: Am—J-Trop-Med-Hyg. 1995 Apr; 52(4): 299—305
AB: In a longitudinal study between 1991 and 1993 in an endemic area in eastern
Sudan j, 85 cases of kala-azar (visceral leishmaniasis) were diagnosed, of whom
48 (567.) developed post—kala-azar dermal leishmaniasis (PKDL). Another four
cases of PKDL had no clinical history of kala-azar. In children, PKDL was more
frequent in the very young: seven of nine ka 1 a—az ar cases (787.) in the group
0-1 years of age and 13 of 16 (817.) in the group 2-3 years of age developed
PKDL. On the average, PKDL occurred 56 days (mean; range 0-180) after the end
of treatment of kala-azar. To assess the severity of PKDL, a classification was
developed using three grades of severity based on differences in density and
distribution of lesions. In young children, PKDL was more severe. Incomplete
reatment of kala-azar may be important in the pathogenesis of PKDL. Thirty-one
patients were followed-up for at least six months; of these, 20 were not
treated (17 healed, two improved, and in one, the condition was unchanged),
three healed after incomplete treatment with sodium stibogluconate, and eight
were cured after trea_tnient
tr^eatment but
but. two required two courses. Con si (..lei' able morbidity
was caused by PKDL and"should
and should be taken into consideration in- the management and
follow-up of kala-azar patients, The high incidence of PKDL may have important
implications in transmission.
3 of 16
£Studies on the effect of deltamethrin bath treatment of hamsters infected
with Leishmania donovani for interrupting kala-azar transmission J
AU: Jin-C: Xiong-G; Hong-Y: Su-Z
ADs Institute of Parasitic Diseases, Chinese Academy of Preventive Medicine,
Shanghai.
SO: Chung-Kuo-Chi-Sheng-Chung-Hsueh-Yu-Chi-Sheng-Chung-Ping-Tsa-Chih. 1994 ;
12(4): 300-2
AB: Phlebotomus chinensis were fed respectively on two groups of Lricetulus
barabensis infected with Leishmania donovani, of which one group had received
deltamethrin bath and the other was not treated with insecticide bath. The
TI :
.
results showed that all the sandflies in the former group died within 24 hours,
while those in the latter qroup had a high survival rate. Among the 16u
sandflies examined. 114 (69.17.) became infected. The promastigotes not only
developed well in the midgut, but also invaded esophagus, pharynx and
proboscis. In the control group, the mortality of sandflies in 24 hours was
5.17. (3/59). According to the data obtained in the present study, the authors
consider that insecticide bath treatment of infected domestic dogs in endemic
villages could be used for interrupting kala-azar transmission.
4 of 16
TI; Indian kala-azar caused by Leishmania tropica.
Jaf-fe—CL; Gupta~AK; Sharma MC; Sinha—SF ;
AU: Sacks-DL; Kenney-RT; Kreutzer-RD;
I
Neva-FA; Saran-R
AD: Laboratory of Parasitic Diseases, National Institutes o-f Allergy and
Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20992,
USA.
SO: Lancet. 1995 Apr 15; 345(8955): 959-61
AB: Kala-azar, or visceral leishmaniasis, in India is generally assumed to be a
result of infection with Leishmania donovani. 15 parasite isolates collected
over the past 10 years from patients with classical disease were typed by
□noclonal antibodies, isoenzymes, and kDNA analysis. 4 were shown to be L
tropica, a species historically associated with cutaneous disease and more
recently a mild "visceralising" disease from the Desert Storm experience. The
results confirm that L tropica is a co-endemic agent of visceral leishmaniasis
in India, and may shed light on the rising frequency of therapeutic
unresponsiveness to sodium antimony gluconate, which complicates tre^lXffl^KLk ®
this lethal disease.
5 of 16
TI: Treatment of atypical leishmaniasis with interferon gamma resulting in
progression of Kaposi's sarcoma in an AIDS patient.
AU: Albrecht-H; Stel1brink-HJ; Gross-G; Berg-B: Helmchen-U; Mensing-H
AD: Medizinische Kernklinik und F'oliklinik, Universitatskrankenhaus Eppendorf,
Hamburg, Germany.
SO: Clin-Investig. 1994 Dec; 72(12): 1041-7
___
AB: Visceral leishmaniasis (ka1 a—az
ar) affecting HIV-infected patient is being
reported in increasing frequency, A 40-year-old German bisexual patient with
is described who presented with Kaposi's sarcoma, epigastric
full-blown AIDS -----------pain, diarrhea, and weight loss but without fever. Leishmania amastigotes were
initially found in biopsies from stomach,•duodenum, and a cutaneous Kaposi's
-arcoma lesion but were later also recovered from bone marrow and lymph node.
ie patient received three courses of a combination of pentavalent antimony and
interferon-gamma. In addition to the common side effects such as fever,
thrombocytopenia, and elevated amylase and lipase, a vivid progression of the
Kaposi's sarcoma was noted. Tumor progression was temporally closely associated
with treatment with interferon-gamma. Because this phenomenon has also been
observed in other patients, we advise caution when using interferon-gamma in
patients with Kaposi's sarcoma.
6 .o f 16
TI: Immunochemotherapy for a systemic intrace 1lu1 ar infection: accelerated
response using interferon-gamma in visceral leishmaniasis.
AU: Sundar-S; Rosenkaimer-F; Lesser-ML; Murray-HW
AD: Institute of Medical Sciences, Banaras Hindu University, Varanasi, I n d i a SO: J-Infect-Dis. 1995 Apr; 171(4): 992-6
AB: To determine if cytokine immunotherapy accelerates the response to
conventional treatment in visceral leishmaniasis (kala-azar). previously
untreated Indian patients were given antimony for 30 days (n = 15) or antimony
plus in ter f eron-gamma (IFN—gamma; n — 16). After 10 days, 10 (6^->Z) of 16
(77.) of 15 randomized to
patients treated with antimony plus IFN—gamma versus 1 (77)
.005). On day 20, 14
antimony alone were considered cured of parasites (P < .005).
'
'■ j ' r "•
(93*/.) of 15 versus 6 (407.) of 15 patients, respectively, were apparent clinical
cures (P < .006), and treatment was discontinued early in the 14 IFN-gamma
treated responders. Day 30 apparent cure rates (1007. vs. 737.) and 6-month
ultimate cure responses (877. vs. 607) were higher in IFN—gamma—treated patients
but not statistically different from controls (P > .05). All 13
IFN-gamma-treated subjects who were cured (12 of whom received therapy for 20
days) have remained healthy with follow-up of 14-24 months (mean, 18.9). These
results indicate that IFN-gamma successfully accelerates the parasitologic and
clinical response to antimony treatment, an effect that should permit,
shortening the duration of conventional therapy in previously untreated
kala-azar.
7 of 16
TI: Correction of serum electrolyte imbalance prevents cardiac arrhythmia
during amphotericin B administration,
AUs Thakur-CF
SO: Nat1-Med-J-India. 1995 Jan-Feb: 8(1): 13-4
AB: Arrhythmias and cardiac arrest have been reported during amphotericin B
administration but no effective technique has been described to prevent them, I
saw two patients with kala-azar resistant to sodium stibogluconate who
developed cardiac arrest after amphotericin infusion (in spite of tolerating a
test dose). Both had low levels of serum sodium, potassium and calcium. After
these were corrected the amphotericin B was restarted and the course of
treatment completed successfully. I suggest that prior to giving amphotericin B
to patients with resistant kala-azar their electrolyte imbalance should be
correc ted.
8 o-f 16
TI: Diagnosis and treatment of ka1a-azar.
AU: Chandra-J: Patwari-AK
AD: Department of Pediatrics, Lady Hardinge Medical College and Associated,
Katawati Saran Children's Hospital, New Delhi.
SO: Indian-Pediatr . 1994 Jun; 31(6): 741-8
9 o-f 16
TI: Phase 2 efficacy trial of an oral 8-aminoquinoline (WR6026) for treatment
of visceral leishmaniasis.
AU: Sherwood-JA; Gachihi-GS; Muigai-RK; Skillman-DR; Mugo-M; Rashid-JR;
Wasunna-KM; Were-JB; Kasili-SK; Mbugua-JM: et-al
AD: Clinical Research Centre, Kenya Medical Research Institute, Nairobi.
SO: Clin-Infect-Dis. 1994 Dec; 19(6): 1034-9
>B: The efficacy of an oral 8-aminoquinoline
(8--CE6—(diethy1 amino)hexy1 JaminoJ—6—methoxy—4—methylquino1ine) (WR6026) in the
treatment of 16 patients with ka1 a azar was evaluated. The first 3 patients
received therapy for 2 weeks at a dosage of 0.75-1.00 mg/(kg.d); 1 patient was
cured, and in,regard to the other 7, a 1-logarithm decrease in the number of
splenic parasites and clinical improvement were noted. The next 8 patients
received therapy for 4 weeks at the same daily dosage (1 mg/Ckg.dJ); 4 were
cured, and for the other 4, 1- to 2-log decreases in the number of parasites
and clinical improvement (in regard to weight, liver and spleen size,
hemoglobin level, and leukocyte count) were noted. The therapy was associated
with minimal toxicity; adverse effects included gastrointestinal distress,
headache, and methemoglobinemia. The fact that one-half of the patients were
cured indicates that future trials with longer regimens and higher dosages are
warranted and should include patients for whom existing treatment methods have
fai1ed.
10 of 16
TI■ Diagnosis of symptomatic visceral leishmaniasis by use of the polymerase
chain reaction on patient blood.*
AU5 Nuzum-E; White-F-3rd; Thakur-C; Dietze-R; Wages-J; Grogl-M; Berman-J
AD: Division of Experimental Therapeutics, Walter Reed Army Institute of
Research, Washington, DC 20307-5100.
SO: J-Infect-Dis. 1995 Mar; 171(3): 751-4
AB: To diagnose symptomatic visceral leishmaniasis (ka1a-azar) using peripheral
blood rather than tissue aspirates, a polymerase chain reaction (PCR) technique
was developed for which the detection limit is 1 Leishmania-infected macrophage
in 8 mL of blood. For Indian, Kenyan, or Brazilian patients with
parasitologically confirmed kala-azar, 57 of 63 cases before treatment had
blood that was FCR-positive (907. sensitivity). None of 40 clinically healthy
persons had PCR-positive blood (1007. specificity). Twelve (927.) of 13
clinically cured Indian patients had negative PCR reactions 1-6 months after
treatment. This PCR procedure can provide a parasito1ogic diagnosis for the
vast majority of kala-azar cases before therapy, may identify patients who have
been successfully treated by chemotherapy, and should substantially reduce the
need for invasive tests.
11 of 16
TI : A combination of sulphadiazine. trimethoprim and metronidazole or
tinidc'azo 1 e in ka 1 a-azar .
AU a Bano-P; Shahab-SM
AD: Sadar Hospital Biharsharif, Nalanda, Bihar.
SO: J-Assoc—Physicians—India. 1994 Jul: 42(7): 535-6
AB: Nine patients of ka1a-azar showed good response to treatment with a
combination of su1phadiazine, trimethoprim and metronidazole or tinidazole
given orally -for 12 to 25 weeks. No untoward side effect was noticed.
Tinidazole sulphadiazine and trimethoprim combination was -found to be safer for
treatment of kala-azar in pregnant women.
12 of 16
TI: Daily versus a 1ternate-day regimen of amphotericin B in the treatment of
k;ala-azar: a randomized comparison.
AU: Thakur-CP; Sinha-GP; Pandey-AK; Barat-D; Singh-RK
AD: Patna Medical College and Hospital, Bihar, India.
SO: Bull-World-Health-Organ. 1994; 72(6): 931-6
AB: Using a randomized study, we compared a daily and an a1 ternate—day regimen
of amphotericin B for the treatment of ka1a-azar. with respect to efficacy,
adverse reactions, cost-effectiveness, and tolerance. The study subjects were80 kala-azar patients, drawn from the first four decades of life and matched by
age, sex, and parasite load. The patients were randomly allocated to treatment
groups A and B (40 patients per group). Patients in group A received a daily
^egimen of amphotericin B, starting with an escalating dose of 0.05 mg/kg body
weight per day until a daily dose of 1 mg/kg was reached; the latter dose was
then given daily till a total dose of 20 mg/kg body weight had been
administered. The patients in group B also started with an escalating dose of
0.05 mg/kg but when 1 mg/kg was reached the drug was given on alternate? days.
All 80 patients using the two treatment regimens were cured, no patient
relapsed in either group in 6 months of follow-up, and their bone-marrow
aspirates were free of amastigotes. Treatment of kala-azar patients with the
daily regimen of amphotericin B at a dose 1 mg/kg body weight was as effective,
not more toxic, equally well tolerated, and much more cost-effective than the
a 1ternate-day regimen and should be adopted for treatment of this condition.
13 of 1 6
TI: Is one year follow-up justified in kala-azar post-treatment?
AU: Nyakundi—PM; Wasunna-KM: Rashid—JR; Gachihi—GS; Mbugua—J; Kirigi-G;
Muttunga-J
AD: Clinical Research Centre, Kenya Medical Research Institute, Nairobi.
SO: East-Afr-Med-J. 1994 Jul; 71(7): 453-9
AB: Sixty-five patients, 51 males and 14 females, with clinical and
parasitological evidence of visceral leishmaniasis were initially treated as
follows: 44.67. were on intravenous sodium stibogluconate (pentostam) 20 mg/kg/d
for 30 days. 35.47. was on a combination of pentostam as above and allopurinol
21 mg/kg/d in three divided doses for 30 days while 207. was on pentostam 10
mg/kg thrice/d intravenous1y for 10 days. All patients were parasitologically
negative by the end of their respective treatment regimen. All patients were
reviewed at 2 months, 6 months., and 12 months periods in order to evaluate the
relapse rates and optimal follow-up period. Thirteen patients (207.) relapsed at
2 months and one patient (1.57.) relapsed at 6 months follow-up periods
respectively. There was no relapse between 6 months and 12 months follow-up
period. The mean liver and spleen sizes in responders showed a dramatic
reduction at 2 months follow-up and thereafter a gradual reduction occurred in
the next 10 months. Weight gain continued throughout the year. Apart from
platelet count which showed a sustained high level from discharge to 12 months
follow-up, the peripheral blood indices stabilized from 2 months follow-up.
Relapses were retreated until parasitologically negative twice and then
followed up, for a period of 12 months. At follow-up the liver and spleen sizes
reduced gradually in the next 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)
14 of 16
TI: Amphotericin versus sodium stibogluconate in first-line treatment of I ndian
ka1a-azar.
AU i Mishra-M; Biswas-UK; Jha-AM; Khan-AB
AD: Darbhanga Medical College and Hospital, Bihar, India.
SO: Lancet. 1994 Dec 10; 344(8937): 1599-600
AB: Patients do not always respond to treatment of visceral 1 e i s ti m a n i a s i s w i t h
pentavalent antimony, and the drug has toxic effects. Amphotericin B might be
useful as an alternative first-line treatment for the disease. We compared the
efficacy of amphotericin and sodium stibogluconate in a prospective randomised
trial in 80 uncomplicated and parasitologically confirmed cases of Indian
kala-azar. None of the patients had received an anti1eishmania1 agent before.
Sodium stibogluconate was given at 20 mg/kg in two divided doses daily for 40
days, and amphotericin in fourteen doses of 0.5 mg/kg infused in 57. dextrose on
alternate days. All 40 patients randomised to amphotericin were cured; of the
40 patients assigned to sodium stibogluconate, 28 (707.) showed initial cure and
25 (62.57.) showed definitive cure (p < 0.001). With amphoteric in, there was
quicker abatement of fever and more complete spleen regression with no serious
adverse effects. Amphotericin is effective in the first-line treatment of
Indian kala-azar and superior to antimony therapy.
15 of 16
TIs A further study of LDT and IFAT tests in evaluating the control of
kala-azar in China.
AU s Bao-V; Wang-ST; Shao-OF
AD 3 Xuzhou Medical College, Jiangsu, China.
SO: J-Trop-Med-Hyg. 1994 "Dec; 97(6): 357-61
AB: Ka1a-azar (KA) used to be highly prevalent in Shandong Province in China
and , according to the survey made in 1950, the average prevalence rate was 350
per million. Through mass treatment and sandfly control, the prevalence rate
was brought down to 3 per 100,000 in 1958 and the disease was basically
eliminated. Since 1972, only 18 residual patients have been detected and no
newly infected cases have appeared. In the meantime, the vector density' had
been reduced to such a low level that sandflies could not be found in 857. of
the villages. For further evaluation of the control measures, an immunological
survey on a relatively large scale was conducted in 78 townships located in 24
counties of 13 prefectures and cities in 1990. A total of 10,239 rural
residents of different ages had the Leishmanin dermal test (LDT). None of the
people under 30 years of age was positive (0/8020), while in those aged above
30, the average positive rate was 4.47. (98/2219). During the survey, blood
samples were also taken from 4232 people for indirect fluorescent antibody test
(IFAT); results were all negative. This indicates that the transmission of KA
had been completely interrupted since the early 1960s and the province is now a
non-endemic area of KA. Further analyses of the data showed that LDT is of
great value in epidemiological investigation of KA, for the evaluation of
control measurements, the ascertainment of the past and present status of the
disease, and detection of subclinical infection.(ABSTRACT TRUNCATED AT 250
WORDS)
16 o -f 16
The
t
reatment
of
k
ala-azar
during
pregnancy.
TI :
AUs Thakur-CP; Sinha-GP; Sharma-V; Barat-D
AD: Department of Medicine, Patna Medical College, Bihar, India.
SO: Natl-Med-J-India. 1993 Nov-Dec; 6(6): 263-5
ia-azar in pregnant women is difficult to treat because for
AB: BACKGROUND. Ka
________
them the two commonly used drugs, sodium stibogluconate and pentamidine, are
not considered safe. We assessed the effect of amphotericin B on pregnancy, on
the foetus and kala—azar. METHODS. Five pregnant women were administered
amphotericin B at a dose of 1 mg/kg body weight daily starting with 0.5 mg/kg
body weight till a total dose of 20 mg/kg body weight was given. The progress
of pregnancy was monitored u1trasonographically and the mothers and children
were followed for six months. RESULTS. All the 5 women were cured of the
disease and there was no harmful effect on the children. CONCLUSION.
Amphotericin B cures kala-azar. during pregnancy with no harmful effects on the
oetus.
PC-SPIRS 3.30
MEDLINE (R)
1994
MEDLINE (R) 1994 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.
1 of 5
TI: Successful treatment of refractory visceral leishmaniasis in India using
antimony plus interferon-gamma.
AU: Sundar-S: Rosenkaimer—F; Murray-HW
AD: Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
SO: J-Infect-Dis. 1994 Sep; 170(3): 659-62
AB: Fifteen Indian patients with relapsing or drug-refractory visceral
leishmaniasis were retreated for 30 days with antimony plus interferon-gamma
(IFN-gamma). All 15 had failure of an initial course of antimony and at least
one additional course of antimony or pentamidine; 7 patients had failure of
three or four prior courses of therapy. During the study, tne^ient was
discontinued in 2 patients because of anemia and congestive heart failure in 1
md intractable vomiting in the other; both subsequently died. In the remaining
13 patients, IFN-gamma plus antimony treatment was associated with daily fever
but no other adverse reactions. After 30 days of therapy, 9 (697.) of the 13
al 1 9 were healthy,
patients were apparently cured. Six months after treatment, all
had parasite—free bone marrow aspirate smears, and were considered cured. None
have relapsed during a mean follow-up of 15.9 +/- 1.7 months. These results
support the use of antimony plus IFN-gamma as an immunochemotherapeutic
alternative for kala-azar patients who have repeated failures of conventional
treatment.
2 of 5
TI: Liver morphology and function in visceral leishmaniasis (Kala-azar).
AU: el-Hag-IA; Hashim-FA; el-Toum-IA; Homeida-M: el-Kaiifa-M? el-Hassan-AM
AD: Department of Pathology, Faculty of Medicine, University of Khartoum,
Sudan.
SO: J-Clin-Pathol. 1994 Jun; 47(6): 547-51
AB: AIM—To study the morphology and function of the liver in visceral
leishmaniasis (Kala-azar). METHODS—Percutaneous liver biopsy specimens from 18
patients with confirmed visceral leishmaniasis were examined under light and
electron microscopy before and after treatment with pentovalent antimony. The
tissue was also examined for hepatitis B surface and core antigens using
mmunoperaxidase staining. Liver function was investigated in nine patients
before and after treatment. RESULTS—Specimens before treatnierrt showed Kupffer
cells and macrophages colonised by leishmania parasites in 407. of cases. A
chronic mononuclear cell infiltrate had affected the portal tracts and lobules.
Ballooning degeneration of the hepatocytes, fibrosis of the terminal hepaticvenules, and pericellular fibrosis were common findings. I he fibrosis was
related to Ito cells transforming to fibroblast-like cells. None of the
patients had hepatitis B infection. All patients had biochemical evidence of
liver dysfunction before treatment. Liver function improved after treatjnent.
CONCLUSION—Visceral leishmaniasis causes morphological and functional
disturbance in the liver. Focal fibrosis rather than cirrhosis occurs. The
exact aetiology of hepatic damage is unclear but may have an immunological
basis.
TI :
AU:
AD:
SO:
AB:
3 o-F 5
Tinea versicolor and visceral 1e i shmani asi s.
Hashim—FA: E1hassan—AM
Physiology Department, Faculty of Medicine, University of Khartoum, Sudan.
Int-J-Dermatol . 1994 Apr; 33(4): 25S-9
BACKGROUND. Visceral leishmaniasis (ML) is endemic in several areas in the
Sudan. The disease is associated with depressed cellular immunity. Tinea
versicolor is a normal tommensal of the skin which can become pathogenic
particularly in patients with depressed cel 1-mediated immunity. Patients with
VL have a high prevalence of tinea versicolor. METHODS. One hundred and thirty
patients with parasitologic confirmation of VL were screened for tinea
versicolor infection. In the suspected cases the diagnosis was made by
demonstrating the fungal hyphae and spores in skin scrapings. All patients were
treated with sodium stibogluconate. RESULTS. Of the 130 patients with VL, 10.87.
were found to have severe tinea versicolor. The fungal infection developed or
became worse with the start of VL. After successful treatment of VL, the tinea
lesions disappeared completely or decreased in severity. CONCLUSIONS. Depressed
cell-mediated immunity that is a feature of VL is the probable underlying cause
for fungal infection. Tinea infection during the course of VL is to be
distinguished from lesions of post-ka1a-azar dermal 1eishmaniasis .
4 of 5
TI: Immunoblotting identifies an antigen recognized by anti gp63 in the immune
complexes of Indian k
ka
a1a-azar patient sera.
AU: Sanyal-T; Ghosh-DK; Sarkar-D
AD: Leishmania Group, Indian Institute of Chemical Biology, Calcutta.
BO: Mol-Cel1-Biochem. 1994 Jan 12; 130(1): 11-7
AB: In SDS-PAGE the immune complexes (IC) of kala-azar patient sera showed
intense bands at 55 kDa and 20 kPa corresponding to heavy and light chains of
immunoglobulins. In immunoblot experiment, kala-azar and normal IC after
treatment with patient sera showed multiple bands of which the band at 55 kDa
was most prominent in kala—azar IC. It is known that in kala-azar sera
antihuman IgG is present, so the heavy band at 55 kDa region may be due to
higher amount of IgG and/or other antigen(s) present at that region. Immunoblot
experiments of kala-azar IC with anti gp63 also developed a major band at 55
kDa. It suggests that the antigen (55 kDa) and gp63 have common antigenic
epitope (s). Normal IC did not react with anti gp63 indicating absence of this
antigen in normal IC. Antigenic similarity between the IC antigen (55 kDa) and
gp63 indicated that the former antigen may have been processed from gp63. In
summary, identification of a parasite antigen (55 kDa) in IC of ka,1 anazar.
patients sera may be useful in developing a serodiagnostic assay for visceral
leishmaniasis.
5 of 5
TI: Treatment of post-ka1a-azar dermal leishmaniasis.
AU: Ramesh-V
AD: Department of Dermatology and Regional STD, Centre Safdarjang Hospital„ New
)elhi, India.
SO: Int-J-Dermatol. 1994 Mar; 33(3): 153-6
PC-5PIRS 3.30
MEDLINE (R)
1323.
MEDLINE (R) 1993 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.
1 of 13
TI: Treatment of Brazilian kala-azar with a short course of amphocil
(amphotericin B cholesterol dispersion).
AU: Dietze-R; Milan-EP; Berman-JD; Grogl-M; Falqueto-A; Feitosa-TF; Luz-KG;
Suassuna-FA; Marinho-LA; Ksionski-G
AD: Tropical Medicine Unit, Federal University of Espirito Santo, Vitoria,
Braz i 1 .
SO: Clin-Infect-Dis. 1993 Dec; 17(6): 981-6
AB: Amphotericin B is an effective but toxic anti1eishmania1 agent.
Lipid-encapsulated amphotericin B should have a high therapeutic index for
visceral leishmaniasis because reticuloendothelial cells, the sole site in
which Leishmania is found, will phagocytize and concentrate the complex.
Amphotericin B cholesterol dispersion (Amphocil; 2 mg/Ekg.dj intravenously) was
administered to 10 Brazilians with kala-azar for 10 days (cohort 1) and to 10
Brazilians with kala-azar for 7 days (cohort 2). All patients were successfully
treated: 19 of the 20 patients were without visible parasites in the bone
marrow; the mean time to afebrility was 4.2 days; spleen size regressed by a
mean of 797. 2 months after therapy; and no patient had clinical or laboratory,
abnormalities by the end of 6-12 months of follow-up. Side effects were fever
and chills accompanied by respiratory distress, but not nephrotoxicity, in
children < 3 years of age.
2 of 13
TI: Leishmaniasis: report of 33 cases and a review of the literature
Ceditorial 3
AU: Bouree-P; Belec-L
SO: Comp—Immunol-Microbiol —Infect—Dis. 1993 Oct; 16(4): 251—65
AB: Leishmaniasis are parasitic diseases in extension. They appear in new foci,
because of important displacements of populations, and they affect
immunocompromised patients (under chemotherapy, transplanted, or HIV infected).
Study of 33 cases of leishmaniasis, 22 visceral and 11 cutaneous, at the
Hopital du Kremlin-Bicetre, France, showed predominant contarnination in Maghreb
and in the south of France. In the case of Kaia-Azar, fever (IB cases) and
lepatosp1enomega1y (19 cases) are frequent, and the serodiagnosis and the
search of parasites by myelogram are always positive. In HIV-infected
individuals, clinical signs are similar, but the serodiagnosis is less
reliable. Evolution is bad in transplanted patients who must remain under
immunosuppressive drugs. In the case of cutaneous leishmaniasis, diagnosis is
based on local sample, while the serodiagnosis remains negative. Treatment is
sometimes long, necessitating repeated treatments.
3 of 13
TI■ EChildhood k al a-azars the c a ses o f a deca d eJ
AU: Lopez-Pena-LF: Clemente-Yago-F; de-1a-Cruz-Amoros-F: Gorostiza-Felipe-P;
Monferrer-Fabregat-R; Escriva-Tomas-P
AD: Servicio de Pediatria, Hospital General de Alicante.
SO: An-Esp-Pediatr. 1993 Sep; 39(3): 199-201
AB: The aim of our work was to review the epidemiological,, clinical and
laboratory features of the cases of Kala-azar in our hospital during a decade
in order to outline data that might be useful in helping to make an earlier
diagnosis and subsequently, earlier treatment. We report eighteen cases of
visceral Leishmaniasis treated in our hospital between January 1981 and
December 1990. The ages of the patients varied between five months and seven
years. In our experience, medullar aspirate was the most effective diagnostic
method. However, it this test is negative, specific serological tests should be
included in the assessment of any pediatric inpatient with fever and
splenomegaly. In our opinion, it is very important to keep this disease in
mind, especially in non-endemic areas.
4 of 13
TI: Leishmanin and tuberculin sensitivity in leishmaniasis in the Sudan, with
special reference to kala-azar.
AU: Zijlstra-EE; el-Hassan-AM
AD: Leishmania Research Group, Medical Research Council, Khartoum, Sudan.
SO: Trans-R-Soc-Trop-Med-Hyg. 1993 Jul-Aug; 87(4): 425-7
AB: The application of leishmanin and tuberculin skin tests was studied in
patients with leishmaniasis in the Sudan. 35 cases of active kala-azar and 3
relapse cases were leishmanin negative. 817. of patients treated for kala-azar
showed a positive reaction after 6 months. 17 of 29 patients with post
kala-azar dermal leishmaniasis (PKDL) were leishmanin positive. 2 of 16
patients with kala-azar tested with tuberculin were positive; one was diagnosed
as tuberculosis. In 7 initially tuberculin negative patients, the tuberculin
test became positive after treatment. A new Leishmania major skin test antigen
(Pasteur Institute, Iran) was more reactive than other antigens in patients
with cutaneous leishmaniasis, mucocutaneous,leishmaniasis and PKDL, but not in
treated kala-azar cases. In a field study in an area of endemic kala-azar, the
new L. major antigen proved more reactive both in individuals previously
exposed to L. major (causing cutaneous leishmaniasis) and in those with past
exposure to L. donovani. The literature concerning skin testing with leishmanin
and tuberculin in kala-azar is reviewed.
5 of 13
TI: K
aia-azar
Ka
1a-azar in western Upper Nile province in the southern Sudan and its
spread to a nomadic tribe from the north.
AU: el-Hassan-AM; Hashim-FA; Ali-MS; Ghalib-HW; Zijlstra-EE
AD: Department of Pathology and Physiology, Faculty of Medicine, University of
Khartoum, Sudan.
SO: Trans-R-Soc-Trop-Med-Hyg . 1993 Jul-Aug; 87(4): 395-8
AB: Since the start in 1988 of the present epidemic of kala-azar (visceral
leishmaniasis) in western Upper Nile state in southern Sudan, the epidemiology
of the disease in all parts of the Sudan where kala-azar has been reported was
reassessed by the Leishmaniasis Research Group in Khartoum. In this paper, the
spread of the epidemic is described among a nomadic tribe originating from
southern Kordofan state, who migrate every year with their cattle to the Bentiu
rea in western Upper Nile state where the epidemic is still raging. 200 cases
from this tribe were seen in Khartoum; another 56 cases were found during a
field trip to the area. In addition, the Bentiu area was visited, where 301
cases were under treatment and another 52 of 1120 individuals screened were
confirmed parasitoTogicalTy. 20 cases of post-ka1 a—azar dermal leishmaniasis
were found. Parasites isolated from the nomadic tribe were of the same zymodeme
as parasites isolated previously from the Nuer in western Upper Nile. The
epidemiological findings in each state are discussed in relation to the tribes
that were affected and the ecology of the area.
6 of 13
in
children
in
Efficacy
of
amphotericin
B
in
multi-drug
resistant
k^.a-azar
TI 5
first decade of life.
AU: Thakur-CP; Sinha-GP; Sharma-V; Pandey-AK; Sinha-PK; Barat-D
AD: Department of Medicine, Patna Medical College.
SO: Indian—J—Pediatr. 1993 Jan—Feb; 60(1): 29—36
AB: Fifty children in the first decade of life, and suffering from multiple
drug resistant kala-azar, confirmed by demonstration of amastigotes in
aspirates of bone marrow or spleen were treated with amphotericin B in
gradually increasing dosage to a total dose of 20 mg/kg. All patients had
classical features of severe kala-azar, and had taken more than one course of
antimony and pentamidine, and three patients had taken one? additional course of
ketoconazole besides many courses of antimony and pentamidine. The clinical
response started just after first infusion in 8 patients, and the patients
became afebrile. By Sth infusion, all looked better and 18 patients became
afebrile. By 15th infusion all patients were afebrile and cheerful. Their
spleens became smaller and body weights and total white cell counts increased.
Forty eight patients had parasitological cure at the end of treatment, and only
2 patients required an additional 5 infusions for parasitological cure. All
patients were ultimately cured. No one relapsed within six months of follow up.
All patients had shivering, rigor and rise of temperature on the day of
infusion, which could be minimized with prior administration of low dose of
hydrocortisone, but could not be eliminated. Eighteen patients had loose
motions during treatment, while 14 patients had decrease in appetite which
improved quickly when the treatment was over. Fourteen patients had transient
rise of blood urea, in six patients serum creatinine also increased and 16
patients had a minor fall in serum potassium.(ABSTRACT TRUNCATED AT 250 WORDS)
7 of 13
TI: The treatment of kala-azar in the Sudan with sodium stibogluconate: a
andomized trial of three dosage regimens.
MU: Zijlstra-EE; Siddig-Ali-M; e1-Hassan-AM; Hofland-HW; el-Toum-I; Satti-M;
Ghalib-HW
AD: Leishmania Research Group, Medical Research Council, Sudan.
SO: Trans-R-Soc-Trop-Med-Hyg. 1993 May-Jun; 87(3): 307-9
AB: In a randomized study in the Sudan, 3 different regimens of sodium
stibogluconate were compared in patients with parasito1ogica11y confirmed
kala-azar (visceral leishmaniasis): 10 mg/kg for 30 d (38 patients), 20 mg/kg
for 30 d (29 patients), and 20 mg/kg for 15 d (37 patients). Treatment failures
were defined as death, partial response, relapse, or the development of
post-ka1a-azar dermal leishmaniasis. The hazard ratio for failure of 20 mg/kg
for 30 d vs. 10 mg/kg for 30 d 2.1 (957. confidence interval ECU = 0.6, 7.6)
and for 20 mg/kg for 15 d vs. 10 mg/kg for 30 d it was 1.7 (957, CI
0,5, 6.1).
No significant difference was detected between the 3 regimens in the rate of
return to normal of haematological criteria, regression of spleen size, or
weight gain. After 15 d treatment parasite clearance with 20 mg/kg for 30 d and
20 mg/kg for 15 d was more profound than with 10 mg/kg for 30 d (P < 0.05), but
the difference was no longer present at the end of treatment. Further
investigation of the effectiveness of short, intensive treatment regimens in
the treatment of
a-azar is warranted.
8 of 13
Visceral leishmaniasis (kala-azar) after a visit to the Mediterranean
region.
AU: Rudi-J; Racz-P; Horner-M; Kommerell-B
AD: Medizinische Universitatsk1inik, Abteilung fur Gastroenterologie,
Heidel berg.
SO: Clin-Investig. 1993 Aug; 71(8): 616-9
AB: The case of a 17-year-old patient is presented who became ill 10 months
after a holiday visit to Malta. Symptoms included fever peaking daily at-40
degrees C, pancytopenia, and splenomegaly. There was no evidence of bacterial
or virological involvement, and probatory treatment with antibiotics followed
by corticosteroids was without success. Examination of bone marrow led to the
diagnosis of visceral leishmaniasis (kala-azar)■ A therapy with pentavalent
antimony brought rapid improvement in clinical symptoms and led to complete
recovery. A short review is presented of the epidemiology, diagnosis, and
therapy of visceral leishmaniasis. The aim of this presentation is to remind
the attendant physician of the clinical symptoms involved with the possible
case of visceral leishmaniasis.
jI:
9 of 13
TI: Amphotericin B therapy in kala-azar■
AU: Giri-OP
AD: Department of Medicine, Darbhanga Medical College and Hospital,
Laherisarai.
SO: J-Indian-Med-Assoc. 1993 Apr; 91(4): 91-3
AB: Twenty-seven adult patients of kala-azar unresponsive to sodium
stibogluconate (SSG) were given amphotericin B in the dose schedule of 0.50
mg/kg body weight on alternate days for a total of 21 to 31 infusions,
depending upon clinical and parasitological response. A 1007 cure rate was
achieved at the end of the therapy and nd relapse was encountered during 12
months follow-up. Only mild adverse reactions were noted on the day of infusion
during therapy. Amphotericin B was found to be an acceptable alternative drug
for treatment of such cases.
10 of 13
TI : Evaluation of amphotericin B as a first line drug in comparison to sodium
stibogluconate in the treatment of fresh cases of kala-azar.
AU: Thakur-CP; Sinha-GP; Sharma-V; Pandey-AK; Kumar-M; Verma-BB
AD: Department of Medicine, Medical College, Patna.
SO: Indian-J-Med-Res . 1993 Jul; 97: 170-5
“n A total of 150 patients of kala-azar matched for age and sex and
parasitologically proved were randomly allocated to two equal treatment groups.
Patients in one group received amphotericin B(AMB) in a dose of 1 mg/kg body
weiglit (BW) on alternate days starting with 0.05 mg/kg/bw on first day with
daily increments, till a total dose of 20 mg/kg/bw was given; the patients in
the second group received sodium stibogluconate (SAG) in the dose of 20
mg/kg/bw, im daily for 30 days. The efficacy, safety and cost-effectiveness of
the two drugs were compared. Apparent cure (afebrile at the end of therapy) in
75 (1007.) and 69 (927.) patients and ultimate cure (no relapse in six months of
follow up) in 75 (1007.) and 60 (807.) patients occurred in the AMB and SAG
groups respectively. The difference between the ultimate cure in the two groups
was significant (P < 0.001). Six (87.) and 9(127.) patients of SAG group showed
primary (with no response to SAG during treatment) and secondary
unresponsiveness (with no response to SAG after relapse) respectively and they
were cured with amphotericin B.(ABSTRACT TRUNCATED AT 250 WORDS)
11 of 13
TI: Post-kala-azar dermal leishmaniasis
leishmaniasis:: a clinical and therapeutic study.
AU: Ramesh-V; Misra-RS; Saxena-U; Mukherjee-A
AD: Department of Dermatology and Leprology, Safdarjang Hospital j, New Delhi,
India.
Int-J-Dermatol. 1993 Apr; 32(4): 272-5
,.d: BACKGROUND. Post-kala-azar dermal leishmaniasis is a condition peculiarly
confined to the Indian subcontinent. METHODS. The clinical features and
investigations in 18 patients of post—ka Ia —azar dermal leishmaniasis were
studied. RESULTS. There was a polymorphic picture from hypopigmented macules to
nodules and plaques. Mucous membranes were affected in five, the lips and glans
penis being the most frequent sites. Histopathologically, a rich dermal
infiltrate was seen in indurated lesions and in macules; it was confined to
perivascular foci in the upper dermis. Leishman-Donovan bodies were seen .in 16.
CONCLUSIONS. The lesions cleared in 4 to 5 months after treatment with sodium
g/day. The
antimony gluconate intramuscu1 ar 1y 20 mg/kg/day up to a maximum of 1 q/day.
drug was well tolerated.
12 of 13
TI: Heterogeneity of cutaneous leishmaniasis with emphasis on the Old World.
AU: Peters-W
AD: Department of Medical Parasito1ogy, London School of Hygiene and Tropical
Medicine, England.
SO: Schweiz—Med—Woehenschr. 1993 Jun 19; 123(24): 1237—49
AB: Leishmaniasis of the integument which may result from infection with a
number of different species of Leishmania can be primary., or can arise as a
late manifestation of systemic infection of the reticuloendothelial organs
(kala-azar)- Infection of the skin and/or mucosae assumes many different
clinical forms which are reviewed here. The immune response is essentially a
cell-mediated one. Even left untreated, the majority of tegumentary lesions
will eventually self-heal but the process may be very prolonged and severe
scarring can result. The main features of diagnosis, prevention and tr e£t^m.enMtt
are discussed. No vaccines are generally available at present. Organic
pentavalent antimonials remain the drugs of choice.
13 o-f 13
TI : Amphotericin B in resistant kala-azar in Bihar.
AU: Thakur-CP; Sinha-GP; Pandey-AK? Barat-D; Sinha-PK
AD: Patna Medical College and Hospital, Bihar, India.
SO: Natl-Med-J-India. 1993 Mar-Apr: 6(2): 57-60
AB: BACKGROUND. During the recent epidemic of kala-azar in Bihar, we identified
a group of patients who were unresponsive to the two commonly used
drugs—sodium stibogluconate and pentamidine. We evaluated the use of
amphotericin B in these patients because it has been shown to be active in
experimental animals against amastigotes and promastigotes, it has been found
:o be useful in South American patients and is now recommended by the World
Health Organization as a second line drug. METHODS. We selected 300 patients
who were unresponsive to sodium stibogluconate and pentamidine (out of 500
patients with kala-azar confirmed by demonstration of Leishmania donovani
bodies in their splenic aspirates). Amphotericin B was given in a dose of 1
mg/kg body weight on alternate days starting with 0.05 mg/kg body weight with
daily increments till a 1 mg dose was reached. A total dose of 20 mg/kg was
given initially and repeated if the parasites persisted. The investigations
done, before and after treatment were splenic or bone marrow aspiration,
measurement of the spleen and liver size, body weight, total and differential
white cell counts, haemoglobin level, total serum protein, blood urea, serum
creatinine, serum potassium, blood sugar, serum alanine and aspartate
transaminase, electrocardiography and a chest X-ray. The efficacy of tceatme£it.
was assessed at the end of treatment and after 6 months of follow up. RESULTS.
After treatment with amphotericin B, 298 (997.) of the patients had been cured
of their disease as evidenced by the disappearance of fever, reduction of
hepatosplenomegaly, clearance of the parasites from the spleen and bone marrow
and an absence of relapse on 6 months of follow up. Two hundred and sixty-eight
(897.) patients required 1 g of the drug, 24 (87.) required 1.5 g and 6 (27.)
required 2 g. All patients had shivering and fever during the infusion. Two had
a cardiac arrest from which they could not be revived. Other complications
ncluded anorexia, stomatitis, jaundice, hypokalaemia and a rise in blood urea.
However, these were only mild and improved after treatment was stopped.
CONCLUSION. Amphotericin B is an effective drug for patients with ka1a-azar.
unresponsive to treatment with sodium stibogluconate and pentamidine, but it
should be administered under close medical supervision.
PC-SPIRS 3.30
MEDLIME (R)
1992
MEDLINE (R) 1992 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.
1 of 16
TI : Treatment of kala-azar in India CeditorialJ
AU: Thakur—CP
SO: Natl-Med-J-India. 1992 Sep-Oct; 5(5): 203-5
2 of 16
(
leishmaniasis
(
k
ala-aza
r)
with
aminosidine
TI : Treatment of visceral
in Bihar,
Bi har < India.
paromomycin)—antimonia1 combinations, a pilot study in
AU: Thakur—CP; (Olliaro-P;
----- . , Gothoskar-S; Bhowmick-S; Choudhury-BK; Prasad-S;
Kumar—M; Verma-BB
AD: Patna Medical College, Tripolia Social Service Hospital,- I n d i a »
SO: Trans-R-Soc-Trop-Med-Hyg . 1992 Nov-Dec; 86(6): 615-6
iB: A 20 d drug regimen of aminosidine (= paromomycin) at 12 mg/kg/d in
combination with sodium stibogluconate at 20 mg/kg/d proved efficacious and
well-tolerated in patients with visceral leishmaniasis in the State of Bihar,
India. Eighteen of 22 evaluable patients achieved an ultimate cure. The
remaining 4 patients, although not cleared of parasites, had their parasite
grade reduced and also improved clinically. This confirms prior findings in
Kenyan patients with kala-azar. and indicates that this regimen is a valid
alternative to antimonial compounds alone in the State of Bihar, where cases of
kala-azar not responding to antimonial drugs and intolerant of pentamidine are
increasingly recorded.
3 of 16
TI: Detection of circulating an tigen by McAb-AST for evaluating the efficacy of
anti-Leishmania chemotherapy.
AU: Hu-X; Lin-F; Kan-B; Yan-W
AD: Laboratory of Parasitology, West China University of Medical Sciences,
Chengdu, Sichuan.
SO: Chin-Med-Sci-J. 1992 Sep; 7(3): 157-60
AB: We have adapted the simple and sensitive McAb-antigen spot test (AST) for
evaluating the efficacy of anti-Leishmania chemotherapy. Serum samples from 37
kala-azar patients were tested by McAb-AST, and all showed definite positive
eactions before treatment. After a course of antimony treatment, 20 turned
negative, coupled with the disappearance of clinical symptoms; another 12 cases
responded with weak positivity accompanied by an improvement, of clinical
manifestations; and the remaining 5 antimony-resistant patients showed strong
positive reactions, with their conditions gradually worsening. Furthermore, all
6 cases in which the diagnosis was missed by the bone marrow smear method
turned McAb-AST negative after chemotherapy. These results suggest that
McAb-AST can be used to evaluate the efficacy of chemotherapy as well as to
avoid missed diagnosis by the bone marrow smear method.
4 of 16
TI : Rapid and sensitive detection of Leishmania kinetoplast DNA from spleen and
blood samples of kala-azar patients.
AU: Smyth-AJ; Ghosh-A; Hassan-MQ; Basu-D; De-Bruijn-MH; Adhya-S; Mallik-KK;
Barker~DC
AD: Department of Pathology, University of Cambridge, UK.
SO: Parasitology. 1992 Oct; 105 ( Pt 2): 103-92
AB: Following sequence analysis of a Leishmania donovani kinetoplast DNA (kDNA)
minicircle, we have developed synthetic oligonucleotides for Use in the
polymerase chain reaction (PCR). With these primers, we have amplified L.
donovani kDMA from splenic aspirates and blood samples taken from kala-azar
patients. Treatment of the samples for PCR requires only limited DMA
purification by lysis in SDS, digestion with proteinase K, phenol extraction
and ethanol precipitation of the resulting nucleic acid. We have obtained
amplified product routinely with DNA prepared from the equivalent of 2.5—25
microliters of splenic aspirate or of 50-500 microliters of blood from infected
patients. In dilution experiments a visible product has been obtained on
amplification of DNA from the equivalent of 2.5 x 10(-7) microliters of splenic
material. We therefore propose the amplification of L. donovani kDNA by PCR as
a rapid and highly sensitive method for the diagnosis of kala-azar.
5 of 16
TI : Visceral and cutaneous leishmaniasis in an European paediatric population.
AU: Mattot-M; Ninane-J; Bigaignon-G; Vermy1en-C; Cornu-G
AD: Department of Paediatrics, Cliniques Universitaires Saint-Luc, Brussel *s.
SO: Acta-Clin-Belg. 1992; 47(4): 231-7
AB: Six children with leishmaniasis, aged 10 months to 10 years, were treated
in the Paediatric Department. Four patients had visceral leishmaniasis
(kala-azar): diagnosis was based on bone marrow examination and therapy
consisted of a combination of Glucantime and Lomidine. The remaining two
children had cutaneous leishmaniasis: diagnosis was made by skin biopsy and the
patients were treated with Glucantime alone. In all children, serology was
clearly positive at the time of the diagnosis and all patients improved. The
only side effects were cough associated with fever in one child, and
supraventricular premature beats in another one. They were ascribed to
Glucantime, and proved reversible after discontinuation of the treatment.
6 of 16
TI: Post kala-azar dermal leishmaniasis in the Sudan: clinical features,
pathology and treatment.
AU: el-Hassan-AM; Ghalib-HW; Zij1stra-EE; Eltoum-IA; Satti-M: Ali-MS; Ali-HM
AD: Leishmaniasis Research Group., Medical Research Council, Khartoum, Sudan.
SO: Trans~R—Soc—Trop—Med-Hyg. 1992 May-Jun; 86(3): 245-8
AB: The clinical features, pathology, immune responses, diagnosis and treatmen.t
of post kala-azar dermal leishmaniasis (PKDL) in the Sudan are described and
discussed. The disease is characterized by maculopapular or nodular lesions on
the face, limbs or trunk. Lesions appear during or within months after the
treatment of visc oral leishmaniasis, but in 2 of 19 patients there was no
previous history of kala-azar. PKDL may be confused with leprosy both
clinically and pathologically, Similarities and differences between the 2
diseases are discussed. Unlike visceral leishmaniasis, the peripheral lymphoid
zells of patients with PKDL respond to Leishmania antigen and some are
leishmanin positive. The response to intravenous sodium stibogluconate (20
mg/kg for 30 d) was reasonably good but some patients required repeated or more
prolonged treatment. Ketoconazole in a dose of 10 mg/kg daily for 4 weeks had
no effect on PKDL.
7 of 16
TI: Oral leishmaniasis associated with kala-azar■ A case report.
AU: Abbas-K; el-Toum-IA; el-Hassan-AM
AD: Dental School, Faculty of Medicine, University of Khartoum, Sudan.
SO: Oral-Surg-Oral-Med-Oral-Pathol. 1992 May; 73(5): 583-4
AB: Mucosal leishmaniasis as an oral disease in the form of chronic
periodontitis with involvement of the oral mucosa is described. Leishmania
parasites were isolated from the oral lesions, lymph nodes, and bone marrow.
The patient had a low-grade fever and hepatosplenomegaly that regressed along
with the oral lesions after treatment with stibogluconate sodium.
8 of 16
TI: Observations on the effect of verapamil with sodium stibogluconate in kala
azar .
AU: Thakur-CP; Kumar-M
AD s Department of Medicine, F'atna Medical College Hospital , I n d i a.
SO: Trop—Geogr—Med. 1992 Jan; 44(1—2): 15—8
AB: 40 parasitologically confirmed cases of kala azar, were randomly allocated
into four treatment groups to assess the effect of verapamil on fresh and
antimony resistant cases of kala. azar. Untreated patients received sodium
stibogluconate only or in combination with oral verapamil. Antimony-resistant
patients were treated with sodium stibogluconate combined with oral verapaxmil
or pentamidine. The patients were followed up for six months. Verapamil neither
shortened the duration of treatme nJ: nor increased parasitological cure rate nor
improved the ultimate cure. In antimony unresponsive patients it did not
reverse unresponsiveness.
9 of 16
a
comparison
with
in
children
from
the
Sudan:
Clinical
aspects
of
kala-azar
TI :
the disease in adults.
AU: Zijlstra-EE; Ali-MS; e1-Hassan-AM: el-Toum-IA; Satti-M; Ghalib-HW
AD: Leishmaniasis Research Group, Medical Research Council, Sudan.
SO: J-Trop-Fediatr. 1992 Feb; 38(1): 17-21
AB: The clinical presentation of kala-azar in 43 children and 45 adults was
spared. In both groups fever, left upper quadrant abdominal pain and
.welling, and weight loss were equally the most common presenting symptoms.
Lymphadenopathy was observed in 86 per cent of children and 76 per cent of
adults. Splenomegaly was absent in 2 per cent of children and 7 per cent of
adults. No significant difference was found in frequency distribution of
symptoms and signs between children and adults. Haematological indices were
compared in both children and adults with kala-azar and their control groups.
In both children and adults with kala-azar, haemoglobin concentration, total
white cell count, and platelet count were significantly lower before than after
treatmen t. Only haemoglobin concentration was lower in children with kaX^ZL^sLE.
as compared with adults with the disease. Children in the control group had
lower haemoglobin and higher total white cell count than adult controls.
Response to therapy was evaluated in 693 patients. 1wo-hundred—and-fifty
children and 373 adults were treated with sodium stibogluconate 10 mg/kg for 30
days; in both groups 12 per cent deaths and 4 per cent relapses occurred.
Thirty children and 40 adults were treated with sodium stibogluconate 2 x 10
mg/kg for 15 days. In children, 3 per cent deaths and 7 per cent relapses were
noted; in adults there were 8 per cent deaths and 5 per cent relapses. No
significant difference in death rate or relapse rate was found between children
and adults in both regimens. Both regimens performed equally well in children
and adults with regard to death rate and relapse rate.
10 of 1 £>
leishmaniasis in HIV infection. A totally opportunistic
TI: CVisceral
infection!
AU: Cabie-A; Matheron-S; Lepretre-A; Bouchaud-O; Deluol-AM; Coulaud—JP
AD: Service des Maladies infectieuses et tropicales, Hopital Bichat-Claude
Bernard, Paris.
SO: Presse-Med. 1992 Oct 24; 21(35): 1658-62
AB: Visceral leishmaniasis occurring in immunocompromised patients, and in
particular during HIV infection, has been described in recent years and differs
from the usual Mediterranean kala-azar as encountered in France. In order to
define the clinical, diagnostic and therapeutic features of the HIV-Leishmania
spp. co—infeetion, we report 8 new cases and compare them with data from the
literature. The co-infection occurs at any stage of HIV infection, usually in
drug addicts using intravenous injections. Clinical manifestations, such as
fever, weight loss, liver and spleen enlargement and po1yadenopathy, and
laboratory findings (cytoponia, inflammatory syndrome) are generally present
but not specific during the HIV infection course. Moreover, some
gastrointestinal and p1europu1monary forms of the co—infection are misleading.
Leishmaniasis serology is negative in 50 percent of the patients. In most cases
the diagnosis is provided by detection of the parasite in bone marrow samples.
Culture must be systematic, and samplings must be repeated if they are
negative. The first-line treatment consists of pentavalent antimony. Almost 80
percent of the patients respond to this treatment, but relapses occur in 50
percent of the cases. This high risk of relapse and the opportunistic behaviour
of leishmaniasis justify a prophylaxis of relapses.
11 of 16
TI: Ka1a-azar: a comparative study of parasitological methods and the direct
agglutination test in diagnosis [see comments!
AU: ZijIstra-EE; Ali-MS; el-Hassan-AM; el-Toum-IA; Satti-M; Ghalib-HW; Kager-FA
AD: Leishmaniasis Research Group, Medical Research Council, Sudan.
SO: T rans-R-Soc-Trop-Med-Hyg . 1992 Sep-Oct; 86(5): 505-7
AB: In a comparative study 88 patients were diagnosed as suffering from
kala-azar (visceral
(viscera 1 1eishmaniasis) using 3 parasitological methods
simultaneously. Splenomegaly was absent in 4 cases. In 84 patients with
splenomegaly, splenic aspiration appeared to be the most sensitive method
(96.47.), followed by bone marrow aspiration (70.27.) and lymph node aspiration
(58.37.). There was no relation between titres in the direct agglutination test
and parasite load as determined by the number of parasitological methods which
were positive or parasite density in splenic aspirates. Splenic aspiration and
bone marrow aspiration were compared as an assessment of cure in ka1a-azar. In
6 (137.) of 46 patients tested, parasites were found, all by splenic aspiration.
Bone marrow showed parasites in one of these. The literature with regard to
parasitological investigations before and after treatment is reviewed.
12 of 16
TI: The treatment of kala-azar: old and new options.
AU: ZijIstra-EE
AD: Department of Infect i ous D i seas e s a n d T r o p i c:: a 1 M e d i c i n e, A c: a d e n i i c: M e d i c a 1
Centre, Amsterdam, The Netherlands.
SO: Trop—Geogr-Med. 1992 Jul; 44(3): 288
13 of 16
TI: Post-kala-azar derma 1 leishmaniasis in the Sudan: peripheral neural
involvement.
AU: E1hassan-AM: Ali-MS; Zijlstra-E; Eltoum-IA; Ghalib-HW; Ahmed-HM
AD: Leishmania Research Group, Faculty of Medicine, Khartoum, Sudan.
SO: Int-J-Derrnatol . 1992 Jun: 31(6): 400-3
AB: Four patients developed post-kala-azar dermal leishmaniasis and neuritis
(PKDL) 1 to 6 months following apparently successful treatment of kala-agar.
The duration of the lesion varied between 1 month and nearly 5 years.
years, The
xesions were macules^ papules, or nodules affecting the face, extremities, and
trunk. The diagnosis was made by demonstration of the parasite in slit smear
and biopsies and by a positive direct agglutination test (DAT). Histologically,
the patients were found to have neuritis affecting the cutaneous nerves in the
lesion only. The nerves showed a 1ymphohistiocytic infiltration and
occasionally parasites. There was no impairment of sensation. Response to
sodium stibogluconate was good. PKDL may simulate leprosy both clinically and
pathologically.
14 of 16
TI: Ketoconazole in the treatment of antimony- and pentamidine-resistant
k1a-azar Cletter!
AU: Wali-JF; Aggarwal-F; Gupta-U; Saluja-S; Singh-S
SO: J-Infect-Dis. 1992 Jul: 166(1): 215-6
i
15 of 16
TIs
AU: Lagardere-B; Che?val 1 ier-B• Cheriet-R
ADs Service de Pediatrie,, Hopital Ambroise Pare, Boulogne.
SO: Ann-Pediatr-Paris. 1992 Mar; 39(3): 159-64
AB: The incidence of infantile visceral leishmaniasis is currently increasing!,
at least in the Mediterranean region. Most cases seen in France occur on the
Mediterranean coast or are imported from Africa. However, contamination in
other regions of France is not an e>iceptional occurrence and may raise
diagnostic problems. The parasite reservoir is the dog population in which the
prevalence of Leishmania infection is particularly high in the Provence and
Cevennes regions. Both teenagers and young children may be affected by this
disease, whose clinical manifestations may be misleading. The typical
symptomatic triad, i . e . „ anemi a-f ever-en 1 arged spleen R may be incomplete!,
especially as a result of the intermittent character of the fever. Patients may
remain afebrile for long periods. Diagnosis rests on demonstration of the
parasite in bone marrow specimens (several biopsies are often required) or in
the spleen. Bacterio1ogic studies using a special medium are helpful. Serologic
tests are sensitive and specific but often become positive only late in the
disease. Management still rests on pentavalent antimonial compounds. Advances
have been made in the understanding of the toxic effects and rules for optimal
use of these drugs. Improved insight into the parasite's biology may result in
use of new forms of treatmen t: allopurinol is at present the only recent
addition to the armamentarium which has been proved effective in humans when
uven in combination with an antimonial compound.
16 o -F 16
TIs CKala-azar■ Is it possible to treat it with aminog1ucosides?J
AUs Tapia-Collados-C: Comino-Almenara-L? Escriva-Tomas-P; Ribera-Delgado-M;
Gonza1ez-Peraba-J; Tapia-Lopez-M; Lopez-Pena-L
AD: Servicio de Pediatria, Hospital General, Alicante.
SO: An-Esp-Pediatr. 1992 Jan; 36(1): 37-8
AB: We report the case of a 13 month old male infant with visceral
leishmanisis. The clinical picture was suggestive of kala-azar, but a bone
marrow aspirate was negative, so treatment was not started. During the course
of the process an urinary infection was documented and therapy with
aminoglycosides was begun. At this time we observed that hepato—and
sp 1 eno—meqa 1 y diminished and then disappeared and clinical m a n i F e s t a t i o n s
in>proved. We later received a p o s i t. i. v e s-i e r o 1 o g y -f o r I. e i s I»m a n i a cl o n a v a n i . W e
review the medical literature in respect to this therapeutic possibility.
PC-SPIRS 3.30
MEDLINE
(R)
1991
MEDLINE (R) 1991 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.
TI :
AU:
SO:
1 of 9
Amphotericin B for second-line treatment of Indian kala-azar Eletter!
Mishra-M; Singh-MP; Choudhury-D; Singh-VP; Khan-AB
Lancet. 1991 Apr 13; 337(8746): 926
2 of 9
TI : Post ka1a-azar dermal leishmaniasis: the Kenyan experience.
AU: Muigai-R: Gachihi-GS; Oster-CN; Were-JB; Nyakundi-PM; Chunge-CN; Kirigi-G;
Rashid-JR
AD: Clinical Research Centre. Kenya Medical Research Institute, Nairobi.
SO: East-Afr-Med-J. 1991 Oct; 68(10): 801-6
AB: Post kala-azar dermal leishmaniasis (PKDL) occurs occasionally after
successful cure of visceral leishmaniasis. Twelve patients with diagnosis
consistent with PKDL were seen at Clinical Research Centre from 19S1 to 1985.
Clinical presentation ranged from macular hypopigmented lesion to generalized
nodular lesions. All lesions cleared either by self-cure or by treatment with
sodium stibogluconate.
3 of 9
TI : Comparison of regimes of treatment of antimony-resistant kala-azar
patients: a randomized study.
AU: T h a k u r - CP: I ■. 1.1 m a r - M ; P a n d e y - A K
AD: Patna Medical College and Hospital, Patna, Eli bar, India.
SO: Am-J-Trop-Med-Hyg. 1991 Oct; 45(4): 435-41.
AB: Three hundred twelve patients with antimony-resistant kala-azar were
randomized into three groups, The first group (A) received pentamidine
isethionate intravenously three times each week until parasitological cure was
achieved. Group B received pentamidine concomitantly with a 20-day regimen of
sodium stibogluconate. Group C received pentamidine injections that were
followed by 20 days of sodium stibogluconate therapy. All patients became
afebrile after 10 injections of pentamidine. Parasitologic cure was achieved in
approximately 987. of the patients who had 33 or more injections of this drug.
The addition of the antimony compound did not appear to enhance the rate of
parasitologic cure. Three patients continued to have parasites after 40
injections of pentamidine. After six months, the rate of parasitologic cure was
significantly higher in Group C (pentamidine followed by sodium stibogluconate)
than in either Group A or B. Forty patients relapsed after apparent
parasitologic cure and were successfully treated with five additional
injections of pentamidine, followed by a course of antimony therapy. Minor side
effects with pentamidine included an uneasy feeling during intravenous
injection (127.), intestinal disturbances (67.), cellulitis (57.), abscess
formation (17.), and allergic manifestations (27.). Major reactions to this drug
included hyperglycemia (107.; reversible in 67. and irreversible in 47.), and
delayed hypoglycemia (87.). Four deaths were associated with the administration
of this compound. It is concluded that pentamidine is an effective but toxic
drug for the treatment of antimony—resistant kala—azar.(ABSTRACT TRUNCATED AT
250 WORDS)
4 of 9
TI: Kala-azar in displaced people from southern Sudan: epidemiological,
clinical and therapeutic findings.
AU: Zijlstra-EE; Ali-MS; el-Hassan-AM; el-Toum-IA; Satti-M; Ghalib-HW;
Sondorp-E; Winkler-A
AD: Leishmaniasis Research Group, Medical Research Council, Sudan.
SO: Trans-R-Soc-Trop-Med-Hyg . 1991 May-Jun; 85(3): 365-9
AB: Six hundred and ninety-three patients with kala-azar were seen in Khartoum,
Sudan, from January 1989 to February 1990. They were almost exclusively from
the Nuer tribe, originating from the western Upper Nile province in southern
Sudan, an area not known previously to be endemic for kala-azar■ Because of the
civil war in southern Sudan no treatment was available locally and massive
migration to northern Sudan occurred; many died on the way. All age groups were
affected; there was a slight male preponderance (56%). In the clinical
presentation, marked generalized lymphadenopathy was prominent (847.).
Splenomegaly was absent in 4% of cases. Patients usually showed anaemia,
leucopenia and/or thrombocytopenia . 623 patients were treated with sodium
stibogluconate, 10 mg/kg for 30 d; relapse occurred in 47. and death in 127..
Latterly, 70 patients were treated with sodium stibogluconate at 2 x 10 mg/kg
for 15 d, with relapse in 67. and death in 67.. The difference between the 2
regimens in the number of relapses and deaths was not significant. The outbreak
may have been caused by a combination of factors: the introduction of the
parasite from an endemic area to a non-immune population, the presence of
malnutrition caused by loss of cattle and unavailability of other food sources,
and possibly an ecological change in favour of the sandfly vector.
5 of 9
TI: Evaluation of efficacy of longer durations of therapy of fresh cases of
ka1a-azar with sodium stibogluconate.
AU: Thakur-CP; Kumar-M; Pandey-AK
AD: Patna Medical College Hospital.
SO: Indian J-Med-Res. 1991 Mar; 93: 103.10
AB: The efficacy and safety of three regimens of treatment for ka1a-azar
(visceral leishmaniasis) with sodium stibogluconate were evaluated in a
randomised clinical trial to ascertain the optimal duration of treatment for
Indian patients. The study included a total of 312 (226 male, 86 female)
patients with fresh ka1a-azar. confirmed by demonstration of parasites in
aspirates from bone marrow or spleen, who were randomly allocated into three
treatment groups of 104 patients in each to receive sodium stibogluconate
intramuscularly. The dose of the drug was 20 mg/kg/body weight/daily with a
maximum of 8.5 ml for 20, 30 and 40 days (groups A, B, C respectively). The
response of treatment was assessed under blind conditions and patients were
followed up each month for a period of six months. The number of patients who
were apparently cured (i.e., those whose temperature had returned to normal at
the end of their respective regimen and aspirates were free of parasites) was
91 (877.) in group A, 98 (947.) in group B, and 102 (987.) in group C. The
difference between groups A and C was significant (P less than 0.01). The
.umber of patients who were? ultimately cured at six months was 74 (71Z) in
group A, 86 (837.) in group B and 98 (947.) in group C. These patients had not
relapsed and were cured as confirmed by a bone marrow aspirate which was free
of parasites. The difference between groups A and C (P less than 0.001) and
groups B and C (P less than 0.05) were significant. However, the difference
between groups A and B was not statistica11y significant.(ABSTRACT TRUNCATED AT
250 WORDS)
6 of 9
TI: Serodiagnosis of Indian kala-azar: evaluation of I FA, ELISA and CIEP tests.
AU: Mittal-V; Bhatia-R; Sehgal-S
AD: National Reference Centre for Ka1a-azar, Zoonosis Division, National
Institute of Communicable Diseases, Delhi, India.
SO: J-Commun-Dis. 1991 Jun; 23(2): 131-4
AB: The sensitivity and specificity of three serological tests viz. indirect
immunofluorescent antibody test (IFAT), enzyme linked immunosorbent assay(ELISA) and counterimmunoe1ectrophoresis (CIEP) for the diagnosis of Indian
<31 a-azar were evaluated. Of the 209 patients in whom Leishmania donovani
parasite could be demonstrated in bone marrow, 207 (99.04 per cent) could be
1
<
diagnosed with IFAT, 203 (96.6 per cent) with CIEP and 208 (99.5 per cent) with
ELISA. None of these serological tests was positive in 40 healthy individuals
and 10 patients each with tuberculosis, toxoplasmosis and malaria. In only one
out of 10 patients with malaria ELISA alone gave false positive result. Of the
119 patients who had clinical features simulating kala-azar but were negative
for Leishmania donovani in bone marrow and responded to treatment other than
that for Indian Ka1a-azar, IFAT, CIEP and ELISA were false positive in three
(2.5 per cent), nil and three (2.5 per cent) cases, respectively. The use of
serodiagnostic tests like ELISA for mass screening and CIEP in less well
equipped peripheral laboratories is suggested.
7 Of 9
TI : Identification of immune complex antigens in sera of Indian kala-azar
patients.
AUs Sanyal-T; Ghosh-DK; Sarkar-D
AD s Department of Cell Biology, Indian Institute of Chemical Biology, Calcutta.
SO: Indian-J-Exp-Bio1. 1991 May; 29(5): 411-5
AB: Level of circulating immune complex (IC) in visceral leishmaniasis is much
higher than that in control sera. In immunob1ot experiment, treatment of
ka 1a-aza r IC with patient sera showed at least 6 bands of which the band around
55 kDa region was most prominent. The band at 55 kDa is primarily due to the
resence of an antigen recognized by its corresponding antibody present in the
patient sera. This was confirmed by using radio!abelled antibody from ka1^-azar
patient serum and antipromastigote serum. The heavy chain of IgG originating
from IC is also present in the same region which was detected by its
recognition with antihuman IgG. The IC gave a band at 55 kDa region with
sea-urchin antitubulin. Ka1 a-azar sera also reacted with purified rat brain
tubulin . The present results suggest that a tubulin like protein is present at
55 kDa region along with the heavy chain of IgG.
8 o-F 9
TI : [Transitory acute kidney insufficiency and insulin-dependent after
treatment of kala-azar with pentamidine and N-methy1g1ucamine antimony3
AU: Morin-D; Dumas-ML; Valette-H; Dumas-R
AD: Service de Pediatrie I? Hopital St-Charles, Montpellier.
SO: Arch-Fr-Pediatr. 1991 May; 49(5): 349-51
AB: Azotemia and diabetes mellitus are now well-known adverse reactions
associated with Pentamidine treatment, especially since? its prescription in
case of Pneumocystis carinii pneumonia. We report the case of a 2 year-old boy,
treated for ka1a-azar with pentamidine and N-methy1 glucamine antimoniate who
developed adverse effects., characterized by a nephrotic syndrome associated
with the classic acute tubular necrosis, and transient diabetes mellitus.
9 of 9
TI: C3 cases of visceral leishmaniasis, one in a HIV-positive man]
AU: Balslev-U; Jonsbo-F; Junge-J: Bentsen-KD
AD: Hvidovre Hospital, Kobenhayn.
SO: Ugeskr-Laeger. 1991 May 27; 153(22): 1591-2
AB: Three cases of visceral leishmaniasis (kala-azar) are presented. One of
these was in a 43-year-old patient with AIDS who was infected in Southern
Spain. Another was in a man aged 25 years infected in West Africa. These cases
are the first two adults to be reported in Denmark. The third case was an 18
month old previously healthy boy, infected in Southern Spain. The
symptomtology, diagnosis and treatment of the disease are discussed and it is
stressed that serological diagnostic tests have limited value in HIV positive
pat ien ts.
s ji ■ /h
ft
mnary Health Care
I
“—
[kala-azar control programme for remote
Iribal communities
^Thakur, Sister Frances, Sister Therese, Sister Victoria, & Sister Puspa
Udigenous people have been trained to provide a culturally
ippropriatekala-azar control programme for the tribal population of
^hibganj, Bihar, India. Cultural resistance to modem medicine has
Ten overcome and the influence of village witch-doctors has been
I countered.
I d
| In the district of Sahibganj, Bihar, India there
; rere 23 670 new cases of kala-azar between
1985 and 1990. Under the auspices of the
j Social Development Centre, Dumka, an
J emergency plan was drawn up to tackle this
atuation. Thirty' village health workers
3 t^rcc’^ay raining course during
’■hich they were taught how to administer
iwium stibogluconate intramuscularly, spray
1, conduct door-to-door surveys, and
ncourage affected persons to go to health
■Hires. Six sisters attached to Christian mis■hh? were given a reorientation course in the
°1 of the disease.
'^reness programmes
the help of headmen, kala -azar
eness programmes were organized in
. aSes- Information on the importance,
ent and control of the disease was
In remote and hilly tribal areas It Is desir
able to have carefully prepared educative,
preventive and curative programmes in
place, backed up by mobile hospitals
carrying simple diagnostic and spraying
equipment.
imparted in the local language. Publicity
materials were supplied by the government. It
was explained to the villagers that the disease
could not be controlled by witch-doctors, and
that spraying the insides of houses was vitally
important. Only after an awareness pro
gramme had been undertaken were control
measures applied in any particular village. It
was found that such programmes had to be
repeated from time to time in order to renew
the confidence of the people in the measures
adopted.
Spraying with DDT
^lleop h-rT1er'tus Pro,essor °f Medicine, Patna Medi=. Sister’o p address is Fraser Road, Patna-800001
■folyCrnso unC?S’ Therese' Victoria and Puspa are with
woss Health Centre. Sita Pahar. Sahibganj, India.
Following an investigation by entomologists
into sandfly prevalence and the susceptibility
of the vectors to DDT, the insecticide was
'^IthForL
vm • /oiume 15 • 1994
245
■
I
Hillel
TlUtJ ml L/dl L
sprayed during January/February and
May/June on the inner walls of houses and
covered cowsheds up to a height of about two
metres at 1 g/m2, using approximately 1.4 kg
DDT per 14 litres of water. The numbers of
kala-azar and malaria cases were estimated
before and after intensive spraying was con
ducted in several remote villages.
Treatment
i
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L
<;
-
■
.-’M:
A survey was conducted in order to discover
persons who had been suffering from fever
for more than three weeks and they were per
suaded to attend the health centres for further
investigation. In each such case, total and
differential counts of white blood cells were
made, the haemoglobin concentration was
measured, the aldehyde test was performed,
and thick and thin blood smears were pre
pared for the detection of malaria parasites.
If the aldehyde test proved positive, treatment
for kala-azar was initiated. Sodium stiboglu
conate was given intramuscularly at 20 mg per
kg body weight daily for 20 days in new cases
and for 40 days in relapsed patients, with a
maximum of of 850 mg. Following diagnosis
and the start of treatment at the centres, treat
ment in the villages was carried out by village
health workers, who were requested to ensure
Ihr ■
It was explained to the villagers that the
disease could not be controlled by witch
doctors, and that spraying the insides of
houses was vitally important.
rf
Bl s 5
that people newly diagnosed as having kalaazar took 20 injections of the drug and that
relapsed cases took 40 injections.
Hi
Patients who failed to respond to the 20-day
course of treatment were categorized as cases
246
of primary' unresponsiveness. Clinical cur
was considered to have been achieved if
patients became afebrile and their spleens
returned to normal size. If no relapse
occurred in the following six months the ®
patients were regarded as having been defini
tively cured.
|
■J.1-—
At the Sohorghati, Kundly, Sahibganj and W
Pahar centres there were respectively one, cl
one, one and three sisters and two, four, W
20 and eight village health workers, and the
patients with kala-azar who were treated M
numbered 191, 84, 403 and 962 respectively.^;
Of the 1640 treated patients, 1592 werecuredj
and of the 48 patients who relapsed and were:
treated again with a 40-day course of sodium:
stibogluconate, eight relapsed a second time.
Forty-four patients became unresponsive ■
to sodium stibogluconate and were sent to •'
hospitals for treatment.
Spraying presented difficult problems in
remote areas, particularly where the equip-j *
ment had to be carried by hand for long
distances. Without great dedication on the .m
part of local workers it would have been
impossible to achieve the desired coverage.^
The spraying operations, performed by the
village health workers and supervised by the
sisters, reduced the incidence of kala-azar
malaria in three villages where monitoring-^,
was carried out; increased numbers or cases^
were recorded in one village, perhaps becaUST^ -.
heightened awareness resulted in more PeC^:
going to their health centre for treatment
Strict supervision was the key to thesucce^O
of the spraying programme.
The ratio of male to female patients was I*.
1, whereas in a hospital-based study a rati^^g
2 to 1 had been reported, possibly
World Health Forum • Volume
AiiiJ’Jz'Ji Cuniiui lil ft- .
i nCy to refer males rather than females to
tai when the condition of patients
^mes serious. People with kala-azar
nded better to drug treatment in newly
areas than in areas where the disease
^appeared in the early 1970s, perhaps
^inadequate doses of the dmg had
j^used in the latter areas, giving nse to
^j‘t-
Clearly, when plans are being drawn up for
the control of kala-azar it is important to take
local circumstances into account. In remote
and hillv tribal areas it is desirable to have
carefully prepared educative, preventive and
curative programmes in place, backed up by
mobile hospitals carrying simple diagnostic
and spraying equipment. ■
X
‘ ' ‘
■H
*1
.
. '
' -O
distance.
^5#*~_____________ ___________ _ __
^0:’>
I
.|Wr >
’
th'.:
fe>
Importance ol the blood supply
I< i'r
F: ■
bloodtransfusion service. No general hospital can be effective unless it can
perform blood transfusion, and if blood is not available from an outside
Source, the hospital itself is obliged to undertake the task of blood collection.
I
The recruitment and selection of blood donors are critical to the success of a
blood programme, and every effort must be made to ensure both the safety
of the donor and the safety of the transfusion for the recipient. The process 0
donor selection is reliable only when information provided by donors can oe
trusted, and experience has shown that this is most likely when there is no
material gain from donation. Problems in donor selection are considerab y
reduced when a blood transfusion service is founded upon the principle 01
voluntary, unpaid blood donation.
<
r-r
J
■ w N Gibbs & A. F. H. Britten, ed. Guidelines for the
organization of a blood transfusion service. Geneva.
World Health Organization, 1992: 1.
& ,^lthForum • Voium€ 15 . 7994
247
■
I
I
I
?
KAI.A-AZAR CONQURED !
r
By
E Varghese SVD1, PP Hembrotn, PV Raj„S Melookunnel & R Tiwary
LI INTRODUCTION
leishmaniasis or Kala-azar (as popularly called in India - KA) is considered as one
of die six dreaded tropical diseases of human beings by WHO. h its briefing on
Leishmaniasis published in 1991 WHO listed 83 countries as affected by
Leishmaniasis. A Briton,
Dr. Lainson reported in 1983 ( Indo-UK Workshop on
Leishmaniasis) dial KA is major public healdi problem faced by the tropical world. He
said there are about 4 lakhs (400,000) new cases of Leishmaniasis registered each year
in die world.
12. KA INCIDENCE IN INDIA
In India KA has been occurring in endemic (restricted to certain pockets only),
epidemic (seasonal like cholera or gastro-enteritis) and sporadic (sudden outbreak)
forms since long It was reported for die first time in 1824-25 in Jessore (West Bengal)
by Dr. Elliot Later between 1854-75 die fever in Burdwan district of West Bengal and
the epidemic fever in Garo Hills in 1870 was described as KA by Dr. Clark in his
sanitary report. First epidemic of KA in Bihar occurred in 1882 and after that a gap of
about 10 years die epidemic shuck in 1891, 1917, 1933. Because of die rising menace
of (lie KA in Bihar, the Government of India constituted an expert committee under the
Chairmanship of Dr. Harcharan Singli in 1985, which recommended urgent setting up of
a National KA Control Programme. But nothing came of it If one goes by the reports
and die data from the field study KA is ever on the increase, particularly in Bihar. Not
even one third of die cases get reported; because, veiy few patients come to the centres
for treatment owing to die distance, high cost of treatment, travel and other expenses;
lack of proper information and utter poverty.
1 Institute of Indian Culture, Mahakali Road, Andheri East, Mumbai 400093 India
1
I
g
r
[f
The eastern belt of the country, specially Bihar is the worst hit by KA followed by West
Bengal and Uttar Pradesh. Dr. C P Thakur (Patna) reported that there were over 250,000
cases in Bihar in 1991-92.
Muzaffarpur, Darbanga, Vaishali, Samastipir, West
Chainparan, Sahibganj, Pakur, Godda and Dunika, are some of the worst hit of the 33
affected districts in Bihar. In West Bengal in 1949 there were 35,147 reported cases,
which in 1964 came down to 804. But in 1982 it was 979 from Maida, Murshidabad
and 24-Parganas alone, showing an upward trend reported Dr. Chowdhury of Rajendra
Memorial Research Institute (RMRI, Patna). An enquiry at the dispensaries that treat
KA in Hiranpui, Sitapahr, and Sohargliatty, lias shown that when Soharghatty liad 720
KA patients, Sitapahar had 1112 and Hiranpur NSM outpost had 175 cases treated in
1996. Sonadani and Magbita villages in Littipara block (Pakur district) have 110 KA
positive cases out of 700 population, i.e. over 15 per cent people of this area are KA
affected reported Dr. Chandrashekhar, Director ofNavjeevan Seva Mandal (NSM).
1.2. THE PARASITE
Leishmaniasis is caused by Leishmania donovani (named after William Leishman and
Charles Donovan (1903) and oriental sore by L. tropica. Species and sub-species of
the genus Leishmania are parasitic protozoa, related to the Trypanosomes. They are
digenetic parasites, completing life cycle in two different hosts - mammals and
phlebotomie sand flies. There is no conclusive evidence of a sexual cycle in the life
history ot Leishmania^ which appears to divide only by simple binary fission in both
the vertebrate and invertebrate hosts. In the vertebrate host it occurs in the amastigote
form. Spread of the infection in the host may occur when infected macrophages divide
and share their parasite among the daughter cells, or on the heavily infected cells and the
ingestion of the liberated amasitgotes from the macrophages by the vectors. The
incubation period in the vertebrates varies from few weeks to months. Since KA is an
immunosupprassant disease the patient is exposed to secondary infections li|ce
tuberculosis. And since the parasite is intracellular unresponsiveness to drug therapy is
.Y
frequent
2
.. 'V
r
f
LI VECTOR
Phlebotomine sand Hies of Phlebotomus and Sergentomyia genus
is the vector.
Phlebotomus argentipes is found in cowsheds and mud walls of thatched liouses. JulyNovember is die time diey are found in abundance. During tliis time about 81 percent of
flies caught were KA positive reported Dr. Hati, of RMRI, Patna. They usually breed in
damp and dark places where the.dead organic matter is available. RMRI, Patna,
recommends die use of mud and lime plaster for an effective ecological approach to
vector control, in the case of sand flies, particularly as Phlebotomus argentipes and P.
papatasi are growing DDT resistant.
L 4. SYMPTOMS & STRAINS
Anaemia, anorexia, cough, dry and rough skin, fever, hyperipigmentation of skin, jaundice
(in some cases) loose motion, loss of weight, swelling feet, hepato and spleenomegaly,
sparse and brittle hair, etc. are some of die common symptoms of KA. It can be classified
into visceral form and cutaneous form. Visceral Leishmaniasis includes Indian KA,
African and Mediterranean KA. The oriental sore, espundia and post Kala-azar dermal
leishmaniasis (PKDL) group under the cutaneous form. According to Locksley there are
four major clinical syndromes
in this, viz. Visceral Leishmaniasis, cutaneous
Leishmaniasis of die old and new worlds, mucutaneous leishmaniasis (espundia) and
diffuse cutaneous leishmaniasis. Tliis project was primarily concerned with the treatment
of visceral leishmaniasis only.
*
»
15. TREATMENT
Researchers say that while Malaria has only 4 major human straini, KA has at least 19
different strains associated with human infection.
rAdded to this, impaired immune
system of the host in visceral leishmaniasis, doctors opine, is one of the main causes of
unsatisfactory chemotherapy, 'there have been attempts al developing a vaccine since a
few years. But no definite result has been reported yet! Following are the frequently
used KA remedies:
I- .
3
i
?
*
1. Sodium Stibo-Gluconate (SSG) or Sodium Antimony Gluconate (SAG): First
line ding and die drug of choice in KA treatment Dosage: daily injection of 20
mg/kg/bw for a period 20-40 days. Dr. C.P. Thakur and others advise longer duration
SSG / SAG therapy for fresh cases.).
2. SSG is the drug of choice in PKDL as well.
■
f.:
- V
?
3. Pentamidine : Could be used in resistant or relapse cases of’KA Dosage? 4
< '
mg/kg/bw intravenously for 35 days. Drug causes diabetes mellitus.
V
4. Amphotericins B : It is a potent drug associated with severe toxicity. Duration of
treatment with this drug is 45 days. It is usually given on a gradually increasing dosage
starting with 0.05 mgAg^w to 1 mg from l-5th day. From the sixth day the injection is
on alternate days a 1 mg/kg / bw. Rigor, shivering and fever are manifested during the
treatment 'Hus drug is to be administered in hospitals with revival facilities only.
Allopurinol, metronidazole, keto-conazole, 8-aminoquinalone, miltoforine, etc. are some of
4 ■
the oral drugs for KA KA patients, once cured, are immune to the viscerotropic fonn of
L donovani. But there is apparently reported cadriotoxicity in cases of KA undergoing
antimony therapy.
16. RATIONALE BEHIND THE CHAI INTHA IIVE
All the above mentioned remedies have severe reactions and toxicity. Besides, since the
most affected people are illiterate, poor and are largely subsistence labourers and
cultivators they cannot afford to go to the nearby dispensaries and hospitals (which are 220 km away) daily to get the injection. Nor can they afford to pay.
Of course the
government has been trying to provide SSG / SAG free of cost through selected outlets
momtored by the Civil Surgeon. But mostly the supply is irregular and such dispensing
centres are far too few for the vast number of people affected. So, for these various reasons
most of them would not complete the prescribed course. Ibis necessitated the search for a
vable, cheap ^d locally available alternative. So the CHAI constituted a project team
comprising of F¥. Meloo SJ (Co-ordinator), Dr. E. Varghese SVD (Principal Investigator)
Dr. PP Hembrom (Indigenous Practitioner), Dr. PV Raj (Professor and Head of the
I
Department of Kayachikitsa, Ayurveda College, Hyderabad,
Honorary Co-PI, and ’
■!
4
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t
c
S;
r
Consultant), Dr. Rnjender Tiwary (Supervising Medical Officer - ayurveda) and other
local co-ordinators and supervisors for running a piljt project on treatment for KA with
herbal medicine. The team improved on the basic formulation of Dr. PP Hembrom and
other local practitioners who claim to have had success in treating the KA cases, and made
a herbo-mineral formulation.
L 7. IMPLEMENTATION
Having already ascertained the need for such an initiative through the member institutions
of CHAI serving in the affected areas it entrusted die work of the project to constituted
expert team. The team did extensive literature survey and background study, consulting
prominent researchers like Dr. C.P. Thakur, Patna, and A Nandy, Calcutta, before
launching die project Culture tests were also conducted with the medicine on the parasite
culture.
It then set up a local Ethical Committee, comprising the Village Headman of Satia village
(Pakur), a practising lawyer, five prominent persons from the locality, under the auspices
of CHAI, a registered Trust 'Hie committee studied the project proposal well and gave the
assent to proceed, considering the benefit and the least risk involved in this. Nodal
agencies were intimated regarding this pilot project, which of course is not required for
using a known drug under the direct supervision of a registered ayurvedic medical
practitioner.
A sample oi 49 patients were selected at five centres, namely Chandnahat and Damuruhat
(Godda distr ict), Kodma and Sitapahar (Sahibganj district) and Soharghati (Pakur district).
The probable patients were serened and selected at these centres as and when patients
1
came in on their own, by the attending physicians, after obtaining the informed consent and
fulfilled other WHO recommendations in pilot projects. KA suspected patients were sent
to the nearby hospitals for laboratory investigations. Those who exhibited the usual clinical
symptoms and tested KA positive in Aldehyde test and DAT, with high ESR were sent for
bone marrow smear test. Those tested KA positive in all these tests were administered.the
medicine prepared under the direct supervision of the project team. Each patient was
I
5
r
I
A';-/.’:
••
...ontaed and
we" l"“i"'ain"1 at
I.iitay »d <*»•* »»
C“,'r’'
After r rwlelir® the st.puhded c»OTe rrldelryde test »d blood test, were done, be.rde.
the improvement in th. general condition and the clinical nynptom. noted earlier.
IhoBe with no fever, no hepnto/sple.nomegaly, no.rnal Wood connt. and negative aldehyde,
and in some cases bone marrow smear lest. and were considered cured.
n.a. HERBO-MINERAL FORMULATION
Number
Botanical Name
Skt / Hindi Name
Part Used
1
Boerhaavia
Punamava
Root
diffusa
Beshakapore
Plumbago
Chitraka
zeylanica
Chitrak
lritex
Nagbail
peduncularis
Charaigorwa
2
3
?
Root
Bark
/?
■i
PREPARATION:
Treat die finely cut pieces of Plumbago roots in lime water for about two hours to purify it
I
before putting it into the mixture. Make decoction of the above medicines taken in 1. 1/2 . 1
proportion and finely cut in 16 parts of water and boil down tn half on slow fire. Afler
sieving the decoction add 10 g of Woodfordia Jmticosa flower powder, 1 g of pepper
powder and 50 g ofjaggery for 1 litre decotion as preservative, yarm it up again for some
time, cool it and bottle it
-
1i .
DOSAGE:
25 ml x twice daily x 45 days. For children give 15 ml instead of 25 ml.
i
To activate the medicine each patient is given 125 mg of Triphala-Mandoor powder once
daily.
?•
■
6
. I
♦
tl.........
.,..1 .4....
. ,1 mol »'• ••
Triphala-Mandoor Preparation:
\
?■
Phyllofithus emblica fruit powder 1 part
Terminalia belli rica seed powder 1/2 part
Tenninalia chebula seed powder ‘/apart
Add 10 g of Mandoor rasa to 100 g of the above mixture to make the triphala mandoor
mixture.
ITT RESULT
In all 49 patients took the treatment (Cahndnahai: 15; Damnjhat: 3; Kodma : 8; Sitapahr:
14; and Soharghalti : 9). Of these 32 completed the course and 26 had positive reslutff,
meaning healed or nearly healed. Ihose who were not healed or those during the course of
treatment wanted to switch over to allopathic treatment for whatever reasons, were given
free stibnite treatment Given below is the patient list from the 5 censes who underwent the
treatment:
PRE-TREATMENT RECORD (Chandnahat Centre)
Village________Remark
Weight
Name of patient
Sex
Age
1. Agnes Tudu
F
18
42 kg.
Chandhna
New Case
2. Babudahan Soren
M
32
35
Langodi
New Case
< 3. Barka Hans'dak
M
16
34
Dumerthari
New Case
4. Bema Hembrom
F
40
44
Chandana
New Case
5. Budhrai Tudu
M
40
44
Sagor
Relapse Case
6. Choto Hansda
M
10
21
Sagor
New Case
7. Chunde Soren
M
40
41
Molianpur
Relapse Case
8. Marcella Hembrom
F
35
42
Chandna
New Case
9. RamaPaharia
M
10
24
Jolo
New Case
10. Sahal Kisku
M
18
26
Sindri
New Case
11. SaibaTudu
F
45
43
Borwa
New Case
12. Salomi Murmu
F
.. 35
40
Borwa
New Case
13. Sarojini Murmu
F
27
40
Langodi
New Case
14. Sonoti Hansda
F
12 ’
20
Borwa
New Case
15. Suleman Murmu
M
35
40
Sagor
New Case
No
Fev.
Liv
TC
Hb
ESR
7
Aide DAT BM
Wt
Date
*
i
«
■■
*
- li
42
070597
4+
35
100197
4+
30
030397
NP
4+
' 35
230397
NP
4+
4+
44
250497
5”
5”
NP
4+
4+
21
020497
104
102
5”
NP
4+
41
161296
7
104
3”
NP
‘4+
42
030297
8
103
3”
NP
4+
24
100397
9
104
5”
NP
+
26
040497
10
104
4”
NP
44-
43
030197
11
12
102
5”
NP
44
40
281296
13
102
5”
NP
44
4-
40
171096
14
103
4”
NP
44
4+
27
030597
15
104
4°
NP
40
251096
1
102
4”
NP
2
103
5”
NP
3
104
y’
NP
4
101
4”
5
104
6
J800
2500
4000
+
116
9.2
150
7
5.2
120
+
+
44
POST-TREAl’MENT REPORT (Chandanahat)
Liv.
TC , Hb
ESR
Aide DAT
BM
Wt
Date
Rem
1”
NP
4200
9.2
65
Neg.
Neg.
45
240697
good
98.8
NP
NP
Neg.
39
280297 good
3
98.6
NP
NP
Neg.
32
200497
4
98.2
NP
NP
Neg.
36
100597 good
5
99
1”
NP
Neg.
Neg.
47
090697 good
6
98.6
3”
NP
Neg.
+
23
140797
OK
7
98.2
NP
NP
Neg.
Neg.
43
080297
OK
8
99.6
r
NP
+
42
200397
impr
•f
i.
9
99
NP
NP
Neg.
26 * 050597
OK
- •.
10
99.2
2!’
NP
Neg.
28
200597
OK
11
98.8
2f’
NP
Neg.
45
200297
OK
12
98.2
NP
NP
Neg.
42
090297• OK
ii ■
No
Fev
1
99
2
3500
7
100
f
8•
OK
13
98.4
NP
NP
14
98.6
2”
NP
15
98.8
1”
NP
Neg.
6
4300
120
Neg
-
Neg
+
42
160197
good
28.5
150797
impr
43
080297
OK
PRE-TREATMENT RECORD (Damruhat Centre)
16. Baju Marandi
M
20
38 kg Pottamdi
New Case
17. Bemabas Hembrom
M
24
39
Kondapur
New Case
18. Ramchoran Soren
M
30
45
Titria
New Case
No
Fev.
Spl.
Liv.
TC
Hb
ESR
Aide DAT
BM
Wt
Date
16
99
3”
NP
5300
8
150
4+
38
081096
17
irreg
2”
NP
9300
11
85
4+
40
211096
18
102
2”
NP
1020
8
160
4+
+
+
+
45
091096
POST-TREATMENT RECORD (Damruhat)
No
Fev
Spl
Liv
TC
Hb
ESR Aide DAT
16
98.4
NP
NP
5300
8.6
20
Neg
17
98.2
1”
NP
9300
11
40
Neg.
18
98.6
NP
NP
6800
8
66
Neg.
BM
Wt
Date
Rem
42
251196
good
Neg
40
121296
OK
Neg.
46
261196
good
PRE-TREATMENT RECORD (Kodma Centre)
19. Chundka Hembrom
M
25
41
41kg.
kg
Mvsol
Mysol
Relapse Case
20. Chundkae Basky
M
7
14
Bethany
New Case
21. Gabriel Tudu
M
50
45
Kodma
Relapse Case
22. Matti Horon
M
8
24
Kodma
New Case
23. Mongol Hembrom
M
18
35
Kodma
New Case
24. Sumi Ibdu
F
12
26
Titalia
Relapse Case
25. TalaBesra
M
8
24
Pakaria
Relapse Case
26. Teresa Besra
F
30
41
Banghi
New Case
ESR
Aide DAT
No
Fev
Liv
TC
Hb
9
BM
Wt
Date
J
.
‘r
19
NP
NP
8.6
60
44-
4-
2+
41
101196
7
68
4+
-4
4+
14
101196
20
>>
4°
1’*
21
102
2»
NP
3900
5.5
45
4+
4-
4+
45’
290497
22
103
3”
NP
5400
6
68
44-
4-
24-
24
060597
23
102
5”
2”
3050
5.2
34
44-
■4
24-
35
080597
24
98.4
4”
NP-
44-
4-
4-
26
131196
25
98.8
6’’
NP
2750
7.2
80
44-
4-
4-
24
071196
26
103
4”
NP
2200
5.6
33
4-
-4
4-
41
071196
POST-IKEATMENT RECORD (Kodma)
!
Hb
ESR Aide
DAT
BM
Wt
Date
Rem
NP
8.6
6
Neg
Neg.
Neg.
43
281296
good
NP
NP
7
16
Neg.
Neg.
Neg.
15
281296
OK
98
NP
NP
RA
RA
RA
Neg.
RA
RA
RA
150697
22
98.6
NP
NP
RA
RA
RA
Neg.
RA
RA
RA
230697
23
98
NP
NP
RA
RA
RA
Neg.
RA
RA
RA
250697
24
98
1”
NP
Neg
28
150197
OK
25
98.4
2”
NP
Neg.
27
221296
OK
26
98.2
NP
NP
Neg
42
221296
OK
Liv
98.6
Sp_l
NP
20
98.2
21
No
Fev
19
PRE-TREATMENT RECORD (Sitapahar Centre)
i.
r;e
:c'
t
4^
TC,
27. Abdul Hamid
M . 8
16 kg Borio
28. Ajnara Khatoon
F
6
12
Udhwa N^w Case
29. Bale Hembrom
F
25
33
Barhait New Case
30. Baso Soren j
M
7
19
Dabdiha New Case
31. Chundby Marandi F
22
35
Barhait NewiCase
32. Clement Kisjai
M
10
24
Talbaria New Case
33. Jetha Hansdak
M
50
48
Satia
34. Lundhya Besra
M
8
15
Shardharia New Case
I
Relapse Case
Relapse Case
K
10
l’;
New Case
35. Munijan Maria
F
20
44
Denja
36. Pamei Khaioon
F
8
16
Jamnagar New Case
37. Simon Malto
M
40
46
AmbarparaNew Case
38. Sukha Kliatoon
F
12
32
Bhaia
New Case
39. Surdliani Hembrom F
26
25
Sabdrka
New Case
40. Susani Muimu
8
19
Sarmapur
Relapse Case
TC
Hb
j
?■ ■
M
No
Fev
27
100
2”
1”
4+
28
99.6
5”
1”
4+
29
98.6
4”
NP
60
30
101
5”
NP
135
31
99.2
3”
NP
Ljv
10
ESR
Wt
Date
16
111096
4-
12
161096
4+
4+
33
181096
4+
3+
19
181096
Aide DAT
BM
4+
35
271196
»
12.3
95
4+
+
24
111096 r
6.2
145
4+
4+
48
091096
NP
4+
+
15
091096
3”
NP
4+
20
041096
102
2”
NP
4+r
■
16
181096
37
99
7’
NP
4+
4*.
46
271196
38
irreg
5*’
NP
4+
31
181096
39
102
4”
NP
4+
28
111096
40
101
6”
3”
19
271196
32
101
2”
NP
33
102
4”
NP
34
trreg
2”
35
99
36
3800
8
155
4+
4+
POST-TREATMENT RECORD (Sitapahar)
No
Fev
Spl
Liv
27
99
r
NP
28
98.8
3”
29
98.4
30
TC
ESR
Aide
DAT BM
Wt
Date
Rem.
2+
16
301096
Dis
1°
4-
14
161196
Dis
4”
NP
4-
33
181196 , Dis
98
3”
NP
18
231296
Dis
31
98.4
NP
4-
36
271296
Neg.
32
98
11”
NP
Neg.
26
161296
good
NP
135
50
Neg.
11
4-
IP
■4 .
33
34
35
98.4
36
g
I.
241096
Dis
NP
2”
NP
Neg.
46
151196
OK
2”
NP
+
16
181196
Dis
4”
NP
48
240197
OK
34
161296
Neg
28
091196
Dis
141296
Dis
38
39
98.6
4M
NP
98.8
3’*
NP
+
40
98
98.6
Dis
2”
Neg.
+
37
231096
85
Neg.
t
r
PRE-TREATMENl' RCORD (Sohaghati)
41. Charles Soren
M
30
49 kg-
Amr ap ara
Relapse case
42. Luki rain Hernbrorn
M
42
44
Rodgu*
Relapse case
43. Manu Giri
M
35
40
Sindrigola
New Case
44. Pargana Munnu
F
30
43
Perak
Relapse Case
45. Ponera Murmu
F
20
33
Amr ap ara
Relapse Case
46. Rahim Mia
M
35
Dengdia
Relapse Case
47. Raju Hansdak
M
40
41
Surejbera
New Case
48. Rani Marandi
F
22
38
Soharghatty Relapse Case
49. Solei Soren
M
36
Margaboni
BM
Wt
Date
4+
+
49
311296
4+
2+
42
281096
35
211196
43
211096
33
021296
40
281096
41
271196
44-
38
041096
44-
41
091196
NO
FEV
SPL
LIV
TC
Hh
ESR
Aide
41
102
4n
NP
1100
7.2
138
42
101
8”
NP
2450
6
120
43
irreg
2”
NP
44
9§T
6M
r
45
100
8”
NP
46
101
6”
NP
47
99.8
8”
NP
48
100
10”
NP
1150
5.4
155
44-
49
102
7,
NP
4600
6
120
44-
DAT
4+
2600*
75
7
4+
4+
44130
6
‘I
■
Relapse Case
4+
4+
4+
♦
12
i
ur,rur ATvnTKrr urrr’nDn
•B
A
. ¥ ‘
t
■
i ,r
f11
rOS r-'HUiA iMEN 1 REUOIID (Sohargliati)
’I
•’
NO FEV
SPL
LIV
4T 99
4”
NP
TC
Hb
ESR
Aide DAT BM
wt
Date
I
49
100)197 Dis
Neg.
Rem
45 » 301296
42
98.8
4”
NP
43
98.6
2”
NP
Dis
44
98.4
4”
NP
251196 Dis
45
99
5”
NP
46
98.6
yf
NP
47
98.6
6”
NP
42
030197 Neg
48
98.4
T9
NP
38
111296 Dis
49
99
5”
NP
41
35
270197 Neg
111296 Neg
111296 Dis
_______ ?
IV DISCUSSION ’
As this was basically a patient-oriented project to popularise natural medicines under
normal living conditions the patients were allowed to be on their own. Ulis had some
negative influence on the proper running of the project. Many discontinued the medicine
after die initial relief and some others were unhappy about the slow improvement, etc. Of
the 49 patients who started taking the decoction only 32 completed the course. Reasons for
this large number of drop outs, in addition to the above mentioned reasons, is that despite
the best efforts to follow up each patient, because of difficult terrain, long distance and
other logistic hurdles kept the patients away from the supervisors and the health workers
I
sent to follow them up.
1,1
In spite of the best efforts possible in the given circumstances the result has not been upto
the expectations, particularly in getting the follpw-up tests dope for the patients who
completed the course, and in getting all the prescribed laboratory jtests done on each of the
r
■■
"
selected patients. There are seveial reasons for this lapse • 1. DAT test was available only
in Taljhari, winch is close to Kodma (while all other centres are far away from Taljhari,
the farthest being 150 kin away. So getting the technicians to collect the sample, sending
someone to get the results, etc. was not practical, as in many centres there were no
organised camps to screen patients and even the screened patients had to be taken to the
13
♦
nearest hospitals for other tests. So except in Kodina die DAT test was not taken, despite
the standing instructions to take DAT. 2. Bone Marrow extraction is a very painfill
procedure which many patients refused to undergo. So only 30 patients underwent BM test
before die commencement of die treatment and 13 after the course was completed. 3.
Another major problem involved in this pilot project was that the centres selected were
very far from each odier so even for the local co-ordinator to visit all the centres usually
took 3-4 days. Secondly the commitment, understanding and availability of each local team
member and die supervising staff in different centres varied, consequent to which some
centres had near 100 percent positive turn out and some centres near 100 percent negative
results. 4. From the patients part, lack of education, various socio-economic
considerations, distance, and poor health consciousness deterred them from completing the
prescribed course, reporting periodically, and doing die required pre and post treatment
tests. Most patients who dropped out after 20-30 days of treatment went away for lack of
speedy recovery, others fell off because the recovery was satisfactory and they regained
the ‘normal health’ which enabled them to work and earn their livelihood. Though the
supervising team sent health workers periodically to follow diese patients up, most of them
were not available at dieir homes - some on visits, odiers in the markets, yet others in the
J
fields or forests! Because of these in many cases a second or third visit yielded no result,
and a reminder to report to the respective dispensing centres only met with ne^tive
compliance Though these were facts known right from the beginning the team kept on, for
the simple reason that we are trying to popularise a medicine which has to be taken in the
most natural and ordinary life-situations of, the patients. 5. Since many of the local
supervisors and health workers, though technically competent and very committed and
promised frill co-operation, were grass-roots level workers, whose only concern is to
promote healing, health and well-being, for some of them the conforming the project
methods and procedures to the exact technical prescription was not a priority. From this
backdrop, the result of this pilot project has been very encouraging and praiseworthy.
26 of those who completed the prescribed course got rather completely cured (those with
remark ‘good’ f) or there is remarkable progress in their over all well being and the clinical
symptoms haviiig disappeared or nearly disappeared (those with the ‘OK’ remark). They
'
*
T
I
14
*
I
still being followed up and even after five months of stopping tire medicine no
symptoms recurred. All of them have improved health and are leading nonnal life. Of the
six negative results, 2 are suspected tuberculosis cases (one show KA negative, except for
spleenomegaly and slight fever. The others too may have other health problems which need
to be treated.
!
Among the 49 patients 16 were relapse cases and others were fresh cases. Even in
allopathic treatment there are several instances where even after 45 injection the spleen
remain palpable. With 26 people getting
cured and. the culture test showing that the
medicine kills the KA parasites, it is ample enough to contend that this formulation is
effective to treat visceral Leishmaniasis / KA. But a more systematic research from the
Allopathic stream fulfilling the ICMR prescriptions would be highly advisable to get wider
i
•1
acceptability and proper recognition for tins new fonnulation.
ABBREVIATIONS USED:
Aide: Aldehyde Test, + : Positive, BM: Bone Marrow, Cox: Tuberculosis, DAT: Direct
Agglutination Test, Dis: Discontinued, ESR: Erythrocyte Sedimentation Rate, Fev: Fever,
Hb: Haemoglobin, Impr: Improving (Report Awaited), Irreg:
Irregular,
Liv: Liver,
Neg: Negative, NP: Not Palpable, OK: Satisfactory, RA: Report Awaited, Rem: Remark,
Spl: Spleen, TC: Total Cell Count, Wt: Weight
REFERENCES
i
Anonymous 1995: Kala-azar in India: A Report on the National Workshop on
KA Cb;?Zrc»/(hereafler referred to as KAIN), New Delhi April 25-26,
Actionaid India
Anonymous 1991: Kala-azar Incidence in Bihar, Office of the Chief Malaria
Officer Bihar, Patna.
Bryeeson, A. 1983: ‘Immunological Priciples in Leishmaniasis”, Proceedings
ofthe Indch UK Workshop. 103-110.
Chandrasekhar] D. 1995: “Kala-azar Malto Project: Status Report 1995”,
KAIN.
Chaturvedi, G. 1995: “Kala-azar in India : Background Note”, KAIN
Chowdhtuy, A. B. 1983: “Recent Resurgence of KA in West Bengal”,
Proceedings ofthe Indo-UK Workshop on Leishmaniasis, RMRI, Patna.
10-19.
15
Desjeux, P. 1991: Information on the Epidemology and Control ofthe
Leishmaniasis by Country or Territory, WHO/LE1SH/91.30.
Dhanda, V, P S. Shetty & R.C. Dhiman. 1983: “Studies on Phlebotomine
Sand Flies as Vectors of KA in Bihar”, Proceedings qflndo-UK Workshop.
128-137.
Guru, F.Y. 1992: “Prospects of Immuno-modulatore from Synthetic and
Natural Products for Effective Cure and Control of Visceral
Jndo-US Leishmania Vaccine Workshop-]992> Bethseda.
40-41.
Ghose, A. C., J. P. Haidar & SandhyaG. 1983: “Immunological Studies on
Visceral Leishmaniasis”, Proceedings ofIndo-UK Workshop. 150-153.
Hati A K. 1983: “Current Status of Leishmaniasis - Vector Biology”,
Proceedings ofthe Indo-UK Workshop. 84-91.
Jain, S.K. 1991: Dictionary ofIndian Folk Medicine and Ethnobotany. Deep
Publications, New Delhi.
Kirtikar K. R. &B. D. Basu. 1994 (Reprint). Indian Medicinal Plants. Bishen
Singh Mahendra Pal Singh, Delira Dun.
Kumar V, S. K. Kesari, N. K Sinha, A Palit, A. Ranjan, K. Kishore, R. Saran
& S. K. Kar. 1995: “Field Trial of an Ecological Approach for tlie Control
of PhJebotonious aigentipes using Mud and Lime Plaster”, Indian Journal
ofMedical Research, 101. April 1995. 154-156.
Lamson, R. 1983: “’Hie leishmaniases as Global Public Health Problem”,
Proceedings ofthe Indo-UK Workshop. 20-35.
Locksley, R.M. 1982: “Leishmaniasis” in Harrison’s Principles ofInternal
Medicine, Vol 1. McGraw-Hill Inc. New York 789-791.
Mahajan, R.C. 1983: “Immunology of Leishmaniasis”, Proceedings ofthe
Indo - UK Workshop. 111-115.
Mallick, K. K, A. K. Hati, A. Nandy. 1983: “Clinical Profile ofKala-azar in
West Bengal”, Proceedings of Indo-UK Workshop. 116-118.
Nadkami K. M. 1982 (Revised Edition): Indian Materia Medica. Popular
Prakashan, Mumbai.
Thakur, C.P, M. Kumm & A.K Pandey. 1991: “Evaluation of Efficacy of
Longer Duration ofllierapy of Fresh Cases of KA with SSCJ'Jndian
Journal ofMedical Research (A) 93. March 1991. 103-110.
Ihakur, C P 1992 : “Diminishing Efficacy of Sodium Stibo-Gluconate and
Pentamidine in KA, of DDT on Sand Flips and Search for a Potent
Vaccine for Prevention”, Indo-USLeishmania Vaccine Workshop-\992.
Bethseda. 27-28.
Ihakur, C.P, G P Sinha, V. Shanna, A.K. Pandey, M. Kumar & B.B. Verpra.
1993. Evaluation of Auphotericine B as a First
First Line
Line Drug
Drug in
in Comparison
Comparison
to SSG in Ireafment of Fresh Cases of KA”, Indian Journal ofMedical
Research (A) 97, July 1993. 170-175.
i
?
»
3
16
■ r
?
!5
Kala-azar Research
Report Update:
Dr. E. Varghese SVD
only antimony compounds as tlie main remedy, which is not available to patients as and
when they need it. Since tliere are several effective herbs that heal many diseases CHAI
constituted a team of experts (Ayurveda doctors, traditional healers and ethnobotanists) to
study the literature and local health traditions and come up with a viable formulation for
KA. Having done extensive literature survey and survey of the local health traditions the
team headed by Dr. E. Varghese under die expert advice of Dr. PV Raj (Professor of
Ayurveda) and Dr P. . Hembrom (Traditional practitioner, whose original formulation
was improved upon) and Dr. Rajender Tiwai i (Local Supervisor) came up with the above
mentioned fonnulation.
The team briefed die Ethical Committee appointed by CHAI (constituted of legal and
medical experts, local Sarpanch, and leaders from various fields in the locality, in al
seven of diem) of die benefits and the zero risk factor in administering die medicine and
appraised die Committee of the probable benefit which is much beneficial to the local
people. After considering the various aspects of die expertise and the credentials of project
team dieir ability to conduct such a project, the logistics, and benefits of such a break
through the Ethical Committee at its meeting held on 25 08 1996 at Paharia Sanity Seva
Office, Sai Village, Pakur Dt, Bihar, approved die project and gave its approval to go
ahead with it.
t
?
Accordingly five dispensing centres were selected and through each of
oi these
mese centres
cemreB
patients were screened and sample selected. Allopathic doctors did the screening of
patients and the suspected cases were sent for pathological investigations. Those turned
positive in the investigations, especially in Aldehyde test, and bone marrow smear test, and
those exhibiting the clinical symptoms were posted for treatment The local team under the
supervision of Dr. Rajender Twari a practising Ayhrvedic doctor, and qualified nurses at
each centre regularly monitored the patients with the progress, chatting the observations
periodically. The patients thus selected wfcre given medicine for one week and were
allowed to go home and be in natural conditions.
*
49 patients who turned out to be KA positive were administered the medicine. Of them 32
completed the course prescribed (for 45 days). Of them 26 got cured with no relapse till
to-date, those who were willing to go for a second round of confirmatory tests for cure
were sent. Others were certified by the doctors as healed for absence of relevant clinical
symptoms and pi onounced improvement in health and physique.
17
r
•r
1„ its second sdting to evahnue
81
by the Principal Investigator and the
Etliical Committee was briefed with
P' V ,
degirous to learn the actual effect
team. Having learned that 16 people got
Colnmittee suggested for a controlled
of the medicine standardise the corns
ciumdanahai Dispensary and Kodma
group of 10 patients to be taken at two cen , * Jungly commenced by March
gispe,OTy And co,“’"Xe ,« X
of pmie.d. »d Kdd.nt «f
1997 and was concluded in July 1997
paharia Samaj Seva gamiti, Sai) the
1-2—preK"bed
course; the reports of which are awaited.
m fte nubile the medicine »» eullnre tested
S
Medicine, Calcutta; which showed that e me mm®
. formulation following
nmd School we willing to do . thorough r.cemch .n W wA ta»
XSZft^SiXi^^^lCS’Xn.toeWd^
A short patter will, the reeult-np-to.dnte wan pre.ented W the S*' “XmXiTS"
„„ Noto,,1 Medicine, held nt1~
SSXKhJ been
™
f„;
to Henlto
Action, and other vernacular periodicals.
Dr. E. Varghese (PI) and Dr. PP Hembrom (Horopathy Consultant) presented the. progress
and die details of the research a meeting of the co-ordinating co,™^ee^prp;^ctor Sr
1 Xc" "toden. oS Xtnitof'SSi - Sr.
Medical Advinor to CHAJ
X c XXnX30 97 During which it w» decided to apply for ptoeot,*
ii?, ,„ toeSicne; to neek eon,potent pemo.m.t to Ink. op . > -“P
*
1
dlop^ie rtrewn »d to r*
allopathic stream and to seek funds for that from various agencies CUI
CSTM (Calcutta) were suggested to be competent agencies to
e up
^ns to explore
C M Francis and Dr. E. Varghese were requested to approach h ’
the possibility of either of tliem taking it up.
r
Sincerely Yours,
/■)
'
»
f/. r'A' /k
Dr. E. Varghese SVI5
Principal Investigator
I
18
?
u
• Ia) I
b
rinolytic and hemoing and 0Her maxi□les. J A ppi Physiol
. Effects of exercise
n clotting and fibririen. J Appl Physiol
7,
for deep venous
2:961. 1977
KG: The pos*-phleew lock In Bet gon
Venous P/ obi&n >s
Sk. 1978. pp 395?nous Thrombosis
ers of the
>hia. Harper & Row,
Exercise and Coronary
Artery Disease
Terence Kavanagh
JP: Physical basis of
in chronic venous
Phys Med Pehab1'
'sen JF. Kiarke M
oxygen
tension
•e in health and in
disease Acta Chir
1986
M Exercise testing
vteriai occlusive
>n clinical exer■ Olin 2 440-454
Blanchard RS:
•sage on the
>re'eg of the
ibil 33 604-
'rinsic conh yesse.s
'□ 4 m j
\insiatic
\7-3d8.
o+ion
I schetnic heart disease is the major cause of death in adult males through
out most of the advanced world. Its three clinical manifestations (angina, myo
cardial infarction, and sudden cardiac death) now seem almost inevitable
accompaniments of our modern life style. The basic pathology' involved, ath
erosclerosis, is a highly complex process which still defies precise scientific
explanation.
Broadly speaking, there are two main theories of pathogenesis. The first
focuses attention on the lipidlike nature of the atheromatous plaque (1) Lowdensity and very low-density lipoproteins are said to infiltrate the arterial wall
and accumulate in excessive amounts, leading to the formation of fattv streaks
and, later, fibrous plaques upon whichhhrombi can form. Initiation of this pro
cess is variously attributed to an inflammatory reaction in the vessel wall, endo
thelial wear and tear due to prolonged hypertension, or tumorlike proliferation
of sick subendothelial muscle cells. Closely associated with tTiis hypothesis is
the now largely held view that abnormalities in the plasma lipid levels are a
major contributor to the process (2), and that lowering total blood cholesterol
levels will reduce the incidence of coronary heart disease (CHD) (3).
The second theory (4,5) proposes that the initial stimulus for atheroma
formation comes not from the lipid accumulation, but from the formation of
thrombi on the endothelium. The consequent aggregation of red cells, plate
lets, and enmeshed lipid material become Incorporated into the wall of the
artery and ultimately evolve into the typical atheroma. Proponents of this school
may place more emphasis on the development of antithrombotic agents than on
measures to lower plasma lipids.
Our lack of conclusive scientific an£ statistical proof as to the exact cause
oi atherosclerosis does not mean that measures should not or cannot be taken
toward primary or secondary prevention. There is now a vast body of evidence
inking certain risk factors with coronary artery disease (6,7). These are.- (a)
male sex; (b) heredity; (c) elevated plasma cholesterol (in particular the lowdensity lipoprotein (LDL) fraction), usually associated with a high dietary
387
388/
Therapeutic Exercise
intake of saturated fats; (d) hypertension; (e) cigarette smoking; (f) diabetes
mellitus; (g) obesity; (h) psychosocial stress; and (i) physical inactivity.
Many of these factors are interdependent, or may even give rise to one
anotlter. Furthermore, the presence of more than one risk factor increases con
siderably the likelihood of developing the disease. It, therefore, seems entirely
reasonable to deduce that a strategem designed to eliminate these risk factors
will reduce the disease’s incidence.
More recently,
ease Control, Atlanta
epidemiological and
concluded that "the
ence that physical ac
CHD.” They went or
be similar in magni
smoking. These obse
physical activity sho
dietary uuxiitication
I
THE ROLE OF PHYSICAL ACTIVITY AS A PROTECTIVE FACTOR IN
CORONARY ARTERY DISEASE
Epidemiological Evidence
Whereas physical inactivity is listed as a risk factor, physical activity can be
viewed as a "protective factor." It is almost 40 years since Morris et al. (8) pub
hshed a report in The Lancet which showed that highly active conductors on
the London double-decker buses had significantly less heart attacks than their
sedentary coworkers, the bus drivers. Since then, a large number of studies have
consistently demonstrated the same finding (Table 20.1 (9-18)). Regular phys
leal activity, either at work, or as part of a recreational program, apparently con
lers a degree of protection from myocardial infarction, both fatal and nonfatal.
1 he reduction in risk lor active persons compared with the inactive is about 3iold Furthermore, the incidence of suddenreardiac death, a major and common
manifestation of ischemic heart disease, is similarly reduced with regular phys
The major criticism leveled against these reports, particularly the early
ones, is their bias of preselection: constitutionally stronger individuals choose
vigorous physical work and/or recreation, while those who are not will choose
a more sedentary life-style. The later published reports, in particular those of
the Paffenbarger group (15,16,20) dealing with San Francisco longshoremen
and Harvard alumni, have refuted the possibility of preselection with elegant
methods of statistical analysis.
I
I
Table 20.1
Epidemiologic Studies: Comparative Risk for Heart
Attacks for Low Physical Activity Members of Groups Compared with
High-Level Members of Same Group
Physical Activity
Author
Morris (UK. 1953) (8)
brumer (Israel, 1960) (9)
Taylor (USA, 1962) (10)
Kahn (USA, 1963) (11)
Brunner (Israel. 1966) (12)
Kannel (USA, 1967) (13)
Shapiro (USA, 1969) (14)
Paffenbarger (USA. 1977) (15)
Paffenbarger (USA, 1978) (16)
Morris (UK, 1980) (17)
Garcia-Palmieri (USA, 1982) (18)
Population
High
Low
I ondon transport
Pout office
Kibbutzim dwellers
Railroad
Post office
Kibbutzim dwellers
Framingham
Insurance clients (NYHIP)
Longshoremen
University alumni
Civil servants
Puerto Rico heart program
10
11)
1.0
1.0
1.0
1.0
1.0
1.0
1.0
1.0
1.0
1.0
2.2
2u
3.0
2.0
1.9
3.0
2.5
4.8
3.0
2.2
2.8
2.0
How much phy
artery disease? Paffe
kcal over a 42-hour
(15). Morris’s bus. c
stairs 60-70 times a <
much energy, with p
climbing (8).
In the workpl:
machine, and so wt
active with inactive,
carried out "dynami
groups, and above t
fewer he an attacks,
some of the activitie
versity graduates stu
protection at total c;
of which at least 21
defined as more th;
taineering, cross-co
The Multiple P
some 12,000 men al
tension and hypercl’
light i 2-4 kcal/min
than •' kcal per mil
and sudden cardiac
compared with the
moaaliiv and suddc
ot i \rn. im’ dalle, tk
mih walk) I hei
to higlii i U vvls
quently than seven
and or intensity' to
St
I
I
A number of
which regular exer
Animal mode
increase coronary'
<' >
mi
Chapter 20—Coronary Artery Disease
making: (f) diabetes
Jcal inactivity.
ven give rise to one
factor increases con
efore. seems entirely
ate these risk factors
IVE FACTOR IN
/389
More recently, Powell and his colleagues (21), from the Centers for Dis
ease Control, Atlanta, subjected a total of 43 such published studies to careful
epidemiological and statistical analysis in order to establish their validity. They
concluded that “the observations reported in the literature support the infer
ence that physical activity is inversely and causally related to the incidence of
CHD.” They went on to observe that “the relative risk of inactivity appears to
be similar in magnitude to that of hypertension, hypercholesterolemia, and
smoking. These observations suggest that in CHD prevention programs, regular
physical activity should be promoted as vigorously as blood pressure control,
dietary modification to lower serum cholesterol, and smoking cessation” (21).
Threshold for Protection
ivsical activity can be
Morris et al <pvb
ictive condtKiors on
art attacks than their
mber of studies have
18)). Regular phvs
ram, app.ur.< on
th fatal and nontatal.
' itiact ive is a bom *
a major an<l <. onunon
xd with regular phys
particularly the early
r individuals choose
■> are not will choose
n particular those of
cisco longsh(;remen
lection with ''k g,ant
■sk for Heart
Compared with
Physica* Activity
Hiph
Low
1.0
1.0
■o
1.0
22
20
3.0
20
1o
3.0
1.0
1u
1.0
1.0
1.0
VO
10
2.5
4.8
3.0
2.2
2.8
20
How much physical activity is needed to provide protection from coronary
artery disease? Paffenbarger’s longshoremen needed to expend at least 8500
kcal over a 42-hour work week, at a minimum effort intensity of 5 kcal/min
(15). Morris’s bus conductors, running up and down the double-decker bus
stairs 60-70 times a day, in addition to walking to collect fares, used at least that
much energy; with peak expenditure of between 6 and 10 kcal/min during stair
climbing (8).
In the workplace, we have seen increasing replacement of muscle by
machine, and so we now must study recreational habits in order to compare
active with inactive. Morris et al. (17) found that civil servants who regularly
carried out “dynamic aerobic activity involving free movement of large muscle
groups, and above the energy required for a training effect” had significantly
fewer heart attacks. Swimming, jogging, brisk walking, and hill climbing were
some of the activities cited; all require peak expenditures of 7.5 kcal/min. Uni
versity graduates studied by Paffenbarger et al. (16) began to develop significant
protection at total caloric expenditures of 7000 kcal over a 42 -hour work week,
of which at least 2000 kcal were spent in a vigorous sport (“vigorous” being
defined as more than 5 kcal/min ayd closer to 10 kcal tnln). logging, moun
taineering, cross-country skiing, swimming, and tennis were given as examples.
The Multiple Risk Factor Intervention Trial (MRFIT), studying a group of
some 12,000 men at high risk for coronary artery disease (smokers with hyper
tension and hypercholesterolemia) over a 7-year period, compared the effect of
light (2-4 kcal/min), moderate (4.5-5.5 kcal/min), and heavy (equal or greater
than 6 kcal per minute) physical exercise on coronary heart disease mortality
and sudden cardiac death. The conclusions were that “the moderately active as
compared with the least active men had 63% the age adjusted rates for CHD
mortality and sudden death” (22). The moderately active averaged 47 minutes
of exercise daily, to burn 224 kcals or 4.8 kcal/min (equivalent to a daily brisk
2% mile walk). There appeared to be no particular benefit, in this group at least,
"to higher levels of activity. Presumably, individuals who exercised less fre
quently than seven times per week would be required to increase the distance
and/or intensity to achieve the same result.
Suggested Mechanisms of Protection
A number of exercise training effects can explain the mechanisms by
which regular exercise protects against coronary heart disease.
Animal models have demonstrated that chronic exercise can significantly
increase coronary artery diameter, t‘ne extent of myocardial capillarization
390/
rherupcuilc i xcrci^e
&
( - Al' t re
KC
C°rO,W Mel,OSi's’ cori,n:,0’ collateral growth
- 2/i Ik Ighlened resistance ol the Ischemic heart to ventricular itbrlil mon
as also> been demonstrated m treadmill-trained rats and dogs (28 29) Non
trained Macaca monkeys fed an atherosclerotic diet developed severe coron irv
atherosclerosis and fatal myocardial infarctions, whereas their treadmill trained
ounterparts, fed the same diet, were found to have large caliber coronary- arter
ies, totally free from atherosclerosis (30).
In man, iit has been shown that regular endurance training increases end
diastolic volume, and that this is associated with
....i an enhanced stroke volume
and a resting and exercising bradycardia (31)
Indeed, the bradycardia is a hall
mark of the trained state, and is due to a variation in the influence of the
autononne nerve supply to the heart. The parasympathetic, or vagal tone is
increased at rest, and the sympathetic tone decreased during exercise (32) This
makes for a more efficient pump, less likely to labor during intense and uZ
peeled episodes of physical effort.
1 Ihe demonstration
of coronary
> . oi '!.
coronary collateralization
collateralization as
as aa result of training has
p.oved to be dtihcult in man, possibly because these collateral vessels are fre
quent y quite small (100-200 mM) are usually located intramurally, and are fre
quently undetectable by clinical coronary angiography. However, there is cir
uimsianual evidence tor collateralization from studies which show higher rale
pressure products (heart rate multiplied by fsystolic blood pressure) after train
tng, lot equivalent levels ot myocardial ischemia (as measured by the onset of
angina or amount of ST segmental depression) (Fig. 20.1) (33 34) Recently
exerc.se scintigraphy has been used to detect the development of exercise
iiKlut.-d tollateralization in man, and favorable reports are already beginning
to appear in the literature (35,36).
6
A number of peripheral changes brought about by. exercise training by
■Il hl ling die established risk I.mors, could explain Hie CHI) protective e'lfecl
blood pressure is reduced as a result of Increased skeletal muscle vascularity
and consequent drop in peripheral resistance (37). This, together with the
training liradycardia, makes lor a reduction in rale pressure product, and thus
myocardial oxygen demand, at equivalent levels of effort (38). Plasma triglyc
eride levels are lowered. There is an increase in levels of HDL cholesterol and
J
I
si
T
BBii
In
rn!
J
Bit
i
I
n
|| i | fl i|f! I
H
/‘oj
KiiLWi
a Kit
iUl
20 ?
aLXsfon
I
•/
1 1U1
rl I
Kti
a (Iccicasc in l.DI. chok
risk, while the Liner is
lioned above, who wit
developed higher HDL
Training enhances lib
improves glucose toler
suess induced levels o
and increases levels ofc
regular exerciser is mo
most capable, of lead in
as obesity, cigarette sm
gether, tins is an impot
exercise protects again,
I
B Kl
Se9"ent resP°nse to zeroise. A. Normal isoelectric ST-segment seen
em‘C chan9es with exercise; 3.5 mm of "horizontal" ST-segmental
I
uiolkjll
■u
""•Rfl
*
EXERCISE
Although Levine :
diac patients as early as
widely accepted throu^
belieis, this aggressive
diac rupture, of left ver
contrary, the benefits c
with recovery', a pov
avoided, with conseqi
tiv> ro<la). we even s
testing being safely cat
lion. .ilV'>'ding the phy
additional psychologic
since the early I'
taiion programs for pa
aoi locoton.uA artery b
noncxcix i>ing cardiac
adjust better to their d
ical v orking capacity,
All or the benefits of
prevention can apply
vivors. In pan.cular, i
given workload, whict
dv cardia also increase
occurs during this ph:
myocardial ischemia,
the considerable alle’
quently reported as a
Other exercise r<
decreased depression
of healthy living, i.e..
ventricular ectopic be
the coronary atherosd
Few would now
acute myocardial infa
Ml
Chapter 20-Coronary Artery Disease
3ry collateral growth
?ntricular fibrillation
dogs (28.29). Non
ped severe coronary
eir treadmill trained
'liber coronarv arter-
ning increases endaced stroke volume
bradycardia is a hall
fluence of the auto
oi
vagal
lofp
p'Hi’hlb. M.'j
I lllh H i
js
fhh
||I* | Hiii'H
'Mill dI irahiing has
eral vessels aie fre
rurally, and are fre>wever. there is cir?h show higher rate
•ressure'i after train
•red b\ the onset of
(33,34) Recently,
pment of exerciseal readv beginning
xercise training, by
D protective effect.
muscle vascukiritv
together with the
'• product, and thus
38). Plasma triglyc
DL cholesterol and
ric ST-s^gmont seen
nJ™:
fo,m" h invers'1’’
/391
“ “D
uoned above, who withstood' the adtrse^ffecTs' o^Hh*
mCn
developed higher HDL cholesterol than th •
f
ather°sclerotic diet,
Training enhances fibrinolytic responsen™1exerc's,n2 counterparts (30).
improves glucose tolerance and increases in.suHniTa(45'44>’
stress-induced levels of cirruLirin
.
sensitivity (45,46), reduces
and increases levels of circulating l-endorpHns
( 47'48 ’’
regular exerciser is more health conscious and s
'°
S,mpler leve1’the
,ret
:
J1* '• “ 1I"P°S|"» "»
xt k Ixr ptotccts against cardiovascular disease.
he’CHS, IX™”,,,'1,',',',
EXERCISE IN POSTCORONARY REHABILITATION
Although Levine and Lown (51) pioneered the early mobilization of car
diac patients as early as 1952, it was not until the 1970s that the practice became
widely accepted throughout the United States and Canada. Contrary to previous
beliefs, this aggressive approach is not associated with an increased risk of car
diac rupture, of left ventricular aneurysm formation, or of sudden death. On the
contrary', the benefits are considerable. The patient equates early mobilization
with recovery, a powerful psychological boost. Severe deconditioning is
avoided, with consequent earlier return to work and everyday physical-activi
ties. Today, we even see reports of medically supervised submaximal exercise
testing being safely carried out in a matter of days after acute myocardial infarc
tion. affording the physician important prognostic information and the patient
additional psychological benefit.
Since the early 1960s, theredaas been a proliferation of exercise rehabili
tation programs for patients recovering from an acute myocardial infarction or
aortocoronary’ artery bypass surgery. The results indicate that, compared with
nonexercising cardiac patients, those who participate in an exercise program
adjust better to their disease, have improved cardiovascular function and phys
ical working capacity, and are more likely to return to active employment (52).
All of the benefits of physical training described in connection with primary
prevention can apply equally to the vast majority of myocardial infarction sur
vivors. In particular, there is the reduction in the rate-pressure product at a
given workload, which decreases myocardial ozygen demand. The training bra
dycardia also increases the period of diastole, and since coronary blood flow
occurs during this phase of the cardiac cycle, the prolongation helps to reduce
myocardial ischemia. Both these mechanisms are the likeliest explanations for
the considerable alleviation and even abolition of anginal symptoms so fre
quently reported as a result of exercise training.
Other exercise related benefits pertinent to the postMl state include: fa)
decreased depression and anxiety (53,54); (b) greater adherence to the tenets
of healthy living, i.e., diet, no smoking, etc.; (c) reduction in the frequency of
ventricular ectopic beats (55); and (d) possibly stabilization or regression of
the coronary atherosclerotic process (56).
Few would now disagree with the claim that exercise rehabilitation after
acute my oca i di.a I infarction or aortocoronary artery bvpass graft surgery greatly
f
392/
Therapeutic Exercise
enhances the patient’s quality of life, improves functional capacity, counteracts
CHD risk factors, and encourages return to work. For these reasons, postMI
exercise therapy is firmly advocated by such bodies as the World Health Orga
nization (57), as well as by many international and national organizations
involved in the primary and secondary prevention of atherosclerotic heart
disease.
A number of prospective randomized controlled trials showing the effect
of postcoronary exercise on cardiovascular mortality and morbidity have now
been published. Like many other secondary intervention trials after myocardial
infarction, c.g., fi blockers, aspirin, the results have been unclear. Some studies
show a statistically significant beneficial effect; others fail to do so. Often the
reason lor this has been methodological, e.g., limited patient entry, insufficient
follow up, high dropout rate, or contamination between control and interven
lion groups. In order to overcome this problem, the method of pooling the
results of similar trials and then analyzing them as a whole has been introduced.
Known as meta-analysis, this technique has been increasingly applied in situa
tions where it is-suspected that the trials, because of the problems mentioned
above, have lacked the statistical power to successfully demonstrate the real
benefit of a treatment.
May (58) was one of the first to review a number of long-term trials of
secondary' prevention after myocardial infarction. With regard to physical exer
cise studies, he found that “although none,of the exercise trials showed a sta
tistically significant reduction in total mortality, all but one had a positive trend
favoring the physical training group that varied from 21% to 32%.’’ On pooling
of the results, he found a statistically significant 19% reduction in total mortality
in the exercising group. He went on to say that “pooling of the results from
these (i.e., exercise) studies may be more acceptable than for other categories
of intervention, as one does not have to account for unknown pharmacological
factors. The differences in exercise schedules between studies are minor, and
the programs were all started at approximately the same time after the acute
event'’ (58).
Subsequently, others have employed the same technique, the most recent
being Oldridge and his associates (59), who subjected the 10 major randomized
prospective trials to meta analysis, and found a highly significant reduction of
25% in recurrent fatal myocardial infarction in the exercising group. This is as
beneficial an effect as has been reported for ^ blockade therapy after acute Ml,
a form of intervention now widely accepted clinically.
EXERCISE TESTING
Exercise testing is now a rapidly growing subject in its own right and there
are a number of excellent texts which deal with the topic in its entirety. Only
the essentials will be dealt with here.
Methodology
Currently, an exercise test is carried out primarily on a treadmill or a cycle
ergometer. The latter is cheaper, quieter, and occupies less space. It allows for
easier blood pressure readings and artifact free electrocardiogram tracings. If
the test includes a collection of expired gas and/or blood sampling, this can
also be carried out with more facility during upright cycling. A drawback of the
-
cycle ergometer is
harder io reach des
lionary cycling dot
treadmill walking,
higher.
1 he treadmil’
this reason, has be
ting. Cycle ergonv
physiology, large<
The purpose
to increasing leve
itored are heart n
ottcn. we collect
gen consumprior
pH, and lactate ar
rather than an ass
I
i.
I
Starting fror
the patient is ext
confirmed by the
rate and oxy gen i
toms or signs ap
test is terminatec
A submaxin
usuailv 8S% of it
he estimated froi
Cycle ergot
stage and steady
>taai \alue, usua
minute (16 watts
arc made in the f
when the ventila
analysis of expin
The steady
duration, the ini
ctlori Measurem
variables are jud
The maxim
can be estimarea
Male
Maximum Powe
Output (KPM)
... .
Chapter 20—Coronary Artery Disease
acirs. counteracts
reasons, post MI
)rld Health Orga
lal organizations
rosclerotic heart
lowing the effect
’bidity have now
after myocardial
•ar. Some studies
do so. Often the
?ntrv. insufficient
*ol and intcnen
1 of
the
>een introduced,
applied in situa
lems mentioned
^nstrate the real
cycle ergometer is that older individuals with weak quadriceps may find it
harder to reach desired heart rates before the onset of quadriceps fatigue Sta
tionary cycling does not result In as high a maximum oxygen consumption as
Ngher' Wa kin8, bUt the difference is smal|i ventilation and lactate are slightly
The treadmill employs the more natural walking action, and possible for
this reason, has become the principal choice of cardiologists in the clinical set
ting. Cycle ergometers tend to be used more by those involved in respiratory
Physwlogy, large-scale cardiac rehabilitation programs, and cardiorespiratonfitness testing.
1
The purpose of the test is to study the subject’s cardiorespiraton- responses
to increasing levels of physical effort. The noninvasive parameters usually mon
ttored are heart rate, blood pressure, and the exercise electrocardiogram less
often, we collect and analyze expired air in order to calculate ventilation, oxv
gen consumption, and carbon dioxide production. Occasionally, blood gases
pH and lactate are also measured. Exercise thallium scintigraphy is a diagnostic
rather than an assessment procedure, and is outside the scope of this chapter.
Exercise Test Protocols
ng term trials of
o physical exer
Is showed a staa positive trend
%.’■ On pooling
n total mortality
the results from
other categories
Pharmacological
are minor, and
after the acute
the most recent
ijor randomized
nt reduction of
roup. This is as
■ after acute MJ,
right and there
entiieiy. ()111y
Im ill or a cycle
e. It aJh.Yws for
am tracings. If
■>ling. this can
■awb.u k • >f the
Starting trom rest, the workload is increased in a stepwise manner until
the patient is exhausted. This is known as a maximal test, and its completion is
confirmed by the fact that, despite a further increase in the workload, the heart
rate and oxygen uptake do not show a concomitant rise. If any untoward symp
toms or signs appear before this physiological maximum Is reached, then the
test is terminated, and is referred to as a "symptom limited” maximal test.
A submaximal test is one carried out to a predetermined target heart rate
usually H5% of maximum. Maximum heart rates, which decrease with ig<- < m’
be estimated from age-related tables (60) or by using the formula (61 )
HR Max — 2IQ — 0.65 X age (years)
Cycle ergometer tests can be divided into two types, progressive multi
s age and steady state. In the former, the power output is'increased by a con
slant value, usually 100 kilopond meters per minute (KPM), or 16.7 watts, every
minute (16 watts) until maximal, or target, heart rate is reached. Measurements
are made in the final 15 seconds of each minute. This test is particularly v lluable
when the ventilatory anaerobic threshold (see below) is being calculated from
analysis of expired air.
The steady state test employs three power outputs, each of f > minutes'
duration, the intensity being usually 25%, 50%, and 75% of estimated maximal
efforr Measurements are made during the last minute of each stage, when the
variables are judged to have reached a constant steady star,The maximum power output for healthy adults fon the cycle ergometer)
can be estimated from the following equations (62):
Male
Maximum Power
= H200 ~
Output (KPM)
in yr X 32.0)J 4- 3.5 X body wt (kg)
2
r
394/
Therapeutic Exercise
Female
Table 2
Test.
Maximum Power
= l^00 ~ (a£e in yf X 14,0)] + 3.5 X body wt (kg)
Output (KPM)
2
~
~
Stage
t
2
3
4
5
6
7
25 watts). A fitter subject might be given a third power output of 900 KPM
(150 watts). At tnittal assessment, cardiac patients are usually given power out
puts of 150 KPM (25 watts), 300 KPM (50 watts), and 450 KPM (75 watts).
Iteadmill testing can be carried out to maximum, or to a target heart rate
and the common protocols in current use differ only in the time it takes for the
nrSslv
J16'
8°alS' THe Balke and NaU«hton Protocols
ptob. bl) best suited to the early postMl patient. The Bruce (probably the most
popular in use today) and the Ellestad protocols are slightly more demanding
but are less time-consuming (Tables 20.2, 20.3).
Table 20.2.
Stage
1
2
3
4
5
6
Protocols for Treadmill Exercise Test.
A, Balke
Stage
1
2
3
4
5
6
f'
Speed
3.3 mph
Grade
(%)
Duration
(mln)
Constant
Constant
Constant
Constant
Constant
Constant
2
6
10
14
2
4
6
in ihe .inseuC*
m.iiU c
oetns
grab rails for suppc
verv slight and occ
should not be toucl
me tn the choice fo
8
10
12
18
22
B. Naughton0
Stage
2.0 mph
Grade
(%)
3.0
Grade
(%)
3.4 mph
Grade
(%)
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
0.0
3.5
7.0
10.5
14.0
17.5
0.0
2.5
5.0
7.5
10.0
12.5
15.0
17.5
20.0
22.5
25.0
27.5
30.0
32.5
The heart rate
increases linearly v
be nottxi that maxi
maximum oxygen i
crepancv when cor
max = 65% HR ma
Physicians sh
responses to each ?
increasing ettort o
“chronotropic incc
disease (63). Ther
heart rates as a rest
Duration
(min)
2.0
4.0
6.0
8.0
10.0
12.0
14.0
16.0
18.0
20.0
22.0
24.0
26.0
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
2
Systolic blooc
age healthy rniddh
cate^ good left vei
so called "inotropi
"Lower speeds suitable for cardiac patients and those with low tolerance.
---- .Jm.
Chapter 20—Coronary Artery Disease
Table 20.3.
Test.
Protocols for Treadmill Exercise
A. B< jce
(kg i
y
/395
d this has to be
d's initial steady
). and
KEM
put of 900 KPM
’iven power out
(75 watts).
target heart rate,
e it takes for the
3n protocols are
obably the most
ore demanding.
Stage
Speed (mph)
Grade (%)
Duration (min)
1
2
1.7
2.5
3
4
5
3.4
4.2
5.0
6
7
6.0
10
12
14
16
18
20
22
3
3
3
3
3
3
3
5.5
B. Ellstad
Stage
i
2
3
4
Duration
(min)
Speed (mph)
Grade (%)
Duration (min)
1.7
10
10
10
10
15
15
3
2
2
3
2
3
3.0
4.0
5
5.0
5.0
6
6.0
In the absence of metabolic measurements, and where treadmill perfor
mance is being expressed with reference to energy cost tables, the use of the
grab rails for support can give spuriously high readings Apart from providing
very slight and occasional support to the very apprehensive subject, the rails
should not be touched during the t^sf, and this exclusion may make cycle ergo
metry the choice for older and more disabled subjects.
4
6
8
10
12
OBSERVATIONS MADE DURING TEST
Heart Rate
Duration
(min)
2
2
2
2
2
2
2
2
2
2
2
2
2
2
^ce
*
The heart rate, which is read from the exercise electrocardiogram (ECG),
increases linearly with workload and oxygen consumption. However, it should
be noted that maximum heart rate (HR max) is reached a minute or so before
maximum oxygen uptake (VOZ max); this asymptote leads to an apparent dis
crepancy when comparable levels are expressed as percentages, e.g., 50% VO.
max = 65% HR max.
Physicians should be thoroughly familiar with the normal heart rate
responses to each stage of the protocol being used, since sluggish response to
increasing effort or, less commonly, failure of the heart rate to rise (termed
“chronotropic incompetence’’ by Ellestad) may be a feature of ischemic heart
disease (63). There can also be profound reductions in resting and exercise
heart rates as a result of treatment with ^-blocking agents.
Blood Pressure
Systolic blood pressure increases linearly with exercise, rising in the aver
age healthy middle-aged subject to 200-300 mm Hg. A normal response indi
cates good left ventricular function, while a sluggish or inadequate response,
so called “inotropic incompetence,’’ suggests left ventricular dysfunction (usu
396/
Therapeutic Exercise
Hon
Whith SeVere coro™ry artery disease) or aortic outflow obstruc
non. Agam, the physician should be familiar with the range of expected
cSeT" 1,1 SySt°11C bl0°d PreSSUre tOr eaCh work s«ge of the protocol
block. WPW syndrom^, c
hypoxemia from otherjC
2 Elevation of the
with areas of ventricular
am angina (coronary an
3. Frequent compb
often issocvitcd with m
cihc as ST segmental eV
4. Increase in R v
some to indicate ischer
The rate pressure product correlates very well with myocardial oxygen
from test to ^ei""8 eXerCiSf?’
USed t0 identify 3 threshold for ^na
exerc^e "k'shoLId h6
Steady> °r may deCrease sli8htly during
a? d b
ted that sometimes in testing young subjects the
Korotkoff sounds can be heard down to 0 pressure.
Electrocardiogram
FCC LhpS>|Stem
’eadK and electr°de Placement used to obtain the exercise
ln the past edition
the testing of cardiac p
has been more general
ment has made the pre
breath by breath analys
me?, sure men rs as oxyg
»c-s| ic
y '<;<<- tidal v
cannel only measure f
the level of etfort at wb
50% m of peak oxyg
old
t Fig. 20.2). Iteilccitve aerobic uaitu
pi\.-pei'ii.m to \ O_> max
evaluating of the pallet-
I. The mos^commonly sought exercise-induced electrocardiographic
finding is depression of the ST segment (Fig. 20.1), It has been convincingly
demonstrated that changes in ST-T amplitude and direction are most readfly
o served in the bipolar CMS lead, in which the positive electrode is placed at
the Vs position and the negative electrode on the manubrium. The configuration
o’n/u/pX8pt9Z?s?Om ‘hiS plaCeme,V;‘a8gerateS the S w;,ve- and all™s
ord (64/
?
f ■•SC811,ent ^normalities present in the full 12 lead rec2 Addition of two oilier leads, eg., V, and III, increases the sensitivity and
allows easier analysis of ectopic beats,
3. While a 12 lead resting electrocardiogram should be carried out before
•e carried out before
■ id after an exercise test, a full 12-lead system of exercise monitoring is prob
ably unnecessary, li will pick up very little abnormality not seen in a suitable 312 1 .“f' i8Uratl°n; and ‘S m°re ti,ne-c°nsuming and expensive. But if the full
■ “ h ele^pcardl°8Min is used for exercise, artifact can be avoided by plac
ing the hmb lead electrodes at the shoulders and iliac crests. Provided they do
not advance too much onto the torso, the ECG tracing will closely resemble the
orthodox resting configuration.
ticuladv wi^h^ analiySiS °f
eXCrCiSe electrocardi«gram is now available, par
ocularly w th regard to mathematical evaluation of the ST-segment depression
However, despite the advances made in this area in recent yets, skilled human
inteipretation still remains indispensable.
Irrespective of the lead system used, Bayes’s theorem will apply (65). The
piedictive value of a positive test (i.e., the percentage of subjects with an exer
c sc induced ECG abnormality who ultimately prove to have coronary artery dis
is an expression of the prevalence of the disease in the population being
s ed. bus. there are more false-positive responses encountered when testing
a group of asymptomatic healthy young people than when evaluating a high
risk group or those with a prior history of myocardial infarction
The c lassical exercise electrocardiographic changes commonly associated
with an abnormal test are as follows:
1 Horizontal or downward sloping depression of the ST segment of 1 mm
or more (measured 80 msec from the “J point”) in any one lead, generally indi
cates myocardial ischemia. However, note that there are a number of nonis
chemic conditions in which this can occur, e g., hypokalemia, bundle branch
70
to
i
"■i
>*
-
40
50
30
40
_ 20
M
10
20
0
10
0
i
Figure 20.2. Determinat
tilatory equivalent (Ve/\.
and the nadir of the Vt/’
min., approximately 60%
Kavanaan T Yacoub MF
tives m Cardiology 4:21-
Chapter 20—Coronary Artery Disease
tortic outflow i .bsir'ice range of expected
age of the protocol
ph’,n"ceu,k’1 a<!™K
2. Elevation of the ST segment, 1 mm or more, may be seen in association
. ............ ■ v“'—- -
n myocardial oxygen
i threshold for angina
Tease slightly during
young subjects, the
3. Frequent complex ventricular arrhythmias (three or more in 10) am
. .................... .»'“«"»-........ »«pe-
.. .x ™
»-«
Analysis of Expired Gases
obtain the exercise
b but the following
H ectroca rd i og ra p h i c
s been convincingly
on are most readily
ectrode is placed at
*n. The configuration
? S wave, and allows
the full 12 lead rec-
s (he sensitivity .md
* carried out before
Monitoring is prob
^een in a suitable 3'ive. But il the full
e avoided bv plac
■ Provided they do
>selyresemble the
/397
breath-by-breath analysts, with graphic display and subsequent printout of such
''p“k'; “b“ d“de
ptratory rate, tidal volume, and respiratory exchange ratio Trom these one
t7en?e7e?XfcTZhTc?7oXykbn ;ptake<V°2 maX)’ bUt Can als° determine
50% 60% of np iL
iik ^e^ins t0 be performed anaerobically (usually
d (l (FKaTTr UPt C)- ThiS.P°int " kn°Wn aS the ventilatorv thresh"
XX -SobiTt in n:pPPrOX'nir: C1OSely ,he leVC1 Of intensify Xired for
ittecttve aerobic training, occurs before maximal effort is reached increases in
valuating of the patient with cardiac disease.
80
ioxv a'cailabk'. par
;ment depression,
rs, skilled Im man
70
60
60
40
50
J
40
d
■S'
20
•>iu
30
1 apply (65). The
acts with an exer>ronary artery dis>opulation being
red when testing
aluating a high-
20
0 J
10
VT w 1.1 L/mlnutc
0
0.5
-i.
f only associated
L’gment of 1 mm
. generally indi
Im her of non is
[bundle branch
1
VO, m*x - 1.9 L/minutr J
1.5
10
1
2.0
O, Intake (L/mlnute)
tilal'o’
and the nadir oMhf
min apPXatelv 60%
th?Sh°ld fr°m Pl0' 0' Ven,"atlon
and
°XV9en
°ke
At the inaction of the Vf line
^7 ,he ven,,tot°^ threshold. In this case. It is b L/
Kavanagh T Yacoub MH TheS'^ r
f/ves fn
1988 )efitS
eXerC'Se
°f 1'9 L/mln <^<^9 from
U°nM
P^-
...... .
f
398/
Therapeutic Exercise
1 80
Peak effort
I
Some ot the inc
160
Peak aftorl
140
» |
I•y•d
'•covary
Catacholamma**
1
120
F-S*
I
1
\
100
80
— Danarvatad heart
i
f
Normal raaponae
• —- Recovery
60
1. Diagnose whe
toms suggest tl
2. loaliLite the r»
disease;
3. A.'i'icss prognot
i Screen tor late
5 Determine lev
program; and
6. Quantitate fur
response to the
i
C-'iitraindicatk
0
2
3
5
6
8
®
410
11
12
13
15
17
18
10
(Minute*)
Stage of Frank-Starling method
ynset of circulating catecholamine eliect
heart transplant patients. Perspectives in Cardiology 4.21-37, 1988.)
« hlgtiL. Take (i‘ntl thUtlhe ventilatory threshold), is relatively unaffected bt
di-tc^henn^C T”’ ‘l
antagOnistS’ no“^orthy tn light of current car
diac therapy. Cardiopulmonary exercise testing is increasingly employed in
XIh? Tl 1C unctlonal capacity of Patients with congestive heart failure
67/ 8 . Fins appears to give a more objective measurement than the New York
eart Association classification, or duration time on an exercise test. Another
applnation is in the exercise rehabilitation of cardiac transplantation patients
> tnm‘(r
\eartt b 5 'O reSP°nCl in a linear fashi0n 10 increases in Power
t U! d ig. _(.3) thus completely invalidating the use in these patients of
tab es which relate heart rate to power output and/or oxygen uptake. Direct gas
analysis allows one to offer clear advice on training intensity (69 70)
Thus, knowledge of both cardiac and pulmonary responses to effort per
mits more precise prescribing of a safe and effective training level. In addition
\ve can utilize pulmonary gas measurements to calculate stroke volume and car
diac output noninvasively (62).
INDICATIONS, CONTRAINDICATIONS, AND REASONS FOR
TERMINATING AN EXERCISE TEST
In the context of this chapter, the major purpose of an exercise test is to
establish a sale and effective level of physical training for the patient with isch
emic heart dtsease. However, there are other indications, some of which are
listed below.
\X ithin 6 week
ried out during
ncart rite oftei
\cute mvocard
3 I nstable angn
4. Complex venu
5. Second- or thii
6 S; -vcre aortic <
obstructive car
’ Severe system;
and
8 Acute infectio
1
Among the rea
1. z\ lai lure of he
increasing effc
2. Systolic blood
sure 120 mm
3. Frequent (3 it
iricular tachyc
a. Sustained sup
5. Development
o. ST segment d
~1. Increasing an
8. \ny adverse c
excessive swe
THE F
An exercise p
activ ity; (b) intensi
Chapter 20—Coronary Artery Disease
/399
Indications
Some of the indications include:
1. Diagnose where the occurrence of chest pain or other cardiac symp
toms suggest the presence of coronary artery' disease;
2. Evaluate the results of surgical or medical therapy in ischemic heart
disease;
3. Assess prognosis after an acute myocardial infarction;
4. Screen for latent coronary' artery disease;
5. Determine level of cardiovascular fitness before entering an exercise
program; and
6. Quantitate functional status inc congestive heart failure, and assess
response to therapy.
Contraindications
Contraindications include:
IS
»9
fuel
increasing effort,
or age. Note Ahe
ed deceleration
le termination of
lefits of exercise
unaffected by
?f current carempkwed in
he/.n fiilure
the New York
test. Another
Uion patients,
ises in power
■«e patients of
=ke. Direct gas
70Y
to effort per. In addition,
ume an'-’ car-
FOR
ise test is to
nt with isch
bf xxhich are
1. Within 6 weeks of an acute myocardial infarction—exercise tests car
ried out during the very early recovery phase are usually low level, the
heart rate often not being allowed to rise above 120 beats per minute;
2. Acute myocarditis or pericarditis;
3. Unstable angina;
4. Complex ventricular arrhythmias;
5. Second- or third-degree heart block;
6. Severe aortic outflow obstruction, as in aortic stenosis or hypertrophic
obstructive cardiomyopathy (HOCM);
Severe systematic hypertension that is not responding to medication;
and
8. Acute infections.
Reasons for Terminating the Test
Among the reasons for terminating the test are:
1. A failure of heart rate or systolic blood pressure to rise, or a fall, with
increasing effort;
2. Systolic blood pressure exceeding 260 mm Hg, or diastolic blood pres
sure 120 mm Hg;
3. Frequent (3 in 10 or more) complex ventricular premature beats, ven
tricular tachycardia;
4. Sustained supraventricular tachycardia or atrial fibrillation-,
5. Development of second- or third-degree heart block;
6. ST-segment depression in excess of 2 mm, horizontal or downsloping;
■7
Increasing anginal symptoms; and
8. Any adverse change in the patient’s appearance or attitude, e.g., pallor,
excessive sweating, confusion, etc.
THE PRESCRIPTION OF ENDURANCE EXERCISE
An exercise prescription requires four components. They are: (a) type of
activity; (b) intensity of effort; (c) duration; and (d) frequency of workout. Each
<
I
II
400/
Therapeutic Exercise
is defined below, with specific reference to the coronary artery disease
II
Type of Activity
««ceor "^^mareLZtlmXscdpS*^
Training
bility routines
Patients shoub
symptoms, etft
with climatk
(73,71).
All exerc
cert ibc'uh in c-
muscJe '"asses. Endllr
are brisk walking, slow jogging (12 mkiiire
‘Z commonly "sed. Examples
long-distance cycling, cross-countt sklng‘od " , '’i^’ re,axed swi'n‘"mg.
there are doubtless more possibilities den 2 teerinS’ circuit training, etc
e„vlro,„„e„, „ J" be ni,^S ?
strengthening regimens, while valuable and eZ that flexibiIity and muscle
are not included in the category of.cardio"
T"
in their
right
the more complex the training activitC ch*
CO"dltlonin8 activities.
require and, therefore, the fewer paden wdlZhi’
m°tOr skiH 11 "'HI
will
since the ability to perform a panicula smon w ie t0 participate- In addition,
I’
I
*
In recent
involved in the
cuLr health. Tt
ability and saiet
advising a phys
assessment for i
have pr. n en coi
!■» <«»!- “‘zz;:x
m
in;:; . ■jr.-h
Hulicr inonito!
ge< Ji. TheyZfbZhi orte »“ ““ Sp°r° “ s"“
■i training effect from vigorous cornnftiHy8
Healthy young adults will get
ketball, and soccer, but the n- i,en?P L
Sp°rtS SUch as te""is. squash has
emly healthy but sedentary middle ag^S7s oZ" dirSe (°r dle appar
els of
.
© male) is often unable to attain the lev
of efinrt
eflon required. Furthermore
1 may be highly dangerous to attempt to do
so without medical clearance
clearance.
References
i.
Virchow RLK:
ihrer B&rgrun
unu pa tnoIoq
lin. Hirschwaic
2.
Goldstein JL.
sis. The low-d
tor hypothes
1977.
3.
Lipid Reseatct
Research Cltni
ven tian Trial
mciaence of <
jAXIA 25 1.351
4.
Rokitansky C v
logical Anaroi
enharn Society
5.
Duguid JO: Tn
sclerosis. Aden
shy Press, 1976
6.
Kanno-’ WB, M*
general cardio
Framingham $
38 46-51, 1976
7.
Epstein FH: Mult
prea.ction of c
Bull NY Acad M8.
Morris JN, Head
Coronary heart
activity ot work
1111-1120. 195
9.
Brunner D, m<
infarction amor
Intensity
80S
<evri
'ng wtth coronary
artery
disease Darien,
< n
a.X,'?W
Um 011
heart rate. When
deal
.he i,7ver
imJnshS
andTi
T° *^
hOt,,d
of c"utn,
duration ol the workouts so as to achiev/th^desi”8/01^ lhi'S by illci'ea!>ill« 'he
‘he intensity should never be greater than ,t .
ed 'raining effect. Obviously,
Patients should be exercised below their threshokl'f d dUring
cxercise test
tschem.c changes, and never in the presence of k , °r an8‘nu or sh segmental
a,ld HO1I„ „o„iMn8 sh P u b “
Duration
dnuous, and las’fo/aUe^ra^Xu^Th^im0^0141 Shh°Uld be Steady’ con'
as to allow lor this duration without causing exceZefaSgLe" Sh°U,d
SUCh
Frequency
TW
S-*- SJ -
»ee^ .o E,„, a„y bclle6l
gams that are not commensurate with Se M
V ?
WiH yield
spare time. However, there will always HeZ l
i;ncroachments on one's
some leeway.
5
CkS When a session has to be
missed, providing
j
Fitness
cannot be StOred’ a‘ld W"l>ln weeks of discontinuing training, a
decline
is apoarem'
apparent.
--k.
J—
Chapter 20—Coronary Artery Disease
n’ .irterv /*ise:ise
/401
Other Aspects
Training sessions should include a warm-up and a cool-down and flexi
btltty routines should be practiced in order to reduce the incidence oHniurie '
eff be instructed in pulse taking, recognition and interpretation of
U ,1
ff
°f,' 1e Var OllS medications exercise tolerance how io cone
(73 70
t,C Cond,,ions' and lh(' Choice Of suitable footwear and dotlth'g
masses. Endu>used. Examples
ixed swimming,
lit training, etc.
genuitv and rhe
ty and muscle
heir own right,
acbv’pv
possession of at least rhe basic
.1 defibrillator should al wavs be
Oto- sk’’l !• wi’]
<te. In addition,
it is difficult to
hing that most
Toronto Reha
eal application
ports or g.nne>
adults will get
s. squash, has
(or the appar
attain the lev> attempt to do
d or the level
-e. When dealde of caution,
icreasing the
1. Obviously,
exercise test.
>T segmental
arrhythmias.
steady, conuld be such
any benefit,
s will \ ield
ts on one *
has to he
training. a
CONCLUSIONS
Tn recent Tyears
’—— ; a greater proportion of the population has become
involved in the type of aerobic activities Ik
c ..own to be associated with eardiriv'ic
cular health. T*T’’1l'~
’ '• •
ability and safety of such endeavors.
....... ........ ’• rh,s chf’Pter has outlined the rationale for
advising a physically active life, and has
J provided guidelines in the areas of
assessment ffor and prescription of exercise,
particularly in those patients who
have proven) coronary artery disease.
s"wif
.ilb
;z
References
i.
Virchow RLK: Die Cellularpathologie In
ihrer Bergrundung auf physlologische
undpathologische Gewebelehre Ber
10.
lin, Hirschwald, 1858.
Goldstein JL, Brown MS: Atheroscleror .
sis: The low-density lipoprotein recep
tor hypothesis. Metabolism 261257
1977.
►JI
Lipid Research Lipid Program: The Lipid '
munal settlements In Israel. Lancet
2:1049-1051, 1969.
Taylor HL, Klepetar E, Keys A, et alDeath rates among physically active
2.
and sedentary employees of the rail
road industry. Am J Public Health
52:1697-1707,1962.
Kahn HA. The relationship of reported
3.
coronary heart disease mortality to
Research Clinics Coronary Primary Pre
physical activity at work. Am J Public
vention Trial results. In Reduction in
Health 53:1058- 1067C 1963.
incidence of coronary heart disease.
12. Brunner D: The influence of physical
JAMA 251:351-364, 1984.
activity on incidence and prognosis of
4.
Rokitansky C von: A Manual of Patho
ischaemic
heart disease. In Raab W
logical Anatomy. London, New Syd
(ed): Prevention of Ischaemic Heart
enham Society, 1852.
Disease: Principles and Practice.
5.
Duguid JD: The Dynamics of Athero
Springfield, IL., Charles C Thomas
sclerosis. Aberdeen, Aberdeen Univer
1966.
sity Press, 1976.
13. Kannel WB: Habitual level of physical
6.
Kannel WB, McGee D, Gordon T: A
activity and risk of coronary heart dis
general cardiovascular risk profile the
ease. (Proceedings of the Interna
Framingham study Am J Cardiol
tional Symposium on Physical Activity
38:46-51, 1976.
and Cardiovascular Health.) Can Med
7.
Epstein FH: Multiple risk factors and the
Assoc J96:811-812, 1967.
prediction of coronary heart disease
14. Shapiro S, Welnblatt E, Frank CW, et al:
Bull NY Acad Med 44 916-935, 1968
Incidence of coronary heart disease in
8.
Morris JN, Heady JA, Raffle PAD, et al:
a population insured from medical
Coronary heart disease and physical
care (HIP). Am J Public Health 59 1activity of work. Lancet 2:1053-1057101, 1969.
1111-1120, 1953.
15. Paffenbarger RS, Hale WE. Brand RJ et
9.
Brunner D, Manelis G: Myocardial
al: Work-energy level, personal char
infarction among members of comacteristics and fatal heart attacks a
I
K
Awareness Through
York, Harper % Row,
■■
icepfs in performing
Handout given as
jis workshops, 1988.
Intelligent Body The
?sslona' Taae T-ehos.
rank Wildman, Ph D.,
ell RG (ed). Rabbi Ben
Age. Old Age New
Brace Jovanovich.
Exercise for Low Bock Pain
David A. McCune and Robert B. Sprague
■Respite recent advances in spinal imaging and diagnostics for clarifica
tion of the medical diagnosis, the conservative treatment of spinal disorders has
held exercise as its cornerstone for decades. This chapter presents various
objectives of exercise and possible mechanisms used in the treatment. Exer
cises, with variations, are presented in the Appendix to this chapter to demon
strate their application to spinal disorders. Unlike in years past when clinicians
prescribed “standard” back exercises, today’s clinician must apply exercise in
a specific and judicious fashion when treating spinal disorders. The use of exer
cise has now been expanded to aidUn clarifying the medical diagnosis, as well
as in identifying a specific pathology. Exercise is an essential part of the treat
ment of acute back pain, chronic back pain, and in prophylaxis
MEDICAL DIAGNOSIS
The specific pathology causing spinal pain frequently eludes even the
most astute clinician. Quantification of structures at fault in back pain often
must rely on a clinical diagnosis. Often, this is determined by assessing the
patient’s response to exercise. Although this chapter is not intended to present
diagnostics, appreciation of the medical diagnosis is necessary for appropriate
application of exercise. In general, there are three categories of spinal pain:
chemical or inflammatory, mechanical, and organic. Patients often present with
a combination of two, or even three of these categories. McKenzie (I) has out
lined two general categories of spinal pain, referring to them as chemical or
inflammatory’ pain and mechanical pain.
Chemical (Inflammatory) Pain
xjrt'ir mir
un aoi move, nor de rhey change with specific
sptnal movements. Generally, if the symptoms associated with an inflammatory
process are to change, they worsen secondary to exercise. Though less effective
lor this type of pain, exercise may be helpful if appropriately prescribed. Wyke
(2) states that burning” is the most common description of chemical pain.
299
300/
Therapeutic Exercise
Mechanical Pain
<» ^2iXbX^X:h'8r"^b''o'p“,“'
complaints
logical function of the intervertebra/disTthe^i,adv5rsely affects the Physio
rounding contractile or nonconrnrriiA • f ’‘ T)OP^yseal joints, or the suralence of any of these pathologies perX!.^ HowewrY6"10”1 tO
preV‘
the vast majority of spinal disorders P.U ■ < \
wever» there is agreement that
“axsx ,ta'
«■
........ ...................
e .se
“
otegory are coZt
;
?
"c US Spinal pai,K Also
»nd d,s.
in
S** b‘“
-...... .
PATHOLOGY CLARJfICATION
exercises for spinal d^sordw^AsZinent anddo^
de,e™’ine aPPr°P‘iate
•nents include the patient’s reXT
documentation of active move
.... .................
be limited to single movements is ..... I.
es^tltlal that .issesstnem not
Pathology by assessing symZn Xn es to
ab°UI lllC 13i“ielll s
stressed the efficacy of assesvtn
■
6 t0 rePeated movements. Cyriax
has outlined a
dZ/ r
mov“
plaints, as summarized in Table 15.1. t'n“‘ite the source of 'he patient's com
Table 15.1.
Particula
are reproduce
This s\ mptoni
seal disc sym
during moveii
others state th
only at vxtrer
tissues.
Once th*
exatn, and test
favorably alter
is not identifie
symptom chan
The use <
clarifying the p
major objective
and (5') prever
L:\vicise 1
Wuious inechu
nun.mon of jp
pain reduction,
appropriate exc
priare, the patie
pain, a decreas<
pain.
Summary of Cyriax’s Soft Tl
issue Evaluation (3)
Amovement-tests all anatomical structures
Findings
Indicate
Active and passive motion is restricted
and/or painful in the same direction
Active and passive motion is restricted
and/or painful in the opposite direction
Relative restriction of passive motion In
various directions
C Resisted mo vemen ts— test all
Arthrogenic lesion
Soft tissue lesion
Capsular pattern
contractile structures (muscle, tendon, periosteum)
Findings
_
Painful and strong
Painful and weak
Painless and weak
Painless and strong
The mech
mechanorecepc
si are of rhe invc
Extensive
enhanced thioi
eral, relief of p;
mg i\ pe i mech
sec., which has
these receptors
_______
Indicate
Minor lesion
Major lesion
Neurological or complete rupture
Normal
The preset
source of pain,
theoretical mod
environment wi
of this continue
spasm. Muscle p
immobilization
Chapter 15—Exercise for Low Back Pain
‘patient complaints
affects the physio
joints, or the sur
mem as to the prev? is agreement that
and that exercises
and is either inter
ates that pressing,
union descriptions
ormalities and dis
i. Also included in
pecific knowledge
» chapter. Exercise
ated problems, but
malities.
{“mine appropriate
)n of active moveing and foil?'’, ing
tat assessment m •:
‘bout the patient s
lovements. Cyriax
iovemems
tie
(he p niem > coin
1 (3)
>. bursas, bona, blood
’Indicate
lesion
sion
*tern
/301
Particular note should also be taken as to whether the patient’s symptoms
are reproduced during the test movement (in range) or only at the end range.
This symptom-range relationship is helpful in differentiating between apophy
seal/disc symptoms and soft tissue symptoms (4). McKenzie states that pain
during movement is indicative of mechanical derangements in the disc, while
others state that the apophyseal joints are at fault (1,5,6). Symptoms reproduced
only at extremes of motion are felt to arise from adaptive shortening of soft
tissues.
Once the source of the symptoms is clarified through history, physical
exam, and test movements, the prescription of appropriate exercise designed to
favorably alter these specific structures can follow. Even if a particular structure
is not identified, exercises may be prescribed and modified based on desirable
symptom changes.
OBJECTIVES OF EXERCISE
The use of exercise in the evaluative stage is essential in (he process of
clarifying the potential source of the pathology. In the treatment process, three
major objectives exist: (1) pain reduction; (2) restoration of normal function:
and (3.) prevention of future recurrence.
PAIN REDUCTION
Exercise for reduction of pain has long been an ;accepted
, . J clinical goal.
Various mechanisms for pain reduction and differing guidelines for the deter
mination ol appropriate exercises have been offered. When using exercise for
pain reduction, three clinical symptoms should be evaluated in determining the
appropriate exercise, and in assessing patient progress. If the exercise is appro
priatc. the patient will report one <»r more of the following: centralization of the
pain, a decrease in frequency of the pain, and/or a decrease in intensity of the
pain.
c
Mechanoreceptors
The mechanisms of pain reduction relate to the effect of exercise on the
mechanoreceptors, muscle spasm, inflammation, and the resting anatomical
state of the involved structure.
Extensive work done by Wyke (7) revealed that pain reduction is greatly
enhanced through appropriate stimulation of joint mechanoreceptors In gen
eral, relief of pain is perceived through prolonged end-range stretch stimulat
ing type I mechanoreceptors and through midrange oscillation frequency of .5/
sec., which has its effect by stimulating type II receptors. Stimulation of each of
these receptors through exercise has been found to function in pain inhibition.
Muscle Spasm
Indicate
Dl or complete rupture
T^e
af tar^ized
soasm has il«?c ir.na ’-e—i
■,
source of pain Mam- authors refer to the pain spasm hypothesis k serve ay a
theoretical model, i.e., if the muscle guarding is prolonged, the altered local
environment will result in further irritation to free nerve endings. The presence
of this continual chemical irritation is believed to perpetuate the muscular
spasm. Muscle guarding or spasm serves its immediate function by reinforcing
immobilization for the involved injured structures. Whether the source of the
t 302/
Therapeutic Exercise
“■ "'",,“dVe
H— W »<-■
»
pain arc present. Over
with medications alone
ally prolong the patient
m e c h a n i c a 1 com po n e n t«
ailment, and advancing
Gentle exercises
once the inflammatory
component may be ide
Relief of
nene
ot the
me muscle
muscle spasm
spasm can be effected through two mechanisms The
» „ .he locabzed
of d.o ,p„,„ ,ot.|f T„i ,„„„™ “oMe
< d. hues, but must also include a lengthening stretch to the involved muscles
hl g T1"^ ° ,tlS!,ues allows for dilation of capillaries and results in increased
ood How to the muscle cells. Removal of metabolic wastes and increase in
local oxygen also result. Though this mechanism may be effective in immediate
ehet of muscle pain, it is not effective if other structures persist as “X
lying cause of the protective spasm. In this instance, treatment of the muscle
spasm only does not address the problem properly
An alternative means of treating muscle spasm is through affecting the
actual source of the spasm. Obviously, if traumatic bony fracture or grostdis
location is present, immobilization will ultimately assist in relief of local mus
e spasm, in the absence of trauma, treatment requires clarification of the
ottendmg source of fire muscle spasm. Williams (8) felt that the primary source
of low back pain is from paravertebral muscle spasm and loading the apophyw rh |O,nlr i'11S 1S "°'.wlly do most Patients with acute low back pain present
i h lumbar flexion deformities? Clinically, we have observed marked reduction
.local mus. le spasm through active or passive lumbar movements other than
I Xion. We must assume, then, that pain redUc'tion in these instances is thro m
i echamsms other than muscular stretch. Quite possibly, we have removed the
c etiding stress from pain producing structures other than muscle.
Chemical Irritation
nerv Pain generated
chemical inflammatory irritation of the nociceptive
nerve endings may be reduced or eliminated by two means- fl) physically
eduemg the chemical irritants; or (2) neurologically reducing the activity in
be noctcept.ve receptor system. In the former, improved clrcula m e u 1 s
m
■ C.L
membranes may also become more permeable, resulting in
discussed later in‘this'chaptJr.
meChaniSm <neuroPhysiological) will be
Mixed Causes of Pain
Mailland (9) implies that patients often present with not only mechanical
<i chemical pain, but with an assortment of both types of pain He further
■mphes that the chemical component of the patient pain may be p-tHly or
wholly caused by mechanical stress. For example, chronic microtraunta to the
um >ai spine created by adaptively shortened structures in the hip joint may
provoke symptoms, both chemical and mechanical in nature, in either the hip
adjacent lumbar spine. Reduction and subsequent elimination of the
m cha.m .tl stress in the hip indirectly reduces the related spinal pain 1 ikewise
eduction and subsequent elimination of any mechanical stress in the lumbar
sj me produces a posttive effect on the chegtical pain. Reduction of the chem
rel ef O1f P°nCnt’
°f phySiCal agents’ Provides only temporary
e"nW"
“'ed ‘O
Probably in some cases, both chemical and mechanical
,te
components of
j
The tmal propos
mechanical stress. All :
bral discs, and the a
McKenzie (1) has pos>
alters rhe state and poi
been confirmed by oth
remove abnormal sires
tionship to the interve
when the intervertebr:
pruuaple of cemralizat
by Donaldson (12). K
shortened structures ai
ing the p tin of stretchi
the level ot pain. In <
cites the reproductior
mechanical stress. Ot
aflects the apophyseal
apophyseal joint, then
cal sires') from any or ;
ceived patient pain.
Using knowledge
cian can prescribe apj
ment, starting position
inate pain
RES
Once pain has b<
restoration of normal j
and peryinicular soft
normal groxs spinal n
hide an abnormal segt
most effective for rest
retaining this mobilin
cific desired effect at
assume that with appr
desired effects of the c
levels. \X hen restorin.
nective tissue and mu
Chapter 15—Exercise for Low Back Pain
sm inav be present to
/303
pain are present. Overemphasis on treating the chemical component either
with medications alone or in some combination with physical agents may actu
ally prolong the patient’s problems. Further consequences of not addressing the
mechanical component include failure of the patient to fully recover from his
ailment, and advancing the chronicity of the problem.
Gentle exercises may be used to reduce inflammation and edema, and
once the inflammatory component is reduced or eliminated, the mechanical
component may be identified and dealt with appropriately.
two mechanisms. The
eatment may include
the involved muscles,
d results in increased
astes and in ere.: . in
■ffective in immediate
persist as the under
itment of the muscle
Mechanical Stress
lhe final proposed mechanism for pain reduction relates directly to
to
mechanical stress. All spinal structures—lhe apophyseal joints, the interverte
bral discs, and the associated soft tissue- have
anatomical resting
have anatomical
resting states.
states.
McKenzie (1) has postulated that appropriate application of exercise actively
alters the state and position of the nucleus of the intervertebral disc. This has
been confirmed by others (11). He feels that it is possible, through exercise, to
remove abnormal stress from the disc and restore the normal anatomical rela
tionship to the intervertebral junction. Reduction of mechanical deformation,
when the intervertebral disc is at fault, is best accomplished by following the
principle of centralization described by McKenzie (1) and further documented
by Donaldson (12). Reduction of mechanical deformation, when adaptively
shortened structures are at fault, is best accomplished by temporarily reproduc
ing the pain of stretching the deformed tissues without permanently increasing
the level of pain. In describing his “postural syndrome,’’ McKenzie (I ) also
cites the reproduction of pain in normal soft tissue simply due to excessive
mechanical stress. Others report that abnormal mechanical stress adversely
affects the apophyseal joints (5,6). Whether it concerns the disc, soft tissue, or
apophyseal joint, there is clinicahevidence that removal of excessive mechani
cal stress from any or all of these structures will result in the reduction of per
ceived patient pain.
Using knowledge of neurology, physiology, and biomechanics, the clini
cian can prescribe appropriate exercises for low back pain. Direction of move
ment, starting position, frequency, and vigor are all coupled io reduce and elim
inate pain.
hrough affecting the
fracture or gross dis
n relief of 1oc.il muss clarification of the
at the primary source
loading th? apophv
back pain present
ed marked i v duct ion
ovements other than
instances is through
ve have removed the
muscle
of the nociceptive
eans: (1) phvsh'al|v
-ucing the activity in
rirculation results in
inens in th
' .t< d
neable. re.-jh.ing in
ysiological’ will be
tot onlv mechanical
of pain. He tun her
n may be partly or
microtrauma.to the
ft the hip joint mav
re, in either the hip
elimination of the
?inal pain. Likewise,
•tress in the iumbar
action of the chemdes only tmnpornrv
ress the underlying
RESTORATION OF NORMAL FUNCTION
Once pain has been reduced or eliminated, the process is directed toward
restoration of normal gross and segmental spinal mobility, muscle coordination,
and periarticular soft tissue length. Exercise is essential in the restoration of
normal gross spinal motion and posture. Apparent normal gross mobility may
hide an abnormal segmental movement. Though passive manual techniques are
most effective for restoration of segmental mobility, exercises are essential in
retaining this mobility. There is little evidence that exercise can produce a spe
cific desired effect at only one segmental level. It is reasonable, however, to
Clinic that with appropriate stabilization ()f superior and inferior segments, the
desired effects of the exercise can be localized to within two to three sequential
levels. When restoring segmental mobility, emphasis is usually placed on con
nective tissue and muscle.
-ical components of
• 1
TherapeuLic Exercise
Stretching
ao?}1*!tTn?"tly
fO‘"* Caps"le c"tUaS'. “d
“'XT “d
f
4
XSXfT10" 7h ,l'r
SSS “TT 'lly “d
»
..... ,.....
XT
'»-■«stretch of->o minn,
•*n<J a sustained
■" rd~XT
F
^du‘*1 len«th with the presence nt h
be’
'4“t: “XT™.'
when
~s«xx-='~r«srses's
Neurophysiologic Approaches
l
neurons. Ar
ability. Spec
threshold of
t-h.rging me
produce bot
on tissue elc
The pri
manipulatiot
muscle spine
b‘ngih chan^
detect chan£
found to assi.
sized that iso
bition of the
relaxation an*
tluough the (.
A secon
antagonist mt
through the S
Deep rot
believed to be
midrange exer
movement. Mt
function. VC'eak
and inactive m
provide the fu
eliminate the c
ening of weak
result in only p
Though it
mobility, norm;
elongation of e:
Complete :
than relief of pc
fence to be succ
length and bala
tonic spinal stabi
posture. Posture
Achieving j
essential in the
muscles are rhe 1
cles Specific stn
sic.ted jor sett tiss
Sp
Recent advai
spine have be con
1
1
*
Chapter 15—Exercise for Low Back Pain
capsule cartilage, and
r in the loss <m mobility
is dependent upon the
ies of collagenous and
bers (IS). ('o||;ig< 'nous
mdon. 1 ht'se hbeis .n-e
)ads. Fewer in number,
tarily and returning to
Connecti\e tissue reorwhile responding to
rcome the p”'■ grossive
?nt through a full and
ssue are not clear. Rec) seconds, though spc■lave demonstrated an
the presence of heat
studies have, reported
)n and frequency (In
duration and range of
-?nificant in long term
ctors. Stolo'.- and Wei
nuscle are dependent
3ns, the sarcolemma.
ociatcd tendons. The
•ment extensjbiluv is
1 that at the extreme
further motion.
>e taken int account
(26) state that exer
.'reasing the collagen
cess of simultaneous
rate of break k wn
lore
nnd less
4ile debilitating scar
aware that excessive
iltant new iniun- and
Iso neurophysiologleuromuscular facil
the neuromuscular
’NF is based on the
i, resistance, irradiaory stimuli decrease
of additional motor
/305
excir
threshold of motor neurons or Jsults'hi 1 "l .S,’'lr(e ',f s,llrmli ihat raises ih<charging motor neurons (30 31) rh,
1' c<1rcasc in ,n|mber of actively dis
■ produce both incr ased st e
and fI "l^.,t,1,Zation of the^ Principles mas
on tissue elongation
8
we refer here only to their efle. t
I he prlmaiy reason for |>nf effectiveness in >1
1
manipulation of the stretch reflex This L
’ 1 “Ll<‘ elongation Iles in the
muscle spindles, which are sensitive
1
'nJo,ves two 'VP65 of receptors:
length changes in the muscle fiber and’cnlni
We" as to the rate of
detect changes in overall tissue tpne" ?
tendor organs (GTOs), which
loundtoass^tinmZe^rZe^sa: hX^T T
sized that isometric contraction followed h. ?!
,
have hypothe
bition of the alpha motor neuron Z 1 Y Z relaxation results in an inhi-
contraction of
.h.oug.beSb„d„8I0„la„ ret.lpr„„
"'"'• ••e’s relaxation
be.leved
midrange exercises done frequently with an emohas-repet'tlOn' low distance,
movement. Muscle imbalances are also helfe Z
restoring coordinated
function. Weak muscles require strenmh
eved t0 contribute to the loss of
and inactive muscles require retraining PriZ t’8h'musc'es require stretching,
provide the fundamental base for addr
P fS described by Sahrmann (36)
eliminate the chronic microuauma pre ent'd8 i Z
t0 redllce or
ening of weak muscles only usitwthe m ost""8 re"7 movement Strength
result in only partial recover of function or ib S"ph!-‘,t,ca,ed equipment, mav
Though it is still unclear what
, absokltelV no ^in whatsoever
mobility, normal range of motion is essentia 1 "to heiH
SP'nal
elongation of existing connective^tissues. ‘ to
g °f new C0,laRen and
PROPHYLAXIS
pZs ;xs"r™tp'nAl'>v
fence to be successful. The objectives for nrev 'r miJSt prevent futl|re recur
length and balance (agonisgJs JXnntfA
t0 reStore: soft
tonic spinal stabilizers; phasic muscle ftreneth C°”rdlnatlon and endurance of
posture. Posture must be addressed from th?'
pr°per bod>’ mechanics and
Achieving a balance of son He
, theilnltial Visit to discharge.
essential in the treatment of back 'disorders
a8°niSt
antaRonist is
muscles are the hip flexors hamstrings i
i
mO'St common)y shortened
des. Specific stretching technique S 8‘ o' m^'eS’ and paraspinal musstated for soft tissue elongation.
'
mentI°ned later using the rationale
Spinal Muscle Deconditioning Syndrome
spine have become'
306/
Therapeutic Exercise
ie quantification of muscle function has pointed to a marked deficit in physical
function m patients with chronic back disorders. The role of this decondition
ing syndiome is becoming more clearly evident (43-45). Weak muscles have
long been considered a contributory factor in back disorders. Many authors
herefore have advocated the use of strengthening programs (40,44,47)
Improvement in one's physical conditioning has been shown to aid in restora
non of normal life-styles following back disorders (31). Isokinetic strength
quantification reveals that normal trunk extension flexion strength ratios range
from 2. : I to 1.1:1 (37), but little has been done to quantify the strength and
endurance role ol the smaller deep muscles of the back. Chronic fatigue in
these deep muscles has been hypothesized to produce low back pain (48 49)
Much has been written about strengthening exercises for low back pain
hese exercises are generally directed to the muscles of the trunk and pelvis'
Despite Ihe nnporlance placed on strengthening, relatively little has been
i< poih-d ^-garding the appropriate use of exercise based on muscle liber type
and function, rhe paravertebral muscles are predominantly red fiber type find
iuncnon
Ingli endurance, low force activities. Muscles such as the abdomln d
and gluteal muscles have greater amounts of white fibers. Respecting these dil
erenct-s, it is then logical to also rehabilitate the paravertebrals for their specific
functions in relation to the spine.
1 he deep paravertebral muscles (rotators and multifidi) have been found
by inserted electrodes to contract moderately and bilaterally symmetrically dur
ing spina rotation and during extension (50). During sitting and standing, they
are slightly active (51). Due to their proximity to the apophyseal joints a cor
ollary (unction may be coordination and guidance of the apophyseal joints dur
mg most movements. With this in mind, the clinician initiates a muscular train
mg program with appropriate endurance training for these muscles. Once
segmental movements are well coordinated muscularly, recruitment of more
powerful muscles (larger paraspinals) should not disrupt normal joint median
ics. f.linna ly, those patients who demonstrate no segmental strength or range
ot monon deficits but complain of a "catch” in their back may be .suffering from
transiem symptoms from apophyseal incoordination and subsequent joint
stiess Muscular retraining includes the motion of rotation through the mid
range using little or no resistance. These motions should be performed with it
least 60 repetitions to take account of the endurance nature ol ihe liber fvne of
Hiv <lc('p ini!.•><.■!<•.•>.
•’
Increases in muscle strength are generally accomplished developing ten
sion in involved muscles against a large amount of resistance for relatively few
repetitions. In general, the fiber type of abdominal and paravertebral muscles
docs not end Itself io this type of stressful training. These muscles must also
be named with high repetitions of movement against low loads (48)
Muscles that are phasic in nature should be trained for strength. Strength
gains have been reported using variations on Delorme’s original progressive
resistive exercise concept (52). Progressive strength gains are achieved through
multiple sets (usually three) of 10 or fewer repetitions.
The final approach to prophylaxis is the’functi'onally specific exercise
These exercises must be designed by the clinician to simulate the patient’s
functional environment. The application of proper body mechanics in this stage
is the basis lor exercise design. For example, if the patient frequently bends and
hits heavy crates at work, weighted boxes will be lifted repetitively to
strengthen needed muscles and reinforce proper body mechanics and posture.
PR
In vieu of t
cess of any treat
relief or on the
back pain, if suet
for back pain. A
strength, endura
posture are not i
To maintaii
gtuh• body lurch
to retain the bet
initially eliiuinat
thru‘.vs k \ercises
preventive progr
must be individu
It should be
reflect our conce
diligently can ea
include both pre
kxerci.ses p
the clinic Each i
ration, and propf
tions. In the text
pain reduction; i
laxis 1 here will
to meet all three
but otter a repres
.u u\ c exeiciscs,
liiiuiauo.n being
Once more
modincation are
of the exerc’se n
mem at the initi
mcdiik'.rdor.s, an
V ::h fc-.v. if any,
erai guidelines ai
simplified terms)
of pain, and alth<
porary increase i
reasonable perio
Objec
Exercises st
lumbar flexion (I
Chapter 15—Exercise for Low Back Pain
d deficit in physical
)f this decondition
Veak muscles have
ders. Many authors
'grams (tO.H.r).
n to aid in restorasokineti- strength
‘ength ratios range
y the strength and
Shronir fatigue jn
'ack pain ( 18, 49).
or low back pain,
trunk and pelvis.
v little has been
muscle fiber t\ pe
rd fiber type and
as the abdominal
pecting those difs for their sj^ecific
/307
PREVENTION OF RECURRENT LOW BACK PAIN
Objective
"T"
«■
relief or on the rapidity of return in w -t, |dRed
°n the acblevement of pain
back pain. If successfully treated a patient will''
abo*ition of futllre lr™'
for back pain. A compJheX• prS^ o7wTk8a'n
,he C'inic
strength, endurance, coordination balance
bact^ exerclses never ends, as
posture are not innately self-perpetuating. ’
° y mecllanics’;,nd Proper
Preventive Management
good body mechanics,^nd rewind baLne'-T* h™5' C°ndnUe to exercise, use
to retain the benefits of the successful treatmeu'^' bXerciscs H10'” or,,,n used
initially eliminate the oain- (?) r ,
,rtatrneint Program are those that (I)
fitness exercises^c"asS^V Sh^“JynCti°n;
O)
^neral
preventive program has its genesi's in
r ?
SP0rtS' Thus’ a successful
must be individualized and perpetuated tCeSSfU treatment ProKram. Exercises
have been found
mmetriealh durad standing, thev
seal joints a corayseal joints dur
a muscular train
muscle^ Once
titmeni of more
al joint mechanrength or range
e suffering from
ibsequent joint
rough the mid
rformed with at
he fibei type of
on posture does not truly
diligently can easily be negated bv non/ C SUb,eCt °f th,s chaPter—performed
include both proper posture and specific exeXs P" SPina' treatmcnt must
recommended exercises
the-'are ^l^ntly used in
the cHnicTcKrbe^
ration, and prophylaxis. Exercises dh baues
1
reductlon’ function restotions. In the text below, exercises are22 ’
g'VCn W"h basic r,irec
pain reduction; restoration of normaMnn r d acc°rd'nK t0 obiectives, namely,
•axis. There wiil be olw ous dupbeado Z""
COOrdinatio^
P-phy
to meet all three objectives Th^e ex ?re ?
eXerCiSeS
be ,,sed
but offer a representative sam. lino f
"T nC"her inclusive nor exclusive,
active exercises, like passive exercises oXobili^r d eXerCi'S?S' The choices of
limitation being the creativity of the practitioner
endless-the mai"
developing ten
r relatively few
lebral muscles
Jcles must also
(48).
ngth Strength
•al progressive
• ieved thrc»ugh
modification^re^-<•
of the exercise must be satisfied and "eXT7 t
mfl"- A’SO’the obiecti'e
ment at the initial and subseciuent rr,.->f d b' sub,ectlve and objective assessmodifications, and additions will deneri ,mtnt scssions- Appropriate deletions,
With few, if anv, '‘correct ’ exercists^or r t
patient’s rcsP°ose to exercise,
oral guidelines and principles guide the skilled chni
cific exe rcise.
1 the patient's
3s in this stage
nly bends and
?petitivcly to
’ and posture.
p-y
Syn'P'onis’ «en
......
pai„, ,hey mU!, produ-™
X
reasonable period of time.
Oblecnve: Poln Reduciton-Suggested Exercises
0.1 A prone lumbar extensmn (Fig. 15.2), side lying rota-
■
■
I
308/
Therapeutic Exercise
‘1“n (Fi8- 15-3). lateral glides (Fig. 15.4), and
prone-lying oscillations (Fig.
References
Objective: Restoration of Function—Suggested Exercises
i
I
f
, r *^ercises suggested for restoration of function are supine lumbar flexion
(Fig 15.1), prone lumbar extension (Fig. 15.2), hamstring stretches (Fig. 15 6)
hip flexion stretch (Fig. 15.7), sitting rotations (Fig. 15.8), side-lying rotations
(Fig. 15.3), and lateral glides (Fig. 15.4).
1 hese exercises are designed to restore full-range movement by stressing
end-range stretch in each of their respective physiological motions. If the
desired effect is stimulation and regeneration of collagen in an injured area the
stretch should be repeated 10 times and'held for 2-5 seconds. For long range
tissue elongation and improved range of motion, stretches should be main
tained for 15-30 seconds.
Objective: Prophylaxis—Suggested Exercises
Exercises suggested for prophylaxis are supine flexion (Fig. 15.1), prone
extension (Fig. 15.2), hamstring stretches (Fig. 15.3), hip flexor stretches (Fig.
>.-i), prone rotations (Fig. 15.5), abdominal strength exercises (Fig 15 6)
paraspinal strength exercises (Fig. 15.7), and gluteal strength exercises (Fig.’
Prophylactic exercises are designed to maintain range of motion and pro
vide muscular strength and coordination throughout the full range of motion.
For tonic muscles (paraspinais), exercises should be performed as tolerated
with an ultimate goal of 30 or more repetitions. Phasic muscle exercises will
best be performed against resistance. Suggested intensity is two to three sets of
10 -15 repetitions.
CONCLUSION
*i
*
Clinical experience has confirmed the beneficial use of exercise programs
for die treatment of low back pain. In this chapter, we have outlined specific
exercises that have been found to benefit the patient suffering from low back
pain. Though many patients lack specific pathological changes, the clinician
must rely on careful assessment of signs and symptoms as well as available
objective findings to determine appropriate guidelines for individualized exer
cises. Where diagnostic precision is demonstrable or probable, the clinician can
proceed with greater assurance to provide relief. The application of therapeutic
exercise to low back pain remains the cornerstone of conservative treatment and
prevention.
iv’iuzKonzic RA: >
Mechanical Diagi
New Zealand. I
1981.
Wyko B in Jayson
2.
and Sack
Mvixk ai Bath. W>
Cyiiax J- OithopQ
3.
more Williams & V
O Jiian JP. Mechc
4.
In Wall PD. Melza<
of Pain. New Y(
store 1984.
Grieve G: Comi
5.
Problems New Y
stone. 1986.
Mooney V, Rober
6.
drome. Clin O
1976
Wyke B: Artici
7.
manipulative the
Manipulative The
coin Institute of H
Williams P: Examii
6.
five treatment tlower spine. Clin
Maitiana G: Ve
9.
ed 5 London. Bu
10. Barnes JF: Myofa
niosacral therap'
Myofascial Reie
York. Dec. 1984.
11. Krag M. Wilder
ment Distriputior
of Human There
nal Motion SeQ
Results and Th
Moncgraph, Dej
Reitab. College
ton. University ot
12. Donaldson R: C«
ito usefuln
e'.’ii'ig sciaticc
Dallas, 1986.
13. Holland GJ: The £
A review of lit
Assoaanon for
cation and Re
tie vie*/ 1968, pi
14. Cormack DH: Int
Philadelphia, JB I
15.. Nardin M, Franke
collagenous tissi
dm M (eds). Bast
Skeletal Sys ten
Feoiger, 1980, p
16. Lehmann JP. De
and superficial
i.
Midrange oscillation affects type II mechanoreceptors and end-range
stretch affects type 1 mechanoreceptors. Muscle spasm is reduced by stretching
the involved muscles or by reducing the mechanical deformation of other non
muscular tissues. Each of these exercises reduces pain by apparently decreasing
the • omintiatioi) of chemicals causing the Inflammation. This is most cflJ
lively accompltshec! by exercising in the pain tree range initially without
exi!,tlnf5 symptoms. Progression is determined by accurate assess
mem. When the patient is generally able to perform each of these movements
through a lull range ot motion without pain, emphasis then moves to restoration
i
......
.4.
-
’ •-"---■------- ---
/
/
0
THY
WILL
i
.... ;
4®B|!
ilfi
RF
DONE
4b
By Emily Benedek
■|w
4-
"’jA—A-'’ '•.-
li
I
8
•V-
'pWfe>»
I®
>■
:
Mo Udall perseveres against the
ravages of Parkinson's disease, the memory
of his wife, and time itself.
■ n its way, Capitol Hill is not unlike high school. Bells
I ring, the men and women of Congress rise from their
I leather chairs and file out of their offices toward the
I chambers of the Senate and the House of Representa
tives. They rattle about the hallways, chat with colleagues,
exchange jokes, pass along rumors, vote. Then they return
until the next set of bells summons them back
The bells ring again and Morris King Udall, U.b.
Representative from Arizona's 2nd District, lumbers down
a marble hallway of the Cannon House Office Building.
Udall's 6-foot-5-inch frame, once the robust body ot a
professional athlete, is stooped by arthritis and the ravages
of Parkinson's disease. He has become frail and thin,
especially in ^he last year. His pants, too big for him now,
are hitched up over his waist with suspenders, and the
cuffs dangle inches above his ankles. Yet this day the tall
|i
W1
S'
w
. ‘A
’t* ii
’4
-J#' r.
1
v- .... 'J/'
........
p..., CrT-rrnc PhOTOCR APHc
I
ft
f
r
Udall is indignant about his capacity being
questioned. He told a colleague, 'The man who can
replace me hasn't yet been born."
man with the unassuming manner is in a hurry. He's got essential to Arizona's future—continues until completion.
For 27 years, Udall has waged these and other battles
his one good eye set on the Capitol (the other was
with
humor, grace and affection, winning a reputation as
removed at age 6 when a childhood pal accidently hit it
a statesman in the grand old sense: funny, erudite, quick.
with a penknife) and he's got to get there in time to vote.
Now he's dug in for his toughest battle, one that requires
He walks fast, very fast.
all his considerable resources. And the stakes couldn't be
The long legs that served him well as a member of
the Denver Nuggets in the old National Basketball League higher. Mo Udall is fighting for his life. Every moment,
are set on cruising speed. The shoes, size 13, pound like he battles with the unrelenting adversary of Parkinson's
disease. He battles with the memory of his late wife, Ella.
paddle wheels beneath the high-water pants. The ath
lete's discipline propels him forward. According to Udall's He battles with time itself.
The toll of Parkinson's, an ugly and chronic neuro
doctor, anybody else with Parkinson's disease of the same
logical disorder, has led some, publicly and privately, to
severity would be in a wheelchair or bedridden. Says an
aide, "If the team needs you, you play. That's how he suggest that Udall step down. No matter: Despite the
ceaseless aches and pains of osteoarthritis and despite the
thinks."
cconfounding of his muscles and sometimes his memory,
Udall is in a good humor this morning. It is primary c_.
day in Arizona and the "Mechamites" have just defeated Mo Udall is running again, and1 on Nov. 8 he will almost
the two most powerful Republican legislators in the state, certainly be returned to a 15th consecutive term in
throwing the party into further disarray. Beneath the Congress.
For most of his career, Udall has run virtually
furrowed brow and the gray hair, within the face that is
unopposed.
This time, he faces a Republican challenger
rendered implacable by his disease, Udall s gaze turns
in
Joseph
Sweeney,
a one-time Democrat and perpetual
mischievous. "Udall's first rule," he says. "Don't interfere
candidate who mounted his campaign with less than
while your enemies are self-destructing.'
Actually, Udall does not find the situation so funny. $5,000. Udall barely bothered to campaign back in his
The Republican turmoil may cost Arizona the $4.4 billion Southwest Arizona district, waiting until Congress adCl. j an appearance. In 1986, Udall was
superconducting supercollider. The Arizona leaders de- journed before___
making
by Luis Gonzales, who confeated in their primary races. House Speaker Joe Lane and challenged in
in the
t ~ primary
p
’i was preventing him from
Senate President Carl Kunasek, had planned to offer state tended that Udall's poor health
fulfilling
his
duties.
Gonzales,
who was defeated by Udall
funding for roads, sewers and other requirements. Now
and who just lost a primary bid for a seat on the Pima
those promises carry no weight.
County Board of Supervisors, today says, "He's slipped.
"I used to be asked how Arizona could produce so
The time is here for him to consider stepping aside and
many influential Americans," says Udall, stepping into the
letting other people have the opportunity to be elected."
members' elevator in the Capitol building, "including a
Udall's physical deterioration has not been lost on his
minority leader, a president of the Senate, two of nine
secretary
of
the
Interior,
Barry
congressional
colleagues. Observes a political reporter m
Supreme Court justices, a !
'
■
'
j
Washington,
"For
about three years, people have been
Goldwater and me. I said well, I thought the reason was
differences
referring
to
Udall
in
the past tense."
we had civilized politics. We could keep our cl.C-------Yet those who work closely with Udall insist that his
on the high road."
second floor and Udall steps work is still top-notch. Says Sen. Edward M. Kennedy of
The elevator stops on the second floor and Udall steps
out. "Maybe we've had our day
( , in the sun," he says, Massachusetts, "He's always led the way to a higher
heading for the floor of the House, "and now we're standard. My brothers recognized this. He's a very, very
important congressman, a very powerful and courageous
slipping back."
individual. He's better than 95% of his colleagues, and the
I
Il II o Udall has had a few of his own days in the sun,
IVI including a substantial run at the Democratic presiIVI dential nomination in 1976. In Congress, he led the
vanguard of reformers who opposed the ossified seniority
system in the House, reorganized the committee structure
and the civil service, and instituted campaign reform. He
has been Congress' most dedicated protector of wilder
ness areas, earning the moniker "Mr. Environmentalist."
And he has been a vigorous advocate for Arizona; he has
ensured, for instance, that funding for the Central Ari
zona Project Canal—a massive public works undertaking
38 • Arizona Trend • November 1988
only appropriate comparison of his abilities is against
himself."
Says Rep. Ben Nighthorse Campbell or Colorado,
who serves on Udall's Interior Committee, "When you
find somebody like Mo Udall, you hang onto him. Every
Democrat would rather have a chairman who wields the
power he does rather than have a rank beginner."
Udall himself is indignant about his capacity being
questioned. "The man who can replace me," he once told
Campbell,
Udall would prefer to ignore the disease. The man
he sees in the mirror is not the man in
i.. his
- mind's eye.
",
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4
Mo and Ella Udall at the Democratic National Convention
in New York City in 1976.
Ian -T
1 athletlc- healthy, a Westerner, an outdoors
man. I ve always pictured him as a masked man who rides
into town on a white horse," says a friend. "He shoots
tTem Wh
neVer kclinS °PPonents' °"ly wounding
them. When he leaves the townspeople ask, 'Who was
at masked man? And I tell them. That's the tall Udall.'"
Udall °U Carni, ta k a, great' optimistic game, like I do,"
Udall says of his condition, "or you can sit around and say
can t stand it. I'll hurt the rest of my life,' and you
now andTf
1 stretched this thing out 14 years
now, and I figure 1 can go on a few more." Udall is
determined to beat this beast. He has subjected himself
to experimental medications, and he adopted a new diet
th such ngor that he lost far too much weight
hk . JUth i tOld^hiS C1°sest friends and Stives believe
that his work in Congress is what keeps Udall fighting
tervf-b20^
4 " MuCCain' "M° is a man whose
heritaee
every fiber is devoted to public service. It's in his
’
s heritage,
in his blood, and it is his sustaining force "
Certainly, Udall's disease sometimes leaves him de
pressed. And since his wife's suicide in August, he has
been grim, even sullen, according to an aide. Udall is 66
years old. He once told Ella that he wouldn't live to 70
His family worries that the prediction will prove true "I
think Mo wants to go out in Congress," says the aide "It's
almost the only way for him to go/'
Courtesy Of M. K. Udall
fl couple from Arizona waits to pay a courtesy call
O on their congressman. The man is a mechanic who
5
tha* Udall flew around
his district. (Udall prides himself on having been an able
pilot for 20 years despite his visual impairment.)
Udall returns from a vote and enters his office suite,
ead raised, with a slightly quizzical expression on his face
He walks past his secretary and into his private office
He needs time these days to get organized, to take his
medicine. He takes five different medications and vitamins
six times a day m an experimental program for Parkin
son s run by the National Institutes of Health. Every three
hours, every day he takes his pills, which his staffers cut
and place m piles for him. Because his illness prevents him
rom setting an alarm on his wristwatch, an aide reminds
him to take his medicine—in much the same way that
and f
k,notte,d _ties for him at h°me, drive him to
and from work and fetch chocolate milkshakes in the
nope that he'll put on weight.
Ready at last Udall emerges to greet the couple. "So
you re the man who rendered those planes useless at any
pead- he teases- breaking the tension a bit. But Udall is
tired. His head is starting to roll, and he hasn't complete
control over his facial muscles. The couple enter his office
Mo reaches down to turn his swivel chair. He can't quite
get it to move. No one offers to help him; this is his
unresno6'dth‘S
knepS h‘m 8°m8' Pushin8 *at
unrespondmg muscle, willing that nerve to transmit its
i
T
■
•■
I
i.
I
I
I
To keep his joints from stiffening and his arthritic back
from aching, Udall tends to stay on his feet and in motion.
message. It is agonizing to watch. Finally, he positions the
chair, puts his hand down on the seat and lowers his body
onto it. His guests are outwardly calm, but their knuckles
are white from gripping the arms of their chairs.
Udall notices it all. He offers a few pleasantries and
a story. He tells the couple about the time he was flying
into Dulles Airport and ran out of fuel nine miles out.
"Congressman," his passenger suddenly asked, "are both
those dials supposed to be on zero?"
The guests laugh more heartily than is necessary.
Mo Udall will never fly an airplane again. After a few
more minutes of catching up on old times, Udall is ready
to conclude the meeting. The visitors don't pick up on his
cues. At last he says, "OK, gang. It's time. School's out."
40 • ARIZONA TREND • November 1988
■V II o Udall has distinguished himself as a man who can
l\fI change votes through the power of affection. He
111 is a master of the art of likability. Says Udall, "John
Dingell [a representative from Michigan] keeps black
books of people who don't vote with him. Others win
things because of love and respect. I chose to go that
way. I had to do it my way. I couldn't be mean. You can
be just as effective using persuasion and affection as the
more traditional games of hardball.
Young liberals regard Udall as a folk hero, and
"Western congressmen look up to Udall regardless of their
party," says Colorado's Campbell. "A suggestion from
Mo is like a mandate from anybody else. He never says,
'1 want you to do this/ He offers suggestions. He's
',
■S*
yAat«■> -illfc <r<,'i>,1»'':SinHiri ■'!
i
"I once tried to oppose the Udall machine," says
a California congressman. "And I stih have
the tire tracks on me to prove it."
Udall advises them to find a committee member who
suggested a few things that I've listened to very carefully."
will support their changes. He doesn't say outright that
Adds Terry Bracy, who ran Udall's presidential cam
he will not fight for them, but that becomes clear.
paign, "When was the last time Udall lost a vote?"
The delegation collects its maps and departs. Later,
"Udall is his best when weighing in on the most
the lobbyist says, "Mo asked one question. He asked about
difficult issues," says George Miller, a Democratic repre
the power output of the dam. If one thing will defeat this
sentative from California. "When an issue gets stuck, the
project, it's that low number. Goddamn, his mind is sharp.
Udall network in Congress is what moves things. He is a
man of principle. When Mo puts his name to the paper, He went right to the heart of the matter."
For bringing his clients to the powerful chairman of
it's on the right side of the issue. Congressmen view him
the Interior Committee, the lobbyist doubtless earned a
as a national figure."
Sen. Kennedy watched Udall chair an October meet handsome sum. Udall told an aide later, I did him a pretty
good favor. He probably earned $25,000 for that meeting.
ing of the Office of Technology Assessment, a bipartisan But this is the name of the game, access to power and
board of heavy hitters, and observed, "He knows when
to press, when not to press. He knows when to listen. influence. These are things Udall possesses.
And sympathy is not the source of his power, either.
He declared that the yeas had it in a vote that was very
"People are distressed to see Mo sick," says California s
close, and no one challenged him to a roll call. People have
Miller, who also sits on the Interior Committee, "but
a sense that if Mo wants it, it s probably right.
—-- --.1
Vnu don't 20 to
While Dingell kept enemy lists, Udall kept jokes. For sympathy won
the
won'*.t get him
....... down
—
—road. -You don t go t
Congress or
or Jesu.ts
Jesuits for
for mercy
mercy. You
30 vears Udall has collected gags and political humor in Congress
You don't
don t go
go to
to the
the well
wel
hf/own black notebooks. He is frequently asked to as
as many
many times
times as
as Mo
L.~ has
— and
---- winbecause people
- , , feel
nrovide a joke or story for his colleagues to use in a speech, badly for you. His illness means very little around here
>
L
i
But Udall is more substantial than a soapbox funnyman, to prove it.
He is an intellectual and a legal scholar. He wrote the
seminal lawyer's handbook, Arizona Law of Evidence, and two
n the paneled walls of the House Interior Committee
guides for lawmakers. The Job of the Congressman and Education
I I are paintings of Indian scenes. Ben Nighthorse
of a Congressman. In 1984, he was voted the most respected
U Campbell, the only Indian House member, requested
and most effective member of Congress by all his peers.
—'
— y-y
.7
which depicted
Even before the onset of disease 14 years ago, Udall that one of the paintings-DeafA Whoop whicU1 depicted
was prone to moods, somet.mes dark moods, but he's an Indian scalping a wh.te
’
never apologized for them. When an aide tells him he has arranged fonts removal <md ca led « ne« conference
been criticized in a newspaper story for brooding too "My esteemed colleague here, he told the press objects
much, Udall shoots back, "So was Abraham Lincoln."
to the surgical operat.on this ind.an'
1 p
forming on this white gentleman. And it he s ottenueu,
then I'm offended."
A
top Udall
aide, now
lobbyist, enters
"It used to be " says Udall's bro*^S‘ydart'„7hha°
M former
former top
Udall aide,
now aa lobbyist,
enters Udall's
Udall s
A
office
with
clients
from
a
small
Western
town.
They
secretary
the Interior under John Kennedy that you
f| office with
clientsanfrom
a small Western
They could readoftranscripts
Mwant
to block
environmental
bill town.
that would
of the meetings Mo chaired an
fl want to block an environmental bill that would
prevent them from building a hydroelectric plant. Udall they were as good as literature. They were humorous and
prevent them from building a hydroelectric plant. Udall
listens to them. He gets up from his chair, walks around
plain t0 see, is Jess
the room. After a few minutes in any stationary position,
sparkling as he chairs a full Interior Committee meeting;
Udall's joints stiffen and his arthritic back pains him.
much of his energy is consumed simply dealing with the
The presentation continues. Udall paces, shuttles
Across the room, over a fireplace, hangs a portrait
around his burrow. When the discussion is almost over, .pain.
------coat__sl’ ^^^
”
- one shoulder, a charis
the charts still held in mid-air, Udall asks, "How much of Udall,
matic
Western
congressman.
It
was painted only four
power will you get from the dam?" A man in cowboy
years ago, but today he looks 20 years older, thanks to
boots and a blazer with decorative stitching says, "200
megawatts." Udall nods. It is a low number. The group is Parkinson's disease.
Parkinson's is a degenerative disorder of the central
quiet.
A P17n\’ a TPPMO • NJovpmb^r lORR *41
jl-
I
I ’
Ella Udall's nickname was Tiger. She was
outspoken, irreverent, quick-witted—and, says
a friend, "terribly, terribly lonely."
I
door to the garage, stepped into her Cadillac and turned
on the engine.
.
Mo Udall, who rarely is able to sleep mornings, awoke
at 10 a.m. He smelled exhaust fumes and, fearing that
something was wrong, walked downstairs. He found Ella
dead in the car. He phoned the neighbors and asked their
sons to come over. They lifted Ella out of the car an
brought her into the house Udall called for an ambulance.
The death was ruled a suicide.
One recent morning, while walking to a vote, Mo
Udall is asked about the ebullient, contrary Woman whose
nickname was Tiger. After her death, he went into
seclusion with his children for two weeks, and the thought
still torments him. "I don't want to talk about it now," he
says softly. "Maybe in a few months.
Ella's many friends are not so reticent. Their reactions
to her life and death involve anger, compassion, but mostly
sorrow—for Ella and Mo.
"She was terribly, terribly lonely," says a friend ot
treltmeSs,
that Ella's. "She wanted him to resign
• i so they could have some
time
to
themselves.
It's
awfully
hard to watch someone
he followed, far too religiously, a special diet thought to
you
love
deteriorate.
help the absorption of dopamine in his brain.
"All the time she asked him to quit," continues the
One frustration of dealing with the disease is the
iixci.d, who as a former congressman's wife knows first
dependence on medication. Udall takes a variety of pills, friend, who
hand that politicians can't always make time for their
the most important ingredient of which is L-Dopa, which
f **
families. "They don't hear. Maybe to him it sounded like
is metabolized by the body into dopamine. Udall must
maintain the strict medication schedule, or the frightening a broken record and it would be better tomorrow.
"Ella was 59," she continues. "At that age, women
Parkinson's symptoms reappear. "It's like an old monkey
need more reassurance; you're getting older, you don t
on your back," he explains. "You never quite get away
from it. When the medication begins to wear off after look like you did at 25 or 35. You need more, attention
three or four hours, you're like an addict. You need your from your husband." However, she concludes, You can J
blame anybody for this. Many wives go through it and
next fix."
z .
Another typical result of severe Parkinson's is an most survive."
Two and a half years ago, Ella kicked her husband
increasing and burdensome dependence on family, for
out of the house; she said she wanted to establish a life
eVen the most menial things. For years, Ella Udall stoically,
of her own. They reconciled, but Ella found the burden
even courageously, dealt with Mo's disease. Because his
difficult, Udall of caring for her husband ever more difficult, and she
arthritic back makes sleeping prone so
Twould often doze off in his chair at home at 11 p.m. Ella blamed Udall's staff for encouraging him to push on. 1
would wake him at midnight for his medication. He'd think she was fearful about the future,' says Rosemary
Cribben, who worked for Udall and was a friend of the
struggle to fall asleep again, typically dropping off by 3
,
. .
. i
a.m., only to be awakened again at 6 by Ella to take more family.
Indeed, for some years Ella's relationship with her
pills. "He'd be groggy and yell at her," says an aide.
husband's staff had been strained. Says one of her friends,
Ella was also called upon to cook for him, lay out his
"She felt tolerated by the staff—just tolerated—and that's
clothes and, at times, help him dress. But increasingly,
friends say, she was resentful of the demands. They a terrible feeling. It's common that staffs look on wives
as meddling, interfering, bothersome objects."
became a wedge between them.
It's not that Ella didn't know how the Hill operated.
She had worked for several congressmen and had served
n the morning of August 13, Ella Udall entered her as staff assistant of the Postal Service Subcommittee of
i I husband's bedroom at 6 o'clock and gave him his the House Committee on Post Office and Civil Service.
chairman
of
V medication: one-half tablet of CR-IV, one-half tablet Udall was
ya. ------ that subcommittee. When they
of Sinemet, one Symmetrel, Vitamin E and Motrin. Then met, Udall was dlv0-----------^
,
Vincent' from
she went into the kitchen and put her dog's food on the whom he had six children. Ella had a son, Vincent,
stove to warm. At some point, she walked out the kitchen a previous marriage. Mo and Ella married in 1968.
nervous system. In its victims, neurons no longer produce
enough dopamine, a neurotransmitter that helps smooth
passage of nerve impulses. There is no known cure,
victims usually experience motor problems, slurring of
speech and, in some, a shuffling gait. The disease takes
different courses. In some patients, it gets very bad very
m inomeib, me
quickly, leaving them bedridden.
In others,
the degenera
ys Udall's
disease
developed
tion is slow. Dr. Targovnick say
’ ’’
'•
slowly and is in its final phase, meaning it probably won t
get worse. Parkinson's is not fatal. Though it can affect
the mental capacity of some sufferers, Targovnick says it
does not affect Udall's.
Mo Udall first noticed telltale signs of the disease
during his run for the presidency. He explained to his
doctor that it felt like his "motor was running too fast."
Within two years, the disease was diagnosed at Bethesda
Naval Hospital. Udall was so disturbed by the diagnosis
that for six months he told no one, not even Targovnick.
11CA J •
42 • Arizona Trend • November 1988
u-/ * i v
•*>•**<•*'•
--
,
I
J
Y
I
A
4
4
From the time he was a child,
Mo Udall has battled adversity and turned
misfortune to his advantage.
IL
1
Problems first surfaced after Udall's 1976 presidential
try. "Ella came back and thought she was going to run the
office," says a staffer. "Finally, Udall told her it was his
office, that he appreciated her input on certain matters.
On personnel matters, for example, he'd say Til ask Ella.'
She was very astute. But he made it clear that he had to
have the final word."
"Ella made the staff uneasy," says Erik Barnett, Udall's
press aide, "because it put them in the position of having
to please Mo and his wife. It almost seemed worse to
displease her." In the end, Ella stayed away from the office.
"She maintained a home, she got a poodle and she
shopped," says a staffer.
Ella Udall was outspoken, irreverent, quick-witted,
mercurial. "She was a very electric person, a spontaneous
t
person," says Cribben. "She loved to play
games." Ella
spoke her mind and eventually tired of social dinners, with
their demands of politesse and diplomacy.
"We thought she'd write the great American novel,"
says Udall's current secretary, Joan Shycoff. "She read
voraciously, she was eloquent, but not well-educated. The
skills she had she could never put in the right place."
"I think Ella was a woman of extremes," says Cribben.
"She had swing moods. Sometimes she liked to be out
socializing. Other times she stayed home for months.
"Nevertheless," Cribben continues, "she enjoyed the
role of Mo Udall's wife—having influential friends, enjoying the perks of power. It was a real coup for her. But it's
hard to accept the good and take the bad, too."
If Ella was the fire, than Mo was the ice. Says Stanley
Kurz, who has been Udall's friend since they served
together in World War II, "People find Mo cold. It's hard
to be intimate. He's kind and he's thoughtful and helpful,
but on a personal basis, you don't swap details of your
personal life. I think it's his strength."
Udall also maintains that distance from his staff. Says
pre^ss aide Barnett, who drives Udall to and from home
and has the most access to him, "I've always tried to
become a friend he could turn to, but he's never let me
be one. I realized it's probably for the best."
Still, by all accounts Mo and Ella were devoted to
each other. "He shared things with Ella that he never
shared with us," says Barnett. Watching her husband's
deterioration distressed her. "She felt that he was not
well enough to do some of the things he did," says a family
friend. Ella was particularly disturbed when Udall re
turned exhausted from the Democratic National Conven
tion in Atlanta.
In the end, says one of Ella's friends, "she didn't have
anything to look forward to." Says Cribben, "I think Ella's
expectations in life were never met. There was probably
not enough give-and-take from both parties. It might
have been that Ella was the least yielding."
In the days before she died, Ella called many of her
friends and relatives. In retrospect, some realized she was
bidding them farewell. But others can't believe she in
tended to die. "She was an inveterate note writer," says
Cribben. "She always wrote notes to Mo. She adored her
son Vince. She would have written him a note."
No note was found. Ella had left the dog's food
warming on the stove. "She loved that dog," says a friend.
"Had she intended to go, she would have fed it first." The
last thing she did remember to do was give Mo his
medicine.
■ n a way, struggling against Parkinson's every day,
I every moment—just to walk, speak, sit, think—and
I succeeding beyond reasonable expectations is pure
Udall. His life has been marked by setbacks that he battled,
and eventually turned to his advantage. He lost an eye as
a child, yet became a star athlete. He was kept out of the
Army because of the disability, yet eventually served and
was discharged with the rank of captain.
In 1954, he deferred to Stewart and decided not to
run for the House seat from the 2nd District; he ran for
a county judgeship instead and lost. But he replaced his
brother in 1961 when Stewart became secretary of the
Interior. Udall launched a symbolic challenge against
Speaker of the House John McCormack in 1969. He lost,
but became? an obvious candidiate for majority leader in
1971. He lost that, too, to the late Hale Boggs, but gained
enough prominence that he was pushed as a Democratic
presidential hopeful in 1976. This characteristic Udall
himself calls "succeeding by losing. Losing and bettering
your prospects."
Now it's Parkinson's to battle while trying to oversee
the final stages of the Central Arizona Project, to make
final determination of water rights along the upper
Colorado River, and to fight for the Arizona Wilderness
bill. "It's a losing fight and he knows it," says his brother
Stewart about the disease. "But he won't admit it. He
keeps on fighting."
And laughing even as he fights. One day recently,
Udall told the story of a hard-working, God-fearing man.
The man was blessed with a lovely wife and several
children. But: one day things began to go wrong. First, his
wife ran <off with his best friend. In his humility, he said
to God, "Thy will be done." Then his daughter took a
shiftless husband who ran the family business into the
ground. "Thy will be done," he repeated. By this time, he
was reduced to working a small plot of land. He suffered
through droughts and crop failures, yet he remained
faithful. "Thy will be done," he would tell God. Finally,
while out plowing under the stalks of his dead crops, he
slipped and fell into the dirt, and his mule kicked him in
the head. The man turned his gaze skyward and said,
"God, Thy will be done. But this shit's got to stop."
ARIZONA TREND • November 1988 • 43
/
i'
GOITRE CAN BE ffiEVENTED
Goitre prevalent all along the sub-Himalayan belt. It is
also seen in the Chhotanagpur plateau, Aravalli range
and the Eastern and Western Ghat ranges. About 3 90 million
people live in these areas and 25 million may be suffering
from goitre. Given below are a few tips on the causes
and prevention of goitre.
Enlargement of the thyroid gland, which is situated in
the neck of a person, is known as goitre.
Goitre is essentially a deficiency disease associated
with lack of iodine in soil or water.
Goitre is prevalent in the Himalayan belt, from
Jammu and Kashmir along the Southern slopes of the Himalayas
to Arunachal Pradesh, Nagaland and Manipur. It is also seen
in the Chhotanagpur plateau, Aravalli range and the Eastern and
Western Ghat ranges.
Nearly ninety million people are living in these areas
and about 25 million people may be suffering from the disease.
How do people develop goitre?
People develop the disease when sufficient amount
of iodine is not available for their thyroid gland to
maintain its normal function. Normally, the thyroid gland
draws iodine from the blood and converts it into the hormone
called thyroxin. This hormone is essential for the functioning
of all body tissues.
How is goitre identified?
Goitre produces enlargement of the thyroid glands
causing swelling in the neck, These may be large enough
to be seen or palpable or can be felt by the hand. The gland
may also not necessarily be large enough to be visible or palpable.
Who gets goitre?
Anybody can be afflicted by goitre, People of all
ages and both sexes can fall a victim. But goitre affects
children most. It is also more common in females than in males.
The size of the thyroid gland normally increases a
little as children grow up. But in goitre, this growth is
progressive and the gland keeps on increasing in size with
age.
... 2
2
Pregnant women are particularly at risk to get
afflicted with goitre, since the demand for iodine is greatly
increased during this period. In areas (villages and towns)
lacking iodine in water and soil, the iodine deficiency conti
nues to increase in the body of women with each pregnancy. This
results in further enlargement of the thyroid gland.
Effects of goitre
Goitre leads to physical deformity. A person with
large goitre presents an/ ugly appearance. In some cases,
the enlarged glands may be large enough to cause respiratory
difficulties, because of the pressure on the windpipe. In
such cases, surgery may be necessary,
z
Goitre may reduce the physical strength of an in
dividual. In pregnant women, insufficiency of iodine can
affect the foetus. Children born on women affected by
goitre are more prone to iodine deficiency than others.
Goitre may also lead to deaf mutism and varying
degrees of mental deficiency in the offspring.
Prevention is possible
Goitre can be prevented. Consumption of iodized salt
regularly is the best preventive measure against goitre, It
supplies the iodine necessary for the thyroid gland to do its
normal function.
Iodized salt is available in plenty from any local
shopkeeper, and it costs just just as much as ordinary salt.
Take iodized salt and prevent goitre.
Remember
* Iodine deficiency is the main cause of goitre.
** Goitre can appear in both males and females and at any age.
***
Regular use of iodized salt in iodine deficiency areas
arstas ensures prevention of the disease.
Source: Swasth hind - May 1980
'T’i'S' i -
JAPANESE ENCEPHALITIS
b'
JAPANESE encephalitis, which has been much in the news
till recently, is a disease of short duration. It is a disease of
the brain caused by a tiny germ called Japanese-B-encephalitis
virus. The virus affects the brain and its meninges (covering
of the brain) and spinal cord.
Signs and symptoms
How does one recognize a case of Japanese encephalitis?
There are some definite symptoms. The victim experiences
sudden rise of temperature. This is moderate to high. There
are also signs of headache, backache and neck rigidity. The
patient may also show symptoms like loss of consciousness of vari
ous grades, such as, confusion, convulsions, coma and paralysis.
How does it spread?
Japanese encephalitis, as has been stated earlier, is
caused by a tiny germ, This diseased germ is transmitted
to man by a particular type of mosquito, Usually, the
infection is confined to birds, pigs and cattle, Interestingly
enough, these birds and animals, when infected, do not show
the disease, Man normally does not harbour the
germ but can get
infected if a germ carrying mosquito bites him.
But it should be
remembered that not <every
--- person bitten by an intected mosquito will
suffer from the disease,
_
According to estimates, the disease
has been found to occur only in a
vety few infected persons.
It has been found that the disease has occurred in less than
one person in one lakh of people.
Another matter to be noted is that Japanese encephalitis
is not contagious, viz., it
coes not spread from man to man.
Or, in other wards, a diseased p*
persons is not of any risk to any
other person. Therefore, there is
no need to keep a patient
isolated.
The^isGaSe also is not spread by eating food, including
eat or drinking of water or milk i.e., food articles do not act
as ‘carrier’ of the disease.
Who gets the disease?
It should be remembered that Japanese encephalitis does
not have affinity to any
,— age
*- group of population, or to any sex.
It can attack people of all
age groups and both males and females a
are equally prone to it.
Preventive measures important
Although Japanese encephalitis is
a disease of short
duration and occurs in a very few infected
persons, it can often
prove fatal, if not managed properly in time,
Hence, preventive
easures are of extreme importance in keeping this disease
qway.
... .2
2
As the disease is caused only by the bite of the germ-carrying
mosquitoes, all possible measures should be taken to eliminate
chances of mosquito-breeding or getting bitten by mosquitoes.
These measures should be followed:
i) Prevent breeding of mosquitoes by taking care to see
that there is no stagnant water in and around houses.
ii) If mosquitoes are seen to be breeding in large pools
of water like ponds, etc., the anti-malaria workers
should be contacted and asked to take remedial
measures.
iii) Get rooms and verandah, where mosquitoes rest,
sprayed by the malaria workers.
iv) Use mosquito nets while sleeping.
v) If the residence is near the places, where cattle
and pigs are kept, ensure that these places are
thoroughly sprayed by anti-malaria team.
It should be- remembered that Japanese-B-encephalitis
often resembles malaria, meningitis, and other diseases with
fever. It is, therefore, essential to make a proper diagnosis.
Hence call for a doctor or health worker whenever there is a
case of high fever, alongwith unconsciousness, or headache
or neck rigidity. Early diagnosis and treatment can save a life.
Source: Swasth Hind - July 1979.
I
I
Message from Dr Hiroshi Nakajima
DIRECTOR-GENERAL OF WHO
WORLD HEALTH DAY 1997
T TNTIL quite recendy there was a widespread feeling that the struggle against infecdous diseases was
J almost won. The means of controlling most of them seemed either available or discoverable without
undue difficulty. Spectacular progress has indeed been made: smallpox has been eradicated and six
other diseases will be eradicated or eliminated soon. But tragically, with optimism came a false sense of
security, which has helped many diseases to spread with alarming rapidity.
Major diseases such as malaria and tuberculosis are making a deadly comeback in many parts of the
world. At the same time, diseases such as plague, diphtheria, dengue, meningococcal meningitis, yellow
fever, and cholera have reappeared as public health threats in many countries, after many years of decline.
In addition, previously unknown infectious diseases are emerging at an unprecedented rate. In the last
20 years, more than 30 new and highly infectious diseases have been identified. They include the virulent
Ebola-type haemorrhagic fever, HIV/AEDS and hepatitis C. For many of these diseases there is no
treatment, cure or vaccine.
Antibiotic resistance is another important threat to human health which has emerged during the last
20 years. Drugs which once could be counted on for protection against many infectious diseases are
becoming less and less useful as resistance to them spreads. In addition, fewer new antibiotics are being
produced, owing partly to the high costs of development and licensing. As the treatment of communicable
diseases becomes less effective, more people need hospitalization, illnesses last longer, treatment costs more
and absenteeism from school and work increases.
There are many reasons for the appearance of new diseases and the resurgence of communicable diseases
once thought to be well under control. These include the rapid increase in international air travel and the
growth of mega-cities with high population densities and inadequate safe water and sanitation. The risk
of foodborne diseases has been heightened by the globalization of trade and changes in the production,
handling and processing of food. Environmental factors can lead to the exposure of humans to previously
unknown diseases. For example, man is destroying forests and moving into previously remote animal and
insect habitats which carry high risks of exposure to disease.
Meanwhile, in rich and poor countries alike, resources for public health are being reduced as limited
funds are spent on other priorities. As a result, the appearance of new diseases, the re-emergence of known
diseases, or the development of antibiotic resistance, may go unnoticed until it is too late. A recent striking
example is the human immunodeficiency virus (FHV) which was recognized only after it had already
infected large numbers of people in many countries. If diseases of epidemic potential are detected early
enough, epidemics and pandemics can be prevented in some cases, in others minimized.
For these very pressing reasons, the theme «Emerging Infectious Diseases - Global alert, Global response*
has been chosen for World Health Day 1997. It is my hope that, by using World Health Day as a catalyst,
countries will be able to take a realistic look at these problems and concentrate on rebuilding the foundations
of disease surveillance and disease control. Both the public and the private sectors must be encouraged
to research and develop better techniques for surveillance and control, and new antibiotics to replace those
which are no longer effective.
We have to face the fact that infectious diseases are a common threat which demands urgent attention,
especially at a time when people all over the world are being brought closer together by international travel
and trade. Communicable diseases respect no frontiers. We must work together globally to control them.
it
fI
S'
Bossssss
WHD 97.1
•A WORLD HEALTH DAY
••
7 April
B
<
:
EMERGING INFECTIOUS DISEASES
What are emerging and re-emerging infectious diseases?
Emerging infectious diseases are those due to newly identified and previously unknown infections which
cause public health problems either locally or internationally.
Recent emerging diseases include a highly fatal respiratory disease caused by a virus called sin nombre; a
variant of Creutzfeldt-Jakob disease, a disease of the central nervous system which is suspected, though not
proven, to be associated with a similar disease in cattle called bovine spongiform encephalopathy; HIV infection
which causes AIDS, with its sequelae of human suffering and economic burden; and diseases such as Ebola
haemorrhagic fever with a potential for international spread. Other examples of new or newly detected infectious
diseases of global concern include a new form of cholera , a haemolytic uraemic syndrome , hepatitis C and
hepatitis E, Legionnaires’ disease, and Lyme disease. Although it is not always possible to know if these
diseases are new in humans, or whether they have been present but unrecognized throughout the years, many
emerging diseases are thought to be due to a closer contact of man with their reservoirs in nature, witli a
successful «jump» of the infectious agent from animal to man across the species barrier.
Re-emerging infectious diseases are those due to the reappearance and increase of infections which
are known, but had formerly fallen to levels so low that they were no longer considered a public health
problem.
I
<■
1
Re-emerging infectious diseases often reappear in epidemic proportions. Tuberculosis is increasing
worldwide due in part to its close association with HIV infection; cholera has been re-introduced into
countries and continents where it had previously disappeared, and where it can spread because water and
sanitation systems have deteriorated; dengue or «breakbone» fever has started to occur in urban areas where
mosquito control has broken down.
Microorganisms resistant to antibiotic drugs emerged and spread soon after the introduction of
these drugs and in parallel with their use. Many well-known antibiotics are no longer effective to treat
common infections such as otitis, pneumonia, gonorrhoea and tuberculosis. At the same time, fewer
new antibiotics are released on the market, partly because of the high cost of developing and licensing
them and because the development of resistance reduces the «useful lifc» of antibiotics. If the arsenal
of drugs against infectious diseases loses its power, the future for patients with even a banal car infection
will become bleak.
J
I
Th'5
information material
produced
by
the Division of Emerging
and
Other Communicable Diseases Surveillance and
Control,
WHO 1
Headquarters, Geneva, is intended for modia/public use and does not constitute an official document Additional copies mav be obtained from
JbV/
Public Information Unit, World Health Organization, Regional Office for South Fast Asia. Indraprastha Estate
New Delhi 110 002, India
^3
Emerging Infectious
Diseases
1
WORLD HEALTH DAY
WHD 97.10
7 April
WWW.WHO.CH ■ the home of WHO on the Internet
How to navigate your way around the WHO home pages
Using the WHO site
Once you have contacted the WHO via the Internet (www.who.ch) the main menu page should appear
quite quickly. The layout of the WHO Web pages will be familiar to anyone who has used the net because
they follow a pattern used by many other users and institutions.
You will see the WHO logo and a
picture of WHO HQ in Geneva but few other graphics as the site has been designed to allow the fastest
possible downloading of information*.
The main menu is linked to other pages in the site by key words or phrases highlighted in blue and
underlined. By clicking on the highlighted section, the desired pages are called up. For example, if you
click on the light blue WHO, you access the page which gives you background information on WHO
and a list of addresses, phone and fax numbers, and e-mail addresses regarding WHO HQ and the six
Regional Offices. It might help to think of our web site as a book. The main menu page is the cover
with the contents listed on it. By clicking on a particular subject on the cover (highlighted and underlined
in blue ), you will go to the chapter on that subject. Then by clicking on a highlighted topic in die
chapter menu, you will see the individual pages of information, and so on.
So, if you want more detailed information on the topic of this year’s World Health Day, Emerging
and Communicable Diseases, click on WHO Headquarters’ Major Programmes (light blue underlined)
in the main menu. This will take you to another menu listing the major programmes including the
Division of Emerging and other Communicable Diseases Surveillance and Control (EMC). By
clicking on this you will see another menu listing various aspects of the work of EMC such as News
of diseases reported to EMC, Cholera and Epidemic Dysentery or Haemorrhagic Fevers (including
Ebola, dengue.tt) If you click on any of the highlighted areas, you will find the latest information
on that subject.
If you have a special interest in a topic and know you will visit the page frequendy, you may like to
bookmark that particular page to save time. How you bookmark a page will vary depending on which
Internet browser you are using. For example, if you are using Netscape and want to bookmark a page
simply click on Bookmarks and then on Add Bookmarks in the box which appears. The page will
automatically be called up every time you select the page from your list of bookmarks.
j
'nformahon
ma ton al jirodacod
by
fho Division
of Emerging and
Other Communicable Diseases
Surveillance
and
Control,
WHO
Headquarters. Geneva, is intended lor modia/public use and docs not constitute an crhcial document Additional copies may lx» obtained from
l\t|>ll< inftMmatuMi Unit 'A.xld llrxilth O(|cini/atKXs Rcaional
o fix '.MitlilaU Amo Indraprastoa f slate
t
(\-llu IIU
((!Ui
As well as information about WHO programmes, the site also gives you access to all of the Organization’s
Public Information materials in most cases both in French and English. These include Press Releases
and Fact Sheets. To reach this information click on Public-Information-Publique on the WHO main
page, there under Headquarters choose the language in which you want to view the information: either
English or Francais. Then choose Press releases or Factsheets or Backgrounders or Notes to the
Press and so on.
From the main page you may also view electronic versions of 10 WHO Newsletters on topics
ranging from chemical safety and noncommunicable disease to changes in medical education and
practice.
The WHO web site is big and getting bigger all die time, but don’t be put off! There is a search
engine installed at the top of the main menu page and on many of the inside pages, such as Public
Information, which will help you find what you are looking for either by key word or concept. This is
particularly useful in the WHO Statistical Information System (WHOSIS) page where there is a great
deal of health and health-related data and information. Also, WHOSIS and some other Programmes
have hypertext links to other non-WHO sources of information such as the Centers for Disease Control
and Prevention (CPC) in the USA and the Global Health Network which also has versions in Japanese,
Portuguese and Spanish.
In addition to the web site at WHO HQ there are links to web sites or e-mail addresses in the six
WHO Regional Offices. These sites will contain information specific to the region. You can link to these
sites or find the e-mail address by cEcking on Regional and other offices.
WHD97.10
Page 2
What causes emergence or re-emergence of infectious diseases?
Several factors contribute to the emergence and re-emergence of infectious diseases, but most can be
linked with the increasing number of people living and moving on earth: rapid and intense international
travel; overcrowding in cities with poor sanitation; changes in handling and processing of large quantities
of food; and increased exposure of humans to disease vectors and reservoirs in nature. Other factors
include a deteriorating public health infrastructure which is unable to cope with population demands, and
the emergence of resistance to antibiotics linked to their increased misuse.
Travel has always been a vehicle to spread disease across the world, and die central protective legislation
edicted in the 14th century by the City-state of Venice has evolved, over the centuries, into the current
International Health Regulations. The volume of travel has dramatically increased in recent years: presendy
well over 50 million people use international air transport each year. The speed of travel ;has;similarly
increased: whereas cases of cholera, plague and smallpox were slowly , transported from one'’continent to
anodier by ship and could be recognized-during the voyage, it is now possible and. quite ,likely , that an
infected traveller will only develop signs of the disease several days after arrival.
- .• ' ->
V.j.
Emerging and re-emerging infections reflect the constant struggle of microorganisms to survive. One
of the ways microorganisms have found of surviving is to overcome the barriers which norrhally protect
humans from infections. This may follow deforestation, which forces forest animals closer"toririafjjri^earch
closer'to man in'search
of food, or failure to control mosquitoes and other carriers of disease’to humans,/dr a breakdd^?iiiwater
and sanitation systems, or failure to detect diseases early, or ffailure
’’-^S of
-r immunization
’■ '
prdgramm^'^r high!
risk human behaviour.
• '
• "■v
All of these have been observed within the past decades, together with a waning concern - arid decreasing
resources - for infectious disease control. During the first half of the 20th century deaths from infectious
diseases declined steadily because of improved hygiene and ^nutrition. This trend was strengthened with
the advent of vaccines and antibiotics during the 1940s and culminated in the late 1970s in the eradication
of one infectious disease, smallpox. Because at that time infectious diseases appeared to be a decreasing
threat, funds for their control were channelled to other problems, experts on infectious disease retired or
left the field and students turned to more rewarding subjects than viruses and bacteria - the infrastructure
for communicable disease control began to crumble.
The global response
Since 1992 alarm over emerging and re-emerging diseases has resulted in a number of national and
international initiatives to restore and improve surveillance and control of communicable diseases. The
Member States of WHO expressed their concern in a resolution of the World Health Assembly in 1995,
urging all Member States to strengthen surveillance for infectious diseases in order to promptly detect
re-emerging diseases and identify new infectious diseases. The World Health Assembly recognized tliat the
success of this resolution depends on the ability to obtain information on infectious diseases and the
willingness to communicate this information nationally and internationally. This resolution has been
translated by WHO into the establishment of the Division of Emerging and other Communicable Diseases
Surveillance and Control (EMC), whose mission is to strengthen national and international capacity in the
surveillance and control of communicable diseases, including those that represent new, emerging and
re-emerging public health problems, for which it ensures a
WHD97.1
Page 2
9
BSE
Bovine Spongiform Encephalopathy (BSE) was first described in the United Kingdom in November 1986 and up to
mid-1996, approximately 160 000 cases had been confirmed.
By mid-1996, BSE had been reported from 10 other
countries and areas; in one group of countries the disease occurred in native cattle, while in another group cases were
only identified in cattle imported from the United Kingdom.
This fatal neurological disease of cattle is associated with a transmissible agent, the nature of which is not yet fully
understood.
It was known that similar transmissible agents caused brain disease in humans, including kuru, and the various forms
of Creutzfeldt-Jakob Disease (CJD). The latter can be sporadic, familial, or occur accidentally as the result of a medical
procedure (injection or graft of infected human material).
On 20 March 1996, the United Kingdom announced the existence of a cluster of 10 persons identified with what
appeared to be a variant of CJD. Full investigation of these cases led to the conclusion that exposure to BSE was the
most likely hypothesis. By late 1996, a total of 14 cases of the variant form of CJD have been reported in the United
Kingdom and one confirmed in France.
The suspicion of a link between BSE, and the new variant form of CJD through the satisfaction of an essential need
such as nutrition, has had important implications for public health and a devastating impact on consumer’s confidence in
beef safety and thereby the cattle industry. It has forced us to think through the links between public health, industrial
development, technology, economic constraints, market and trade practices, public information and consumer safety.
In the case of BSE and the. new variant form of CJD, advancement of our scientific knowledge should permit
policy-makers to ensure both the continuation of economic activities dependent on the cattle industry and the safeguard
of public health.
Hepatitis C
Viral hepatitis is a major global public health problem. The discovery of the hepatitis C virus (HCV) in 1989 ended
a period of intensive international research efforts aimed at the elusive «Non-A, Non-B» virus, which was well known as
a cause of post-transfusion hepatitis. Although HCV is not as infectious as hepatitis B or HIV, as many as 80% of infected
people can become chronically infected and risk serious long term effects such as liver cancer which places HCV among
pathogens of primary concern to humanity.
As with all recently discovered diseases, there is considerable controversy within the scientific community regarding
prevalence, incidence, natural course, patho-biological implications, socio-economic burden and management of acute and
chronic hepatitis C. However, the route of transmission through transfusion with unscreened blood, through the use of
inadequately sterilized equipment or through needle-sharing among drug-users is well documented. Sexual and perinatal
transmission have been reported but are uncommon. Additional studies are needed on possible alternative transmission
modes.
Based on prevalence rates ranging from 0.1% to 33% in different countries, WHO estimates today that as many as
3% of the world’s population could be infected with HCV and that there may be some 200 million chronic carriers who
are at risk of developing liver cirrhosis and/or liver cancer.
Although the socio-economic impact of chronic hepatitis C has only been partly studied, the costs are likely to be
high, as was found in studies dealing with chronic hepatitis B. Treatment with interferon is effective in about 20% of
patients. For the remaining 80%, international research efforts should focus on combined antiviral therapy. It is clear
that 90% of patients who are in need of treatment today cannot afford it.
No vaccine is available, but most HCV infections can be prevented by:
■ Screening of blood and blood products worldwide.
S Destruction of disposable medical material and adequate sterilization of reusable medical material.
■ Promotion of public education about the risks of using inadequately sterilized material.
■ At a time when traditional public health activities are weakened and when conditions in public health laboratories
are deteriorating, the challenge of a new disease places extensive pressure on the medical community and additional
financial burdens upon society.
WHD97.1
Page 3
TUBERCULOSIS-a global emergency
Alarming outbreaks of tuberculosis caused by multidrug-resistant strains in the United States have lately stirred public
interest. In Minneapolis, a person with tuberculosis infected 41 people in a neighbourhood bar. In Western Canada, a
health care worker infected 100 other people. In recent years, outbreaks of tuberculosis in wealthy countries have been
investigated in discotheques, churches, subways, schools, airplanes, court rooms, and even on a riverboat casino.
Tuberculosis is easily transmitted from person to person. One-third of the world's population - nearly two thousand
million people, from New York City to New Delhi - has already become infected. The infection with the tuberculosis bacillus
may lie dormant for many years; some people may not even progress to the disease at all. Active tuberculosis has a
better chance of developing when the person's immune resistance is weakened, as is the case for women suffering from
hormonal and nutritional stresses of pregnancy or for people living with HIV/AIDS. People dually infected with the tuberculosis
bacillus and with HIV are 30 times more likely than HIV-negative individuals to become seriously ill with tuberculosis.
i
In 1993, the World Health Organization declared tuberculosis a global emergency. Tuberculosis is now the leading
infectious killer of adults, and will have killed at least 30 million people within the next ten years if current trends continue.
It is likely that no other infectious disease is creating as many orphans and devastating as many families as TB. This
huge toll is the price the world is paying for complacency.
A cost-effective and proven drug treatment exists, but careless tuberculosis treatment practices are triggering bacilli
that are resistant to once-effective drugs. Multidrug-resistant tuberculosis develops when doctors or other health workers
prescribe the wrong drugs or the wrong combination of drugs. It also occurs if the right anti-tuberculosis drugs are not
taken on a consistent basis, or are not taken for the entire six months of treatment. Powerful tuberculosis drugs should
not be prescribed without ensuring that they are taken correctly.
That is why the Global Tuberculosis Programme of WHO is urging all countries to adopt the DOTS (directly observed
treatment, short-course) strategy, in which health workers or volunteers watch tuberculosis patients under their care swallow
each dose of the medicine for at least the first two months of treatment and monitor their progress toward cure. The
strategy is already showing remarkable success in many countries.
WHO is vigorously promoting DOTS: it trains key health workers, assists governments and health ministries worldwide,
promotes research into effective ways to cure tuberculosis, contributes to the cure of tuberculosis patients, and mobilizes
funds and political commitment to address the pandemic adequately.
The existing BCG vaccine prevents severe tuberculosis in children, but it does not have much impact on the disease
in adolescents and adults. Research to develop a new and more efficient tuberculosis vaccine is under way. A range of
candidate vaccines is now available, for clinical evaluation studies.
WHD97.1
Page 4
I
Io
Emerging Infections
diseases
\ WORLD HEALTH DAY
WHD 97.2
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w
7 April
I
EMERGING AND OTHER INFECTIOUS DISEASES:
PARTNERSHIPS TO MEET A CHALLENGE
THE LOGO
t
A worldwide partnership of countries, non-■governmental organizations, international organizations, and
/Aindividuals is required to respond to the threat of emerging and re-emerging diseases by ensuring
rapid detection and effective containment. The logo selected for the
Division of Emerging and other Communicable Diseases - Surveillance and
Control illustrates this partnership. The arrow on the logo begins with a
point or points on earth which signal a global alert - the re-appearance of
a known disease such as yellow fever, cholera, meningitis or plague, or the
appearance of a newly identified disease such as hepatitis C, AIDS or Ebola,
or a disease resistant to usual antibiotic treatment. The arrow then increases
in width and extends to encircle the earth, as do the increasing number of
parmers required to ensure a global response of maximal containment for
communicable diseases, with minimal disruption.
The World Health Organization, as one of the parmers in this global
effort, is strengthening global monitoring systems to serve as part of the overall detection system. Three
independent systems cover the globe, bringing together specialized laboratories and disease surveillance
systems from all countries, and feed information electronically to die World Wide Web and other international
electronic and printed media.
WHO COLLABORATING CENTRES
The first global monitoring system is that of the WHO Collaborating Centres, specialized laboratories
and institutions with expertise in infectious disease diagnosis and epidemiology. During recent epidemics
it has become clear that the WHO system of Collaborating Centres could no longer fully respond to
global needs. Some centres, for example, had failed to keep up with changes in technology and were unable
to provide the diagnostic support necessary to confirm the etiology of disease outbreaks. Some of the
centres specializing in infectious disease epidemiology had failed to develop expertise in some of the newer
infectious disease challenges. There are not enough Collaborating Centres in developing countries to ensure
regional self-sufficiency. WHO is asking governments to provide the resources necessary to bring the WHO
Collaborating Centres up-to-date. WHO is also facilitating exchange of information and reagents among
Centres, increasing die number of Centres in developing countries, and ensuring that all centres are linked
electronically and regularly exchange information.
This
vl&SjjW
information
material
produced
by
the Division
of Emerging
and Other Communicable Diseases Surveillance
and Control.
WHO
Headquarters, Geneva, is intended for media/public use and does not constitute an official document. Additional copies may be obtained from
Public Information Unit, Wodd Health Orqanuahon Req.onai Olko fix South fast Asia. Indranrastha Estate. Naw Dolb 110 002 'ndm
7
ANTIMICROBIAL RESISTANCE MONITORING
The second global monitoring system includes the WHO networks for monitoring and containing
antimicrobial resistance; WHONET for die monitoring of antimicrobial resistance in general, and the
programme for monitoring gonococcal antibiotic susceptibility (GASP). Antimicrobial resistance is rapidly
increasing worldwide, facilitated by inappropriate prescribing by health workers, poor compliance by patients
to prescribed dosage, and failure to control the availability of antibiotics by limiting them to pharmacies
and health facilities. Antimicrobial resistance results in higher costs due to the use of more expensive
combinations of aptibiatics,/ to increased rates of hospitalization for infections- once easily treated on an
outpatient basis, and to time lost from work or school until cure. At the same time pharmaceutical companies
are less willing to take the risk of developing new antibiotics, because the high cost of research and
development and the potential of rapidly developing resistance jeopardize the recovery of investments made
in research and development. Through WHONET and GASP, WHO regularly obtains standardized
information of known quality on the current state of. antimicrobial resistance, helps countries^ use this
information nationally for sound drug policies, and internationally uses the information to identify problems
and advocate research and development on antibiotics.
?
INTERNATIONAL HEALTH REGULATIONS
The third system is represented by the International Health Regulations (IHR), currently the only
international public health legislation which requires mandatory reporting of infectious diseases. Three
diseases are covered by the IHR - cholera, plague and yellow fever. Reporting these diseases, however, is
often associated with negative repercussions such as restrictions to trade and travel. Some countries therefore
do not report and WHO has no legal mandate to force reporting. In addition diseases such as haemorrhagic
fevers and pulmonary disease are not included in the IHR. To turn the IHR into a working global alert
system, where reporting will be encouraged and all globally important diseases will be reported, WHO is
rewriting the IHR. This will eventually require an initial reporting of clinical syndromes of potential
worldwide importance to ensure an immediate and appropriate international response, followed by causal
reporting once the diagnosis is known, when modifications in the response may be made as necessary.
Clear and concise guidelines for countries are also being developed, describing both appropriate and
inappropriate responses once a syndrome is reported.
In addition to partnership in global monitoring, WHO is working in countries to strengthen national
disease detection and response through improved surveillance systems and specialized training in epidemic
preparedness and response. In this parmership WHO provides overall technical guidance through its
international consensus policies on surveillance and control strategies; it facilitates bilateral or multilateral
activities of governments and non-governmental organizations in enlarging the critical mass of epidemiologists
and public health laboratory specialists, and its advocates for government commitment to provide the
resources necessary.
A final role of WHO in this partnership is to help ensure a coordinated global response to infectious
diseases of international importance, often with the technical expertise of the WHO Collaborating Centres
or other centres of excellence. At other times the WHO response requires involvement of WHO staff at
the field site to begin surveillance and containment activities while facilitating the arrival of technical
expertise from other international partners, and to remain after containment to plan and implement activities
for the prevention of future outbreaks.
To enter the 21st century and meet tomorrow’s challenges of new, emerging, re-emerging infectious
diseases, or even to meet the challenge of well-known diseases, WHO will continue to participate in and
syncrgisc global partnerships by ensuring strong national disease surveillance and control programmes,
global networks to monitor and alert the world to infectious disease and related public health problems,
rapid information exchange through electronic links, and rapid response to contain epidemics of international
importance.
WHD97.2
Pago 2
v Oiseases
A WORLD HEALTH DAY
WHD 97.3
fl 7 Aprilr r®T@^b.Id
^88
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.
_______
PROTECTION WE TAKE FOR GRANTED
j lie routine immunization activities of WHO prevent an estimated 3 million deaths per year. In addition,
| at least 750,000 children are protected from blindness, mental retardation, or other disabilities. In
1995, almost 80% of children throughout the world were immunized against six vaccine-preventable
diseases - diphtheria, tetanus, whooping cough, measles, polio, and tuberculosis. This achievement involves
over 500 million immunization contacts throughout the year; at the same time, immunization activities
provided opportunities for other primary7 health care interventions, such as health education for mothers,
growth monitoring, administration of vitamin and mineral supplements to children in need/deficiency, child
spacing and routine health checks. This again helps prevent diseases, disability, suffering and deaths.
An important key to the success of this ongoing preventive activity is the promotion of good disease
surveillance and monitoring. As high immunization coverage is attained and the number of cases declines,
disease surveillance becomes critical to monitor the changing patterns of vaccine-preventable diseases and
to guide changes in immunization strategies. Disease surveillance is also critical to pinpoint pockets of
poor performances and high risk so that public health action can be enhanced in these areas. For instance,
incidence and immunization c overage data can help identify7 areas at high risk for neonatal tetanus and
ensure that resources are channelled to these areas. Sur\7eillance data can also be used as an early warning
svstem to monitor trends in the number of new cases of a disease arid predict where and when epidemics
may7 occur. Specific action can thus be taken in time to prevent an epidemic. Surveillance systems also help
detect and prevent die re-emergence of vaccine-preventable diseases such as yellow fever and diphtheria bv
identifying sub-populations and certain age groups at high risk.
Monitoring systems determine ways to boost immunization coverage rates and improve service delivery7
and related costs. For example, for vaccines to be effective, it is crucial that they7 be kept cool at all times
of die supply chain (cold chain). By7 improving and developing good surveillance and monitoring systems,
poor programme performance can be detected and corrected before public confidence in immunizadon is
undermined.
information
material
produced
by
tbo Division
of Emerging
and Other Communicable Diseases Surveillance
and Control,
WHO I
Geneva, is intended for media/public use and does not constitute an official document. Additional copies may be obtained from:
Public Information Unit, World Health Organization, Regional Office for South East Asia, Indraprastha Estate. Now Delhi 110 002, India
Control of influenza
Unlike other acute respiratory diseases, influenza can cause severe illness complicated by pneumonia. Elderly persons
or persons with underlying health problems are at increased risk for these complications. The severity of influenza is
reflected during major epidemics by large increases in the number of cases admitted to hospital and in the number of
deaths from influenza; the increase in deaths during influenza seasons is in some countries used as a measure of the
impact of influenza epidemics.
Influenza occurs globally and epidemics are registered in regions of temperate climates every year. Three to four
times per century a new influenza virus appears which causes worldwide epidemics (pandemics) and some of them have
been associated with extremely high mortality rates. The most severe pandemic this century occurred in 1918-1919 and
killed at least 20 million. The last influenza pandemic started in 1968 with the appeareance of the A/Hong Kong influenza
strain. It is clear that new pandemics will occur and it is equally evident that the preparation for this global threat has
been insufficient.
Two measures can reduce the impact of influenza: vaccination and treatment with anti-viral drugs. Because of the
cost, side effects and limited availability, drug treatment is not applicable on a global scale. Vaccination of persons at
high risk therefore remains the most effective measure to reduce the impact of influenza. As the virus mutates continuously,
vaccination must be repeated annually before each influenza season with an updated vaccine to assure a good match
with the circulating influenza strains. Influenza vaccine can prevent severe influenza and deaths and it is therefore strongly
recommended for persons aged more than 65 and those at risk to develop severe complications - especially those over
6 months of age with underlying conditions such as chronic heart or lung disease, renal or metabolic disorders.
WHO coordinates the global influenza surveillance which is built on a network of 110 national influenza centres in 80
countries and four WHO Collaborating Centres for Reference and Research on Influenza in Atlanta. London, Melbourne
and Tokyo. The surveillance ensures the collection of epidemiological data and of viral isolates for rapid characterization
and international comparisons. The annual recommendations for the influenza vaccine are based on the information
obtained through this surveillance system. This regular and continuing influenza surveillance programme will also most
likely detect a pandemic threat.
To prepare for the forthcoming pandemic, national and regional plans should be developed now. These plans should
take into account that in case of a pandemic a vaccine might not be available or available only in insufficient quantities.
The plans should set priorities and objectives to guide control strategies, operative decisions and allocation of resources
at the national, regional and district levels
Jj jh:GLj01J-3
WHD 97.4
WORLD HEALTH DAY
7 April
EXAMPLES OF SUCCESSFUL PREVENTION AMD OUTBREAK CONTROL
THE PAST
Smallpox
One of mankind’s greatest triumphs is the eradication of smallpox. Under the leadership of WHO, all
the countries of the world united to destroy the killer virus.
Although a vaccine to fight smallpox had already been discovered 200 years ago, the disease was still
endemic in the 1960s. In 1967, WHO launched a global smallpox eradication campaign, systematically
vaccinating entire populations in endemic countries - an enormous and complex exercise. The strategy'
soon became «surveillance and containment: every time a new case was discovered, it was isolated and
contacts of die patient traced and vaccinated. Where cases were detected, local immunization was intensified.
The last case of naturally acquired smallpox was reported from Somalia in 1977, and in 1980, WHO
declared die world free from die scourge. In its 1996 session, die World Health Assembly recommended
that die last smallpox stocks would be destroyed in 1999.
THE FUTURE
lust as die\' eradicated smallpox, WHO and its partners are optimistic that diey are on the right track
to eradicate or eliminate odic infect ous diseases bv the year 2000, in particular poliomyelitis, leprosy and
guinea-worm disease (dracunculiasis).
Poliomyelitis
Poliomvelitis is an infectious viral disease that attacks rhe central nervous system, causing permanent
paralvsis of the muscles and frequently death. It mainiv arfects voting children. In 1988, WHO established
a target to eradicate polio by the vear 2000. The strategy; used rests on two basic activities: surveillance
and immunization. Surveillance data are used to gear immunization activities towards populations at higher
risk for polio. Worldwide, almost half of the children under 5 were immunized against the polio virus in
1995 in the course of National Immunization Davs.
An estimated USS700 million are needed to reach the target of eradicating polio by the year 2000, to
save manv lives and avoid much human suffering. The projected savings of more than USS1 500 million
a year thereafter far outweigh this expenditure. WHO is confident that the drive for the eradication of
poliomyelitis is on target.
Tins
information
material
produced by the Division
of t merainq and Other Communicable
Diseases
Surveillance and
WHO
Control
Headquarters. Geneva, is intended for media/puNic usa and does not «onshtufo an official document Additional copies may lx? obtainoa ’tom
' •hlic Information I’ml Wi»dd H^iilh < iqanica'ion
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Leprosy
Leprosy is a disfiguring but curable disease. It is caused by an organism which mainly affects nerves
and skin and is spread from person to person by droplets from the nose of an infected individual.
In 1996, the number of registered cases of leprosy in die world has fallen below one million. This
offers striking evidence that WHO’s strategy for eliminating leprosy as a public health problem is on course
for success. There were an estimated 1.8 million people with leprosy compared with 5.5 million in 1991
and 12 million in 1985.
WHO pursues a two-fold strategy against leprosy: treating patients with a combination of three drugs
(multidrug therapy - MDT) combined with case-finding. There is evidence that the elimination strategy
has already had a significant impact in terms of a dramatic and constant reduction in morbidity. This
approach has also increased the priority accorded to leprosy control activities in highly endemic countries;
it has also improved case detection through better coverage with MDT (a free supply of drugs was provided
through WHO to countries in need), and focused attention on difficult-to-reach populations.
Guinea-worm disease (dracunculiasis)
This is caused by the parasite Dracunculus medinensis, commonly known as the guinea-worm, which
is transmitted by drinking water infested with the intermediate host of the parasite. The worm, ingested
with drinking water, migrates through the body and eventually emerges slowly through the skin causing
fever, nausea and vomiting, frequendy for several months.
Although there are no drugs to treat the disease nor a vaccine to prevent it, dracunculiasis may be
totally eradicated from the world in the near future. The strategy advocated by WHO combines a variety
of interventions and approaches but emphasizes two primary measures: the strengthening of surveillance,
which implies establishing or strengthening case-containment activities in all endemic villages with intensified
community participation, and the mobilization of decision-makers, including village chiefs to improve
community awareness and participation in making drinking water supplies safe and other eradication efforts.
Campaigns to control guinea-worm disease have been instituted by most of the 18 endemic countries,
mainly in Africa.
Proven strategies exist to reach the targets for all three diseases; their implementation requires more
political commitment and financial resources. Together with WHO and UNICEF, Rotary International,
for example, is raising funds to advance the polio eradication initiative. Global 2000, UNICEF, bilateral
agencies, several non-governmental organizations, WHO and countries themselves are furthering guinea-worm
eradication activities. More such expanded parmerships are needed for investnients to be rewarded by
significant economic, social and human benefits of eradicating these diseases.
WHV97A
Page 2
^gseases
WHD 97.5
WORLD HEALTH DAY
7 April
EMERGING INFECTIOUS DISEASES - CHALLENGES AND SOLUTIONS AHEAD
Vision for the 21st Century
A world on the alert, able to contain communicable diseases through:
■ strong national disease surveillance and control programmes
■ global networks of centres, organizations and individuals to monitor diseases
■ rapid information exchange through electronic links to guide policies, international collaboration, trade and travel
■ effective national and international preparedness, and rapid response to contain
■ epidemics of international importance
Between the world of today and this vision for the 21st Century lies a huge gap. The likelihood of
bridging this gap depends on how well committed partnerships can be forged between individuals and
countries, with the backing of WHO and other agencies within and outside the UN family.
Recent outbreaks of Ebola haemorrhagic fever, meningitis, plague, and yellow fever illustrate the
challenges to making both the global alert and the global response a reality.
CHALLENGE: EARLY DETECTION OF EPIDEMICS
In a poor public health environment an unusual disease event may not be detected until it has become
a major threat to the population and cannot be contained with national resources. Public health laboratories,
even if they exist, are often poorly equipped or unable to diagnose common diseases and assess their impact
on the community.
International response required:
Improve the national infrastructure for routine surveillance of common diseases. Assess national
surveillance systems, strengthen public health laboratory services, support training in epidemiology
and laboratory techniques to increase the pool of staff capable of maintaining routine surveillance
on a national scale. Surveillance will provide the background data against which uncommon events
can be identified.
This information
' '/
material produced
by
the
Division of Emerging and
Other Communicable Diseases Surveillance and Control,
WHO
Headquarters, Geneva, is intended for media/public use and does not constitute an official document. Additional copies may be obtained from
Public Information Unit, World Health Organization, Req.onal Office for South East Asia, Indrapmstha Estate. Now Delhi 110 002. Ind.a
'3
CHALLENGE: RAPID NATIONAL RESPONSE TO UNUSUAL DISEASE EVENTS OR OUTBREAKS
An unusual disease event or outbreak may have been reported to local or national health authorities
but may not trigger a response, or only trigger an inadequate or late reaction.
International response required:
Train key national staff, assess surveillance systems and prepare plans to contain future outbreaks
before they become international emergencies. In addition to these long-term activities, WHO may
be required to play an active role in the management of outbreaks with its partners through the
provision of expert advice, diagnostic reagents, vaccines and drugs, an international response team
if needed, within 24 hours. Once the outbreak is brought under control, WHO and its partners
assist countries in evaluating the outbreak and the way it was handled, to improve future
performance.
CHALLENGE:
EFFICIENT AND VIABLE NATIONAL SURVEILLANCE SYSTEMS
Many countries lack a national, uniform surveillance system for the routine monitoring of communicable
diseases. There may be a surveillance system dedicated to monitor one disease or a series of uncoordinated
systems for different diseases. Data and information from a fractioned and poorly integrated system do
not provide for disease alerts and for the global monitoring of communicable diseases, nor do they help
national authorities in setting public health policies.
International response required:
Develop surveillance guidelines with internationally accepted case definitions; stimulate the use
of these guidelines through workshops for regional and national key4 staff. Facilitate and coordinate
the flow of information to and from national surveillance systems within a global network.
Collaborate with international initiatives for communicable disease surveillance to ensure an efficient
and cost-effective collection of data that can be compared internationally.
CHALLENGE: TIMELY HEALTH INFORMATION
Outbreaks of communicable diseases have become news; the media are often the first, and sometimes
the only source of information on outbreaks. In the absence of official information from the country
concerned, inaccurate reports have triggered panic situations which made it difficult to evaluate the true
situation and the need for intervention. Official information, which could temper exaggerated or inaccurate
reports, has sometimes been difficult to obtain, either because it does not exist or because it could not be
cleared for release.
International response required:
Advocate an open, responsible exchange of information and facilitate national reporting of outbreaks.
Make available reliable and relevant information on diseases and outbreaks to the world community
through electronic and conventional media. Supplement this with appropriate advice to people
living in or going to affected areas.
CHALLENGE: SOUND INTERNATIONAL REACTIONS TO OUTBREAKS
The international community sometimes reacts with panic to outbreaks of cholera, Ebola haemorrhagic
fever, and plague in recent years. Extraordinary and inappropriate measures have been instituted, and
barriers set up against travel and trade, including quarantine at airports. These measures cause heavy losses
in tourism and export widiout providing much real protection against the potential import of the disease
into die country. Quarantine is a poor protection against the import of a disease. Travel time is short and
an infected person can board a plane in apparent good health and arrive at a new destination days, if not
weeks, before symptoms appear.
WHD97.5
Page 2
International response required:
Revise the International Health Regulations to provide an internationally-agreed code of practice
and control of the international spread of potentially dang'erous infectious diseases, according to
today’s epidemiological and economic realities. Provide guidelines on the application of the
Regulations to minimize the disruption of travel and trade which has been a strong disincentive
to give alert in the past.
CHALLENGE:
CRUMBLING INTERNATIONAL INFRASTRUCTURE
As public healtli priorities changed in the 1970s and 1980s,
became scarce and the necessary infrastructure weakened.
resources for communicable diseases
International response required:
WHO’s network of Collaborating Centres is an important component in this infrastructure. The
Centres are laboratories selected for their degree of excellence and willingness to cooperate
internationally. Together they make a network which can handle a broad range of communicable
diseases with a high degree of specialization. Strengthening of the WHO Collaborating Centres is
required to provide high quality reference service for diagnosis, training and intervention in
outbreaks. Identifying new laboratories to extend the network to new areas (subject and geographical),
and establishing electronic links to facilitate the flow of data and information within, to, and from
the network are also required.
CHALLENGE: SPREADING ANTIMICROBIAL RESISTANCE
Antibiotic-resistant bacteria appeared almost as soon as antibiotics began to be used. The emergence
of resistant bacteria has accelerated in the past two decades and some infections have become difficult and
expensive to treat. The problem is compounded by the slow appearance of new antibio-tics on the market.
They cost much to develop and license and the problems of resistance gives manufacturers only a short
time to recuperate these costs. A major cause is a massive misuse of antibiotics in humans and animals.
The result is increasing health care costs and longer hospitalizations.
International response required:
Extend the use of WHO-developed programmes and others that accurately monitor the frequency
and geographical distribution of antimicrobial resistance. Link users of the programmes in an
international surveillance network to generate the data needed to develop national and global
strategies and guidelines for the appropriate use of antimicrobials in humans and animals. Stimulate
and support research to improve the number of drugs available on the market and to develop
alternative ways of preventing and treating infections.
CHALLENGE: DISEASE EMERGENCE THROUGH CONTACTS WITH ANIMALS
Animal farming and food production has intensified and increased the risks that diseases in the animals
are transmitted to humans through the food chain. Another reason why new infectious diseases have
emerged in die past two decades is diat more humans risk coming in contact with animals carrying diseases,
for example when forest areas are cut and destroyed and animals living there seek other habitats closer to
human populations, or when humans penetrate deeper into the remaining forest areas for leisure or work.
International response required:
Strengthen surveillance of communicable and zoonotic diseases, seek international consensus on
policies to prevent and contain transmission of animal diseases to humans and prepare guidelines
for die use and management of animals reared for human consumption.
WHD97.5
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WHD 97.6
WORLD HEALTH DAY
FA
7 April j
AAA
WORKING TOGETHER TO FIGHT DISEASE:
THE RED CROSS AND WHO
EBOLA
Kikwit, Zaire 1995
Tn May 1995, joint action by ±e Red Cross, the World Health Organization, Medecins sans Frontieres
JjBelgium), Institutes of Tropical Medicine (Belgium), Sweden, South-Africa, and Centers for Disease
Control and Prevention (USA) teams and local non-governmental organizations proved quick and
effective in containing a deadly epidemic of haemorrhagic fever caused by an outbreak of the Ebola virus
in the town of Kikwit, Zaire.
The combination of medical advice from WHO and its partners and the capacity of the Red Cross
Society7 of the Republic of Zaire (National Society) to access all levels in die community dirough its
thousands of volunteers proved particularly efficient in stopping the spread to the rest of Zaire of a disease
which left 245 people dead in and around Kikwit. National Society7 volunteers were on the front line,
transporting die sick to quarantined sectors of hospitals, collecting the bodies of victims and burying them.
Five Zairian Red Cross volunteers became infected and died in the line of dun7.
With support from the International Federation of Red Cross and Red Crescent Societies (die Federation),
the Zairian Red Cross mounted a vast public information campaign. Posters and leaflets in die four national
languages of Zaire and in French explained how to avoid infection. One poster recommended avoiding contact
with blood or other bodily fluids of a patient. A second advised people against washing the bodies of die dead,
wliich is a traditional part of burial ntes. A third warned that used syringes must be burned. A fourth recommended
diat patients' clothes be handled only with gloves on and that they be boiled before being washed.
All activities were coordinated by7 an international monitoring and surveillance team which was set up
as soon as die disease was diagnosed. It included representatives from the Zairian Red Cross, the Federation,
WHO and its parmers, die Government of Zaire and otiier non governmental organizations. Research
also began in order to identify die natural host of the Ebola virus.
After rhe epidemic, die National Society helped families who had lost members to the disease, and
who were shunned by’ neighbours afraid of contagion. Volunteers distributed short term material assistance
(such as food) to die affected families. They also informed neighbours that dierc was no risk in allowing
these people to go about their ordinary business and diat diey should be re integrated into the community.
Mayibout, Gabon 1996
The Federation and WHO joined forces again together with die French government co help the
Gabonese national authorities and the Red Cross fight an outbreak of the Ebola virus in February 1996.
A massive information campaign included information sheets on how to fight Ebola, designed for medical
personnel and produced by the Federation and WHO. Protective wear for all those in contact with patients
(gloves, aprons, masks and goggles) as well as disinfectant was immediately shipped to Gabon. The epidemic
was quickly stemmed, but left 16 people dead.
This
hv
.nformation
nxitcnal
M-vxiquartnis i \meMi
1
produced
hy
iho
Division of Emerging and Other Communicable Diseases .Surveillance
s mtixxlivl (or tnodia/pulJic use and docs not constitute an emcial (Aummt Additional . x)i» s ■
• -tid I <•*11111 1
■■ ani/ahon
'<v|ionai < th' r i t ' .'util I
•■• a
na 1 • i'p
’ •-.v
and (iwitrol
WHO
av !<■ i4'?tiinivj •
At the beginning of March 1996, at an international conference on Ebola convened by WHO in the
Zairian capital of Kinshasa, some 140 medical specialists and representatives of NGOs discussed ways to
combat future outbreaks of the fatal disease. The Zairian Red Cross received a special citation of gratitude
for its work from WHO and the memory of the five Red Cross workers who lost their lives after contracting
the disease was honoured. It was also decided to begin studying the usefulness of blood from survivors
of the Ebola outbreak at Kikwit (some 60 people survived) in treating others with the disease. WHO
has so far collected 13 samples which are being tested for antibodies to the disease. Plans are under way
to have the Zairian Red Cross collect blood from those who still have high antibody levels.
DIPHTHERIA in the former Soviet Union 1995
For decades, diphtheria, thanks to widespread immunization, had become a controlled, almost forgotten
disease. The sense of control changed abruptly in the early 1990s, as a diphtheria epidemic broke out in
the Russian Federation and Ukraine. This was linked to die destruction of die Former Soviet Union, to
heavy population movements and to social and economic stress. Diphtheria rapidly spread to all other
Newly Independent States (NTS); by the end of 1994, a total of 47 802 reported cases and 1 746 deaths
had been reported. Worse seemed in store for 1995. Only mass immunization efforts could slow and
finally did control die epidemic.
In 1995, Estonia reported 19 cases of diphtheria, Landa 369 cases, Lidiuania 43 cases, Belarus 322
cases and Ukraine 5336 cases. In June 1995, the Federation launched a combined appeal with WHO and
UNICEF calling for resources to control die diphtheria epidemic. The funds requested for this appeal were
as high as USS 33 million.
Under die strategy drawn up by the three organizations, the Federation has taken on operational
responsibility- for die three Baltic States of Estonia, Lama and Lidiuania, and for Belarus and Ukraine, by
providing vaccines, syringes and needles, cold chain equipment, antibiotics, antitoxin and human resources
for implementing and monitoring die programme.
Under die responsibihty of the Federation, with funding from ECHO (European Community’
Humanitarian Office) and other donors, approximately 31 million doses of vaccines were shipped into die
countries and mass vaccination campaigns took place in autumn 1995 and spring 1996. As an effect of
diese mass vaccination campaigns, die case load and mortality are stabilizing in some countries and decreasing
in others.
The whole programme was planned in close collaboration with the National Red Cross Societies and
the Ministries of Healtii. The Red Cross Societies were responsible in particular for social mobilization
efforts, for training seminars for health staff, for printing posters, leaflets and other information material
about diphtiieria, vaccination places and dates. The nauonal ana local media got involved throughout the
whole programme. Other institutions, such as churches, schools, transport companies, big enterprises and
police were also mobilized bv the Red Cross for spreading out information to the public. Vaccination
rooms were established in all polyclinics, and medical personnel was trained and instructed on die Federation's
requirements in reporting and data collection.
A big challenge for die Red Cross Societies was how to contact die so-called hard-to-reach groups, such
as the unemployed, homeless, gypsies, and alcoholics. Mr George Weber, Secretary General of die Federation
said, "infectious diseases have become die biggest killer these days, and poor and vulnerable people are more
affected than odiers. We in die Federation have therefore given high priority to die control of epidemics,
particularly in diosc groups which arc hard to reach. This is possible tiirough die widespread network of Red
Cross volunteers”. For die vulnerable groups, soup kitchens and secondhand clothes distributions were organized,
market places and dormitories were xisited and many home-bound and disabled persons were vaccinated in
their homes. These efforts increased vaccination coverage by at least 20%.
WHO acts as the secretariat for the Interagency Immunization Co-ordinating Committee (IICC) which
is addressing the problem of diphtheria in the former Soviet Union and coordinates the implementation
of the programme. UNICEF has taken on responsibility for carrying out the programme in other countries
of the NTS. The partnership between these organizations and the Federation is very close and well
functioning. Much has been learnt on how* to combine different institutional cultures and management
styles, and future plans for controlling the epidemic arc jointly discussed. This big operation is now well
under wav, the epidemic is under control in rhe Baltic Stares and Belarus, and vaccinations arc continuing
in all six countries.
•VHDQ’
■
\y
i
fi
Emeraiog Infectious
\ Diseases
'1
WORLD HEALTH DAY
7 April
WHD 97.7
‘J ®
’iI:’-
PERSONAL ACCOUNTS
The control of the outbreak of Ebola haemorrhagic feverl:
the account of a WHO medical officer
Z^Vi 9 April 1995, a 35 year-old male laboratory worker from Kikwit H hospital was transferred to
y^/Kikwit General Hospital with severe bloating and high fever. Surgery was performed the next day
and abnormal bleeding was diagnosed. Unfortunately, and despite a second operation, the patient
died three days later, on 14 April. Although this could have been the end of an unfortunate medical
concern, it was in fact, for most health workers, nurses and physicians involved in the operation, the silent
beginning of an epidemic.
On 7 May 1995, rumours about a possible outbreak of Ebola haemorrhagic fever in Zaire, together
with a request for assistance reached WHO, Geneva. The diagnosis was rapidly confirmed by the Centers
for Disease Control and Prevention (CDC) in Adanta, Georgia, a WHO collaborating centre. On 9 and
10 May an international team with members from WHO and WHO collaborating centres assembled in
Kinshasa and flew to Kikwit, where the national experts were fighting the outbreak under difficult conditions.
The WHO team led and coordinated the international response, working closely with the local authorities
and Non-Governmental Organizations (NGOs) such as Medecins sans Frontieres (MSF), the Red Cross,
and die local Catholic Mission. Additional expertise for laboratory diagnosis, viral diseases, epidemiology,
clinical management, public education, information, engineering, disaster relief, arrived in Kikwit from
CDC, WHO, MSF, the International Federation of Red Cross and Red Crescent Societies, Sweden, South
Africa, Belgium and Zaire. A strict isolation ward was set up; an agreed definition of an Ebola case was
approved and used to sort patients and provide them with appropriate care. After a few days, die management
of cases was under control.
It was dien time for a more thorough investigation, to collect information from die population. The
international team investigated reported deadis, suspected cases, unusual events or anything which could
clarify the complex chains of transmission of the disease and lead to the source of the epidemic. Every
day, special investigation teams checked rumours, by foot, on bicycle, driving miles in a 4-wheel drive
vehicle. Daily radio contact witii remote villages outside Kikwit was needed to monitor the entire region.
Tills effort led to the identification of a 35 year-old charcoal maker who had died on 13 January 1996 in
Kikwit General Hospital and who, retrospectively, seemed to be die first in a series of cases which had
occurred over four mondis until the dramatic outbreak in the hospital.
Excerpt from World Health, January-February 1997
s
Uli,
Infomohon
motenol
Headriuorten, Gone™,
>
produced
by
ibo
Diviiion of Emerging and
Olber Communicable Oseases Surveillance
and
Control,
WHO
intended for media/public uro and doos no< constitute an official document Additional copies may bo obtained from
Public Information Unit, World Hnallb CXqanization, Regional Office for South East Asia
Indmprnsiba Estate. New Oi'llu I 10 00? India
Operational support from WI IO headquarters in Geneva to the field operations faced complex logistical
problems, because of the geographic inaccessibility of the outbreak zone, the poor state of the local
infrastructure, particularly in telecommunications and transport, the high turnover of field staff; the high-level
media interest in the epidemic intensified some of these problems. A satellite link with WHO headquarters
in Geneva maintained the communication flow.
By late May, about two weeks after the alert, the epidemic was under control, although additional
waves of patients were still expected. The last case occurred on 14 July 1995. A regional surveillance
system for Ebola haemorrhagic disease was fully functional and the emergency phase was over. The epidemic
command post, from which the international team of physicians and scientists had successfully controlled
the outbreak, remained in place until October 1995.
The epidemic was declared over after 24 August 1995, once 42 days (twice the maximum incubation
period of the disease) had passed without a case. The epidemic toll was 316 cases, of whom 124 women
and 121 men lost their lives. A long-term surveillance system was set up in the Kikwit area, looking for
any suspected case, particularly of haemorrhagic disease, or any unexplained death.
Dr Guenael Rodier
Division of Emerging and other Communicable Diseases Surveillance and Control
Meningitis: the epidemic of the century in Nigeria
The account of a physician working for Medecins Sans Frontieres
Nigeria: the states of Kano, Katsina, Bauchi... Three million people vaccinated, 30000 people treated.
We did it! We would never have imagined we could carry out such a massive vaccination campaign in
two months.
Since the beginning of 1996, Nigeria has been dogged by a meningitis epidemic of unprecedented
scale. It is the first time that we in Medecins Sans Frontieres have had to deal with an epidemic situation
in such a densely populated region. There are two million inhabitants in Kano, the country’s economic
ner\re centre, which we chose for our first mission.
When we arrived at Kano, the situation in the big 650-bed hospital was catastrophic: people with
meningitis were laid out on mats, some people who were lying on the bare ground were in convulsions.
The most serious cases were usually children. In mid-February 1996, when the situation deteriorated
suddenly, 120 patients were arriving at the hospital every7 day. The staff were run off their feet and medicines
and vaccinations had dwindled to nil.
There were too many cases in a very short space of time for the Nigerian health system to cope with
the epidemic without outside help. Health structures were in place and the staff were quaEfied, but material
resources were limited. Very soon, effective cooperation between Nigerian health teams and the international
team from Medecins Sans Frontieres helped provide suitable treatment and launch the vaccination campaign.
The challenge in Nigeria was, quite simply, enormous. In the diree states of Bauchi, Kano and Katsina,
with a total of 15 million inhabitants, several million people needed to be immunized. The race against
time began on 7 March when 30000 vaccinations were given in one day at 20 centres. Armed with
megaphones, we went round markets and places of worship in an effort to mobilize the population, and
carried out a comprehensive information campaign.
Despite the operation’s success, with 3 million people vaccinated and 30000 patients treated we are
still slightly disappointed: of the eight Nigerian states that were particularly affected by the epidemic, we
were able to help only three. Slow international mobilization, both in die media and at an operational
level, more than likely deprived tens of thousands of patients of treatment*.
Elisabeth Le Saout
Meningococcal meningitis is found right across the world. It is the only form of bacterial meningitis that causes epidemics, with the most serious of
which occur in sub-Saharan Africa. The
disease is caused by a bacteria which is transmitted mainly through contact with the droplets given off by
the respiratory tracts of persons infected. Meningitis is characterized by the sudden onset of headache,
'ith fever, nausea, vomiting, photophobia and
stiffness of the neck. Other symptoms of the disease are lethargy, delirium, coma and/or convulsions.
’Recognizing these difficulties, WHO and its partners launched an African meningitis initiative in 1996 with the objective of strenthening surveillance
and response to prevent future epidemics of this size.
WHD97.7
Page 2
Emerging iofectioos
Diseases
WHD 97.8
A WORLD HEALTH DAY
■■
7 APril ; K
-
WHO NETWORK ON ANTIMICROBIAL RESISTANCE MONITORING
WHO is establishing a global network of laboratories
that generate standardized, quantitative data on antimicrobial susceptibility testing.
Data are used locally for containment of resistance and internationally to develop
better drug policies and advocacy for new antibiotic development.
l.BACKGROUND
The long-term goals are to:
■ encourage policies and practices that will
ensure better infection control and patient
care at local level
■ prolong the useful
antimicrobials
life
■ support rational selection
essential drug lists
of
available
of regional
■ detect and contain the emergence of new
and major multidrug resistant bacteria
WHO headquarters, in close collaboration with the
Regional Offices and WHO Collaborating Centres, is
establishing a global network of laboratories to monitor
antimicrobial resistance.
WHO is also developing a global data bank to help
identify antimicrobial resistance problems of local,
regional and global priority, seek consensus on how
to tackle these problems, and initiate and coordinate
appropriate control and containment measures.
■ standardize interpretation of antimicrobial
resistance tests
■ support those involved in antimicrobial drug
research, development and advocacy.
This information
material
produced
by tho Division
The establishment of this Network represents a new
stage in the global surveillance of antimicrobial
resistance. Funds from both WHO regular budget and
external sources are being made available and the first
laboratories have been enrolled.
of Emerging and
Other Communicable Diseases
Surveillance
and Control,
WHO
Hoadqvartors. Gmtw is intended for media/public use and does not constitute an official document. Additional copies may lx) obtained from
I’ubhc Information Unit Wodd Health Organization
Rcqional Office fix South fast Asia ’ndraprastha Estate, New IVlhi 110 00?
viia
WHO will support laboratories which:
■ participate in an initial Quality Control pilot
project
Q routinely conduct quality control tests and
process their test results in a computer
database
use standardized susceptibility tests
(pre-ferably as outlined by WHO guidelines)
and process quantitative measurements
S process test results with a software
compa-tible to WHONET (WHO supports
provision of interfaces)
■ participate in routine proficiency testing
In order for the Network to generate data which
arc of regional and global significance, core network
laboratories are applying standardized laboratory
techniques so that the data arc accurate.
The Network will:
■ be temporally and geographically representative
H
be flexible enough to react to changing trends
■ be open
to
both
hospital
and
community
laboratories
■ include important bacteria and antimicrobial drugs
become sustainable.
2. CHARACTERISTICS OF THE NETWORK
Network laboratories are in command of die skills required to conduct standardized and quality
controlled antimicrobial susceptibility tests.
Tlrrough training courses, external quality control and proficiency testing, local support.
Results of antimicrobial susceptibility testing are locally processed and analysed and data are routinely
submitted to WHO for incorporation in the WHO data
Fifty laboratories will provide standardized,
bank. Laboratories participate in a quality assurance
quantitative antimicrobial susceptibility testing
programme.
Tbrotigh local qziality control, on-site evaluation, data
bank and report monitoring, periodic proficiency testing.
data to WHO by the end of 1997. The Network
will be expanded to 60% of WHO Member States
in 1998 and to 80% in 1999.
WHO manages its data collation ensuring, feed-back
and publication of information. It expands die Network with its parmers and establishes national WHO
working groups on antimicrobial resistance monitoring for identification of priority areas for research and
development and policy formulation.
3. INSTITUTIONAL FRAMEWORK
External quality control and proficiency testing is conducted by the Ginters for Disease Qmtrol
and Prevention, Atlanta, USA. A second centre is being identified for continuous external proficiency
testing, which will be able to support a growing network of laboratories.
Training courses are conducted by WHO teams using training material developed in collaboration
with WHO partners.
On-site quality control, local advice and training are provided by WHO consultants.
The WHO data bank is managed within WHO.
Overall management and coordination of the WHO Network and routine publication of results arc
the responsibility of the Division of Emerging and other Qjmmunicablc Diseases Surveillance and Gintrol
(EMC) in WHO. EMC liaises with national authorities, the pharmaceutical industry and other interested
parties.
WHD97.8
Paqe 2
21
WORLD HEALTH DAY
WHD 97.9
-"/'A ‘
7 April!
;,7.T
THE INTERNATIONAL HEALTH REGULATIONS:
MAXIMUM PROTECTION, MINIMUM RESTRICTION
INTRODUCTION
In 1377, Venice wrote the first recorded quarantine legislation to protect itself from rats on ships
arriving from foreign ports. Later legislation in Europe and elsewhere led to the Paris inter-national sanitary
conference in 1851, which laid down the basic tenet protection against the international spread of infectious
diseases: maximum protection with minimum restriction, a tenet still valid today. A full century lapsed before
the International Sanitary Rules were adopted, in 1951; these were amended in 1969 to become the
International Health Regulations (IHR).
Three communicable diseases - cholera, plague, yellow fever - must currently be reported under the
IHR. International enforcement of reporting is not a feasible proposition under the IHR, however, and
reporting is far from complete. Countries fear economic consequences when they report (see below); for
new diseases with potential for international spread, the IHR do not apply (see box).
In 1995, the World Health Assembly called for a revision and updating of the IHR to make them
more applicable to infection control in the 21st century. Over the years, the policing sense of the Regulations,
reflected in the emphasis on quarantining of cases and contacts, has given way to public health measures
in order to minimize the risk that an imported infection establish a new focus. The application of die IHR
has been affected by changes in the global health situation and die increase in international travel. The
control of infectious disease at the international level through improved surveillance and intervention
strategies is more effective than die application of quarantine practices. The basic principle of the revised
IHR should continue to be to ensure maximum security against the international spread of diseases with
minimum interference widi world traffic and trade. The IHR will be revised along the lines shown in the
following box:
Immediate reporting for only three diseases should be replaced by immediate reporting to WHO of defined
syndromes representing disease occurrence of international importance and of the basic epidemiological information
that will be useful in control of disease. The IHR should be accompanied by a practical handbook facilitating
their use and defining the requirements for international reporting. The revised IHR should be integrated into all
epidemic surveillance and control activities at global, regional and national level. The IHR should include a
mention of inappropriate or unnecessary interventions and provide clear indications as to why their actions are
not required.
This
v\47'JiI W
information
matonal
produced
by
the
Division of Emerging and
Other Communicable Diseases Surveillance
and
Control,
WHO ’
Headquarters. C-encvo is intended for modia/public use and does not constitute an official document Additional copies may bo obtained from
Public Intnrrrwifion Unit World Hralth Organization Regional Office for South East Asia Indraprastha Estate. New Delhi 110 00?
India
~iy
The IHR also describe health facilities and personnel that should be available in ports, and w^at
maximum measures national healdi authorities should institute to protect their territories. The IHR allow'
national authorities to dispense with those measures which arc not appropriate in die national context, j
The revised draft will be submitted to the World Healdi Assembly for ratification in 1998, and widely
diffused along with its operational handbook; these documents have great potential to serve as a global
alert system for diseases of international importance, and to ensure maximum protection with minimum
restriction.
Examples of misapplication of the IHR
Cholera in Latin America. When cholera was identified in 1991, Peru notified die disease at once,
as specified by die IHR. Help was immediately forthcoming, but during that year alone cholera infected
over 300 000 persons and caused 3000 deaths in Peru. In addition to its public health impact, the epidemic
led to losses in trade and travel estimated at US$ 700 million at least due to excessive measures imposed
by other countries.
e
Plague in India. In 1994 an outbreak of presumptive plague occurred in India. India reported die
outbreak to WHO after information had been diffused by the international press. The outbreak led to
much economic disruption and concern worldwide: in some countries airports were closed to aeroplanes
arriving from India, and Indian guest workers were forced to return even diough some had not lived in
India for several years. Imports of foodstuffs from India plummeted; the overall loss was estimated at
nearly US$2000 million.
Examples of irrelevance of the IHR in new diseases
Ebola in Zaire. In 1995 an outbreak of Ebola haemorrhagic fever occurred in Zaire (316 cases and
245 deaths). The immediate official reaction was to close the road leading to Kinshasa, the capital city
500 kilometres away, but the airport near the outbreak site was not part of the quarantine and a case of
Ebola did arrive in the capital city by air. Strengthened disease surveillance in Kinshasa, however, immediately
detected the case and no local spread occurred. Even if this case of Ebola had boarded an international
flight in Kinshasa, the IHR would have had no application since the disease does not fit under their
mandate.
Hantavirus Pulmonary Syndrome in the United States. In 1993 an outbreak of a disease characterized
by fever, muscle aches and intestinal complaints followed by of shortness of breath and rapid progression
to death was first identified in the southwestern United States, then in other states. The cause was found
to be a newly identified virus in the Hantavirus family. The deer mouse is now known to be the reservoir
of this virus. Despite national alarm as a result of this outbreak and concern about die possibility of
cross-border transmission, the IHR again were not applicable.
The revision of the IHR is being undertaken witii such scenarios in mind in order to ensure an orderly
and appropriate response to outbreaks of infectious disease of global importance.
WHD97.9
Page 2
/
r^fej^kXxi^KA^^. 'ilniH^*saiariijf.J«-w*. .■ .
32
e reduction of dental caries
;uppl., pp. 1311-1316(1982).
ries in Irish schoolchildren
■1317-1320 (1982).
tlal caries in the Netherlands:
and 1 l-15-year-old children,
uppl., pp. 1321 -1326 (1982).
al caries in New Zealand. J.
Cartology Today. Int. Congr. Zurich 1983. pp. 33-39 (Karger. Basci 1984)
Dental Caries in Underdeveloped Countries
Aubrey Sheihain
Ilic London Hospital Medical College, London, England
nee in Norway. J. dent. Res.
Scotland. J. dent. Res. 61:
Dental caries is a sugar-dependent infectious disease. Therefore
n Sweden. J. dent. Res. 61:
SeltTed^
:ntal caries in US schoolchil351 (1982).
sing and filled teeth among
PO. Washington 1967).
sing and filled teeth among
JPO, Washington 1981).
ies in United States children.
tries where sugar consumption is falling [27], Industrialized countries
can absorb little more sugar so underdeveloped countries are c0™ing four-fifths of what they produce. 50 years ago they exported fourfifths of production [31]. In addition to home produc .on, in some
underdeveloped countries, sugar is the second largest food ncm^.mportcd Sugar is one of the first foods to respond to a rise in income in lowincume countries and the percentage of sugar consumed in hmden
forms rises progressively with rising income and increasing total sugar
of United States children.
I
d caries, oral hygiene status,
398 404 (1976).
of root-surface caries in a
>ot caries. 3. t\ Clinical study
I
evalcnce in adults with life
str. 552: (1980).
at surface caries among inEpidemiol. 8: 84-88 (1980).
i
1« i» consumption „ sotig^d
in countries which had a per caput consumption of less man zu kg/ytai
[29] The bigeest users of sugar in underdeveloped countries arc the
subsidiaries of large multinational food and drink PJ0“ssinS
panics and include cake and biscuit manufacturers and th o t dr nk
industry. Soft drinks are probably the most important factor in the
sharp increase in sugar consumption in countries as diverse as Iran and
Venezuela. In Mexico, nearly live bottles of soft drinks are consumed
per man, woman and child every week [9].
Increases in Dental Caries
Deteriorating dental health is seen as a necessary consequence of
economic growth which in itself is assumed to be a desirable goal tor
USA)
I
34
Shciham
_______ Yet the extent of the deterioration will reflect the priorities
everyone.
is toe
~
and severity of de,...I caries
pidly i» underdevriopsd countries; of 20 eoun.ncs -«he e
Dental Caries in
consumed per pci
other. He found t
attack increased.
Shimatmira [21] ii
changed with inc.
at a given level
differentially.
mS 1321 In those coumries which have repotted >««»». *• *
caries
, A/itn IS between 1966 and 198Z in
creases in DMFT were from 0.
$ Mcxic0>
1:4 200 would be needed to ticat 12-ycai oks wi
tict-nonulaone de^st and wo
^dScrTnc^DMF Vf 0.7 to 3.5 would
requkeanTx'tra 700 dental operators per million children [2]. A levJ
achieve in countries in
of dental manpower which is impossible to
health is less than 5 USS
which the annual per capita expenditure on
’ : majority
of the
the cost of one restoration per child would exhaust the
._
health budget. What chance is there of treating children in J , f
neaim uuubv
‘At six years of age only 11.4 /o
fillings 73% required two-surface fillings,
I
i
In underdeve
with rising sugar
In the permanen
levels [10]; the s
molars [1]- Will
second molars :
consuming com
caries becomes
environmental
factors. They ca
[22].
In some tm
very young an<
young and roo
Socio-Den
In undcrd
social class ai
group and lc\
The influ
Ethiopian ch
four times im
as many pern
differed by cl
i
I
I.
Sugar and Dental Caries
What is the cause of this frightening increase in dental caries in
underdeveloped countries? The consensus view-is that refined sug s
and in particular sucrose is the princ.pal dietary cause 13 19 25]
Sreebny [25] found a strong association between the quantity of sugar
and a higher
pattern of ca
to high inco
company.
Urbaniz
ly to consul'
nr*
Dental Caries in Underdeveloped Countries
34
iect the priorities
ity of dental caries
20 countries where
me years apart, 15
China) showed no
? had a decrease in
increases, the in1966 and 1982 in
4 years in Mexico,
years in Lebanon
been reported by
s [2] described the
ics as ‘absolutely
I years in Kenya,
■ears in Thailand,
verted into treatpulation ratio of
i DMF of 3.0. If
cdcntist:popula0.7 io 3.5 would
Idren [2]. A level
' in countries in
less than 5 USS
e majority of the
dren in Fiji, for
age only 11.4%
ired one-surface
cd thrcc-surface
urfaccs. 29% of
e of caries’ [24].
Jen tai caries in
refined sugars
se [13, 19, 25].
antity of sugar
35
consumed per person per day on the one hand and the DMF on the
other. He found that at levels above 50 g/day the intensity of the caries
attack increased. Schnlerud [18] in Norway and Takeuchi [26] and
Shimamura [21] in Japan had previously shown that the caries pattern
changed with increases in sugar consumption. Takeuchi [26] found that
at a given level of sugar consumption specific teeth were affected
differentially.
In underdeveloped countries the first change in the pattern of caries
with rising sugar consumption is an increase in the primary teeth [16].
In the permanent teeth pits and fissures -are mainly affected at low sugar
levels-[10]; the second molar being more frequently carious than first
molars [1]. With increases in sugar consumption the ratio of first to
second molars affected is one - similar to that found in high sugar
consuming countries [6]. At the higher sugar levels proximal surface
caries becomes more common. These patterns of disease indicate that
environmental factors arc more important than genetic predisposing
factors. They cast further doubt on Jacksons’ theory of caries aetiology
1:1
I
J22].
In some underdeveloped countries dental caries is a disease of the
very young and the middle-aged [20], coronal caries occurring in the
young and root caries in the older group [15].
Socio-Demographic Variables
In underdeveloped countries the distribution of caries varies with
social class and acculturation, level of urbanization,, gender, ethnic
group and level of fluoride consumption.
The influence of social class is strong [5]. Olsson [14] found that
Ethiopian children from more affluent high social class families had
four times more caries in primary teeth than poorer children and twice
as many permanent teeth with caries. She found that the caries pattern
differed by class. Upper class children had more anterior teeth affected
and a higher number of both proximal and smooth surface lesions. This
pattern of caries was associated with the increased availability of sugar
to high income families since the establishment of a national sugar
company.
Urbanized populations in underdeveloped countries arc more like
ly to consume refined sugars than those in rural areas. Therefore it is
1
j
■
II r
I!
!
r
i
I
i
i
I-
|
Shciham
I
Dental Caries ir,
36
not surprising that caries rates arc higher in urban populations. In the
Sudan, Emslie [4] found seven times more caries in 15- to 19-ycar-old
urban children, where the annual per capita sugar consumption was
over 1001b, than in rural children living in an area where the sugar
consumption was below 5 Ib/year/person. Similar trends were found in
Mozambique [7]. Swaziland [8] and South Afiica [3].
Females usually had a higher caries rate than males [10]. And there
arc differences in caries ratesln different ethnic groups within a country.
In Malaysia, Chinese children had a much higher caries rate than
Malays and Indians [11]. Similar trends existed in Singapore despite
water fluoridation [12]. In Fiji, Indians also had lower canes rates than
Fijians. This difference was mainly due to the diflercnces in the ages of
exfoliation of primary teeth and eruption of the permanent teeth [24].
Fluoride levels in water and foods have been shown to be related
to caries rates. Studies in underdeveloped countries, some with low
levels of sugar consumption, offer an opportunity to assess the effect
of fluoride with differing levels of sugar consumption. In an extensive
study of populations living on 14 South Pacific islands, Spcake ct al.
[23] did not find a clear relationship between enamel fluoride levels and
caries prevalence when comparisons were made between islands, yet a
significant relationship did exist within island populations. This sug
gests that where environmental factors were similar, fluoride did have
an effect. They found that where sugar levels were high, the influences
of fluoride were outweighed by dietary factors. It was possible to
develop a predictor chart of caries rates from enamel fluoride levels and
sugar consumption levels [23].
Public Health Aspects
should include z
imports and alte
To summarr
health problem i’
Swaziland, the <
resources are ho
disease [8]. The
when compared
should be rcme
require about 2
training and en
considerable an
many underdev
Increases ir
the intensity of
affected.
The major
refined sugar. '1
control the risi
tries, primordi
refined sugars
needed.
Reference?
1
2
3
4
The increases in caries in many underdeveloped countries arc very
rapid. The principal reason for the increase is the increase in consump
tion of sugar-containing foods, drinks and confections. The conven
tional methods of preventing caries used in industrialized countries are
not appropriate for underdeveloped countries. The cost of fluoride
toothpaste, paper cups for fluoride rinses and toothbrushes are beyond
the means of the vast majority. Therefore the logical public health
strategy is primordial prevention; preventing the emergence of patterns
of eating that are known to contribute to caries [33]. The strategy
5
6
7
8
Akpata, E.S
molars in ur
Barmcs, D. ?
Barmcs, D. E
dent. Ass. I.
EmsHc, R.L'
167-178 (19
Enwonwu, <
countries. C
Hirshowitz,
health and
Johanncsbu
Hobdcll, M
Republic o'
Klausen, B
Community
I
1
!
j
I
36
Denial Caries in Underdeveloped Countries
populations. In the
15- to 19-year-old
■ consumption was
?a where the sugar
ends were found in
37
should include a national food and agriculture policy, controls on
imports and alternative useful uses of sugar.
To summarize, dental caries is rapidly becoming a severe puplic
health problem in underdeveloped countries. In some countries such as
Swaziland, the dental caries rate is as high as in Denmark but the
resources arc hopelessly inadequate to cope with the treatment of the
disease [8]. The increases in dental caries may not appear to be great
when compared to the caries rates in industrialized countries but it
should be remembered that every increase of 1 in the DMF would
require about 200 dental operators per- million children. The cost of
training and employing such an increase in the dental workforce is
.considerable and beyond the educational or financial capabilities of
many underdeveloped countries.
Increases in dental caries appear to have a well-defined pattern; as
the intensity of the disease increases different teeth and tooth sites are
aflcctcd.
The major factor associated with the increase in dental caries is
.refined sugar. Therefore if worthwhile efforts are going to be made to
control the rising epidemic of dental caries in underdeveloped coun
tries, primordial prevention aimed at controlling the availability of
refined sugars and sugar-containing foods, drinks and. confections, is
needed.
ales {IO]. And there
>s within a country,
r caries rate than
Singapore despite
er caries rates than
mces in the ages of
manent teeth [24].
town to be related
?s, some with low
o assess the effect
•n. In an extensive
nds, Speake ct al.
fluoride levels and
veen islands, yet a
la lions. This sugfluoridc did have
igh, the influences
\ was possible to
fluoride levels and
I
I
l!
I
References
countries are very
case in consump3ns. The convcnized countries arc
cost of fluoride
ushes are beyond
cal public health
gence of patterns
33]. The strategy
5
1
I.
2
3
5
6
7
8
Akpata, E.S.; Jackson, D.: Caries vulnerability of first and second permanent
molars in urban Nigerians. Archs oral Biol. 23: 795- 800 (1978).
Barmes, D.E.: Epidemiology of denial disease. J. clin. Pcriodont. 4: 80-93 (1977).
Barmes, D.E.: Oral health status of children - an international perspective. J. Can.
dent. Ass. 12: 651-658 (1979).
Emslic, R.D.: A dental health survey in the Republic of Sudan. Br. dent. J. 120:
167-178 (1966).
Enwonwu, C.O.: Interface of nutrition and dentistry in pre-industrialized tropical
countries. Odont. Stom. Trop. I: 19-42 (1978).
Hirshowitz, A.S.; Rashid, S.A.A.; Clcaton-Joncs. P.E.: Dental caries, gingigal
health and malocclusion in 12 year old urban black schoolchildren from Soweto,
Johannesburg. Community Dent, oral Epidemiol. 9: 87-90 (1981).
Hobdcll, M. H.; Cabral, J. R.: Dental caries and gingivitis experience of the People’s
Republic of Mozambique (1978). Odont. Stom. Trop. 3: 111-126 (1980).
Klauscn, B.; Fanoe, J.G.: An epidemiologic survey of oral health in Swaziland.
Community Dent, oral Epidemiol. 11: 63-68 (1983).
iI
i
i
<
I
■
Shciham
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
Dental Caries in Ur.t
38
Lappc, F.M.; Collins, J.: Food first. The myth of scarcity, p. 234 (Souvenir Press,
London 1980).
Legler, D.W.; Al-Alousi, W.; Jamison, J.C.: Dental caries prevalence in secondary
schoolchildren in Iraq. J. dent. Res. 59: 1936-1940 (1980).
Ministry of Health, Malaysia: Dental epidemiological survey of adults in Peninsular
Malaysia (Dental Division, Kuala Lumpur 1978).
Ministry of 1 Icallh, Republic of Singapore: National dental health survey of school
population - 1970 (Dental Branch, Singapore 1973).
Newbrun, E.: Sucrose in the dynamics of the caries process. Int. dent. J., Lond. 32:
13-21 (1982).
Olsson, B.: Dental health situation in privileged children in Addis Ababa, Ethiopia.
Community Dent, oral Epidemiol. 7: 37-41 (1979).
Powell, R.N.: Cutress, T.W.: Changing patterns of caries prevalence in Tongatapu.
Odont. Slom. Trop. 4: 221-227 (1981).
Russell, A.L.: World epidemiology and oral health; in Krcshovcr, McClure, En
vironmental variables in oral disease, pp. 21-39 (Am. Ass. Adv. Sci., Washington
31
32
33
34
World Development
WHO: Oral health g:
Oral Health Unit, 6
WHO: Prevention o
1982).
Yassin, I.; Low, T.:
in West Malaysia. C
1
l966)-
Sardo infirri, J.; Barmes, D.E.: Epidemiology of oral diseases - difTcrcnces in
national levels. Int. dent. J., Load. 29: 183-190 (1979).
Schulcrud. A.: Dental caries and nutrition during wartime in Norway (Fabritius &
Sonncrs, Oslo 1950).
Shciham, A.: Sugars and dental decay. Lancet i: 282-284 (1983).
Shciham, A.; ElTcndi, I.; Noi, B.K.: Assessment of denial needs: pilot studies in
Indonesia. Odont. Slom. Trop. 2: 45-53 (1979).
Shiinamura, S.: A cohort survey on caries attacks in permanent teeth during a
period of approximately 20 kg of annual sugar consumption per person in Japan.
J. dent. Hlth 24: 46-52 (1974).
Sofacr, J.A.: Genetics and site attack in dental caries. Comments on Jackson’s
theory. Br. dent. J. 152: 267-273 (1982).
—
Spcakc, J.D.; Cutress, T.W.; Ball, M.E.: The prevalence of dental caries and the
concentration of fluoride in the enamel of children in the South Pacific. N.Z. dent.
J. 75: 94-106 (1979).
Spcakc, J.D.; Singh, D.; Ligani, M.: Caries, periodontal disease and the treatment
requirements among urban school children in Fiji. Odont. Slom. Trop. 3: 47-63
(1980).
Srcebny, L.M.: Sugar availability, sugar consumption and dental caries. Commu
nity Dent, oral Epidemiol. 10: 1-7 (1982).
Takeuchi, M.: On the epidemiological principles in dental caries attack. Bull. Tokyo
dent. Coll. 3: 96-111 (1962).
Third World Sugar Forecast. African Business (Jan. 1981).
Viton, A.; Pignalosa, F.: Trends and prospects of world sugar consumption. Part I.
Mon. Bull, agric. Econ. Statist. 9: 1-10 (1960).
Viton. A.: Pignalosa, F.: Trends and prospects of world sugar consumption. Part II.
Mon. Bull, agric. Econ. Statist. 9: 1-12 (1960).
Walker, A.R.P.; Dison, E.; Walker, B.F.; Segal, A.F.: Contrasting patterns of
caries profile and dental treatment in pupils of 16-18 years in South African ethnic
groups. Community Dent, oral Epidemiol. 10: 69-73 (1982).
F
Dr. Aubrey Sheil
The London Hos;'
I
I
I
r
1
I
I
38
Dental Caries in Underdeveloped Countries
p. 234 (Souvenir Press,
31
32
i prevalence in secondary
3).
vey of adults in Peninsular
33
34
Ha! health survey of school
39
World Development Movement: Sugar: crisis in the Third World (London 1980).
WHO; Oral health global indicator for 2000. Dental caries levels at 12 years (WHO
Oral Health Unit, Geneva 1982).
WHO: Prevention of coronary heart disease. Tech. Rep. Ser. 678 (WHO Geneva
1982).
Yassin, I.; Low, T.: Caries prevalence in different racial groups of schoolchildren
in West Malaysia. Commun. Dent, oral Epidemiol. 3: 179-183 (1975).
:ss. Int. deni. J., bond. 32:
in Addis Ababa, Ethiopia.
prevalence in Tongatapu.
Kreshover, McClure, En>s. Adv. Sei., Washington
diseases - differences in
i
: in Norway (Fabritius &
(1983).
d needs: pilot studies in
‘rmanent teeth during a
on per person in Japan.
I
Comments on Jackson’s
i
of dental caries and the
oulh Pacific. N.Z. dent.
f
i
sense and the treatment
. Stom. Trop. 3: 47-63
L
dental caries. Connnu-
♦
>
lies attack. Bull. Tokyo
1
ir consumption. Part I.
•consumption. Part II.
onlrasting patterns of
i South African ethnic
I
I
I
I
Dr. Aubrey Sheiham, Department of Community Dental Health,
The London Hospital Medical College, Turner Street, London El 2AD (England)
J
I
r
1
i
I-
11-117
4 •
Routine Medical Management of Acute
Myocardial Infarction
Lessons From Overviews of Recent Randomized
Controlled Trials
Salim Yusuf, MB, DPhil, MRCP, Peter Sleight, DM, FRCP,
Peter Held, MD, PhD, and Stephen McMahon, PhD, MPH
In recent years, several large randomized trials have clarified the role of various interventions
in acute myocardial infarction. There is clear evidence that thrombolytic therapy, aspirin, and
0-blockers reduce mortality. Both aspirin and 0-blockers also reduce reinfarction and stroke.
Of the thrombolytic agents, comparative trials have established that tissue plasminogen
activator and streptokinase have similar effects on mortality, morbidity, and left ventricular
function. There appears to be an increased risk of cerebral hemorrhage with tissue plasminogen
activator. The benefits of heparin in copjunction with aspirin and a thrombolytic agent are
unclear and, at best, are likely to be modest Heparin increases the risk of hemorrhagic
complications twofold. Although trials of vasodilators conducted before the widespread use of
thrombolytic therapy and aspirin have been promising, newer trials are needed to evaluate their
effects among patients receiving these agents. The aggregate of all trials of the routine use of
calcium antagonists or antiarrhythmic agents indicates that these agents dojiot improve
survival. (Circulation 1990;82(suppl
11-134)
uring the last decade, emphasis on the man
agement of patients with acute myocardial
infarction (AMI) has shifted from ap
proaches focused largely on the prevention or man
agement of malignant arrhythmia to strategies
aimed at reducing the extent of infarction, prevent
ing reinfarction, and promoting myocardial healing.
This change in emphasis has been due, in part, to
better understanding of the factors influencing the
course of experimental and clinical infarction and,
in part, to our increasing ability to evaluate reliably
the benefit-risk ratio of new interventions in large
well-designed randomized clinical trials. This arti
cle reviews pharmacological interventions in AMI
and does not review the trials of percutaneous
transluminal coronary angioplasty (PTCA). Despite
its theoretical appeal, all the trials of routine PTCA
have consistently failed to demonstrate benefit; in
From the Clinical Trials Branch, Division of Epidemiology and
Clinical Applications, National Heart, Lung, and Blood Institute
Bethesda, Md (S.Y., P.H.), the Cardiac Department, John Rad
cliffe Hospital, Oxford, England (P.S.), and the Clinical Trials
Research Unit, Department of Medicine, University of Aucidand,
New Zealand (P.S.).
Address for correspondence: Salim Yusuf, MB, DPhil, MRCP,
Clinical Trials Branch, Division of Epidemiology and Clinical
Applications, National Heart, Lung, and Blood Institute,
Bethesda, MD 20892.
\
fact, there is a trend toward increased mortality and
morbidity in several trials of routine PTCA.1-3 The
results of these trials have been reviewed by Ryan4 in
this supplement.
Rationale for Interventions in Acute
Myocardial Infarction
Deaths in patients after AMI are usually due to
one or more of the following causes: 1) Large infarcts
that lead to deteriorating pump function and second
ary arrhythmias, 2) primary or drug-induced ventric
ular tachyarrhythmias or asystole, 3) cardiac rupture,
4) reinfarction, and 5) infarct expansion and ventric
ular dilatation.
Deaths after AMI might therefore be reduced by
any one of a number of potential interventions. The
size of an infarct can be reduced by improving the
balance between oxygen supply and demand through
increasing myocardial blood flow (dissolving an
obstructing clot or improving collateral blood flow)
or by reducing oxygen demand by reducing cardiac
work. Antiarrhythmic drugs could be used to
decrease the risk of death due to arrhythmias
although these drugs may themselves confer an
increased risk of asystole and heart block. Some
antiarrhythmic agents are known to have a negative
inotropic effect and may even exacerbate arrhyth
mias. Cardiac rupture and arrhythmias might be
11-118
Supplement II
Circulation
Vol 82, No 3, September 1990
prevented by reducing myocardial wall stress. Rein
farction could be prevented by preventing reocclusion or by reducing oxygen demand. Infarct expan
sion and ventricular dUatation may be prevented by
reductions in afterioad and preload or by promotion
of infarct healing by preserving blood supply to the
infarcted area. In this article, we review the data
from randomized trials of a number of commonly
available interventions and discuss their results in the
context of their mechanisms of action.
In the last few decades, there has been a growing
acceptance of the randomized controlled trial as the
preferred method to evaluate most treatments. It has
also become apparent that most successful or adverse
treatments in cardiovascular diseases typically have
only moderately sized effects (10%, 15%, or 20%) on
such major outcomes as death or myocardial infarc
tion. To detect such differences reliably (10% mor
tality reduced to 9% or 8.5%), studies with a few
thousand events are usually required. Individual
small trials of a few hundred patients often show
misleading and conflicting results. When only one of
a number of similar trials testing a treatment shows
statistical significance while others are unpromising
or equivocal, the reader should not base judgment on
a single “positive” trial. An unbiased and more
representative estimate of the effect of treatment can
be obtained by a formal overview (or meta-analysis)
of all relevant trials. This approach requires a metic
ulous search for the relevant data on all randomized
patients in ail trials, careful and unbiased extraction
of data, and use of valid statistical techniques that
preserve the randomized comparisons. Such analyses
have sometimes found convincing evidence of an
effect of treatment or the lack of effect, even when
the separate trials have appeared to be contradictory.
The significance levels from a trial or from an over
view should be interpreted cautiously unless they are
dramatic (say, p<0.001). Details of the general and
statistical methods and the advantages and limita
tions of meta-analyses are outlined elsewhere.5
Thrombolytic Therapy
Among patients with the early clinical signs sug
gestive of acute transmural MI, about 80% have
thrombotic occlusion of the coronary arteries.6-7
About three fourths of these occlusions can be
dissolved by intracoronary infusion of a thrombolytic
agent.7 If the obstruction is cleared early enough,
some salvage of ischemic myocardium, and, hence,
improvement in ventricular function is likely. Only
about 1,000 patients have been studied in all trials of
intracoronary thrombolysis.8 These trials appear
superficially conflicting, but pooling these results
suggests a non-significant 18% lower mortality
among the treatment group.
Even if intracoronary thrombolysis were effective, its
widespread use would be impractical and expensive.
The delays caused by the need for angiography may
further limit its value. Most efforts at thrombolysis have
therefore focused on rapid intravenous infusion of a
high dose of streptokinase (SK) or, more recently, of
the second-generation agents such as tissue-plasmino
gen activator (t-PA) or anisoylated plasminogen
streptokinase activator complex (APSAC).
In addition to salvaging ischemic myocardium,
thrombolytic agents may reduce mortality by a num
ber of additional mechanisms. For example, in exper
imental infarction, reopening of the ligated coronary
artery several hours after myocardial salvage is pos
sible, prevents infarct expansion, and promotes
healing.9 SK and APSAC markedly reduce circulat
ing fibrinogen levels.10 This reduces plasma viscosity
and blood pressure.11 These mechanisms may
increase myocardial blood flow through collaterals
and may also decrease myocardial oxygen demand. In
addition, circulation of anticoagulant fibrin degrada
tion products may prevent rethrombosis.
Effect on Mortality
Although the newer agents appear to be more
effective than SK for rapidly recanalizing coronary
thrombi,12-13 their effects on mortality and major
morbidity have been evaluated much less extensively
than for SK. During the past 25 years, at least 31
randomized trials involving about 41,000 patients
with suspected AMI have compared the effects of
intravenous SK with those of standard treatment. In
1985, we reviewed data from 20 of the earlier trials,
which included about 5,300 patients? These analyses
showed that treatment reduced mortality by 24%
(95% confidence interval [CI] ’from -34% to -12%,
p<0.001). In addition, these analyses suggested that
the reduction in mortality occurred regardless of
routine anticoagulant use and occurred even among
patients treated 6-12 hours and 12-24 hours after
the onset of symptoms. Subsequently, two very large
trials, Gruppo Italiano per lo Studio della Streptochinasi nellTnfarto Miocardico (GISSI)14 and the Sec
ond International Study of Infarct Survival (ISIS2),15 each demonstrated significant reductions in
mortality of about 20-25% (at 21 days, 628 deaths
among 5,860 patients in the SK group compared with
758 deaths in 5,852 controls, p<0.001 in GISSI; and
at 35 days, 791 deaths among 8,592 treated patients
compared with 1,029 deaths among 8,595 controls,
p<0.001 in ISIS-2; Figure 1). In addition, the
collective data available from several small or mod
erately sized trials show a significant reduction in
mortality.16-24 An overview of all the available
studies indicates that early (^2-5-week) mortality
was 12.8% (2,614 of 20,371) in the control group
and only 10.0% (2,062 of 20,634) in the SK group.
The estimated 24% reduction in the risk of death
has a relatively narrow 95% CI (-20% to -29%)
and is highly significant (p<0.0001). Long-term
follow-up of patients entering the two largest trials
demonstrates that the short-term reduction in mor
tality is maintained for at least about 1-2 years.15 25
Recently, data on the effects of t-PA and APSAC
on mortality have become available. The AngloScandinavian Study of Early Thrombolysis
♦
Yusuf et al Routine Medical Management of AMI
4 '
500-
Placabo infusion and taMata:
568/4300 (13J*»
-X*
461/4296(10.7*1
A^irin:
Straptotunaw:
448/4300 (10.4*1
I"
; Soo
’s .
Straptokinaaa and AapMn:
343/4292 (8.0*1
200-
100-
o-io
7
14
21
28
36
Day* from randomisation
FIGURE 1. Vascular mortality curves at 5 weeks in ISIS-2.
There were similar numbers of nonvascular deaths in the
streptokinase group compared with placebo but fewer nonvas
cular deaths among those allocated to aspirin. Since the
number of nonvascular deaths are very few (about 1%), the
data for total mortality are essentially unchanged. See text for
explanation of trial name abbreviation. (Reprinted with per
mission from Reference 15.)
(ASSET),26 a trial of 5,000 patients, studied the
effects of intravenous t-PA or placebo given within 5
hours of onset of pain. All patients received intrave
nous heparin for over 24 hours. In this study, t-PA
reduced mortality by 26% (95% CI, -11% to -39%;
p<0.001). A similar trend has been observed in an
overview of seven small trials of t-PA in a total of
1,700 patients (33% reduction; 95% CI, -54% to
-3%).27-33 A British study of APSAC (APSAC In
Myocardial infarction Study [AIMS]) given within 6
hours was terminated prematurely, after randomiz
ing 1,200 patients, because of an apparent 50%
reduction in mortality (pcO.OOl).34 Combining data
from all available APSAC trials involving a total of
about 2,000 patients suggests a 52% reduction in
mortality (95% CI, -33% to -65%;p<0.001).35 The
available data (Table 1) from the trials of t-PA and
APSAC should be interpreted cautiously and should
not be used to assess the relative efficacy of the
agents because the apparent effect sizes observed
with SK, t-PA, and APSAC in different trials might
be influenced by differences in patient selection,
timing of treatment, and co-interventions. The effect
of patient selection is illustrated by the relatively
large effect of similar magnitude in the subset of
patients in ISIS-2 that were selected by the entry
criteria for the AIMS trial (Table 1). Moreover, the
Cis of the overall estimates with each agent overlap,
such that it would be prudent to await the results of
trials that directly compare these agents. (For exam
ple, ISIS-3 will compare SK, t-PA, and APSAC, and
preliminary data from GISSI-2 comparing t-PA with
II-119
SK will be discussed later.) Thus, at present, the
available data are more useful in showing that throm
bolysis is effective, rather than providing reliable
information as to which agent, if any, is most effective.
Effect on Left Ventricular Function
Table 2 summarizes the data from 20 randomized
trials of intravenous SK,161719"24-36 t-PA,27 29-32 and
APSAC37-41 compared with placebo regarding the
effects of early treatment on left ventricular ejection
fraction measured by contrast arijgiograms. In most
trials, an improvement in left ventricular ejection
fraction of about 2-6% (absolute units) has been
observed with each agent. Only one small study
examined the effects of intracoronary SK on left
ventricular ejection fraction when treatment was
started late.46 This study reported a significant
improvement in left ventricular ejection fraction in
patients treated with intracoronary SK who had
preexisting collaterals. However, the results of this
study should be interpreted cautiously until confir
matory evidence from other studies is obtained. t-PA
has been directly compared with SK in four
trials42’43-45-47 and with urokinase in one trial.44 In
none of these trials was ejection fraction significantly
different in patients treated with t-PA compared with
those treated with SK or urokinase. Of these studies,
the most data are available from the Italian compo
nent of the second GISSI trial, which included more
than 12,000 patients.47 There was no difference in the
proportion of patients who had an ejection fraction
less than 35%, who developed left ventricular failure,
or who had a QRS score greater than 10 (an indirect
electrocardiographic measure of the extent of infarc
tion). These data conclusively prove that there is no
appreciable difference in the effects of these agents
on ejection fraction.
Expanding Indications for Fibrinolytic Therapy
There is consensus that treatment with any one of
the available fibrinolytic agents in patients presenting
within 6 hours of symptom onset, with ST-segment
elevation on the electrocardiogram, and less than 70
years of age will reduce mortality by about 25-30%.
However, such patients represent only about 2030% of patients presenting with suspected MI.26 If
thrombolytic therapy can be shown to have a similar
or even a smaller (e.g., 15-20% reduction in the risk
of death) but worthwhile net benefit in other catego
ries of patients (e.g., those presenting late or in older
high-risk patients), then the clinical and public health
value of such treatment would be considerably
greater. In this context, it should be emphasized that
trials designed to assess the effects of a treatment in
the overall population rarely have adequate power to
detect a benefit in every subgroup that really benefits.
Moreover, the larger the number of subgroups exam
ined, the greater the likelihood of finding spurious
effects in one or the other subgroup simply by
chance. Therefore, it is usually worth placing greater
reliance on the overall results of the trial, and
t
Circulation
11-120
Supplement II
Tabli 1.
Effect of Intravenom Thromboiytfc Agents on Short-term Mortality When Administered Within 6 Hours of Onset of Symptoms
Zo/ 82, Na 3, September 1990
Deaths (n)/patients (n)
Reference
Active
Control
105/622
495/4,865
471/5,350
623/4,878
648/5,360
113/1,730
1,184/12567
(9.4%)
Odds
ratio
O-E
V
44.1
247.4
0.70
-9.8
-63.2
-88.0
131/1,525
0.72
-18J
55.3
1317/12327.
0.74
-179.5
597.3
Streptokinase
Yusuf et al®
GISSI’4
ISIS-213
Nir\e small to
moderately sized
trials16-24
Subtotal
streptokinase
ji
115/564
0.80
0.77
250.5
(12.3%)
95% confidence interval of 0.68 to 0.80, p<0.0001
t-PA
ASSET26
Seven small trials 27-33
Subtotal t-PA
182/251626
48/874
245/2,495
70/870
230/3,390
(6.8%)
315/3,365
(9.4%)
0.72
0.67
0.71
-32.4
97.7
-11.2
-43.6
27.5
125.5
95% confidence interval of 039 to 0.84, p<0.001
I;
■
APSAC
AIMS34
11 small trials33
Subtotal APSAC
40/625
77/630
0.50
-183
265
33/583
55/536
73/1,208
(6.0%)
132/1,166
(11.3%)
0.55
0.52
-12.1
-30.4
20.2
46.7
-63.3
111.6
-253.5
770.0
95% confidence interval of 0.39 to 0.69, p<0.001
ISIS-2 “AIMS”
Cohort*
180/2,745
(6.6%)
310/2,783
(11.1%)
0.57
95% confidence interval of 0.47 to 0.68
Total all agents
(streptokinase+t-PA
+APSAC)
1,487/17,165
(8.7%)
1,964/16,858
(11.7%)
95% confidence interval of 0.67 to 0.77, p<0.0001
O-E, observed minus expected; V, variance; t-PA, tissue plasminogen activator; APSAC, anisoylated plasminogen-streptokinase
activator complex. See text for explanation of abbreviations of trial names.
‘Consists of patients who presented with ST-segment elevation <6 hours after onset of symptoms and who were <75 years old.
accepting that this result tends to provide the best
estimate of the direction of the effect within each
subgroup, rather than trying to scrutinize the results
of each subgroup separately. In the next few sections,
we will examine the effects of treatment on a number
of important subgroups and demonstrate the general
consistency of the data.
Time from onset of pain. An overview of the ran
domized trials conducted before 1984 demonstrated
that intravenous SK reduced mortality by about 25%
and that the reduction in mortality observed was
approximately similar among patients starting treat
ment within 6 hours, 6-12 hours, or 12-24 hours
after onset of symptoms.8 This conclusion seemed
controversial, especially since GISSI demonstrated
steeply diminishing benefit with increasing delay
from onset of pain, with little apparent benefit after
6 hours.14 However, GISSI randomized only about
2,000 patients after 6 hours (17% of all patients
randomized), so that the statistical power to detect
even a 20% difference after 6 hours was low, and the
95% Cis of the actual result included fairly sizable
benefits (e.g., a 15-20% reduction). The ISIS-2
study15 tested the effect of late treatment by deliber
ately randomizing about 10,000 patients after 4 hours
(58% of all patients randomized) and observed ben
efit in patients treated both early and late. However,
the benefit decreased with increasing delay to treat
ment from the onset of symptoms (odds reductions of
35±6% [mean±SD] at 0-4 hours [p<0.0001],
16±7% [p=0.01] at 5-12 hours, and 21±12%
[p=0.04] at 12-24 hours). The mortality reduction
I
Yusuf et al
Routine Medical Management of AMI
11-121
Table 2. Left Ventricular Ejection Fraction After Intravenom Thrombolytic Therapy
Ejection fraction (%)
Patients
randomized (n)
Patients with
angiograms (n)
Time window
(hr)
Active
Control
A
Streptokinase vs. control
Heikkila et al22
Durand et al24
White et al17
Schreiber et al21
ISAM16
Kennedy et al19
Wisenberg et al23
Binaghi et ai36
Olson et al20
?
64
219
38
1,741
368
66
251
52
130
45
194
24
848
170
59
206
46
<3
<3
<4
<5
<6
<6
<6
<12
<12
59
57
55
47
57
54
54
57
44
49
49
50
42
54
51
47
54
43
+ 10*
+8*
+5*||
+5
+3t
+3
+7
+3
+ 15
t-PA vs. control
O’Rourke et al30
Holmberg et al32
Armstrong et al33
Guerci et al27
Australian Heart Foundation29
Van der Werf et al31
145
352
118
138
144
721
126
295
105
117
103
577
<2Vi
<3
<3%
<4
<4
<5
61
59
54
53
58
51
54
55
48
46
52
49
+7tU
+4*
+6*
+6*
+2*
APSAC vs. control
Been et al37
Buchalter et al38
Meinertz et al39**
Taeymans and Mateme40**
Bassand et al41**
32
43
313
82
230
22
<3
<3
<4
<4
<5
41
35
55
55
52
33
29
56
54
47
+8
+6
-lit
+1
+5t
Reference
Comparison of agents
White et al42
PAIMS43
Neuhaus et al44
Sheehan et al45
GISSI-247
7
256
68
?
I
t-PA
58
55
55
50
SKJUK
58
0
53
+m
55
0
49
+1
<6
Similar
055
A, Active minus control ejection fraction; t-PA tissue plasminogen activator; APSAC, anisoylated plasminogen-streptokinase activator
UK, urokmasc.
urokinase. See text for explanation of abbreviations of trial names
complex; SK, streptokinase; UK
*p<0.05, tp<0.01, Xp<0.001.
§ Radionuclide left ventricular ejection fraction.
|| Data for all patients randomized were derived from the data on those with and without previous myocardial infarction provided
separately in the article.
^Ejection fraction was also measured using radionuclide angiography. There was a 4% higher ejection fraction in treated patients
270
171
246
290
12,381
240
152
239
145
?
<3
<3
<6
•’Control group received heparin.
ttMean ejection fraction for each group derived from data provided in article by site of myocardial infarction
56%tn7heSet,-Pl'Joeunp^mpaJed^h^ Hthe'sK^ur3'’'’10 ejeC,i°n
VentnCU‘ar ejeC,iO" fraC,i°B
- action
for patients entered between 6 and 24 hours was
highly significant overall (18±7%, p=0.01) and was
also observed among patients with initial ST-segment
elevation (22±10%, p<0.025). The mortality data
from all trials of intravenous SK in which treatment
was given later than 6 hours are summarized in Table
3 and indicate that the combined results of the old
trials, GISSI, and the ISIS-2 pilot are almost identi
cal to the ISIS-2 results (17±5%, p<0.001).
The evidence for benefit in patients entered late is
reinforced by the data from the APSAC and t-PA
trials. Although none of the trials of intravenous t-PA
or APSAC randomized patients 6 hours after the
onset of pain, the “slope” relating mortality reduc
tion to treatment delay within the early period pro
vides clues that later treatment might still be benefiC^’ F°r example, if a steeply diminishing effect were
observed within 4j
hours, it would be logical to
I
11-122
Supplement II
Table 3.
Short-term Mortality in Patients Treated >6 Hours From Onset of Symptoms With Intravenous Thrombolytic Agents
Circulation
Time
window (hr)
Reference
Vol 82, No 3, September 1990
Deaths (n)/patients (n)
>
SK
Control
Odds
ratio
109/712
133/985
19/146
261/1,843
154/724
0.67
134/961
9/67
297/1,752
318/3,241
579/5,084
375/3,235
672/4,987
O-E
V
P
-19.5
-2.1
-0.2
-21.8
51.1
57.6
5.3
114.0
0.01
0.96
0.96
0.83
0.83
0.83
-28.8
-50.6
155.0
269.0
0.01
0.001
Streptokinase
>
Yusuf et al®
GISSI14
ISIS-2 pilot18
Subtotal
6-24
-
6-12
6-24
ISIS-2^
6-24
TOTAL
>6
>
NS
NS
0.05
Typical odds ratio of 0.83; 95% confidence interval of 0.73 to 0.93. .
No data are available for tissue plasminogen activator or anisoylated plasminogen-streptokinase activator complex.
Note that both ISIS-2 and the pool of previous trials each indicate a 17% reduction in mortality, so that these two sets of data reinforce
each other.
See text for explanation of abbreviations of trial names.
i
■
assume that after 8 or 9 hours, there could be little
benefit. On the other hand, if there is no such slope
or only a gradually diminishing effect in patients
treated within 6 hours, it would be reasonable to
expect that treatment a few hours later might provide
some benefit. Therefore, we examined the effects of
treatment by time in the two largest trials (other than
those in Table 3). In ASSET, t-PA reduced mortality
by 26% when given within 3 hours (81 of 992, or
8.1%, vs. 107 of 979, or 10.9%) and by 24% when
given at 3-5 hours (99 of 1,504, or 6.5%, vs. 129 of
1,488, or S.6%).26 In AIMS, APSAC reduced short
term mortality to a similar extent when given within
4 hours (18 of 334, or 5.4%, vs. 30 of 326, or 9.2%;
41% risk reduction) and when given 4-6 hours (14 of
168, or 8.3%, vs. 31 of 176, or 17.6%; 53% risk
REFZT1ME (hl
NO. PLATHS/FATM MTS
Acw v Corttroi
A. Yuul W M 86
0 80
04
106/822 » 115/884
6-12
86/M8 w 70/341
,0.82
12-24
53/3^ v 80/421
6. GISSI
278ZB18 » 388^071
0-3
,0.61
>34
217/1848 « 2S4/18Q0
,0J8
>8-12
133/888 v 134/881
C. ISIS-2
0-3
207/2881 v 311/2587
—»2i-
>3-6
284/7788 v 337/2803
,082
>6-24
320/3242 v 381/3238
0 ASSET
81'982 v 107/878
0-3
)0.74
>3-8
98/1504 v 128/1488
E AIMS
^.57
0-4
18/334 « 30/326
42±-----
>4-8
02
0.4
0.6
14/188 v 31/178
08
1.0
17
1.4
ODOS RATIO ANO 96% CONFIDENCE INTERVAL
FIGURE 2. Chart showing mortality reduction (odds ratio
with 95% confidence interval) in four large recent trials of
thrombolytic agents and the overview of old trials subdivided
by the time to treatment from onset of symptoms. See text for
explanation of abbreviations of trial names.
reduction).33 These data from ASSET and AIMS
show little evidence of a slope within 6 hours and
strongly imply, therefore, that treatment even after 6
hours is likely to reduce mortality (Figure 2). This is
consistent with the data from the intravenous SK
trials, which provide clear evidence that treatment
with a thrombolytic agent more than 6 hours after the
onset of symptoms will lead to a worthwhile reduc
tion in mortality. Although a few small trials like the
Western Washington trial19 or the European Coop
erative trial31 appear to contradict this, the number
of deaths in these studies were too few to reliably
assess the overall benefits of treatment, let alone the
effects in various subgroups.
Although in experimental infarction, myocardial
salvage may be possible only if reperfusion is
achieved within a few hours of coronary ligation,
there may be important dissimilarities in human
infarction, so that benefit may be achieved by a
number of additional mechanisms: 1) Late reperfu
sion may prevent infarct expansion and promote
healing.9 2) Coronary occlusion has been shown to be
intermittent in humans; this may prolong the period
of myocardial viability.48 3) In patients with collater
als, it is possible that the period of myocardial
viability is prolonged. 4) The onset of symptoms in
humans is difficult to time, and it is possible that a
period of subtotal obstruction that causes ischemia
and severe pain (unstable angina) may precede total
obstruction and infarction. (In the ISIS-3 study,
although 70% of patients were admitted >3 hours
after onset of pain, 94% of patients were entered
within 3 hours of the cessation of pain, indicating that
most patients had repeated episodes of pain and,
presumably, ischemia.)
Age of the patient. In all four large trials, older
patients still benefitted from thrombolysis. These
data are summarized in Table 4. Although ASSET
and AIMS included only patients less than 75 years
old, both the relative and absolute risk reductions
were greater in older patients. Moreover, ISIS-2
randomized about 3,400 patients older than 70 years
F
i
Yusuf et al
4
Routine Medical Management of AMI
11-123
Table 4. Effect of Thrombolytic Therapy on Short-term Mortality by Age Groups in Four Large Randomized Trials
Reference/
Deaths (n)/patients (n)
age group (yr)______ Active
Control
Streptokinase
GISSI
S65
291/3,784
217/3,824
65-75
>75
ISIS-2
<60
60-69
2>70
t-PA
ASSET
s55
56-65
66-75
APSAC
AIMS
<65
>65
**
Odds
ratio
Deaths (n) prevented by
treating 100 patients
0.72
2
0.90
1.5
I
0.82
4.2
0.71
1.6
0.70
3.8
0.81
3.3
0.87
0.6
0.81
1.4
(5.7%)
240/1,444
(16.6%)
171/592
(28.9%)
(7.7%)
261/1,442
(18.1%)
206/623
(33.1%)
162/3,864
(4.2%)
320/3,033
(10.6%)
309/1,695
(18.2%)
224/3,856
(5.8%)
435/3,023
(14.4%)
370/1,716
(21.6%)
29/748
(3.8%)
63/963
(6.5%)
90/827
(10.8%)
33/745
(4.4%)
71/896
(7.9%)
140/852
(16.4%)
0.62
5.5
21/405
(5.2%)
11/90
(12.2%)
35/411
0.59
(8:5%)
26/86
0.34
(30,2%)____________
3.3
18*
e^iri^HXZer^^S^
a.g'an.dth"e “ benefit
”
lhese trial8. However, the absolute numbers of lives saved increases substantially with increasing age ' “ ‘
aniS°ylated
activator compiex. See text for
in in“tin^
and observed a highly significant reduction in mor
tality among them (309 of 1,695, or 18.2%, vs. 370 of
1,716, or 21.6%;p<0.01). In this trial, the benefits of
SK were additive to those of aspirin (in the whole
population and among the elderly), so that with their
combination, the absolute mortality reduction was
substantial (135 of 854, or 15.8%, vs. 203 of 852, or
23.8%; p<0.001 among those >70 years; Figure 3).
Other subgroups. Several studies have shown reduc
tions or improvement in left ventricular function or
mortality in patients with anterior or inferior MI, those
with and without previous MI, and those with and
without ST-segment elevation.15-26^ Although it is pos
sible that the relative and absolute risk reductions in
certam subgroups of patients, such as those with an
inferior MI or those without ST-segment elevation, may
be somewhat smaller, it is still likely that these patients
may experience a worthwhile benefit from treatment.
tO **<,Uite Sma11' “P8^in AIMS'
should >* ‘aken
Therefore, it appears that the categories of patients
that might benefit from fibrinolytic therapy are fairly
broad and probably include about 70-80% of patients
presenting with suspected AMI. Several trials (e.g.,
Estudio Miocardio Estreptoquinasa Republic Ameri
cas Sul [EMERAS], Late Assessment of Thrombolytic
Therapy [LATE], and ISIS-3) are currently seeking
further evidence of the value of treatment in a number
of subgroups in which the effects of treatment are less
well accepted (e.g., patients presenting 6-24 hours
after onset of symptoms or with no ST-segment eleva
tion on the electrocardiogram.
Adverse Effects of Fibrinolytic Therapy
Reocclusion and reinfarction. In the recent trials of
short-duration, high-dose infusions of SK, lysis of
intracoronary thrombus has been observed to pro
duce an excess risk of reinfarction. In cases where
11-124
I
30
Supplement II Circulation
<80 YRS
8MB YRS
Vol 82, No 3, SepterTlber 1990
RHYRS ;
*
Ia 20
2
J
I
g
io ■
0
FIGURE 3. Bar graph showing percent mortality reduction by
streptokinase (S), aspirin (A), and their combination in ISIS-2
by different age groups (yrs, years). Note that the absolute
numbers of lives saved by any one of the three treatments
increase substantially with increasing patient age. P, placebo.
II■r
treatment was prolonged for 24-48 hours (as in the
old trials), significantly fewer patients suffered reinfarction, whether or not anticoagulants were rou
tinely used.8 These data, however, do not indicate
that anticoagulants are without value. Data on rein
farction are available from seven of the eight trials of
t-PA. Surprisingly, these data indicate only a small
excess in reinfarction (321 of 3,317 among treated
patients compared with 299 of 3,298 among the
patients receiving placebo; 9.7% vs. 9.1%). No data
on reinfarction are available from the trials of
APSAC. In ISIS-2, which employed a 2x2 factorial
design (one fourth of patients received SK; one
fourth, aspirin; one fourth, both; and one fourth,
neither), aspirin prevented the excess reinfarction
observed with SK (reinfarction rates: placebo, 3%;
aspirin, 2%; SK, 4%; and aspirin+SK, 2%).15 In the
Thrombolysis in Myocardial Infarction (TIMI)-IIb
trial, immediate administration of /3-blockers was
found to reduce the incidence of reinfarction among
patients treated with t=PA (6-day reinfarction: 2.3%
among 696 patients allocated to immediate P'
blockade compared with 4.5% among 694 patients
allocated to receive /3-blockers after the sixth day;
p<0.02).2 No other intervention has been demon
strated to reduce the risk of reinfarction after throm
bolytic therapy. In particular, several trials of imme
diate (at admission) PTCA or deferred PTCA (1848 hours after thrombolytic therapy) versus usual
care have each shown a trend toward excess mortality
and excess reinfarction in those randomized to an
“invasive” strategy.1-2 Although heparin has been
routinely used after a thrombolytic agent in some
trials, little controlled data exist to support its use in
conjunction with thrombolytic therapy and aspirin.
Preliminary data from GISSI-2 indicate little additive
benefit from the addition of heparin to a regimen
consisting of a thrombolytic agent, aspirin, and /3-
blockers. (See also a following section on heparin.47)
ISIS-3 is further evaluating this question.
Hemorrhage. In ISIS-2, minor bleeding occurred
more commonly in the SK group (3.5% vs. 1.0%).is
There was also a small excess in the number of
patients with hemorrhage requiring transfusion
(0.5% vs. 0.2%). The excess in bleeding was unre
lated to the use of aspirin but was closely related to
the use of heparin (absolute excesses in minor and
major hemorrhagic episodes were 5.3% and 0.7% in
the SK and control groups, resjiectively, with planned
intravenous heparin; 2.6% and 0.4% with planned
subcutaneous heparin; and 1.5% and 0.0% with no
heparin use planned; also see the section on hep
arin). In ASSET, in which all patients received
heparin for 21 hours, 6.3% of patients given t-PA and
0.8% of patients given placebo had a minor bleeding
episode.26 The proportion of patients developing a
major bleeding episode was 1.4% and 0.4%, respec
tively. The incidence of bleeding in the various trials
should not be used to compare the effects of the
different agents because of differences between stud
ies in definitions and ancillary drug use. Of note, no
particular subgroup (e.g., the elderly) was at higher
risk of suffering episodes of major bleeding in the
treatment group compared with controls in ISIS-2.
Stroke. In ISIS-2,15 GISSI,14 and ASSET,25 there
was no overall excess in stroke. However, in all these
trials, there was a significant excess of early and
presumed hemorrhagic strokes, which was balanced
by a similar decrease in late, presumably thrombotic
strokes. No excess in stroke was observed among
elderly patients treated with SK compared with those
allocated to the control group in ISIS-2.
Hypotension. In ISIS-2, there was an excess of
hypotension and/or bradycardia (10% SK vs. 2%
placebo) and allergic reactions (4.4% vs. 0.9%).15
None of the allergic reactions were considered to be
due to anaphylactic shock. The bradycardia and
hypotension may be the result of production of
vasoactive kinins by the less-specific SK-based drugs
and is therefore likely to also be seen with APSAC.
This may not necessarily be harmful since in ISIS-2,
there was no excess mortality in patients with this
condition. The incidence was not reduced by the use
of prophylactic steroids.15 Similar results have been
reported from GISSI.14 The incidence of hypoten
sion, bradycardia, and allergic reactions appears to
be lower with t-PA.42-47
Cardiac rupture and arrhythmias. In almost all SK
trials, there appears to be more deaths among the
treated patients than controls during the first day.
For example, in GISSI, there were 120 deaths in
those allocated to receive SK compared with 76
deaths among those allocated to receive placebo
within 6 hours of onset of symptoms.48 Some deaths
were due to arrhythmias, but a high proportion was
reported to be due to electromechanical dissociation,
raising the possibility that treatment might cause
myocardial hemorrhage and cardiac rupture.
Detailed analyses from ISIS-2, ASSET, and AIMS
i
c
4
Yusuf et al
are not yet available. In ISIS-2, there was a similar
excess of deaths in the SK group in the first 24-36
hours. However, data from the discharge forms sug
gest that the numbers of patients who suffered car
diac rupture overall were similar in the two groups.
In all four major trials“.15.26.34 of thrombolytic agents,
there was no excess in the incidence of ventricular
fibrillation or cardiac arrest. On the contrary, in at
least two trials, there was a significant reduction in
nonfatal cardiac arrests.
Comparison of thrombolytic agents. Several studies
have directly compared the effects of “clot-specific”
thrombolytic agents (e.g.; t-PA, pro-urokinase) with
the nonspecific agents (e.g.; SK, APSAC, or uroki
nase). In most studies, the proportion of patients
demonstrating recanalization or patency 90 minutes
after initiation of therapy was greater with the former
class of agents.i2-13’50 However, angiograms per
formed at 24 hours or later did not reveal any
significant differences in patency.42.4350 In one study
comparing pro-urokinase with SK, while there was a
difference in patency at 60 minutes, there was little
difference at 90 minutes.50 In the TIMI study, the
differences in recanalization rates were more marked
when treatment was initiated after 4 hours after the
onset of symptoms, whereas with earlier treatment,
the differences were only modest.12 These data indi
cate that although clot-specific agents produce more
rapid thrombolysis, especially with “old” clots, these
differences narrow after about 90 minutes. The rele
vance of the early difference in recanalization to
mortality or ejection fraction has been assessed in
several studies.
There have been five randomized trials that com
pared the effects of t-PA with SK or urokinase on left
ventricular function.42-44 ^.47 jn none of the studies
was there a difference in left ventricular ejection
fraction. The GISSI-2 study,47 along with its interna
tional counterpart, randomized 20,749 patients in a
2x2 factorial design to receive t-PA alone, SK alone,
t-PA plus subcutaneous heparin (started 12 hours
after randomization), and SK plus subcutaneous
heparin. All patients presented within 6 hours of the
onset of pain and had ST-segment elevation. All
patients without contraindications received aspirin
and intravenous ^-blockers. There were 926 (8.9%)
deaths in the t-PA group compared with 887 (8.5%)
in the SK group. In the group receiving t-PA plus
heparin, there were 475 (9.2%) deaths compared
with 408 (7.9%) deaths among those receiving SK
plus subcutaneous heparin (started 12 hours after
randomization). While this difference in favor of SK
is statistically significant (Z=2.41,p<0.02), this result
may be due to the play of chance. However, it makes
it unlikely that t-PA is superior to SK, even if a more
intensive regimen of earlier and intravenous heparin
is used in all patients. This conclusion is indirectly
supported by 1) the similarity of effect on mortality of
t-PA and SK compared with placebo in separate
trials. (Most of these t-PA trials used an aggressive
regimen of intravenous heparin.) and 2) the similar
Routine Medical Management of AMI
11-125
ity of effect on left ventricular function in trials that
directly compared the agents against a background of
intensive intravenous heparin therapy.
In GISSI-2, the incidence of minor hemorrhagic
episodes was significantly higher with t-PA compared
with SK, whether or not heparin was used. In both
groups, the risk of these minor hemorrhagic episodes
was increased by the use of heparin. The incidence of
major hemorrhagic episodes was significantly higher
with SK, but this was largely due to an excess among
those given heparin (0.8%, t-PA-►heparin vs. 1.2%,
SK+ heparin). Among those not given heparin, there
was little difference in major hemorrhagic episodes
between 4he two groups (0.5%, t-PA alone vs. 0.6%,
SK alone). There was a significant excess in stroke
among those treated with t-PA (139 events, or
1.35%) compared with 99 events (0.95%) among
those treated with SK (p<0.01). The excess in stroke
in the t-PA group was due to those classified as
hemorrhagic or undefined (82 with t-PA vs. 51 with
SK), with no difference in the incidence of ischemic
strokes (57 in both groups). Heparin did not appear
to increase the risk of stroke in either group.
Therefore, it appears that both t-PA and SK have
similar effects on ejection fraction and mortality.
However, t-PA increases the risk of hemorrhagic
stroke. The higher incidence of major bleeding epi
sodes with SK is largely prevented by avoiding the
use of heparin.
Aspirin and Other Antiplatelet Agents
ISIS-2 randomized about 18,000 patients not only
to SK or placebo but also to relatively low-dose
aspirin (160 mg given on the day of MI and continued
for 4 weeks) or placebo in a 2x2 factorial design.
Mortality was reduced by 23% (804 of 8,587 in the
aspirin group compared with 1,016 of 8,600 in the
control group; 95% CI, -15% to -30%; p<0.0001).
In addition, there was a 44% reduction in nonfatal
MI (83 vs. 170; 95% CI, -41% to -61%; p<0.0001)
and a 46% reduction in nonfatal stroke (27 vs. 51;
95% CI, —26% to —65%; p<0.01). The combined
benefits of SK and aspirin yielded considerably
greater benefit than either treatment alone. Their
combined use resulted in a 42% reduction in mortal
ity (5-week mortality of 8.0% in those given SK and
aspirin, 10.7% in those given aspirin alone, 10.4% in
those given SK alone, and 13.2% in those given
placebo) without any excess in major bleeding com
plications (Figure 1). The effect of aspirin, unlike
that of SK, was independent of the delay from onset
of symptoms to time of treatment (odds reduction at
0-4, 5-12, and 13-24 hours: 25±7%, 21±7%, and
21 ±12%, respectively). Aspirin added to the benefit
of SK in all subgroups examined. In particular, in
patients older than 70 years among whom these drugs
might have been considered contraindicated, the
combination markedly reduced mortality (135 of 854
[15.8%] vs. 203 of 852 [23.8%], p<0.001) without
increasing the risk of hemorrhage or stroke (Figure
3). Thus, because older patients are at high risk of
11-126
I
J
Supplement n Circulation Vol 82, Na 3, September 1990
death, the absolute numbers of lives saved by treating
those older than 70 years is substantially greater than
treating younger patients (based ^on ISIS-2, the num
ber of deaths prevented for every 100 treated
patients less than 60 years old is 2.5; for those 60-69
years, 7; and for those older than 70 years, 8).
The Antiplatelet-Trialists Collaborative Group51
recently reviewed all the long-term trials of antiplatelet.agents in secondary prevention (including patients
with unstable angina and cerebrovascular disease).
Ten trials evaluated aspirin or other antiplatelet
agents started some months or years after MI and
continued for a year or two. Six trials evaluated
aspirin and dipyridamole, and two evaluated
sulfinpyrazone. In the 10 post-MI trials in a total of
18,441 patients, antiplatelet treatment reduced the
risk of vascular death by 13% (7.9% in the active
group compared with 8.8% in controls; p<0.01), of
nonfatal MI by 31% (5.5% and 7.4%, respectively;
p<0.0001), and of nonfatal stroke by 42% (1.1% and
1.9%, respectively; p<0.0001), with no effect on
nonvascular deaths (0.8% and 0.9%, respectively).
Overall, treatment reduced the risk of developing a
major vascular event by 25% (95% CI, -19% to
-31%; p<0.0001). This benefit was observed in all
subgroups examined (e.g., by age, sex, blood pres
sure, and presence or absence of diabetes). This
benefit in preventing major vascular events observed
in both the early and late post-MI trials is consistent
with the results of trials in patients with cerebrovas
cular diseases (22% risk reduction, p<0.0001) and
unstable angina (36% risk reduction, p<0.002).
The data from an overview of the trials suggest that
aspirin alone is just as effective as aspirin plus dipyr
idamole or sulfinpyrazone. The benefits of aspirin
appear to be similar in the trials that evaluated doses
of 160 mg/day, 300-325 mg/day, 0^900-1,500 mg/day.
Data from the UK trial51 of transient ischemic attacks
suggest that lower doses of aspirin were associated
with two thirds fewer gastrointestinal side effects but
were equally effective in reducing cardiovascular
events. In conclusion, it is reasonable to recommend
aspirin at 160-325 mg/day or 325 mg on alternate days
to patients with AMI, starting early, and continuing
for at least a year or two. The best dose is not precisely
known, but this should be considered a minor issue
compared with the decision to use aspirin.
Heparin
Until recently, there were only limited data on the
use of heparin in conjunction with thrombolytic
therapy and aspirin. Before the recent results from
ISIS-2 clearly indicated benefit from aspirin, many
investigators had routinely used intravenous heparin
during or after fibrinolytic therapy with the expecta
tion that reocclusion and reinfarction would be pre
vented. The pilot study to the ISIS-2 trial, in which
about 600 patients were randomized to heparin or
control, observed a trend toward less reinfarction
among treated patients but found no difference in
mortality.18 Similar effects on mortality and excess
reinfarction have been observed in the thrombolytic
trials in which anticoagulants were routinely used
and those in which they were not, indicating that it
may not be absolutely essential to follow throm
bolytic therapy with heparin. In ISIS-2, there was a
trend toward greater mortality reduction by SK when
more intense anticoagulation was planned (risk
reductions of 31% when SK was used with intrave
nous heparin, 27% when used with subcutaneous
heparin, and 12% with no heparin). However, as
stated earlier, both major andhninor bleeding epi, sodes were more common with the more intense
heparin regimen.15
Thefe have been several trials of subcutaneous or
intravenous heparin completed before the common
use of aspiria and/or thrombolytic agents. These
have been reviewed by MacMahon et al.53 The odds
of suffering death or subsequent infarction were
reduced by 16±7% and 22±10%, respectively (both
about p=0.02). In addition, there was a halving in
the incidence of strokes, pulmonary emboli, and
deep vein thromboses. These trials do not address
whether these beneficial effects will be realized
when heparin is given after fibrinolytic therapy
and/or aspirin and whether the risks of bleeding will
be a major problem.
Several small trials have evaluated the role of
heparin in maintaining coronary artery patency after
thrombolytic therapy. Topol et al54 randomized 131
patients to receive t-PA only or t-PA plus heparin 90
minutes after initiation of therapy. The patency rates
in the two groups were identical (79%). Bleich et al55
randomized 93 patients 3 hours after initiation of
t-PA therapy to receive heparin or no heparin. None
of the patients received aspirin. Angiography per
formed at a mean of 57 hours later showed a trend
toward greater patency with heparin (71% vs. 44%;
two-tailed p=0.08). In an Australian study,56 195
patients received t-PA followed by heparin for 24
hours. Patients were randomized to continue heparin
therapy or to receive aspirin for 7 days. Patency was
the same in the two groups (80%). Ross et al57
randomized patients to receive t-PA alone or t-PA
plus heparin for 1 week. Angiography performed at a
mean of 7 hours after randomization indicated higher
patency in the latter group. However, aspirin was
used in a dose of 80 mg daily orally. It is therefore
possible that after a single dose of 80 mg aspirin
orally (unlike the 160 mg aspirin chewed in ISIS-2),
little immediate antiplatelet effect is observed. Con
sistent with this possibility, in this study there were
fewer reocclusions in the aspirin group compared
with the heparin group among patients who had an
angiogram performed 1 week later.57 The Studio
Sulla Calciparina nell’angina e nella Trombosi ventricolare neil Infarto (SCATI) group randomized 360
patients to receive 12,500 units of calcium heparin
subcutaneously twice daily and 351 patients to no
heparin.58 None of the patients received aspirin; 433
patients received prior thrombolytic therapy. There
was no difference in reinfarction, but mortality was
Yum/ et al
significantly lower (21 of 360 vs. 35 of 351; d<0.03).
Similar results were observed in the subgroup of
patients who had previously received SK. The above
data suggest that while heparin is likely to be valu
able after thrombolytic therapy, heparin may not be
superior to aspirin. Moreover, it is unclear whether
heparin provides additional benefit when added to
aspirin and thrombolytic agents.
The GISSI-2 study evaluated the role of subcutane
ous heparin in addition to thrombolytic therapy and
aspirin in 20,749 patients.47 There were 883 deaths
among the 10,353 patients allocated to receive heparin
compared with 930 deaths among the 10,396 allocated
to receive no heparin (odds ratio of 0.95, with a 95%
CI of 0.86 to 1.04). While these results are still
consistent with a 10% reduction in mortality, it defi
nitely indicates that in the presence of aspirin, the
benefits of heparin may be only modest. There was no
effect on reinfarction (285 vs. 301) or stroke (118 vs.
120). However, there was a significant increase in
patients experiencing minor and major hemorrhagic
episodes (863 vs. 471 for minor episodes, pcO.001).
These data do not rule out the possibility of a modest
reduction in the risk of death of about 5-10%. For the
moment, it would be prudent not to use heparin
routinely, at least until the results of ISIS-3 become
available in late 1990 or early 1991.
0-Adrenergic Blocking Agents
^-Blockers reduce oxygen demand by lowering
heart rate and blood pressure; they also counter the
direct adverse effects of catecholamines and also
have antiarrhythmic properties. Thus, 0-blockers
may cause a reduction in infarct size, decrease myo
cardial wall stress, and prevent cardiac rupture.
Reductions in indirect indexes of myocardial damage
(such as enzyme or electrocardiographic changes) in
humans have been observed in at least nine studies in
which intravenous treatment with a 0-blocker was
started within 12 hours of onset of pain.
Data are available from at least 28 randomized
trials including about 27,500 patients.5960 In the
largest of these studies, ISIS-1,60 vascular mortality
was reduced by about 15% during the 7 days of
treatment (3.9% in the 0-blocker group, 4.6% among
controls; p<0.05) (Figure 4). After 7 days, the differ
ence in mortality between the treated and control
groups increased slightly; this may be due, in part, to
the modest excess of continued use of /3-blockers
after discharge in the treated group compared with
controls. Almost identical mortality results were
observed in another large trial, the Metoprolol In
Acute Myocardial Infarction (MIAMI) study.61 Pool
ing the results of all 27 available randomized trials
indicates that such treatment reduces mortality by
13% (95% CI, -2% to -25%) in the first week
(p<0.02). The mortality reduction when analyzed by
separate time intervals was most marked in the first 2
days (—25%), so that maximum benefit is likely to be
obtained by initiating treatment early (Table 5). Data
on nonfatal reinfarction and nonfatal cardiac arrests
Routine Medical Management of AMI
500r
IL 127
483
480.'
44orJ
GROUP ALLOCATED
CONTROL
f 400
o
420|r
404f-
[423
_f406
388
366,r“‘
3421
i
o
300 •
r
2®2* __ p
[M7
200
iE
4j
GROUy ALLOCATED
ATENOLOL
[36
fTi
l
i
3
i
I
J
_J346
331
[313
1 1
100
:i ’21
’?■
ivfe
5mg
End of trsatmant
period for thoM
allocated atenolol
0 i '2 ’3'4' s 'a ' 7' s'9'lo'ii'u'ia'iA'
D«y« from Randomisation
FIGURE 4. Vascular mortality curve at 7 days (period of
therapy randomized to control or atenolol) and for the next
week in ISIS-1. Note that the mortality curves diverge early
and then remain parallel See text for explanation of trial name
abbreviation. (Reprinted with permission from Reference 60.)
V
%
in hospital suggest that early treatment reduces risk
by about 19% (p<0.01; 95% CI, -5% to -33%) and
16% (p<0.02; 95% CI, —2% to —30%), respectively.
The available data on all patients suffering death,
nonfatal cardiac arrest, and nonfatal reinfarction
indicate a 16% reduction in the risk of suffering one
of these major events (1,110 vs. 1,298,p<0.0001) and
provide strong evidence that treatment is indeed
beneficial. Retrospective analyses of the causes of
deaths in ISIS-1 suggest that the reduction in mor
tality is due chiefly to prevention of cardiac rupture
and ventricular fibrillation.62 A trend toward fewer
deaths due to cardiac rupture was also observed in
both the MIAMI trial and the earlier trial from
Goteborg.63 The benefit with early intravenous /?blockade was particularly apparent in the first 24-36
hours after drug administration, unlike thrombolytic
therapy, where in both GISSI and ISIS-2 there was
an excess number of deaths in this early period.
These data suggest a complementary role for
blockers after thrombolytic therapy.2 There has been
only one small trial of 0-blockers given after throm
bolytic therapy. In this trial, although the numbers of
deaths were similar at 6 days with ^-blocker and
control groups (17 of 696 vs. 17 of 694), the 95%
confidence interval is quite consistent with the pre
viously observed reduction in mortality of about 15%.
In this trial, there was a significant reduction in early
nonfatal reinfarction (16 of 696 vs. 31 of 694,p<0.05)
and in recurrent ischemic episodes (107 of 696 vs. 147
11-128
Supplement II
Circulation
Vol 82, No 3, September 1990
Table 5. Mortality in Trials of Early Intravei•nouM 0-Blocfcer Followed by Short-term Oral Treatment Divided by Time to Death After
Myocardial Infarctions
Deaths (n)
2-3 days
0-1 days
'
I i;
I 1
d
I ij
■j!
r ’
0-7 days
BB _______ Con
BB
Con
BB
Con
ISIS-1
MIAMI
26 small trials
121
29
55
205
91
21
25
137
92
23
38
153
105
29
37
171
104
29
37
Total mortality (n)
Total patients (n)
I
4-7 days
Trial_____________________
171
41
51
263
Approximate percent change
in odds (±SEM)
170
BB _________ Con
317
367
79
93
117
126
I
513
586
13,815
13,721
-23±8
-u±ir ___________ -1±U , -_____________ -14±6
BB, 0-blocker; Con, control; SEM, standard error of the mean. See text for explanation of abbreviations of trial names. (Modified with
permission from Reference 51.)
of 694, p<0.005), providing some direct evidence of
additional benefit with 0-blockers when added to
thrombolytic therapy.
In addition to the short-term benefits of 0-blockers,
several independent trials have clearly demonstrated
that long-term therapy with 0-blockers for a year or two
reduces mortality and reinfarction by about one
fourth.59 Examination of the results in various sub
groups based on baseline characteristics such as MI
location, Q- or non-Q-wave MI, age, heart rate, or
blood pressure do not suggest any significant heteroge
neity of effect. Therefore, a policy of starting 0-blockers
intravenously within the early hours of MI, followed by
long-term oral treatment, should be considered in all
patients who have no contraindications.
Calcium Channel Blockers
Calcium channel blockers reduce oxygen demand by
lowering blood pressure and myocardial contractility.
They dilate coronary vessels and prevent calcium over
load of ischemic cells. While the above mechanisms
may be expected to reduce the extent of myocardial
injury, several of these drugs produce adverse effects
that could potentially offset the benefit. For example,
nifedipine can cause reflex tachycardia and coronary
vasodilatation of vessels supplying nonischemic areas.
This could lead to a diversion of blood from the
ischemic zones (“steal”). Verap il and diltiazem have
the potential to cause sinoatr and atrioventricular
block and depression of m jardial contractility,
thereby causing heart failure. Therefore, the net benefit
of these agents can only be assessed in carefully con
trolled randomized trials.
In total, data are available from 21 randomized
trials of varying sizes.64 Altogether, these trials stud
ied about 17,800 patients. Five trials included more
than 1,000 patients each, while most studies had
fewer than 200. This means that most trials were
individually too small to be able to detect even large
differences in mortality and major morbidity.
Only one large short-term trial has been re
ported,58 while two other studies started treatment
early and continued treatment for 6 months.59-60 In
the nifedipine study by Wilcox et al,65 4,491 patients
with suspected MI were treated for 1 month.
Almost 70% of patients were entered into the study
within 8 hours of the onset of chest pain. A similar
number of patients in each treatment group (64%)
developed an MI, and the mortality was 6.3% in the
placebo group and 6.7% in the nifedipine-treated
group. Reinfarctions were slightly more common in
the treated (2.2%) than in the control (1.5%) group
(p=NS). The Secondary Prevention Reinfarction
Israeli Nifedipine (SPRINT)-2 trial66 was stopped
early after randomizing 1,358 patients due to a
trend toward increased early mortality in the nifed
ipine group. The 6-month mortality wa$ 15% in the
treated groups compared with 13% among controls.
The number of patients developing MI in the
nifedipine and control groups (84% compared with
87%) was similar. In the third large trial, verapamil
or placebo was administered intravenously in 3,498
patients and continued orally long-term at a dose of
120 mg three times daily in patients who developed
an MI and who could tolerate the study drug (42%
of the patients in each group).67 The withdrawal
rate due to side effects during long-term treatment
was high, 42% in the verapamil group and 34% in
the placebo group. At the end of the 6-month
treatment period, 8.6% of the verapamil-treated
patients had died compared with 8.4% in the con
trol group. There were 50 reinfarctions in the group
randomized to verapamil compared with 60 in the
placebo group (p = NS). Enzymatically estimated
infarct size in a subgroup of 100 patients was not
significantly different between the groups. A fourth
study, the Multicenter Diltiazem Post-Infarction
Trial (MDPIT), randomized patients to receive
diltiazem or placebo starting 2-4 weeks after AMI
for 2-3 years.68 There was no significant difference
in the proportion of patients who suffered death
(166 active vs. 167 control) or reinfarction (99 vs.
116, p=NS). Subgroup analyses suggested that
treatment appeared to be significantly harmful for
patients with large infarction, depressed left ven
tricular function, or pulmonary congestion, whereas
there appeared to be a nonsignificant favorable
trend in patients without pulmonary congestion or
i
i
Yusuf et al
non-Q-wave MI. The authors of this report wisely
caution that their analyses do not provide conclu
sive results but only suggest hypotheses for future
trials. A further small trial of diitiazem in patients
with non-Q-wave infarcts demonstrated no effect
on mortality but claimed that treatment reduced
nonfatal reinfarction.*’ This result is not significant
if a standard'two-sided p value is used, which has
been used in most trials. Moreover, there was an
excess of adverse effects such as Mnoatrial irrest
and atrioventricular block. Similar excess occur
rences of sinoatrial arrest and atrioventricular block
were observed in the Danish verapamil study.67
In addition to the above four studies, 14 smaller
studies in which treatment was started early included
about 1,800 patients. An overview of the results from
all 18 trials provides reliable estimates of the likely
effects of treatment.64 In the studies in which treat
ment was started within 24 hours, 3,258 of 5,352
(60.8%) patients treated with calcium channel block
ers developed MI compared with 3,289 of 5,356
(61.4%) among controls (p=NS). An overview of the
mortality results from trials in which treatment was
started early indicates a nonsignificant increase in the
calcium blocker-treated group. This adverse trend is
observed in both the short-term studies (200 of 3,121
[6.4%] in the calcium-blocker group died compared
with 185 of 3,150 [5.9%] among controls) and the
studies in which treatment was started early and
continued for several months (251 of 2,409 [10.4%]
and 235 of 2,396 [9.8%], respectively). Because the
various calcium antagonists differ in some of their
pharmacological properties, we stratified the analy
ses by agent. With no agent was there a significant
reduction in mortality or reinfarction. The trials with
diitiazem suggest a trend toward fewer reinfarctions
(113 of 1,557 among actively treated patients com
pared with 142 of 1,560 among controls; p=0.10).
However, this trend is not significantly heteroge
neous compared with the overall results (x2 for
heterogeneity=NS). Moreover, there does not
appear to be any reduction in mortality with dii
tiazem (180 of 1,574 vs. 181 of 1,577, respectively).
These data indicate that prophylactic use of cal
cium channel blockers during the early phase of MI is
I.V.
201- 13® : 193
lisa
<15.
I 105
Heparin
^07?
Aspirin
0.4
0.5
0.6
0.7
0.8
0.9
♦- REDUCTION IN MORTALITY
25,000
<0.00001
6,700
<0.001
Z300
<0.001
<0.001
27,000
2.000
<0.001
-----------------------------------
6,000
N.s.
-------------------------- ---------- -
8,500
N.S.
27,000
<0.02
18,000
<0.0001
^0.87
0.80
p
10,000
0.98
Lidocaina
1
21±19
N.S.
31±8
<0.001
Nitrates
No.
Patients
Calcium Channal blockara
%
7^,
1X1
Intravenous Nitrates
Nitrates reduce oxygen demand and myocardial
wall stress by reduction of both afterload and pre
load; nitroglycerin might additionally increase blood
supply by relieving coronary „spasm. Intravenous
sodium nitroprusside has been evaluated in three
trials and intravenous nitroglycerin in six trials in
approximately 1,000 patients each.70 Lower mortality
was observed in all three trials of nitroprusside, with
the difference being statistically significant in one
trial. Lower mortality was observed in five of six trials
with nitroglycerin; in two, the differences were sta
tistically significant (p<0.05). Overall, the pooled
data indicate a 12% mortality rate among the 1,009
treated patients compared with an 18% mortality
rate among the 1,004 control subjects (pcO.OOl).
This represents about a one third reduction in the
risk of death (95% CI, -18% to -49%). The risk
reduction in the six nitroglycerin trials (45%) appears
somewhat greater than that in the three trials with
O.M
IV Nitratw
iej
not likely to be beneficial and may well be potentially
harmful in some high-risk patients.
IV StreptokinaM >6hrs
IV Batablockm
%
Overail
192 : 257
Figure 5. Bar graph showing short-term mortality reduction
(%) in randomized trials of intravenous (I. V) or oral nitrates
in acute myocardial infarction. Active, a; placebo,
SD,
standard deviation; NS, not significant.
I 0.71
IV APSAC
Oral
56:64
[l2J
I i
fl
oi—I
Reduction %
35±9
(±S.D.)
<0.001
^0.74
IV t-PA<6hrs
II-129
%
25r
Agaffl
IV StreptokincM < 6tvs
Routine Medical Management of AMI
1.0
1.1
1.2
1.3
1.4
INCREASE IN MORTALITY
ODDS RATIO AND 96% CONFIDENCE INTERVAL
<0.02
Figure 6. Chart showing summary
of effects of various treatments on
mortality in acute myocardial infarc
tion. Odds ratios and their 95% con
fidence intervals are plotted The size
of the square is related to the variance
of the data. Larger squares reflect
more data, and narrower confidence
interval indicates more precise esti
mates of treatment effect. IV, intrave
nous; t-PA, tissue plasminogen acti
vator; APSAC, anisoylated plas
minogen-streptokinase activator com
plex; NS, not significant.
11-130
Supplement II Circulation
kb/ 82, No 3, September 1990
sodium nitroprusside (23%). This difference,
although not statistically significant by conventional
criteria, is consistent with clinical and pharmacolog
ical data that suggest nitroglycerin is likely to be the
more beneficial agent.
Oral Nitrates
At least five trials with oral nitrates have been
published.71 Overall, there was a 10% short-term
mortality among 560 patients randomized to oral
nitrates compared with 12.3% among 521 controls.
This 21% risk reduction (95% CI, +16% to -46%) is
not significantly different from the results of the
intravenous nitrate trials.
Overall (oral and intravenous treatment), there
were 192 (12.1%) deaths in nitrate-treated patients
compared with 257 deaths among controls (16.7%)
(31% risk reduction; 95% CI, -7% to -47%; Figure
5). Subgroup analyses of these trials by such variables
as location of infarction and time from onset of pain
did not consistently reveal benefit in any particular
subgroup. These data suggest that intravenous ni
trates (in particular, nitroglycerin) and probably oral
nitrates reduce mortality when given early to patients
with moderate or large Mis.
I ■
hl;
I
F ir
h-
Lidocaine
In the early hours after an MI, death due to
ventricular fibrillation is common. To prevent ven
tricular fibrillation and hence to reduce mortality,
physicians often treat patients, especially those with
complex ventricular arrhythmias, with a prophylac
tic antiarrhythmic agent such as lidocaine. At least
14 randomized trials with a total of 9,155 patients
have studied lidocaine.72 Nine trials evaluated
intravenous lidocaine infusions in 2,194 patients
during a 24- to 48-hour period, whereas five trials
evaluated intramuscular lidocaine injections in
6,961 patients and followed them up for 1-4 hours.
In the 14 trials, 89 nonfatal and 14 fatal cases of
ventricular fibrillation were reported. In three trials
no event was recorded, and in seven trials there
were fewer cases of ventricular fibrillation in the
treated group; in only one trial was this difference
statistically significant. In the four remaining trials,
there were more events among patients treated with
lidocaine. Overall, the data from all trials indicate a
35% reduction in the odds of developing ventricular
fibrillation (95% CI, -56% to -3%) but with only
borderline statistical significance (p<0.04).
In the 14 trials, 137 deaths were reported. In
neither the trials individually nor overall was there
any significant difference in mortality. Indeed, early
mortality was about one third greater among
lidocaine-treated patients, but the 95% Cis include
the possibility of no effect as well as the possibility of
harm (38% excess risk; 95% CI, -2% to +95%;
p<0.10). There was no heterogeneity in the results
between the intravenous and intramuscular trials
regarding the effects of lidocaine on ventricular
fibrillation and mortality. Data on fatal or nonfatal
asystole were available from only seven trials. There
was an excess of fatal asystole (10 vs. 5,p=NS), fatal
asystole plus asystole requiring resuscitation (34 vs.
13, p<0.01), and total asystole (54 vs. 25, p<0.01).
However, because of the incompleteness of the data
on asystole, biases in end-point ascertainment cannot
be ruled out. However, if prophylactic treatment
were to double the number of early deaths from
asystole (given a rate of three asystolic deaths per
1,000 observed among controls in the trials), then this
could outweigh the benefits of 4 one third reduction
in ventricular fibrillation, especially among patients
at low.risk for this event and when so few cases of
ventricular fibrillation are fatal (one per 1,000 among
controls in the trials). Therefore, routine use of
prophylactic lidocaine in patients with suspected MI
should be avoided in situations where facilities for
resuscitation are available.
The need for caution in routinely using antiar
rhythmic drugs is further emphasized by the results
of the Cardiac Arrhythmia Suppression Trial
(CAST),73 which demonstrated that among post-MI
patients with frequent ventricular arrhythmias, sur
vival was significantly shortened by the use of two
class-Ic antiarrhythmic agents despite excellent sup
pression of ventricular arrhythmias (encainide and
flecainide: 56 of 730 [7.7% ] deaths or cardiac arrests
among actively treated patients compared with 22 of
725 [3%] in the placebo group; pcO.OOl). The two
large trials of mexiletine also demonstrate a trend
toward an increase in mortality.74-75
It is possible that in certain types of patients (e.g.,
those with prolonged ventricular tachycardia or those
resuscitated from ventricular fibrillation) or in certain
situations where facilities for resuscitation are limited,
the benefits of preventing ventricular fibrillation by
lidocaine might outweigh the potential for harm. How
ever, routine use of antiarrhythmic drugs in other
situations could potentially result in excess mortality.
Discussion
During the last 5-10 years, the emphasis in the
treatment of AMI has moved from the era of moni
toring, arrhythmia management, and circulatory sup
port to a new and very promising approach based on
reperfusion and damage limitation. In the past, rec
ommendations for therapy have been based largely
on either a presumption of benefit by extrapolating
from experimental work or the effect of an interven
tion on certain mechanisms or surrogate end points.
Instead, current recommendations are based on
direct evidence of the effects on clinically important
outcomes after careful evaluation in large welldesigned randomized controlled trials (Figure 6).
Such trials have been made possible by the selfless
collaboration of hundreds of investigators in common
protocols around the world. These trials have pro
vided clear proof of benefit for some agents and lack
of benefit or even evidence of harm with other
interventions. Often, the results of these trials could
)
YiGuf et al
Table 6.
De.crip.io, of M^or Tri„, of
Myo<:Irdlj| t,toaio.
Routine Medicaj Management of AMI
11-131
CondMct(<| „ |n
1
Reference
Tv™i
Expected
Principal outcome
Status of study as
—
—
yP0 °f trial
study size_________ of interest
of April 1990
Value of thrombolysis among subgroups where there is no consensus
-----------------------------EMERAS
> 6 hr after onset; SK vs. placebo
4,000-5,000 5-wk mortality
3,000 recruited
LATE
> 6 hr after onset; t-PA vs. placebo
5,000 Short-term mortality
800 recruited
ISIS-3
Patients who, in the opinion of their12,000-15,000 5-wk mortality
20,000 overall
physicians, have no clear indications
(25% in this
or contraindications to thrombolytic
part of the
therapy (SK, t-PA, or APSAC vs.
study)
placebo)
TIMIT
Unstable angina, non-Q-wave MI
2,000 Combined end points of ?300
mortality, reinfarction,
and- ECG evidence of
ischemia
Other trials
ISIS-3
Comparison of t-PA vs. SK vs.
APSAC; factorial: heparin vs. no
heparin
50,000—60,000 5-wk mortality
GUSTO
<6 hr; ST-segment elevation;
comparison of t-PA vs. SK vs.
t-PA+SK; all patients on i.v.
heparin
CONSENSUS-2 Enalapril vs. placebo
March 1991
1992
March 1991
1992
March 1991
30,000 Short-term mortality
Planning
1993
9,000 6-mo mortality
Recruitment
underway
1991
Recruitment
underway
Recruitment
underway
Pilot underway
1992
1993
Planning
1993
Chinese study
Captopril vs. control
10,000 Short-term mortality
SMILE
Zofenopril vs. placebo
ISIS-4
2x2x2 factorial design of captopril
vs. control, nitrates vs. control,
magnesium vs. control
Lisinopril vs. control
3,000 Mortality or heart
failure in hospital
30,000 5-wk mortality
GISSI-3
20,000
Expected
report date
10,000-12,000 Short-term mortality
1993
and T-PA
not have been predicted from prior theories or study
from data that focused solely on mechanisms.
Perhaps the most surprising result of the large
trials is the remarkable efficacy of a simple inexpen
sive agent such as aspirin and that the substantial
short-term gains of thrombolysis and aspirin therapy
are maintained for at least 1-2 years, and probably
longer, without large-scale intervention with coro
nary artery bypass graft surgery or PTCA. It may be
that early thrombolysis gives time for the rapid
development of collaterals, which then exert a pro
tective effect, so that rethrombosis is less likely to
lead to reinfarction. Moreover, the use of simple
measures such as aspirin and /3-blockers appear to
substantially reduce the risk of reinfarction and
recurrent ischemia.
It also appears that thrombolytic treatment is
beneficial in many categories of patients who were
previously excluded from some of the earlier trials,
such as elderly patients, patients with shock or hypo
tension, patients with inferior infarction, and patients
seen 4-6 hours after symptom onset. Reductions in
mortality by SK among patients entered into treat
ment late after onset of MI or reductions in mortality
by aspirin given in the acute phase were not pre
dicted based on hypotheses, theories, or dogma prev
alent a few years earlier. Subsequent to publication
of the results from some recent trials, claims of
mechanisms to explain the above findings are now
being proposed! These experiences suggest that the
approach to entering patients into trials, while rec
ognizing existing theories, should not be unduly
restrictive. Instead, investigators should be willing to
test the validity of such opinion by randomizing a
broader range of patients with the condition than has
been the practice in some studies and among whom
the effects of treatment are uncertain (“the uncer
tainty principle”).76 The safety of thrombolysis with
modem regimens makes it plausible to consider its
use in patients with other conventional contraindica
tions, for example, hypertensive patients after control
of blood pressure or those with a history of ulcer or
stroke in the distant past, so long as the patient is
considered to have a high risk of dying of the AMI.
However, it should be emphasized that decisions
should be taken in light of benefit-risk ratios for each
individual patient based on reliable evidence from
large clinical trials.
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Supplement II
Circulation
Vol 82, No 3, Septemfer 1990
Finally, one should reemphasize the importance
of general preventive measures after MI, such as
stopping smoking, lowering cholesterol, controlling
hypertension, reducing weight, and encouraging
regular exercise.
Future directions (Table 6)
Current trials such as ISIS-3 in conjunction with
further analysis of GISSI-2 will resolve which of the
three available thrombolytic agents (SK, t-PA, or
APSAC) is preferred. ISIS-3, the South American
EMERAS trial, and a trial of late thrombolysis with
t-PA (LATE) will provide more information on those
categories of patients (e.g., presentation with equiv
ocal electrocardiograms or late entry into treatment
after pain onset) in cases where there may still be
some controversy about potential benefit. ISIS-3 will
provide further information regarding the role of
heparin after different thrombolytic agents. Several
large trials studying the effect of angiotensin convert
ing enzyme inhibitors and nitrates should provide
further information on vasodilators and their role in
preventing infarct expansion, ventricular dilatation,
and death. Approaches to preventing reperfusion
injury, such as free-radical scavengers, or to prevent
ing reocclusion by blocking specific platelet receptor
sites with monoclonal antibodies appear promising
but are yet to be investigated in humans. The role of
magnesium in prevention of arrhythmic deaths in
AMI appears promising and deserves to be evaluated
in large-scale trials.
Recommendations
Based on an overview of all available randomized
trials in AMI, the following general strategies for the
treatment of patients can be recommended, so long
as there are no contraindications to the administra
tion of a particular agent. A thrombolytic agent
administered intravenously within 24 hours of onset
of symptoms is likely to reduce mortality. Since the
benefits appear to be greatest when thrombolytic
agents are administered very early, every reasonable
effort (such as minimizing the time of patient admis
sion to a coronary care unit or administering therapy
in the emergency room) should be made to initiate
treatment promptly. If a patient presents 6-12 hours
after onset of symptoms, thrombolytic therapy should
still be considered if there is clinical evidence that the
infarction is still evolving (repeated episodes of chest
pain, presence of R waves on the electrocardiogram,
etc.). The currently available data indicate that there
is no appreciable difference between t-PA and SK
although comparative data with APSAC are lacking.
Therefore, it would be reasonable to administer any
one of the three agents until the results of ISIS-3,
which is expecting to randomize 50,000-60,000
patients, are available. The addition of aspirin to SK
(or presumably to other thrombolytic agents) results
in further reductions in mortality, reinfarction, and
stroke without an excess of serious bleeding episodes.
Intravenously administered ^-blockers, when given
to patients without contraindications, reduce mortal
ity (probably by preventing cardiac rupture and fatal
ventricular fibrillation), reinfarction, nonfatal cardiac
arrests, and recurrent ischemic episodes. Both aspi
rin and /3-blockers should be continued long term in
appropriate patients since further reductions in mor
tality and reinfarction can be realized. Thrombolytic
agents, /3-blockers, and aspirin can be safely used
together. They are thought to produce benefits by
quite different mechanisms, and because the avail
able data suggest no appreciable adverse but proba
bly beneficial interactions, using them in combination
is likely to be more beneficial than any one used
alone. Vasodilators (intravenous or oral nitrates)
may benefit patients, especially if they have large Mis
and pulmonary congestion. Based on the available
data indicating little benefit and possibly an increase
in mortality with calcium channel blockers, lidocaine,
other antiarrhythmic drugs, and PTCA, these inter
ventions should not be used routinely.
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Key Words • myocardial infarction • clinical trials
(
i
I
Yusuf et al
mittee Meeting. May 29, 1987: In Streptokinase-IV treatment
for acute myocardial infarction. Vol I:pl55-177
12. The TIMI Study Group: The Thrombolysis in Myocardial
9%
Pha“ ’ findings- N Engl J Med
1 70J, J 1L. 7JL— 7JO
13. Verstraete M, Bernard R, Boiy M, Brower RW, Collen D, de
Bono DP, Erbel R, Huhmann W, Lennane RJ, Lubsen J,
Mathey D, Meyer J, Michels HR, Rutsch W, Schanff M,
Schmidt W, Uebis R, Von Essen R: Randomized trial of IV
recombinant tissue-type plasminogen activator versus IV
streptokinase in acute myocardial infarction. Lancet 1985;
1:842-847
14. Gruppo Italiano per lo Studio della Streptochinasi nelf
Infarto Miocardico (GISSI): Effectiveness of thrombolytic
treatment in acute myocardial infarction. Lancet 1986-1:
397-402
15. ISIS-2 (Second International Study of Infarct Survival) Col
laborative Group: Randomized trial of intravenous streptoki
nase, oral aspirin, both, or neither among 17187 cases of
suspected acute myocardial infarction: ISIS-2. Lancet 19882:349-360
16. ISAM Study Group: A prospective trial of Intravenous Strep
tokinase in Acute Myocardial infarction (ISAM): Mortality,
morbidity and infarct size at 21 days. N Engl J Med 1986314:1465-1471
’
17. White HD, Norris RM, Brown MA, Takayama M, Maslowski
A, Bass NM, Ormiston JA, Whitlock T: Effect of intravenous
streptokinase on left ventricular function and early survival
after acute myocardial infarction. N Engl J Med 1987317:850-855
18. ISIS Pilot Study Investigators: Randomized factorial trial of
high-dose intravenous streptokinase, of oral aspirin and of
intravenous heparin in acute myocardial infarction. Eur Heart
J 1987;8:634-642
19. Kennedy JW, Martin GV, Davis KB, Maynard C, Stadius M,
Sheehan FH, Ritchie JL: The Western Washington intrave
nous streptokinase in acute myocardial infarction randomized
trial. Circulation 1988;77:345-352
20. Olson HG, Butman SM, Piters KM, Gardin JM, Lyons KP,
Jones L, Chilazi G, Kumar KLA, Colombo A: A randomized
controlled trial of intravenous streptokinase in evolving acute
myocardial infarction. Am Heart J 1986;3:1021-1025
21. Schreiber TL, Miller DH, Silvasi DA, Moses JW, Borer JS:
Randomized double blind trial of IV streptokinase for acute
myocardial infarction. Am J Cardiol 1986;58:47-52
22. Heikkila J, Luomanmaki K, Ventila M, Virtanen KS, and the
MISS Study Group: Early intravenous thrombolysis prevents
myocardial damage in large evolving myocardial infarction, in
Parker J, Fitzgerald P, (eds): Thrombolysis Bulletin. London,
Current Medical Literature, 1987, p 6
23. Wisenberg G, Finnic KJ, Jablonsky G, Kostuk, WJ, Marshall
T: Nuclear magnetic resonance and radionuclide angio
graphic assessment of acute myocardial infarction in a
randomized trial of intravenous streptokinase. Am J Cardiol
1988;62:1011-1016
24. Durand P, Asseman P, Pruvost P, Bertrand ME, La Blanche
JM, Thery C: Effectiveness of intravenous streptokinase on
infarct size and left ventricular function in acute myocardial
infarction prospective and randomized study. Clin Cardiol
1987;10:383-392
25. Gruppo Italiano per lo Studio della streptochinasi nell ’Infarto
Miocardico (GISSI): Long-term effects of intravenous throm
bolysis in acute myocardial infarction. Final report of the
GISSI study. Lancet 1987;2:871-877
26. Wilcox RG, Von der Lippe G, Olsson CG, Jensen G, Skene
AM, Hampton JR: Trial of tissue plasminogen activator for
mortality reduction in acute myocardial infarction. AngloScandinavian Study of Early Thrombolysis (ASSET). Lancet
1988;2:525-530
27. Guerci AD, Gerstenblith G, Brinker JA, Chandra NC, Gott
lieb SO, Bahr RD, Weiss JL, Shapiro EP, Flaherty JT, Bush
DE, Chew PH, Gottlieb SH, Halperin HR, Ouyang P, Walford
GD, Bell WR, Fatterpaker AK, Llewellyn M, Topol EJ, Healy
B, Siu CO, Becker LC, Weisfeldt ML: A randomized trial of
Routine Medical Management of AMI
11-133
IV tPA for acute myocardial infarction with subsequent ran-
iwTin'iu-iTis*^ coronary an»i0P,asty- N En^ J
28' XCTo etC M’ B,eife,d w’ Browcr RW« charbonnier B, Collen
D deBono DP, Dunning AJ, Lennane RJ, Lubsen J, Mathey
DG, Michel PL, Rayaud PH, Schofer J, Vahanian A, Vanhaecke J, Van de Kley GA, Van de Werf F, Von Essen R:
Double-blind randomised trial of IV tissue-type plasminogen
activator versus placebo in acute myocardial infarction. Lancet
1985;2:965-969
29. National Heart Foundation of Australia Coronary Thrombol
ysis Group: Coronary thrombolysis yd myocardial salvage by
tissue plasminogen activator given up to 4 hours after onset of
myocardial infarction. Lancet 1988;1:203-208
30. O Rourke M, Baron D, Keogh A, Nelson G, Barnes C, Raftos
J, Graham K, Hillman K, Newman H, Healey J, Woolridge J
Rivers J, White H, Whitlock R, Norris R: Limitation of
myocardial infarction by early infusion of recombinant tissue
type plasminogen activator. Circulation 1988;77:1311-1315
31. Van de Werf F, Arnold AER, and the European Cooperative
Study Group for Recombinant Tissue-Type Plasminogen Acti
vator: Intravenous tissue plasminogen activator and size of
infarct, left ventricular function, and survival in acute myocar
dial infarction. Br Med J 1988;297:1374-1379
32. Holmberg S, Hartford M, Herlitz J, Luepker R, Swedbcrg IC
Very early thrombolysis with rt-PA in acute myocardial infarc
tion (abstract). Circulation 1988;78(supp| II):II-U01
33. Armstrong PW, Baigrie RS, Daly PA, Haq A, Gent M,
Roberts R, Freeman MR, Bums R, Liu P, Morgan CD
(TPAT): Tissue plasminogen activator Toronto placebo con
trolled randomized trial in myocardial infarction. J Am Coll
Cardiol 1989;13:1469-1476
34. AIMS Trial Study Group: Effect of intravenous APSAC on
mortality after acute myocardial infarction: Preliminary report
of a placebo-controlled clinical trial. Lancet 1988;2:545-549
35. Yusuf S, Collins R, Held P, Anderson J: Effect of APSAC on
mortality in acute myocardial infarction: An overview of the
randomized trials (abstract). Circulation 1988;78(suppl
II) •11*277
36. Binaghi G, Campolo L, Casari A, Repetto S: GISSI: The
coronary artery and ventriculography study. Giomale Italiano
di Cardiologia 1987;17:89-100
37. Been M, de Bono DP, Muir AL, Boulton FE, Hillis WS,
Hamung R: Coronary thrombolysis with intravenous anisoylated plasminogen-streptokinase complex BRL 26921 Br
Heart J 1985;53:253-259
38. Buchalter MB. Bourke JP, Jennings K, Adams PC, Kenmure
ACF, Chan Wah Hah, Reid DS: The effect of thrombolytic
therapy with anisoylated plasminogen streptokinase activator
complex on the indicators of myocardial salvage. Drugs 1987
23(suppl 3):209-215
39. Meinertz T, Kasper W, Schumacher M, Just H (for the
APSAC multicenter trial group): The German multicentre
trial of APSAC versus heparin for acute myocardial infarction
Am J Cardiol 1988;62:347-351
40. Taeymans Y, Materne P [on behalf of the Belgian Group of
the European Multicentre Study]: Assessment of Left Ven
tricular function in a randomized study of FV anisoylated
plasminogen streptokinase activator complex versus heparin in
acute myocardial infarction. Drugs 1987;133(suppl 3):216-220
41. Bassand JP. Machecourt J, Cassagnes J, Anguenot T, Lusson
JR, Wolf JE, Ducellier D, Borel E, Peycelon P: A multicenter
double-blind trial of IV APSAC versus heparin in acute
myocardial infarction (abstract). Final report of the APSIM
study. J Am Coll Cardiol 1988;11:232A
42. White HD, Rivers JJ, Mastowski AH, Ormiston JA, Takayama
M, Hart HH, Sharpe DN, Whitlock RML, Norris RML: Effect
of intravenous streptokinase as compared with that of tissue
plasminogen activator on left ventricular function after first
myocardial infarction. N Engl J Med 1989;320:817-821
43. Magnani B, PAIMS Group: The Plasminogen Activator Ital
ian Multicentre Study (PAIMS): Comparison of intravenous
single chain rt-PA versus streptokinase in acute myocardial
infarction. J Am Coll Cardiol 1989;13:19-26
11-134
>
1
r1
E .r
J
:l
Supplement II
Circulation
voi 82, No 3, September 1990
44. Neuhaus KL, Tebbe U, Gottunck M, Weber MAJ, Feuerrer
W, Niederer W, Haere W, Praetorius F, Grosser KD, Huhmann W, Haepp HW, Alber G, Sheikh-Zadeh A, Schneider B:
IV recombinant rt-PA and urokirfase in acute myocardial
infarction: Results of the German Activator Urokinase Study
(GAUS). J Am Coll Cardiol 1988;12:581-587
45. Sheehan FH, Braunwald E, Canner P, Dodge HT, Gore J,
Van Natta P, Passamani ER, Williams DO, Zaret B: The
effects of intravenous' thrombolytic therapy on left ventricular
function: A report on tissue-type plasminogen activator and
. streptokinase from the Thrombolysis in Myocardial Infarction
(TIMI Phase 1) trial. Circulation 1987;75:817-829
46. Rentrop KP, Feit F, Sherman W, Stecy P, Hosat S, Cohen M,
Rey M, Ambrose J, Nachamie M, Schwarz W, Cole W,
Perdoncin R, Thornton JC: Late thrombolytic therapy pre
serves left ventricular function in patients with collateralized
total coronary occlusion primary endpoint findings of reperfu
sion trial. J Am Coll Cardiol 1989;14:58-64
47. GISSI 2: Results of a trial comparing streptokinase and tPA
with and without heparin in acute myocardial infarction.
Lancet (in press)
48. Hackett D, Davies G, Cherchia S, Maseri A: Intermittent
coronary occlusion in acute myocardial infarction. N Engl J
Med 1987;317:1055-1059
49. Mauri F, de Biase M, Franzosi MG, Pampallona S, Forcsti A,
Gasparini M: In hospital causes ot death in the patients
admitted to the GISSI Study. Giomale Italiano di Cardiologta
1987;17:37-44
50. PRIMI Study Group: Randomized double-blind trial of
recombinant pro-urokinase against streptokinase in acute
myocardial infarction. Lancet 1989;1:863-868
51. Antiplatelet Trialists’ Collaboration: Secondary prevention of
vascular disease by prolonged antiplatelet treatment. Br Med J
1988;296:320-331
52. UK-TTA Study Group: UK transient ischemia attack aspirin
trial: Interim results. Br Med J 1988;296:316-320
53. MacMahon S, Collins R, Knight C, Yusuf S: Reduction in
major morbidity and mortality by heparin in acute myocardial
infarction (abstract). Circulation 1988;78(suppl II):II-389
54. Topol EJ, George BS, Kereiakis DJ, Stump DC, Candela RJ,
Abbotsmith CW, Aronson L, Pickel A, Boswick JM, Lee KL,
Ellis SG, Califf RM: A randomized controlled trial of IV tPA
and early IV heparin in acute myocardial infarction. Circula
tion 1989;79:281-286
55. Bleich SD, Nichols T, Schumacher R, Cooke D, Tate D,
Steiner D, Brinkman D: The role of heparin following coro
nary thrombolysis with t-PA (abstract). Circulation 1989;
80(suppl II):II-113
56. National Heart Foundation of Australia Coronary Thrombol
ysis Group: A randomized comparison of oral aspirin/
dipyridamole versus IV heparin after r-tPA for acute myocar
dial infarction. Circulation 1989;80(suppl II):II-114
57. Ross AM, Hsia J, Hamilton W, Chaitman B, Roberts R,
Kleiman NS: Heparin versus aspirin after recombinant tPA
therapy in myocardial infarction: A randomized trial
(abstract). J Am Coll Cardiol 1990;15:64A
58. The SCAT! Group: Randomized controlled trial of subcuta
neous calcium-heparin in acute myocardial infarction. Lancet
1989;2:182-186
59. Yusuf S, Peto R, Lewis J, Collins R, Sleight P: Beta blockade
during and after myocardial infarction. An overview of the
randomized trials. Prog Cardiovasc Dis 1985;17:335-371
60. ISIS-1 (First International Study of Infarct Survival) Collabo
rative Group: Randomized trial of intravenous atenolol among
(16,027) cases of suspected acute myocardial infarction: ISISI. Lancet 1986;2:57-65
61. The MIAMI Trial Research Group: Metoprolol in acute
myocardial infarction (MIAMI). A randomized placebocontrolled international trial. Eur Heart J 1985;6:199-226
62. ISIS-1 (First international Study of Infarct Survival) Collabo
rative groups: Mechanisms for the early mortality reduction
produced by beta-blockade started early in acute myocardial
infarction: ISIS-1. Lancet 1988; 1:921-923
63. Hjalmarson A, Elmfeldt D, Herlitz J, et. al.: Effect on mor
tality of metoprolol in acute myocardial infarction: A double
blind randomized trial. Lancet 1981;2:823-827
.64. Held P, Yusuf S, Furberg C: Effects of calcium antagonists on
initial infarction, reinfarction and mortality in acute myocar
dial^ infarction and unstable 'angina. Br Med J 1989;299:
1187-1192
65. Wilcox RG, Hampton JR, Banks DC, Birkhead JS, Brooksby
LAB, Burns-Cox CJ, Hayes MJ, Joy MD, Malcolm AD, Mather
HG, Rowley JM: Trial of early nifedipine in acute myocardial
infarction: The TRENT study. Br Med J 1986;293:1204-1208
66. The SPRINT study group: The Secondary Prevention Re
infarction Israeli Nifedipine Trial (SPRINT) II: Design and
methods, results (abstract). Eur Heart J 1988;9(suppl l):350
67. The Danish Study Group on Verapamil in myocardial infarc
tion: Verapamil in acute myocardial infarction. Eur Heart J
1984;5:516-528
68. The Multicenter Diltiazem Post Infarction Trial Research
Group: The effect of diltiazem on mortality and reinfarction
after myocardial infarction. N Engl J Med 1988;319:385-392
69. Gibson R, Boden WE, Theroux P, Strauss HD, Pratt CM,
Gheorghiade M, Capone RJ, Crawford MH, Schlant RC,
Kleiger RE, Young PM, Schechtman K, Perryman B, Roberts
R, and the Diltiazem Reinfarction Study Group: Diltiazem
and reinfarction in patients with non-Q wave myocardial
infarction. N Engl J Med 1986;315:423-429 A
70. Yusuf S, Collins R, MacMahon S, Peto R: Effect of intrave
nous nitrates on mortality in acute myocardial infarction: An
overview of the randomized trials. Lancet 1988;1:1088-1092
71. Held P, Teo KK, Yusuf S: Effects of beta-blockers, calcium
channel blockers and nitrates in acute myocardial infarction
and unstable angina pectoris, in Topol EJ (ed): Interventional
Cardiology. Philadelphia, WB Saunders Co, 1990, pp 49-65
72. MacMahon S, Collins R, Peto R, Koster RW, Yusuf S: Effects
of prophylactic lidocaine in suspected acute myocardial infarc
tion. An overview of results from the randomized, controlled
trials. JAMA 1988;260:1910-1916
73. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators: Increased mortality due to encainide or flecainide in a
randomized trial of arrhythmia suppression after myocardial
infarction. V Engl J Med 1989;321:406-412
74. Chamberlain DA, Jewitt DE, Julian DG, Campbell RWF,
Doyle D McC, Shanks BG: Oral mexiletine in high risk
patients after myocardial infarction. Lancet 1980;2:1324-1327
75. IMPACT Research Group: International mexiletine and pla
cebo antiarrhythmic coronary trial I. Report on arrhythmia
and other finding. J Am Coll Cardiol 1984;6:1148-1163
76. Yusuf S, Held P, Teo KK, Toretsky ER: Selection of patients
for randomized controlled trials: Implications of wide or
narrow eligibility criteria. Stat Med 1990;9:73-86
Key Words • myocardial infarction • clinical trials
I
26
Traumatic Paraplegia
and Quadriplegia
%
DONALD A. NAGEL, M.D.
The word paraplegia, according to Dorland's Medical Dictionary means
paralysis of the legs and lower part of the body, both motion and sensa
tion being affected. Quadriplegia means paralysis of all four limbs
hese conditions, broadly speaking, could be caused by congenital abnor
mahties. infections, tumors, or chemicals, as well as by injury (trauma)
laumatic paraplegia and quadriplegia are the subject of this chapter ’
heie are many causes of traumatic paraplegia and quadripte&ia
Birth injunes can produce it; accidents about the home or school. Xh
mort lnC
fa ’S.frOm a height. can produce it; and bullet wounds
Of o 1 fJ“5leS’ 3nd lnjUrl®s from motor veh>de accidents can produce it’
Of all of these, motor vehicle accidents are perhaps the most frequent
cause. As younger people are increasing their exposure with high-speed
bicycle^ motor-driven bicycles, motorcycles, and sports cars it is antS
pared that the number of children who have traumatic paraplegia and
quadriplegia will increase.
P^apiegia and
From ancient times this injury has been noted as one of the most
devastating. It is frequently associated with fractures of the bones of the
spinal column-but not always; the spinal cord can also be damaged bv
%
°ne l0™ UP°n the °ther’ without an>’ signs of fracture (Fig
-6-1), and there also are many fractures of the back (spine) that do nft
nerve'6
The(?aral-VSls ls ca-ed by an imerrupdon of the
ner,eS and pa hwa>
from the bram tQ
pathways are located in the spinal cord, which passes through the bones
vertebiae, that comprise the spinal column (Fig. 26-2). The function of
I
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413
PHYSICALLY HANDICAPPED CHILDREN
Copyright V 1982 by Grune & Stratton.
ISBN: 0-8089-1391-3
All rights of reproduction in any form reserved.
.BRRBI 1 'WMJIHiriwmiiw
414
DISLOCATION OF THE
CERVICAL VERTEBRA
FRACTURE AND DISLOCATION
OF LUMBAR SPINE
TEAR
ALLOWING
DISLOCATION
FRACTURE
Fig. 26-1. Injuries to the spinal column. Dislocation and fracture dislocation of the spinal
column may or may not cause serious injury to the spinal cord.
ft
SPINAL CORD
(SHADED)
INSIDE
■VERTEBRA
Fig. 26-2. Normal spinal column and spinal cord. The spinal
column is composed of 7 cervical. 12 thoracic, 5 lumbar, and 5
fused sacral vertebrae through which the spinal cord and its
branches pass.
Traumatic Paraplegia and Quadriplegia
415
SKIN
SPINAL CORD
(CROSS SECTION)
I
I
MUSCLE
Fig. 26-3. Nerve pathway. Sensory nerves bring impulses into the cord, where they
can be transmitted to the brain, and motor nerves carry impulses from the cord (and
brain) to various muscles.
I
these pathways may be disturbed because of pressure exerted on the spi
nal cord by bony fragments or, in rare instances, soft tissue from the
cushions (discs) between the vertebrae. If the pressure can be removed
quickly enough and the blood supply to this area restored, then occasion
ally the nerves will begin to function again. Spinal cord pathways that
have been completely torn apart by the injury will not regrow with our
present repair techniques, however, and the resulting paralysis will be
permanent. Research is ongoing in this area, and hopefully the future
will hold discoveries that will allow us to repair these injuries success
fully. Nerves located outside the spinal cord, which either bring impulses
from the skin or carry impulses to muscles from the spinal cord, can be
successfully repaired (Fig. 26-3).
ACUTE CARE
I
<
The handling of the patient with an injured spinal cord immediately
following the injury can, in some cases, make the difference between an
incomplete injury, which may recover, and a complete injury, which will
not. Injured athletes or persons injured in a motor vehicle accident who
are conscious but complain of being unable to move their limbs very well,
or note an electric type of pain shooting into their limbs, should not be
moved until they can be moved by people who have been trained to take
care of such injuries. Such patients should be moved on a board that has
attachments to fasten the head and body so that the head will not rotate
in the process of moving. These patients must not be allowed to sit or to
416
Donald A. Nagel
have their heads elevated to take a drink, and they must not be allowed
to walk, even though they desire to. If transportation cannot be arranged
quickly, patients who have little or no sensation and no motion in their
extremities should be protected from shock.
Once these patients have reached a hospital, they should be placed in
the hands of a physician knowledgeable in the care of such injuries. The
patients injured spine should be protected during the process of obtain
ing x-ravs. Treatment will be based on the history, physical examination,
and the x-ray findings. In injuries to the neck, tongs are usually placed
into the skull so that traction can be applied to bring about a reduction or
a realignment of the fractured bones. Injuries to the spine at the chest
and at the abdominal level are usually cared for in special beds. Rubber
tubes (catheters) are inserted into the bladder to allow drainage of urine,
and care is given to see that the patient continues to have bowel move
ments. Of special importance is frequent turning so that the skin does not
break down. There is some disagreement as to whether or not operations
should be done on patients who have complete paralysis and loss of all
nervous functions below the level of the injury. There is uniform agree
ment, however, that if the patient has some neurologic function, and if
this diminishes during observation, the patient should have an operation.
The operation usually consists of a decompression of the spinal cord, and
may, in addition, be accompanied by a spine fusion. Depending upon the
type of spine fusion, the patient will have to be immobilized in some type
of device while the fusion becomes firm. This will take 6 weeks or longer.
REHABILITATION
Rehabilitation should begin shortly after injury. Perhaps the most
important aspect of this is the patient's morale. Generally speaking, pa
tients who develop traumatic paraplegia and quadriplegia have been ac
tive individuals. They should be encouraged to continue in their active
approach to life. The seriousness of their injuries should not be ignored,
but the fact that the personality of the individual and his or her mind are
more important than any physical loss should be stressed. Patients
should be encouraged to set goals for themselves, such as self-care and
locomotion. If they can be treated in a spinal cord injury unit, where the
personnel are geared to handling the problems of this type of patient and
where the patients can see other people with problems as serious as theirs
who are making progress towards their goals, then they will be encour
aged.
Patients who are quadriplegic will have to set lower goals for them
selves than patients who have the use of their arms. Nevertheless, such
patients should be able to feed themselves with the assistance of various
special devices, and locomotion should be possible, at least with a motor
ized wheelchair.
Paraplegic patients, in addition to being able to feed themselves,
should learn to take care of their bladder and bowel functions. Many
paraplegic patients develop some control of their bladder without the in
sertion of a tube. This involves the use of their hands on their abdomen to
push out the urine. Male paraplegic patients will require the use of a
urinal, and females generally use pads with special types of pants. The
bowels are usually easier to regulate than the bladder; this is accom
plished by means of suppositories or enemas. Even when the level of the
spinal cord injury is high, paraplegic patients should at least be in
structed in the use of crutches for ambulation. They may later choose to
use the wheelchair as their primary means of locomotion, but if they have
Traumatic Paraplegia and Quadriplegia
the option of using crutches in particularly difficult situations, they will
be better able to cope with their environment. Paraplegic patients will be
taught a swing-to or a swing-through type of crutch walking and will be
fitted with long-leg braces.
A major step in patients’ rehabilitation occurs when they leave the
hospital to return home; yet another occurs when they return to school.
Patients must be accepted in each of these situations as individuals, and
at times this will be quite awkward for patients, as well as family,
teachers, and friends. They must be encouraged to take the positive ap
proach—to seek out new friends and experiences and to develop their
minds to the fullest so that they can become self-supporting in the future.
Literature is available for these young people (some is listed at the end of
this chapter), and. in many areas, associations of patients who are para
plegic and quadriplegic have been formed. There are, in fact, interna
tional wheelchair Olympic games (Fig. 26-4), and young athletes might be
encouraged to join organizations that participate in such activities.
There are problems to be faced and adjustments for family and
teachers to make. Specifically, patients will need more time than the av
erage for self-care and for attention to their bladder, bowels, and skin.
They will probably need a special bed, wheelchair, and braces. Other as
sistant devices will be necessary. Patients should be encouraged to care
for themselves as much as is physically possible and should not allow
themselves to become dependent and depressed. They should seek guid
ance in vocational planning and training so that the employment that
they plan for is obtainable for them. They should remain in close contact
with the physician, who understands their problems completely. Urinal
ysis should be performed at least monthly, and x-rays should be taken
yearly to evaluate the possibility of kidney-stone formation. In contradis-
I
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I
I
F'ig. 26-4. Wheelchair
games. Games are impor
tant to some paraplegic
patients.
I
hr
■s
CS)
418
Donald A. Nagel
tinction to adults, younger patients may develop deformities in the spine
and in the extremities if they have asymmetrical muscle pull. Many pa
tients with quadriplegia and paraplegia develop pain and muscle spasm.
Various new medications are becoming available almost monthly. If
these do not solve the problem, then neurosurgical consultation should be
obtained to evaluate the possibilities of removal of scar from around the
traumatized area or of other neurosurgical procedures to eliminate the
pain.
One of the most important decisions that patients will make is what
vocation to pursue. Patients who can become self-supporting are well on
the way to an independent, fruitful life. It is recommended that each indi
vidual work closely with a vocational counselor and read the Handbook
for Paraplegics and (Quadriplegics. The following is quoted from the
Handbook with the author’s permission:
Among some of the jobs or businesses that paraplegics and quadriplegics
have successfully had are as follows: switchboard operator, secretary, sales
man. teacher, watch repairer, jewelry designer and repairer, woodworkers,
artist, bookstore operator, accountant, office manager, lawyer, doctor, physi
cal therapist, architect, publicity man. actors, disk jockey, book reviewers,
copy readers, writers, mail order businesses, stationery and greeting-card
store, gift store, magazine agency, florist, weaving, hydroponic farming, stat
istician. IBM operator. Comptometer operator, plastics manufacturer, elec
trical assemblers, radio and TV repair, wheelchair repair, civil service, sew
ing machine operator, embroidery, leathercraft, photography, bookbinding,
hobby shop, philatelist, real estate, phone solicitation, answering service,
addressing envelopes, advertising, taxidermist, research worker, clipping
service, designers, draftsman, and many others. These jobs and businesses
are not conjecture, in each case at least one paraplegic or quadriplegic has
worked or is working in the classification. If anything about them should
impress you, it should be the variety of employment.
Setting realistic vocational goals and then setting about their
achievement with determination should make living a successful adven
ture.
BIBLIOGRAPHY
Department of Health. Education and Welfare. What You Should Knoiv About
Paraplegia. Publication No. SRS-RSA-119-70. Washington, D. C.. Govern
ment Printing Office, 1970.
Department of Health. Education and Welfare. Spinal Cord Injury—Hope
Through Research. PH Service Publication No. 1747. Bethesda, Md., Na
tional Institute of Neurological Diseases and Stroke. National Institutes of
Health. 1968.
Frost, A.. Handbook for Paraplegics and Quadriplegics. Chicago. National Paraple
gia Foundation, 1964.
National Paraplegia Foundation. Hoic to Get Help If You Are Paralyzed. Chicago.
National Paraplegia Foundation.
Norton. P. L., and Foley. J. J.. Paraplegia in children. Journal of Bone and Joint
Surgery 41A:1291, 1959.
i
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bo
THE SCOURGE
The Indian plague epidemic of 1994
V. K. Ramachandran
in Bombay
I
t
TN the first week of September 1994.
Xthe first laboratory-confirmed cases
of human plague in India since 1966
were reported in Beed district in
Maharashtra.
By September 29.
according to oificial reports, there were
328 suspected cases of plague in an
area with a radius of 30 km in Beed,
and there were 325 suspected plague
cases in no less than 23 out of 29 dis
tricts in the State. On September 22.
an epidemic of pneumonic plague
spread rapidly in the city of Surat in
Gujarat. By September 30, according
to official figures, there were 752
plague patients m Surat, and 44 per
sons were killed by plague. Surat
remains the worst-affected centre of
the current epidemic.
From Surat, the disease spread to
Maharashtra, and. in addition, by
September 29. 62 cases were reported
trom West Bengal. 21 confirmed cases
and 43 suspected cases from Delhi,
five cases from X’aranasi (Uttar
Pradesh-), three from Haryana and one
each from Punjab and Kerala. Three
suspected cases were reported in
Bangalore on September 30. On
October 1, it was reported that there
were more than 2,800 suspected cases
countrywide, and more than 4,000 on
October 2. Putting together evidence
from press reports of officials figures,
by October 1, the total plague-related
mortality was 54 persons in Gujarat,
and, on September 25. Maharashtra's
Health Secretary Ramanand Tiwari
told Frontline that there had been one
plague death in Dhule district. Two
persons died of plague in Delhi on
September 30. and. on the same day. a
youth from Khar in Bombay died in
the isolation ward of the Kasturba hos
pital.
The plague epidemic has had inter
national repercussions. By September
30. the Gulf Cooperauon Council had
banned flights to and from India; the
United Arab Emirates had stopped the
import of foodstuff from India and the
berthing of ships from India at its
pons; Russia had declared a six-day
quarantine on passengers from India;
and Air Lanka. Emirates, Pakistan
International Airlines,
Bangladesh
Biman, and Aeroflot had suspended
services to India (some airlines have
since resumed some flights). On
September 30, European airlines
decided not to suspend flights to India.
I he United States State Department
announced that the risk of internation
al travellers being infected by plague in
India was low, and the British Foreign
Office said there was no cause for con
cern in the major tounst destinations,
while advising people not to risk
plague-affected areas. Some European
countries have introduced limited con
trols at airports.
On September 29, plague cases were
still spreading, although cases were
being cured, and plague mortality had
fallen sharply in Surat. In New Delhi
on September 28. Union Health
Secretary M. S. Dayal said that mortal
ity had been controlled (two plaguerelated deaths occurred in New Delhi
the next day), that the infective stage of
the outbreak would end in a week, and
that treatment of affected persons
could take another three weeks or so.
4
Frontline, October 21,1994
I'.
K J \i=
(Facing page) In a hospital corridor in Siirat, alert
with personnel of the Rapid Action Force:
removing a body.
‘
1
At the same press briefing, ±e repre
sentative of the World Health
Organisation (WHO) in India, N. K.
Shah (who is a citizen of Nepal),
expressed
confidence
in
the
Government of India’s estimate that
the number of plague-affected persons
was about 1,100. and said that, barring
a fresh outbreak of plague, the current
one will be over in three weeks.
The epidemic began in Beed dis
trict. There were some tremors in the
district during the earthquake in the
Latur-Osmanabad region in 1993.
Although outside the main earthquake
area, many people left their homes and
old houses were used to store gram.
Reponers have been told that these
storage-places became infested with
rats. Early in August. Sonaji Kashinath
Lange, sarpanch of Mamala village,
Majalgaon taluk, informed the Kuppa
health centre that a swarm of fleas flew
out ot a house that was unlocked after
being closed tor a long time (subse
quent reports contirm significant rat
falls in the \illage). On August 26. the
first suspected human plague case
appeared in Beed. On September 2,
the
National
Institute
of
Communicable Diseases (NICD) was
called in by local authorities. On
September 15, a front-page piece in
The Times ofIndia by Kalpana Jain and
Subhas Kirpekar reponed four cases of
plague from Beed. (Asked to com
ment, Maharashtra Chief Minister
Frontline, October 21,1994
' 'I
. z’
; ’'i
Pictures: By special arrangement
Sharad Pawar said he was unaware of
the news.)
Although no deaths have been
reponed, the number of cases erf
bubonic plague in Beed and Sholapur
continues to rise. One case of pneumonic plague has also been reported
from the Beed civil hospital.
On September 22, after a day on
which rumours went through Suraj
city that the public water supply was
poisoned, an epidemic of pneumonic
plague began. Repons of the number
of deaths on the first day - even from
official sources - varied: The Times
India cited an official repon that 24
people died; another “official figure”
cited was 45; and the Chief Secretary
to the Government of Gujarat said 17
deaths had been reported by the
evening of September 22. Two promi
nent persons, however, differed; Union
Health Minister B. Shankaranand said
that until a team of the NICD submit
ted its repon, “it could not be said that
the deaths were caused by plague,”
and Gujarat Chief Minister Chhabildas
Mehta declared that the virulence in
Surat was “not plague at all.” In
Bombay, Doordarshan’s Marathi news
telecast made no mention of the Surat
epidemic.
In Surat, nevertheless, officials con
firmed an epidemic of plague on
September 22, and by September 24,
six cases were reponed from
Ahmedabad,
six
from
Baroda
(Vadodara), four from Bhuj, and one
<each
’ from
"
Gandhinagar, Palanpur and
Cambay
’
in Gujarat. By Sunday,
September 25, Ahmedabad, Baroda,
Amreli.
Bharuch,
Ankleshwar,
Jamnagar and Bulsar were declared
plague-threatened. The areas worst
affected in Surat were Katargam and
Ved Road. Cases were also reponed
from the Ghodod, Mithikhadi and
___ ,
Chimini
Tekra
areas,
from
Sanjaynagar and Rajivnagar of the
Udhna industrial suburb, from slums
around the Elbee Cinema, from the
working-class
„
>
Limbayat
and
Ruderpura areas, and from the com
mercial areas of Chowk Bazar and
from a centre of the diamond cutting
industry in Varachha. Although the
epidemic is one of pneumonic plague,
three cases of bubonic plague were
reported on September 24.
Epidemiologists suggest that plague
could have been brought to Surat by
migrant workers from Maharashtra
(Biswaroop Das’s study of Surat slums
shows migration to Surat of workers
from Jalgaon. Nashik, Dhule, Nagpur,
Buldana,
Bhandara.
Raigad,
Aurangabad. Akola, Ahmednagar and
Beed districts in Maharashtra) or could
have originated in Surat after the
floods, when carcasses were left to rot
in the streets, or by a combination of
these two lines of transmission.
For at least three days, the health
and general administrations in Surat
5
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A patient being brought to hospital.
I
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were in chaos. Large numbers of pri
vate doctors fled the city, the coordina
tion between public health authorities
and health personnel in hospitals was
poor, supplies of antibiotics were
attacked and looted, and spokesmen of
the Government spoke in different
voices. A large-scale exodus of persons
from Surat began. One newspaper cal
culated that 2"0,000 persons left Surat
in the three days between September
23 and 25; others have estimated that
400,000 persons, or about one-quarter
of the cin-’s population, left the city.
Buses and trains were packed and tick
ets were sold at very' inflated rates; a
friend from Economic and Political
Weekly reponed that the price of a bus
ticket from Surat to Bombay was Rs.
1,500 on September 25.
A lesson from the first four days of
the epidemic in Surat was that where a
fear-stricken population has little faith
in the public health system, isolating
patients is difficult. iVIore than 100
patients ran away from hospitals in
Surat in the early days of the epidemic.
On September 25, the Rapid Action
Force was deployed in Surat, and the
Government announced an <eight-point
'J
“action plan” to control the epidemic.
In practice, hospitalisation and the
provision of antibiotics are the most
imponant measures of control at jpresent. After September 25, the number
of deaths declined, although the dis
ease continued to spread.
Although many doctors, particularly
doctors with private practice, fled the
city, many stayed on, particularly in
public hospitals. At least five doctors
and three nurses from the Surat civil
hospital were infected by plague;
8
die crisis in Surat; the administration in
Bombay did not consider it necessary
to take public health security measures
in the city in response to the outbreak
of plague in Beed.
An attempt is being made to screen
entrants to Bombay from Surat and to
fumigate incoming trucks, but given
the volume of traffic and the diversity
of modes of transport, these cannot be
even remotely comprehensive. The
Bombay Municipal Corporation and
the Government of iMaharashtra have
discussed the possibility of invoking
the law to seal the city’ from entrants
from Surat; this too is unlikely to be
successful. (It is of some interest that a
similar measure failed in the last centu
ry as well. On October 19, 1897, a
telegram
from
the
Government
ordered that all third-class railway pas
sengers from the plague-affected areas
of Surat and surrounding areas be
stopped. The Plague Committee noted
that the order did not work mainly
because they were evaded “(I) by pas— sengers booking second class and (2)
Index of real per capita public health
passengers travelling down the line
expenditure in India on public health
from Surat, and buying
tickets to
.
and on the prevention and control of
Bombay from Broach and other unin
diseases. 1984-85 = 100
Year
Index
I fected stations.”) The Corporation has
announced that it would increase
Public prevention
rodent-killing in the city’ and that more
and health control
garbage-collecting trips were being
of diseases
organised. It also announced that, by
1984- 85
Too
100
September 26, two million people had
1985- 86
101
94
been surveyed and that 600 “contact”
1986- 87
100
94
persons - that is, in contact with immi
1987- 88
95
98
grants from Surat - had been identi
1988- 89
97
100
fied.
1989- 90
103
103
Of the different methods of plague
1990- 91
100
94
control,
Bombay’s
administration
1991- 92*
95
87
appears to be concentrating on three
1992- 93**
____________ 94______
83
sets of measures;, first, large-scale pub
• revised estimates
** budget estimates
lic announcements; secondly, identify
Source : V.B. Tulasidhar. ‘Expenditure
ing patients, organising hospital beds
Compression and Health Sector Outlays',
and hospitalising patients; and. thirdly,
Economic and Political WeeKfy. November 6. 1993.
stocking up on antibiotics, particulariv
tetracycline and especially for prophy
among those on the honour-roll of per laxis (there was panic buying of tetra
sons infected while treanng others were cycline in Bombay as soon as news of
Avinash Dave, S. Sharma, Kalpesh
the Surat crisis appeared: as in Surat,
Bavsar and Sudeep Nair.
the price of tetracycline rose sharply, to
The epidemic in Surat is a special prices the poor cannot afford).
threat to Bombay. There is enormous
Bombay’s
Deputy
Municipal
traffic between Surat and Maharashtra
Commissioner in charge of health,
and between Surat and Bombay Sudha Bhave, expressed confidence
(according to one official estimate,
that the supply of hospital beds and
more than 55,000 persons migrated drugs would be adequate. At present,
from Surat to various parts of the State
the public mood in Bombay can be
during the present crisis). Bombay is
described as tense, but there is no
rodent-ridden, and one-half of its pop
panic.
ulation is homeless or slum-resident,
It has been noted that the real per
and lives in conditions of bad sanita capita public expenditure in India on
tion, congestion and general depriva public health and disease-control pro
tion that are conducive to the rapid grammes has been cut back in recent
spread of infectious disease.
years (see Table). V. B. Tulasidhar, an
Aleasures to control plague have economist at the National Institute of
been taken in Bombay in response to Public Finance and Policy, has noted
Frontline, October 21,1994
1
COVER STORY
that “real expenditure on disease con
trol programmes remained virtuallv
stagnant during 1985-91 and fell
steeply during the adjustment period”.
Tulasidhar considers the overall
impact of adjustment programmes on
medical and public health budgets to
have been marginal; at the same time,
“due to cuts in specific-purpose health
sector grants to States, the burden of
compression was mainly on preventive-cype disease-control measures...
mainly meant for controlling infectious Arunkumar Bhatt
diseases which afflict mainly the poor.” in Surat
In addition to general cutbacks in
expenditure on public health and the
'HIS time round, the people of
control of infectious diseases, in 198~
Surat panicked. Nearly half of the
the Government of Maharashtra began 22-lakh population in this industry
explicitly to dismantle the institutions rich city- in Gujarat fled their homes of plague prevention and control in the by road, rail, air - in the last week of
State. The plague control unit under September. They ran from pneumonic
the Department of Public Health was plague and carried yvith them the infec
abolished. Despite repeated advice, tion to other parts of the State, and
despite warnings regarding the possi other States. The plague became an
bility of rodent-bome infections after epidemic.
the earthquake, and despite having
Officially, 48 persons have died of
agreed in principle to re-establish the pneumonic plague in Surat and 55 per
unit, the Government did not re-estab cent of 600-odd cases admitted with its
lish the unit. (After the epidemic m symptoms in the local hospitals tested
Surat. Ramanand Tiwari told Frontline positive for it.
it would be revived.)
The normally resilient Suratis. yvho
In 1989. the Government-run took in their stride an outbreak of
Haffkine
Bio-Pharmaceutical cholera in 1988 which claimed 102
Corporation ceased production of anti lives and an outbreak of hepatitis B in
plague vaccine. On September 25, 1989 which claimed 129 lives, were
Tiwari told Frontline that a remaining
i
devastated this time by the very- name —
batch of 14.000 vaccines, with
...di an plague. The Government’s inability’ to
expin- date of November 1994. were tackle the problem, its attempts to
being tested for their potency (the first underplay the gravity’ of the situation,
batch of 10,000 vaccines was present and the media’s exaggerated reports of
ed by the chairman of the Haffkine death, compounded their fears.
Bio-Pharmaceutical Corporation to the
Mayor of Bombay on September 30).
The Health Secretary- said a lead time A
of “about a month” was required to
begin production of the vaccine. It has
since been announced that the first
100,000 doses of fresh vaccine would
be ready by October 30. Asked to
comment on the cutbacks and on the
abolition of the plague control unit, the
Health Secretary told Frontline that,
given the conditions at the time,
“investment in plague was like invest
ment in dinosaurs.”
Shocked,
shattered Surat
l
1
Among the first to leave were doc
tors, particularly those with a roaring
practice, executives and businessmen.
A Government given to imposing curfeyv at the slightest provocation did not
'bother
'
to impose restrictions on entry
to and exit from the city; the question
ol putting Surat in quarantine was not
even considered.
The chic authorities and a local
newspaper. \'av Giijarai Times, under
took a campaign telling the people chat
pneumonic plague was curable and
advising them not to leave. But no one
was willing to listen.
“How can you stop people running
for their lives when you do not provide
either medicines or treatment, or even
clear the filth?” asked a civic official in
Ahmedabad. Besides, said a police
officer, it the people had been prevent
ed from leaving Surat, it would have
led to a law and order problem. So. ±e
Government opted to allow the epi
demic to spread.
Traditionally a centre for business,
Surat is also among the filthiest cities in
India, largely the result of rapid industrialisation and haphazard'
,
1 growth.
WTien the waters of ±e river Tapti,
★ ★ ★
Plague can be prevented, controlled
and cured. The prevention, control
and cure of plague are basic tasks of
the public health authorities, and the
occurrence of an epidemic of plague in
the late 20th century represents a fun
damental failure of a health system in
modem society-. The Indian plague”
epidemic of 1994 must be controlled
and ended, and health policy and
investment must ensure the prevention
and control of avoidable infectious dis
ease among the people of India. ■
When the exodus began, a scene at a railway station.
Frontline, October 21,1994
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which had inundated die city in the
second week of September’, finally
receded barely 10 days before the dis
ease broke out, it left behind stinking
puddles, slush, garbage, sewage and
carcasses, ideal conditions for an out
humans through house rats. The
Sanjeev Unhale
break of diseases. However, in spite of
rodent population had increased
protests from residents demandins that
manifold in the entire Marathwada
the city be cleaned up. neither the
f | ’’HE Government of India, and region after the earthquake.
municipal
authorities
nor
the
1 the people in general, had bv and
When this correspondent visited
Government took any notice. let alone
large ignored the threat from plague the plague-affected villages, including
initiate action.
in the comforting belief that the killer Mamala, Salimba and Laxmipur, the
The pneumonic plague was first
disease had become extinct in the pungent smell of pesticides hung in
reported from Ved Road, where seven
subcontinent way back in 1966. Even the air. Walls and houses were cov
persons believed to rhave been
suffering
----- .—**^**“&r
the detection of a significant, though ered with graffiti and posters appeal
--n hours £
| isolated, case which indicated the
within hours of one another on t presence of the Yersinia pest is bacte- ing to the people to eliminate rats. A
September 21. Three of them were , ria in 1976 by the Beed district health number of dead rats had pea-sized
from Maharashtra. Suresh Bokade. 20, I authorities had no effect on the gov- nodules on them, indicating that they
of the Lakshminagar Housing Society, I emment machinery’. The Rip Van were infected with plague. Villagers
was perhaps the first victim - he died ' Winkle-like slumber continued till the said some cats and dogs which had
eaten the rats had died.
on die way to hospital alter passing
pestilence claimed its first batch of
Village sarpanch Sanaji Kashinatha
blood in his sputum.
victims in Mamala village of the same Langhe recalled that the first sign of
By September 22. 1" people had
district in Maharashtra, in August this danger was noticed by one Vashitha
died in quick succession. The symp
year. However, it took one more Langhe in the first week of August.
toms were the same: high fever, blood
month for the authorities to acknowl The moment he opened his house
in the sputum, cough, luns congestion
edge the existence of a plague epi which had remained locked for a long
and severe body pain. The municipal
demic.
time, a swarm of fleas covered him
corporation's Chief Medical Officer,
For the first time, 38 persons were and soon spread in the area surround
Dr. R. P. Sinh, and Deputv .Municipal
identified as showing positive symp ing the house.
Commissioner (health) Dr. Mohanty
toms of plague in Mamala, a hamlet
The sarpanch said he had informed
suspected it was pneumonic plague.
with 53 houses, in iMajalgaon tehsil. the Kuppa health centre of this on
But in the capital, Gandhinagar, the
haly<T dur'ngJhe September 30 August 5. Only when aa uuu
doctor, who
entire matter was kept under wraps. A
earthqunfc in rhe AUraihwada region, visited the place 10 davs later was
senior Minister, not from the Health
the village had received tremors and covered. with
. . fleas
~
did the authorities
Ministry, told the bureau chief of a
the entire population was rehabilitat realise the seriousness of the problem.
news agency under cover of anonymity
ed in makeshift shelters away from The villagers were unaware of plague
the toll in Surat was 200. Immediately,
their houses which were since used to though they were showing symptoms
the news was wired and was picked up
store grain and fodder. One theory’ of lymph adenitis in their armpits.
b\ the national and international
put forward on the emergence of The district administration started
media. In Surat, the people panicked
plague
is that the rodent population in spraying DDT in the last week of
further.
the fields migrated to human habitats August. By that time, 38 persons had
As tar as they were concerned, the
on account of the destruction of their been affected in Mamala. On
fact that even the BBC had reported
holes in the subterranean upheavals Sepetmber 1, their blood samples
this figure was enough. Given’ the
and passed on the epidemic to were sent to Pune and Bangalore for
administration s abysmal record in
providing sanitation facilities, fearful
memories of plague kept alive through plague.”
gists had done blood cultures and
fact and tolk tale, and the ravages of
The Chief Minister's argument was
the flood and the Government’s tardy that plague first attacked the rodent established that it was pneumonic
response, the non-availabilitv of medi population which then died en masse. plague. As Mehta prevaricated; the
cines, the lack of infrastructure to iden What he did not reveal, which the NICD confirmed the finding. Dr. A.
tify quickly those affected, and the research paper did, was the fact that K. Mukherjee, Director-General of
unhygienic conditions in public hospi these deaths could occur elsewhere, Health Services, and Union Health
Secretary’ M. S. Dayal also put the toll
tals resulted in the exodus from Surat.
not necessarily in the affected area. His
Gandhinagar made things worse by second argument was that the inci in Surat at 44.
Thus when Mehta finally announced
withholding information. Often its ver dence was typically confined to a par
sion contradicted the information ema ticular neighbourhood and did not that 35 lakh capsules of tetracvcline
nating from Surat. As the official death occur in the scattered manner it struck had been rushed to Surat and 34 lakh
toll went up from 17 to 27, Chief in Surat. This, however, is more typi capsules of tetracycline and 8.000
Minister Chhabildas Mehta told the cal of bubonic, not pneumonic plague injections of streptomycin were being
press in Ahmedabad that the killer dis spread by inter-human transmission. airlifted from Ahmedabad, there was
ease was possibly viral pneumonia. He Besides, it had been confined to Ved anger among the people. The drugs
quoted a research paper published bv Road, Katargam and Chhatrabhata. were in short supply and their prices
Dr. Saraljit Sehgal and Dr. Rajesh The third point was that the family had risen three to four times; a strip of
Bhatia of the National Institute of members of victims had not been 10 cost Rs. 80. Many’ thought the dis
ease was water-borne; as a result even
Communicable Diseases (N1CD) say infected.
mineral water, at Rs. 25 a bottle, cost
ing, “The preliminary circumstantial
However, before his arguments more than double.
evidence suggests that it cannot be the could reach Surat, two local patholoFor five days, confusion reigned in
The starting point
10
Frontline, October 21,1994
■.-J’-.-*»
■
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testing. The samples tested positive.
All this was over in the first week of
September, but ±e officials of the
Central Government pressured the
State machinery not to announce the
return of plague, to avoid panic. The
State health officials were confused
±ough they had started distributing
tetracycline tablets. The situation
went out of control after September
15.
Half a century- ago, the spread of
any epidemic used to be restricted to
a particular town and could be con
tained there by controlling the entry
and exit of people. Considering this,
the administration launched an inten
sive plague prevention drive in 50 vil
lages falling within a radius of 15 km.
However, this time, because of the
increase in the population and speedi
er means of communication, their
task was difficult and the disease w’as
transmitted to seven adjoining dis
tricts.
By September-end 200 cases of
bubonic plague were identified in
Beed district, 35 in Parabhani, 33 in
±e quake-affected Latur district, 29
in Nanded, 16 in Aurangabad and
four in Jalna. But the severity of the
calamity was felt by the au±orities
only when the disease took a heavy
toll in Surat. The return of more than
1,000 labourers to Marathwada, who
were working in Surat, intensified the
A red alert was now sounded.
Teams of doctors were deployed at
entry points such as railway and bus
stations. Civic bodies and ±e Public
Health Department were geared up to
spray pesticides in vulnerable areas
like slums. Regular garbage removal
from the streets and bylanes was
ordered. Non-governmental organisa
tions such as the Janarth in
Aurangabad and the Manavlok in
Beed have initiated, among other
things, mass campaigns to educate the
public.
However, these had an unexpected
response: people started buying and
using tetracycline tablets. In a tragic
case in Malegaon town, an infant died
after it was administered tetracycline
by panic-stricken parents. Many peo
ple are consuming tetracycline as a
preventive measure, which is danger
ous. Surprisingly, the Government,
some experts say, is giving out mis
leading advertisements regarding pre
ventive measures. A prominent
advertisement given by the National
Institute of Communicable Diseases,
published through the Directorate of
Advertising and Visual Publicity
(DAVP, 94/352) in almost all the
newspapers, suggests a preventive
dose of 500 mg of tetracycline every’
six hours for five days. This has been
contradicted by experienced physi
cians, who say this dose is too high
and the medicine is curative.
Likewise, a.syrup suggested for chil
dren was banned a decade, ago, they
point out. ..r
*
,
Amidst all this, the'common* man
____________________
feels the health
and local authorities
do something only when ^crisis, like
■
’
the
present plague,
presents ; itself;
otherwise they pay scant'attention to
the need to maintain the environment
clean, which is their immediate
responsibility. Once the epidemic
recedes, and the hue and cry raised
through the media ouuaiuca,
subsides, “im
Rip|
Van Winkle” will go back to sleep. ■
the city. One Surati, fleeing for his life,
was rirtually looted by transporters,
druggists and roadside dhaba-owrners.
Families even refused to give shelter to
relatives from Surat. In some villages in
Saurashtra, lathi-wielding patrols were
organised to keep out Suratis until they
took the plague test at district health
centres
and
reported
negative.
Urfortunately, none of these centres is
equipped to carry out these tests.
If the Suratis who fled to their native
villages became outcasts there, in the
city they were dubbed traitors. The
original Suratis reviled them for
encroaching upon the city’s services
and comforts, for ruining the environ
ment, for engendering disease and,
finally, when called upon to lend a
hand, for turning tail. According to
Kashiram Ran, a Lok Sabha member
from Surat, “The social relations with-
in Surati society will perhaps not be the
same anymore.”
As the plague moves elsewhere and
±e city struggles to overcome the
residue infection by swallowing tetra
cycline and shovelling filth, the people
are hard put to get their economy
together. The city’s trade, commerce
and industry’ have invested in Rs.
40,000 crore worth of art silk, textile
processing, diamond, dyes and chemi
cals and suppon engineering units.
Most of them are now closed. Workers
fled on the eve of pay-day, September
22, leaving behind pay-packets
totalling Rs. 100 crore. Factory owners
have fled to Bombay; some diamond
merchants have gone abroad. Doctors’
suggestion that factories be shut down
to prevent the spread of the epidemic
was read as an official order. And
although by September-end some peo
panic.
Frontline, October 21,1994
ple were returning to Surat, it will take
a month at least before activities are on
an even keel.
The president of ±e Southern
Gujarat Chamber of Commerce and
Industry estimated that the daily losses
in Surat’s industries amounted to Rs.
51.65 crore, including an export earn
ing of Rs. 2.5 crore. The largest indus
try, art silk and fabric, is losing Rs. 25
crore a day, the diamond industry Rs.
15 crore, dyes and chemicals Rs. 5
crore and engineering Rs. 3.85 crore.
Trade turnover loss is estimated at Rs.
20 crore. The exchequer is losing Rs.
3.35 crore daily - Rs. 2.10 crore by
way of excise, Rs. 25 lakh by way of
octroi and Rs. 1 lakh by way of sales
tax.
The total loss suffered by various
industries and trades is estimated at a
staggering Rs. 1,200 crore, a major
blow for the thriving but small econo
my. The diaifiond industry', for
instance, has piled up stocks of rough
stones (raw material) worth Rs. 3,000
crore. Delayed processing and export
would add to the interest burden.
Many units in all the sectors are smallscale and the apprehension is that thenworking capital may have been wiped
out. In fact, the Rs. 30 to 50 crore
annual turnover of private couriers
(angadia) benveen Surat and Bombay
is a fair gauge of the volume and pace
of commerce in the city.
But, of course, the heaviest blow has
fallen on the workers, who comprise
about 10 lakh of Surat's population.
While the 2.5 lakh diamond cutters
and polishers are losing Rs. 1.25 crore
in wages daily, about 4.5 lakh textile
workers are losing, daily, Rs. 2.25
crore. They earned between Rs. 80
and Rs. 250 a day in Surat; now in
their native villages most of them are
unemployed. The current financial cri
sis is bound to erode the wage struc
ture considerably.
The tragedy is that the epidemic and
its aftermath could have been avoided
had timely measures been taken. The
plague has not yet been eradicated.
Doctors Sehgal and Bhatia recall the
experience when “a disease simulating
pneumonic plague hit Tangnu village
in Himachal Pradesh in 1983. The sus
pected human pneumonic plague with
well-defined inter-human transmission
involved 22 cases and 17 deaths. The
outbreak lasted three weeks and
abruptly stopped after the suspect
cases and contacts were effectively
treated and control measures initiat
ed.” If this was possible in an obscure
village nestling 3,000 metres high in
the mountains, there is no excuse for a
bustling city like Surat to have gone the
way it did.B
11
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V. K. Ramachandran
is a major centre of
O industrial growth in Western
India, and is a metropolis that has
grown very rapidly. The growth
of industrial production has been
on a substantial scale, by means
of small industry, carried on in
workshops, rough sheds, manu
factories and households in dif
ferent pans of the city. Among
the important industries that are
and0^01^’ Pardy in 1116 smaJI
and less-regulated or “informal”
sector are textiles - including the
production of artificial silk (Surat
produces 60 per cent of India’s
artificial silk) and zari, textile pro
cessing and the production of
Par5s or textile and garmentmaking machinery’ - diamond
cutting (30 per cent of India’s
HBK ■ /J f
£™^Verim this sector is frorn
Street after the outbreak^fague.60' 6’ Municipal employees with insecticides on
a
12
Surat), plastics, engineering, and
chemicals and dyes. There has
also been growth in the highmvesttnent organised sector
notably chemicals and petro
chemicals, and in the financial
service and transpon sectors.
rhe growth of Surat’s popula
tion has been extraordinary: it
Frontline, October 21,1994
increased from 317.519 at the Census
of 1961 to an estimated 1.7 million at
p.e beginning of 1993. A study by
A ghost town
SmXs°0P ?’S °f the Centre for S°^
Studies in Surat published this year
esumates that 28 per cent of Surat’s
population lives in slums. Migrant
labour is a most striking feature of
Surat s labour force, and according to
one recent newspaper estimate,
SXT
C'°Se 10 75 per Cenl Uf
A Special Correspondent
control. The textile factories and the
———— ----diamond-cutting industry have
<i
are individually clean and SuteT oT’rfr°m Other
W communally
’
largest groCp
fOnnmg
SingIe
and
SKXSi " bj«
few days back, it occurred to
Jurats population: in Das’s study,
**e probably got that insight
'T6 mr18rants from Gujarat,
a 21 ashtra’ Uttar Pradesh. Orissa.
c -------you
approach
awav “P
™£y hve in sh“tv
approach the
the town,
town, from
from 55 km
km awav
Andhra Pradesh, Himachal Pradesh
itself
there
are
hillocks
of garbage on rirer^A f™8
Canals and the ’
itself there are hillocks of
Rajasthan. Bihar'and other States. Ian
mer. A large percentage of the ;
either
side
of
the
road.
The
river
St??3" A°f the Centre for Asian
apti has been turned into one vast city- s 2.2 million people live in !
Studies, Amsterdam, who has worked
sewer
and along both banks are slums. One estimate says that just on I
m Surat and other parts of Gujarat
5’000 s,ums '
sprawling
slums. Of all the cities I o 2gkR°ud there
as^o^h351 30 }-earS’ describes Surat
nd
that
huts
spring
up
in these set- i
>
as one big transit camp” of workers, i have seen, this is easily the filthiest. dements at the rate of 100 a day.
I
much
worse
than
Varansai
or
hh haxe here a reserve army of
The urban influx, coupled with
Kanpur.
If
at
all
plague
had
to
break
labour moving around in an economic
the newly-found wealth, has given i
out, it had to be here.
jungle, a predominantly male force of
When I visited Surat on nse to a number of housing colonies i
aliens with no or meagre skills... forev
September 25, the fourth day of the around the city, many of them unauer kept on the run and worn out in a
epidemic,
it was like a ghost town, thorised. So thev lack basic civic I
ruthless work regime."
amenities. The draiiinage system cov- |
lhe shops were all closed though ers
The growth of urban living facilities
only a small area of the town.
some
autorickshaws
were
on
the
and civic amenities remains far behind
Garbage is jijust■ thrown
’
by the road- i
road. Remarkably, the State trans side and s
Bremf0'^- °f Surat’S Population.
sewage
flows into the i
port buses were plying, ferrving peo
Breman writes: “The roads remain
ir* rn/-'l l
i
«
streets. Basic
facilities needed
for a i
ple out of the city.
onpa'ed in the new neighbourhoods,
decent life get a short shrift in all the
The
railways,
the
telecom
and
the
a l surface water is thoroughly polluted,
postal sendees were functioning. ciues of Gujarat, but this is much I
plants and trees are nowhere to be
Most
of the private doctors had fled more pronounced in Surat.
seen, power failure is the order of the
Piles of garbage, rotting carcasses
the
city
and the government doctors
day and night, sanitation and drainage
and
cesspools of sewage can be seen
of Surat and some from other parts
rot1",! !Smal State and-- malaria has
on the mam thoroughfares. Rats and
of
the
State
were
working
round
the
come back to the urban milieu with a
clock. These are the lowly govern bandicoots multiply in this situation.
vengeance. Even a longer list would fall
TTey were all flushed out of their
ment senants who are often remem
Shon of conveying the overwhelming
holes by the recent floods. Cattle and
bered
only
for
their
faults.
There
impression of filth, ugliness and
were no voluntary agencies at work donkeys roam the thoroughfares
decrepitude that meets the eve of the
If the disparity between the rich
except
some Bajrang Dal workers
newcomer on leaving the railway staancI the poor is the highest in India,
who
were
cleaning
up
some
streets
n. urat is said to be the dirtiest city
and the Church’s Auxiliary’ for wnthm ±e country it is the highest in
of Its size in the whole country.’
Social Action (CASA) from Delhi Surat. Side by side with those who
Nexertheless, the municipal authorities
that was distributing medicines in take a flight to Bombay in a private
boast .hat real estate prices are nearly
aircraft to have lunch and get back
the slums.
high as in Bombay, hardly less
there
are children who, without a
Surat has a tradition of business
n^f V1311 in the most ProsPerous
stitch on, are raised along the rail
and
it
was
here
that
the
British
estab
pans of the world.” A municipal offi
way lines.
lished their first trading post in A.D.
cial has been cited as saying that the
As we were leaving the city, I saw
1813 and the Dutch in A.D. 1820
citj generates 1,000 tonnes of garbage
a group of children frolicking in
Though
the
city
has
one
of
the
oldest
a day, of which 500 tonnes is collected
water, at the edge of the Tapti. Thev
municipalities, set up in 1852 and _have
by municipal staff.
nowhere to go, plague or no
made a corporation in 1966, in
v«ACC?rding t0 Bisvvaro°P Das’s sur
plague. They are from the shanty
recent
decades
it
had
grown
out
of
vey, about 80 per cent of the slum
town on the bank. ■
andSrih°,dt U?Cd °Pen Spaces’ canaJ
a d n?er banks' roacis and rail tracks
and other places other than latrines for water rose about 60 cm. Carcasses emphasised repeatedly the connection
defecation. “The attention is now were left to rot in open spaces after the between the current economic policies
xv-ater receded. According to a newspaocussed on the plague, as well it per
report, at a- recent
recent (before
(before the
the Cui C G^'emrnent of India and
should be, Breman told Frontline.
plague
epidemic)
meeting
between
curTer«
hettlth
meeting between msis-T^
But we must also remember that Surat’s
Deputy
Municin^
I „ e ,ep?dem,cs ha' e to do with
malaria and hepatitis may have claimed
Commissioner in charge of health and of a no hl'°f St3>? and the absence
X^e.”
S
Year
the hospitals and 250 doctors and iour^l hLt pul?llc1 sPheJe> he said. Public
ists. doctors warned the municipal off!
mim’1”8
pub,‘c health were not
Early in September floodwaters were Cial
“that epdemics of c“otera and
p™nues at all and “the state
m the town, and, in the Ved Road area
eventoplague
wereeimminent
’’
pretence of being an
one of the main areas of plague - possibly
Speaking
PCr/^
“™
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Paying the price
and Qatar suspended all flights
between their countries and India. One
Air-India flight to Jeddah, with 240
passengers on board, had to be recalled
after take-off, and pandemonium
resulted at the international airpons
when thousands of passengers were
Praveen Swami
was in place., either, for Delhi residents told their flights had been cancelled.
in New Delhi
who had returned from business trips Dubai, Abu Dhabi and Pakistan soon
followed suit. Malaysian Airlines
CCqr'HE only good business to be to Surat or other plague-affected cities: stopped operations to India, and
nor was an epidemic control plan in
in, one Delhi businessman place.
recalled staff working for Jet Airways.
recently said, “is the the tetracycline
The implications of these actions
On
September
25,
United
States
business. W eeks after the first reports
soon
became evident. Though most
Ambassador Frank Weisner
W eisner called on
or a plague outbreak came in. the
European and Asian countries did not
Onion
B
Health
Minister
national costs of India's worst recent
stop traffic, media coverage had its
Shankaranand
and told him Indians
-------- public health disaster are 1
inevitable impact: tourists in Delhi
e
g
fr0I
7
P[
a
S
u
e-affected
areas
to
evident. Reports indicate that the
could be seen walking around with sur
the
U.S.
would
have
to
fill
up
special
plague may have an abiding impact not
gical masks on. One major German
only on its victims and their families, forms on their arrival. Tour operators tour operator, Der, canceUed a tour of
out on a spectrum of Indian domestic read this as an advance warning of India. Major British tour operators like
and international business activity. If impending curbs on travel, particularlv Thomas Cook and Lunn Polly, too,
the Central Government believed the if the plague hit Delhi or Bombay, the are offering refunds to anxious trav
suffering of plague victims in Gujarat. major traffic hubs, in a big wav.
Over the next two days, as the num ellers. “At the moment,” says one rep
Maharashtra and Delhi would, like
ber
of reported cases . grew, several resentative of the Indian travel agent
other national calamities, soon be
Sita World Travel, “there is no major
erased from collective memory, that countries announced plague-related drop, and charter flights to Goa, for
restrictions
on
Indian
travellers.
From
smug assumption has been shattered.
example, are arriving on schedule. But
The first sign that the outbreaks in September 25, aircraft from India were if this plague scare continues, particu
Beed and then Surat would have fumigated on arrival at airports in larly in Delhi, which is the hub for trips
Rome and Milan, and passengers were
national implications came days after
to Jaipur and Agra, it will be disas
cases of suspected plague, later con subjected to special health checks. In trous.”
Frankfurt, doctors checked passengers
firmed. were reported in Delhi on
The September 29 decision by the
September 24. Within a week, the before being allowed to disembark. United Arab Emirates to suspend all
5irn
il
ar
restrictions
were
announced
bv
number of cases was to cross 120. The
cargo transhipment from India has put
the Bangladesh Government.
outbreak was. perhaps, predictable
trade with one of India’s major markets
Other
countries
reacted
in
a
more
Thousands of people from Gujarat
in jeopardy. The principal victim so far
drastic
manner.
When
on
September
had come to the city, and little effort
has been Air-India, which has been los
an international alert was declared
had been made to identify or monitor
ing
Rs. 2 crore a day. Indian Airlines
them. No surveillance infrastructure against air passengers from India. also has reported massive losses, which
Saudi Arabia. Kuwait, Bahrain, Oman
have been initially estimated to run into
“several crores”, and domestic opera
TTmTiMlJlJaMU.
TJ_.
tors like East West, too, have reported
declining traffic.
ini
The domino-effect provoked by the
breakdown in Gulf transhipments has
been enormous. Union Finance
WiaiQ
Secretary Tejendra Khanna has said
the “panic reaction” may retard Indian
expons by as much as 2 per cent, or
Rs. 1,400 crore. Agri-exporters have
been sharply hit by rhe loss of their
rSKSali
principal market, the Gulf, and their
SESSS-i
scrips have been steadily plunging. A
spectrum of commodities, ranging
from frozen meat to fruit and basmati
nee, can no longer be shipped to West
Asia. Bilateral trade with the United
Arab Emirates alone is estimated at 3
billion a year: Qatar alone impons over
five lakh tonnes of Indian fruit daily.
* Similarly, remittances from the Gulf
g to Kerala have been hit (see box)
< Alternatively, several Indians have
iowpriori^6G-B' Pant H°SPital inDeIhigets
been standed in the Gulf, though visa
extentions have been granted. While
Emirate nationals whose visas were
^orig history of apathy
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14
Frontline, October 21,1994
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expiring have been evacuated from
India on a special flight, Indians wish
ing to return to work in the Gulf or join
new jobs there have not been able to
go.
Bindu Bhaskar
Two thirds of India's oil imports
Bangladesh and the Philippines
come from the Gulf, and no one is cer
would fill up vacancies. Many who
tain whether Indian tankers will be
r | ’’HE Gulf ban on air landings has came home for the Onam festival,
allowed to dock at Gulf pons. While a
J- heaped losses amounting to sev
are worried about not being able to
Shipping Corporation of India tanker
eral crores of rupees on the aviation, return before their visas expire.
arriving from Korea was allowed to
travel and export sectors operating
Remittances from expatriates have
pick up oil and proceed to India, o±er
through Kerala. Flights of six airlines come under a shadow. Thousands of
tanker operators have been warned
ferrying 8,000 passengers on the households are affected as postal
their ships will not be allowed into the
Gulf route and generating a daily links are cut off.
territorial waters of the Gulf
business of Rs. 3.75 crore have
Canara Bank, which manages Rs.
Cooperation Council. If the situation
ground to a halt. A drop of Rs. 2 880 crore of non-resident Indian i
persists, India will be forced to dip into
crore a day in customs revenue has remittances from the Gulf even- j
its buffer oil stocks, which can only last j also been estimated.
45 days.
month, has tied up with three i
Caught in the grip of a severe cash
These losses are likely to be com ; shortage owing to flight cancella- exchange companies in Dubai, Doha j
pounded byr a loss of international | tions, travel agents and tour opera and Bahrain to facilitate financial i
transactions electronically.
investor confidence. In London,
tors, employing roughly 40,000
With ships from South-East Asia
Indian Global Depository Receipts
people, have requested airlines to skipping the port, tonnes of tea, cof
(GDRs) crashed after the BBC and
defer demands for payment and to fee and foodstuff remain in storage
CNN began carrying regular reports
refund unused tickets. October- in Kochi. Garments from Tirupur,
on the plague situation in Gujarat and
March is their peak season and all Tamil Nadu, sent to various destina
/Maharashtra. The Japanese trading
the major agencies are in the throes tions through a sea-air link via
giant Mitsui is evacuating its staff from
of a ‘zero-revenue’ situation.
Dubai, have also piled up in Kochi.
Bombay and Delhi; Israeli software
At least 25 per cent of the passenis also a setback to the hortiexpert Ayelet Rosenweig has cancelled , ger traffic to the Gulf consists of job- There
cultureJ trade. Nearly 40 tonnes of
CaQl.'nvo A «
_ 1Z*
i
a high profile visit to Bombav; a tour
seekers. As Gulf employers are vegetables and fruits worth Rs. 30 to
by the Mauritian Minister for Tourism
unlikely to wait indefinitely, there is Rs. 40 a kg routine!v find their wav
has been postponed, and foreign
concern that recruits from' Pakistan, to the Gulf. ■
experts at the Essar Gujarat steel plant
in Hazira have left the country.
Director of the National Institute of
Is this international reaction hysteri Urban Affairs, Dr. Dinesh Mehta, has granted for tetracycline impons to
cal.-' Union Petroleum Minister Satish argued that the central problem in ensure availability at reasonable prices,
Sharma told journalists in London the Surat was that revenues from high- and the Finance Minister announced
plague threat had been handled irre value businesses had been pumped that Rs. 20 crore would be kept aside
sponsibly by the international media. into land rather than infrastructure. to meet plague-related expenditure.
Could this situation have been
This argument, however, misses the High land prices and poor infrastruc
key point: that the international ture resulted in overcrowding arid poor avoided? As Dr. Saraljit Singh, a
response merely mirrors the break sanitation. Surat, Dr. Mehta argues, plague expen and adviser to the \X orld
Health Organisation, points out,
down of public confidence within was a disaster waiting to happen.
“plague breaks out fairly regularly
India. The problem has been that State
The Central Government’s interven
governments have shown little clarity tion, when it came, was also limited. around the world.” Exactly 13,366
of purpose. As late as September 20, Initially, no effort was made to limit the plague cases were reported" globallv
when bubonic plague spread from exodus from Surat: only after the out between 1980 and 1992, 206 of these
Mamala to several adjacent villages, break in Delhi did trains bypass the m an advanced country like the United
Maharashtra Deputy Health Minister ciC’• “Health is a state subject,” argues States. What went wrong in both Beed
I aban Ghatowar made the incredible National Institute of Communicable and Surat was the absence of a con
claim that the outbreak was minor, Diseases (NICD) Director K. K. tainment apparatus. “It is true the
since it was “of the bubonic variety, Datta, “so our role could only be advi warnings were not heeded,” argues
Duua. “It is true that Maharashtra shut
not the fatal pneumonic variety.” sor}’.
The Central Government
Similarly, on September 26 after cases instead used financial aid and drug down its plague monitoring facility in
had been reponed from around availability programmes as its instru 1987. But please remember, there are
Gujarat and two deaths recorded in ments. On September 24, the Union other demands. Polio, cholera, malaria,
V adodara, the Chief /Minister insisted Health Ministry’ set up a central control people die of all of these. And
that “not a single case of pneumonic room under the supervision of the resources are few.”
“Today”, admits Delhi Health
plague was registered anywhere in Prime Minister.
Minister Dr. Harsh Vardhan, “there is
Gujarat except Surat.”
More positive action decisions, when no epidemic control or disaster man
Why did the State governments made, were clearly firefighting mea
respond in this way? One possible rea sures devoid of any direction other agement masterplan either in this city
son is that they had no infrastructure to than ensuring drug availability. By late- or nationally. We deal with situations
deal with the crisis they were facing. September it was decided to’ despatch as and when they emerge. ”
The capital city’s response to its
Critics, however, argue that the 10 million tetracycline capsules and
response was entirely consistent with 2,000 tonnes of die powerful insecti near- 7 00 cases of suspected plague has
official attitudes to health and urban cide Gammexane to /Maharashtra and been chaotic. Figures given out by var
development policy issues. The Gujarat. Total duty exemption was ious authorites were often at odds.
Until recently, hospitals like the All
Frontline, October 21,1994
15
Kerala concerns
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India Institute of Medical Sciences
were not even reporting cases to the
monitoring authority. More criticallv.
no proper information on the plague
was put out by the authorites, leading
to a mad rush for surgical masks, tetra
cycline and even quack remedies
At the central Infectious Diseases V. K. Ramachandran
Hospital, patients walked in and out
freely, unrestricted by nervous pohee- ■pLAGUE is an infectious fever
men simng a safe distance away from X caused by the bacillus Yersinia
the building. The hospital itself is a Pestls (the information here on the etidecrepit,. rat-ridden colonial buHdin^ ni°g'’ preVention and control of
™ J' E' Park and
with an iirritable and overworked stm!' K T
- the ’body
.2. of a patient
„
in one case,
aban- o' .Pa^' T^book of Preventive and
doned by his family' was allowed toX disease
'19915'Ir ls Primarily a
on a bed for five hours before it was
n
r°den?’ Emitted bv the
removed.
1 "aS fat flea-.
which human beings
Once schools and public entertain
/?ome ln™lved. In India, the wild
ment faciHties were closed, complete fieri
haS heen idendpamc ensued, with commuters disatT
Th
reservoir of Plague.
peanng off buses and shoppers walk
of7
mam cllnical forms
mg around with surgical masks The nnb S“e m human bemgs: bubonic.
Official cleanliness drive failed n 7
t p"eumonic
septicaemic
improve conditions for the urban poor fuffcU" ririb°^C PiagUe' the patient
Incising a bubo—1482, Nurenberg.
particularly in East Delhi's sprawling 7
sudden fever, chills, headache
rodent
fleas, peridomestic rodent fleas,
slums. "Do you know." X DePh! nori27b7'°?'
enlarged iymph
commensal
rodent
fleas-humans;'
Ch-ef -Minister M. L. Khurana, "that the 77 7^ 1^1
lp
numans-human fleas-humans; and
the
groin
and
the
neck.
Pneumonic
until recently, garbage was not even
is high humans-humans (as in pneumonic
c eared out of slums because thev were plague, which affects the lungs,
hv -irr>7
PlaSue?- The incubation period of
ly
infectious
and
spreads
I
’
illegal colonies?”
by droplet
bubonic plague is two to seven davs, of
infection;
it
generally
follows
as
a
com
This story of chaos, confusion and
s as a com- pneumonic plague one to three’davs
of
bubonic-septicaemic
apathy has been mirrored at all levels. plication
and of septicaemic plague two to seven
plague.
Plague
bacilli
exist
in a pneu- days.
Union Health Minister B. Shankarmomc
plague
patient
’
s
sputum.
anand has been holed up in silence
The prevention and control of
There are at least five types of trans
since the plague broke, and repeated
plague
involves the control of plague
attempts to contact him proved unsuc mission of plague to human beings: cases, the control of fleas, the control
commensal
rats-rat
fleas-humans;
wild
cessful. The Minister has not, so far,
ot rodents, vaccination, chemoprophy
seen it fit to hold a press conference. rodents-wild rodent fleas or direct con laxis, surveillance and health educa
tact-humans;
wild
rodents-peridomesSimilarly, the Prime Minister has not
tion. Measures to control plague cases
seen any need to address the nation to tic rodents, commensal rodents-wild include early diagnosis, notification,
calm the widespread panic, justified or
isolation, treatment and disinfection'
otherwise. Foreign journalists and tour
1 reatment is started without waiting
Definitions of plague
operators have been offered free travel
tor confirmation of the diagnosis. The
and hospitality’ to “see the situation for
drug of choice is streptomycin admin
"PLAGUE is an infectious fever
themselves,” but there appears to be
istered
intramuscularly; tetracycline
X caused by the bacillus Yersinia
few takers.
administered orally is'an alternative
pesns.,
transmitted
by
the
rat
flea.
It
If there is one lesson from the plague
bulphnomides are used when other
is a disease of rodents, and epi
outbreak, it is that a coherent system of
drugs are not available and in certain
demics
in
human
beings
originate
prevenuve medicine, urban planning
other cases. Oral tetracycline is also the
ana disaster
aisaster management
would
’^fntact wid} the fleas of infected
and
--------- - have
drug of choice for chemoprophylaxisproved less expensive than contain^g
2±er W°Jds’ p,ague is
the alternative is sulphonamide.'
the epidemic. Delhi is now snendinf
Pnmanh a disease of rodents and
Immunisation with the plague vaccine
Rs. 2 crore for a rapid urban c^ean-up
th^cvd^Th^d' incident^ly int0
(the vaccine was developed in India in
programme, an
an expenditure
has 71 cMo™S;'n
programme,
expenditure rendered
1897 by Haffkine and modified in the
necessary by the decades-old degener20th century by Sokhey) is an impor★
Bubonic
plague
is
characat*°n.ot 1^le c^’’s urban infrastructure
tant preventive measure.
terised
J by
‘ J a swelling of the lymph
Critically, the plague is not the only
Park and Park write that there is a
nodes.
nrHnlAm
__ _i
....
problem confronting the public health
great deal of evidence of plague
*
Pneumonic
plagut
system:
over
u
.,
k
.
is
one
system: over 1,200 people are believed
remaining “silent” for periods of 10
where the lungs are extensively
to have died in the last four months of
years or more in respect of plague in
involved.
cholera in Bihar, Uttar Pradesh, ’
certain areas, followed by “sudden
★ Septicaemic plague is one in
Himachal Pradesh and Jammu and
explosive outbreaks of rodents or
which
the
blood
stream
is
so
Kashmir, an epidemic that rages large
human plague.” Mean temperatures
invaded by Yersinia that death
ly’unreported. If the lives lost are not
between 20 deg. C. and 25 deg C
occurs before the bubonic or
adequate reason to address these
and a relative humidity of 60 per cent
pneumonic
forms
have
had
time
^sues the crores of rupees wasted
are considered favourable for the
to appear. ■
will hopefully provide an added
spread of plague; these are roughly the
incentive. ■
climatic conditions that obtain in west'
em India from November. ■
A disease of rodents
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The route to humans
duced as a rule by the bite of infected tion of the disease.
rodent fleas, and also called enzootic
Sadanand explains: “To prevent
T)LAGUE took a very heavy' toll of plague. Persons with bubonic plague this, the wild rodent population
suffer
from
a
swelling
in
the
neck,
J- human life in the latter part of the
should be kept under surveillance.
19th century and the early part of the groin and axilla (arm-pits) and then Plague control units (in various
from high fever. The incubation peri
20th century. In India alone, more
States) do this by collecting wild
od for humans is two to six days.
than 10 million people perished from
rodents, taking out their blood and
Sadanand said: “After the bubonic
plague between 1896 and 1918
testing it in the laboratories. Once we
There was a steady decline in the stage, it becomes a pneumonic stage find any wild foci, we perform anti
when
the
bacteria
invade
the
lungs
of
incidence of the disease from the
rodent and anti-flea measures. While
middle of this century in India and man. Once that stage is reached, rodent control is done by fumigation
transmission can take place from man of rat burrows, flea control is done bv
human plague cases almost ceased in
1967. It has now erupted again, first to man easily by droplets, that is, bv
benzene
hexachloride
at Mamala village in Beed district, spitting saliva. This transmission (BHC, Gammexane). That is why
does not require fleas. Sometimes the
xMaharashtra, and a few days later in human blood stream will be full of we have to continue the existence of
Surat, Gujarat. While victims at
plague control units. We are doin^
Mamala were ’ ' '
this in Tamil Nadu. We established
the more iTJlT
i’
pneumonic
^eads through the flea {Pulex ^irri- the Institute of Vector Control and
has stalked Surat.
Zoonoses at Hosur in Tamil Nadu in
According to A. V. Sadanand.
1984.” (Zoonoses are animal diseases
Although plague was considered a transmitted to man.)
Vice-President
of the Indian
public heal± menace which had been
“What is important is ±at people
Academy of Entomology and retired
eradicated, the risk of its spreading to
Chief Entomologist, Tamil Nadu domestic rodents has remained. This should be educated immediatelv to
take precautionary steps and ’ use
— drugs. If the treatment starts
within 24 hours of the onset of
the disease, nobody need die.
In olden days, there were no
antibiotics and people used to
die like flies. Now we have
/wild mmn\
IfleaL
potent drugs. People having
[fle a ] ENZOOTIC [flea] /
\
/WILD ROD£NT\
fever, headache and swelling in
Jrodent]
the neck, groin, etc. should
Timrrnl
rod ent I
V epizootic?
peridomestic \
--------immediately take tetracycline.
FLEA] RODENT [flea] xffkEAL
The second most important
flea
' ENZOOTIC y /pEglDOME5Tlc\
thing is that the medical profes
sion should be alerted because
Ml’JJ.Til [rodent] RODENT (rodent
V EPI ZOOTIC?
/ PNUEMONIC \
most of them have forgotten
what is plague. They should be
MAN | EPIDEMIC Iman
JFLEA5.
1FLEA
educated to analyse the cases.
Thirdly, in places like Madras,
( Bubonic
mam] epidemic
where the rodent population is
MAN]
MAN
very high, the municipal corpo
ration should take rodent con
/SEPTICAEMIC\
' endemic \
FLEAS,
trol measures. Once the rodent
a] PLAGUE [flea]
FLEAS] plague
population is controlled, the
flea population goes down
MAN
automatically.
MAN
“Most imponant is that pre
viously endemic areas such as
— Karnataka, Andhra Pradesh
Goyemment, plague first starts with
and Maharashtra should revive
is essentially because plague organ their plague
control units. Bv watch
wild rodents, that is, rats in the field,
isms have been present in wild
ing the rat density and flea' density
lhe flea gets it from ±e wild rodents
but does not die. When the flea bites rodents. A public health problem and performing serological tests and
domestic rodents, the disease spreads could surface following natural clami- rodent blood tests, we will be able to
ties such as flood, earthquake or war.
among the latter. Thus “rat falls’' All these disturb the natural ecology^ predict the onset of plague. Port
cities, where foodgrains come by
occur. When rats fall and die, ±e
that is, the normal habitat of wild ship, are at risk because along with
fleas leave them and attack people. So
rodents. With these beginning to the grain, rats also come in. The main
it spreads from man to man. This is
called bubonic plague, that is, pro- migrate to domestic or peri-domestic thing is people should not panic and
areas, there could be a sudden erup- run away.” ■
T. S. SUBRAMANIAN
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™a,b,rxs™S'p'™.“ss
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NATURAL HISTORY OF PLAGUE
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Frontline, October 21,1994
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T. S. SUBRAMANIAN
Plague, through
the centuries
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T3LAGUE has killed huge numbers
JL of people at different periods in
history, and has played an enormous
role in human social and demographic
history as well as in our language and
collective memory. The 14th century
plague epidemic in Europe, the Black
Death, is estimated to have killed 25
million people, or one-fourth the pop
ulation of Europe.
In a 1986 paper on plague in
London in the 16th and 1 “th centuries.
Paul Slack, a historian of plague in
England, noted that plague was a “reg
ular visitor” to London between the
Black Death of 1348 and the epidemic
of 1665-66. “Nearly a quarter of the
city's inhabitants died in 1563,” Slack
writes. “In 1665 more than 80,000
people died; that is, equivalent to the
total populations of contemporary
Norwich. Bristol, Newcastle. York and
Exeter... Nothing in the modern world,
short of nuclear catastrophe, could
match that. Yet these figures... under
state the extent of those disasters.”
In 1894. plague in Canton and Hong
Kong killed 80,000 to 1,00,000 people,
and was transmined from south
Chinese ports to different parts of the
world. The epidemic of the 1890s and
early 20th century of plague in India,
particularly in west and south India,
was pan of this third pandemic of
plague. David xAmold estimates that
the plague epidemic that began in 1896
- “massive in scale and fraught with
political, social and demographic con
sequences” - claimed, by 1930, more
than 12 million lives.
According to the World Health
Organisation (WHO), in 1992, nine
countries recorded 1.582 cases of
plague in humans, and there were 138
plague deaths. Brazil. .Madagascar,
Vietnam. Myanmar and the United
States reported plague cases almost
every year between 1983 and 1992.
With respect to India, J.E. Park and K.
Park (Textbook of Preventive and Social
Medicine, 1991) state that there has
been) no laboratory-confirmed human
plague since 1966. In 1984. there were
two “suspected outbreaks”, in areas on
18
the Tamil Nadu-Andhra Pradesh bor
der and in Himachal Pradesh. Positive
sera specimens from rodents “were
observed in 19"9 in Kolar and in 1976
in xMaharashtra. where suspected
human cases were reported earlier in
Bhir (sic.) district.”
THE WORST-HIT
Given the means by which plague is
transmitted, it is inevitable that the
poor, particularly those who are illhoused and live in insanitary condi
tions. arc affected worst by it. Paul
Slack writes of the London epidemic of
1665-66: “Plague was not only con
centrated in time. It was concentrated
socially and geographically. Since the
disease was carried by rats and fleas,
people in the most dilapidated, over
crowded houses and with fewest
changes of clothing were most vulnera
ble: the poor, in other words, who were
‘pestered’ together in those sheds, cel
lars and subdivided tenements which
contemporaries recognised as the foci
of infection.”
In Bombay in the 1890s, too, the,
worst-off areas were those where peo
ple were “forced to live in miserable
shanties, dark, low, small, and built on
insanitary sites, without plinth, added
to which... 16 to 20 persons will sleep,
eat and work in a space hardly suffi
cient for the requirements of four” which, although a description taken
from the report of the Bombay Plague
Committee of 1896-97, is a reasonably
accurate description of the living con
ditions of about half of Bombay's cur
rent population.
Describing in 1993 some areas
where plague broke out in 1994 in
Surat. Jan Breman of the Centre for
.Asian Studies. .Amsterdam, who has
worked in Surat and other parts of
Gujarat over the last 30 years, wrote:
“On my wandenngs through the slums
of Katargam. Limbayat, Udhana and
Pandesara. my eyes never fail to fill
with tears and my nose does not stop
running... Adjacent to workshops are
labourers’s hutments and dormitories
owned and given out on rent by slum
lords. The work-sites and sleeping
places are not far apart and sometimes
even coincide.” ■
T)LAGUE is a disease of great antiq1- uity: it existed several centuries
before the birth of Christ. Central Asia
is considered the cradle of plague.
The first recorded epidemic was
among the Philistines in 1320 B. C.
And the first reported pandemic was in
A.D. 542.
“This pandemic appears to have
originated from Pelusium in Egypt,
and it lasted about 50 to 60 years and
' spread to all parts of the world. The
next recorded pandemic, called the
Black Death, started from Central Asia
during the 14th century and its wave
swept through Europe, India, China
and other Asian countries,” says a
report published by the Directorate of
Public
Health
and
Preventive
Medicine, Tamil Nadu, during the
15th
All-India
Inter-State
Coordination .Meeting on Plague held
in Madras on August 27 and 28, 1982.
In India, there is a reference to
plague in the ancient Sanskrit poetical
work, Bhagavath Purana, which
warned people to leave their homes as
soon as rats fell from the roofs and
died. Says the well-researched report:
“The definite recorded history’ of
introduction of the disease into India
was in 1031-1032 A. D. from Middle
Asia, following the invasion by Sultan
Mohamed Ghazni. The first epidemic
was in Calcutta in 1895 and in
Bombay in 1896. The total number of
deaths due to plague in India from
1896 to 1918 was more than ten mil
lion... The endemic centres in the
South probably got established after
the Bombay city’ epidemic of 1896.
Andhra Pradesh got involved in 1898
and the Nilgiris in 1903.”
Plague made its entry into Bombay
city’ in August 1896. “At first, diffusion
was comparatively gradual, but by the
middle of 1898, the disease had spread
over the greater part of the Bombay
Presidency, where it had been the
reported cause of some 90,000 deaths.
Infection was also carried to Mysore,”
says the Mysore Gazetteer , Volume I,
edited by C. Hayavadana Rao, printed
at the Government Press, Bangalore, in
1927.
There is a vivid description of how
plague swept through Bombay city and
the havoc it wrought in a book entitled
A Tour Through the Famine Districts of
India by F. H. S. Merewether, Reuter’s
Famine Commissioner, published by
A. D. Jones and Co., London, in 1898.
Merewether wrote:
“Bombay has earned another title to
our respect, and may be justly called
Frontline, October 21,1994
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The pandemics in Bombay, Mysore
Bombay the Busy... One of the first
things that strikes the newcomer is the
enormous mass of humanin’ which
throngs the city; vviiich crowd is intensi
fied tenfold in the native quarters of the
town... In the native quarters at night the
footway is simply impassable, owing to
the masses of shrouded natives who use
it as their sleeping-place. In the vicinity
of the Crawford markets and in the
quaner of Cammatepura, they simply
line the pavement, and wrapped closely
in their dirty-whiie chuddahs, look like
bales of merchandise. But the destroying
angel of plague altered all this. In streets
where even towards midnight it was
impossible, owing to the crowds, for a
liccagharry to proceed beyond a walking
pace, a battery of artillery might have
galloped in safety down the now-desert
ed thoroughfare. I went on a tour of
inspection when the disease was at its
height, and found whole streets in the
busiest portion of the native town practi
cally deserted. The shops were all
closed, and the occupants had disap
peared en bloc. It was calculated at that
time that nearly two-thirds of the inhabi
tants had fled from the pest-stricken
island to the mainland. This enormous
exodus on the part of the people did
incalculable harm to the Presidency, and
without doubt caused the spread of the
fell disease into the country districts of
the province.
“At a later period on my tour, I found
in one remote village of the Konkan that
more than forty’ people had died of the
plague which had been imponed by a
sufferer from Bombay...”
There is a striking similarity
between what Merewether wrote in
1898 about Bombay and what has
now happened in Surat and in Beed
district, Maharashtra. He observed:
“In the earlier stages of the epidemic,
the (Bombay) municipality auempted
the disastrous plan of concealment; and
it was mainly due to the fearless policy
and tone of The Times of India in laying
bare the actual facts of the case, and
especially in tracing its abnormal mortal
ity to its true cause, that the Government
was forced to take the strenuous repres
sive measures it subsequently did. If
from the first the nettle had been
grasped firmly, and a cordon established
round Bombay, the disease would not
have attacked Kurrachee nor been so
widespread as it eventually became. The
Plague
Committee
which
the
Government too tardily formed, had it
been in existence sooner, would doubt
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Frontline, October 21,1994
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less have achieved at an earlier stage a variability’ in the State than else
still more brilliant success. With such where,” it adds.
To give an all-India break-up, while i
popular and indomitable chiefs as
General Gatacre and Dr. Pollen, the 60,32,693 people died of plague from
1896 to 1906, another 42,21,528 lost '
dread monster would have been sooner
their lives between 1909 and 1918.
quelled.”
The mortality caused by the “Angel and yet another 17,02,718 perished
of Death”, as Merewether described between 1919 and 1928.
The number of deaths went down
the plague, was “enormous” in
by a quaner between 1929 and 1938 - .
Bombay. He wrote:
“When a case occurred or proved it stood at 4,22,880. It went down fur- i
1948, |
fatal, a circle was placed on the door ther between 1939 and
for
2,17,970
lives, i
post of the house, and in one house accounting
alone the number of rings shown up Between 1949 and 1958, 59,056 per- ;
adds up to forty’-three. There was also sons died of plague while only 678 fell j
an oart or square where this number was to the disease betweem 1959 and
1968.
exceeded... Hospitals sprung up on all
On a global level, though there was j
sides like mushrooms in a single night.
The wail of the mourners was heard on a drastic decline in the incidence of
every side, and one could not pass down plague because of the introduction of I
a street without meeting one or more rodent control by cyanogas fumiga
funeral procession. The burning ghauts tion in the 1930s and organochlorine
were strained to their utmost capacity, insecticides for flea control in the late
1940s, about 30 countries were affect
and the Mahommedan burial-grounds
could not hide beneath the earth suffi ed by plague between 1986 and 1979 ,
ciently fast the Moslem victims. On with 46,987 human cases. In 1967, |
Mahim sands, if in ordinary times you 6,004 cases were recorded, nearly 94 ■
ride out there in the early morning, you per cent of these from Viemam. In
may generally find the dying embers of 1953, 78 per cent of the human cases
one fire. In the times of the plague, the in the world were from India. whole sea-shore was clothed with the However, India has been free from the
human plague since 1967.
fires of innumerable funeral pyres...”
Just as the plague has now hit hard
the textile and diamond industries in FOCI OF THE INFECTION
According to the report published
Surat, the plague in Bombay left its
“indelible mark” on the city’s “com by the Tamil Nadu Directorate of
Public
Health
and
Preventive
merce and enterprise”.
When the infection spread to Medicine, however, the natural foci of
Mysore, more than 2,24,476 people this infection remained entrenched in
died in Mysore State between July the following three areas: “(i) the sub1898 and June 1918 - more than Himalayan focus comprising Punjab.
11,000 deaths a year. “Formidable as Uttar Pradesh, Bihar and north of the
this total is, it certainly falls short of Ganga; (ii) the central Indian focus
the truth. It is probably a closer comprising the water sheds of the
approximation to the actual number, Vindhya, Bhanrer and Maikal ranges
however, than is common in the case and, the Mahadeo Hills; and (iii) the
of other diseases,” says the Mysore focus along the Deccan plateau of
-peninsular India consisting of three
Gazetteer.
“The State has been persistently centres in the South as follows: (a) the
affected with plague during the whole water sheds of the Western Ghats in
of the twenty’-year period and no Maharashtra and Karnataka States;
month has been completely free from (b) the water sheds located in the dis
plague since July 1898. Altogether tricts of Periyar, Dharmapuri. Nilgiris
2,24,476 plague deaths were reported and North Arcot in Tamil Nadu; and
for twenty years, 2.1 per cent of the (c) Chinoor district of Andhra
all-India mortality and equivalent to a Pradesh.”
At present, the focus in the South is
death rate of 39.21, or a mean annual
rate of 2. The climate of the Mysore believed to be confined to the south
plateau is more equable and uniform ern half of the hilly Kolar district in
than that of any other part of India south-eastern Karnataka, adjoining
and perhaps as a result of this climatic Dharmapuri and Periyar districts of
peculiarity', the annual incidence of Tamil Nadu and Chittoor district of
plague has presented a lesser degree of Andhra Pradesh. ■
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COVER STORY
Less than vigilant
Plague surveillance in India
Ravi Sharma
in Bangalore
i
T)LAGL’E surveillance in India exists
-L only in its rudimentary form. The
country s only surveillance unit is in
Bangalore. Established in 1975, it
works under the National Institute of
Communicable Diseases (NICD),
India s central plague laboratory and
nodal centre for the control of the dis
ease.
The Bangalore Plague Surveillance
Unit carries out research in epidemiol
ogy and the detection of plague and
other rodent-borne diseases like lep
tospirosis. A team of officials from this
unit have gone to Mamla (the
Maharashtra village where the first
cases of the current epidemic were dis
covered) and also to Surat.
Its operation is restricted mainly to a
geographic area located at the junction
of Karnataka, Tamil Nadu and Andhra according to experts like Dr. Saraljit
Pradesh, States which have been long Sehgal, Director, NICD, was till the
perceived as the plague zone of India - recent outbreak, “the last known
especially the rocky delta districts of focus” of plague in India. He had cau
Kolar in Karnataka, Chittoor in tioned at a workshop in Bangalore in
Andhra Pradesh and Dharmapuri in November 1992 that the fact that
Tamil Nadu.
plague persisted in rodents in these
The decision to position the unit in States meant plague was “simmering
Bangalore was taken for two reasons. beneath the surface.”
First, the last reponed case of human
The Bangalore unit coordinates the
or domestic plague (defined by the activities of the State plague control
World Health Organisation, or the
units located in Kolar (Karnataka),
WHO, as “plague that is intimately Hosur (Tamil Nadu) and Palamner
associated with man and rodents living (Andhra Pradesh). These units are
with man, and has a definite potential manned by around 600 personnel
of producing epidemics”) as opposed
r-* *— whose main job is to trap rodents,
to s viva tic or win
> ”’ ’
“nlam
C
c^tc^ rat fleas, collect sera samples and
the WHO
as
“
plague
that
exists
in dispatch them to the Bangalore Plague
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nature ^
i dIpendem
_____
.of ky1?31? P°Pula- Surveiflance Unit, from where, after
tions and their activities”) in India was bacteriological diagnosis, ±e positive
reported in 1966 from Mulbagal taluk samples are sent to the NCID’s central
of Kolar district.
laboratory’ for reconfirmation. The
Secondly, sylvauc foci continued to JState units in tandem with the surveilbe active in these three States and, lance unit also investigate rat falls and
r------c? — —
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A rat being caught in its burrow, trapped and combed for fleas.
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suspected cases of human plague. The
Bangalore unit also trains health offi
cers from all the States in measures to
combat plague.
According to Dr. Shyamal Biswas,
Assistant Director, NICD, currently
heavy infection because it will tend
Java Shreedhar
heading the Plague Surveillance Unit,
to disseminate infection and also
the unit regularly does random sam
hinder the progress of development
pling of wild rodents for the plague
TT was 1925, and we were in the of natural immunity to plague
bacilli and over the past few years there
JlArmy station at Trimulgherry, among the local rat population.
has been a “positive occurrence of sylnear Hyderabad. The Army was
Today, as part of the Tamil Nadu
vatic or rodent plague”. Says Biswas,
always on the alert for suspicious Government’s anti-plague measures,
“We have been doing tests since 1976,
incidents. The first evacuation order a plague surveillance and monitoring
but it was only in 1989 that we got the
came following a rat fall in one of the cell functions round the clock. All rat
first positive samples (plague-infected
houses. We immediately set about falls are to be immediately reported
rodents).”
collecting our children and belong to this cell (phone 454269 in
In 1989, of 28,561 rodents tested
ings and assembled at the maidan, Madras) or to the Deputy Director
three proved positive; in 1990, of
disinfected and readied for us. We of Health Services or the nearest pri
32,644 four tested positive; in 1991, of
pitched our tents or built crude huts mary health centre. Dead rodents are
45,301 rodents 50 tested positive, in
and stayed there, sometimes for as to be carefully packed in several lay
1992, of 54,626 rodents 135 were pos
long as three months, till it was ers of paper or in plastic bags. Tne
itive; and in 1993, of 51,427 tested five
declared safe to return to our homes. neck of the bag should be tied to pre
tested positive. In the first eight
Shops in the bazaar opened at 9 a.m. vent the escape of fleas. The bag
months of this year, of 30,000 rodents
and were closed by 4 p.m. People should then be placed in an empty
tested, 30 (20 from Tamil Nadu, two
had to be back in the maidan by box or tin and packed with cloth or
from Karnataka and eight from
evening and were not allowed out at cotton to prevent leakage of any flu
Andhra Pradesh) were positive for sylnight. Relatives or friends were not ids. The box should then be labelled
vatic plague.
allowed to visit for months together. giving details of when and where it
Biswas, however, says emphasis
We were all given a single injection was found and forwarded to the cell.
should not be given to the numbers,
and our houses were
__ sprayed with
----According to Dr. N. C. Appavoo,
since “even one positive case is bad
pesticides. This happened nearly six Additional Director, Department of
enough, and it showed sylvatic plague
times, about every two years, till the Public Health and Preventive
activity was going on in the area”.
rat falls stopped,” said 88-year-old Medicine, “The prevailing chaos is
But, as Biswas says, the incidence of
Saraswati Benegal, recalling the due to the time lapse between the
rodent plague does not necessarily
plague epidemics of the 1920s and recognition of the problem and
mean that an epidemic is just around
1930s.
responding to it systematically. It will
the comer. It happens “only when an
Immediate evacuation to a con take a mere fortnight to get the epi
infected wild rodent (a permanent
trolled environment, inoculation demic under control with weapons
reservoir and a relatively resistant host)
with Haffkine’s vaccine, rat destruc like tetracycline at our disposal.”
comes in contact with semi-domestic
tion and sun or chemical disinfection Meanwhile, rats are being trapped
rodents, which in turn transmit the dis
were the temporary' measures to be and screened for plague antibodies
ease to commensal rodents (both of
adopted in an infected locality, and vehicles are being fogged with
which are highly susceptible), and then
according to a memorandum on pesticides to eliminate fleas.
to man.” As Sehgal says, “Rat fall is
Plague Preventive Policy, dated
Rat flea surveys are carried out to
the harbinger of the domestic rodent
April 30, 1934. Fumigation of rat assess flea indices which will indicate
plague and a sign of imminent out
burrows with cyanogas ensured the the effectiveness of spraying opera
break of the epidemic bubonic plague
complete destruction of rats and tions. The average number of
in humans.”
fleas and this was <extensively and Xenopsylla cheopis fleas per rat is
Curiously, blood samples are not
successfully carried out in endemic used to foretell the potential explo
taken from States other than
ar^Wike Cumbum in Madurai dis- siveness of the situation, during an
Karnataka, Tamil Nadu and Andhra
tricnFramil Nadu.
outbreak.
Pradesh. An NICD unit, which was
The memorandum, however,
It may be vital to desist from
functioning in Maharashtra, was shut
strongly deprecated the practice of importing plague metaphors from
down in 1987 as it was considered
“commencing rat destruction at the the past if we are to deal effectively
expendable. As a doctor at the NICD
onset of plague and stopping it at the with this epidemic. Evoking bleak
says, that line of thinking could be a
first signs of subsidence of plague images and the odour of death and
thing of the past now. Sources in the
cases.”
devastation may hamper sensible
Plague Surveillance Unit aver that after
It is considered dangerous to efforts to put a system in place to
the
experience
in
Surat
the
attempt rat-trapping in the midst of combat the epidemic. ■
Government might well decide to set
up units similar to the one in Bangalore
in other States.
says, control ot
of human plague never ics. My field staff are full-time employ
The surveillance unit, as Biswas arose since plague was looked as more ees. Besides, we pay Rs. 200 for every
explains^ only detects plague; it is not of an “academic problem”. He says the rat caught.”
equipped or meant to control it. But, as State Government had brought down
As experts say, plague, like any epi
Dr. M. T. Hema Reddy, Director, the staff strength in both the Bangalore zootic disease, cannot be eradicated or
Health and Family Welfare Services, and Kolar units to skeletal levels, but controlled: “It can only be monitored”.
Karnataka, under whose directorate unlike other States had not abolished And India hardly has an effective sur
the plague units in Karnataka function, the units. “It is a question of econom veillance network. ■
The first steps
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A recent Health Ministry study shows that
over a lakh Indian women die each year due
to anaemia. Dr SHANTI B. RANGWANI
provides a few tips on how to improve your
energy levels
N THE Third World, where eyesight, poor memoiy. general
female nutrition levels body weakness, frequent dizziremain low, anaemia is one ncss. fatigue, shortness of
of the main causes of breadi on exertion, headache, j
fatigue among women. In and depression.
India, an estimated 83 per
Except in the case of heavy”
cent of the adult female bleeding, anaemia doesn't come
population would qualify about overnight. To overcome it,
as anaemic. Anaemia or iron supplements are essential but
dcncicncy means that the blood so is a proper diet.
does not have enough haemo • Common foods rich in naturglobin, the oxygemcarrying iron al organic iron are wheat, brown
compound that gives human rice (rice with husk), green leafy
blood its characteristic red vegetables, cabbage, carrot,
colour. With reduced oxygen beet, tomatoes, and spinach.
availability, the body is unable Apples, being rich in iron,
to burn off sugar
sugar, to produce arsenic and phosphorous are
enough energy, and a study has recommended. Other fruits rich
proved that on an average, jn irori aj-g bananas, grapes,
anaemic women couid stay on a dates and peaches.
treadmill for eight minutes less • A small but essential amount
than normal women.
of copper contained in apricots
An unbalanced and low iron and almonds acts along
diet depletes iron reserves as with iron and vitamins as a
does the consumption of devi 'catalyst in the synthesis of
talised refined foods and over- haemoglobin. Copper also
processed foods lacking in life- boosts iron absorption.
giving ingredients. Iron may
have nothing to do with energy • Supplements of trace ele
’ production directly, but it is a ments. Vitamin B-12 and folie
mineral crucial to the transport acid are necessary for the prop
of nutrients and oxygen as it is er production of haemoglobin.
Folic acid deserves a special
one of the chief compo
mention. In a study in which
nents of the
women received
haemoglobin
either
iron
molecule.
alone,
or
folate
Iron is diffi
alone, or iron
cult
to
and
folate
absorb — a
together,
only
I Oi •
person can
26 per cent of
absorb
no
those
who
more than 2
received
a
mg a
day.
single
nut
Thankfully, it
rient showed
is also difficult
1 a
rise
in
to eliminate.
!
haemoglobin.
Iron
defi
9 Foods like
ciency is gen
mangoes,
Sr
erally found
raisins.
red
among young
beets, spinach
women with
and lettuce sup
menstrual
ply a good form
problems and
of
vegetable
among those S
haemoglobin.
who have been ’
s’”-W*Jra| • One cup of
continuing i
freshly-sproutwith a faulty
*' -
n
'Si
111
111711
Cl I x.
I1CU 1 Cl 1 1 Cl .J,
CAj7X-Kj,
anaemic women could stay on a dates and peaches.
treadmill for eight minutes less • A small but essential amount
than normal women.
of copper contained in apricots
An unbalanced and low iron and almonds acts along
diet depletes iron rcseives as with iron and vitamins as a
does the consumption of devi catalyst in the synthesis of
talised refined foods and over haemoglobin. Copper also
processed foods lacking in life boosts iron absorption.
giving ingredients. Iron may
• Supplements of trace ele
have nothing to do with energy
ments. Vitamin B-12 and folic
1 production directly, but it is a
acid are necessary for the prop
mineral crucial to the transport
er production of haemoglobin.
of nutrients and oxygen as it is
Folic acid deserves a special
one of the chief compo
mention. In a study in which
nents of the
women received
haemoglobin
either
iron
molecule.
1
alone, or folate
Iron is diffi
alone, or iron
cult
to
folate
and
absorb — a
together, only
person can
26 per cent of
absorb
no
those
who
more than 2
received
a
mg
a
day.
single
nut
Thankfully, it
rient showed
is also difficult
’A
i a
rise
in
to eliminate.
I haemoglobin.
Iron
defi
• Foods like
ciency is gen
mangoes,
erally found |8
1 raisins,
red
among young
beets,
spinach
women with
and lettuce sup
menstrual
ply a good form
problems and
of
vegetable
among those
haemoglobin.
who have been
• One cup of
continuing
___
freshly-sprout
with a faulty
diet for some months. Heavy ed moong seeds, taken early
blood loss due to serious injuiy, morning on an empty stomach,
or ailments such as piles and also helps. Alternatively, make
heavy menstruation can also an emulsion of black sesame
lead to anaemia. Even normal seeds by grinding them and
periods drain iron, pregnancies adding water. To this, add just
sap^it and weight-reducing a dash of milk and jaggery. Take
diets cut down its intake.
half a cup on an empty stomach
Anaemia can also be a result eveiy day.
of sustained emotional strain • Though many naturopaths
and anxiety, which affect the ask anaemics to eschew fasting,^
•
“ i of
production of hydrochloric microscopic examination
cf
acid essential for the assimila blood before and after fasting
tion of proteins and iron. Again, has shown an overall improvea variety ol
dings, such as ment in the quality of blood
of drugs,
aspirin and steroids, if taken in after fasting.
excess, can destroy beneficial • Ayurveda offers the most
intestinal flora and this in turn comprehensive
cure
for
hampers the assimilation ofcer- anaemia. Special Ayurvedic iron
tain vital vitamins and minerals, preparations are humanised,
including iron. Vitamin E, espe- non-toxic iron oxides, prepared
cially, is veiy sensitive to the by repeated incineration of iron,
effect of drugs, and the absence as well as by cooking it in vari
of this vitamin leads to poor ous herbal substances. As iron
supplements weaken the digesblood quality.
The normal level of haemoglo- tion, they should be taken with
bin in a person is 15 gm per 100 compensating herbs such as
cc of blood. Since haemoglobin ginger and cinnamon to improve
is the oxygen carrier of the body, digestion. Good formulas> are
the famous shatauari and the
adequate levels are vital for res
” l
compound.
piratory and metabolic efficien- ashwagandha
cy. Lack of haemoglobin can Chyavanprash. has also been
w
make yon look haggard
and can used for curing anaemia for
also lead to premature wrinkles, thousands of years.
The absence of a vital blood • Two glasses of carrot and
ingredient like haemoglobin spinach (palak) juice in the ratio
also results in slow clotting and 3:1 every day with breakfast are
in slow healing oi wounds, weak good lor anaemlcs.
a /
I
■I
Wk
—‘VAX
11
y V
M
A njnexure - j j j
List of sub—
1
Tuberculosis
Dr. S.P. Pamra , Hony.Advisor
, TB Association of India,
New Delhi.
Dr. G.A. Panse,
Joint Director (Planning
Dental College Building^ b
' SS0”™"1 and
Director, n.T.I. Bangalore (Karnataka) °
-
Dr. S.P. Gupta,
ADG(TB) Dte.CHS. ,New Delhi/
°
..CONVENOR
a^ ^13juaza£i„J^anese Einceghalit.is
-.filarias is
2•
1. Dr. A.N. Raichowdhuri, Director,
9
Dr o P.K. RaiaaoneiA"
Rajagopalan, Director,
NICD, Delhi
VCRC, Pondicherry
Dr. S.K. Sharma
9
Director of Health Services
9
Haryana
Dr. S.N. Saxena
9 Director 9 CRT, Kasauli (HP)
Dr. G.K. f
Sharma (.o,
Dro O.K. Rao
"-J
(**) .
.•.CONVENOR
...CONVENOR
) Director
o U
o
o
• o
S)TrARIVnd
f«)
y
i ccTor(H) for other Diseases.
3. Hj-ar3Lhoea 1 d i^s e a s os
Dr. S.Ko Sengupta
DDG(P), Dte.GHS,
9
Nfrman Bhavan, New Delhi
o. Banerjee 9 OADG(Diarrhoeal) ,
Dte.QHS, New Delhi
Dr. KoC0 Nandy,
Nandy Asstt.
Asstt. Director of
Die. of Health Services
RHe^th Services(Malaria)
->y i/r iters’
Building Calcutta
Dr. SoC.Pal, D±±ecTc
Director, NIC a ED, P-33
XM, Calcutta-700010.
, CIT Road Scheme
4- ^■^^lLX...2ransmittejl,^
d y
—- —
r. Dharam Pal, Advisor (STD)', Dte.GHS,
5
New Delhi
^ineav^grm
NICD, Delhi.
6‘
imye litis-
Dr’
Jacob John, Prof a „
« Head Deptt.of Virology
and Immunology, CMC Hospital
? VELlore-632004.
Dave’ Director fEnterovirus
'
Hesearch Centre,
me Institute, BOMBAY-400012.
...p/2
I
' <
7
Rabies control
j
Dr o V.R o
Ka1ayanaraman 9 Director ? Pasteur Institute,
Coonoor□
8
Vaccines; 0 Prod_uctior\ .anjl
Dr. K.H. Dave, Director, ERC, Bombay
Dr, V . h. Kalyanaraman? Director, Pasteur Instt. Coonoor
(HP)
1
Dr 3 X Saxena, CRI, Kasauli
Vellore.
Jacob John,
Dr
Dr <* I n d 3?a B h a rg.a v a , Dy. Commissioner(MCH) Niuin. of Health
and E.U , Nirman Bhavan y New Delhi.
CONVENORo
Dr „ SJ.<. Sengupta, DDG(P), Dte. GHS..
9
i'XPhoi£ and_
n/testdal_J?JLL
iXes
Chakravarti
Chakravarti,, Prof, of Epidemiology
Prof. A.K.
<
AIlaPH, Calcutta -7000073.
Delhi
10
11. Epi^mi^o_logj.£a_l service^
Dr. S.K. Sengupta, DDG(P),, Dte.GHS Nirman Bhavan,N.Delhi
-doDr. Mahendra Singh, Director
Director,, CBHI
Dr. Harcharan Singh/Dr.
)r. N.K. Sinha
(Jt. Advisor(H)
(Dy. Advisor(H),Planning Commission
New Delhi.
Dr. Rajyalakshmi,Director, Institute of Preventive
Medicine and Lab. Services, HYDER ABAD'(AP)
Dr. G.A. Panse s Joint Director of Health Services
(PDE) Bombay.
Dr. A.N. Raichowdhuri, Director, NICD, Delhi.
Dr. A.K. Chakrabarti, Professor of Epido AIlaPH
Calcutta.c. ..o ...... . ....... J ........CONVENOR
12. Environmental Sanitation and Industrial Health
.. .
*•
r
r i.-
«
N
'*
•
»
Dr0 B.B. Chatterjee, Director, National Institute of
Occupational Health, AHI7IEDABAD (Gujarat) ,
Dro B.B
Sunderesan, Director, NEERI, NAGPUR
Drc K.j. Nath, Prof
o
Calcutta.
of Environmental Sanitation, AllaPH9
...CONVENOR
o
o o
13
Dr. Madan , Mohan, Advisor (Ophthalmology) Govt
India, Dte. GHS, Nirman Bhavan, New Delhi.
14. .Leprosy
Dr. K.Co Das, ADG( Leprosy). Dte OGHS
Nirman Bhavan, New Delhi-110011.
4
of
I
2 3
Financial inputs during sixth plan*
4
Results of evaluation
5„ Health Programmes which have made spectacular/
adequate progress.
6
Reasons ibf increasing or stable incidence/prevalence
of some diseases and remedial measures suggested
for improving the situation.
7
Changes in the strategies, if any, with justification
(backed up by pilot trials, research studies or
experience inside or outside the country)
80 Components that are required as vertical health
programme^) set up and those that can be integrated
with horizontal health services.
9. Resources required for the seventh plan period
commensurate with the performance and impact objectives.
10. Goals/targets that are related to control of communi
cable diseases as mentioned in the national health
policy.
.Indicators:
Infant mortality
Current level
125(1978)
1985
(105)
1990
(87)
02)
(104)
Crude death rate
(14)
Pre-school child
(1-5) mortality:
(24)
(20-24)
(15-20)
Maternal Mortality rate
4-5
3-4
2-3
Leprosy:
(Z disease arrested
cases out of those
detected)
20
40
60
T uberculosis
(Z disease arrested
cases out of those
detected)
50
60
75
1.4
1.0
0.7
Blindness
(incidence Z)
»
VI
Guidelines for preparing Seventh Plan proposals in
respect of control of communicable diseases and
Blindness.
i
j
i
>
The following facts be kept in mind
ji
8
m
' ~ J?
o
o
CD
• JP
CO
'■
ET GJO) —
"O
I
A. The National Health Policy accepced by the Government
of India envisages to provide universal, comprehensive,
primary health care services, relevant,, to the actual
needs and priorities at a feasible cost.
o
n cxj o 5
_ ■£
C9 id £Q
B. The 20-point programme of the Prime Minister includes
Water supply, sanitation, tuberculosis, Iprosy control
and Blindness.
C. The Government of India isa signatory to the declara
tion 'Health for all by the year 2000 AD'.
D. Development of primary health care system in the
country, so that the planning and implementation of
health programmes where feasible is through the
organised involvement and participation of the community.
Status Paper
1
f
Review of the infrastructure as will be existent
at the end of the VI Plan period with a view to
consider for their continuation during the VI Plan
period.
2. Review of the existing health programmes in the
light of mid-term appraisal of VI Plan.
3. Approach to VII Plan and identification of thrust
areas for VII Plan.
4. Improvement of communicable diseases surveillance/
services.
6. Identification and initiation of new disease control/
eradication programmes.
6O Strengthening of institutions/organisations in order to
a) develop trained manpower for the programmes
b) undertake applied research based on feedback •
for the programme implementing agencies
c) assist in problem solving :
d) undertake periodic independent evaluation of
the programme.
Sub-group reports may focus on the following:1
The problem as it exists today and before the
implementation of disease control measures if any.
2. Year of commencement of disease control.
p/2
7
3,
Dr. K.H. Dave , Director, Enterovirus Research
Centre, Haffkine Institute, Bombay.
♦
Dr. T.Jacob John9 Profe a Head, Deptt. of Virology ex
Immunology, CMC Hospital 5 VELLCRE-632004
9.
Dro O.K
Rao, Deputy Director (H) NICD, Delhi.
10c. Dr. C.Mo Habibullah, .Pref. of Gasteroenterotology y
Institute of Medical Sciences, Osmania Medical
College a Hospital,y HYDERABAD-500012(AP).
11
Dr0 B.B. Sunderesan, Director, National. Environmental
Engineering Research Institute, Nagpur-440020.
12. Dr. C.R. Krishna Murti 9 MADRAS (Tamilnadu)
13. Dr. S.C. Pal, Director, National Institute of
Cholera a Enteric Diseases, Calcutta-i700010o
14. Dr. S.K. Sharma, Director of Health Services,
Haryana - CHANDIGARH
15
Dr. G.AO Panse, Joint Director of Health Services(PDE) 9
Dental College Building , BOMBAY
16. Dr. B.B. Chatterjee, Director, National Institute of
Occupational Health, Meghani Nagar, AHMEDABAD-380016.
i'
17. Dr. Dhar.am Pal 9 Advisor, STD, Dte. GHS, New Delhi.
18. Dr. KoJ. Nath, Professor of-Environmental Sanitation,
AIIHcxPH, Calcutta
19o Dr. Harcharan Singh, Joint Advisor (Health) 9
Planning
Commission, New Delhi.
20. Dr. S. Sriramachari, Addl. DG, ICMR, New Delhi.
CO-OPTED MEMBERS
1.
2.
3.
4.
5.
6.
Dr. A.K Chakravarty, Professor of Epid. AIIHctPH, Calcutta
Dr. Mahendra Singh 9 Director, CBHI, Dte.GHS, New Delhi.
Dr. V.R. Kalyanaraman, Director, Pasteur Institute,Coonoor.
Dr.(Miss) Jotna Sokhey,DADG(EPI),Dte.GHS, New Delhi
Dr. S.K.5engupta,DDG(PH), Dte.GHS, New Delhi.
Mr M.S. Madhava Rao,. Senior Research Officer,
Planning Commission , Yojana Bhawan, New Delhi.
Annexure-IL
.. .....
.III
WM
%
Terms of Reference of the Working Group on control
of Communicable Diseases _an.d control of Blindne_ss_
c
(i)
To assess the present status regarding prevalence/
incidence of communicable diseases like malaria,
filaria, tuberculosis, leprosy and diarrhoeal
diseases and the arrangement for monitoring thereof^
(ii) To examine the strategies adopted in the 6th plan
for control/eradication of these diseases and the
operation thereof in the field situations and to
advise how deficiencies, if any, in the strategies
or operations could be rectified and the programmes
made more result-oriented and cost effective, keep
ing in view the long term goals for the control/
eradication of these diseases in the health policy
statement and to achieve Health for All by 2000 AODO
(iii) To identify the additional manpower and training
needs and advise to what extent they could be
fitted into the ongoing health sectors programmes and
to what extent additional training programmes would
be necessary:
(iv) To identify the areas of research thrust and
development of appropriate technologies and their
application to strengthen the ongoing p'rogrammes
towards the objective of health for all by the
year 2000 A.D.
„
(v)
fo quantify the requirement in the 7th five year
plan of financial and material resources for
effective control/eradication of these diseases and
define the respective roles in financing and
implementing these programmes.
Members of Working Group
Chairperson - Shri P.K. Umashankar, Addl. Secretary (Health)
Convenor
- Dr. A.No Raichowdhuri, Director, NICD.
Members
1.
Dr. Madan
r
Mohan, Advisor (Ophthalmology) Govt, of
Indiaa, Dte. G.H.S., Nirman Bhavan, New Delhi-110001
2. Dro G.K. Sharma, Director, NMEP, 22-Sham Nath Marg,Delhi
3. Dr. SoP. Gupta
ADG(TB), Dte.GHS, Nirman Bhavn
New Delhi
4. Dr. S.P. Pamra , Hony. Technical Advisor, TB Association of India, New Delhi.
5. Dr. KoC. Das, ADG (Lep), Dte.GHS, Nirman Bhavan New Delhi
9
6. Dr. M.S. Nilakantha Rao, Bangalore (Karnataka)
....p/2
4
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i *
*
♦
*
*
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*
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*
*
REPORT OF THE WORKING GROUP
*
*
ON
*
*
CONTROL OF COMMUNICABLE DISEASES
*
*
i
*
*
*
*
*
*
*
*
♦
AND
CONTROL OF BLINDNESS
*
*
*
*
*
*
*
National Institute of Communicable Diseases 9
22-Shamnath Marg Delhi-110054.
""
♦
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****************************************************************i
....
4
-
•
■; ■
■
«
Report of the Working Group on Control of Communicable
Diseases and Control of Blindness.
St
•
•
•
f
Forewbr’cl
Contents
Pag c/ s
I.
INTRODUCTION
1
II.
CURRENT STATUS
(i) Leprosy
(ii) Tuberculosis
(iii) Malaria
Civ) Filaria
Cv) Blindness
1
r
3
3
4
4
Mid-term appraisal
5
III.
BROAD ISSUES EMERGED
5-6
IV.
APPROACH TO THE ISSUES
6-7
V.
RECOMMENDATIONS
7-9
1. National Leprosy Eradication Programme
10-12
2. National Tuberculosis Control Programme 13-14
3. National Malaria Eradication Programme
14-15
4. National Filaria Control Programme
16-17
5. Diarrhoeal diseases Programme
17-18
6.
National Programme for control of
Blindness
18-20
7. Development of Epidemiological Services 20-22
8
GuineaWorm Eradication Programme
22-23
9. YAW eradication programme ‘
23
lO.Kala-azar control programme
24-25
11.Poliomyelitis control programme
25-26
12.Sexually transmitted diseases
26-27
13.National Programme for Vaccine Prod.
28-31
14»Viral Hepatitis
31-32
. •«• p/2
2-
r
15. Acute respiratory diseases
32-33
16. Typhoid Control Progranune',
- 33-34
17. Intestinal parasitic diseases\ .
35-36
18. Measles Control Programme
36
■ 19v Rabies control programme
20. Japanese encephalitis.
Annexure
I
Annexure
II
Annexure
III
I
36-39
i
T
SQ-ilO
ji
.
}
■' i'
:
r
■
•V
r
A
Fbre-word
/o^he.P2-arLnlng Gc^ission, vide their letter Ifo.HLH.
2C2)/839 dated the 18th August,1983 constituted eight gro
ups for the formulation of proposals for the 7th five
year plan, ■which included the group on control of commu
nicable diseases and control of blindness. The terms of
reference and composition of this group are given in
Annexure-I.
o
members of the Working Group were requested to
theJstaPus Papers on their specialities within the
guidelines developed (Annexure-II) in accordance with the
bv“p°i^ Programme and the National Health Policy approved
n-no-n
v
"• cl-If1 cUTl 1*1 U
28th11nH
were presented and discussed in
°f the
group held on
I /SIs
given in Annexure-III.
5
5
17th
meGting of the working group was held on
17th and 18t^ January,1984 to review the draft proposals
presented by the sub-groups/officers who were assigned the
tasks. The proposals for the different programmes - on
going and new were discussed in depth and suggestions were
made by the members to further modify the proposals. A
Drafting Committee was constituted to prepare a comprehenth^dr^^n
SVight
n s^stions made submStS
th^ draft report that was finally adopted in the meeting
n? ?h°n 2M*84
h3-1984- I must thank the m^bej?
i working group for their unstinted cooperation and
involvement. A special word of thanks is due to Dx
Dr.A.N.
Haichowdhuri, the convenor for his untiring efforts and
hard work in giving a final shape to our proposals.
I have great pleasure in submitting the report of the
■working group for consideration of the Planning Commission.
working
//J ?£ -
i./ "
P.K. UMASHANKAffi
Additional Secretary (Health) and
Chairman of the Working Group on
Control of Communicable Diseases
and Control of Blindness.
I, Introduction
The Constitution of India envisages the raising of
the level of health of the people as among its primary
objectives by ensuring adequate opportunities and facili
ties.
The health infrastructure has been expanded through
planned development during the previous plan periods and now
a fairly extensive net work of primary health centres,subcoritres, dispensaries, hospitals etc, is functioning in the
country. The problem of communicable diseases is a major
public health problem. Some of the communicable Diseases
that were controlled, for example, malaria, kala-azar, cuta
neous leishmaniasis etc. are again posing a serious threat
to the health pf the people. The infant and child mortality
rate in the country is still high compared to developed
countries. Majority of these deaths are due to preventable
communicable diseases.
In view.of the Prime Minister's directive - "The need
of many should prevail over the need of a few", it is imper
ative to make.the health services responsive to the needs of
many. The Prime Minister's new 20-point programme lays emphas.f on control of communicable.diseases which are sapping the
vioality of the nation. The National Health Policy document
rightly draws priority attention to nutrition, prevention of
food adulteration, water supply and sanitation, environmental
protection, immunization against preventable diseases etc.
Indeed, attention to these areas will undoubtedly go towards
at
control of communicable diseases , and is in tune with
the Nation's commitment to health for all by 2000 AD.
11 Current situation
Before the 6th plan period, the control programme was
mainly cirected against diseases like smallpox, malaria,tubercu^osis, leprosy, filaria, venereal diseases,, trachoma and
cholera. The country has been able to a.chieve eradication of
smallpox, substantial reduction- in morbidity and mortality due
o malaria and as a collateral benefit, virtual elimination
of plague, kala-azar and cutaneous leishmaniasis. The reduct
ion m mortality due to cholera and control of explosive epi
demics was also achieved. This is reflected in the reduction
of iniant mortaiity rate 1161 to 120), reduction of death
:2?°4 to 14.8) and increase in average.life expectan
cy (30 to 54 years)
Encouraged by the results achieved, the disease control
programmes were extended during the 6th plan period to cover
other conditions as well as to expand the scope of the ongoing
programmes. Accordingly, the chplera. control programme was
re-designated as diarrhoeal diseases control, trachoma control
as prevention of blindness and venereal disease control as
prevention of sexually transmitted diseases. The DPT and TT
immunization were incorporated in the Expanded Programme on
Immunization.
....p/2
:-2-:
The current situation regarding the five major National
health programmes are roviewod below:1. Lepro sy
About 400 million people live in areas where the
prevalence of the disease is 5 and above per 1000 .popu
lation. The estimated number of cases in the country is ab
out 4 million, out of which 20$ cases are of infectious
. type, 25$ have some sort of physical deformities and about
20$ belong to child age groups. About 0.4 million..cases
are detected additionally every year and about O.'S
million cases are discharged from the list as cured or dead.
Till 1977, tho programme was run as 100 per cent centrally
sponsored scheme under category I. From 1978-79 to 1980-81,
it was converted to category II scheme with financial res
ponsibility being shared between centre and state on 50:50
basis. During this period it was observed that achievements
and progress of the programme was tardy and slow. Hence,
from 1981-82 onwards, it was reconverted to category I,
i.e. 100 percent centrally sponsored scheme by the Plann
ing Commission. Tho national leprosy control programme was
also renamed as national leprosy eradication programme
from April 1983 in pursuance of the recommendation of the
Swaminathan Committee report.
During the 6th plan period, 15.18 lakh cases have been
detected till December, 1983 against the target of 17.20 lakhs,
out of which 14.31 lakhs cases have been brought under treat
ment. During tho same period, 8.87 lakhs cases have been
discharged as disease arrested/cured against the target of
11.10 lakhs. During, the same period, 17 leprosy control
units have been set up against the target of 15; 202 urban
leprosy centres have been set up against tho target of 50;
865 survey-education-cum-treatment centres have been estab
lished against the target of 200. 64 temporary hospitali
sation ward of 20 beds each have beon started against the
target of 50 and 65 district leprosy officers’ unit have
been established against tho target of 50. 290 .other units
(reconstructive surgery’units, sample survey-cun-assessment
units, training centres etc.) have also been established
against the target of 233. Figures show that the targets
fixed for each of the components have been substantially
exceeded as a result of concerted effort made to complete
the accummulated backlog of earlier plan period.
The budget provision of,.Rs.40 crores was made-for tho
entire 6th plan period. Out of this, an amount of Rs.24.07
crores have been utilised till Decemb or,1983 to meet the
expenditure on plan components under the programme.
....p/3
s-3-:
2. Tuberculosis
Fully equipped and staffed district TB centres to
undertake district-wise TB programmes in collaboration with
General Health and Medical Institutions, have been establi
shed in 354 districts of the country. In addition, nearly
300 TB clinics are also functioning and about 45,000 TB
beds are available for treatment of seriously sick TB pati
ents.
During the 6th plan, the schemes of establishment of
district IB centres and IB beds has been included in the
state plan sector, while the.schemes of supply of material
and equipments/anti-.TB drugs have, been Classified as a cent
rally ‘sponsored scheme on 5C&50 sharing basis between the
centre and the states. The scheme of supply of material and
equipment/anti-TB drugs to the TB clinics run by voluntary
bodies has been classified as 100% centrally sponsored sche
me. An amount of Bs.700 lakhs was initially provided for the
implementation of these schemes during 6th plan. Upto the
end of 1983-84, it is .expected that about 1090 lakhs would
be spent on the implementation of the schemes. A sum of
Bs.1050 lakhs has been provided during 1984-85 and thus it is
expected to spend about
2100 lakhs for the implementation
of the schemes"during 6th plan period against the initial
allocation of Bs.700 lakhs. With the inclusion of tuberculo
sis programme in the 20-point programme, a new thrust has
been given for the expansion of the essential activities
and targets were laid for the first time for detecting one
million TB cases during 1982-83 which was fully achieved.
During 1983-84 target has been laid for detection of 1.25
million new TB cases and for conduction of sputum examination
of the new chest symptomatics at the primary health centres.
During 1984-85, it is proposed to increase the target of
detection of new TB cases to 1.375 million cases.
3. Malaria
The incidence of malaria was. brought down to 0.1 mil
lion by 1965 as a result of malaria eradication programme
actiti^ied. However, there wa.s resurgence of malaria and in
1976, the incidence? was 6.5 million cases which was again
brought down to 2.1 million cases in 1932 as a result of
implementation of modified plan of. operation. Daring the
above period, there was extended coverage of the community
for detection of malaria cases as reflected by the increase
in the number of .blood smears examined from 55 million
•in 1976 to 62.64 million in 1982. The spread of P.falciparum
infection which was posing a serious problem is being
tackled with the introduction of a new strategy. Ihere are,
however, localised, problem of P.falciparum to commonly
used drugs. The resistance to DDT and BHC has also been
recorded in vectors of malaria in different parts of the
country. Against an outlay of Bso224 crores, the anticipated
expenditure is Pso296 crores during the sixth plan.
<
:-4-:
4. Filaria
e3^1S^n^^e‘oSn?JoOr=2t“nS
■;
' '
•
o
The National Filaria Control Programme has an approved outlay ofBs.300 lakhs for the
t.
sixthplan period to meet
the 50 per cent of the material- and equipments required for
urban filariasis activities and 50 per cent total
rural filariasis projects, A sum of ks.200 lakhs is cost of
expected
to-be spent till the end of the year 1983-84.
5. Blindness
was
eye
Pr08r^e the
s:
programme the following infrastructure has
Vlth plan Achievement
target
upto 1983-84.
Expected achio
vement
1984-85
Mobile Units
80
78
2
.Primary Health Centres 2000
1670
330
District hospitals
400
354
' 46
Medical colleges
60
42
18
Training schools for
Ophthalmic assistants
37
35
2
Regional institutions
6
4
2
;r
In 1982? tl.
2
the Govt.of
India set up a working group under
the chairmanship of Dr.M^s.Sw^inathant
L
.
This group suggested
speedy augmentation °L
of s^vicos at various
obfS
levelZwith
•
0,13
object to reduce the incidence of blindness from 1.4$—-1 in
1975
to. 0.5 by 2000 AD. inese^recommendations included development
of eye banks in each medical
<_
>- district mobile units
encouragement to volunta•Ohal eye care ^cllXiesfiP
f°r aUSmQ“tation of instituti-
the programme
was
cSJo
3ft
an ^ituX tm%ig84thhast&e^.?6266
croresSo Allocation for the financial year 1984-85 is rs.7.5 crs.
...p/5
5 -•
Mid-term appraisal
/
ibe mid-term . evaluation of the 6th plan programme
with respect to malaria, tuberculosis, and control of blind
ness revealed the following trends
a. The incidence of malaria declined from 6.5 million
cases in 1976 to 2.1 million cases in 1982. The
spread of P.falciparum’infection which was posing
a serious probTem is Hieing tackled with the intro
duction of Pofalciparum containment programme as
a new strategy.
'
b. Bae treatment regimens in respect of tuberculosis and
WQr° rao<Ufied to reduce the duration of treat
ment through short-term chemotherapy and multi-drug
regimen respectivelyo
c. With regard to control of blindness, ophthalmic
iacilities have been strengthened at various
levels and 7.8 lakhs of cataract operations have
been done in 1982.
III. Broad Issues emerged
nning Commission as also the terms of reference, the broad
issues that emerged during the working group discussions
follow^1Oerati°n in the seventh Plan Proposals are as
a.
^segment of population who are affected mostly
and scope of introducing innovative measures and
appropriate technology should be considered.
b.
Primary health care system should be'optimally utilised
for comprehensive health care and for better die else su
rveillance and control in view of the -national health
Ali‘’Cbya2000hAD?OIDC|i^ent °f the nation to 'Health for
c.
^senses which could be eradicated or reduced to a
great extent with the existing technological knowledge
namely yaws, guineaworm, rabies should.be considered? ’
d.
Onerging/re-emerging health problems like viral henatiti^
Japanese B encephalitis, kala-azar,
*
kala-azar acute respiratory
attention" chlldren belo'w 5-> years' should receive
...P/6
:-6- :
e.
Necessary research infrastructural facilities
should be devcloped/augmcntOd to meet the cha
llenge of future needs of control of communicable
diseases.
f.
Fbr effective control/eradication programme, inter
sectoral collaboration should be ensured - (i) for
development of modern bio-technology and (ii) im
provement of environmental sanitation and indust
rial hygiene.
g.
Self-reliance in respect of production of vaccinesj
drug$, chemicals and planned development of ancillary industries needed for the purposc should bo
achieved through inter-sectoral collaboration
h.
Effective implementation, monitoring and evalua
tion of various disease control programmes should
be ensured through development of epidemiological
services.
IV. Approach to issues
Keeping in view tha broad issues outlined above. a
rational approach should include a®
Effective and efficient implementation and streng
thening of multipurpose workors’ scheme is essen
tial pre-requisite for successful implementation
of communicable disease control programmes in the
7th plan period.
On-going disease control programmes should be stren
gthened to produce impact on the disease incidence.
c.
Identifying new and emerging health problems and
working out strategies for their co nt rol/pr even
tion through national/regional programmes.
de
Steps be taken to establish a permanent mechanism
of the nature of cabinet sub-committee and.also a
health advisory committee for achieving ‘Health for
All1 by 2000 AD with administrative authority
for establishing intor-sectoral collaborations with
other ministries such as works and'housing,. agricul
ture, irrigation, environment, social welfare,
education, industry, science and technology,
chemical and fertilizer and information and broad
casting.
o<
Vaccine production and quality control should be
taken as a major plan project in providing incuts
(.financial and material) to central and state
institutes with a view to stabilise and diversify
...p/7
*
z-7-:
the production and quality c_^_l
udiagnostic
G°n^r9'?'
reagents and immunologicals for disease
"--- ; investigations and for expanded programme of immunization
respectively.,
f.
Establishment of epidemiological services as an
Integral part of primary
- health
- --1 care system for im~
piementation,’ “o^ito^ing and evaluation of various
health activities should bej taken up as a national
programme.
g.
!!SaSS?hshoUld be develop^ for active involve
ment of the community, allied institutions, volun.tary organisations, professional associations and
1
delivirv
medical Practitioners in the health
-i ” care
uu. x v tn V .
h.
A built-in health education component in all the
progr mmes utilizing all available media Including
mass media for proper motivation of the com^unit^
£tUiessQthan°5F3oftth* {^ Programme should provide
J-ess than 5/ of the total outlay for this purpose.
1.
■,f?r GOntinued education through preand ln“service job oriented training of
health manpower should be provided on the lob nna
through the existing institutions und by osSbl^h
S,
ln%tlt“«ohs. Training of the traineSt
J0061^ 2“° “Wsls- Adequate provision
should bo made for thls^purpose in the plan progra-
J.
Health services research for more effective imnlP
mentation of the programmes should be SZn S Oner
ational research technique should be adopted/’ °P
k... bri
T* en/e2,hnoi°F
bio-technology need to '
be
introduced
for
4-f u ■ 9r 1nec. _or improving the current production
improving the quality of
V.
immunodiagnosti-c immuno-biologicals,drugs etc.
R e c o m m e
n<lations-
ena/n/iew,-2f the issUes raised and the approaches
2ibh 2ted’
reGOmendations of the Working Group
with respect to identified areas are given b^low?-
a*
/nHi//mtional hQalth Programmes, national malaria
eradication programme,.national filaria control proleZfiy^SZitS^g^s31/: diarrhoeal d^™
...p/8
:-8~:
will be significant reduction in the morbidity/mortality from the current level of malaria,tuberculo
sis, filaria, diarrhoeal -diseases, sexually trans
mitted diseases during the 7th plan. Guineaworm
will be eradicated and preparatory phase for eradica
tion of leprosy will be completed. The production
of different vaccine will be coordinated to meet
the requirements of the national health programmes.
b.
Now efforts will be mounted to control and contain
the following diseases which are of national and/or
regional importance, namely Japanese encephalitis,
kala-azar, viral hepatitis,' typhoid,'intestinal
parasitic diseases, yaws, measles and acute respi
ratory illoss in children below five years.
c.
Establishment of epidemiological services at all
levels of health care would be necessary for proper
Implementation and monitoring. Every programmes
should have an inbuilt provision independent evalua
tion.
a.
Effective inter-sectoral coordination need to be
established for potable water supply, sanitation,
solid wastes, sullage and storm water disposal,
water and air pollution control between the
ministries of health, works and housing, depart
ment of environment and other related organisations*
Such collaboration is absolutely essential to make
a dent in the control of communicable diseases such
as cholera and diarrhoeal diseases, typhoid and in
testinal parasites, viral hepatitis, malaria, ence
phalitis, filariasis etc.
e.
A permanent and continuous system of monitoring and
evaluation of public water supply system including
that in mass transport systems shouldbe introduced all
over the country. This should preferably be carried
out by the health services departments of the state
in close coordination with local governments, pub
lic health engineering and other department^ concer
ned with community water'supply. This would go a long
way in improving the quality of drinking water and
vpuld contribute significantly in controlling communieable diseases.
f.
g.
i
-
Health education component of all diseases con
trol programmes should bo given full attention to
enlist individual as well as community support.
Each programme should,therefore, make provision of
not less than 5% of its total outlay for this pur
pose.
.
Mechanism should be evolved to ensure that the
central assistance for implementation-of the various
national health programmes are utilised for the
specific purpose for which the assistance is made.
.,.p/9
:-9-:
h.
The 7th plan allocations for various identified
programmes should be done as per priority given
D © J_O W •
i) Leprosy
-cjHxuay, tuberculosis, malaria, filaria, diarrhoreceiveGhigh pri ^it^01 °f blindness should
11)
Development of epidemiological services as a '
■national programme should be taken up in the
7th plan.
111)
Guineaworm and yaws eradication and kala-azar,
poliomyelitis,, and-sexually transmitted disease
control programmes should be continucd/started.
where applicableo
iv) A national programme for vaccine production and
quality control should be included in the 7th
plan.
v) Beginning should be made towards development of
new health programmes on viral hepatitis, acute
respiratory diseases in children below 5 years,
contro! of typhoid fever and intestinal helminB^encephalltls^’ measlas’ rabl«
Japanese
4.4^The t’rlef description
of the- proposals in the
,
identified areas, Gusci
’ibing the
ghg c
describing,
current status>
objectives and strategy in the
x, 7th pian proposals and
areas of research rare given in the next few pages.
•
•
..p/10.
1* National Leprosy. Eradication Programme
1.1 Current status - Please, refer to page
2.
1.2 Objective and strategy
• During the 7th plan period, we expect to detect 1.5
million additional cases and treat about 4 million cases
including . old and new cases. At the some time about 2 mill
ion cases are expected to be discharged from the list so as
to gain start towards negative balance. As a result it is
expected that by the end of 7th plan, the- tdtal number of
cases on record will be about 2 - 2.5 million achieving a
substantial control of the disohso in some districts. This
is also expected to be reflected in the reduction in the
prevalence rate, deformity rate and now .case detection rate.
The strategy in broader aspect will remain unchanged
but during the 7th plan emphasis will be given to wider
coverage of multi-drug campaign trial in 100 high endemic
leprosy districts, intensive health education through all
types of mass communication.media and community participa
tion, inclusion of welfare and rehabilitation services,
introduction of monitoring and concurrent evaluation with
periodic and practical assessment of the programme,free
supply of specific anti-leprotic drugs, introduction of
new training courses for social welfare,.and managerial sk
ill for senior non-medical supervisors and nursing staff,
wider participation of voluntary organisations and inter-’
national agencies and establishment of new training centres
and regional institutes for augmentation of action orien
ted research both in the field and laboratory.
1»3 Seventh plan proposal
1.3»1 Manpower development
a) Strengthening of Directorate
The office of the programme officer at the centre
will be strengthened by giving him additional technical,
secretarial and statistical help.
Similarly staff in the office of the state leprosy
officer and district leprosy officer will be adequately
strengthened.
b) Strengthening of field organisation
To cover the high endemic areas where the prevalence
rate of the disease is 5 and above per thousand it will be
necessary to provide trained leprosy technicians at the
rate of 1 for every 20-25 thousand population, 1 trained
non-medical supervisor (NMS) for every 5 leprosy technicians,
physio-technician and health educators - 1 each for every
4 such Non-medical supervisors covering a population of
...p/ll
about 4 lakhs in rural areas and. about 4-6 lakhs in urban
ar^as. Other ancilliary staff for secretarial support,
supervision, assessment, will also be. needed,
1.3.2 - Training.,- Training -will be organised through regu
lar and short orientation courses and also by conducting
workshops ano seminars. There are 41 leprosy training contres including one central and two regional institutes®
i£ ?nrek^^-ni^
nodical officers, 4 wnths' tr^in' ■'?a-,-ninS for Para-medical workers,
mon uh s- tj.a..ning xor laboratory technicians, 9 months'
for physio-technicians and 2 months' training for leprosy
LSP T,GCa-U°-rs and orie year Gaining for Assistant Leprosy
i'3”'! Oe,
during the plan period by providing
stipunos uo the uranneos. A few regional training-cHm-refe
rral instituues wi-l also be established in the country.
SfJ? 08
campaign will also be impacted through
aiscrlct and sub-district level before 6
the district is taken under the campaign.,
1»3*3 7 3^1ih_education - Health education through mass
communication and audio-visual aids.to.be introduced throu§ ^- specificcomponent to the scheme by involvement t^rou
^oal^4 e™Gation, mass communication and media expert s.
fVnds.prov^®d at; central, and state levels for central airectorate, state directorate and voluntary agencies
can take up action straightway,
7 agencles
rf and rehabilitation - Welfare and rehabilita' nbn o^, pa^ien^s w.iH form a .specific component of the 7th
p an scheme and integrated with case detection and case tr
eatment programme for a meaningful life to the patient in
the context of repeal of Leprosy Act and- correction of
physical_defprmityo ■Th© existing socio-economically dislo
cated patients will be specially taken care of in addition
to . those the community „
.juuigiuu
■
7 WWOfc treatment in the
lorn ol a dictrict-wise campaign for 3 years for a comorehens re case detection supervised treatment with a view to ear
ly cure, preventing deformities, preventing drug resistant
germs and achieving interruption of transmission of the di
sease in the community will be introduced as the main thrust
vfirnS Programme„ 100 such districts having leprosy pre^lercc rate above 5/1000 prevalence rate will be covered
So^idtrto ^b-bn?eTdf'?Ulti”drUg Vr'eatment will also’be
t? Patients being treated in indoor institutions
having trained medical and laboratory services.
1.3,6 - Monitoring and evaluation
a) IHe states will be advised to monitor the programme
through theix' Staue Leprosy Eradication Board.
The effective implementation of the programme
and adjustments in operations^ as necessary^ in
oeP/12
s-12-:
different areas of the state will be made- by the
State Board.
b)Ihc concurrent evaluation of the programme will be
made by the authority who is implementing the
programmCo This evaluation will be made at least
twice a year0
^^ual and more infrequent evaluation will be done
44.“^pendent team who are not directly concerned
with the implementation.
Attempts will be made to send a central evaluation
°naG
yGars to hyper-endemic states for evaluation and making recommendations.
1*3.7 - Material and equipments
a) Equipments, vehicles, microscopes, calculators,
Projection equipment, duplicator and typewriters
will be needed. Construction of clinic building,
training centre, hospital wards will also be requiredo
b) Anti-leprotic drugs and drugs for treatment of
reactions and associated complications or other
diseases for treatment of leprosy patients will
will
De needed. Laboratory reagents dressing materia
ls, protective shoes and prosthetics will also
be required. Drug like Refampicin, Clofazimine
are not manufactured inside the country. Hence
these have to be imported.
i*?:8 “ Ztolglal implications - Rinds will be needed for
full implementation of the units,established during the 5th
plan period and for establishment of some more new units
to complete coverage in high endemic areas and to provide
technical and supervisory support to lesser endemic areas
for introduction of multi-drug campaign. Funds will also
oe needed to meet operational cost, salary of the staff,
supply of drugs, materials and equipment, transport and
construction of buildings particularly of functional type
als2 for. staff quarters in tribal, hilly and backward
areas where houses are not available on rent.
1.3.9 - Areas of research
1) Vaccine
il) Operational
iii) Chemotherapy
iv) Chemoprophylaxis
v) Investigation into drug resistance
...p/13
:-13- :
National Tuberculosis Control Programme
2.1 Current status - Please refer to page 3.
2.2 - Ob j ective and $trat e.^y
, . To achieve detection of 2.5 million cases per year
which will approximately be equal to estimated incidence.
augment and strengthen the treatment activity so
that cure rate rises from 40 per cent toQabout 80 per
cent.
F
2.3 Seventh plan proposal
The main objective during the 7th plan period would
be to continue the expansion and strengthening of TB
case finding activities at all levels and arranging su—
pply of anti-TB drugs in sufficient quantities for treat
ment of diagnosed TB <3 patients.
'
(a) The following schemes are suggested for impletoentation:D Establishment of fully equipped and staff district
TB4. vne?trGS in thic£1y populated districts and
establishment of mini TB centres with basic mini
mum staff and equipment in thinly populated distnets where there is no such centre;
Establishment of additional district TB centres in
of oJSClS Sllionr dlstricts haVing a Population
Jteplacemont of old sots of X-ray equipments with
Odelca cameras which have outlived their utility
and considered unserviceable or uneconomic for re-
pair s;
iv) Provision of X-ray unit with Odelca cameras to the
TB clinics run by voluntary bodies;
V) Jentre?6^ °f 10° °ld VGhicles
district TB
vi) Provision of miniature X-ray film rolls in suffici ent quantities for use at the equipped district
TB centres;
vii) Provision of additional laboratory
technicians
at the primary, health centres where the -workload is considered extremely heavy;
#lii) Establishment of 2000 TB beds specially in those
districts where they are not available or the
existing number is insufficient;
....p/14
:-ld-:
ix) Supply of standard anti-TB. drugs to. sWes/union
territories/voluntary body run organisations.
x) Introduction of - short -course chemotherapy drugs
regimens containing Rifampicin and Pyrazinamidc
in a phased manner - 75' districts each year so
that by the end of 7th plan about 375 districts in
the country are covered under these regimens.
The group recommended that the items at sub^paras
Cv) 5 Cvi); (ix) and (x) be taken up as 100$ cen
trally sponsored schemes and the remaining may be taken up
by the states/union territories under their own budget to
quality for central assistance.
(b) Die following activities will be taken up as purely
central schemes
i) Production of health education material^
ii) strengthening of TB sections, Dte.GHS to undertake
proper monitoring of the programme and for shoulder
ing additional responsibilities involved.
iii) National TB institute , Bangalore - It is proposed to
augment substantially the research and training
activities of the institute during the 7th plan
period. Pbr this it would be essential to provide .
additional building blocks, machinery and equipments
in various sections, replac-ement of old vehicles and
manpower in various sections of the institute.
3.
3• National Malaria Eradication Programme
3.1 Current status - Please refer to page 3.
3.2 Objectives and strategy
___Ihe objectives of the modified plan of operation - NMEP
will remain unchanged during the seventh plan period, They
are -
a) to prevent deaths due to malaria and reduction in
the period of sickness.
b) maintenance of status of industrial development and
green revolution due to freedom from malaria,deaths
and reduction of morbidity.
c) to consolidate the achievements obtained so far.
To achieve the above objectives, the residual insecticides
spray in rural areas as well as in peripheral areas of town
ships and anti-larval operations in urban areas will continue
...p/15
:-15-:
to be adopted. Similarly for. detection and treatment of
malaria cases, the' pbriodio ‘surveiilahce on fortnightly
basis -with microscopic examination of blood smears and
administration of anti-malarial drugs’1 'will-'continue to be
in force during this period. .. No major deviation in the
technology of malaria ccntrcl-is envi sag fed'during' the seventh
plan period. But research on operational aspect of
Malaria control for*developing alternate integrated
methods of control will be given high priority.
Special-programme for containment of Plasmodium falciparum
namely P.falciparum Containment: Programme, to prevent
deaths and spread of resistant strain of/ Plfalcibarum to
commonly used drugs in new areas will continue with the ass
istance from SIDA/WHO.
3.3 Seventh plan proposal
~ Requirements - The spray and surveillance operation
be continued and the present pattern of assistance may
be modified in view of the fact that the surveillance acti
vities will be carried out through multipurpose workers
and this should be reflected in the budget which will be
earmarked, for development of multipurpose workers scheme
during the seventh plan; period, whether it is decided to
be centrally sponsored or the state liability. However, the
component for spray operation, i.e. district level and the
seasonal staff for spray operations, material and equipment
(.insecticides, pumps, vehicles and anti-malarial drugs) may
be made 100 per cent centrally sponsored as was in force
.prior, to 1979-80.
However, it will'be necessary to strengthen the perinheral services by additional staff for supervision of delivery
of services to the community, monitoring and reporting under
NMEP will also be made more effective by strengthening the
services with appropriate staff component. This is all- the
more necessary, consequent to introduction of MPW scheme on
a horizontal, basis and increase in population.
For the above purpose, suitable augmentation of staff,
at peripheral, district, state and central level will be
effected.
3.3.2 Areas which need research are a. Research oft operational aspect of malaria cpntrol;
with a view to develop alternate integrated methods
of control.
- y.■
•.
b. Ecological and' control of vectors of malaria.
c. . Chemotherapy of malaria.
d. tJr^ug resistance in malaria parasite.
e. Serology of malaria.
f. Cultivation of malaria parasite. .
g. Immunological aspect of malaria.
....p/16
:-16-5
• National Filaria Control Programme
Current__status - Please refer to page 4O
^•2 Objectives and strategies
copbinbe the ongoing antilarval measures and
detection and treatment of mf. carriers in 177
control units located in the urban areas*
J
<■
b) To extend filariasis control activities in the
'
1? of ^^tment of clinical cases through the
health guides to the total rural population
The strategies to’be followed-are given below:The main strategy of the programme-in urban areas is to
SnthaivT?r “OS£lui^ breeding by carrying out recurrent
tSvnTa Th
chemical larvicides at weekly inZ i
?esne methods are envisaged to control‘also the
vectors of malaria and other mosquitoes. To reduce the sou
rce of infection quickly 102 filariasis detection and treat~f?ms are operating in some control units to treat
microfilaria carriers and filaria cases»
The present strategy of detection qnd treatment of mfB
Cppri?fs
DEC Is not cost effective. The only possible
iJfeDFrVJvmiQ?hb? for/eyeing the filaria disease is by makS ?EG available under the primary health care system for
treatment of clinical cases of filariasis. DEC reduces the
frequency of future qcute attacks and thereby chronic disea
se. Pilot studies during the last one year in two endemic
arvaSnT?nOWeC\thQ village health guides. (VHGs) could
PF3 available to suspected cases of .filariasis without
affecting their other activities*
4.3 ■Seventh plan proposal
” Every village health guide or in his
equivalent or.in their absence multipurpose worbpr^T.i?r11a8+-f:L3;afia4-enc]emiG ^lstricts in the country would
with
and fcweat cliniGal cases of. filariasis
with DEC in their-areas* Necessary addition would be made
in the training manual for village health guides. DEC would
h® rn?Lenished t? ,V?Gs periodically. Posts' of District Filar*a Gf£lcers
be
created where neceJ?
entrust coordination and guidance of the programme
activities in endemic districts. Total cost oT DEC would be
borne by the Government- of India. The existing NFCP units
and deuection-cum-treatment centres evolved in urban areas
and survey units in endemic states would continue and their
cost would be shared between centre and the states on 50:50
oasis as for- hMEP.
nh3!1 "
.... p/17
4»3.2 - Areas for research
a) Operational aspects of control' would cpnfinue to be
identified and studied.
b) Medical social science research.
c) Integrated vector control measures.
5. Control of Diarrhoeal disease^ programme
5.1.1 - Current status A
—
Acute
diarrhoeal disease is
one of the major causes of morbidity and mortality
—in children below 57 years of age. •"•u.+uuj.a,
In India, 13.8%
"/ of the-total population, i.e.
l.e. 94 million are in the age group of 0-4 years.
Since the average number of diarrhoeal episode
child per year, about 188 million episodes.of Diarrhoea takes
place among the group.'
group. 10/ of thesepatients,
these patients, i.e. 18.8 mi
llion need rehydration therapy and 1/ i.e. 1.8 million are
in the grave
alisation^
76 risk>
rlSk’ zone facing mortality
mortality and require hospit(Tkl-i 4 *1 A!
— _
__
.
-L_
he
■
Hiring, the fourth five year plan, 46 cholera combat teams
W4Sr?xfet: up in the cholera endemic states and laboratory fa
cilities were augmented. Hiring the fifth plan, the programme
was transferred to the state sector. Hiring 1983-84, a pro
vision of Rsi3 lakhs exists for preparation of health educa
tion materials. In view of the. magnitude of the problem, it
is essential that the present diarrhoeal disease control pro
gramme should not only continue but requires to be further
--strengthened. in .0.11 aspects.
:,v _
_ .
?•
- Obj ectives and strategies' - Hi e short term objective
is the reduction of mortality through effective implementa?r51 rQhydration therapy at the peripheral level.
This includes production and distribution of the ORs packets,
training of medical and para-meeidal health personnel as
u ix.jp education of mothers and community and operational/
52^ rS?rV1ices Ietearch jor identification of suitable stra
tegy of implementation,.. The long term objective of reduction
i”
..Provision of .safe water and
sanitation facilities.
. "
5.3 - Seventh plan proposal - Operational studies at
community leve.!1 P?7® i^icated .the efficacy of OHS and training^ of adequate number of health workers
wuxn-surs, it will be possible
ril^ d°wn the mortality rate during the seventh plan by
50%.
5.3.1 - Production of ORs packets - Present production of
ORS packets is around 5 million per year. This need be in
creased. to 10 million by 1984-85 and 40 million packets
..p/18
by the end of the 7th plan, so that atleast 100 packets
could be distributed by each village health guide each
year.
5.3.2 - Training - About 18,000 doctors working'in the pri
mary health centres are to be trained at the district level
training courses. This can be achieved during the first two
years of the 7th plan. The paramedical staff working at the
primary health centres can be trained at the PHC level in
batches by the doctors who have already been trained at
district level. Training of the state level offiders will be
arranged at national level. The education of the mothers
. and the community members, are to be arranged through the sui
table audio-visual aids on proper feeding of the children,
breast, feeding, weaning, personal hygiene etc.
•r
5.3.3 Financial Outlay - Provision’ should have to be made
for purchase of 40 million packets of ORS, development of
supply system upto peripheral level, strengthening of diagno
stic facilities and establishment of clinical management
system in hospitals and other treatment centres plus educa
tional materials and other treatment centres plus educatio
nal materials for the community.
5.3.4 - Argas for research
a) Etiology, pathophysiology,mode of transmission,
role of safe water supply;
b) Operational research to determine the best, means
for successful implementation of the programme.
6. National Programme for control of Blindness
Summary of VIIth plan proposals - ~~~
6.1 Current status --Please refer to page 4.
6.2 - The objective will be implementation of Swaminathan
Committee's recommendations and reduce the incidence of
blindness from 1.2$ in 1985 to 1$ by 1990. The strategy
will be as recommended in the Swaminathan Committee's report.
6.3 Seventh plan proposals - The Tilth plan proposals are
broadly based on the recommendations of the Working (Eroup
which aim at -
i) completing the infrastructure at PHC block, Taluka and
district levels. It is envisaged that.^atleast one Oph
thalmic surgeon and one ophthalmic assistant should be
available for rendering eye care services to population
of 50,000.
-' J.....
...p/19
5-19-I
ii) Adequate number of eye beds be provided at district
hospitals and community health centres with a ratio
of 1 eye bed for 20,000 population.
iii) All medical colleges be covered with specialised, treat
ment and diagnostic facility for comprehensive eye care
including the development of eye banks.
iv)- Adequate training/research facility be created in all
the medical colleges in the country.
o
v)
Training facilities for training of Ophthalmic Assistants
be augmented to meet the requirement of Ophthalmic Ass
istants to man all PHCs, Distt.Hospitals, Mobile Units
etCo
vi)
Voluntary sector be encouraged both for eye camps and
for establishment of permanent eye care facilities.
vii) Management and monitoring component of the programme be
adequately strengthened.
viii) Intensification of eye health education measures o
ix)
Vision research and Bio-Ophthalmic Research for develop
ment of research in instrumentation and Bio-Ophthalmics.
x)
Ten regional institutes including those already establi
shed be established for development and strengthening
of sub^specialities, ophthalmic training and. research.
xi)
Dr..Rajendra Prasad Centre for Ophthalmic Sciences,
New Delhi be developed as the National Institute of Oph
thalmology to provide technical leadership for planning
and implementation of the programme and for development
of super specialities, operational and basic science
research and manpower development.
xii)
Mobile units be establishecT'at district level for streng
thening preventive and promotive aspects of the programme
including provision of services for children screened for
ophthalmic care through ongoing school health scheme.
•
•
•
.
jO
xiii)
Ophthalmic instrument workshop be established''to provide
base for quality.control, repairs maintenance of equip
ment and.to provide training to the staff in maintenance
and repairs of ophthalmic instruments/equipments.
xiv)
Provision of spectacles to-cataract operation cases.
Areas of rgsearc h.
■■ ■
a. Epidemiological research on cataracts corneal ulcers
and nutritional blindness.
....p/20
;-20-s
b. Basic science research on cataract and essential oph
thalmic drugs.
c» Operational research on mobil-e ophthalmic health care
delivery in rural areas including eye camps and
school eye health.
i
d. Development of ophthalmic instrumentation and
implements and corneal substitutes.
7o Development of EpidemiologicalServices
7.1 Current status - The integration of preventive and curaative aspects oFhealth care delivery as a national objective
has been identified and acted upon during earlier plan period.
It has made steady progress culminating into development of
primary health card programme for providing comprehensive hca_th care to the people*. But development of epidemiological
services as an integral Part of primary health care has not
been given serious consideration. Without any mechanism o
epidemiological services it will not be possible to tackl the various disease problems in the country on horizontal
basis.
7.2 Objectives and strategies - The obj ective^ -will be to
establish the nation-wide epidemiological services where in
the pivotal role will be played by the district, state and
national levels with a strong organisational set up, wirn a
view to implement, monitor and evaluate various health pro
grammes being delivered through-the primary health care sys
tem.
In evolving the strategy main considerations will be given
to available health infrastructure. For implementing the
programme, a two-fold strategy is required vis. administrative and technicalo
The administrative strategies will be to a) launch a
centrally sponsored scheme;-b) appoint a programme officeis
at the national/and state levels; c) restructuring/reorganising/redefining the job requirements of functionaries at
various levels.
The technical strategies will involve a) setting, up an
organisational structure to meet the requirements of disease
b) ensuring prompt service and availability of rapid diag
nostic facilities; c) training of personnel7.3 Seventh plan proposal
ructui*y-5 In suggesting the orga7.3.1 Organisation and structure*
full
should he given to
nisational pattern, full consideration
c.
•.p/21
s-21-s
the requirements of the epidemiological services at the
SSSaSSSarK-K.
possible that the broad.staffing structure required for
establishment of the epidemiological services may possibly
be made partly by suitably restructuring/reorganising and
redefining job responsibilities of the various'personnel
already available at different levels.
Rational level
As has been pointed out in the strafpvpi a?P°intfiient
a Programme officer at the national
level with appropriate staff will have to be made.
Cb) State level - Every state at the headquarters will have
eP^iological coll headed by a senior office^
?ral3ed in epidemiology and supported by statisJ S’ .^oratory and other ancilliary components. Ihe
state epidemiological cell will have facilities for data
collection, processing, analysis and feed back.
Cc) District level i) District is the implementing agency unit of all
health programmes. Each district will,therefore,
have an epidemiological wing with surveillance
and disease Investigation unit and a data processrng unit with inbuilt facilities of feedback.
This wing will be headed by a suitably trained
person m epidemioliogy;
ii) Community health centre/PHC level - At this level,
epidemiological services will be taken care of by
imparting appropriate training to all health persohhel in the principles and practice of epidemio
logy and disease , control.
iJ-uemxu
(y1) —population - The Government of India is keen to
strengthen the health care services in urban slums and Jhe
scheme in that regard has already been finalised. For corP^abioh which have, epidemiological wing, the same .needs to
e s leamlinecl and in view of the government’s decision to
provide comprehensive health care to the urban slum popuiatiph. Additional inputs may have to be provided after ne
cessary appraisal of the situation. Fbr corporations wi?h
qpdi^nd+-hPidemiO^?glCal services» the same is to be organi
sed on the same lines as envisaged for a district.
n^Pitals are an important source for moriimortality data but these data are rarely
iZ ml'Sia
anal^is and thus valuable information
s missed. It is, therefore, necessary to have medicnl
record sections in all district hospitals.Te medial
• p/22
<
:-22-:
record technician with the assistance of statistical assis
tant will compile and analyse the data and submit the report
to the Medical Superintendent for onward transmission to dis
trict epidemiological wing.o
7.3.3
Materials and equipment
Prompt services are the key to success for effective epi
demiological service. Brerefore, provision of^transport faci
lities with POL, rapid data processing with the help of elec
tronic computers, adequate stationeries, typewriters, dupli
cating machines, display boards etc. and rapid diagnostic kits
for outbreak investigation should be given adequate budgetary
support.
7.3.4 Training
Training requirements of the programme is categorised under
two, heads, viz. continued education through inservice training
programme and continued education in improving professional
skill by encouraging personnel to take professional examination;
such as the one taken by the National Board of Examiners.
Training is to be provided to three broad levels of health per
sonnel, viz. managerial level, mid-level and lower level. To
impart this training, national and state training institutions
will be Identified and strengthened^
7.3.5 Areas of research
One of the important functions of epidemiological services
will be to conduct health services research for improving
planning, better implementation, monitoring and evaluation
of disease control programmes. It is obvious that the acti
vity cannot be efficiently discharged without adequate resear
ch into the dynamics of health care delivery. Consequently
resources will be required to foster and sustain this activity.
Guinea-worm Eradication Programme
8.1 Current status - Dracunculiasis or guineaworm disease is
endemic in seven states, namely Rajasthan, Madhya Pradesh,
Maharashtra, Andhara Pradesh, Karnataka, Gujarat and Tamil
Nadu in that order. The disease being rural in distribution
occurs in drier areas with low rainfall and deep water table
where step wells, ponds or tanks form drinking water sources.
About 13 million people living in about 13,000 villages dis
tributed in 85 districts are exposed to this disease. This
disease is transmitted by drinking only contadiinated water.
8.2 Objectives_________________
and strategies - The objective-is to interrupt
the transmission and ensuring disease free status for a con
tinuous period of three years before eradication is declared.
...p/23
The current strategy of provision of protected drinking
water, health education of communities, -chemical treatment
of unsafe water sources, surveillance and training would
continue..
8.3 Seventh plan proposal*
8.3.1 Provision of safe water - FUnds towards provision of
safe water to guineaworm affected villages'' without such a
source would continue to. be a high priority programme under
rural water supply programme. Chemical treatment of unsafe
water sources, case searches and printing and distribution
of health education material should also be provided for.
9. Yaws Eradication Programme
9.1 Current status - "No reliable estimate of extent of yaws
problem in the country is available. Anti-yaws teams are
currently working in Orissa and Andhra Pradesh and resur
gence of yaws has been reported from Madhya Pradesh. The
problem needs attention as it is technically and administra
tively feasible to eradicate the disease. Yaws.mainly affects
the population living in tribal'areas. In view of the Govern
ment's commitment to uplift the socio-economic dondition of
the tribal people the programme should receive adequate su
pport.
9.2 Objectives and strategies a) Active search operation be carried out in erstwhile
endemic areas to delimit the problem and identify
population at risk.
b) Training of medical and paramedical personnel
in yaws case detection, diagnosis and treatment.
c) Strengthening of laboratory facilities where needed.
9.3 Seventh plan proposal
The essential requirements are provision
undertaking the following activities
of .funds for
a) One mobile team will be established . for 0.5 million
population at risk.
b) Functional responsibilities of the organisational
structure at each level. Arrangement for treatment
with Pa for each detected case has to be made.
c) Training of personnel.
,...p/24
10. Kala-azar Control
10.1 Current status --Kala-azar—was vif-tually eliminated
from the country as a collateral benefit of insecticides
spray under NMCP/NMEP, .A. large' outbreak occurred with many
deaths in several areas of Bihar in 1977. Number of_cases
and deathp reported from Bihar since 1977 is as followss-
1977
1978
1979
1980
Cases
Deaths
0 O Q
18589
41953
25473
12623
13801
0 3 0
9956
n a o
9986
229
62
28
18
37
31
‘ 91
• o c
O J o
cf O ''
0 0 3
1981 ■
1982
1983
(Upto Nov)
Imported sporadic cases of kala-azar were also reported
from Assam, J & K, Tamilnadu,
Tamilnadu Gujarat and Delhi during the
j.
Large
number of indigenous cases are also
recent tears
reported
from
some
districts
of West Bengal during^ the last
i
_______
_
two years. From the trends seen it appears^likely, that di
areas particularly
sease may spread 'to other
"
" " 1in the ,eastern
region unless special efforts' are made to contain this.
10.2 - Objectives and strategies a) To reduce the incidence and level of transmission
of kala-azar.
b) To prevent deaths
c) To prevent the spread to adjoining unsprayed districts.
Strategies include »
a) Early detection and treatirient of kala-azar cases by
establishing good surveillance system.
b) Timely indoor residual spray of DDT in all the
affected areas.
c) Training pi'ofessionals ^nd paramedicals in kalaazar control.
10.3 - Seventh plan proposal
x
10.3.1 Strengthening of NICJ) - The NICD viould be strengthe-
ned to take up the additional responsibility of
guiding this programme and research;
„.,p/25
:-25-s
10.3.2 Supply of materials - Timely supply of DDT in adequate
quantity would be ensured to the states of Bihar and
West Bengal. Adequate funds would be made available
to the states to ensure appointment of spray staff
and availability of drugs.
10.3.3 Areas of research
a) Role of PKDL in the spread of kala-azar.
b) Methods for predicting the areas that would be
affected dhring the next one/two years*
c) Establish the presence and nature of animals in
volved in the spread of kala-azar, if any.
11. Poliomyelitis control programme
11.1 Current status - Polio vaccination programme has been
introduced as a part of national immunization programme from
1979. During 1982-83, 37 lakh children benefitted with three
doses of oral polio, vaccine. Bee National Sample Survey
carried out by the DirectorateGeneral of Health Services in
1981 and 1982 has estimated that every year, 1.5 lakh child
ren get poliomyelitis in the absence of vaccination programme.
The survey has also indicated that it is as serious a public
health- problem in rural areas as in the urban areas. 85^ of
the cases get the disease before three years of age.
U.S Objectives and strategies - Considering the residual
disability due to poliomyelitis, it is proposed to have faster
expansion of the polio vaccination programme. It is proposed
to cover 100% of the new-borns by 1987-88 as a part of the
Expanded Programme for immunization. Ihe proposed vaccination
target9 percentage of coverage of new-born and requirement of
vaccine (including, booster dose) year-wise during the 7th
plan is given belowsYear
■
1985- 86
1986- 87
1987- 88
1988- 89.
1989- 90
Nocof beneficlaries (in
lakhs)
140
170
228
233
238
Percentage of
new-born.
60
76
100
100
100
Requirement of vaccine
(in lakh doses)
500 .
600
800
800
800
. .,..p/26
: -26-s
Three doses of oral poliovaccine at a minimum int9rva?o? one month starting at the age of 3rd month »11
be folloved. A booster dose vlll be given 1- to 18 months
after primary vaccination^ In addition to the fixed centres
strategy (clinics) annual outreach campaigns will be or
ganised for wide coverage..
11.3 Seventh plan proposal
11.3.1 Augmentation_ofproduction in the country
The need of polio vaccine for the programme at present
is meVby importing bulk concentrate separate!/ for type I,
type II and type III.. It is expected teat the in i&enous
production of oral polio vaccine vail start at HaitKinc mo
phar^coutionl corporation WJ. (BBPC) Pombay from lg5,
to 20 21 1S a)S03.
Vith an
o? ^\irqi£Synt3norf''tbe programme has to be met
by importing bulk concentrate for the present. A voeo
unit for ‘blending and importing of imported oral polioinfill bP organised to meet the expanding requirement
of°the P
r— in )he fiell arrangements for maintenance
of COM oXaln by providing not only eQUlpmonts ^t also
ensuring their maintenance has to be
as
to be provided with mobility so that all the chlioren
f three doses of oral polio vaccine by fxrst birth day.
Ibis will involve community participation to be achieved by
large scale health education programme using; various mass
IX t financial outlay will be included in the-MCH
budget of Department of Family-.Welfare.
11.3.2 Research needs.._-
a) Usefulness of killed poliovaccines;
b) Blending of killed poliovaccine with DM
manufactured in India<>
12c Sexually. transmitted diseases (STD)
12.1 Current status,- The number of cases of STD reported
oThealth Services during the last five years
to Dte.General
—— —- - is given belo-ws-
Year
Total number of STD cases...
1978
1979
4,79,687
5,69,676
7,12,262
5,57,992
4,60,939
1980
1§81
1982
p/27
:~27-s
™om yhe-.-figures, it a-ail be seen that for the years
1978-80, there has been a rising trend in the number of
||rX^ea?sd198£^f ^h^gj Fdec“ Sis^F5 ’
line probably is due to the late submission of the statis
tics by the various centres.
12.1.2 A. small fraction of the patients suffering from STD
report at ho spital/tr eatm ent centres arid--thus the above
ilgures do not indicate- the. exact nature of the problems.
The majority of STD cases are syphilis, chancroid, gono
rrhoea, lymphogranuloma venerieum and granuloma inguinale.
12.2 Obj ectives and strategies - The objective of reducing
the incidence of STD in the country is proposed to be ach
tbe
ieved through a) serological screening of all pregnant women-attending,
antenatal clinics run by states, union territories,
voluntary organisations and civil bodies.
E^uigments. - V.D.R.L. testing are being provided
to district hospitals and later to primary health
centres.
b) Training of medical and Pai'a-medical personnel
on STD in five regional training centres.
Training of laboratory technicians in five reference
laboratories.
d) Provision of health education about STD, to the
target group - students community, labour force,
industrial workers, general public patients - pati
ents attending family welfare clinics etc.
e) Establishment of a nodal centre - D.G.H.S. for moni
toring coordination and dissemination of scientific
information to various centres involved in the STD
control programme.
f) Assess the magnitude of the problem of STD through
f-our survey and mobile STD units - Evaluation of
the programme.
I2*3 |eyenth plan proposal - It is envisaged to arrange for
detection of more cases suffering from STD at PHCs, district
ho spit.als, civil hospitals. The above will be achieved by
strengthening the regional training centres, reference la
boratories and survey-cum-mobile units.
....p/28 .
s-28-:
13. National Programme for Vaccine Production
13.1 Current situation - India is self sufficient in the
production of DPT, DT, TT, BCG and typhoid vaccine. The need
for polio vaccine is met by import of bulk concentrate of
polio vaccine, separate for type I, type II and type III.
It is then diluted, blended and empouled for distribution
to the field. The working group on maternal and child
health have worked out the year-wise tentative vaccination
target and on that basis estimated the annual requirements
of different, vaccine.
13.2 Objectives and strategies
The objectives are to
a) make the country self-sufficient and self-reliant
in its vaccine requirement for expanded programme
of immunization;
b) induct modern biotechnology for production of better
quality of existing vaccines and introduction of new
vaccines which are epidemiologically necessary for
the country;
c) establish an independent quality control laboratory
at the national level;
The strategies •will be to
a) start a national programme on the same line as na
tional disease control programmes for vaccine pro
duction and quality control in order to develop and
d-iversify the production in the state and central
institutions;
b) channelise on a national basis the international
.aiiBs available in this area;
c) separate the final quality control and certification for release of immunobiologicals from the
production establishments;
d) augment training facilities for providing trained
manpower at various levels in this field.
13.3 - Seventh plan proposal
13.3.1 DPT vaccines, DT and TT vaccines The tables
below present the likely availability of DPT, DT and TT
vaccines from public sector institutes by providing addi
tional inputs, during the various years of seventh plan.
....p/29
g-29-s
i) Likely availability of DPT .vaccine from public sector
additional
institutes with ai'l'l
—7 inputs
' 7 " during 7th plan (in
million doses)»
87-88
88-89
89-90
Institutes
1985--86
B6-87
CRI Kasauli
PII Coonoor
HBPC Bombay
13.0
7.5
7.0
Shortfall
25 o 3
18.0
18.0
16.0
16 = 0
-15.0
13.5
12.0
10c0
will increases in"ph- 10.0
ases
23.7
23.9
23 o4
22O1
(This shortfall will be made_up by private^sector supplies.
of DPT from Bengcal Immunity not known)
The production capacity
< ...
ii) Likely availability of DT vaccine from public sector in
stitutes with additional inputs during 7th plan (in
million doses).
Institutes
1985-86
86=87
CRI
PIIC
HBPC
Short fall
16.0
5.0
6.0
2.7
16.0
6.0
6.0
2.8
87-88
13.0
7.5
6.0
88-89
89-90
13.0
8.0
13.0
10.0
6.0
6.0
(This shortfall will be made up by private sector institutes).
iii) Likely availability of TT vaccine from public sector institutes with additional inputs during 7th plan (in mi
llion doses).
Institutes
1985-86
88-89
89-90
CRI
PIIC
HBPC
State institutes
Shortfall
22.0
22.0
22.0
22.0
8.0
7.5
5.0
5.0
8.0 Will increase in phases
9.0
9.0
9.0
9.0
9.0
26.2
14.8
21<,1
26.2
26.0
22.0
10.0
14.0
9. 0
20.0
86-87
87-88
(Shortfall will bo made up by private sector supply)
The production capacity of Bengal Immunity is not known.
13.3.2 - BCG Vaccine - The National requirements of the BCG
vaccine during the 7th plan period can be met adequately by
the BCG vaccine institute at Madras by providing extra faci
lities for filling and freeze-drying of vaccine.
.,.p/30
5-30*’ 5
.
13.3.3 Poliomyelitis vaccine (oral) - This programme is of
national importance nric“nt presenF"£he oral poliovaccine is
imported in ■bulk’and blended by. only one source (HBPC) in
the .country. It is highly desirable that an alternate source
be organised at the earliest. At the same time, steps should
be taken to augment the existing blending and bottling faci
lities in the BHPC to meet the need. Indigenous production
of oral poliovaccine has commenced in HBPC and"5 million
doses of oral polioVaccine is expected to be available.by
1984-85, It is a-lso expected that this unit will be able to
step up the production during the 7th plan period to 20 mi
llion doses.
13.3.4 Measles.vaccine - It is proposed during the 7th plan
period To commence"the immunisation against measles starting,
with a coverage of 2W and achieve atleast 73$ coverage
at. the end of 7th plan.
At present the measles vaccine is not produced in the country
and hence has to be imported. The approximate cost of measles
vaccine is around Rs.16/- per 10 dose vial.
A measles vaccine production unit is being proposed with
•CRI Kasauli under the 7th plan and the project reported is
under the preparation for envisaging a production of 2 mi
llion .
13.3.5 Ratios v.-iccinp The Pasteur Institute Coonoor.has
submitted a" project proposal for 7th plan to the Ministry of
Health & FW. towards production of one million doses of the
tissue culture vaccine in vero-cells per annum at a reasona
ble cost for the use of common man. This project should be
provided with sufficient plan aid to go into production.
13.3.6 Japanese encephalitis vaccine - The unit has "been
established at the CRT Kasauli under Indo-Japanese collabonition for production of this vaccine during 7th plan
period. The unit will produce 2 million doses per annum o
13.3.7 Quality control of vaccines ~ Immediate steps should
be taken to set'up an independent-new institute for standar
dization and quality control of immunob io log i cals in the
country and also to meet the needs of providing trained
manpower in this important field. A project report in this
regard is being drawn up by the Vaccine Production Board.
13.3.8 Areas for research -
ae Towards production of newer vaccines like MMR
vaccine, hepatitis vaccine, etc. for the future.
o o o
p/31
b. Towards application of modern bio-technology in
vaccine production.
c. In view of the trend towards alternative strate
gies in control of- poliomyelitis using injectible
poliovaccine particularly in combination with DPT
vaccine for development of quadrapie .vaccines,
steps need to be initiated to develop expertise
and infrastructure* towards such a goal in the
public sector.
14. Viral hepatitis surveillance
,-L4,1 CUiirppt. situation - Viral hepatitis is one of the lead
ing causes of morbidity'and mortality in the country. Pre
sently the diagnosis is mainly based on clinical information.
to th?
bureau of health intelligence,
180974 cases and 228 deaths were reported in 1980. In view
of the deficiency in reporting of cases, these figures are
perhaps the tip of the iceberg of the real extent of the
problem.
Based on epidemiological investigations conducted
in different parts of the country, iL
it has
has been
been ’observed thatViral hepatitis is expanding health problem andI affect both
urban and rural areas;
14.2 - Obj.ectives and strategies - The objective is to begin
a new health programme for broadly delimiting the problem’viral hepatitis both in urban and rural areas through survei
llance and laboratory confirmation.
In order to effectively tackle the problem, the following strategies ■will be
as under:-
a. identification of viral hepatitis surveillance centres
in different parts of the country and providing them
with diagnostic facilities* Such centres may be
identifier; in the central as well as state sectors.
ba to develop laboratories at medical*'colleges and dis
trict level to act as sentinal centres for survei
llance.
c. to make available suitably trained personnel to man
these laboratories and centres.
d.
strengthening of research capabilities of these cen
tres to undertake research in the priority areas
including surveillance and control activities.
..p/32
s-32-z
14.3
Seventh plan proposals.
. Resource allocation -will be required for the follow
ing activities:• ?'
14.31Strengthening of viral hepatitis centres - At present
9 such centres have been identified in the country. But due
to paucity of funds? adequate facilities could not be pro
vided in these institutions and as such they have not been
in a position to function as desired. During the 7th plan,
it is proposed to augment the facilities in these centres
with manpower and equipments for effective functioning. In
addition.it is also proposed to identify moro centres for
the purpose.
14.3.2 Expert committee meetings - An expert committee will
be set up to develop/model training modules on viral hepati
tis surveillance and laboratory’diagnosis.
14.3.3 Training - Training courses will be organised and con
ducted to provide trained manpower to these centres.
14.3.4 Area of research -
a . delimination of hepatitis problem in urban and rural
population;
b. Dynamics of three hepatitis virus transmission in
the context of socio-economic and cultural settings.
c. Operational strategy for control of the clisease.
15. Acute Respiratory Illness (ARI)
15.1 Current situation- ARI is a great killer particularly in
early childhood. 'This constitutes a major cause of illness
in infants and pre-school children. Very little is known aboout the current status of ARI. A number of viruses, bacteria,
chlamydia and other agents are the causative agents. Of
this expanded programme of immunisation takes care of
Diphtheria and Pertusis and it also envisages some action
against measles during seventh plan. For the remainer, prac
tically nothing is being done. It is necessary for some spe
cific remedial actions to be integrated with the primary
health sare programme.
15.2 - Objectives and strategies - The objective will be to
reduce mortality and morbidity Tn children below 5 yxears of
age.
p/33
? ••-33- s
. Ihe strategy -will be (a) training of medical and paramedical personnel for early detection" of clinical cases and
their domiciliary treatment; (Co); development of referral
system for cases th-1 cannot be'at
at "home"
, tended
. - -- —
(c) immunisation of target population . ? Cd)
strengthening’ of five
regional laboratories for providing diagnostic laboratory
aeute respiratory illness and (e) health educa-
tion of mother and the
—j community»
u
15.3 Seventh plan proposal
gaining - Training courses will be organised for
medical and paramedical officers in case detection Sd ?bnt
?S/sflsservloe for patlents “d
x cig,
o J- o •
. roTiMog'®4-
15.3.2 Drugs - Drugs £ required for the first line of treatment will be provided to all PHCs.
13.3.3 Laboratory services - Identification of five regional
laboratories - Five regional laboratories, each one in"
bo
western, northern and southern zones will
i entified an< strengthened with equipment, personnel and
necessary reagents for laboratory diagnosis for acutS respiratory illness. Rapid diagnostic kits will also be madf a?3-L-Cl kJ
'U/
r
15.3.4 Health education.,- Health education material will be
prepared and distributed to all 'concerned.
Hegey/h needs - (a) development of-local rapid diasystbChFlts f° ayte resPiratory illness should be taken ''
up with urgency. Ihe.micro organisms responsible for acute
idlntifie^fJTyy in
b’elow
yQars should be
tetter understanding of the transmission dy
namics of these diseases"^. , (b) Simple and cost effective tre-itment schedule for these diseases, -will be searched*
16
Typhoid control programme
-"ntx.sus “ In India? the incidence of typhoid fever
dUe toinadequate provision of protected water supply
nhnlHrrPer station services/ Ihe exact incidence of ty- ‘
t qid fever in India is not knowno Reports received by cenoTthroTlnkh o
th int?1lieence.,(GBHI) indicate occurrence
oi three lakh cases and eight hundred deaths every year.
However, the acqual incidence is certainly much higher. Con
sidering the public health importance control of typhoid fever
^hebthne exPanded Programme of immunisaohhoJ* ,
on ™lth b;LValent typhoid vaccine is being
carried out for primary school entrants«
..p/34
s-34-s
16.2 Objectives and strategies - The objective will be
to" Ca) provide medical aid/relief to the needy through pri
mary health care system; Cb) protect by active immunization
children, adolescents and young adults; Cc) improvement of
food and personal hygiene through extensive health education
measures.
The strategy would entail (a) strengthening of the exist
ing primary health care system with provision of antityphoid
drugs; (b) necessary training of taedical and paramedical
personnel for case detection and treatment methodology of
health education of the family/community , particularly those
employed in food establishments; Cc) development of simple
field laboratory tests for confirmation of clinical diagnosis
and detection of carriers; Cd) immunization of the tarbet
groups and Ce) testing of water samples and education of
food handlers.
16.3 Seventh plan proposal -■ Adequate budgetary provisions
will have to be made for the following activities
16.3.1 Drugs - Drugs for treatment of typhoid cases will be
provided to the districts and PHCs.
16.3.2 Immunization - Typhoid immunization will be extended
to the target groups.
16.3.3 Training - Training of PHO medical and paramedical
officers in clinical detection of typhoid cases, their la
boratory confirmation and reporting will be undertaken.
16.3.4 Inter-sectoral collaboration - Inter-sectoral colla
boration will be aimed for providing safe drinking -water
and improvement of environmental sanitation for monitoring,
quality of water supply, establishment of laboratory facil
ities for testing water samples in each district will be re
quired.
16.3.5 Arms of research -
a. Develop rapid diagnostic kit to detect resistant
strains of chloremphenical.
be Develop simple laboratory test for quick confir
mation of diagnosis.
t' ..
e. Evaluation of effectiveness of the available
vaccines.
....p/35
35 -s
17• Intestinal parasitic clisense control
17.1 Currant status - Common intestinal narasltoa -in
SBE?™ s® “iiH a ».»•;.
1-iiR^a.B-S •= ■«£•i,
Z fnt spe4es of Parasites are available oX S Pl
oSpr^ J°n/teritQries- The magnitude of the problem 1S ?he
other states/union territories would be delimited Thp-wron S
SUlnf“SlSOlsStav»ll“fer SUrWS ln the
pation.°n
sSn X^S-in"10
reatmQnt ancl also to ensure community partlci-
n^7enth,plan ProP°sal - Suitable budgetary provision
wil1 ^required for the following activitieti- provision
J7*3*J Drueg^- Provision of adequate quantity of drugs to
Of
s to treat persons "ith
spXs
■'"...
*
17’3-2 Training ■- i_
Preparation of manual for PEG; medical
officer .and staff to help in diagnosis
fferent species of ’parasites/~6WOXri and Raiment of di-
17.3*3 Sa f e dr ink i ng wa t or - Proviqinn nf
+.
envisag^Tto be achieved during the 7th plan period wou^T
help towards control of this group of infection^
* S°
17.3.4 Areas of research a. to develop methods for quick and easy laboratory
diagnosis.
••.p/36
1
‘
s-s&i’-
b. to determine the relative effectiveness of different
methods of controls
c. to develop methods of surveillance of these infections.
18
Measles control programme
18.1 Current situation - The attack rate of measles is 100$
■with clinical measles in about 75$. The case fatality rate
is between 1 and 3 per cent. In other words, 15 million cases
of measles with about 1.5 to 2.4 lakh deaths occur every year
in the country. The disease leads to ill health of children
by - - , precipitating malnutrition and secondary infection.
25.2
,
strategies - A pilot study.in 36
lc?.2 Objectives and
medical colleges in India indicate..the necessity for intro
duction of measles vaccination in the national immunization
programme. Measles vaccine is safe, effective and gives pro
longed immunity with one injection, which may be considered
as life long. It is suggested that measles vaccination be
introduced in a phased manner by giving priority to those areas
where the case fatality rate is high and large size outbreaks
occur periodically. To achieve a high coverage rate, in addi
tion to services through fixed centres, it will be necessary
to qrganise annual outreach campaign. Vaccine will be given
to the most susceptible group of children, 9 months to 2 years
of age.
18.3 - Seventh plan proposal - At present, measles vaccine is
not produced in the country. Measles vaccine has to be imported
to initiate the programme. The CRI Kasauli is proposing a
project for measles vaccine during the seventh plan with a
production capacity for 20 lakhs doses by 1990. The Ministry
of Chemicals and Fertilizers is examining the proposal for
establishing a viral vaccine production unit, which will pro
duce measles-vaccine. The cost of measles vaccine is expected
to be about Bs.1.50 per dose in a lo-dose vial. The area and
population to be covered by auxiliary mid-wife has to be de
creased so that this additional workload of measles vaccination
can be integrated with the general health services.
19* Rabies control programme
19.1 Current status
1. There is at present no comprehensive rabies control progra
mme executed in our country. In India, Agriculture minis
try has launched Canine Control Programme during the.
Sixth Plan period.
...p/37
<s
:-37-:
2. Atleast 15,000 human deaths from rabies occur every
year in India but even
■ this recording is too
low, since the recorded deaths are based on very limited
reporting.
J
3*
a$-*-eas^ 5 lakhs persons bitten by presumably
rabid animals undergo antirabies treatment annually.
4. About 55.6% of the persons bitten by proved rabid animals
30^t^fCfhthG ?isease after refusing the treatment. Atleast
sasPec^ to be rapid contain the virus
salivary glands and are capable of transmitting the
diseases in nature. ',
-5. .The -bitting ^nimal involved in most instances in our coun
try is the dog (95.4$). In wile! life jackles, • foxds,wolves,
mangoose, bandicoots etc. are involved.
s’wu-Lves’
6. Atleast two types of inactiyated antirabies vaccine for
human use are produced in our country - the 5$ BpL inac
tivated vaccine and'5$ phenol!sed vaccine.-Both are pre
pared from the brain of sheep. The total quantity of the
vaccine produced is around 200 lakhs ml.of BPL vaccine and
i/o lakhs ml.,
z as phenolised vaccine. These vaccines
carry a risk of post-vaccine neuro paralytic accidents at the
rate of 1/5000 to 1/12000. Neural vaccines allo ha?e a
shorter shelf life of 6 months*
7. At present a small quantity of tissue culture anti
rabies vaccine is imported in our country at a very
high cost ■which is beyond the reach of common man.
This vaccine, of course, is non-reactogenic, highly
effective and given as 5 to 6 dbses, of 1 ml. -each.
The shelf life of this vaccine is long since this
is freeze-dried.
S. Pilot project studies on the feasibility of producing
this vaccine indigenously is being carried out at *
- Pasteur Institute of India with WHO/UNDP aid. The
resell? are encouraging. Project report for production
oi VhRO celltissue culture rabies vaccine at a reason
able cost within the reach of common man during the 7th
institute has been drawn and submitted to tire
Min.of Health & F.W.jGovt.of India.
9. At present the country does not have adequate supply
of potent.single dose tissue culture vaccine for the
immunization of the pot .dogs and other pet animals.
...p/38
:-38-?
19o2 Objectives and strategi^s
<
=SClturoCanOrSier
SoUJ
for better surveillance of the disease.
health education and
education and
information and broadensuingc
— ” ) required.
19„3 Seventh plan proposal .- Plan'provisionjwillbe
activities
under
the programmesfor carrying out the folio wing <—
19.3.1 In termini st erial coop era uiQJL-jfpr setting up* of field
ir^ a structure.
exHtent in theyoiolr>g cannlne rabies control programme of
the ministry of agriculture.
19.3.2 Vaccine p.roduction
" The Pasteur Institute of
another vaccine pro-
Snt»fS^arS^i£r Seine
for man and animals required for the programme. .
19.3.3 Expansion of laboratory diagnostic facilities.
All medical colleges and ID hospitals in the country will
be strengthened with this service.
19.3.4 Health education
Health education measures emphasising the
treatment of animal
“S' X oommnlty
ohPp°?pt
JoS. U1
Ing will bo involved.
O
o
.p/39
i-39-:
i
%
19*3.5 Areas of research
a. Operational research on canine rabies control by
education/immunization of dogs under local con
ditions in different parts of the country.
b. The main reservoir species in wild life must be
determined before the campaign for eradication of
the disease in wild .life ig launched^. Representa
tive surveys are urgently needed. After determining
the main reservoir species, the most effective way
of halting the disease by .reducing the species po
pulation etcc have to oe formulatedo
c» Surveillance efforts must be concentrated on the main
species by estimation of population density at
regular intervals which might forecast the potential
danger and intensity of rabieg outbreaks in wild
life.
d. Efficacy of oral immunoprophylaxis of wild life
population using oral rabies vaccine in baits.
e. The areas of research outlined require establish
ment of a. permanent mechanism with administrative
authority for ensuring inter-sectoral collaborat
ion such as with the. Ministry of Agriculture,
Forest department and like.
20r Japanese encephalitis (JE) control
20.1 Current situation - Outbreak of JE have been reported
from West Bengal, Uttar Pradesh, Bihar, Andhra Pradesh, Tamil
Nadu and Karnataka* The disease has a high case fatality
rate of about 50 per cent and the survirors are always
permanently disabled.-.
20.2 Objectives and strategies - The objective will be to
develop a better surveillance system for timely treatment
and control measures in the event of an outbreak.
The strategy follcwecl -will be Ho
early detection and treatment of cases -would
continue* For this laboratory facilities would be
created/augmented at the national,regional,state
levels.
b. Production and use of JE vaccine.
c. DteoNMEP would continue to support control measures
against vectors*
....p/40
*
s-40-?
i
d. Malaria or communicable diseases bureaus in the
State health directorates continue to undertake
measures of prevention and control -with the exist
ing resources.,
e. Antilarval measures are not practical an$ vaccine
available is of limited effectiveness. However,
high risk groups would be brought under vaccina
tion.
20.3 Seventh plan proposal
20.3.1 Institution strengthening - Central research Insti
tute, Kasauli has planned to produce the^vaccine jy
1986. Epidemiology division of NICD be strengthened
to take up early detection and forecasting.
20.3.2 Areas of research -
a. Institutions with facilities would continue to
investigate the outbreaks of JE and to develop
reliable methods for forecasting of outbreaks.
b. Studies would be developed to forecaste the out
breaks. Vector surveillance and sero-surveillance
form important components.
c. Relative effectiveness of different methods If
controls namely immunization, personal prophyla
xis, surveillance and anti-mosquito measures
•would be determined.
• w
t
-k
/ (o
. I)
THE PIONEER 3
Medical apathy terrorises patients
Staff Reporter
New Delhi
_
IN THREE incidents of negligence
and high-handedness reportedJ
from various parts of the city over
the past few days, a woman died
at the operation table of a quack,
a patient jumped to death from
the second floor of the Deen
Dayal Upadhyay Hospital and the
Mr Gupta said that Vijaya '——----------Lakshmi, who claims to have
passed class XII and to be a grad
uate in the Ayurvedic system of
medicine, was neither qualified
nor had the requisite facilities in
her clinic to perform an abortion
■
• ”
on a woman in the advanced
stage of pregnancy. Even other
wise, an abortion in such an ad
vanced stage is fatal, he added.
Lr
---------- ------ --------- — doctor and two of his brothers
Man jumps to death frustrated who were running a private
n“gXmealSaraiR0hiJ,ain
over hospital insensitivity
The man was thrashed re
:PerACr said that Jarawati, the
.
------ J
tiVlllKlll
'
portedly after a dispute over an
exorbitant" medical bill for his
three-year-old daughter’s treat
ment.
The police said that Manoj
Kumar, a Sarai Rohilla resident
had taken his daughter to the
Dewan Nursing Home after she
fell down while playing and sustamed a cut on her chin.
The doctors put three stiches
•1 on the chin and handed a bill of
] Rs 2.200 to Mr Manoj Kumar.
3
When Mr Kumar objected to
I the bfll, saying it was exorbitant
the nursing home staffers insist
floor.
Finding that no one was at ed that they would let him take
tending on him, he reportedly away the child only after the bill
was cleared. This led to an al'■
'
7'
Q6-month
6-m»„PX,t
rmS abO,tiOn
°n
pregnani
o-month pregnant
woman
Mangolpuri, was already a moth
for refusing to pay "exorbitant" er
of four.
medical bills.
Realising that they could not af
In the first incident, a 35-yearold woman who was six months ford to have the fifth child, the
Pregnant, died on the operation couple went to Saar Clinic run by
table of a quack at Mangolpuri in Vijaya Lakshmi and asked her if
north-west Delhi on Monday it was possible for an abortion
The quack allegdly told them
while undergoing an operation to
that it was very much possible
terminate her pregnancy.
DDU Hospital Dr C R Viswas con
Additional Commissioner of and admitted Jarawati at her firmed the incident but denied
clinic.
The
woman
died
of
ex
Police (northern range) B K
that there was any negligence on
Gupta said that the quack Vijaya cessive bleeding during the op the part of the hospital authoreration.
Lakshmi has been arrested and
In the second incident, a 32- ites. "The man was a little dis ±efoUo^gdna« b^XnsZ
charged under sections 304 A
oriented," he said. The police has scolded by Ute nurses
and 314 for causing the death of year-old rickshaw-puller Ram not registered any case since no
Babu,
undergoing
treatment
at
Frustrated by the apathy, Ram
Jarawati.
complaint has been lodged by any
Babu then jumped from the
Section 304 A pertains to Deen Dayal Upadhyay Hospital, of the patient's relatives.
death caused by a rash and neg- jumped to death from the second
Ram Babu had reported to the lloor. He sustained multiple frac
floor of the hospital on June 17
Bgeatact and section 314 deals allegedly
hospital
with symptoms of malar tures and was referred to
due to the hospital
Safdarjung Hospital, where he
withZXieath caused by an act
ia
and
pneumonia
on June 16
dpne with intent to cause mis- staffs's apathy towards his wors and was admitted to the casual- died on June 18.
ening condition.
In the third incident, a 28-year/Carriage."
Chief Medical Officer of the ty dePartment. He was later old man was beaten up and critshifted
to
ward
8
on
the
second
<
ically injured on Sunday by the
Doctor th
father for
t.s?
*
*v
er.^f >ris*
Rent’s
lrcation !:oi'owingB“s
Dewan
Wan and his
hk brothers
hr°‘h^’ allegedly
J*
attacked Mr Kumar and hit him
on the head with iron rods.
Mr Kumar sustained head in
juries and was rushed to Bara
Hindu Rao Hospital, where he is
stated to be in a critical condi
tion. The Sarai Rohilla police
have registered a case against the
three brothers and are investi
gating.
iphi.m
■
s.
r
AIDS victim’s death sets alarm bells ringing in Meerut village
____
w
S Raju
Meerut < l__2____ I
A PANIC button has been pressed
at a village in Meerut following the
news that a young villager died of
AIDS acquired after the local
quack administered a shot
using a contaminated
syringe.
Many of the villagers who went
to the quack for treatment now re
call having been given
Injections. They fear contaminated
Syringes might have been used on
them too.
The village is situated on
Baghpat-Chandinagar road and is
hardly 40 kilometers from Delhi
Chandinagar is an important base
of the Indian Air l;or< e
After Jogendra’s death on Max
’
this year, the almost sleepy vil
lage has woken up (o the danger of
AIDS. There was no knowledge of
Ithe virus until then.
j The village is home to more than
20.000 people, majority of whom
belong to the Jaat community. The
village comes under the Baghpat
constituency which is represented
by former Cabinet Minister Ajit
Singh in Parliament.
Jogendra. whose painful death
was witnessed by the villagers,
was the second son of Chaudhary
Jaipal Singh.
Since his death the villagers
have only this to talk of. Lal Singh,
a farmer in the village, said that
Jogendra died a painful death.
Jogendra was almost bed-ridden
fro seven months and did no
work.
(»nre known as an active boy he
slowly became dull and sick.
Nothing seemed to work and no
body could do anything to cure
him. Sardar Singh and Master
Stikhpal also had the sim’lar things
People suspect quack used contaminated syringe
to say. They also quizzed this re
porter about the cure of the dis
ease and the source of the infec
tion, as if trying to confirm the
truth in the village gossip.
When the reporter told them
that contaminated syringes could
transfer the infection from one
carrier to another, their faces
paled. Lal Singh, Sardar Singh,
Sukhpal and Sanjeev said that
many
villagers had been given injections
by the quacks with used
syringes.
They said that Jogendra was
suspected of carrying the AIDS
virus since last six years.
It was only confirmed in
February this year when he was
admitted to All India Institute Of
Medical Sciences (AIIMS) following
a deterioration in his health from
November 1996.
The villagers said he was treated
for various diseases by the local
quacks who are known to use
same syringes on many patients.
Jogendra. they suspect, was infect
ed during when given a shot with a
contaminated needle.
The village pradhan. Mr
Dhanpal. accused the quacks of us
ing syringes without sterilisation.
"The villagers are in a panic and
everybody is afraid of being an
AIDS carrier." he said.
However. Jogendra's father com
pletely ruled out that his son was
treated by any local doctor. But a
village doctor. Rajendra, refuted
the claim and said that in 1994 he
treated Jogendra when he suffered
from some skin allergy and gave
him two shots of penidulc with the
disposable syringes. The doctor
said: "How can we claim that local
doctors were aware of infected sy
ringes three to four years ago
when they are still in the practice
of applying same syringe on differ
ent patients without proper sterili
sation.
The name of a certain quack
practising in the village is also do
ing rounds.
He is known to be in the habit of
using syringes and other apparatus
many times over.
When quizzed, the quack said he
was properly sterilising the sy
ringes. He also said he had never
treated the deceased. Later, he re
canted and admitted to treating
Jogendra once nt his father's re
quest.
It is alarming that most of the
quacks practising in the village
have assumed the titles of
doctor.
Mr Dhanpal charged the Health
Department for the situation and
said that due to the negligence of
the health officials the MDBS doc
tor of the primary health centre
visits the village once or twice a
month.On the other hand, the
Jogendra's father claimed that his
son became infected after being
given a blood transfusion at the
Narendra Mohan Hospital followed
an accident in 1994.
Then in November 1996 his
health started failing. Then the
family consulted a doctor in
Ghaziabad where Jogendra's elder
brother is a transporter. But
Jogendra's condition did not im
prove. Someone suggested that he
should be taken to Apollo Hospital
in Delhi.
Then they contacted Mr Ajlt
Singh in Delhi, who fixed an ap
pointment with Dr Ajay Niramjan
of Apollo Hospital. Dr Ajay thor-
oughly investigated the case and
suggested the patient be removed
to AIIMS.
Jogendra was at AIIMS for 11
days before the doctors disclosed
his state. They also told his family
that he would not survive for
long.
He died on May 25 leaving be
hind two daughters and a widow.
Jogendra's father said the widow's
blood has been sent for ELISA test
and the report was awaited.
He said that he is thinking of
getting the rest of the family exam
ined too.
The villagers too are looking for
help to test their blood.
Meanwhile. Chief Medical Officer
(CMO) Dr Rajendra Prasad has or
dered a survey of the village. Dy
CMO Dr J Prasad has been given
the task of monitoring the opera
tion. The nodal officer of the AIDS
control prograni in the district. Dr
S K Srivastava. is to assist him.
i
o
/O
p
'I
THE PIONEER 3
City.
TBspreading on wings of ignorance
Rahul Gupta
New Delhi
TUBERCULOSIS IS a great leveller,
It
h torments not only people living
..... ~of
p
u Walled
'
in a maze
gullies in•the
(.ity but also those living in aircondHioned comfort in south
e 11
.
A general physician in
Balhmaran area of the Walled City
Dr lalat Aziz says, "1 get at least
five or six new cases of TB every
month. 1 here is a very high incidenee of 1 B and even higher is the
number undiagnosed cases." He
adds that these cases act as a
reservoir lor spreading the dis,
Another private practitioner in
Sitaram Bazar, Dr Chitra
/Astax ans, says that almost 35 per
emu of the patients coming to her
SUl!! r *roni 1
1 he crowded lanes of Old Delhi
harbour an astonishing number of
people. t > alls and industries.
Lanes are so nariow that shoul-
ders brush and hands collide if the walls chrry red marks of pan most of the bacteria. Still, a few
two people pass by.
and zarda. A person suffering remain in the body in dormant
Tucked away in these lanes are from TB can easily spread the dis- form. During their lifetime, when
various industries. Carpenters^ emie by his incorrigible habit of ever the resistance of these peohammering away al stubborn
spitting piOToveE*^*"*^^’’’ pie declines, the dormant bacte
nails, printing presses reeking of
The TB bacteria has extended ria multiply and cause tuberculo
paper
paper and
and ink,
ink, sewing
sewing machines
machines
its reach even to the posh locali- sis. Stress and tension, smoking,
whirring,
whirring, artisans
artisans making
making mirror
mirror ties. Secretary general of the alcoholism and even diabetes
frames
frames and
and many
many other
other mechanmechan Delhi Medical Association (DMA) overpower body resistance and
ical
*cal works.
Dr G S Grewal, who practices in the TB bacteria take over."
Factories operate in single New Friends Colony, says that hyDr Grewal says, "Because of
rooms
rooms that
thatalso
alsoserve
serve as
asaccomaccom giene is coming down even in posh
pollution and the rise in suspended
modation
modation for
forfamilies.
families.With
Withsuch
such areas. "One can find a big garbage
particulate matter (SPM), the air
overcrowding,
overcrowding, one
one can
can imagine
imagine dump right in the middle of a posh
has become heavier. As heavy air
how
how much
much air-sharing
air-sharing isis taking
taking locality. And poor hygiene is agmoves slowly, the movement of
place.
place. .And
.AndTB
TB isisan
an airborne
airbornedisdis gravated by slums on the fringes "
bacteria slows down and more TB
Fjnding a solution t0 TB is a lall bacteria are inhaled."
ease.
While trudging in the gullies one order. Fifty per cent of the people
He also observes that "we have
comes
comes across
across various
various medical
medical in India are infected by the mirelapses occurring after ten years.
practitioners.
One
"doctor"
who
practitioners. One "doctor" who crobacterium TB. Doctors say People who took incomplete treat
has
has been
been practicing
practicing in
in Ballimaran
Ballimaran that these people run a high risk ment a decade back are now re
has
has not
not received
received aa single
single TB
TB papa of succumbing to the dreaded disporting with tuberculosis." He
limit
!e betient in
in the
the last
last three
three years.
years. 1He
be ease.
adds that earlier bacteria were not
According to senior consultant as strong but now bacteria strike
lieves that TB is on the decline.
rh<*
gullies
of
old
Delhi
shelter
in
the
Department
of
Respiratory
The gullies of old Delhi shelter
fast and relapses occur faster.
quite aquite
few such
a few"doctors".
such "doctors". Medicine at Apollo Hospital Dr
Dr Chawla says that he comes
Dr Aziz
Aziz stresses
stresses that
that in
in the
the Rajesh Chawla, "The body's deDr
across nearly 50 TB patients in a
Walled City,
l.ity, the
the culprits
culprits are
are poor
poor fence mechanisms in these 50 per
Walled
week. ".Almost all of them are
hygiene
hygiene and
and paan
paan chewing.
chewinc. "/All
"All cent cases are able to overcome
from the affluent sections. Not all
are new cases, a lot of them are
referral patients."
The biggest hurdle for doctors
is that people still don't regard TB
as a curahh?JHness,..lt is consid
ered a stigma even in educated
families.
Dr Aziz says. "Initially we find
it difficult to convince people that
they are sufiering from TB, and
later on to convince them to con
tinue the treatment till its full
course."
Medicine is so effective that
symptoms of TB disappear with
in no time, which wrongly en
courages a patient to give up the
medicine.
Doctors say that education has
to be imparted on a war fooling
not only to the masses but also to
the upper classes.
The Government will have to
provide free medicine, whatever
the cost.
This also means that even MDH
medicines, though prohibitively
expensive, will have to be pro
vided.
/
X.
iiurter.
.
No couniry is srfe from threat
sss&cy
WHO^
pp»t;
igSSBS
BPS;
S-S2
-S'Stesa^;
However, he
Thailand have
cases of CJD but7ue
currence of its trai
the disease has r.oRuling out the
fever ln India, he said 7t
came to India as it r -- ’••
western Africa. nough’/as'Trha^
^Bs<may move to-
:O“'~ rs:-5 ®r>XwSs;.
levels
and ,nternalional
of ^mplacency since new
^°ni^^nu",^^S1'engese
region
™xS^S?X‘S-
?^oSn?,n^?e=SH"v “ ^^-“‘houXtoVa^ 5^00^0“^
^idh^in
3=un^--^s
sSBS?s sr"“"s»®x'
Nafrona^
•■noVh'0'08* 'ns,i,ufe »ug!
no threat to Indians”, he
^hsaYdH^“-
rSi-aara sax™sS!
Taiwanese blame China
for epidemic 0 ,3.
7
TAIPEI (Taiwan). April 20.
If truth is the first casualty of war. trust must
be the second, especially between old enemies
like mainland China and Taiwan. To prove it.
plenty of Taiwanese apparently suspect that the
epidemic of hoof-and-mouth disease now ravag
ing their pork industrv could have been an act of
economic sabotage by China.
"A lot of people here have been saying they
believe the mainland sent this disease over here
deliberately.” said Ms. Shen Yi. a radio talk
show host.
Was it just a coincidence, she asked, that the
outbreak began at about the time the Dalai La
ma visited? Beijing views the exiled spiritual
leader as a separatist promoting Tibetan inde
pendence from China, just as it accuses Tai
wan’s President. Mr. Lee Teng-hui. of promoting
Taiwan's independence.
When two adversaries have spent so much
time in the last 50 years eyeball to eyeball from
armed ramparts on cither side of the Taiwan
Strait, it is no surprise that the arrival of disaster
on Taiwan's shores has incited some dark
thoughts.
Tens of thousands of Taiwanese pig farmers
^.irc looking for someone to blame for the billions
■o^ dollars' worth of devastation caused by the
outbreak, which is leading to the greatest ani
mal slaughter on the planet since "mad cow"
disease struck Britain.
So far. more than 1.5 million of Taiwan's 14
million pigs have been destroyed, and more than
1 million more are scheduled for execution.
Some experts are guessing that half or more of
Taiwan's pig population will be wiped out by the
plague, which could take a year or two to arrest
fully. The disease is very contagious and deadly
to livestock but harmless to humans.
I’he industry, which generates S1.5 billion a
year in business, much of it for supplying Ja
pan's \oracious appetite for pork, has ground to
a halt, endangering the jobs of 1 ()().()()() workers
raising hogs and 6()().()()() in related industries.
Last year, the Japanese market bought the
meat from 6 million pigs in Taiwan, represent
ing 95 percent of the islands pork exports. But
Tokyo froze
shipments last month, and Singa
pore and'South Korea followed suit.
"It is just devastating." said Mr. Wesley Yu. a
local assemblyman in southern Taiwan's largest
city. Kaohsiung. "And the Government has
handled things poorly. But no one will lose their
job. In Taiwan culture, no one 1^ s to admit
that they made a mistake.”
Opposition legislators accuse the Government
of being unprepared and incompetent in fight
ing the viral onslaught. A month into the crisis.
Taiwan's agricultural bureaus have failed to gel
adequate supplies of vaccines to farmers, even
though vaccines are abundant in international
markets.
Some Opposition politicians say the Govern
ment’s handling of the crisis will be a factor in
crucial local elections later this year. In those
elections, candidates who forsake claims to the
mainland could seize a majority of municipal
and county offices.
Mr. Lee. worried that the blame might settle
on the shoulders of his governing Nationalist
Party, went before the television cameras last
week to munch on a feast of pig knuckles and
declare. "Eating pork is healthy and safe." Bud
his constituents weren't buying. Pork priced
have declined more than 60 percent since ihe
epidemic broke out.
4
In an unsubtle attempt to point the finger. Mr.
Ix?e said Taiwan would have to do a much belter
job stopping the smuggling of pigs from China
as if that were the only place that the contam
ination could have come from. Malaysia and the
Pb'i/ppines have also had hoof-and-mouth out
breaks of late.
Many Taiwanese, as well as some prominent
experts, apparently believe that the most likely
source of the hool-and-mouth plague was across ;
the l()()-mile Taiwan Strait. Mainland pigs arc
banned from Taiwan because China refuses to
comply with international reporting standards
on the incidence of hoof-and-mouth disease,
and rumors ol epidemics in ITijian and Zhejiang
provinces have reached here.
The mainland has been silent, except in its
offer to sell vaccines al a good profit to its bclea
guered neighbour. But the quality of mainland ;
vaccines is suspect.
It is certainly true that Taiwanese and Chi
nese smugglers have been caught plying th<
strait in the dead of night with loads of piglets
destined for the Taiwan market, where they can
bring double the price they fetch on the main
land. One of those boats could well haw landed
a Trojan pig. — New York Times
THE time;
IF INDIA, MUMBAI
Victims
demand justice
By Rakesh Bhatnagar
deavour to bring about prohibition of
NEW DELHI. In a historic agree consumption, except for medicinal
ment, the US tobacco industry has •purposes
* — of
— intoxicating drinks or
undertaken to cough up a whopping $ dnj8s which) are injurious to health.”
•>08 billion as compensation for
...............
But
the ban on sale of liquor can
treating people with smoking-related
C°nSutrued 35 8oi"g against the
diseases.
itizens right to profession, which
The industry would also concede also means right to livelihood
that tobacco is addictive, a fact which
Consumption of liquor or smokino
it was always shy of accepting.
may pose a serious threat to one’s
hie, but our laws lack teeth when it
In a belated realisation that smok Ut°emCS t0 aCtUa,ly ’dementing
ing can cause cancer and other health
problems various state governments
Therefore neither the breweries
m India have resolved to declare cer nor the cigarette industry in India can
tain public places as “no smoking ever face a situation which the US
«>nes ; many have imposed certain tobacco companies have found them
restrictions on the free sale of ciga selves in.
rettes and children below 14 have
darr,ages had been
been barred from either vending or panted m only two tobacco-related
smoking
cigarettes.
Thp ’rumCaSeS’
flrSt was the Cipollone
ne Delhi government has dede case’ wh,ch was reviewed by the US
Glared public places including railway SuPreme Court. In that case, a federal
stations,
a ,ons’ public transport, cinema W in
’n 1988 awarded $ 400 000 to
halls and restaurants
on
reTUTtS to
t0 name a few,
few’
C !1USband Of Rose Cipollone, who
out of bounds of smokers. There
sm°ked for 42 years and died of lune
at other
the age
of 58.
F
LEGAL VIEW ——j rcancer
_In lhc
case,
the jury
awarded
to -a-----man w
who
smvjkv. for
..
ho smoked
seems to be an urge for implementing 44 ycars before developing lune
canthe law but the administrations lacks ccr II
It found
found that
that tho
the cigarette ubrand
political will to do so, except a few he
okcd was
’<
he sm
smoked
was aa udefective
product
instances when ‘no-smoking’ slogans and the manufacturer
were painted and some persons were U
* not‘ informing
‘ "
by
the public about
caught “red-handed’ and fined. Else health risks of smoking.
where in the country, no one has so
These were the personal injury
tar been caught “red-handed" while cases in which adequate compcnsasmoking and made to pay a fine for ion was granted by US courts. But in
something which has been an age-old India such eases get bogged down by
habit.
procedural law and loopholes which
Any legal challenge of the ban on enable the ‘culprits’ to
escape pun
smoktng tn the Capital may not sue- ishment. Thus the first
casualty is
cced as the conns have declared on justice.
many occasions that the government
IS responsible for the upkeep of citi
Fire tragedies, road accidents in
zen s health.
volving government vehicles, ncgliOn « k k •
gC.nCe by g°vcrnrnent doctors or even
hasO^Pr?^bUl°n’ 016 COUT1’S view rGlerS’
civic authorities' negnas been that it cannot interfere with hgence which result in accidents arc
«- cgislation because it is meant to some of the cases which, despite their
better the people’s standard of living.
8ravity. invariably drag on for years
Article 47 of the Constitution cmthe delinquent is punished or
phatically states that it is the duty of ac<iuitted for lack of evidence
t e State to raise the level of nutrition
Sornc laws arc so obsolete that
n^ hC k?"^ °f ,iving and lo im- rCna,n accidenls could not have been
prove public health.
foreseen when the legislations were
I.
U
enacted.
It elaborates: “The State shall re
gard the raising of the level of nutri
However, with progressive US
tion and the standard of living of its
case laws as examples, people here
people and the improvement of pub
lic health as among its primary duties are coming to have greater expecta
tions from the judiciary in administer
‘ind, m particular, the State shall ening justice in cases of negligence. >
Nurse charged
over death of
^^^ents
London: v A British nurse has
been charged with the attempted
murder of two elderly patients
and incitement to murder anoth
er. police said Friday.
Ms Kathleen Ann Atkinson,
47. of Wallsend, Tyne and Wear,
in the northeast of England, was
dismi ssed from her job as a nurs
ing sister in the intensive care
unit at Newcastle’s Royal Victo
ria Infirmary in March 1996 over
allegations that life-supporting
drugs to critically-ill patients
were withheld.
On Tuesday, after a year-long
police inquiry, she was arrested
and questioned over a number of
deaths at the hospital, and Friday
she was charged with the
attempted murders of Mary Burdon. 69, in February 1991 and
Miriam Egen. 60, in February
1992. and incitement to murder
of Thomas James Luke, 77. in
December 1995.
A police spokeswoman said a
file of evidence on other matters
was being prepared for submis
sion to the state prosecutor’s >4
! office. (AFP)
I
r
7
iil>^
5 die of food
poisoning
„
<HTC)
11 kn>
nn^f
M has b^n
Tple of 'h'
lamination. HowTv?/ <jj'e,nical I
has been registered
J
Russia sitting on Alps bomb
Rise in intravenous drug use Ohos/sfxlal habits lead
Russians to a medical catastrophe, reports Fred Weir
O USSIA is facing an epidemic
-1'Vof sexually-transmitted dis
eases, particularly the deadly ac
quired immuno-deficiency svndrome (AIDS). The crumbling
medical services and public educa
tion system are totally unprepared
tor this experts warn.
spread. These things are driving a
guaranteed opportunities and job
catastrophic upsurge in AIDS and
security for women.”
other diseases,” he says.
They also warn that the postDue to the breakdown of the
Soviet social environment has fuel
Russian health system and the so
led an upsurge in popular cynic
cial stigma that still goes with re
ism. with accompanying patterns
porting a sexually-transmitted dis
of sexual promiscuity and devilease, experts believe the numbers
may-care attitude to the consequ
of registered HIV cases reflect as
ences.
“We are observing an exponen
little as a tenth of the actual num
tial increase in people infected
The obvious causes that have led
bers of infected people.
MTk r|hKT ^Ir)S virus’” says
to this drastic rise in sexually“
If
the
present
rate
of
increase
Mikhail Narkevich, head of the
transmitted diseases is the fact that
continues, we can expect 800,000
Russian Health Ministry’s AIDS
sex and pornography are widely
to a million HIV-infected Russians
unit. “In the first five months of
advertised by the mass media,”
by the end of this decade,” says Mr
this year, the number doubled. We
argues a recent article in Russia’s
Narkevich.
“
That
in
itself
isa
huge
expect it to double again over the
mam medical journal, ‘Meditsinsmedical catastrophe, for which we
summer.’’
ky Kourier’. “One of the consequ
are utterly unprepared.”
ences of the propaganda of sexual
The USSR’s first case of infecThe incidence of syphilis has in
emancipation is the increasing
creased by a staggering 40 times
number of pregnancies among
Iqo? *,DS> was registered in
since 1989. Syphilis infection now
teen-agers. As many as 95 per cent
SnvL iS!X yCarS ago’ when the
stands at 177 per 100,000 people —
of the pregnant women of the age
et ,U",on elapsed, the couna rate that is more than 50 times
from 18 to 20 have no permanent
tpHiad fewer than ten HIV car
higher than most European coun
jobs, 70 per cent are not married,
riers.
tries. Gonorrhea, trichomoniasis
and 50 per cent have sex with
and chlamydia infections have
chance partners."
Russia currently has 4,200 offishown
similar
patterns
of
explo
-rCialiy registered cases of HIV inOver the past two years, howev
sive growth.
! Action and 290 people with the
er, intravenous drug abuse has ex
“We have noticed a direct link
full-blown AIDS condition.
ploded in Russia and. with shared
between syphilis and HIV infec
syringes, AIDS transmission has
tion,
”
says
Mr
Narkevich.
These numbers are small bv
gone through the roof.
Public education about the
comparison with many other coun
At the end of 1995 there were
health risks of unprotected sex is
Ines, but experts say that’s onlv
only 3 cases of HIV-positive drug
virtually non-existent Russia’s
because Russia had a late start on
addicts, says Mr Narkevich. A
first attempt to introduce sex
the epidemic.
year later there were almost 800.
education classes for teenagers be
Health officials say that 70 per cent
‘The Soviet Union was a closed
gan only last year, with a modest
of new cases are now found among
society and that to some extent
pilot project in a handful of
drug addicts.
insulted us from the epidemic that
schools.
Russia’s estimated 600,000 in
was sweeping the world,” says Mr
Until 1995 about 80 per cent of
travenous drug abusers are the
Narkevich.
all new HIV cases in Russia were
pipeline bringing the AIDS
traced to sexual transmission. Ex
epidemic in full force to Russia. At
“But now intravenous drug use
perts point to the dramatic rise in
the same time deteriorating public >
is sharply on the rise, and loose
prostitution since the end of the
health institutions are less abl&<
sexu^ habits are more widecommunist welfare system, with its
than ever to cope.
r
X'a^
i
i
19 die in Malaysia virus menace
Kuala Lumpur: The death toll frofiPnew vfillWn in Malavsia\
asswar*h"
Sarawak state director of medical and health senices department
mnrpamfied Taha AnJ WaS cluoted bV the papers as saying dial two
sa?d 29^ H SUCCUmbed to ,he Coxsackie B virus on Thulsdav He
*aid 29 children were m an isolation ward at the general hosni'tal in
FnrlnHp f°aSla l°Wn ,n_Sarawak stale officials have said Svmptoms
include fever, nervous fits, paralysis and finally heart failure.'X™)
f
'Di-S
OU7
.1
COMM^ity health
!
CELL
SEA/EPI/79
fiangalore-56QQ3z
India
CONTENTS
Page
1.
INTRCWCTION
1
1.1
Role of Outbreak Investigations
1-?
Use of Data Collected During Outbreak Investigations
1
1
2
2.
EPI TARGET DISEASES
2
2.1
2.2
2.3
Epidemiological Features
Criteria for Diagnosis
Verification the Diagnosis
2
2
2
3.
PROCESS OF OUTBREAK INVEST I GAT I (MS
3
3.1
3.2
3.3
Identification of the Existence of a Possible (Xitbreak
Criteria for the Number of Cases That Constitutes an Outbreak
Criteria for Investigating an Outbreak
3
5
6
4.
FIELD INVEST I GAT I (MS AND ANALYSIS OF REPORTS
6
4.1
4.2
4.3
4.4
4.5
4.6
Case-Finding Through Active Surveillance
Line-Listing, Defining and Counting of Cases
Descriptive Epidemiology
Determination of Immunization Coverage in the Community
Determining Who is at Risk of Disease
Follow-up Visits
6
10
10
12
12
5.
CONTROL MEASURES
12
6.
WRITE UP AND REPORT RESULTS
14
1.2 Diseases Covered by The Field Guide
6.1 General Information
6.2 Background Information
6.3 Details of Investigation
6.4 Descriptive Epidemiology
6.5 Description of Control Measures Taken
6.6 Description of Measures for Follow-up Visits
6.7 Problems Encountered
6.8 Factors Contributing to the Outbreak
6.9 Estimates of Vaccine Efficacy
6.10 Conclusions and Reconmendations
6.11 Reporting Procedure
6.12 Dealing with the Public and the Media
14
14
15
15
15
16
16
16
16
16
17
17
SEA/EPI/79
Page ii
7.
PLAN PREX'ENTIVE MEASURES
17
8.
INVESTIGATION OF ADVERSE EVENTS
18
8.1
8.2
8.3
8.4
8.5
Adverse Events Following Vaccination
Measures to Minimize Risk
Field Investigations and Analysis of Reports
Write-up and Report Results
Reporting Procedure and Dealing With the Public and the Media
18
19
19
20
22
9.
ACKNOWLEDGEMENT
22
10.
REFERENCES
22
ANNEXES
1.
Epidemiclerical features of vaccine preventable diseases
23
2.
Case definition of vaccine preventable diseases
24
3.
Laboratory investigations of vaccine preventable diseases
27
4.
List of cases
28
5.
Investigation of neonatal deaths
29
6.
Clinical observations of lame children
30
7.
List of cases with adverse reactions
31
8.
Calculation of vaccine efficacy
32
COMMUNITY HEALTH CELL
32b, V Main, I Block
Koramongala
Bangalore-560034
India
SEA/EPI/79
1.
INTRODUCTION
1.1
Role of Outbreak Investigations
The primary purpose of an outbreak investigation is to control the
outbreak, limit its spread to other areas and assess how prevention
strategies could be further strengthened to reduce or eliminate the risk of
such outbreaks in the future. Control measures are most effective when
selective interventions are applied early to provide maximum impact with
minimum diversion of scarce resources required for achieving and sustaining
high inmunization coverage levels.
This field guide is designed to help the immunization programme
managers at district and PHC levels in making decisions regarding field
investigations, specific interventions and follow-up measures. The general
approaches and recommendations of the field guide may need to be adapted to
specific situations, geographical locations, immunization coverage levels
and resources available. The maximum benefit from these guidelines can be
derived if:
the field guide is studied thoroughly and clarifications, if
any, are sought before circumstances compel its use.
an inventory is made of the facilities available before an
outbreak actually occurs, such as manpower and vehicular
resources; names of experts who could be requested to
assist; referral treatment centres and laboratory facilities
and source of transport media
(in situations where
laboratory facilities are available for confirmation of the
diagnosis).
a list of indications for outbreak investigations is
established. Some indications are suggested in this field
guide and may be conmon to all areas. In places with high
inmunization coverage levels, programme managers may wish to
include additional items, including the criterion that even
a single case may be considered an outbreak.
1.2
Diseases Covered by This Field Guide
This field guide covers the vaccine preventable diseases included under
the Expanded Programme on Inmunization (EPI)\ viz., diphtheria, pertussis,
tetanus, poliomyelitis, measles and childhood tuberculosis. An attempt has
been made to prepare a common methodology and format for the investigation
of these diseases to simplify its use.
Tetanus differs from other diseases because it is not transmitted
person to person. The level of neonatal tetanus cases tends to remain
relatively constant in areas with a low quality of obstetric care and
without adequate immunization. An investigation should be conducted,
however, if there are increases in the number of cases which cannot be
attributed to improved surveillance.
SEA/EPI/79
Page 2
A section on serious adverse events following vaccination is included
so that prompt investigation of these events can also be undertaken. A
report of even a single case of severe adverse event following vaccination
is an indication for investigation.
1.3
Use of Data Collected During Outbreak Investigation
Data collected during outbreak investigations can serve many important
functions, including better understanding of the epidemiological features of
the disease; estimation of vaccine efficacy in field use; surveillance
system weaknesses and identification of high-risk areas and age-groups.
Outbreak investigation data, such as other forms of surveillance data, are
information for action. The results of outbreak investigations should lead
to action in improving and sustaining immunization services.
2.
EPI TARGET DISEASES
2.1
Epidemiological Features
It is necessary to know the epidemiological features of the diseases to
effectively investigate and control outbreaks. For easy reference, the
major items have been simmarized in tabular form (Annex 1).
2.2
Criteria for Diagnosis
The criteria used for diagnosis (case definitions) is important. A
suggested set of standard case definitions is shown in Annex 2. The case
definitions include only major signs and symptoms of typical cases.
First reports of outbreaks may often come from the general public or
recognition of
of the
peripheral1 health workers. It is expected that the recognition
diseases by these health workers or members of the conounity will be based
lisloxy, which, in some of the vaccine preventable diseases,
primarily on history
can be typical.. The
_ diagnosis should be confirmed by a medical officer based
on history and clinical investigations. Laboratory confirmation of the
diagnosis would be needed only under special circtmstances and suggested
tests have also been included in the table of case definitions.
2.3
Verification of the Diagnosis
The first principle of outbreak investigation is to confirm the
diagnosis of as many reported cases as possible. Much time and effort may be
wasted due to misdiagnosis.
(1)
Clinical diagnosis
The reported cases should be investigated by a medical officer to
confirm the diagnosis. The majority of the cases should fall within the case
definitions given in Annex 2. In situations of doubt about whether an
illness meets the case definition, a second opinion may be sought.
*
SEA/EPI/79
Page 3
(2)
Laboratory confirmation
Laboratory confirmation of clinically-diagnosed cases is usually not
essential. Laboratory tests for diphtheria, and tuberculosis meningitis may,
however, be helpful if such facilities exist.
Although laboratory tests are not required for confirmation of the
diagnosis of paralytic poliomyelitis, such tests are necessary for
classification of the type of polio virus.
Laboratory tests may be useful for the detection of carriers and
infected asymptomatic persons and, in the post-epidemic period, may help
assess the extent of silent infection resulting in immunity. Although such
studies may provide useful epidemiological data, they are not directly
relevant to outbreak control.
The details regarding the types of tests,
transportation procedures are shown in Annex 3.
3.
PROCESS OF OUTBREAK INVESTIGATION
3.1
Identification of the Existence of
a Possible Outbreak
sample
collection
and
Outbreaks of vaccine preventable diseases usually occur in areas with
low immunization coverage. When large outbreaks are reported from areas with
high immunization coverage, it is important to reliably verify these
reported coverage levels through such methods as careful review of records
of immunization performance over the previous few years and vaccination
coverage evaluation surveys, Outbreaks in highly immunized conmunities are
usually localized to certain population sub-groups or places which did not
receive adequate immunization coverage.
An outbreak or epidemic is defined as the occurrence in a community of
cases; of an illness clearly in excess of expected numbers. Increases in the
total number of cases do not, however, necessarily indicate increase in the
incidence of diseases. Variation in the number of reporting sites,
completeness of reporting, geographical size of the catchment area and size
of the population are factors that must be taken into consideration while
analysing reports.
Outbreaks can sometimes be forecast in areas with reliable surveillance
systems. Many infectious diseases have cyclic patterns and outbreaks are
observed after regular intervals of one, two or more years depending on the
di se&se and imrmmi z-ation coverage levels in the conmunity. Cyclic peaks of
measles and poliomyelitis, for example, have been observed every second or
third year in many states of India. Graphs on the incidence rates of
measles and poliomyelitis (Figures 1 and 2) illustrate this point. If
similar graphs are plotted for each district, preventive measures can be
taken in advance and the treatment centres can be alerted to provide an
early warning should an outbreak occur. Intervals between epidemic peaks may
increase and the magnitude of the peaks fall as immunization coverage levels
increase.
SEA/EPI/79
Page 4
FIGURE 1. Incidence of Beasles, India 9 1975-1987
320
300 -
288
269
280 z
o
I
260 -
261
257
24
240^
1
220 -1
'9
/
D
L
200 -
O
O
180 -
□
160 -
o
o
□
140 -
ir
120 -
a
100 -
in
id
in
4
O
80 -
Av
2?0
J
K
185
I
1985
1986
1987
I
1986
1987
Id
60 40 -
20 -
0
jI~
1975
1976
—I—
1977
I
1978
I
1979
Ii
1980
I
1981
I
1982
I
1983
I
1984
i
Year
FIGURE 2. Incidence rate of polio in a State, 1975-1987
6
5 -
z
o
H
5□
4 “I
D.
3.5
0
a
O
o
o
o
o
K
UJ
Q-
3 -
2 -
V)
Id
</i
<
o
1
0
I
1975
1976
I
1977
—I—
1978
I
1979
I
1980
I
1981
Year
I
1982
I
1983
I
1964
I
1985
SEA/EPI/79
Page 5
Sentinel centres, institutions that promptly and reliably report all
cases of disease under surveillance, may be particularly useful for
forecasting and early warning of outbreaks.
All health workers must be aware of the major signs and symptoms of the
vaccine preventable diseases,, They should be encouraged to report these
officer of the concerned PHC. Any unusual increase must
casesj to
i— the
— medical
—
be notified inroediately. Such information should also be reported
immed lately by the medical officer to the concerned district officer,
Reports of outbreaks can also be received from members of the community.
Incidence of diseases should be an agenda item in the monthly meetings
at PHC and district levels so that any unusual reports can be identified and
discussed. Even relatively small increases in the incidence of diseases seen
in individual PHCs may indicate serious problems in the district as a whole
if such increases are noted in several of the PHCs. Moreover, neighbouring
PHCs can be alerted to the possibility of potential outbreaks in their
catchment areas and they can take preventive measures.
It is obvious that sensitivity, reliability and timeliness of the
source of reports and alertness of the local staff are very important. In
areas with poor surveillance systems, outbreaks are sometimes identified
only towards the end when preventive measures are least effective.
3.2
Criteria for the Number of Cases That Constitute an Outbreak
The number of cases which are needed to be called an outbreak varies
according to several factors. It depends on past historical patterns of the
disease, virulence of the disease (toxigenic strains of C.diphtheriae, for
example) and iinnunization status in the community. In places with
established epidemic cycles, it may be worthwhile to initiate necessary
preventive measures and alert treatment centres in the area in anticipation
of an outbreak.
'
'
States and districts should establish
criteria
oni the number of cases
local-----situations. These criteria
that constitute an epidemic based on 1their
--- ----could include:
a 25 per cent increase in the number of cases reported as
compared to the corresponding period (month or quarter) of
the previous year. This may not, however, be sufficiently
sensitive in the year that follows an outbreak;
a 25 per cent increase in the number of cases reported as
compared to the average number of cases over the last four
non-epidemic years for the corresponding period;
five or more cases or a single death reported by a health
worker from his area in a month or 2 or more cases in a
week;
a single case in an area which has had no case during the
previous 12-month period, and
a single oaRP in an area with reported inmunization coverage
levels of 80 per cent or higher.
SEA/EPI/79
Page 6
The reporting centres and medical officers in the OPDs should be
encouraged to report any unusual increase in the nunber of cases without
waiting for the submission of their routine monthly report. Si mi larly, while
the current nvmber of cases should be compared with the previous month or
quarter, if the number exceeds the criteria for an outbreak, it is not
necessary to wait for the completion of the monthly or quarterly period to
declare an outbreak. This is important in avoiding any delay in starting
control measures.
3.3
Criteria for Investigating an Outbreak
After an outbreak has been confirmed, a decision must be made as to the
amount of resources (manpower, time, monies etc.) that should be conmitted
to investigating it, or even if it should be formally investigated at all.
If it is known, for example, that immunization coverage levels in the
comnunity are low, then outbreaks should be expected to occur. If resources
are limited, it may be counter-productive to the routine immunization
service that is trying to improve coverage if all activities are stopped to
focus only on the outbreak.
The decision whether or not to investigate and the depth of
investigation must be made at the level where the outbreak occurs.
occurs. The
decision should be based on factors that include immunization coverage in
the conmunity (whether or not an epidemic could be expected to occur);
severity of the disease; effectiveness of control interventions; duration of
the epidemic to the time it has been recognized, importance of investigating
vaccine efficacy and better understanding of the epidemiology of the
disease, etc.
It is the responsibility of the local medical officer to arrange for
the treatment and follow-up of cases and contacts. It should be noted that
during an outbreak a higher percentage of more severe forms may also occur.
4.
FIELD INVESTIGATIONS AND ANALYSIS OF REPORTS
4.1
Case-Finding Through Active Surveillance
After establishing the existence of an outbreak and verifying the
diagnosis, it becomes important to accurately define and count the cases.
During the period of the outbreak, all the cases of the disease under
consideration occurring in that area should be identified and listed.
Active surveillance is necessary to obtain more accurate and complete
information. Active surveillance refers to actively seeking out cases. This
may include visits or telephone calls to all the medical facilities or
private practitioners that might expect to admit or attend cases of the
disease. Depending on the disease and the resources available to investigate
the outbreak, it may even be desirable to conduct house-to-house visits
(especially in the homes of contacts of cases) to find cases. In some
circumstances, comnunity assistance may be enlisted for house-to-house
visits.
SEA/EPI/79
Page 7
Active surveillance also provides a means for standardizing and
increasing the amount of information about each case. In this way it may be
possible to develop a more complete line-listing, including data on
iumunization status, residence, age, symptomatology, etc. This supplementary
information is especially helpful in outbreak investigations to assess
vaccine efficacy, determine complication rates, and further understand the
epidemiology of the disease.
Active surveillance, once initiated, should be maintained until the
outbreak is over. Developing a regular schedule of daily or weekly
(depending on the urgency of the situation) visits or telephone calls to
concerned institutions or individuals will help maintain the flow of
surveillance information to those analysing the outbreak and directing
control activities.
4.2
Line-Listing, Defining and Counting of Cases
It is important that information from surveillance be recorded in a
standardized manner. Persons who are ill and meet the case definition for
the outbreak disease should be entered onto what is called a ’’line-listing".
This is a list of all cases with the relevant data on each case which
provides the basis for counting of cases. It is the data-base on which the
descriptive epidemiology of the outbreak can be made and it can serve as the
basis for other, more sophisticated, analytical epidemiological studies,
such as risk-factor analysis, vaccine efficacy, etc.
The line list suggested for field use is shown in Annex 4. Summary
tables have been included (Tables 1-5) to facilitate analysis of data. Forms
for investigating individual cases of poliomyelitis and neonatal tetanus are
given in Annexes 5 and 6.
TABLE 1. Weekly distribution of cases and deaths
Week ending
Total
Number of cases
Ntmber of deaths
SEA/EPI/79
Page 8
TABLE 2. Determining high-risk age-groups
Age-group
Female
Total
Male
%
% No.
No.
% No.
Population in Attack rate
the age-group per 1 000
0-11 months
12-23 months
24-59 months
5 -9 years
10-14 years
15+ years
Total
TABLE 3. Inmunization status of the cases, by age
Age-group
0 dose
No. %
C-ll months
12-23 months
23-59 months
5+ years
Total
Immunization coverage
NK
2 doses 3 doses > 3 doses
1 dose
No.
%
% No. %
No. % No. % No.
Total
No.
%
SEA/EPI/79
Page 9
TAPI J? 4. Complications within six weeks of measles
Complaint
Mild
Nisher of cases
Moderate
Severe
Died
Total
Diarrhoea
URI
Pneumonia
Conjunctivitis
CNS complications
Others (Specify)
TABLE 5. Reported vaccination coverage
Year
Population
Estimated
infants
____ Vaccination performance
0 dose 1 doses 2 doses 3 doses 3+/B
Percentage coverage - lt2 or 3 doses (as appropriate) x 100
Estimated number of infants
Percent
coverage*
SEA/EPI/79
Page 10
4.3
Descriptive Epidemiology
In investigating an outbreak, it is necessary to develop a detailed
description in terms of time, place and person, as follows:
(1)
Cases by time
The onset of illness of the cases should be graphed by days, weeks or
months, as appropriate (example in Figure 3). This type of graph is commonly
referred to as an epidemic curve. The epidemic curve can 1be ’helpful
\
’ in
identifying the index (first) case or cases, generation of disease (peaks of
disease separately by troughs during incubation period), and may even
suggest patterns or modes of transmission.
It is also useful to present previous year’s information or possibly an
average of several previous years for comparison on a line graph. Such
graphs help to demonstrate the magnitude of the outbreak compared to the
previous reported incidence, how rapidly the disease is spreading and if
control efforts are succeeding.
(2)
Cases by place
A map of the area or even a rough sketch can be drawn showing where
each reported case resides to indicate geographical distribution of cases
(example in Figure 4). In some situations, serial spot maps, by week or by
month (or by disease generation) may provide insight into the pattern of the
spread of the disease over time.
Cases tend to cluster and it may also be useful to mark affected
schools or other institutions on the map in addition to residential locations. Such mappings may assist in identifying the sources of infection.
(3)
Cases by person
Cases should be described in terms of age, sex, vaccination history and
other relevant data. It is usually sufficient to group cases by age-groups
like 0-11 months, 12-23 months, 24-59 months, 5-9 years, 10-14 years and 15
years and above. Sex differentiation may also be helpful.
Immunization status is an important descriptive as well as analytical
parameter. The immunization status of each case must be carefully
investigated to ascertain the number of doses of the vaccine received by the
patient. Immunization cards or ininunization registers should be checked to
verify the immunization status. Verbal history should be used only if such
records cannot be obtained. Ideally, the place of immunization should also
be examined for quality of the cold chain.
4.4
Determination of Immunization Coverage in the Community
The immunization status in the cotnnunity can be assessed through
records
available at the PHC.
Percentage
immunization performance
estimated
by
dividing
the
total
number
of doses
immunization coverage is
third
doses
(OPV
and
DPT)
of
the
vaccine
administered
(measles and BCG) or
• ’ s total population of that age-group in the
to a specific age-group by the
village. The data may be stiunarized as in Table 5.
SEA/EPI/79
PMe 11
FIGURE 3. Polio epidemic in a district, July 1986
20 -■
19 18 17 16 -
to
u
to
<
o
o
it
kJ
m
2
□
z
15 14 13 -
14
12 11 10 9 8 7 -
7
6
6 5 4 3 2 1 - 0
0 -*■
T
1
4
3
3
3
1
2
0
T
3
0
o
T
4
5
6
8
7
9
10
Day
FIGURE 4. Example of spot map
11
12
13
0
T"
14
0
15
SEA/EPI/79
Page 12
The age-groups vaccinated should be carefully assessed as inclusion of
older children may give a false sense of higher coverage. The imunization
activities, including periodicity of the inmunization sessions, quantities
of vaccines received and cold chain system, should be reviewed.
Information on immunization coverage may also be available through past
vaccination coverage evaluation surveys. If no such coverage evaluation
surveys have been performed recently, if estimates of inmunization coverage
by reports of doses administered are unavailable or suspect, or if a large
number of vaccinations are given by the private sector and are not reported,
then it may be useful to conduct a coverage evaluation survey as a part of
the outbreak investigation which may also be used to facilitate estimation
of vaccine efficacy.
4.5
Determining Who is at Risk of Disease
The descriptive epidemiology will help to define the population groups
at high risk of disease in terms of age-groups, geographical location,
activity (school, mela, etc.), and imnunization status.
It is more iappropriate to determine attack rates rather than absolute
numbers because rates take into account variation in the population size of
different age-groups. Such rates are generally computed by dividing the
number of cases by the population size for the same age-group.
Example:
There are 45 cases of poliomyelitis among 11 000 children less
than 5 years of age in the affected town.
Attack rate =
4.6
= 0.004 or 4 cases per 1 000 population less
45
than 5 years of age
11000
Follow-up Visits
It is important that arrangements are made for follow-up visits so that
late cases are not missed. Some
I--- of
_ the
— diseases, especially measles, can
in
children.
lead to secondary infections
children, Prompt treatment of these
secondary infections in such children can save many lives. Post-measles
complications, most commonly diarrhoea and pneumonia,, can occur at any time
up to six weeks after the onset of the illness. However, since these
diseases can also occur in chi1drpn without measles, records of the diseases
in children following measles and without measles should be maintained
separately.
5.
CONTROL MEASURES
A sensitive surveillance system, prompt investigation and pre-defined
control strategies are helpful in the successful control of the spread of
the outbreak, limiting the total number of cases and providing proper
medical attention to those already affected. Such measures are most
effective when started as soon as possible.
SEVEPI/79
Page 13
For most of the vaccine preventable diseases, imnunization of the
susceptibles is the first priority. While close contacts of cases should not
be excluded from ininunization, they are likely to have already experienced
their highest risk of acquiring the infection. For neonatal tetanus,
although immunization of pregnant women will control the disease, it is
important that delivery practices in the area are reviewed and necessary
corrective steps taken to reduce the risk of tetanus immediately. For
tuberculosis, chemotherapy is a major feature of control measures.
An appropriate cut-off age for vaccination is determined from the
public health and epidemiological perspective based upon case analysis and
ininunization coverage data. Immunization should be directed to achieve
the maximum impact in the most susceptible age-group. There are several ways
to determine this cut-off age. One possible method is to direct all
ininunization activities to the age-group that contains 85 per cent of all
cases, and to allow immunization, on demand, to older age-groups that
contain between 85 to 95 per cent of the cumulative total cases.
Inmunizations provided to the age-groups containing the remaining 5 per cent
of total cases are not of epidemiological importance for containing the
outbreak, and may actually divert scarce resources and manpower away from
the high-risk groups.
At the initial stages of an outbreak, before precise data are known
about the age distribution of cases, the cut-off age may be determined from
data f rom the non-epidemic years or from a previous epidemic of the
disease.
A dose of vaccine should be provided to all children who have not
completed a full ininunization series even if less than four weeks have
elapsed since the last dose of a multiple dose vaccine. If the dose given
during the outbreak was at an interval of less than four weeks for the
multiple dose vaccines, then it should not be counted as one of the primary
series of three doses. Such children should be advised to return to complete
the course.
Records should be kept of immunization administered during an outbreak.
Ideally, these records can be the same immunization registers used for the
routine programme. If this is not possible, relevant data may be entered in
the registers subsequently. Ideally, the immunization data should also be
recorded on the immunization card of the child.
The affected areas and villages/wards in the immediate neighbourhood
should be covered. Contacts should be traced if they have moved outside the
affected area and such village(s)/ward(s) should also be covered.
All control measures should help to strengthen the existing
ininunization delivery system. Outbreak ’’campaigns" of immunization, moving
from
from one
one area
area of low coverage to another and leaving no sustainable routine
ininunization delivery system in place is disruptive and will simply lead to
other outbreaks in the future when sufficient number of susceptibles
accumulate.
Elective surgical procedures and injections, including immunization,
should be discontinued during an toutbreak of poliomyelitis to avoid the
possibility of surgical or injection-associated paralysis. It is important
SEA/EPI/79
Page 14
that such postponement is done only during the period of an epidemic.
Inmunizations should continue in areas of endemic poliomyelitis, even during
the seasonal peak, so that the routine services designed to reduce other
vaccine preventable disease incidence will not be compromised. It should be
recognized that the risk of injection-induced poliomyelitis is insignificant
if children are irmunized at the earliest recommended age-group while still
under the protection of maternally-acquired antibodies. The risk is further
reduced as coverage levels in the community increase.
Appropriate treatment of patients and contacts should be started. Such
treatment may be life-saving and should not be delayed pending laboratory
confirmation of the diagnosis. This will also serve to reduce transmission
while the outbreak is investigated. The treatment procedures are available
in standard medical texts and should be undertaken ideally in consultation
with a peadiatrician.
While there is no
no specific treatment for poliomyelitis and measles,
proper medical attention can, however, reduce complications and early
treatment of secondary infections can be life-saving. All patients with
fever should be advised to take adequate amounts of fluids to avoid
dehydration. A normal diet should be encouraged.
Isolation of patients is difficult and rarely effective. However,
potentially susceptible visitors should be discouraged from entering the
household of a patient during the period of comnunicability.
6.
WRITE-UP AND REPORT RESULTS
The following is a suggested format for writing up the results of an
outbreak investigation:
6.1
General Information
State
District
Town/PHC
Ward/Village
Population
6.2
Background Information
Person reporting the outbreak
Date of report
Date investigations started
Person(s) investigating the outbreak
SEA/BPI/79
Page 15
6.3
Details of Investigation
Describe how
how the
Describe
the cases were found (may include: (a) house-to-house
searches in the affected area; (b) visiting blocks adjacent to the affected
households; (c) <conducting
------- - record reviews at local hospitals; (d) request
ing health workers to report similar cases in their areas, etc.):
6.4
Descriptive Epidemiology
Cases by time, place and person (attach summary tables and
relevant graphs and maps).
Age-specific attack rates, mortality rates and complication
rates.
Immunization status of
levels in the community.
cases
and
immunization
coverage
High-risk age-groups and geographical areas.
6.5
Description of Control Measures Taken
Depending
applicable:
on
the
disease,
all
or
some
of
the
following
may
No. of households visited:
No. of children examined:
No. of cases treated:
.
of
contacts of cases treated (if applicable):
No.
------No. of children hospitalized: ---- ------------No. of children vaccinated during the outbreak
(see Table 6 below):
—
TABLE 6. Vaccination of children, by age
Age-group
0-11 months
12-23 months
24-59 months
5+ years
No. of children vaccinated (by prior status!
0 dose
1 dose
2 doses
3 doses
NK—
Population
in age-group
be
SEA/EPI/79
Page 16
6.6
Description of Measures for Follow-up Visits:
6.7
Brief Description of Problems Encountered
(During Outbreak Investigations and Control):
6.8
Factors Which, in Your Opinion, Contributed to the
Outbreak (may include: low unnunization coverage;
cyclic recurrence; local festival; common
nursery/school; etc.):
6.9
Estimates of Vaccine Efficacy:
6.10 Cone 1 usions and Recommendations
For future outbreak investigations and control:
For improvement in inmunization services to minimize
recurrence of outbreaks:
Date
(Namd and Designation)
SEA/EPI/79
Page 17
6.11 Reporting Procedure
Infomation on the existence of an outbreak should be reported
inmediately7 to the next higher level (by courier or by telephone and
Such action is necessary to keep the authorities
telegram, if
i. available).
—
so
that
they
are
able to provide timely assistance and alert
informed
others, if necessary.
Information
Information on
on the outbreak should also be provided to the other nearby
health units to alert them of possible increase in ntmbers of cases in their
areas.
Copies
Copies of
of the
the investigation report should be sent inmediately and
directly to the concerned district, state and central officers.
Feedback should be provided to the community leaders in the area
regarding the outcome of the outbreak investigation and preventive action
planned for the future.
6.12 Dealing With the Public and the Media
Reports of outbreaks often appear in the newspapers and can create
panic. It is, therefore, advisable that accurate information is provided m
a timely manner to the news media regarding the numbers of persons affected
and the control measures undertaken. The press and other news media can be
of great assistance in informing the public of the services available and
where they can receive them. The government procedures for dealing with the
press should be followed and necessary information provided through a
nominated government spokesperson.
7.
PLAN PREVENTIVE MEASURES
--- 1 that outbreaks do not recur
Long-term measures are necessary to ensure
future.
The
epidemiological
data
collected
during investigations
in the future. The epidemiological data
operations
,
utilized
for
streamlining
operations,
directing programme
should be utilized for streamlining
and
determining
future
strategies
for
improving
immunization
activities and determining future strategies
in high-risk age-groups and geographical areas.
coverage in
to ensure high quality of
Regular
Regular field monitoring is essential
false
sense of security and be
services. The worst situation is to develop a
that
should
be checked regularly
caught unawares. Some of the parameters t-include the following:
_
Uniformity of high coverage levels. Pockets of unvaccinated
children and pregnant women should be identified since
outbreaks are likely to occur in such areas.
Adequacy of cold chain. Breaks in cold chain can result in
reduced potency of vaccine and low vaccine efficacy.
Estimates of vaccine efficacy, use of cold chain monitors
and testing potency of field samples of OPV may be useful in
monitoring the quality of the cold chain.
SEA/EPI/79
Page 18
AdpfniRny of sterilization procedures. Improper sterilization
can result in ’"outbreaks"
’outbreaks of adverse reactions
techniques can
.
abscesses)
and,
if
injection
equipment is not allowed
(e.g. ------also
of reduced
— a
- source
sufficient time to cool, may i--- be
vaccine potency.
______of~ immunizations,
‘
, If doses of
Proper recording and reporting
vaccine given on demand to children over 12 months of age
are recorded and reported as given to children under 12
months of age, an inaccurately high estimate of vaccination
coverage levels in infants may lead to a false sense of
security.
Routine use of vaccination coverage evaluation surveys.
Such surveys will provide a better estimate of true
inmunization coverage and will also indicate the source of
vaccines and reasons for failure to fully inmunize which may
help direct programme operations to improve coverage.
Completeness of the disease surveillance systgm. Most
routine surveillance systems need strengthening and the use
of sentinel surveillance during the period of strenghthening
of the routine system may be useful in ascertaining disease
trends.
Data obtained from monitoring these indicators should be actively used
in the planning process to improve immunization coverage.
8.
TKVESTIGATION OF ADVERSE EVENTS
8.1
Adverse Events Following \accination
The adverse events that follow vaccination may be coniDon or rare
2. Such reactions are known and are
reactions to the vaccines administered.
instances, convulsions or collapse after DPT
v^SmtLnVy^ur^UnX such^DDumstances, subsequent needed doses of
dS
aX replaced with a dose of DT. It is im^rtant to understand, however,
compared to the morbidity
that the risk of these adverse reactions is
t_ small
-and mortality due to the vaccine preventable diseases.
Severe complications and even death may result if the guidelines .or
the handling and administration of vaccines are not followed. The m^st
is the formation of abscesses following the use of
i^dequately sterilized syringes and needles. Abscesses require Pad
attention from health workers since, in some instances, such abscesses can
le2 to death in the absence of adequate medical care. Abscesses are also
an 'indicator’ of poor programme implementation and follow-up measures are
^ces^y to ensurTtha? these do not continue to occur. Such events are
totally avoidable.
onset of severe diarrhoea, vomiting and fever within a few hours
of melSL vaccine administration has been reported. 'Hie case-fatality rate
inrirWq was high with death occurring within 24 to 48 hours alter
tae o^et of symptoms. Although the precise cause of the symptoms and deaths
SEA/EPI/79
Page 19
has not been identified, the roost likely reason appears to be contamination
and then reuse of the vial of measles vaccine.
i age when infections
Vaccines are usually administered to children at an
have
only a temporal
may h
are common. Some of the adverse events 'reported
cause
of
the
adverse
event being
relationship to vaccination, the primary
administration.
Investigations
are
necessary
to
unrelated to vaccine 2—-----------’
‘
.
It
is
important
that
children
of
the
same
establish the causal relationship,
age-group in the area 1who
—did
-- -not receive vaccines are also examined.
to have a standing
The state health authorities may be advised
microbiologist
on call
‘, a peadiatrician and a
coniTiittee of an epidemiologist,
adverse
events
.
thorough investigation of severe
to ensure prompt and
1-- -------
8.2
Measures to Minimize Risks
The following measures will help to minimize risks of adverse events
following vaccination:
Procedures for sterilization of syringes and needles should
be scrupulously followed and monitored.
A single, sterile syringe and a
should be used for each injection.
single,
sterile
needle
Measles vaccine should be discarded at the end of the
session. Opened vials of measles vaccine should not be used
the next day under any circumstances.
for measles vaccine should be kept separate from
Diluent
potentially
harmful injectable drugs.
other ]
Training programmes for all categories of personnel should
receive the highest priority to ensure high quality of
services.
Field monitoring of the services should be regular and any
deficiences should be noted and corrected in a timely
manner.
8.3
Field Investigations and Analysis of Reports
of outbreaks can be
The basic principles of field investigations first prin^ipl^ 'S
! S to
‘ , The
adopted for the investigation of adverse events,
All
children
diagnosis.
examine as many cases as possible to confirm
<----session
should
be
followed up and relevant
inmunized during the particular l-- 7;,
It
is important that non
details entered in the line list (Annex 7).
in the locality are also examined
inmunized children of the same age-group
-to rule out temporal relationship.
of the data should be made, by time, place and personl in
An analysis as described in section 4. The details of children
c.-the same manner
vaccinated may 1be
— sunmarized as shown in Table 7.
SEA/EPI/79
Page 20
TABLE 7. Ntmber of children vaccinated, with reactions
and nuaber of deaths
Date of
vaccination
Vaccine
NvnJoer
vaccinated
No. with
reactions
Date(s) of
reaction
No. died
Date(s)
of death
for a session) and frequency and quality of routine field monitoring of
services.
unexpected and not easily explainable, it
Where the adverse events are
of each case are carefully noted,
is important that the signs and symptoms
investigations is of prime importance.
The promptness and completeness of :----the national control
' ' 'bej sent for testing to
Vaccine samples should
courier.
should be well packed in ice and sent by awhich
laboratory. The samples
i
the
should clearly state the circumstances under
---- —
The forwarding note
used
vial
with
the
remaining
sample (s) is sent. It is important that the
with unused vials of the same batch.
vaccine is sent for testing along
--'
sent\ iimiediately to the
A report on severe adverse events should be
decision
regarding possible
concerned state and central officers so that a (-----batch of vaccine can be taken pending
holding or recall of the concerned
<-----A.
*
-- -----------------------
A
e
___ J
4
**
o
laboratory investigations.
8.4
Write-up and Report Results
A report should be
with general
This report should start witn
geneinx
investigations conducted.
the pise. where
SEA/EPI/79
Page 21
the event occured. The name of the state, district and PHC/ward should be
clearly stated. The following points should be covered in such a report.
report:
(1)
Cases
How and when were
reported the event?
Who conducted
started?
the
the
first
observed and
symptoms
investigations
and
when
were
who
they
How were the investigations conducted?
type of reactions
Number of children vaccinated and the
observed. The line list and summary tables should be
attached to the report.
Whether any children of the same age-group in the area, who
were not vaccinated, had similar symptoms.
(2)
linical aspects
Detailed clinical picture.
Treatment provided to the children.
Outcome of illness.
-
(3)
Diagnosis by clinicians and observations,
them.
i f any, made by
Operational aspects
How are inmuni
zat ion services generally provided
immunization
area? Procedure followed on the day of the event.
m
the
When and from where the vaccines were received? How were the
vaccines stored and transported?
How many syringes and needles arej available and procedures
of the equipment?
followed for the sterilization
-----Who administered
received?
the
vaccines
and
the
training
they
Have similar reactions been observed in the past and were
not reported?
(4)
laboratory investigations
-
Samples sent for testing and the names of the laboratories.
The testing of the vaccine can take 2-4 months depending on
the vaccine and the tests.
SEA/EPI/79
Page 22
(5)
Suggestions and recocmendations
What was the likely cause of the adverse event?
Measures recotamended to minimize the risks in future.
Date
8.5
(Name and Designation)
Reporting Procedure and Dealing With the
Public and the Media
Iliese are the same as for reporting and dealing with an outbreak of the
disease. However, there is often a greater emotional sensivity when adverse
events occur following vaccination since it is perceived that the health
worker has performed an act that has injured or killed an otherwise healthy
child. It is important that the community’s concerns are dealt with in a
professional but sympathetic manner.
9.
ACKNOWLEDGEMENT
The writers gratefully acknowledge the assistance received from
Dr Indira Murali, Associate Professor (MCH), National Institute of Health
and Family Welfare, New Delhi, and Dr Prema Ramchandran, Deputy DirectorGeneral, Indian Council of Medical Research, New Delhi, in the initial
drafting of the field guide.
REFERENCES
(1)
Benenson, Abram S.
S. Control of communicable
American Publi c Health Association,
1015
Washington DC. Fourteenth Edition, 1985.
(2)
Kim-Farley, R. and Sokhey, Jotna. A simple screening method for field
evaluation of vaccine efficacy, J.Comm.Dis 1988, Vol 20, No.l: 32-37.
(3)
Kim-Farley, R. and Sokhey, Jotna. Issues
J.Comm.Dis. 1988, Vol 20, No.2: 70-77.
(4)
Sokhey, Jotna; Bhargava, Indra and Basu, R.N. A
immunization programme, Ministry of Health and
Government of India, 1984
(5)
Sokhey, Jotna; Kim-Farley, R. and Bhargava, Indra: Case definitions in
the surveillance of vaccine preventable diseases. Ind Paed. 1988, Vol
25, No.7: 599-604.
(6)
Sokhey, Jotna and Kim-Farley, R. Evaluation of vaccination coverage
through sample surveys. J.Conn.Dis. 1987, Vol 19, No.4, 341-348.
(7)
Strasburg, M.A. Guidelines for the investigation
outbreaks of EPI target diseases. EPI/GEN/84/Revl
diseases in man,
Fifteenth Street
in disease
The
NW,
surveillance.
handbook on the
Family Welfare,
and
control
of
Annex 1
EPIDEMIOLOGICAL FEATURES OF VACCINE PREVENTABLE DISEASES
Disease
Causative
agent
Reservoir
I Mode of
!
; transmission !
'.Man
Poliomyelitis [Polio viruses JTaecally
[types I,II and ! contaiinated J
! saterial
!
! Ill
'Pharyngeal
!
I secretions !
Major
complications
Specific
treatment
Iwunity
J Incubation
!
period
! Coitunicabi1ity !
[7-14 days
!(range 3-25
! days)
[First week before!Residual paralysis {Hone
! I after onset of! of liibs
! syiptois
[Paralysis of
[(range 3-6 weeks)5 respiratory muscles !
[
! can lead to death J
[Type specific
[lifelong
.’life-long
Measles
SNeasles virus
[Air-borne
[Man
[Direct contact !
1 with nasal or [
! throat
!
! secretions !
I8-13 days
[Slightlybefore [Diarrhoea
! prodromal periodlPneumonia
! to 4days after [Otitis media
! rash
[Conjunctivitis
[
[Encephalitis
[
'Malnutrition
jHone
Diphtheria
[Man
SCorynebacteriui JAir-borne
[Direct contact !
Jdiphtheriae
!2-5 days
.'2 weeks or less [Respiratory
■ obstruction
[Myocarditis
[Nerve palsies
[20,000 -100,000 [Clinical disease!
! lay not provide!
! units of
! antitoxin
! life-long
'
! immunity
!
•Antibiotics
Pertussis
'Bordetella
[pertussis
[Air-borne
[Man
[Direct contact !
Tetanus
ICIostridiui
[tetani
IBroken skin
[Spores found in!3-21 days
[ soil
!
[Not transmitted [Death
! directly
!
Tuberculosis
’Mycobacteriui
'tuberculosis
I'M.afr icanua
IM.bovis
[Air-borne
[Raw ailk
[Man
[Cattle
[Variable (as
[Progressive pulmonary[Antimicrobals: 'Variable
! long as tubercle! disease
Hzoniazid and !
I bacilli being [Meningitis
! one or lore of:'
! discharged) - JHeiatogenous(iiliary)[Rifampicin,
!
'
■' streptoiycin '
!
[ ethaibutol or !
!
! pyrazinaiide !
[7-10 days
[Early cattarrhal [Brain daiage
[Antibiotics
[(not exceeding ! stage to 3 weeks!Secondary infections !
! 21 days)
[ after onset of [Malnutrition
!
!
! syiptois
!
!
[4-12 weeks
!(iay persist
! life-tiie as
! latent
[ infection)
!Prolonged
[Sedatives
[Clinical disease!
[Muscle relaxants! does not give !
[Antibiotics
! inunity
!
.'Tetanus iuune !
!
[ globulin
!
[
£ft £
M
Annex 2
<8 52
NJ
CASE DEFINITION OF VACCINE PREVENTABLE DISEASES
{ Classification !
Suspect
Physician confined
Laboratory confined
Personnel
Lay Public/ HPHs
Medical Officers
Medical Officers
Methods
History
History ♦ Clinical Investigations
Laboratory Identification
t
{Neonatal tetanusJNonal suck or cry for first 2 days
'
{Onset between 3-28 days
!
{Inability to suck
!
{Stiffness or convulsions
{Tetanus
{Injury or ear infection
{Difficulty in opening icuth
{Stiffness or convulsions
{Trisius
{Generalised luscle rigidity
{Convulsions
{Trisius
{Generalised luscle rigidity
{Convulsions
None
None
SPolioiyelitis {Fever
{Flaccid paralysis
{Positive virus culture for polio virus I
{
{Abrupt onset of weakness or paralysis {No sensory loss
{Positive serology (4-fold or greater
{
{ of the leg(s) or an(s)
{Muscle tenderness
! rise in serui polio antibody titre)
{
!No progression of paralysis after first {Absent or depressed deep tendon reflexes !
!Asyiietrical findings
!
{
{ three days
{Wasting of affected lusdesdate findings)!
!
{Paralysis not present at birth or
!
! associated with serious injury or
{Residual paralysis 60 days after onset of {
!
! aental retardation
! illness should be added as a criteria in!
! areas of low incidence
!
{Measles
{Generalized blotchy rash lasting 3 or {Generalized laculopapular rash
{Positive serology (4 fold or greater
{ lore days
{Fever 38'C. (101’F) or lore
{ rise in serui antibody titre)
{Fever
{Cough, coryza, conjunctivitis or Koplik’s !
{Cough, runny nose or red eyes
! spots
{
{Exposure to a suspect case of leasles in!
{
! the previous 2 weeks or an epideiic of!
{’
! leasles in the area
!
!
W
i
{Whooping cough
{ (pertussis)
•
;
;
}
|
•
'Diphtheria
{Prolonged coughing followed by apnoea,
'Cough persisting 2 weeks or more
'Fits of coughing which may be followed { cyanosis or vomiting
{Typical ’whoop’in older infants and
{ by vomiting
! children
'Typical ‘whoop’ inolderinfants and
{Subconjunctival haemorrhages
{ children
i
{Exposure to asuspect case inprevious
' 2 weeks or epidemic of whooping cough I
', in the area
{White blood cell count with 15000
{
5 lymphocytes/cu mm or more (supportive !
’ of diagnosis but non-specific)
!
{Positive culture or immunofluorescence |
I of nasopharyngeal secretions for
■
! Bordetella pertussis bacteria.
I
!Grey ish-white memorane
teibrane in inruai
throat (uith
{Sore throat (with or without difficulty {Greyish-white
u.
• in swallowing)
• or ,,ithout
in breathing)
fever
{Acute pharyngitis, naso-pharyngitis or
{Greyish-white membrane in throat (with ! laryngitis
’ or without difficulty in breathing) {Airway obstruction
{Exposure to a suspect case of diphtheria{Myocarditis or neuritis (paralysis)
{ in the previous 1 weeks or epidemic of! one to six weeks after onset of
{ diphtheria in the area
! symptoms
JCoiion alternative diagnosis excluded !
! by appropriate tests.- negative throat !
I culture for group A streptococci,
!
! negative blood test for lononucleosis I
JPositive culture of Corynebacteriui
!
! diphtheriae (demonstration of toxin !
! production recommended but not
!
! required)
'
microscopic examination of a direct
!
) smear of a clinical specimen is not 1
! sufficiently accurate to substitute !
! for a culture
!
•xj tn
££
ft)
bJ -u
Ln t-4
oq
‘.Tuberculosis
1 (childhood)
(Listle
(Loss of w
(Prolonge' . >. p ide fever
(Tubercuh
in hilly or close
! neighc
:brain - Dazed condition, stiffness of
neck, convulsions, severe
headache, fever
(GLANDS - lyiphadenopathy in neck and
!
axilla which lay suppurate
(LUNGS - Fever, cough, weakness, poor
!
appetite
(BONES - Fever, pain, swelling and
(
crippling of joints
(Microscopy or culture of tubercle
1 bacilli, identified as lycobacteriui
( tuberculosis, from secretions or
( tissues
(CSF findings consistent with IB
(Suggestive radiological appearances on
! fills of chest, bones or joints
(Suggestive histological findings in
! biopsy laterial
i'And any one of the following.-
IPositive reaction on tuberculin testing
! ()10 ii induration)
(Favourable response to anti-TB therapy
Note: Children lay coie for . : leasles/pertussis secondary infections
A history of possible antecedent measles or pertussis in the last six weeks should be taken for all children
with pneumonia or diannoei (for measles)
Record iuunization status of all cases
Investigate all suspeit idses of neonatal tetanus and poliomyelitis within two days to confirm diagnosis
I
(
I
!
>
SEA/EPI/79
Page 27
Annex 3
LABORATORY INVESTIGATIONS OF VACCINE PREVENTABLE DISEASES
Disease
Spec lien
Perlod
Polioiyelitis !1. Stool 2-5 g {As early as possible in
■' the acute phase
{ (72 hours to 6 weeks)
{As early as possible in
52. Pharyngeal
{ the acute phase
! swabs
2 (36 hours to 10 days)
!3. Blood 5-10 al{Two saaples {- at onset (acute)
or 3-4 al
{- one aonth later
serui
! (convalescent)
I...... --I..........
!1. Blood 5-10 al{Two saaples Measles
{- at onset (acute)
or 3-4 al
!- one wonth later
serua
{ ^(convalescent)
{Two saaples 12. Blood on
! filter paper {- at onset (acute)
{- one aonth later
! (convalescent)
Transportation
•ediui
{Not necessary if
! transportation tiae
! less than 48 hours
{Buffered broth with
{ 1Z protein and
{ antibiotics
{None
{(Serua should be
! separated to prevent
! heaaolysis)
I.................................
{None
{(Serua should be
{ separated to prevent
! heaaolysis)
{None
1 Refrigeration I
!4-8 ’ C
{Virus isolation and i
! type identification!
IFreeze
{Virus isolation and {
{ type identification!
14-8 ’ C
!CFT
{neutralization
14-8 ’ C
;hi
!
{None (can be !HI
{kept at rooa t'l
Diphtheria
{Throat swab
{As early as possible
{Loeffler serua aediua {4-8 ’ C
{ (before treataent with ! coabined with tellurite!
{ antibiotics)
!Aiies or Carey Blair or !
{
! silica gel
!
Pertussis
{Throat swab
{Nasal swab
{As early as possible
{Bordet-Gengou
{ (before treataent with {Charcoal agar
! antibiotics)
!
Tuberculosis a 'CSF
iSputui
{As early as possible
Test
14-8 ’ C
{Isolation
{Toxin production
{Culture
{Nicrosopy
{Culture
a - Skin test - an intraderaal tuberculin test with 2 TU PPD shows an induration
of 10 aa or aore, 48-72 hours after injection. Children witn mn, aimny moercuiosis or severe
aalnutrition aay not respond
a - Radiological findings
SEA/EPI/79
Page 28
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SEA/EPI/79
Page 29
Annex 5
INVESTIGATION OF NEONATAL DEATHS
To be completed by the Medical Officer on all Infants who died within
the 1st month of life (a separate form for each neonatal death).
I.
GENERAL INFORMATION
1. State/U.T.
2. District
3. Town (Moha]la)/PHC/Village
II.
BACKGROUND INFORMATION ON NEONATAL DEATH
1.
2.
3.
4.
5.
III.
4. Physician’s Name
5. Da t e
6. Cluster Nc.
Na me of child
Sex of child
Fa ther’s name
Head of household
Date of birth of child
6. Address of child
7. Name of person interviewed
8. Relationship of person
Interviewed to child
9. Date of death of child
SYMPTOMS PRECEDING INFANT*S DEATH (Please circle appropriate answer)
1. Was the infant able to suck milk after birth?
2. Did the infant stop sucking milk when illness began?
3. Did the infant have a fever?
4. Did the infant have convulsions?
5. Was the infant noted to be stiff?
IV.
Yes
Yes
Yes
Yes
Yes
No
No
No
No
No
INFANT’S CARE SINCE BIRTH (Please circle appropriate answer)
1. Who delivered the child?
Doctor/LHV/ANM
Dai (trained)
Dal (untrained)
Non-dai family members
Other (please specify)
2. Where the child delivered?
Hospital/Health centre
Home
In the fields
Other (please specify)
3. When the child became ill, who
treated the child?
V.
Government health centre
Resitered Physician (Allopathic/
Ayurvedic/Homeopa thic)
Un-registered Physician
No treatment was received
MOTHER’S IMMUNIZATION HISTORY
1. Does the mother know about vaccination with TT?
2. Number of doses received during this pregnancy
VI.
No
(Circle)
Yes
No
(Circle)
OTHER INFORMATION ON MOTHER
1. Is the mother alive?
2. If dead, date of death
3. Symptoms preceding death
VII.
Yes
MEDICAL OFFICER’S DIAGNOSIS
1. Cause of neonatal death_
2. Cause of mother’s death
Signature of Medical Officer
SEA/EPI/79
Page 30
Annex 6
CLINICAL OBSERVATIONS OF LAME CHILDREN
To be completed by the Medical Officer on all lame children (a separate form
for each lame child).
I GENERAL INFORMATION
1. State/U.T.,
4. Physician*! Name
2. District
5. Date
3. Town (Mohalla)/PHC (Village)
6. Cluster No..
II BACKGROUND INFORMATION ON LAME CHILD
1. Name of child.
5. Date of birth of child
2. Sex
6. Address of Child.
3. Father’s Name
7. Person interviewed.
4. Head of Household
8. Relationship of person interviewed to child.
III HISTORY OF ILLNESS RESULTING IN LAMENESS OF THE CHILD
1. Date of onset of lameness
2. Address of child at onset of lameness (Outside the district or not)
3. Number of doses of polio vaccine received by child preceeding onset of lameness.
4. Medical care during illness resulting in lameness—(circle correct answer)
(a) Registered physician (Allopathic/Ayurvedic/Homoeopalhic)
(b) Health Centre.
(c) Un-registcred physician
(d) Other (please specify)
(e) No treatment received
5. Did the child have fever at the time of onset of lameness ?
Yes
No
6. Was the onset of the lameness acute ?
7. Did the lameness progress (increase) after onset 7
Yes
No
No
Yes
IV PHYSICAL EXAMINATION OF CHILD (Circle correct answer)
1. Paralysis of lower limb present
2. Affected Limb
Left
4. Sensation in affected limbs
Flaccid
Normal
5. Muscle atrophy (wasting) in affected limb
6. Gait
normal
impaired
Yes
requires assistance
3. Type of Paralysis present
No
Both
Yes
Right
No Paralysis
Spastic
Impaired
No
unable to evaluate
V EVALUATION OF LAMENESS (circle appropriate answer)
1. Lameness not present
2. Lameness present
(a) docs not require mechanical aid to walk
(b) requires mechanical aid to walk
(c) unable to walk
VI PHYSICIAN S DIAGNOSIS ON CAUSE OF LAMENESS (circle appropriate answer)
1. Poliomyelitis
2. Trauma (please specify)
3. Congenital deformity (please specify)..
-
4. Other tpleasc specify)-------------- --------------------------------------- ------------Medical Officer's Signature
’1
Annex 7
LIST OF CASES WITH ADVERSE REACTIONS
JsiJ
Address
Nane
;no.;
’.Age
Time of
of
:. s» : 2"
i onset
M*Jor •1»n’ *"d
tereda
___________ •.................
......... {
Renarks
;D1,,no,u
•
—......... — •
i
s
------
!—
;—•-----
I
r
—:
!
—:------
aGive name of vaccine and the dose (1, 2, 3 or booster, as relevant).
V)
I
I
I
00
(!)
5
SEA/EPI/79
Page 32
Annex 8
CALCULATION OF VACCINE EFFICACY
of theSti1rZ^n+°f Vaccine efficacy is an important measure of the quality
of the immunization programme and indicates that potent vaccines arebei™
properly administered. Vaccine efficacy is measured by the following formulf
rates ^I^rd
Percentage reduction in the incidence rate? (attack
persons
disease among vaccinated persons compared to unvaccinated
A Ov/llO •
VE = IPPV)(PCU) - (PPU) (PCV)
(PPV)(PCU)
*
where:
VE - vaccine efficacy
PCU = proportion of cases unvaccinated
PPU - proportion of population unvaccinated
PCV = proportion of r
.
. with the number of doses
cases vaccinated
being
examined for vaccine efficacy
PPV = proportion of population vaccinated
with the number of doses
being examined for vaccine efficacy
shoR-nIin1thAPOfnnle- tO calcYlate vaccine efficacy using this formula as
shown in the following example: Suppose that an outbreak of poliomyelitis
chil^en^r^to^-T 1thrlCt;
inmuni2ation coverage in the dis^ict in
hildren 12 to 23 months of age as determined from a vaccination coverage
survey isknown to be 60 per cent for OPV3 and 25 per cent of children are
unimrnunized (15 per cent of children had received only one or two doses)
areCsufferini2ftO 23 '?°nths.of age who are residents of the district and who
three doses^f
■ it
it is
is found
found that
that 15
15 per cent had received
ee doses of OPV vaccine and 75 per
unimmunized (10
per cent
cent were
were unimmunized
(10 per cent of
children had received only one or two doses). Using the aboJJ fZula
or two doses). Us i ng the above
vaccine efficacy would be estimated to be:
1
VE - I»60)(,75)-(.25)(.15) = .450 - .0375
= .4125
(.60)(.75)
.450
.450
.92 or
92%
\Si^Liati°n_ wher1e on}^. one dose of vaccine is required (e.g., BCG
and measles), or where only efficacy of the third dose
vaccine (e.g., COPV3 and DPT3) is desired and --- -- j of a multiple dose
the drop-out rate from the
first to third dose is relatively small, then the formula can be further
simplified as follows:
VE =
ppy - pcv
PPV - (PPV)(PCV)
It IS
is possible.to
possible to simply
simply calculate
calculate vaccine
vaccine efficacy using this formula
as j
^2 5*^ f?1}°ying examPle - Suppose that an outbreak of measles has
.occurred in a
~ district. The immunization coverage in the district is known
to be 75 per cent for measles vaccine in children 12 to 23 months of age as
SEA/EPI/79
Page 33
determined from a vaccination coverage survey. Of children 12 to 23 months
of age who are residents of the district and who are suffering from measles,
it is found that 20 per cent had received a dose of measles vaccine. Using
the above formula, vaccine efficacy would be estimated to be:
.75 - .20
VE =
.75 - (.75)(.20)
.75
.55
.55
.92 or
.15
.60
92%
If this simplified formula is graphed for different values of the three
variables, it is possible to develop a set of curves to easily estimate
vaccine efficacy in the actual field setting. By knowing values for PPV7 and
PCX7, vaccine efficacy can be estimated by looking at where the lines
intersect on the graph. An example using the same outbreak data given above
is illustrated in the figure below.
Percentage of cases vaccinated (PCV) per
percentage of population vaccinated (PPV),
for 7 values of vaccine efficacy (VE)
100
100
so
so
80 - —
so
70 J
70
60 4
SO
O 50 -■
90/^5. — 50
F
T
4 0----
40
30 -
30
20 -
10
10
0
0
102b
30
40
50
PPV
Source:
60
70
80
90
—* 0
100
?pv= 75%
Weekly Epidemiological Record, No.18, pp 133-136
Position: 1761 (3 views)