Dr - LRS Institute of Tuberculosis & Respiratory Diseases

Emeritus Editor:
Dr. P.K. Sen
Editor:
Dr. S.P. Pamra
Editorial Board:
Dr. G.V.J. Baily
Dr. M.D. Deshmukh
Dr. H.B. Dingley
Dr. D.N. Gupta
Dr. S.K. Jain
Dr. K.V. Krishnaswami
Dr. A.N. Malaviya
Dr. M.L. Mehrotra
Dr. D.R. Nagpaul
Dr. A.G. Patel
Dr. K.N. Rao
Dr. S.P. Tripathy
Dr. S.N. Tuli
INDIAN JOURNAL OF TUBERCULOSIS
Official organ of the
Tuberculosis Association of India
Vol. XXIX : No. 3 July 1982
Contents
Editorial : Pathogenesis of Tuberculosis … 131
Epidemiology of Tuberculosis in India
— G.D. Gothi ... 134
Why Integrated Tuberculosis Programmes have
Not Succeeded As per Expectations in Many
Developing Countries — A Collection of
Observations
— D.R. Nagpaul ... 149
Tuberculosis in a Rural Population of South
India; Report on Five Surveys
—A.K. Chakraborty, H. Singh, K. Srikantan,
K.R. Rangaswamy, M.S. Krishnamurthy
and J.A. Stephen ... 153
Lower Lung Field Tuberculosis
—Ram Chandra, Jitendra Nath, G.N. Agrawal,
V K. Srivastava and P.K. Mukerji ... 168
Fungal Superinfection in Pulmonary Tuberculosis
—S.K. Jain, R.L Agrawal, Dev Ashish Sharma
and Manju Agrawal ... 173
Plasma Copper and Zinc Levels in Pulmonary
Tuberculosis
—B.K. Khanna, R. Kumar, P.K. Mukerji,
A.R. Chowdhury and V.P. Kamboj ... 179
Plasma Erythocyte and Leucocyte Free Alpha
Amino Nitrogen Alterations in Pulmonary
Tuberculosis And Effect of A Glucose Load
On These Parameters
—S.C. Seth, Harbans Lai, A.S. Saini and
M.S. Parmer ... 185
Serum Mucoprotein (Tyrosine) Level And
Lactic Dehydrogenase Activity In Childhood
Tuberculosis
—S.D. Singh and N.M. Jain … 189
Posterior Fossa Cystic Arachnoiditis: An
Uncommon Presentation of Neuro-Tuberculosis
—V.K. Srivastava and G.N N. Reddy ... 193
Lupus Vulgaris (Verrucosus) Associated with
Pulmonary Tuberculosis
—T.R. Kapur … 200
Book Review … 203
T.A.I. Gold Medal … 204
Obituary—Dr. R. Viswanathan … 205
News & Notes
Published quarterly in the months of January, April, July & October
Annual Subscription Rs. 40/-, £ 4.00, $ 10, Single copy Rs. 12/-.
Published on behalf of the Tuberculosis Association of India,
3, Red Cross Road, New Delhi-110001.

The
Indian Journal of Tuberculosis
Vol. XXIX New Delhi, July 1982 No. 3
PATHOGENESIS OF TUBERCULOSIS
Robert Koch, in his famous dissertation announcing the discovery of
Tubercle Bacillus, said : “Tuberculosis has so far been habitually considered
to be a manifestation of social misery, and it has been hoped that an improvement
in the latter would reduce the disease. Measures specifically directed
against tuberculosis are not known to preventive medicine. But in the future
the fight against this terrible plague of mankind will deal no longer with an
undetermined something, but with a tangible parasite, whose living conditions
are, for the most part, known and can be investigated further”. Robert Koch’s
pronouncement presaged a complete break from the past thinking and suggested
an entirely new direction towards the control of tuberculosis. However,
subsequent observations showed that even Robert Koch was not completely
correct and his prophesy was the result of dogmatism and over-enthusiasm.
Nageli and, subsequently, Opie and Ghon showed the presence of obsolete
tuberculous lesions at autopsy in persons who had never suffered from tuberculosis
in their life time. What is more important, many of these
lesions contained viable tubercle bacilli. In other words, infection and
mere presence of the aetiological agent in the tissues of the host is not
sufficient per se to determine the development of manifest disease. A
question naturally arises - why do only some of the enormous number
of infected individuals develop the disease ? What are the factors which influence
the development of disease, once infection has taken place ? Could it be
that the very factors which Robert Koch decried are the factors which decide
whether infection will go on to disease or not?
The association of heredity and tuberculosis has been the subject of discussion
for ages. We may not believe that one inherits tuberculosis but one
also cannot deny that heredity can and does influence resistance against disease.
Hill’s hypothesis of the speed of reaction is merely old wine served in a
new bottle. It does not elucidate at all as to what makes the body react and
what determines the speed of reaction.
Knowledge regarding the mechanism through which the natural resistance
operates and factors which augment or depress this is crucial but unfortunately
still lacking. It has been hypothesised that the degree of natural resistance
is dependent in part on ability to develop acquired resistance. But then,
why does primary infection itself heal and the subsequent re-infection some
times progress to disease inspite of the natural resistance being further
augmented by acquired resistance ?
Ind. J. Tub., Vol. XXIX, No, 3

132
The increased susceptibility of household contacts of an open case of
tuberculosis is well-known and attributed to one or other of the three factors
viz. intensity of exposure, heredity, adverse environmental factors. Seemingly
valid arguments can be adduced for and against each of these factors.
Inherent ability of an individual to maintain resistance at a high level may
be, and very probably is, governed in part by heredity but the maintenance of
a satisfactory degree of resistance is also influenced by many environmental
factors. The influence of ‘psyche’ is being increasingly incriminated in the
problems of ‘soma’. But, whether a given unfavourable factor actually depresses
the mechanism of natural resistance or whether the mechanism remains unaltered
but conditions are introduced which thwart it or prevent it from functioning
effectively is, of course, not known. Since many of these factors which influence
the outcome of infection are intangible, the fate of the individual remains
unpredictable.
Mode of reinfection is another moot point in pathogenesis. It is common
knowledge that most of the progressive pulmonary disease is not the
direct result of primary infection but follows re-infection, sometimes many
years after the primary infection. Is reinfection endogenous or exogenous ?
Arguments for and against both have been many and fascinating. Consensus
appears to be in favour of endogenous reinfection being more likely
and more plausible though it cannot be proved that exogenous reinfection
is not possible. This controversy is not merely an exercise in intellectual
polemics without any practical implication. Prevention of tuberculosis does
seem to be linked with this problem. If endogenous reinfection was the only
mode, isolation of an open case from individuals already infected is meaningless.
If on the other hand, exogenous reinfection is possible, then isolation
from both infected and uninfected is imperative.
Endogenous reinfection is also linked with the problem of dormant bacilli.
What makes the bacilli dormant ? Our knowledge in respect of growth requirements
of the bacillus and its metabolism is still limited. Is dormancy governed
by some inherent and intrinsic character of the bacillus or is it in response
to some altered state of the tissues in which the bacilli are lodged ? We are
still ignorant about the mechanism which triggers dormancy and subsequent reanimation.
A substance called “Hibernation Induction Trigger” has been
isolated from the blood of hibernating animals. Could it that some such
substance is involved in dormancy of the tubercle bacillus also ?
The importance of the dormant bacillus is not merely because of its role
in reinfection and relapse but also because of its influence on epidemiology.
When tuberculosis started declining rapidly in the western countries, the high
priests of epidemiology prophesied that eradication of tuberculosis was imminent.
Their optimism was more wishful than rational. As long as there is but
one human being in the world who has but one dormant bacillus inside his
body, he can generate, at least theoretically, a new epidemic of tuberculosis
even if the previous one had completely died out. This has been corroborated
by a number of small localised epidemics that have occurred recently in developed
countries where tuberculosis has declined tremendously.
Ind. J. Tub., Vol. XXIX, No. 3

The unsolved problems in pathogenesis of tuberculosis are many and
varied. Rich summarised the position admirably in 1951. What passed for
knowledge about pathogenesis was more a matter of belief based on reasoning
from analogy rather than a conviction based on valid statistical and scientific
proof. And there the matter rests even today!
133
Ind. J. Tub., Vol. XXIX, No. 3

REVIEW ARTICLE
EPIDEMIOLOGY OF TUBERCULOSIS IN INDIA
Tuberculosis is known to have existed in
India since ancient times and has been mentioned
in classical literature including Ayurvedic
Samhitas. However, quantitative information
about its epidemiology has become available
only in the last half century. Unlike western
countries, where a more or less efficient notification
system has existed for a long time,
India has been lacking in even approximate
data about the prevalence and incidence of
tuberculous infection and disease as well as
mortality rates. One of the earliest official
documents in which data regarding tuberculosis
have been given is the Bhore Commission
Report, 1946. The general impression at that
time was that tuberculosis was mainly an urban
problem and that younger persons, specially
females, were more prone to it than others.
Although the relevant facts regarding the
present day epidemiology of tuberculosis in
India have not yet been fully elucidated, a
considerable amount of information, of varying
degrees of reliability and accuracy, has accumulated
during the course of the last 30 or 40
years enabling us to see at least the outlines of
the problem and furnishing the basis for future
action.
As is well known, infection and disease are
not synonymous in tuberculosis. We have, thus,
two parameters to consider, both interdependent,
even though the extent of interdependence
is itself an enigma.
Prevalence of tuberculous infection
Prevalence of infection is measured by the
proportion of tuberculin reactors in the total
population at any point of time and is usually
expressed as a percentage. However, in the
absence of a well defined test, available information
on this point is highly variable. Because
of the use of different types of tuberculins,
different dosages and methods of testing,
considerable variations in the reading of reactions
by different workers, imprecise knowledge
about the exact size of tuberculin induration
that should be regarded as evidence of
tubercular infection, the possibility of a boosting
effect due to earlier tuberculin testing and the
prevalence of non-specific tuberculin sensitivity
in some areas, the interpretation of tuberculin
G.D. GOTHI*
test reactions is a highly complex job. In view
of these limitations, it is not possible to compare
infection rates reported from time to time by
different workers from different areas. A review
of literature reveals that, unaware of the limitations
of the test, different workers have used
different strengths and types of tuberculin and
arbitrarily set critical values for separating
tuberculin reactors and non-reactors.
The earliest report on prevalence of infection
in India is by Ukil (1930) who found 11%
tuberculin reactors in the 0 to 4 age group and
75% among persons aged 10 years or more in
a survey carried out in areas of Bengal, Bihar,
Assam and Madras. The observed rates were
much higher -in the urban areas. Benjamin
(1938-39), surveying a sample population in
the rural and urban areas of Chittoor district
and in Saidapet (in the suburbs of Madras),
made similar observations although, contrary
to the then current general impression, he
concluded that villages were not free from tuberculous
infection. Rist and Rose (1938) carried
out a survey among Muslim girls in Ludhiana,
Ilahi Baksh (1939) in the rural population of
Jullunder and Rao and Cochran (1943) repeated
a tuberculin survey in Saidapet. All
these reported a high prevalence of infection
in towns, semi-urban areas and villages. High
infection rates were also reported by Frimodt-
Moller (1949) in Madanapalle town and surrounding
rural areas.
More extensive data regarding infection
rates became available as a by-product of the
mass BCG vaccination campaign undertaken
by the Government of India. Analysis of data
showed a high prevalence of infection even at
the young age of 5 years in West Bengal,
Bombay and Uttar Pradesh. The tuberculin
reactor rates at this age in the three states were
23.0%, 32.2% and 27.4% respectively for
males and 21.5%, 32.2%’ and 22.8% for
females. It was found that by the age of 10,
more than half the males and over 45 % of the
females had already been infected. In the hilly
regions, half the population was infected by the
age of 15 years as against the age of 10 years
in the plains. Infection rates in the industrial
towns were higher than elsewhere, 50% level
of infection having been reached before the
age of 10 years.
*Director, New Delhi Tuberculosis Centre, Jawahar Lai Nehru Marg, New Delhi-110002.
Ind. J. Tub., Vol. XXIX, No. 3

EPIDEMIOLOGY OF TUBERCULOSIS IN INDIA 135
Several other studies carried out at the same
time (Sikand and Raj Narain, 1952 in Faridabad
township, Hertzberg, 1952 in Trivandrum city
and Frimodt-Moller in Madanapalle town and
surrounding villages) also revealed a very high
rate of tuberculintzation. Frimodt-Moller (I960)
carried out a large scale tuberculin survey
among a population living within 10 miles
radius of Madanapalle. Using 5 TU PPD
(XIX, XX and XXI with a reaction of 10 mm
or more taken as an evidence of infection),
he found that at the ages of 10 years, 20 years
and 30 years, the infection rates were 10%,
21% and 31% respectively. Using 1 TU and
considering an induration of 6 mm or more as
an evidence of infection the rates at the same
ages were slightly lower.
Considering a reaction of 10 mm or more
to 1 TU PPD RT 23 with tween 80 as positive,
Raj Narain et al (1963) found an overall infection
rate of 38.3% in a sample population
of Tumkur district (42.8% among males and
33.9% among females). Infection rates in the
rural and semi-rural areas were 37.9% and
43.9% respectively. The overall prevalence of
infection in 119 villages of Bangalore district
(based on the same tuberculin and reaction
as above) was found to be 30% (35% among
males and 25% among females) (National
Tuberculosis Institute (NTI), 1974). The infection
rates for both sexes increased with
age upto ‘45 to 54 years’ (66% to 72% for
males, 47% to 50% for females). The rate of
increase in females, unlike males, slowed down
after the age of 15 years. Repeated tuberculin
testing of the same population at intervals of
1-1/2 years to 2 years did not show any change
over a period of 5 years. In a recently conducted
study in Chingleput district of Tamil Nadu,
Tuberculosis Prevention Trial (TPT, 1980),
using 3 TU of PPD-S and considering an
induration of 12 mm or more as evidence of
infection, reported an overall prevalence rate
of infection of 50% (males 54%; females 46%).
Among males, the infection rate rose rapidly
upto the age of 25 years (reaching 80 %) whereas
in females the rise continued upto 35 years
(reaching 70%). In both sexes the rate levelled
off after the peak had been reached. In the
Kashmir valley, infection rates were found to
be considerably lower than, say, in the south
Indian states of Karnataka and Tamil Nadu.
(Unpublished material 1980).
In Tumkur survey, the prevalence rates of
infection in the age groups 0 to 4 years, 5 to 9
years and 10 to 14 years were 2.7%, 5.5% &
25.4% respectively (Raj Narain, 1963). Gothi
et al (1979) found nearly the same rates among
children and adolescents in the same population
after 12 years.
Udani (1968) reported a prevalence rate of
4.7% in the age group 0 to 6 years on the west
coast. In the semi-urban areas of Delhi the
rate was 4.6% (Dingley, 1979) in the age group
0 to 4 years but among school children (5 to
14 years) in the city, the figure was 40.7%
(Singh, 1960). Figures for school children
of Nagpur were reported as 24.4% by Majumdar
(1960). At the age of 15 years, Benjamin
(1951) found the lowest infection rates in
Assam (51% among males and 36% among
females) and the highest in U.P. (males 75%,
females 74%). In the Tuberculosis Prevention
Trial (1980), the rates for age groups 1 to 4
years, 5 to 9 years and 10 to 14 years were
4.9%, 7.9% and 16.5% respectively, males in
general showing a higher prevalence than
females. Krishnaswami (1978) reporting on the
urban slums of Madras found a very high
rate of infection for children below 5 years.
In another congested urban areas of Madras,
Narmada et al (1973) reported rate of 7.3%
in the 0 to 4 years age group.
Although data available from various
sources are not strictly comparable, nevertheless,
there are some common features viz. (i) infection
rates increase with age and are higher in males
than in females (ii) the difference can probably
be explained by the fact that males in general
lead a more active life and mix with people in
a much wider circle, thus coming across more
chances of acquiring infection, (iii) infection
rates, in general, are more or less the same in
urban and rural areas, although they are somewhat
higher in congested urban areas and
industrial towns.
Incidence of infection
The conventional method of estimating the
incidence of infection is by repeated tuberculin
testing of the population. Persons classified as
non-reactors at an earlier tuberculin testing who
become reactors at a subsequent testing can be
considered to have acquired tuberculous infection
in the intervening period and incidence
of infection is calculated per annum by expressing
the latter as a percentage of the former.
Several attempts have been made, mostly in
south Indian states, to estimate the incidence
of infection.
Bogen (1957) used age specific prevalence
rates of infection for his estimate of 5.3 % per
year for all ages. Using similar data, Frimodt-
Moller (1960) estimated the annual incidence
of infection as lying between 4.7% and 6.2%
for different ages and Raj Narain et al (1963)
between 0.9% to 2.4%. Partly these differences
may be accounted for by different standards
Ind. J. Tub., Vol. XXIX, No. 3

136 G.D. GOTHI
adopted for judging tuberculin positivity.
Frimodt-Moller (1960), however, also gave a
different estimate of the incidence of infection
(2%) per year by direct observation i.e. after
repeated tuberculin testing at intervals of 2-1/2
years. Narmada et al (1977) reported 3%
annual incidence of infection in 0-12 years age
group.
Serious doubts about the validity of the
studies mentioned above arose as a result of
the findings of Raj Narain et al (1965) wherein
they proved that a previous tuberculin test
boosts the induration of any subsequent tuberculin
test reaction. Also, it was found that the
prevalence of non-specific sensitivity (Frimodt-
Moller 1960; Raj Narain et al 1965-72; Chakraborty
et al 1976) may interfere with the
estimation of the incidence of infection. Raj
Narain (1966) found a method for overcoming
this difficulty and suggested a new approach for
identifying the newly infected persons. By
this method Raj Narain (1965) and Gothi et al
(1972) estimated the incidence in the age group
‘0 to 4’ years at 0.9 % per year and for the age
groups ‘5-9’ years and ‘10-14’ years, 1.4% and
2.1% respectively. National Tuberculosis Institute
(NT1-1974), using the same method reported
that the average annual incidence of
infection for all ages was 1 %, that for the age
group ‘0 to 4’ years being 0.8%. The incidence
rates increased with age. For the age group
‘35 years and above’ the figure varied from
1.3% to 3.16% during three periods. Adopting
the same method of calculation, TPT (1980)
found a much higher annual incidence of infection,
3%, 4% and 6% per year for the age
groups ‘1 to 4’ years, ‘5 to 9’ years and ‘10
to 14’ years, respectively. A plausible reason
for such differences could be the considerable
difference in the prevalence of bacillary disease
in the two areas (4 per 1000 in the NTI study
area and 11 per 1000 in the TPT area).
Tuberculosis Morbidity
Two principal indices are generally used
to measure tuberculosis morbidity in any
community, the prevalence of active disease and
fresh incidence of disease among previously
healthy persons. As in the case of studies
relating to infection, there is a considerable
paucity of data in respect of tuberculosis morbidity
in India and in practically all developing
countries. In western countries, tuberculosis
has been a notifiable disease for a long time
and the system works fairly efficiently. As such,
some data (more or less precise, depending on
the efficiency of the notification system in any
particular country) relating to the prevalence
and incidence of disease have been available
Ind. J. Tub., Vol. XXIX, No. 3
for a long time, even though these statistics are
based only on ‘known’ cases. Although these
data do not take into account the undetected,
asymptomatic cases of tuberculosis, nevertheless
they provide very valuable information
about TB morbidity and trends in the community.
For several decades, these were the
only statistics available even in the western
countries for evaluating the tuberculosis problem.
In India, on the other hand, practically no
reliable data, were available till the early fifties
about the prevalence or incidence of tuberculosis.
One of the earliest estimates made by
Benjamin (1945), based on findings of a small
scale survey in the suburbs of Madras city,
and certain other observations, placed the total
number of active TB cases in the country at
about 25 lakhs, the estimated total TB mortality
in a year being of the order of 5 lakhs (Bhore
Commission Report, 1946).
It was only in the early 1950s that, with the
availability of mobile mass miniature radiographic
facilities, one acquired the means for
evaluating the tuberculosis problem by carrying
out surveys in various groups. In the last 30
years, a number of surveys (some in representative
community groups and others in selected
groups) have been carried out and although
data available are still not sufficient, considering
the size of the country, they provide a
useful basis for planning tuberculosis control
strategies.
It must not be presumed, however, that
with the availability of mass radiography and
sputum examination (the main tools employed
for tuberculosis morbidity surveys) all problems
relating to estimation of TB morbidity have
been solved. Both chest radiography and
bacteriological examination have their limitations.
In addition, the diagnostic problems of
tuberculosis are so complicated that no two
studies are, strictly speaking, comparable and
for that reason it is not possible to make any
general statement about the country as a whole
by taking into account the various studies
carried out in different regions. It would be
useful at the outset to consider all these limitations
to serve as caveat before drawing any
rash and possibly unjustified conclusions from
the various studies carried out at different
centres.
The first difficulty arises from limitations of
the two principal diagnostic tools viz. radiography
and bacteriological examination. Radiological
assessment of chest shadows, as is well
known, is highly subjective and is influenced

EPIDEMIOLOGY OF TUBERCULOSIS IN INDIA 137
by the competence of the x-ray reader and his
impression about the prevalence of other
pulmonary diseases in the region concerned.
A number of studies have brought out the
extent of ‘reader variations’, both intra-individual
and inter-individual, in intrepretation
of chest x-rays (Yerushalmy et al 1950, Sikand
et al 1962, Raj Narain et al 1962, Karan 1962,
Gothi et al 1974). An additional difficulty in
large scale surveys is that usually it is not
possible to have anything more than a single
miniature film to decide the aetiology and
activity of abnormal shadows. This is often
not an adequate basis on which to arrive at a
conclusive diagnosis. A number of procedures
for radiological assessment of miniature films
have been evaluated empirically and the system
commonly followed in the better planned
studies, nowadays, is to have two independent
assessments by two readers with a third ‘umpire’
reading by another reader to settle the
differences between the first two. It has been
found after experimentation that this procedure
is fairly adequate for minimizing errors of
both under-reading and over-reading.
In well planned surveys, all persons with
abnormal chest x-rays are subjected to a set of
bacteriological examinations. The fact that
intensity of such bacteriological examinations
varies from place to place and from time to
time is an additional factor which makes it
difficult to compare or combine results of
studies carried out at different centres. Many
centres lacking culture facilities have perforce no
option but to depend entirely on direct
microscopy of sputum. Some carry out both
direct smear and culture examination of a
single specimen. Some others are in the fortunate
position of being able to examine more than one
specimen at different intervals of time and
sometimes even repeat the chest x-ray, if
indicated. It is natural in this situation that the
final assessments would lack comparability. An
idea of how much difference this would make
can be had from the study of Chandra-sekhar et
al (1970) wherein it was shown that if 4
bacteriological specimens were examined in a
survey, nearly 25% of the bacillary cases were
added by the third and fourth specimens. Nair et al
(19761 have also shown that the rate of bacillary
disease increased by an additional , 39 % if eight
specimens were examined instead of two. It is
thus obvious that unless suitable ‘corrections’
are made, data obtained from one study would
not be directly comparable with any other study
with a different intensity of bacteriological
examination.
Further problems arise because of the fact
that there is no commonly agreed definition of
pulmonary tuberculosis (Raj Narain, 1968).
Except for bacteriologically proved cases, there
is always an element of doubt about cases
adjudged tuberculous merely on radiological
basis. To overcome this difficulty and to provide
a sort of lowest common denominator, the
WHO Expert Committee in its VIIIth Report
(1964) recommended that only sputum positive
patients should be considered as ‘cases’ of tuberculosis
and all others labelled as ‘suspects’.
This definition too is not, however, free from
faults. Bacteriological diagnosis, although highly
specific, is not sensitive enough and it is well
known that a large proportion of tuberculosis
patients with minimal disease are bacteriologically
negative to start with. This, besides the
difficulties enumerated earlier, detracts somewhat
from evaluation of tuberculosis problem
based only on bacteriological confirmation of
diagnosis.
So far as the prevalence rates are concerned, a
certain comparability can be achieved between
various studies by comparing the rate of bacillary
disease. Where estimation of incidence
rates among previously healthy persons is
concerned, a further difficulty arises. Since
there is no agreed definition of a tuberculosis
case, it follows that there is no agreed definition
of a non-case. In a longitudinal study, in which
prevalence of only bacteriologically confirmed
disease at the first survey has been calculated,
the remaining population including bacteriologically
unproved but radiologically active
patients, persons with inactive disease and
those with clear chest x-ray would form the
denominator (population at risk) for calculation
to further incidence. In another study in which
prevalence is calculated on the basis of radiological
and/or bacteriological evidence, the
people at risk which would form the denominator
for calculation of incidence would be
only persons with a clear chest x-ray. Since the
attack rate in the two types of ‘non-cases’ in
the two studies is likely to be different, it is
obvious that incidence rates would also not be
comparable.
Inspite of the difficulties and handicaps
mentioned above, surveys based on examination
by various procedures and techniques
have contributed valuable fundamental knowledge
about tuberculosis morbidity in the
country.
Prevalence of disease
Prevalence is defined as the number of
patients at a given point of time and is expressed
either in absolute numbers or as a
rate per 1,000 or per 100,000 of population.
Ind. J. Tub., Vol. XXIX, No. 3

138 G.D. GOTHI
Prior to 1950 only a few small scale surveys
were carried out in some parts of the country
to ascertain prevalence of tuberculosis. Benjamin
et al (1939) surveyed a population of 3,309 in
Saidapet, a suburb of Madras. Persons having
a strongly positive tuberculin test reaction or
having suspicious symptoms were physically
examined and 241 out of these were picked up
for x-ray. The disease prevalence thus estimated
was 2.3%. Another survey (Lai et al, 1943)
carried out in an urban population at Serampore
in Bengal showed a morbidity prevalence of
7% of which sputum positive disease accounted
for 3%. In both these surveys, because of
meagre x-ray facilities, only a small adult
population was examined. It is easy to see that
the figures do not reflect the correct tuberculosis
prevalence even for the limited areas covered.
Mobile miniature radiography was first
used by Aspin in 1945 to survey Gurkha recruits
for the Army and labour units. All those
examined were aged 18 years or more. In
Gurkha recruits the prevalence of tuberculosis
was found to be 1 % and among labour recruits
3.4%. Obviously, these figures cannot be considered
representative. Besides the fact that
they were all adults, recruits presenting themselves
for appointment in the Army were
expected to be healthier than the community
to which they belonged. In 1947, Frimodt-
Moller surveyed a population of 10,000 in
Madanapalle town and reported a prevalence
of 0.7% bacillary disease. This figure was
confirmed by a series of 5 longitudinal surveys
carried out by Frimodt-Moller in the same area
between 1950 and 1955 in which the population
studied was about 60,000. In 1951. the New
Delhi TB Centre surveyed Faridabad township
(housing displaced population) and found
active disease prevalence rate of 13.6 per 1000
among persons aged 5 years or more (Sikand
and Raj Narain, 1952). Other surveys carried
out about the same time in selected groups at
Madras and Trivandrum were reported by
Phillips (1952) and Hertzberg (1952). These
were the best available data on the subject till
about 1954-55. On the basis of personal impressions
and limited data obtained from
surveys, the general belief about this .time was
that tuberculosis was commoner among younger
people rather than the aged, females rather than
males, and cities and towns rather than villages.
Studies carried out during last 30 years have
disproved these beliefs. The first doubt about
these hypotheses arose from the data obtained
as a by-product of the mass BCG programme
carried out throughout the country starting in
1951. Tuberculin testing of the rural population
revealed an unexpectedly high prevalence of
tuberculous infection in the villages (Benjamin,
1951) suggesting the probability of a substantially
high prevalence of tuberculosis in the
rural areas as well.
To verify this impression, the Indian Council
of Medical Research (1959) organized a large
scale Sample Survey to assess the tuberculosis
situation in urban, semi-urban and rural areas
in various parts of the country during 1955-57.
The survey was carried out in 6 zones of the
country and covered a sample of nearly 300,000
persons aged 5 years or more. All persons
included in the sample were offered mass miniature
radiography. Sputa of persons with
abnormal chest shadows were examined by
direct microscopy and by culture. The main
findings of the survey were (i) the rate of
radiologically active pulmonary tuberculosis
varied from 13.5 to 26.6 per 1,000 population
in different zones and within each zone from
cities to small towns and rural areas, (ii) the
prevalence of bacillary disease varied from
2.4 to 8.2 per 1,000 (iii) prevalence of disease
in rural areas did not differ significantly from
the urban areas, (iv) prevalence of disease
showed a continuous rise with age in both
sexes but for females there was a decline from
the age of 45 years onwards. Nearly 2/3rd of
the total disease was in males. Villages accounted
for nearly 80 % of the total cases (the same
proportion as the rural population bore to the
total population).
Further information about prevalence rates
is available from longitudinal studies carried
out in Delhi, Bangalore, Madanapalle and
Chingleput. The surveys in Delhi and Madanapalle
(the former in an urban and the latter in
a rural areas) confirmed the findings regarding
prevalence rates obtained from the earlier ICMR
survey. In the Delhi study, carried out in a
congested old city area and covering a population
of about 30,000, the prevalence was
found to be 13.2 per 1,000 (bacillary : 4 per
1.000). It is interesting to note that in the Delhi
survey the rate of bacillary disease in the 6
surveys carried out from 1962 to 1977 varied
from 2.1 to 4 per 1,000. Tumkur survey (Raj
Narain et al 1963) carried out in a rural population
of 36,000 showed an overall prevalence
of 19 active cases per 1,000, of which 4 per
1,000 were bacillary. The NTI (1974) found
practically uniform rate of bacillary disease
(3 to 4 per 1,000) in rural population of
Bangalore district during the 4 surveys carried
out between 1962 and 1968.
In the Chingleput study (TPT 1980) where a
rural population of about 300,000 was under
surveillance in connection with a BCG trial,
the prevalence of bacillary disease was
Ind. J. Tub., Vol. XXIX, No. 3

EPIDEMIOLOGY OF TUBERCULOSIS IN INDIA 139
extremely high (17 per 1,000 for males, 4 per
1,000 for females and 11 per 1,000 for both
sexes).
A number of studies carried out in special
groups have also brought forth interesting data.
These include a survey of Delhi Police (Sikand
et al, 1954-1959), Civil Servants in Delhi
(Pamra et al, 1968), Textile Workers (Sikand
and Raj Narain, 1953). Also of interest is a
study carried out in a rural population in
Bangalore in which 22,957 persons were examined;
the prevalence of bacillary disease was
3.0 per 1,000 (Gothi et al, 1976). In Bangalore
city in a small slum population a low prevalence
of bacillary disease (2.6 per 1,000) was reported
(Chakarborty et al, 1979). The low prevalence
in the city slums is probably a reflection of the
better epidemiological situation in Bangalore,
a fact which was also marked in the ICMR
(1959) survey.
Since radiological and bacteriological examination
of children below 5 years is impracticable,
no authentic information on prevalence
of respiratory disease in this age group is
available. However, judging from the infection
rates it can be safely presumed that prevalence
of disease too must be low. Prevalence of disease
(including primary disease) in the age group
5 to 14 years in the rural population of
Bangalore was reported as 0.3% (bacillary
disease 0.1%) by Gothi et al (1972). Similar
figures for Chingleput rural area (TPT, 1980)
in the 10 to 14 years age group were 0.36%
(bacillary, 0.04%). Prevalence, in general, was
somewhat higher among male children. The
surprising finding was that although the prevalence
of infection in the 10 to 14 years age
group in Chingleput was almost twice that
in Balgalore rural area, the morbidity rates were
not different.
It was also found that children with large
tuberculin test reactions (greater than 20 mm,
1 TU PPD-S with RT 23) had more disease
than those with small induration. As expected,
the prevalence of respiratory TB in children
was much less than among adults.
Although extra-pulmonary tuberculosis is
believed to be more common in children than
adults, no authentic information about its
prevalence is available from any large scale
community survey. A study carried out in the
slum population of Bangalore (Gothi et al,
1974), in which all systems of the total child
population were examined, showed a very low
prevalence of all manifestations of tuberculosis
(0.35%) in the age group 0 to 14 years.
Incidence of disease
Incidence of bacillary disease is defined as
the number of new bacillary cases occurring
annually at subsequent re-examination among
1,000 persons either with normal chest x-ray
or healed x-ray abnormality but bacteriologically
negative at the previous examination (NTI,
1974). The incidence of abacillary disease is
the number of new radiologically active but
bacteriologically negative cases arising annually
among 1,000 persons with a normal chest x-ray
at an earlier examination.
Information regarding incidence of tuberculosis
is available from four areas of the
country, Madanapalle, Delhi, Bangalore and
Chingleput. In the congested areas of Delhi,
the overall annual incidence of bacteriologically
confirmed tuberculosis was found to be 1.3 %
per year (Pamra et al, 1973, Goyal et al, 1978).
In rural area of Bangalore (NTI, 1974) the
rate varied from 0.9 to 1.3 per 1,000 per year.
Frimodt-Moller reported an incidence of 1.3
per 1,000 per year in the rural population of
Madanapalle. On the other hand, Tuberculosis
Prevention Trial (1980) has shown a very
high annual incidence of 2.5 per 1,000 between
the first two surveys carried out in Chingleput.
In all areas, incidence of bacillary disease
was higher among males than in females. All
four studies had shown a rising incidence with
age for both sexes. Of the total ‘incidence’
cases arising more than half were contributed
by persons more than 35 years of age among
males and less than 35 years of age among
females.
In the Delhi study (Goyal et al, 1978) the
incidence of abacillary disease among previously
healthy persons was found to vary from 1.5 to
3.8 per 1,000 per year at different periods,
whereas in Madanapalle it was of the order of
4 per 1,000 per year. The follow up of persons
with healed inactive disease in Delhi showed
that their breakdown rates varied considerably
from One period to another, the rate of fresh
bacillary disease ranging from 4 per 1,000 to
14 per 1,000 per year and of active abacillary
disease from 7 per 1,000 to 21 per 1,000 per
year between 1962 and 1967.
Also worth reporting is a study carried
out by New Delhi TB Centre in Delhi Police
(Sikand et al, 1959). It was found that in this
group an average of 7.8 per 1,000 previously
healthy persons (obviously all adults) broke
down every year with tuberculosis, either
bacillary or abacillary.
Ind. J. Tub., Vol. XXIX, No. 3

140 G.D. GOTHI
Gothi et al (1978) analysed the breakdown
rate among previously healthy persons according
to size of tuberculin reaction. They found
that among non-reactors (0 to 9 mm), 0.41 per
1,000 per year developed bacillary disease
whereas among reactors (10 mm or more), the
rate was 1.73 per 1,000 per year. The annual
incidence rate among persons with normal
x-ray chest and a tuberculin reaction between
10 and 19 mm was lowest (0.27 per 1,000).
It was highest (1.9 per 1,000) among those
with a tuberculin reaction of 20 mm or more
(NTI, 1974).
The follow up of persons with inactive
tuberculous or non-tuberculous lesions in the
same population (Gothi et al, 1978) showed
that 3.73 per 1,000 developed bacillary disease
every year. It was also found that among untreated
persons with radiologically active or
probably active tuberculous lesions the annual
breakdown to bacillary disease was 26 per
1,000. An analysis of the total bacillary
‘incidence cases, showed that 76% arose from
the group of previous tuberculin positives. The
population with normal chest x-ray at an
earlier examination contributed 48% of the
total new bacillary cases.
Krishnamurthy et al (1976) found that
the attack rate of disease among recently infected
persons was 7 times higher than among
those infected for more than 9 months.
However, of the total new cases, 72% arose
from the previously infected population, a
finding which corroborates the results obtained
by Frimodt-Moller (1960) and several other
workers in other countries.
Raj Narain et al (1972) & Gothi et al (1976)
calculated the annual incidence of bacillary
disease among persons with low grade tuberculin
sensitivity (reaction O to 9 mm to 1 TU
PPD RT 23 but more than 10 mm in the former
and 8 mm in the latter study to 20 TU) which
is presumed to be due to infection with Mycobacteria
other than tuberculosis. The five
year incidence in this group was found to be
1.4 per 1,000 which was significantly lower
than among reactors to 1 TU PPD RT 23
(10.8 per 1,000 per year). Among non-reactors
to 20 TU PPD RT 23 it was 2.6 per 1,000
(Gothi et al. 1976).
A point of some importance is the length
of interval between two consecutive surveys
in longitudinal studies. In the studies reported
above the intervals varied from one to 2½
years. While calculating incidence rates between
any two surveys one always takes into account
symptomatic breakdowns occurring during the
Ind. J, Tub., Vol. XXIX, No. 3
interval. However, it is not inconceivable that,
if the interval is long, some cases may develop
the disease and die or get cured without treatment
and thus miss being counted in the calculation
of incidence rates. To that extent,
calculation of incidence rates from longitudinal
surveys could be regarded, theoretically, as an
under-estimate. To assess the extent of this
possible under-estimate, Gothi et al (1978)
carried out a study in Bangalore rural population
in which a group of 30,576 was examined
after a short interval of 3 months. The incidence
during the 3-month period was .99 per 1,000
as against the reported annual incidence rates
of 1.3 per 1,000 in some other studies (Frimodt-
Moller, 1976; Pamra et al, 1978; NTI, 1974).
From this, it would appear that there is probably
a significant imprecision in the estimates of
annual incidence as calculated in the studies
referred to above, in which re-examination of
population was carried out after long intervals.
Another possible source of error is the fact
that the second survey may bring to light healed
lesions among persons who had a clear x-ray
at the first survey. Such persons must have had
active disease sometime between the surveys
and must not be ignored while calculating
incidence rates.
Incidence of disease among children is a
parameter of special interest. Gothi et al (1972)
reported the incidence in 5 to 9 year and 10 to
14 year age groups as 0.5 and 1.0 per 1.000
respectively. Children with a large tuberculin
reaction (>20 mm) were found to have a higher
incidence as also those who had been newly
infected between the two surveys. It is possible
that the newly infected lack resistance with the
result that containment of infection takes a
long time and disease manifests itself within
a short period after infection leading to high
morbidity and mortality. New disease was
also seen among children who continued to
remain non-reactors to tuberculin. A plausible
reason for such findings could be (i) tuberculin
test being given in pre-allergic phase or (ii)
overwhelming infection which suppressed the
hypersensitivity.
Narmada et al (1977) reported an incidence
of 2.8 per 1,000 per year in the age group 0-12
years in a congested area of Madras and 1.2
per 1,000 per year among the non-infected and
8.8 per 1,000 per year among the infected.
The high rates in this population reflect the
unhygienic conditions as well as the chances
of acquiring massive and repeated super-infection
among children of poor nutritional status.
The low rates prevalence and incidence
of infection and disease suggest that respiratory

EPIDEMIOLOGY OF TUBERCULOSIS IN INDIA 141
‘
tuberculosis is not a major problem of childhood.
However, it appears that recently infected
children and those with a strong tuberculin
reaction have higher risk of developing disease
and dying of it.
Tuberculosis mortality
In the absence of notification regarding
cause of death, very little is known about
tuberculosis mortality rates in India. One of
the earliest reports on the subject is by Sir
Leonard Roger (quoted by Lankaster, 1920)
who, on the basis of 22 years’ post-mortem
records of Calcutta, concluded that 17% of
the total deaths were due to tuberculosis and
estimated the annual tuberculosis mortality
as 800 per 100,000 of population. Lankaster
(1920) on the basis of Roger’s data and some
other available information reported that
Ahmedabad had an annual tuberculosis mortality
of 591 per 100,000 and put forward a speculative
estimate of at least 400 per 100,000 per year
for most Indian cities. Benjamin et al
(1949) on the basis of the Saidapet study put
the estimate at 462 per 100,000. McDougal
(1949) estimated the annual mortality in India
at about 200 per 100,000 and in the same year,
Frimodt-Moller arrived at a rate of 253 per
100,000 on the basis of Madanapalle study.
Frimodt-Moller (1960) reported that tuberculosis
mortality in the area declined from 64
per 100,000 in 1953-54 to 21 per 100,000 in
1954-55. The marked reduction was probably
due to incomplete recording of deaths as natural
decline and intensive treatment could not have
achieved it in so short a time.
Chakarborty et al (1978), from data collected in
Bangalore area estimated the mortality rate at
84 per 100,000 and further found that the rate
was higher in males and in the older age groups,
(a finding which corroborates earlier results of
Frimodt-Moller, 1960). Among females the
highest mortality was in the age group 30 to 39
years. It may be mentioned that data collected
in the Bangalore area represented the natural
trend since anti-TB services could not be
provided in the area concerned. Goyal et al
(1978) reported an annual mortality rate of
about 40 per 100,000 in a congested area of
Delhi where good domiciliary treatment service
was provided. It must, however, be pointed out
that in this calculation no correction was made
for any possible deaths due to non-tuberculous
conditions among tuberculous patients who
died.
Even taking into account the varying reliability
of the data collected at different periods
of time by different workers, there is little doubt
that tuberculosis mortality is much less to day
than it was in the forties. It is however not
possible to comment on the factors responsible
for the decline which could be due to one or
more factors such as (i) natural decline as a
result of increased resistance and socio-economic
betterment, (ii) availability of more effective
specific anti-TB measures or (iii) increase in
the number of patients coming forward for
treatment in the wake of efficient chemotherapy.
Little is known about tuberculosis mortality
in children. Raj Narain (1975) compared the
crude mortality rates among infected and noninfected
children on the assumption that the
differences in the two could be ascribed to tuberculosis.
Tuberculosis mortality among children
aged 1 to 4 years on this assumption was found
to be 5.5, 5.2 and 23.9 per 10,000 children in
rural Bangalore, Chingleput and Choolai
city area of Madras respectively. The mortality
rate was significantly higher among children
with a tuberculin reaction of 20 mm or more,
specially in the O to 4 years age group. Raju
et al (1971) reported a higher mortality rate
among infected compared to non-infected
children below 5 years. Gothi et al (1972)
reported that of the total deaths from any
cause in the age group O to 14 years, 19%
could be ascribed to TB.
INH resistance
In recent years, a new index has been added
to the usual indices employed for assessing the
tuberculosis situation in any community. This
is the prevalence of primary drug resistance
(specially to INH) in any community. Although
a number of antimicrobial drugs have been
in use during the last 30 years, INH is, for
several reasons, the most important and widely
used of all the drugs and forms part of all regimens
being prescribed anywhere. Primary
resistance to INH may be regarded mainly as
a consequence of unsatisfactory therapy of
infectors (the only other reason being mutation
of bacilli) and is a reflection on the quality of
anti-TB services provided to the community
and availed of by the patients. Although the
significance of INH resistance is still a moot
point, yet the prevalence of primary resistance
in the community is now considered a factor
of considerable epidemiological importance.
As in the case of other indices there is
considerable lack of uniformity in the data
available. This arises due to a number of factors
such as (i) differences in the techniques used
and standards adopted for defining drug resistance
and (ii) difference in the care taken to
elicit history of previous treatment.
Ind. J. Tub., Vol. XXIX, No. 3

142 G.D. GOTHI
Findings on the subject have been reported
by different workers. Frimodt-Moller (1962)
found INH resistant strains in 6% of the untreated
sputum positive patients in Madanapalle
area. Parthasarthy et al (1967) estimated the
prevalence of disease with primary INH resistant
strains as 0.9 and 0.8 per 10,000 in the rural
population of Rayachoty and Madanapalle
respectively and in Madanapalle town, 6 per
10,000. In the rural areas of Bangalore, Raj
Narain et al (1967) reported prevalence of
INH resistance among bacteriologically confirmed
cases as 12%, 15.4% and 25.4% during 3
surveys carried out between 1961 and 1966.
One fourth of these were considered as primary
resistance. However due to unreliable history
of previous treatment this finding can be
considered questionable.
A number of reports are available regarding
prevalence of INH resistant strains among
persons reporting for treatment. Menon (1963)
reported a figure of 15% from Hyderabad
which in the subsequent year rose to 21 %
(Menon, 1964); Pamra (1967) reported a figure
of 14.1 % from Delhi. Rao et al (1967) reported
that among sanatorium patients, 53.7% were
INH resistant, the corresponding figure in
patients attending a clinic being 27.5% in
rural primary health centre, 32.5%, in selective
house to house case finding programme in rural
areas, 15.5%, and in general population surveys,
11.2%. The history of their previous treatment
was not reported.
In 1967, Gangadharam reported the results
of a co-operative investigation sponsored by
the ICMR among previously untreated patients
attending 9 urban clinics in the country situated
in Delhi, Bombay, Calcutta, Madras, Bangalore,
Patna, Nagpur, Hyderabad and Amritsar.
Among untreated patients the overall figure
for INH resistant strains was 16%. Among
treated patients the corresponding figure was
46%, nearly three times as high as in untreated.
It may be worth pointing out that history
of previous treatment was probably not uniformly
reliable in this investigation.
In the longitudinal surveys carried out by
NTI in rural areas, the proportion of sputum
positive patients with INH resistant strains
rose from 11.2% at the first survey to 21.6%
at the 4th survey. The increase was ascribed
to longer survival of the resistant cases of earlier
surveys and the emergence of resistant strains
due to insufficient treatment among those who
had earlier shown sensitive strains. Among the
newly discovered (‘incidence’) cases the percentage
with INH resistant strains during three
successive inter-survey periods was 11.4 %,
Ind. J. Tub., Vol. XXIX, No. 3
10.0% and 6.4% whereas in the Delhi study
there was no significant change in the primary
resistance pattern over a 15 years’ period.
Fate of TB patients in the community
The rural population of Bangalore was
surveyed 4 times during a period of 5 years
at an -interval of 1J and 2 years. The patients
discovered in this study could not be offered
treatment for want of resources and facilities.
Pamra (1966) and Goyal et al (1978) have also
reported on the fate of cases from their longitudinal
study conducted in a congested city
area of Delhi. In this study all patients discovered
were offered good intensive ambulatory
domiciliary treatment. Another study by
Frimodt-Moller (1961) gave similar data about
the rural area of Madanapalle distinct where
too the patients were provided satisfactory
service. Raj Narain reported a tuberculosis
case fatality of 34% and sputum conversion of
11 % in patients 1½ years after the first survey;
24% continued to remain positive. The fate
of direct smear positive culture negative patients
was somewhat better, death rate being 18.4%.
A 5 year study reported by NTI (1974)
shows that of the 178 sputum positive patients,
126 could be followed up. Of these 49.2%
died, 18.3% continued to remain bacillary and
sputa of 32.5% became negative. Death rates
were reported to be highest during the initial
1½ years period of observation; subsequent
survivors continued to live longer and remained
bacillary. Of the new sputum positive cases
discovered during subsequent surveys amongst
the abacillary population of the first survey,
sputum conversion rate during the 1½ years
was 52%, mortality 14.3%; 33.3% remained
sputum positive. The fate of old cases of
previous surveys which were considered as
‘prevalence cases’ was poorer than that of new
cases discovered in the subsequent surveys.
Frimodt-Moller, on the basis of the longitudinal
survey, reported a high mortality
(31.1%) amongst advanced cases in a year;
18% improved. It was further seen that the
mortality in the other category of cases was less.
As for the fate of patients of doubtful activity
judged to be not requiring treatment, 7 to 8 %
developed active disease and 13% showed
clearing of the lesion whereas of the persons
with inactive disease, 1 % developed active or
probably active disease. The overall intensive
treatment given to the patients for a period
of about 1 year in the rural areas by Frimodt-
Moller did not show any change in the tuberculosis
prevalence over a period of 5 years.

EPIDEMIOLOGY OF TUBERCULOSIS IN INDIA 143
He reported the same prevalence rates in the
‘treated towns’ as in the ‘untreated
towns’.
Patients discovered in Delhi longitudinal
surveys were offered treatment under a good
domiciliary chemotherapy service. Of these
74 % became sputum negative, 15 % continued
to remain positive and 11 % died during a 2½
year follow up. The outlook for patients who
were regular in treatment improved but the
prevalence rates, even after good chemotherapy,
did not vary significantly over a period of
15 years.
The Delhi and Madanapalle studies have
shown the course of disease under good chemotherapy
in the community whereas the Bangalore
survey provides information on the natural
course of the disease among tuberculosis
patients without treatment. No change in the
prevalence of the disease in any of the three
areas suggests that probably there is something
other than treatment which is necessary for
making an impact on the problem of tuberculosis.
However, a good treatment service
brings down the mortality amongst sputum
positive cases considerably and also leads to
sputum conversion in a fairly large proportion
of patients even though 15 to 17 % continue
to remain bacillary.
Of the x-ray negative abacillary cases discovered
in the longitudinal survey at Bangalore
(Raj Narain 1966) 6% became sputum positive,
42% got well without any treatment, 26%
remained active abacillary and 5.2% died over
a period of 1 j years. For some patients followed
for a period of over 5 years, the fate was studied
by the NTI (unpublished data). It was observed
that over a period of 5 years, there was a mortality
rate of 26%, breakdown rate to sputum
positivity of 5% and cure rate of 29%. The
remaining 20% continued to have active abacillary
disease.
The fate of active abacillary cases reported
by Pamra and Goyal was found to be much
better under chemotherapy (cure rate of about
65% and death rate of about 5%). Sputum
positivity was not different in this material
as compared with that of the NTI material
where no treatment could be offered. Frimodt-
Moller (1960) found mortality rate of 13.1 %
in a year among x-ray cases with advanced
disease; improvement was recorded in 18%.
In other categories, namely, those with minimal
or moderately advanced disease, the mortality
was less. The comparison of Pamra’s findings
with the NTI observations points to the
achievements that are possible under Indian
conditions with and without good treatment
ment service. Somewhat poor outcome even
under good treatment service could be attributed
to low literacy, poverty etc. leading to incomplete
and irregular treatment.
Tuberculosis in Industry
The beginning of industrialization influences
the epidemiological curve of tuberculosis in
any country. Tuberculosis morbidity, at this
point, gets a sudden spurt due to urban influx,
over-crowding, insanitary living conditions,
hard work, poor nutrition and lack of rest and
recreation. The virgin population moving from
villages to cities gets infected and succumbs
quickly on account of poor resistance and
stresses and strains of urban life. Many of
these break down and contract tuberculosis,
migrate back to their villages carrying with
them infection and disease. With the passage
of time the immunologically deficient and
highly susceptible population is weeded out
further. As industrialization progresses, the
economic and environmental conditions of the
workers improve, helping them to build up
their health and acquire resistance against
infection, leading in course of time, to reduction
in morbidity. India during the last 3 decades
has been passing through this phase which may
account for any apparent decrease.
Apart from the usual hazards of urbanisation
and industrialization there are certain
industries, specially those involving risk of
inhalation of dust, fumes, gas and other respiratory
irritants etc. in which tuberculosis morbidity
is generally much higher than among nonindustrial
workers. Silica is known to alter
susceptibility to tuberculosis. Clinical studies,
animal experiments and surveys have shown
that silicosis lowers the resistance to tuberculosis.
Reports No. 3, 11 and 20 from the office
of the Chief Adviser of Factories indicate that
tuberculosis is a major cause of death and
disability among pottery and ceramic workers.
This is also corroborated by the Bihar Factory
Inspectorate, Labour Department, Government
of Bihar. A survey among coal mine workers
of Raniganj and Jharia also revealed a high
prevalence of tuberculosis among workers
who had pneumoconiosis. Deshmukh et al
(1967) reported a prevalence of 1.32% in coal
mines in Chanda district, no significant difference
being found between surface workers and
underground miners. These rates are not higher
than those in the general population. Several
surveys in coal mining industry have shown
a high prevalence of particles in the working
environment which have an adverse effect on
the lungs. Steel workers (Billimoria, 1967)
Ind. J. Tub., Vol. XXIX, No. 3

144 G.D. GOTHI
although working under unfavourable environmental
conditions did not have a particularly
high prevalence of pulmonary disease (2.57%)
which was not significantly different from
comparable economic and ethnic groups working
in other professions. According to Billimoria,
the environment, as far as steel industry is
concernad, has very little to do with the
incidence of tuberculosis.
Sikand and Raj Narain (1953) carried out
a survey among textile workers of Delhi and
found that the percentage varied between 2%
and 3%. This was higher than in the printing
industry (Government of India Press, Delhi)
which was also surveyed about the same time.
The rates were also higher than the overall
rate for Faridabad township but since the latter
contains all age-groups, a direct comparison
may be misleading and only age-specific morbidity
rate would be comparable. Patel (1967)
reported a high prevalence (160 per 1,000)
of tuberculosis among textile workers of
Ahmedabad. However, the authenticity of this
finding is questionable since the diagnosis
was based only on radiology and very few
bacteriological specimens were examined.
On the other hand, Gupta and Kulkarni (1963)
in a small scale survey of textile workers in
Ahmedabad found a prevalence of 186 per
1,000 in the spinning department and 147
per 1,000 in weaving and other departments.
These findings are unexpectedly high. Sikand
and Raj Narain (1953) and Gupta and Kulkarni
(1963) reported a higher prevalence among persons
who had worked in the industry for longer
periods. This could of course be a reflection of
the higher morbidity rate among older persons
who would, naturally, have a longer duration
of service.
The prevalence of tuberculosis among bidi
workers as reported by Deshmukh (1967)
was fairly high i.e. 3.9% (5.6% among females
and 3.1% among males). The high morbidity
in this group may be attributed to poor socioeconomic
conditions, lack of facilities for
employment, medical examination and subsequent
medical care, and insanitary working
environment besides the fact that being sedentary
and not requiring any particular skill,
the job attracts the already physically weak
persons.
Tuberculosis trends
As in the case of other infectious diseases,
the epidemic curve of tuberculosis follows
a definite course over a period of time. The
morbidity and mortality curves are composed
of two unequal segments, one a short steep
Ind. J. Tub., Vol. XXIX, No. 3
ascending and the other a long slow descending
limb interposed with a plateau. Unlike acute
diseases which have a short time span, the
epidemic curve of tuberculosis is spread over
several centuries with the result that changes
over a short period, say 10 or 20 years, cannot
be perceived.
Information on tuberculosis trends is
obviously of vital importance for planning a
control programme. In the absence of notification
data, reliance has to be placed once more
on repeated tuberculosis surveys or epidemetric
models for providing data regarding tuberculosis
trends.
The decline of tuberculosis in almost all
developed countries had started even before
the application of specific control measures;
the morbidity and mortality had reached a
low level on the descending limb of the tuberculosis
epidemic curve (Grigg, 1958). The
factors that influence the trend of tuberculosis
in any country are (i) changes in the socioeconomic
conditions (ii) the rate and extent
of tuberculinization of the population (iii)
immigration and emigration (iv) war and pestilence
(v) industrialization (vi) prevalence level
of disease and infection (vii) specific anti-TB
measures.
Some limited data are available from repeat
surveys carried out in general population groups
as well as selected groups by several workers
in various regions of the country. Some of
these are summarised below.
In a selected group in Delhi comprising
Delhi Police, Government Press employees
etc., Sikand and Raj Narain (1954 & 1959)
did not find any change in the prevalence of
bacillary disease over a 15 months period.
The overall abacillary disease at two surveys
was 1.5% & 2.0% respectively. It may be pointed
out that the group survey consisted entirely
of adults.
In a 5 year study of 15 villages (population:
9,537) in Karnataka, Raj Narain (1962) did
not find any change in the prevalence of bacillary
disease (4.3% in 1956, 4.5% in 1961). The
prevalence of abacillary active disease at the
two points was 1.7% and 1.8% respectively.
Reviewing the various studies carried out
in differents parts of the country, specially
the 3 longitudinal studies in Madanapalle,
Delhi and Bangalore, there does not appear
to be any discernible change in the overall
prevalence of disease. The prevalence of
bacillary disease which was around 4 per 1,000

EPIDEMIOLOGY OF TUBERCULOSIS IN INDIA 145
in the middle fifties continued to remain at
almost the same level till about 1974. Frimodt-
Moller (1960) observed a lower prevalence
of active disease in younger age in the 1955
survey as compared to the 1950 survey. Similar
reduction in the disease prevalence and incidence
were reported by Pamra (1973) and NTI (1974)
for age group “5 to 34” years although the
differences were not very marked. The longitudinal
survey conducted by NTI showed a
significant decline in the prevalence of infection
in the O to 24 years age group and incidence
of infection for all ages over a period of 5
years. In almost all surveys very little tuberculous
infection was reported in younger children
below 5 years of age. This observation was
corroborated by Gothi et al (1978) who surveyed
a slum population of Bangalore city.
The slight fall in the prevalence and incidence
of infection and morbidity in the younger age
group mentioned earlier is offset by the higher
incidence in older age group and their longer
survival than before. Probably due to chemotherapy,
there are a considerable number of
patients who are neither cured nor converted
but continue to survive, thus helping to maintain
the status quo in regard to tuberculosis prevalence.
From the Bangalore longitudinal study,
where treatment facilities were non-existent,
it was found that nearly 20 % of bacillary cases
die every year, which may be a social failure
but could be considered as an epidemiological
gain. Another 14% of the cases become
abacillary during the course of the year either
without any treatment or with sufficient treatment—an
epidemiological benefit. The depletion
of these 34% cases from the existing pool is
however made up by the fresh incidence of
disease from the healthy population. The
prevalence rate of tuberculosis is thus maintained
from year to year at more or less the same
level. It is thus that inspite of various anti-TB
measures taken during the last 30 years, no
appreciable dent seems to have been made on
the problem.
Gradual problem reduction is possible
if a large scale war is waged against tuberculosis
by finding and treating a considerable proportion,
say at least 40% of the total cases every
year. However, no control measures can be
expected to give quick results (as, for example,
in the case of small pox) since almost half the
population is already infected and new cases
shall continue to arise from amongst these.
Improvement in environmental conditions,
nutrition, etc. will ultimately play a major role
in reducing the tuberculosis problem as was
the case in most western countries where rapid
decline started in late 19th century even before
effective specific control measures were applied.
It would thus appear that although there is
no consensus about the trend of tuberculosis
in our country, there is some indirect evidence
suggesting that the disease is entering the
endemic phase and is possibly on the decline.
This may be deduced from the following:
(i) fall in the prevalence of infection and disease
in the younger age groups in the longitudinal
surveys (ii) change in the clinical picture of
tuberculosis from the acute fulminating exudative
type of yester-year to a more chronic type
with milder symptoms and almost complete
absence of complications like TB meningitis,
enteritis, tumorous suppurative glands in the
neck (Sikand, 1958), (iii) less disease among
young people and in women, (iv) primary
infection and primary disease occurring with
equal frequency among adolescents and adults
and in early childhood. From the history of
tuberculosis in western countries it can be seen
that such changes in the pattern of disease
occur when disease is in the endemic phase and
on the decline. These surmises are also supported
by the fact that prevalence and incidence is
higher in the older age groups, specially males,
that prevalence in towns and villages is nearly
the same and that there is a wide gap between
infection and disease rates (40% and 0.4%
respectively). On the basis of these observations,
Nagpaul (1978) and Aneja (1979) have expressed
the opinion that the tuberculosis epidemic
in India is on the decline, probably slowly,
in view of the prevailing poverty, malnutrition
and over-crowding.
Epidemetric Models
One of the main purposes of epidemiological
studies is to make predictions about tuberculosis
trends in future from past trends. This
cannot be done by considering prevalence,
incidence or mortality rates etc. piecemeal.
An overall view can best be had by the use of
suitable epidemetric models. This, however,
requires accurate or near-accurate calculation
of a large number of ‘transfer rates’ from
one epidemiological group to another. It is not
often that reliable data for such studies are
available from the same study and for this
reason not many reports on this subject are
available for India. Waaler et al (1974) have,
however, prepared a model based on the longitudinal
studies carried out by NTI (1974) and
Raj Narain et al (1963), The model indicates
that with case finding coverage of 30%, completion
of treatment by cases discovered and
with BCG vaccination coverage of 30% the
Ind. J. Tub., Vol. XXIX, No. 3

146 G.D. GOTHI
incidence of disease can be reduced by 26%
after 25 years whereas if measures to combat
the disease are not taken, the tuberculosis
problem is not likely to be reduced even after
100 years. On the other hand, with case finding
coverage of 66 % and treatment completion of
discovered cases the tuberculosis morbidity
could be brought down from 4 per 1,000 to
1 per 1,000 in 60 years.
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Ind. J. Tub., Vol. XXIX, No. 3

148 G.D.GOTHI
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Ind. J. Tub., Vol. XXIX, No. 3

WHY INTEGRATED TUBERCULOSIS PROGRAMMES HAVE NOT SUCCEEDED
AS PER EXPECTATIONS IN MANY DEVELOPING COUNTRIES—A
COLLECTION OF OBSERVATIONS 1
D.R. NAGPAUL 2
Summary : Hard work is still needed to make integrated tuberculosis services, and integration
in general, acceptable to health workers and to improve all the support systems for integrated
tuberculosis services to the extent that the envisioned fruits are borne simultaneously with the
introduction of these services through primary health care.
Now that case-finding and treatment for
tuberculosis are being considered for introduction
into primary health care, it is relevant
that the experience gained from integration of
vertical tuberculosis programmes into the
general health service be reviewed critically.
It would be unwise to let the problems and
weaknesses of integrated national tuberculosis
programmes (NTP) flow into the new emerging
primary health care system without batting an
eyelash.
It could be stated at the outset, and with due
emphasis, that there really is no alternative
to an integrated tuberculosis service, all its
drawbacks notwithstanding. The point at issue
is that the present form of integrated TNPs
need not necessarily be the basis of application
of tuberculosis control technology through
primary health care.
Success with integration has been patchy so far
In the 1960s, when WHO started recommending
NTPs, especially for developing countries,
the epidemiological, socio-economic and operational
reasons in its favour were indeed compelling
(W.H.O. 1964, 1976). After over two
decades, it cannot be truthfully said that NTPs
have succeeded; nor that they have failed. The
old justifications have not changed since, but
the manner in which integration was brought
about has provided a fresh perspective.
It is true that a tuberculosis patient out in a
village has a much greater chance today than
before of being diagnosed and treated, but the
proportion being missed, misdiagnosed and
improperly treated is uncomfortably large.
And, it appears, nothing much is being done by
the integrated health services to correct the
situation. True again, that a newborn baby,
infant, or school entrant has a far greater
probability of getting BCG vaccinated under
the integrated health services, compared with
the BCG mass campaign days. But, vital aspects
like maintaining the potency of the vaccine
and proper vaccination technique were neglected
by general health workers to the extent
that some special programme aspects had to
be reintroduced under the Expanded Programme
on Immunization to make BCG meaningful.
In some countries even voluntary/private
agencies have joined hands with the government’s
integrated NTP but specialized institutions,
both under public and private sectors,
still maintain that they purvey a much superior
kind of tuberculosis service compared with what
general health institutions have to offer. A
degree of competition exists between general
and specialized health institutions in securing
preferential attention of the public, despite freeflowing
bilateral referral provided under the
NTP. This should be enough to confuse the
health workers and the public alike.
Integration is great to talk about
Health officials and workers often talk
about integration knowingly and with enthusiasm
but, like the talk about weather,
nobody does anything about it. The number
who “know” what is wrong with integration is
legion. But it is not for them to find out the
reason thereof and do something, albeit at
their own levels.
Compartmentalized thinking, attitudes, and
functioning abound at all the levels of the health
infrastructure. Strangely enough, those presently
charged with primary health care do not
appear to be above all this. To many, it is the
newest health technology and those not directly
involved could be kept at arm’s length. Is
primary health care gradually and unconsciously
being regarded as a new speciality?
Philosophy of integration is understood but not
really accepted
Integration is most visible in the grassroots
level rural health institutions because that
is where in the estimation of most health
1 Also issued as WHO/IUAT/JSG/BP/81’4 document.
2 WHO Medical Officer, WPRO, and formerly Director, National Tuberculosis Institute, Bangalore, India.
N.B. Views expressed in this article are the author’s own views--Editor.
Ind. J. Tub., Vol. XXIX, No. 3

150 D.R. NAGPAUL
officials, integration is most suited and needed.
In cities and higher levels of the health organization,
integration is either missing or cosmetic,
because it is regarded as unnecessary there.
Despite the welcome success of integration in
rural health institutions the attitudes and
practices of rural health staff are not always
helpful. Poor attitudes could be the reason for
the sizeable misdiagnosis and mistreatment in
respect of tuberculosis under the integrated
health service. By training and the examples of
peers, health workers face serious problems in
forming the needed attitude towards “integration.
Besides, integration conceptually is not
meant for rural areas alone. Attitudinal and
functional changes have to take place at all
levels of the health infrastructure, for success
even for the most peripheral level (W.H.O.
1965 and D.G.H.S. 1967).
The widespread covert non-acceptance of
integration at all levels is there, perhaps, because
integration cuts across the present-day medical
sociology and health services politics. The
apprehensions, insecurity, and confusion generated
by integration among health workers are
just too many. The absence of a strong logical
support to the fears is what is making the nonacceptance
covert and non-vocal.
Highly placed officials, who often exercise
disproportionately large influence on account
of expert clinical services rendered by them to
those in political power, are the ones espousing
the idea that integration needs to be confined
only to the rural health institutions; that people
need and are demanding the establishment of
many more specialized and prestigious centres
and that no country can afford to lower its
medical expertise and not have at least a few
centres equal to the best in the world. In this
way they try to meet the “threat” posed by
integration to their positions/prestige acquired
through a different system. The element of
truth in their statements conveniently is not put
in the perspective that could often be achieved
only by denying the simplest health services or
rendering second-class services to the millions
to provide what is first-class to a few. It is done
perhaps because it is a question of survival for
them.
The purpose of the above suggestion is not
to denigrate but to ascribe the often noted
“weak” political will behind many a public
health programme, the re-separation after the
passage of some years of departments, bureaux,
posts and functions that had been integrated
earlier, the continued opening of new tuberculosis
hospitals and centres when their nonessentiality
has been amply demonstrated, etc.
Ind. J. Tub., Vol. XXIX, No. 3
to just one causation, namely, non-acceptance
of integration. None can afford to be overly
critical or cynical. It is those, who are either
pushing forward integrated health services,
primary health care, etc. or have to sit in judgment
over their success, that must search their
minds. Must planning for the better health of
the people brush aside the felt-needs of the
professional staff who have to carry out the
plans?
Need for acceptability studies
At the time when integration of health
services was being recommended, a pilot project
or two in every country helped to demonstrate
to the local workers that the strategy is feasible
and works well. The mental walls appeared
much later. One after another even promising
NTPs got bogged down with difficulties. The
pilot project approach is also being used to
promote primary health care, to attain the goal
of “Health for All by Year 2000”. This is good,
but when will we learn that what is feasible is
not necessarily acceptable?
Time and effort must be spared now for
acceptability studies regarding integration. No
sooner had difficulties arisen with integration
in respect of NTP than health services research
should have examined its pragmatic basis.
Pragmatically planned programmes are essentially
short-term expedients, but for one reason
or another they succeed in eluding scientific
scrutiny for varying periods. If this note is
regarded as overly critical or unrealistic, pragmatism
will win once again.
This is not to suggest that nothing should
be done until the studies are completed. There
is also no denying that a long time is needed to
bring about a major change from specialization/high
technology of the vertical programmes
involving concentration of “line” and “staff”
functions in the hands of the same persons, to
the people-oriented integrated services with
stress on decentralization, prevention and costbenefit.
The points being made are that a
quarter of a century has elapsed and we do
not have unlimited time at our disposal since
primary health care services have to be pushed
forward now and that we are in a stalemate
with regard to integration and do not have
sufficient awareness as well as knowledge about
what to do.
There was inadequate preparation
A part of the blame for the poor attitudes
and practices among general health workers

WHY INTEGRATED TUBERCULOSIS PROGRAMMES 151
must be borne by those who had the responsibility
for bringing about integration. Compared
with what was demonstrated to them in pilot
projects, the preparations they made for the
extension phase were either deficient or grossly
inadequate, in order perhaps to attain the set”
extension targets. Some programme extensions
comprised merely an administrative order and
despatch of supplies. Training quite often was
improperly organized with the result that untrained
staff rendering the services, some trained
staff awaiting equipment and supplies long
enough to forget their training, and microscopes
lying around in packing cases for years,
were observed quite frequently. The seminars/
workshops that were organized for training
laid far more stress on technology and too
little on the change of attitudes. The people in
general were hardly prepared for the integrated
services and its enshrined referral system. It is
not clear how during the pilot phase the comparative
inadequacy of organizational/training
capabilities, available generally to tackle the
enormous task of extension, was not foreseen
and something done about it. It is hoped that
history will not repeat itself when it comes to
extension in respect of primary health care.
Other observations
Besides poor acceptability of integration,
and inadequate preparation for its implementation,
there is :
(a) unexplained, almost paralyzing, lack
of sustained interest/enthusiasm among
general health workers in respect of
tuberculosis services; perhaps some
other programmes as well. Compared
with acute diseases and physical injuries,
the beneficial results from tuberculosis
services do not become visible quickly,
which may lead to a general state of
disinterest. But, in some cultural milieu,
the apathy tends to disappear when a
family member, friend, or a person with
a “letter of reference” approaches for
the service, suggesting that a part of
the explanation is insufficient social
consciousness among health workers.
Therefore, the apathy needs looking
into and not merely explained away.
(b) Health workers are prone to regard the
functions connected with their “category
training” for entry into service as
“legitimate duty” and other duties
given to them as multipurpose workers
merely as “extra work”. This psycho
logy of extra work perhaps is behind
persistent demand for “incentive pay”
when other duties are entrusted to
them in the wake of integration, on the
grounds that they are overworked. A
number of studies has demonstrated
that all categories of health staff in
rural health centres, including medical
officers, are in fact under-utilized. Yet
the myth of overwork continues to
thrive, and is generally accepted. No
sooner are more hands provided to
help reduce the overwork, than the
staff tend to revert to the unipurpose
system of work, sometimes by private
arrangements among themselves. If
supervisors would not allow it openly,
they are ready to turn a blind eye
towards it.
Under some health programmes the
grant of incentive pay is permitted on
the grounds that health workers in
most developing countries get poor
salaries. There is no reason why health
workers should get less salary than
comparable other categories, but linking
this up with the aim of achieving
higher targets in respect of a high
priority health programme, which indisputably
leads to neglect of other
activities and duties in health institutions,
borders on the undesirable.
Ironically, in spite of the incentive pay
the achievements may turn out to be
fictitious if supervision is lax or cannot
be . exercised for a period. Primary
category training as “multipurpose
health worker”, to cover all the integrated
health duties as the terms of
service at entry, better salary, and good
supervision may resolve the problem.
(c) One of the reasons for NTPs not
succeedings as per expectations could
be that the expectations are unrealistic.
After all, these expectations are those
of the overseeing specialized workers
who are not really familiar with the
structure and dynamics of a general
health service. Replacement of population/prevalence-based
targets with
operational ones within the reach of
multipurpose health workers might
provide the answer.
(d) The “oil crisis” facing the world,
especially the developing countries, may
yet prove a blessing in disguise for the
integrated services. Parenthetically,
transport is an essential prerequisite
for implemtntors/supervisors of a public
health programme. The role of transport
Ind. J. Tub., Vol. XXIX, No. 3

152 D.R. NAGPAUL
as an image builder of health workers,
however, became apparent when attempts
were made to apply management
principles leading to the optimal use
of all roadworthy vehicles belonging
to any health programme in an area.
Marked reluctance was observed for
programme functionaries to travel by
public transport when necessary,
share the vehicle with others from
sister health programmes, and agree
to the allocation of roadworthy transport
according to optimal utilization
and not merely status of those using
them. The most frequent reaction to
“pooling of vehicles” practice was for
the supervisors to forego supervision
duty on one plea or another. Now,
with increasing problems of maintenance
of vehicles and rising price of
gasoline, coupled with insufficient
budgets for supervisory travel, a pattern
of small radius supervision exercised
from each successive level in a
step-ladder fashion might help resolve
the problem.
(e) The supervision of NTPs by general
health workers has been decidedly
infrequent, and at times even incorrect,
making it altogether grossly insufficient.
Quite often, there is great enthusiasm
at the time of introduction of integrated
tuberculosis services in a health centre,
but very soon hardly any case-finding
or treatment are left to be seen, as if
the service had never been introduced
at all. The specialized “staff” officers
in the higher levels often try to correct
the situation by exercising supervision
at all levels, which is obviously an
impracticable proposition. Tf proper
supervision of integrated tuberculosis
services by the general health service
“line” officers cannot be expected at
present, it would take a long time to
make tuberculosis services meaningful
under primary health care.
Not by studies alone
An impression might have been given that
nothing could be done to correct the present
not so satisfactory position of NTPs until the
operational studies have been completed. That
technology of tuberculosis control has reached
the peripheral level is a gain which should not
be thrown to the winds while awaiting scientific
studies. Until then, the status quo should
continue with whatever could be done to
improve poor attitudes, weak programme support
systems, inadequate training and super-
vision, and the general climate of confusion and
apathy. No cut-and-dried solutions for the
interregnum are offered on purpose, not because
it is not possible to offer some suggestions. The
temptation has been resisted. If the earlier
pragmatism and successful pilot projects did
not quite succeed, more time should not be
lost in trying some new pragmatic solutions,
thus tinkering with the problems instead of
tackling them systematically.
Tuberculosis control technology and philosophy
of primary health care
However, there is one basic point between
NTPs and the primary health care systems that
needs a pragmatic rationalization now. Under
the philosophy of primary health care, people
have the right and duty individually and collectively
to participate in the planning and
implementation of their health care activities.
It has to be remembered, however, that at
times people’s perception of the health “threats”
facing them and their participation in meeting
the hazards has to be moulded through health
education. Tuberculosis and leprosy have a
long history of “stigma” which even today
makes individuals and families deny that the
hazard exists for them. They may agree to
these diseases being a community problem, to
which they may accord a low priority. True,
comparatively fewer persons in the community
are afflicted with tuberculosis, but those few
suffer a lot more than others having most other
diseases (Nagpaul et al, 1966). And, before
dying, they infect healthy contacts—about ten
in the case of tuberculosis—who may develop
the disease much later. There has to be a kind
of understanding, at this stage, on the point of
educating the public suitably, because faced
with the enormous and difficult task of ushering
primary health care in the context of a low
perception of tuberculosis as a health hazard,
whatever gains NTPs have already registered,
may be allowed to wither away. That would
mean a real failure of integration.
REFERENCES
1. Directorate General of Health Services, Govern
ment of India, New Delhi; Committee on Integra
tion of Health Services. Report; 1967.
2. Nagpaul, D.R. et al; Suffering in tuberculosis :
Proceedings of Tuberculosis and Chest Diseases
Workers Conference, Hyderabad, India; 1966.
3. WHO Expert Committee on Tuberculosis. Eighth
Report; Tech. Rep. Ser. 290, 1964;
4. WHO Study Group on Integration of Mass
Campaigns against Specific Diseases into General
Health Services. Report; Tech. Rep. Ser. 294; 1965.
5. WHO Expert Committee on Tuberculosis. Ninth
Report; Tech. Rep. Ser. 552; 1976.
Ind. J. Tub., Vol. XXIX, No. 3

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA:
REPORT ON FIVE SURVEYS
A.K. CHAKRABORTY 1 H. SLNGH 2 K. SRIKANTAN 3 K.R. RANGASWAMY 4 M.S.
KR1SHNAMURTHY 8 AND J.A. STEPHEN 6
Summary : The trend of tuberculosis in a sample of 22 villages observed over a period of about 16
years (1961-77). is reported. Distributions of tuberculin indurations did not show a clear cut demarcation
between infected and non-infected. The choice of demarcation level, therefore, is somewhat
arbitrarily made on the basis of the distributions and these varied from survey to survey; between 10
mm at survey I and 16 mm at survey V. The method adopted to demarcate the cut off point has been
described in detail. The actual and standardised infection rates showed more or less declining trend
in 0-4 years, 5-9 years and 10-14 years age groups, The prevalence of cases was not significantly different
from survey to survey (varying from 3.96 to 4.92 per thousand from first to fifth survey). However,
there was a shift in the mean age of cases, and better survival rate of cases diagnosed at later
surveys.
Introduction
For the study of epidemiology of tuberculosis,
it is necessary to obtain information
on its long-term trend, either natural or following
the control programme. In the absence of a
well distributed, adequate and reliable diagnostic
service and reporting system for pulmonary
tuberculosis in India, data on the disease
compiled from the records and reports available
with the health services cannot be considered
representative of the community situation. The
house to house surveys, repeated at intervals
in the population of the same geographical
area, therefore, form the principal means to
study the trend of the disease. However, repeated
surveys in a systematically selected
countrywide sample of population, required
to study the trend of infection and disease, can
be considered a virtual impossibility under the
existing conditions in India; even the one time
prevalence survey has not yet been carried out
for the entire population till todate. The information
on the trend of the tuberculosis
situation in India is therefore usually obtained
from the few isolated repeat surveys conducted
in some areas (Frimodt Moller 1960, NT!
1974, Goyal et al 1978, Gothi et al 1979),
problems of extrapolation of the findings to the
country as a whole notwithstanding.
One such epidemiological study conducted
four times in a period of 5 years among a rural
population of Bangalore district, South India
from 1961-68 (NTI, 1974) has indicated a dec-
line in prevalence rates of infection in the age
groups 0-14 and 15-24 years and in its incidence
in overall as well as in 0-34 years. The prevalence
and incidence of bacteriologically proven
disease also showed a decline among population
aged 5-14 and 5-34 years, during first
three surveys. This trend appeared to be arrested
during the last survey, presumed to have been
caused by conditions of deprivation in the
population consequent upon a severe drought
in the study area.
The data on prevalence and incidence of
infection and disease obtained from the above
study have since been purposefully utilised in
order to project and study the long-term disease
trend in the population by constructing epidemetric
models (Waaler et al 1974, Nair 1977).
Nevertheless, the rather brief period of the
study coupled with the uncertainty about the
observation caused by drought before the last
survey, may not permit firm conclusions to be
drawn regarding a secular trend of the disease
from the study material itself. Moreover, the
projections and conclusions drawn from the
model may require revision on the basis of
further actual observations obtained through
surveys of the population of the same geographical
area from time to time.
Objective
In view of the above, the present study was
designed to repeat the survey in the same geo-
1 Senior Medical Officer
2 Statistician
3 Sr Statistical Officer
4 Team Leader
5 Team Leader
6 Statistical Section
National Tuberculosis Institute. Bangalore
Ind. J. Tub., Vol. XXIX, No. 3

154 A.K. CHAKRABORTY et. al.,
graphical area as for the four surveys between
1961 and 68 (NTI, 1974) to:
(A) obtain information on:
(i) prevalence of infection & bacillary
case
(ii) fate of the bacillary cases
(B) study changes in tuberculosis situation
over a period of about 16 years, in terms of
changes in prevalence rates of infection and
cases.
Study Area & Population
In 1961 the selection of the villages for the
study of dynamics of tuberculosis was made in
such a manner that independent samples were
drawn, consisting of 22 and 119 villages, the
former also forming part of the succeeding
sample. The population in the bigger sample of
119 villages was surveyed four times between
1961-68. While planning survey V, it was intended
to cover 119 villages, material from
which has been reported already (NTI, 1974).
However, owing to paucity of resources, it was
decided to stop the survey after completing
work in the sample of 22 villages only.
The material reported here is thus obtained
from a survey carried out in 1977-78 among the
population in a random sample of 22 villages
of the 3 taluks (sub-divisions) of Magadi,
Channapatna and Nelamanagala in Bangalore
district of South India. The data pertaining to
the V survey have been compared with those
from earlier four surveys in respect of the
22 villages only. The population registered for
the 22 villages was 3% of the total population
in 3 taluks in 1961 and 2.6% in 1977. Till 1975,
no organized anti-tuberculosis services were
available in the area in the form of diagnosis
and treatment of tuberculosis cases and BCG
vaccination of susceptible population. Such
services were also not offered to the population
by the survey teams. The District Tuberculosis
Programme was implemented in the area only
in 1973, following which antituberculosis
services were generally available through dispensaries
in the area and direct mass BCG
vaccination was started for the first time.
Time Table for the Surveys
The data collection for the survey V was
completed in a year and half starting from
February 1977. The interval between the IV
and V surveys was 11 years and that between
I and V surveys was nearly 16 years. The order
in which the villages were surveyed earlier was
unchanged at survey V.
Method
The entire population in each of the 22
villages was registered on individual cards by
visiting them in their houses. Each registered
person was invited 1o attend the examination
centre set up for the day at a convenient place
in the village for tuberculin test and X-ray.
On attending the centre, he was identified with
the help of the card prepared and both his
shoulders were examined for BCG scar. Persons
for whom the minimum examinations for BCG
scar were carried out, formed the ‘response
group’, as distinct from the ‘non-response
group’, who did not present themselves for the
scar reading. Each person was given a tuberculin
test with 1 TU RT 23 with Tween 80 on
the upper third of the dorsal aspect of the
right forearm, a site previously not used for
testing. After the test he was subjected to a
70 mm miniature X-ray of chest.
The induration to tuberculin test was read
by a trained reader between 72-96 hours of
testing, by visiting the persons in their homes.
Longitudinal diameter was measured and the
measurement entered on the respective card.
The tuberculin tester and readers were the same
only for last two surveys. However, the testers
and readers for all the surveys had similar
training and assessment at the NTI before they
undertook testing/reading in the surveys.
The X-rays were interpreted, as in the
previous surveys (NTI, 1974) by two readers
and an umpire. Persons with any chest X-ray
abnormalities were eligible for sputum collection.
Sputum was also collected from persons
who were diagnosed as cases in any of the
previous surveys.
Sputum samples were processed, cultured
and examined at the NTI, following techniques
identical to those adopted at the earlier four
surveys (NTI, 1974). These were examined by
fluorescence microscopy and Ziehl Neelsen
techniques, homogenised with 4% NaOH and
cultured on LJ medium slopes. A person with
positive culture and satisfying identification
test criteria of Mycobacterium tuberculosis was
diagnosed as a case, provided he also had a
chest X-ray abnormality at the current survey
(‘cases’).
Material
Registered population
Age sex distribution of the registered popu-
Ind. J. Tub., Vol. XXIX, No. 3

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA 155
lation in the five surveys reveals significant
differences here and there between age composition
from survey to survey, which did not
indicate an overall pattern and were generally
small in magnitude (Table not presented). There
was an overall increase in the population in
about 11 years after the survey IV at the growth
rate of 1.82 % per year. It was 1.23 per year for
the entire period of 16 years, lack of population
increase between II and IV surveys being the
reason for the observed lower values for the
entire period.
The permanent residents (de jure population)
in the villages constituted between 95 and 98 %
of the total population (Table 1). Their age and
sex composition was different from survey to
survey and children aged 0-9 years were significantly
less in proportion at survey V (P <
0.05) compared to any other survey (Table not
presented).
Coverages
Whereas all registered persons in the villages
were eligible for tuberculin testing and reading,
only those aged 5 years and over were eligible
for X-ray examination. Only the persons with
chest X-ray abnormality were eligible for sputum
collection and such eligibles were found to
be the lowest (6.6%) during survey V. The
proportions of X-rayed persons who were found
eligible for sputum collection were 9.6 %, 15.3 %,
17.9% and 10.7% at survey I, II, III and IV
respectively.
Coverages for tuberculin test reading, X-ray
and sputum examination of eligibles were
uniformly high in all the surveys. Coverages for
tuberculin testing and reading (86.4%) and for
X-ray examination (89.0%) were highest in I
survey and coverage of sputum collection among
the eligibles were the highest (97.5%) in V
survey.
Population with BCG scars
As mentioned earlier, persons for whom the
minimum investigation of reading of the BCG
scar was carried out were taken as the response
group. Overall size of response groups ranged
in five surveys from 91 % (I survey) to 84.8%
(III survey) of the de jure population.
De jure population without BCG scars
have been taken up for detailed analysis in this
report for calculation of prevalence rates.
Their sexwise distribution is presented in Table
2. Between 0.6% and 4.3% of the population
in response group among the de jure population
TABLE 1
Registered Population According to Sex & Residential Status During Five Surveys
Residential
status
Sex
I Survey II Survey III Survey IV Survey V Survey
No. % No. % No. % No.
%
No. %
Permanent
resident
Both sexes 12088 95.6 12370 96.6 12418 96.6 12078 95.9 14382 95.1
Male 6172 97.2 6271 98.1 6293 97.9 6100 97.0 7277 96.5
Female 5916 94.0 6099 95.1 6125 95.3 5978 94.7 7105 93.6
Temporary
resident
Total
Both sexes
Male
Female
Both sexes
Male
Female
556
181
4.4
2.8
438
124
3.4
1.9
437
136
3.4
2.1
521
189
4.1
3.0
744
262
4.9
3.5
375 6.0 312 4.9 301 4.7 332 5.3 482 6.4
12644 100.0 12806 100.0 12855 100.0 12599 100.0 15126 100.0
6353 100.0 6395 100.0 6429 100.0 6289 100.0 7539 100.0
6291 100.0 6411 100.0 6426 100.0 6310 100.0 7587 100.0
Ind. J. Tub., Vol. XXIX, No. 3

156 A.K. CHAKRABORTY et. al.,
TABLE 2
Distribution of the ‘Response’* Population by BCG-Scar status in 5 Surveys
Survey
No BCG Scar BCG Scar Total
Male Female Total Male Female Total Male Female Total
I 5574
(99.4)
5369
(99.4)
10943
(99.4)
31
(0.6)
32
(0.6)
63
(0.6)
5605 5401 11006
II 5204
(95.3)
5209
(96.9)
10413
(96.1)
255
(4.7)
165
(3.1)
420
(3.9)
5459 5374 10833
III 5052
(94.6)
5005
(96.5)
10057
(95.5)
290
(5.4)
184
(3.5)
474
(4.5)
5342 5189 10531
IV 4867
(94.7)
4961
(96.7)
9828
(95.7)
271
(6.2)
167
(3.3)
438
(4.3)
5138 5128 10268
V 4235
(69.4)
4600
(74.2)
8835
(71.8)
1865
(30.6)
1599
(25.8)
3464
(28.2)
6100 6199 12299
Note : Figures in bracket show the percentages
*Response—those in whom reading of scar status was done
had BCG scars between survey I & IV, but for
survey V such proportion was 28.2%. Age sex
structure of the de jure population without scar
was significantly different from survey to survey
(Table not presented.)
Results
Choice of level of demarcation to classify
infected:
the
Distribution of tuberculin indurations: As
expected and in line with the earlier observation
already reported (NTI, 1974), distribution of
tuberculin induration size for all ages both
sexes in any of the surveys did not show a
clear bimodal pattern. To decide on any level
of demarcation to classify the infected and noninfected
among the tuberculin tested population
aged 15 years and over on the basis of
histograms of tuberculin indurations was not
feasible, due to the fact that almost the entire
population in this age group are already infected
with some mycobacteria or other
(Chakraborty et al 1978). In view of this,
demarcation into negative and positive reactors
on the basis of distributions of indurations
could only be attempted in children aged 0-14
years. The demarcation level so arrived at, was
extrapolated to higher age groups, though such
extrapolation may be regarded as hypothetical.
Distribution of indurations in population
aged 0-4, 5-9 and 10-14 years for surveys I-V
are presented in figures I-III. Even in these
curves of distributions pertaining to younger
age groups, the antimodes are not clearly
defined. However, by fitting normal curves
depicting either of the two likely modes, the
anti-mode could be more or less reasonably
hypothesised to lie at around 10 mm for I
survey (Fig. I, II, III : A). The distributions for
surveys II to V (Fig. I, II & III : B, C & D)
were such that it was even more difficult than
in I survey to define two separate modes in
them. Dips in curves of distributions of indurations
which could be taken as antimodes,
could probably be expected to lie around 11 or
12 mm at II survey, 11 or 12 mm at III survey,
10 to 12 mm at IV survey and 14 to 15 mm at V
survey. Based on the above observations, the
demarcation level to classify infected persons
could be < 10 mm,

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA 157
indurations among the sputum positive tuberculosis
cases diagnosed at each of the I to the
V surveys are presented in Table 4. On the basis
of mean minus one SD, if 17 mm is chosen as
the minimum induration of I survey cases, the
chances of misclassification of tuberculosis cases
as tuberculin negative would be about 15%
(P < 0.3); but if 10 to 13 mm (mean minus
2 x SD) is chosen, such chances would be almost
eliminated (P < 0.05). This would justify
selection of the demarcation line to be anywhere
between 10-13 mm. However, the level of

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA 159
tion levels were also separately worked out
(Method b : to be reported in a separate paper)
on similar lines as followed in the earlier report
on four surveys (NTI, 1974), by making allowances
for the differences of mean indurations of
subsequent surveys over the first. The computed
levels are presented in Table 3: row b. These
are, additionally, in line with distribution of
indurations in cases.
Prevalence of infection
Table 3 also presents the prevalence of
infection by age and sex from surveys I to V,
worked out on the basis of the two sets of
demarcation levels, one on distribution and the
other computed. Estimates on prevalence rates
with the population of first survey as standard,
are presented in table 5 for the sake of comparison
from survey to survey after making
due allowance for age sex differences in population.
Prevalence rates of infection, as in the
previous surveys, were higher in males than in
Ind. J. Tub., Vol. XXIX, No. I

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA 161
females except in children in age group 0-14
years (not presented on table). The prevalence
rates were found to rise continuously with age
in all the surveys.
There was a decline in the observed prevalence
of infection between I-V surveys in
0-4 years old children (Table 3). The trend was
significant when the demarcation level to classify
the infected was decided by method ‘a’ (0.05 >
P>0.02); but it just missed being significant
by method ‘b’ (0.10 > P > 0.05).
In 5-9 years age group there was declining
trend in prevalence after II survey by method
‘b’ (0.05 > P > 0.02); in 10-14 years also there
was decline in trend after the II survey both by
method ‘a’ (P < 0.001) and ‘b’ (P < 0.001).
The standardised infection rates were compared
in 0-14 years and all age groups (Table
5). It will be seen that for 0-14 years age group,
there was declining trend after the II survey
both by method ‘a’ or ‘b’. However, the overall
standardised rates showed a rise between I-II
Ind. J. Tub., Vol. XXIX, No. 3

162 A.K. CHAKRABORTY et. al.,
TABLE 5
Agewise Prevalence Rate of Infection (Standardised) l-V Surveys
Age
Survey
Standardised prevalence rate of infection
Population* I II III IV V
1 2 3 4 5 6 7
0-14
years
a 4679
b 4679
6.48 7.84
6.48 8.06
7.84
7.48
6.48
6.06
8.43
4.72
All Ages
A 10369
b 10369
23.35 27.49
23.85 27.58
30.16
27.52
27.76
25.79
27.95
27.18
* Standard population of I Survey
a On the basis of frequency curve by induration size
b By adding, at each survey, mean difference over I Survey
surveys, but were more or less stationary
thereafter with small fluctuations in between
(rates at II, III & V surveys being similar by
‘b’ method, and at II, IV and V surveys by
‘a’ method). This is due to the influence of the
highly significant rising trend in infection rates
observed between I and V surveys in population
aged 15 years and over.
Prevalence of cases
Unfortunately the number of cases found in
each of the surveys was small, the highest being
37 at II survey and lowest 25 at III survey
(Table 6). This did not permit a detailed study
of prevalence rates in various ages and sex
groups. Only a few broad patterns are therefore
pointed out below:
There were fewer cases detected among
population in younger age groups than in the
older, in any survey. Of the total cases, the
proportion detected in population aged upto
20 years was consistently falling with time,
from the highest level of 13.5% at the II survey
to 2.9 % at V survey (Fig. IV). Partly this could
be explained by the difference in population
sizes in different age groups at V survey as
compared to earlier surveys.
At survey I, half the total prevalence cases
were in persons aged 5 to 39 years and the other
half in 40 years and over age group (1 : 1).
At survey IV, the proportion was 1 : 1.4 and
at the survey V it was 1 : 4. This shows increasing
concentration of cases in higher age group
with time.
Of the total cases detected, the proportion
of cases in the females showed a rising pattern
with time, especially in those aged 40 years and
over. Of the total cases in this age group,
females were one out of 18 or 20 at surveys I &
II; and one out of 6 or 4 at surveys IV & V
(Not presented in table).
Owing to small numbers, the prevalence
rates are presented for all ages both sexes and
in two broad age groups, i.e., 5 to 39 years,
and 40 years and over (Table 6). In none of the
age groups or in overall, the difference in rates
between surveys were significant.
The all ages both sexes case prevalence
rates were 3.96 per thousand at survey I and
4.92 per thousand at survey V, the last being
the highest overall rate observed at any survey.
The rates in 5 to 39 years age group for both
sexes were 2.68 at survey II as the highest, and
1.57 per thousand at survey V as the lowest.
In 40 years and over age group the rates for
both sexes ranged from 6.7 at III survey to
10.5 at survey V.
The standardised prevalence rates, on the
basis of standard population of survey I, as
presented in Table 6 were similar to the observed
Ind. J. Tub., Vol. XXIX, No. 3

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA 163
Ind. J. Tub., Vol. XXIX, No. 3

164 A.K. CHAKRABORTY Ct. al.,
rates. The prevalence rates showed a continued
reduction through the surveys, from
2.62 per thousand at I survey to 1.18 at survey
V, in 5 to 39 years age group. On the other
hand continued rise in the rates was observed
after the III survey (6.59 per thousand) to V
survey (10.98) among population, 40 years and
over in age. Whether with larger number of
cases, the differences in rates from survey to
survey would have been significant or not cannot
be commented upon.
Fate of Cases
Out of 36 cases found at the I survey, 31
have been followed up (Fig. V) for a minimum
period of 1-1/2 years (I-II survey) and also
for 5 years (I-TV survey). Among 29 cases
diagnosed at IV survey, 26 were followed up
after 11 years at survey V. The number of
deaths observed were 4, 12 and 17 respectively
in the three periods mentioned above. The
proportion of cases dead were 387 per thousand
in 5 years as compared to 654 per thousand in
11 years. Annual case specific mortality* rate
is calculated to be 77 per thousand and 59
*Deaths due to all causes among cases of tuberculosis.
Ind, J, Tub., Vol. XXIX, No. 3
per thousand, estimated from the observations
made in the first five and subsequent 11 year
periods respectively. The outcome in terms of
survival was better for cases diagnosed at IV
survey than that in the I survey.
Discussion
In the epidemiological survey carried out in
119 villages forming a sample of the 3 taluks
of Bangalore district South India (NTI, 1974),
it was observed that the natural trend of the
disease showed a decline in 5 years, as revealed
from a downward trend of prevalence and incidence
of infection in younger age groups and a
slight decline in prevalence and incidence of
cases in the younger age groups. The trend
as studied from prevalence rates from survey
to survey, tended to be arrested at the time of
the last survey owing to unfavourable economic
situation obtaining at that time in the area.
The observations, made on the basis of data
collected in a relatively short span of 5 years,
gave rise to speculations as to whether these
represented a long-term epidemiological trend
of tuberculosis for the area.

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA 165
The present study extending over nearly a
period of 16 years, appears to confirm the
earlier observation of the declining trend of the
disease though in a smaller sample of population.
The points in favour of a declining
trend of the disease can be summarised as (a)
descending prevalence of infection rate in
paediatric age group (b) very few cases in
younger age group upto 19 years of age, relative
concentration of cases in higher age groups
and higher mean age of the prevalence cases
diagnosed in the later surveys (indirect
evidence); (c) even the unchanged prevalence
rates of the cases from survey to survey may
indirectly indicate decline.
The entire situation probably represents a
natural trend of tuberculosis, though organized
anti-tuberculosis diagnostic and treatment
services were made available in the area in
1973 and direct mass BCG vaccination to the
eligibles was carried out after that. This is
because an implemented programme may not
be expected to influence the natural epidemiological
course in the population in a short time
(Gothi et al 1979).
An important problem concerning the choice
of demarcation level merits discussion here,
since it has considerable influence on the interpretation
of the trend of tuberculous infection.
The mean induration sizes from survey I
through survey V are found to be progressively
rising in 0-14 years population (Table not
presented). It may also be pointed out that
children aged 0-9 yrs. of survey V were never
tested with tuberculin previously. Such progressive
rise in mean induration sizes of tuberculin
reaction has been observed by other workers
also (Edward et al 1965). Further, it should be
appreciated that there is a significant increase
in the proportion of individuals with the indurations
size of 10-14 mm in 1977, as compared
to those in 1962. For example, among
children aged 5-9 years with > 10 mm tuberculin
induration size, about 7.7% and 92.3%
were having 10-14 and 15+ mm sizes respectively
in 1962. At the V survey in 1977, these proportions
were 56.7% and 43.3% respectively.
Considerable increase was observed among
children aged 0-4 and 10-14 years also, though
comparatively less pronounced in the former
(Table not presented). Thus the increase in the
proportion of reactors beyond 10 mm at V,
survey over that in I survey was mainly due to
the substantial increase in the proportion of
Ind. J. Tub., Vol. XXIX, No. 3

166 A.K. CHAKRABORTY, et al.,
the intermediate reactors only, i.e. those lying
between 10-14 mm induration sizes. This could
be interpreted as due to factors other than
specific tuberculous infection; otherwise it was
expected to be distributed in all 10 mm and
over reaction ranges. These observations further
necessitated choice of a separate and higher
demarcation level as compared to that at 1
survey, to compensate the increase of intermediate
reactors at V survey. Such compensation
has, in fact, been made for each survey
to the next varying the demarcation level from
survey to survey, based on the distribution of
indurations. The possible explanations for this
phenomenon would be: different readers
employed at different surveys, intra-reader
variation for the same reader performing test
readings at different times—resulting from
constant practice and experience gained from
survey to survey; a possibility of rising incidence
of infection with other mycobacteria and to
varying potency of tuberculin supplied at different
times. Boosting, thought to be an important
factor in the earlier studies (Raj Narain et al
1966), is no longer considered contributory to
the increase (Raj Narain *et al 1979), especially
since the surveys are conducted at more than
3 months interval from each other. In any case,
the question of boosting is irrelevant to 0-4 &
5-9 year old children of V survey, who were
not even born at the earlier survey.
It is, no doubt, interesting to compare the
infection rates at 1962 and 1977 surveys, in
case the demarcation levels are kept constant
at both the points. In Appendix Table such an
exercise has been carried out, with 10 mm and
14 mm levels. There is no change in the prevalence
rate of infection for 0-4 as well as 0-14
year age group, with 14 mm demarcation
level at both surveys. This prevalence of infection
corresponds to the annual risk of infection
of about 0.8 % (ITS, 1981). On the other
hand, enormous increase in the prevalence
rate for the 1977 survey for 5-9 and 10-14 year
age groups will be estimated, if 10 mm is selected
as the demarcation level for both 1962 and 1977
surveys. In any case, for the reasons mentioned
earlier, especially keeping in view the distribution
of tuberculin induration, it appears
logical to select varying demarcation levels from
survey to survey as suggested in the paper,
rather than select the same demarcation level
for all surveys,
Prevalence rate of cases was found unchanged
at all the surveys, which, however, is
not of much significance owing to the small
number of cases involved. The prevalence rate
of bacillary cases being small, a large population
size is required for the study of its trend
(Chakraborty, 1973). By itself, therefore, the
study of prevalence of cases did not yield
sufficient data to enable one to comment on the
trend of the disease. However, the age wise
proportional distribution showing relative concentration
of cases in higher ages (Figure IV),
may be interpreted as supportive of the hypothesis
of a declining course of tuberculosis in
the community.
Acknowledgement
The authors are grateful to the International
Tuberculosis Surveillance Centre, The
Hague, Netherlands and particularly to
its Research Director Dr. M.A. Bleiker, for
the courtesy in offering valuable assistance and
suggestions after an independent review of the
material. The authors express their indebtedness
to Dr. Raj Narain & Dr. G.D. Gothi,
former Epidemiologists NT1, who were associated
with survey I-IV; Dr. Gothi was additionally
associated with survey V also in its
initial phases. The hard work in the field put
in by Epidemiological teams deserves special
acknowledgement. The authors are thankful
to Mrs. Anuradha & other statistical staff, to
Messrs Narayana Prasad & Nagraj for the
drawings and Mr. P. Perumal for Secretarial
assistance.
REFERENCES
1. Chakraborty A.K.; NTI Newsletter; 1973, 10,
57.
2. Chakraborty A.K., Ganapathy K.T., Nair S.S.,
Kul Bhushan; Indian J. Med. Res., 1976, 64, 639.
3. Edwards L.B. & Smith D.T., Amer. Rev. Resp.
Dis., 1965, 92(1), 43.
4. Frimodt-Moller J; Bull. Wld. Hlth. Org., I960,
22, 61.
5. Gothi G.D., Chakraborty A.K., Nair S.S., Ganapathy
K.T. & Banerjee G.C., Ind. Jour. Tub.,
1979, 26, 121.
6. Goyal S.S., Mathur G.P., Pamra S.P., Ind. Jour.
Tub., 1978, 25, 77.
7. International Tuberculosis Surveillance Centre,
The Hague; Personal Communication, 1981.
8. Nair S.S., Indian I. Tub. Hlth., 1977,21, 111.
9. National Tuberculosis Institute; Bull. Wld. Hlth.
Org., 1974, 51, 473.
Ind. J. Tub., Vol. XXIX, No. 3

TUBERCULOSIS IN A RURAL POPULATION OF SOUTH INDIA 167
10. Raj Narain, Nair S.S., Ramanatha Rao G., 12. Tuberculosis Prevention Trial, Madras, Indian J.
Chandrasekhar P. & Pyare Lai : Bull. Wld. Hlth. Med. Res.- 1979, 70, 349.
Org., 1966, 34, 622.
11. Raj Narain, Gothi G.D., Ganapathy K.T. &
Shyamasundra C.V., Indian J. Med. Res., 1979, 13. Waaler H.T., Gothi G.D., Baily G.V.J. & Nair
69, 886. S.S.; Bull Wld. Hlth. Org., 1974, 51, 263.
APPENDIX TABLE
Agewise Infection Rates in Children At I & V Surveys. Selecting the Same Demarcation Levels at Both Surveys
at 10 mm
at 14 mm
Demarcation level
Age Group
Survey I* Survey V* Survey I* Survey v*
With Infected With Infected With Infected With Infected
Induration (No.) Induration (No.) Induration (No.) Induration
( %)
(%)
(%)
(No.)
0-4 33 2.1 36 2.4 31 1.9 24 1.6
5-9 91 5.7 127 15.4 87 5.5 60 7.3
10-14 179 12.0 159 32.1 159 10.7 75 15.2
*For number of test read children see Table 3.
Ind. J. Tub., Vol. XXIX, No. 3

LOWER LUNG FIELD TUBERCULOSIS
RAM CHANDRA, JITENDRA NATH, G.N. AGARWAL, V.K. SRIVASTAVA AND P.K. MUKERJI
Summary : Prevalence of lower lung field tuberculosis was found to be 1.3% among patients
of pulmonary tuberculosis, nearly three times more in females (2.3%) than in males (0.9%). Onset
was mostly insiduous and duration less than 6 months. Right lung was involved more often. Consolidation
with cavity was seen in 28.2%, productive infiltration, exudative infiltration and consolidation
in 14.1 % each. Microscopic sputum smear was positive in 57.7% of the cases and 92.0%
of them showed sputum conversion at the end of four months treatment.
Introduction
It is a well known fact that post primary
tuberculosis originates in the apices of the lungs.
Only in a few patients it starts in the bases of the
lungs and produces lot of confusion in the
diagnosis of the disease, specially in the absence
of positive sputum.
Most of the reports on basal tuberculosis
became available only after 1920 (Feber, 1931;
Dufault, 1932; Anspatch, 1934; Hamilton and
Freed, 1935; Reisner, 1935; Gorden, 1936;
Viswanathan, 1936; Busley, 1939; Sokoloff,
1940; Andosca and Foley. 1943; Ossen, 1944;
Romendic et al., 1944; Dock, 1946; Ostrum
and Saber, 1949; Fries, 1955; Johnson, 1959;
Segarra et al., 1963; Tripathv and Nanda,
1970; Mathur et al., 1974). Only a limited
number of studies have been conducted in our
country (Viswanathan, 1936; Parmar, 1967;
Tripathy and Nanda, 1970 and Mathur et al.,
1974). In the present report an attempt has
been made to study the problem of lower lung
field tuberculosis and its clinical features,
bacteriological status, radiological presentation
and response to therapy.
Material and Methods
The material for the present study was
selected from patients of pulmonary tuberculosis
admitted to Kasturba T.B. Hospital,
K.G.’s Medical College, Lucknow, during
the period January 1969 to December, 1978.
Of the total patients of pulmonary tuberculosis,
only those patients who had radiological
shadows confined to lower lung field, either
with history of contact and clinical features
suggestive of tuberculosis and/or a positive
sputum smear for A.F.B. were considered as
patients of lower lung field Tuberculosis(LLFT).
Since sputum culture for mycobacterium tuberculosis
was done only in a few cases, its results
were not considered in the present study.
The lower lung field has been defined as
that area on P A view of the chest which extends
below the imaginary horizontal line
traced across the centre of hilar or parahilar
region (Segarra et al 1963). This area includes
middle lobe or lingula in addition to lower
lobe (Parmar, 1967).
The following types of patients were excluded
from the present study:
i) Those with either ipsilateral or contralateral
involvement of both upper and
lower lung fields.
ii) Pleural effusion and thickening, unless
associated with parenchymal lesion in
the area described.
iii) Possibility of non-tuberculous lesion
occuring in the lower lung fields.
iv) Those below 14 years of age.
The clinical and radiological features of
the cases were studied and the response to
therapy was assessed in terms of sputum status
and radiological changes at the end of four
months’ treatment.
Discussion
It is a well-known fact that post-primary
tuberculosis is located in the apices of the
lungs, but in certain proportion of patients,
the disease may start from lower lung field
(Segarra et al., 1963; Parmar, 1967; Tripathy
and Nanda, 1970). In the present study the
prevalence of lower lung field tuberculosis
was 1.3% of the total cases (Table I). A review
of literature shows a great variation in the
reported frequency. It varies from 0.003%
(Colton, 1923) to 18.3% (Ross, 1930). Reports
from our country indicate that prevalence
* Department of Tuberculosis & Respiratory Diseases,
** Department of Radiology,
*** Department of Social & Preventive Medicine, King George’s Medical College, Lucknow-226003.
Ind. J. Tub., Vol. XXIX, No. 3

LOWER LUNG FIELD TUBERCULOSIS 169
TABLE 1
Prevalence of Lower Lung Field Tuberculosis (LLFT) according to age and sex
Age group
(years)
Total patients of pulmonary
tuberculosis
Prevalence of LLFT
Male Female Total Male Female Total
No. % No. % No. %
Below 20 591 406 997 2 0.3 12 2.9 14 1.4
21-29 371 699 2070 12 0.9 15 2.1 27 1.3
30-39 1081 400 1481 10 0.9 10 2.5 20 1.3
40 & above 1108 258 1366 13 1.2 4 1.5 17 1.2
Total 4151 1763 5914 37 0.9 41 2.3 78 1.3
varies from 0.63% to 6.4% (6.4% Viswanathan,
1936; 3.4% Parmar, 1967; 5.1%
Tripathy and Nanda, 1970 and 0.63% Mathur
et al., 1974). The discrepancy in these figures
may be due to confusion in the terms used
viz. basal, lower lobe, parahilar, lower lung
field tuberculosis and variation in the type of
material (hospitalized or ambulatory patients
and sputum positive or negative cases). The
prevalence of 1.3% observed in the present
series seems to be quite low as compared to
other studies. This is probably because of the
fact that Kasturba T.B. Hospital, from where
the study material has been taken is a Centre
which receives patients, from the neighbouring
places usually in advanced stages.
Parmar (1967) observed that most of his
patients were generally young, especially below
the age of 20 years (46% well below the age of
20 years). In our series lower lung field tuberculosis
was seen oftener in younger age groups but
not statistically different from other age groups
(P>0.05). On the other hand the frequency of
lower lung field tuberculosis was 2.3 % in females
in comparison to 0.9 % in males, the difference
being statistically significant (P

170 RAM CHANDRA, ET AL.,
TABLE II
Clinical features of 78 cases of lower lung field tuberculosis
the other hand Viswanathan (1936) reported
chest pain only in 0.95 % of cases. Our findings
are much lower than those of Lathrop and Lyman
(1924), who reported chest pain in as many
as 50% of their cases. In the present study,
only a small percentage (7.7%) of patients
of lower lung field tuberculosis had dyspnoea
and that too exertional.
Fever was seen in 91.0% of the patients
in our series. Viswanathan (1936) noted fever
in 100% of his patients. On the other hand only
half of the cases of Mathur et al. (1974) had
fever. Other toxaemic manifestations such as
loss of weight and appetite were observed in
23.1 % of our patients. Middlestone and Taylor
(1954) observed these symptoms in 21% of
their patients. Parmar (1967) was also of the
view that toxaemic manifestations are common
features in the patients of lower lung field
tuberculosis.
Radiological study revealed many interesting
features (Table III). In half of the cases (51.3%)
of lower lung field tuberculosis, the right lung
above was involved. In 26.9% cases, only
the left lung was involved and in the remaining
(21.8%) both lungs were involved. Similar
observations were made by Parmar (1967)
and by Mathur et al (1974). Many other workers
failed to observe any marked predominance of
any side (Reisner, 1935 ;Sokoloff, 1940; Weidman
and Campbell, 1937; Romendick et al, Segarra
et al, 1963 and Tripathi and Nanda, 1970).
In our study 32. 0% of the cases had far
advanced lesion and in 46.1% of cases lesion
was moderately advanced (Table III). The
figures are more or less comparable to those
reported by Tripathi and Nanda (1970) and
Mathur et al (1974).
As shown in Table IV, most of the patients
had consolidation with cavity (28.2%) followed
by productive infiltration, consolidation and
exudative infiltration with cavity (14.1% each).
Lower lung field tuberculosis is probably due
TABLE III Radiological (PA view) Features
Ind. J. Tub., Vol. XXIX, No. 3

TABIF IV
Radiological nature of lesion
to the ulceration of a bronchus by tuberculous
caseous lymph node with spillage of tuberculous
material into terminal bronchioles
and alveoli, or progression of primary focus
situated in lower lung field, this may commonly
lead to consolidation and cavity formation.
LOWER LUNG FIELD TUBERCULOSIS
71
Evidence of cavity was seen in 62.8% of
cases and its size was less than 4 cm in 43.6%
cases (Table V). Nine patients (11.5%) had
features suggestive of tension cavity. Cohen
(1935) noticed cavities in 70% of his cases,
while Hawkins (1946) noticed cavitation in
as many as 90%. Most of the workers have
reported cavitation in more than 60 % of their
patients (Rothstein, 1949; Johnson, 1959;
Segarra et al., 1963; Parmar, 1967 and Tripathy
and Nanda, 1970). Segarra et al. (1963)
obsered that majority of cavities were larger
than 3 cm in diameter and were of tension
type. In the study of Mathur et al. (1974) the
size of the cavity was 4 cm or more in 31.2% of
the cases as compared to only 19.2% of the
patients in the present study.
Out of the total 78 patients, 45 (57.7 %)
were sputum positive (smear only) and the
remaining (42.3%) were negative for acid fast
bacilli. Patients of lower lung field tuberculosis
showed a favourable response to antitubercular
treatment. Only 25 sputum smear
positive cases could be followed for four
months and sputum conversion was seen in 92
% of these (Table VI). Almost all the patients
showed radiological improvement. 28%
patients showed cavity closure while others
showed appreciable decrease in the size of
the cavities. Parmar (1967) advised that such
cases should be put initially under intensive
chemotherapy for eight to nine months and if
the cavity persists, sputum remains positive and
residual bronchi-actasis is left behind,
patients should be considered for resection.
Poor results of the treatment observed by
earlier workers were due to mechanical
factors and non-availability of chemotherapy
(Mathur et al., 1974).
TABLE V
Cavitary Status in 78 Cases of Lower Lung Field Tuberculosis
Ind. J. Tub., Vol. XXIX, No. 3

172 RAM CHANDRA, ET AL.,
T
TABLE VI
Sputum A Status for A.F.B. in cases of LLFT at the end of four months therapy
REFERENCES
1. Andosca, J.B. and Foley, .T.A., Jour. Thor. Surg.;
1943, 12, 258.
2. Anspatch, W.E., Am. Jour. Dis. Child.; 1934, 47,
1011.
3. Busley, J.F., Amer. Rev. Tub.; 1939, 40, 692.
4. Cohen, R.C., Brit. Med. Jour.; 1945, 1, 662.
5. Dock, W.M., Amer. Rev. Tub.; 1946, 58, 297.
6. Dutault, P.. Amer. Rev. Tub.; 1932,25, 17.
7. Feber, K., Acta. Med. Scandinav.; 1931, 75, 403.
8. Fries, J.W., Jour. Meil. Med.; 1955, 54, 1310.
9. Gorden, B., Internal Clin.; 1936, 1, 67.
10. Hamilton, C.E. and Fredd, H., Jour. Am. Med.
Ass.; 1935,105, 427.
11. Hawkins, F.S. and Thomas, G.O., Tubercle;
1946, 27, 82.
12. Johnson, J.H.P., Brit. Jour. Dis. Chest.; 1950,
52, 385.
13. Lathrop and Lyman, Quoted by Hamilton and
Fredd, J. Am. Med. Ass.; 1935, 105, 427.
14. Mathur, K.C., Tanwar, K.L. and Razdan, J.N.,
Ind. Jour. Chest Dis.; 1974, 16, 31.
15. Middlestone, H.J.H. and Taylor, A.J., Thorax,;
1954, 9, 344.
16. Ostrum, H.M. and Saber, W., Radiology; 1949,
. 53, 42.
17. Ossen, E.Z., New Eng. J. Med.; 1944, 230, 693.
18. Parmar, M.S., Amer. Rev. Resp. Dis.; 1967, 95,
310.
19. Reisner, D., Arch, Int. Med,; 1935,56, 258.
20. Romendic, S.S., Friedman, B. and Schwartz,
H.F. (1944) Quoted by Tripathi and Nanda (1970).
21. Rothstein, E., Amer. Rev. Tub.; 1949, 59, 39.
22. Segarra, F., Shetman, D.S. and Rodriguiz-Agnero,
J., Amer. Rev. Resp. Dis.; 1963, 87, 37.
23. Sokoloff, M.J., Radiology; 1940, 34, 589.
24. Tripathy, S. and Nanda, C.N., Jour. Ass. Phys.
Ind.; 1970,18, 999.
25. Viswanathan, R., Brit. Med. Jour.; 1936, 2, 1300.
26. Weidman, W.H. and Campbell, H.B. (1937)
Quoted by Tripathy and Nanda, J. Ass. Phys. Ind;
1970, 18, 999.
Ind. J. Tub., Vol. XXIX, No. 3

FUNGAL SUPERINFECTION IN PULMONARY TUBERCULOSIS
S.K. JAIN, 1 R.L. AGRAWAL, 2 DEV ASHISH SHARMA 3 AND MANJU AGRAWAL 4
Summary : One hundred forty patients of pulmonary tuberculosis were studied to find out (he
prevalence of fungal superinfection. Fungus positivity was found in 53 % of cases. It was higher in
the treated (chronic) group that in the fresh untreated cases of tuberculosis. Fungal growth was found
to be independent of extent of lesion. Positivity was influenced mainly by the duration of previous
antitubercular treatment, duration of disease, chronicity of lesion and associated illness such as
diabetes mellitus.
Introduction
The prevalence of mycotic involvement in
pulmonary tuberculosis is well documented
(Beatty & Saliba, 1963; Shome et a], 1969,
1976; Sandhu et al, 1964, 1966; Chakravarty
et al, 1964, 1967), but there is no comprehensive
study to find out the correlation of fungus
superinfection with that of duration of previous
antitubercular treatment, duration, extent and
severity of pulmonary tuberculosis. An attempt
was made to investigate the above problems.
Material and Methods
One hundred and forty patients (age range
10-64 years) were randomly selected for the
present study amongst the diagnosed pulmonary
tuberculosis cases admitted in Government
Tuberculosis Hospital, Allahabad from January
1979 to February 1980. They were divided into
two groups: (1) Fresh or untreated group,
comprising cases who had taken none or less
than one month’s antitubercular treatment,
and (2) chronic or treated group—cases who
had antitubercular treatment for more than a
month.
Early morning sputum was collected from
each case after a proper mouth wash with hot
saline water and with proper aseptic precautions.
It was homogenized with the help of sterile
glass beads for smear and culture for fungus.
Direct smear examination for fungal elements
was carried out with 10% KOH or lactopHenol
cotton blue and/or grams staining. For culture
of fungus, a sterile platinum loopful of sputum
was inoculated on three different slopes of
Sabouraud’s dextrose agar medium prepared
by Emmons’ modification (1977) vi/. (1)
Sabouraud’s dextrose agar (SDA) plain, (2)
SDA with antibiotic (Chloramphenicol 0.04
mg/ml), and (3) SDA with antibiotic and
actidion (Chloramphenicol 0.04 mg/ml and
cycloheximide 0.5 mg/ml). To exclude air contaminants,
a plain Sabouraud’s dextrose agar
culture tube was kept as a control along with
slants of each case. Evaluation of the amount
of growth was done according to Kahanpaa
(1972). Criteria for diagnosis of secondary
mycoses in the present study were as follows:
(1) heavy growth of fungus in culture repeatedly
for at least three times, and (2) fungus positivity
by direct smear examination.
Identification of fungal species was made in
accordance with criteria laid down by Mackenzie
(1966), Ajello et al (1966), Conant et al (1971),
and Emmons et al (1977). Candida albicans
was recognised on the basis of pseudomycelia,
blastopore and chlamydospore formation on
cornmeal agar with tween 80 media, and formation
of germ tube (R.B. effect)—serum tube
method (Taschdjian et al, 1960) Candida albicans
along with other species of Candida
were distinguished by biochemical reactions.
Detailed morphology of filamentous fungi
CAspergillus. Rhi/opus, Penicillium) was studied
by slide culture method and/or by Czapeck
media in petri dish. Cryptococcus was identified
by demonstration of thick walled yeast cells
in sputum and sensitivity to actidion. Capsule
of yeast is better seen in India ink preparation.
Results
The fungus positivity by direct smear and
culture was found in equal number of cases
(Table 1). In treated group, the fungus was
found in higher percentage (59 %) than in the
fresh group (37.51%).
Out of 140 cases. 6 were suffering from
diabetes mellitus. Fungus was isolated in all
the 6 (100%) diabetic cases, while in the remaining
134 fungus was isolated in 68 (about 50%).
Aspergillus was the commonest fungus
Professor and Head of Department of Tuberculosis & Respiratory Diseases.
2 Ex-Registrar
3 Lecturer in Statistics and Demography, Post-partum Programme
*Lecturer in Anaesthesia From : Moti Lai Nehru Medical College,
Allahabad-211001.
Ind. J. Tub., Vol. XXIX, No. 3

174 S.K. JAIN, R.L. AGRAWAL, DEV ASHISH SHARMA AND MANJU AGRAWAL
TABLE l
found in both fresh and treated groups, followed
Results of direct smear and culture examinations for by Candida, Penicillium, Cryptococcus and
fungus in pulmonary tuberculosis
Rhizopus (Table 2). Double growth of fungus
was seen in 8 cases of chronic (treated) group.
Table 3 shows the correlation of fungus
positivity with the duration of previous antitubercular
treatment. The positivity was in
39% (35/90) of cases who gave a history of
previous antitubercular treatment for less than
one year, while it was in 78 % (39/50) in those
who had taken more than one year treatment.
The difference was statistically significant.
X 2 = 5.30, df = 1, P < 0.05, S. 3
Correlation between duration of illness and
fungal positivity was also worked out. The
difference in fungus positivity among patients
with duration of illness below 3 years and above
3 years was statistically significant (Table 4).
TABLE 2
Fungal Isolation
Ind. J. Tub., Vol. XXIX, No. 3

FUNGAL SUPERINFECTION IN PULMONARY TUBERCULOSIS
TABLE 3 TABLE 4
175
Isolation of fungus in relation to duration of antitubercular
Isolation of fungus in relation to duration of illness
Comparison was made between upto 1 year and above
one year duration of treatment.
Duration of illness upto 3 years and above 3 years were
compared.
TABLE 5
Fungal Isolation in Relation to the Extent of the Lesions
Extent of lesion Fresh group Treated group Total
No. +ve % No. +ve % No. +ve %
1. Minimal 8 50 9 67 17 59
2. Moderate 10 30 11 45 21 38
3. Far advanced 22 36 80 60 102 55
Total 40 37.5 100 59 140 53
Table 5 shows correlation of growth of fun- in the fresh and the treated group (Table 6),
gus with the extent of lesions. Statistically, the but difference was not statistically significant,
chance of isolating fungus was irrespective of
the extent of the lesions.
Discussion
Fungus was found in a higher proportion
of cavitary cases than non-cavitary cases, both
Superinfection with fungus was significantly
higher in treated (chronic) group than in the
Ind. J. Tub., Vol. XXIX, No. 3

176 S.K. JAIN, R.L. AGRAWAL, DEV ASHISH SHARMA AND MANJU AGRAWAL
TABLE 6
Fungal Isolation in relation to Cavitary Status of the lesion
Type of lesion Fresh group Treated group Total
No. — ve % No. — ve % No. — ve %
1. Cavitary 13 54 60 60 73 59
2. Non-cavitary 27 30 40 57.5 67 46
Total 40 37.5 100 59 140 53
X 2 =2.19, clf-1,
P>0.05, NS.
fresh group. A comparison of results of
secondary fungal infection in the sputum of
pulmonary tuberculosis cases reported by
various authors is given below in a tabulated
form:
Author with year
No. of Fungus positivity in
cases %
Smear
Culture
Grower & Junnarkar
(1965) 100 30.0 58.0
Shome et al (1976) 860 28.3 18.0
Khanna et al (1977) 110 34.3 36.4
Present study 140 52.9 52.9
— Fresh cases 40 37.5 37.5
— Treated cases 100 59.0 59.0
Percentage of Candida species in sputa
of patients with pulmonary tuberculosis has
been reported in the literature to vary from
8 to 80 per cent (Norris, 1933, 8.5% Shome
et al, 1976, 9.19%; Schwarting & Skinner,
1949, 20%; Gonzalez Mendoza, 1958, 23%;
Burt & Ketchum, 1941, 42%; Grower &
Junnarkar, 1965, 42%; Chakravarty et al,
1960, 80%), Aspergillus species, however, has
been found less frequently (Shome et al, 1976,
0.69%; Grower & Junnarkar, 1965, 6%;
Ind. J. Tub., Vol. XXIX, No. 3
Khanna et al, 1977,
10%). In contrast, we found Aspergillus more
frequently (29.28%; 41/140) than Candida
(23.57%; 33/140).
Antibiotics, corticosteroids, antimetabolites
and radiation therapy, etc. influence the
incidence of both primary and secondary
fungal infection (Wood, 1951; Jha et al, 1974;
Shome et al, 1976). Relationship with the
duration of previous antitubercular therapy
has also been mentioned in the literature.
Khanna et al (1977) found higher incidence
of fungus positivity in the treated group cases
than the fresh group. Gonzalez Mendoza
(1958) did not find any difference in the prevalence
of Candida species in pulmonary tuberculosis
cases before and after the availability
of streptomycin. In the present study the
incidence of positivity was significantly higher
(78%) in cases who had had antitubercular
treatment for more than one year than those
who had it for less than one year (39%).
A correlation of the duration of illness
with the fungus positivity was also seen in this
study, the percentage increasing with the
duration of illness (P0.05).
Schwarting & Skinner (1949) also reported that
the degree of tuberculosis had no influence on
the incidence of Candida.
Fungus positivity was higher (59%) in

FUNGAL SUPERINFECTION IN PULMONARY TUBERCULOSIS 177
cavitary group than in the noncavitary group
(46 %). but the difference was not statistically
significant (P>0.05). An interesting finding of
our study was that the percentage of positivity
was high even in the noncavitary cases of the
chronic (treated) group (58 %) than the cavitary
cases (54%) of the fresh group. It is concluded
that chronicity of illness plays a more important
role in superinfection with fungi rather
than the cavitary status of the lesions. Khanna
et al (1977) were also of the opinion that yield
of fungi in pulmonary tuberculosis is related
to chronicity of lesion.
The predominance of fungal infection in
diabetic patients has been reported by Jha et
al (1974) and Khanna et al (1977). Fungus
superinfection was found in cent percent diabetic
cases in our study.
The authors are of the view that factors
mainly responsible for prevalence of fungal
superinfection in pulmonary tuberculosis are:
1) duration of previous antitubercular treatment,
2) duration of illness, 3) chronicity of
diseases, and 4) associated disease such as
diabetes mellitus.
Acknowledgements
The authors are grateful to the Director,
V.P. Chest Institute, Delhi for the kind permission
and Dr. H.S. Randhawa, Ph.D., Head
of Medical Mycology Department for his
valuable guidance and training given to one
of the authors.
REFERENCES
1. Ajello, L., Georg, L.K., Kaplan, W., Kaufman,
L.; CDC Lab Manual for Medical Mycology,
U.S. Department of Health, Education and Welfare
Public Health Service Communicable disease
centre; 1966.
2. Beatty, O.A., Saliba, A.; Coexisting Pulmonary
Fungus Infection and Tuberculosis at District two
State Hospital; Kentucky Med. J.; 1963, 61, 502.
3. Burt, K.L., Ketchum, H.M.; Classification of
Strain of Candida isolated from Sputum; Am.
J. Trop. Med.; 1941, 21, 427.
4. Chakravarty, S.C.; Incidence and significance of
Fungi in Sputum in bronchopulmonary diseases;
Acta Tuberc. Scand.; 1964, 45, 295.
5. Chakravarty, S.C.; Clinical aspect of Bronchopulmonary
Candidiasis; Proceedings of the 22nd
Tuberculosis and Chest Diseases Workers’ con
ference, Hyderabad, 1967, p. 262.
6. Chakravarty, S.C., Randhawa, H.S., Roy, B.K.,
Viswanathan, R.; Candida species in Throat swab
culture of Normal people and in the Sputum of
Patients with Bronchopulmonary Diseases; Calcutta
Med. J.; 1960, 57, 127.
7. Conant, N.F., Smith, D.T., Baker, R.G., Callway,
J.L.; Manual of Clinical Mycology, III Ed.
Saunders, W.B. Company Philadelphia; 1971.
8. Emmons, C.W., Binford, C.H., Utz, J.P., Kwon-
Chung, K.J.; Medical Mycology, Ed. III. Lea &
Febiger, Philadelphia; 1977.
9. Gonzalez-Mendoza, A., Bojalil, L.F.; Incidence of
C. albicans in the sputum of Tuberculous Patients;
Am. Rev. of Tuberc. & Pulm. Dis.; 1958, 77, 543.
10. Grower, S., Junnarkar, R.V.; Mycological flora in
Patients suffering from Bronchopulmonary Diseases;
Ind. J. Med. Sc.; 1965, 19, 823.
11. Hill, A.B.; Principle of Medical Statistics 7th ed.
The Lancet Ltd., London; 1961. p. 139.
12. Jha, V.K., Joshi, M., Sen, P.C.; Significance of
Isolation of Fungi from Sputum in Broncho
pulmonary Diseases; Presented at 9lh Eastern
Region Tuberculosis Conference and 29th National
Conference on Tuberculosis and Chest Diseases,
Delhi; 1974.
13. Kahanpaa, A.; Bronchopulmonary occurrence of
Fungi in Adults; Acta Path, et Microbiol. Scand.;
1972, SOB, 1.
14. Khanna, B.K., Nath, P., Ansari, A.H.; A Study
of Mycotic flora of Respiratory tract in Pulmonary
Tuberculosis; Ind. J. Tub.; 1977, 24, 159.
15. Mackenzie, D.W.R.; Lab. investigation of Candida
infections; In : Symposium on Candida infections.
Ed. H.I. Winner and R. Hurley, Livingstone,
Edinburgh; 1966.
16. Norris, J.C.; Further observations on pathological
yeasts; J. Med. Ass. Georgia; 1933, 22, 250.
17. Sandhu, R.S., Jaggi, O.P., Randhawa, H.S.,
Sandhu, D.K., Gupta, I.M.; Isolation of cryptococcus
neoformans from a patients without clinical
sings of Infection; Ind. J. Chest Dis.; 1964, 6, 93.
18. Sandhu, D.K., Sharma, N.V., Sandhu, R.S.,
Damodaran, V.N., Randhawa, H.S.; Broncho
pulmonary Aspergilloma; Indian J. Chest Dis.;
1966, 7, 198.
19. Schwarting, V.M., Skinner, C.E.; Candida in
Sputum of Patient with Tuberculosis, Mycopathologia;
1949, 4, 349.
Ind. J. Tub., Vol. XXIX, No. 3

178 S.K. JAIN, R.L. AGRAWAL, DEV ASHISH SHARMA AND MANJU AGRAWAL
20. Shome, S.K., Gugnani, H.C., Sirkar, D.K., Murty,
D.K., Raghavan, N.G.S., Rao, P.U.; Cryptococcosis
associated with Pulmonary Tuberculosis;
Indian J. Chest Dis.; 1969, 11, 45.
21. Shome, S.K., Upreti, H.B., Singh, M.M., Pamra,
S.P.; Mycoses associated with Pulmonary Tuber
culosis; Ind. J. Tub.; 1976, 23, 64.
22. Taschdjian, C.L., Burchall, J.J., Kozinn, P.P.;
Rapid identification of Candida albicans by Filamentation
on Serum and Serum substitute, J.
Dis. Child; 1960, 99, 212.
23. Wood, J.W., Manning, I.H., Patterson, C.N.,
Durham, N.C.; Moniltal infections complicating
therapeutic use of antibiotics; JAMA; 1951, 145,
207.
Ind. J. Tub., Vol. XXIX, No. 3

PLASMA COPPER AND ZINC LEVELS IN PULMONARY TUBERCULOSIS
B.K. KHANNA, R. KUMAR, P.K. MUKERJI,* A.R. CHOWDHURY AND V,P. KAMBOJ**
Summary : A study of plasma copper and zinc level was conducted in 46 normal subjects and 94
patients of pulmonary tuberculosis. 64 patients had received specific anti-tuberculosis therapy for over
one month and 30 were previously untreated. Plasma copper and zinc levels were recorded initially in
all patients and subsequently after 1, 2 & 3 months chemotherapy in the latter group ouly. Itwas found
that pulmonary tuberculosis is characterised by rise in level of plasma copper and decline in plasma
zinc level. Only 14 patients did not register any alteration in their levels Highly significant correlation
was established between the level of these trace elements and the presence of acid-fast bacilli in the
sputum, extent of pulmonary involvement, and the nature of lesions seen on chest X-ray. Clinical,
bacteriological and radiological improvement following effective therapy led to partial reversal of
these changes. The depression of plasma zinc level was found to be more pronounced and a highly
sensitive index of tuberculous activity compared to elevation of plasma copper level.
Introduction
Elevation of plasma copper and/or depression
of plasma zinc level (Tani 1965, Halsted
and Smith 1970, Underwood 1971, Beisel,
Pekarek and Wannemacher 1974, Bogden et
al 1977) has been reported in pulmonary tuberculosis
and in many other chronic diseases.
Most of the studies on these two biochemical
parameters relate only to one of them. For
example, whereas Tani (1965) has emphasised
the importance of measuring serum copper
as a useful biochemical modality in pulmonary
tuberculosis, Halsted and Smith (1970) have
demonstrated reduced plasma zinc level. Bogden
et al (1977) have drawn attention to the importance
of measuring both the parameters simultaneously
in these cases, although in most of
their cases, high copper concentration and
low zinc level was not encountered simultaneously.
Pulmonary tuberculosis has a wide spectrum
of presentation. The lesions, radiographically,
may range from acute pneumonic form to that
of chronic fibroid lesion. Likewise, the symptoms
may also vary from severe to none. It
is well recognised that many patients, especially
those following chemotherapeutic treatment,
may not excrete tubercle bacilli in their sputum,
though they continue to suffer from active
pulmonary tuberculosis. Consequently, it is
expected that the basic metabolic alteration,
encountered in this disease, will vary according
to the mode of presentation, severity of the
disease and presence or absence of tubercle
bacilli in the sputum. Adaptation of a single
criterion for the diagnosis of pulmonary tuberculosis
e.g. isolation of T.B. from the sputum,
will necessarily restrict the spectrum of case
studies (Bogden et al 1977). Furthermore, the
authors felt that correlation of these biochemical
parameters, with the clinical, radiographic and
bacteriological status of the patient may be
essential. Further, an effort has been made in
this study, to record the effect of anti-tuberculosis
chemotherapy, administered for 3
months, on plasma copper and zinc concentration.
Material and Methods
The material for the study was selected
from human volunteers (controls) and from
proved patients of pulmonary tuberculosis
admitted to the indoor wards of the department
of tuberculosis and respiratory diseases.
The control group included doctors, nurses
and other staff members working in the department.
They were thoroughly examined and
had a negative medical history. They were not
receiving any medication (46 subjects).
94 patients of pulmonary tuberculosis were
included in the study. 46 patients were sputum
positive (by smear examination) at the time of
admission to the study, while 48 patients were
reported to have been sputum positive in the
past, though negative at the time of the study.
Patients who had hepatic or renal disorders,
diabetes mellitus, hypertension, rheumatoid
disease, lymphoma, myocardial infarction,
pernicious anaemia, hyperthyroidism and
chronic alcoholics were excluded. Women who
were pregnant or were taking oral contraceptives
were also not included.
Detailed history, particularly relating to
previous therapy, was taken. On the basis of
history of previous anti-tuberculosis treatment
the patients were divided in two groups:—
(a) The random group: Patients who had
*Department of Tuberculosis, K.G’s Medical College, Lucknow-226 003 (India).
**Division of Endocrinology, Central Drug Research Institute, Lucknow-226 003.
Ind. J. Tub., Vol. XXIX, No. 3

180 B.K. KHANNA, et al.,
had anti-tuberculosis therapy for more
than a month prior to their induction
in the study (64 cases).
(b) The follow up group: Patients who had
not been treated previously, or who had
taken less than one month of antituberculosis
chemotherapy. After initial
observations, these patients were put
on specific anti-tuberculosis therapy;
comprising of either streptomycin 1
gm. I.M.I, once a day. I.N.H. 300 mg.
orally once a day and PAS 10 gms.
orally (S-f P+H in 6 patients) or streptomycin
and I.N.H. in the same dose as
above and thioacetazone 150 mg./day
orally in place of PAS (S+T+H in
21 patients) or streptomycin + I.N.H.
in the same dose as above and Ethambutol
1000 mg. by month/day (S4- H+E
in 2 patients) or streptomycin + I.N.H.
in the same dosage as given above
(S+H in 1 patient).for a period of
3 months. All the clinical and biochemical
observations were recorded in
these patients at the end of 1, 2 and
3 months of therapy (30 patients).
Observations recorded in these patients
included detailed clinical examination, routine
laboratory investigations including sputum
smear examination for A.F.B. and special
investigations such as plasma copper and zinc
estimation.
The method for assessment of plasma copper
and zinc was the same as that employed by
Bogden et al (1977). The blood samples were
withdrawn between the hours of 10 A.M. and
4 P.M. which coincided with the working
hours of the department.
Observations
A. Correlation between plasma copper and
plasma zinc levels in tuberculosis patients
and control subjects:—
Correlation between plasma (Cu) and Zinc
(Zn) in relation to normal values at the time
of admission to the study.
A significant rise of 22% in plasma copper
level (154.5 ug% ± 33.6) took place in the
patients in contrast to controls (t = 6.04,
df = 138, P < 0.001), while the decline in the
plasma zinc level (63.6 ug% ±17.8) was 28.8%.
The difference was highly significant (t = 10.22,
df = 138, P < 0.001). The reduction in zinc
level was more pronounced. However, no
significant difference was observed in plasma
copper and plasma zinc level between treated
and untreated patients (t = 1.24, df = 42,
P > 0.05).
Out of 94 patients, there were 69 males and
25 females. Their age varied from 10 years to
50 years. No statistical correlation could be
obtained between plasma copper and plasma
zinc values with relation to age and sex of the
patients.
The dietary level of copper and zinc in this
study was not estimated, though all the patients
continued to receive the standard hospital diet.
B. Copper/Zinc ration in tuberculosis patients
and control subjects:
Copper/Zinc ratio was estimated in 46
controls and 94 tuberculosis patients. The ratio
was 2.61 ± 0.85 in tuberculosis cases, while it
was 1.44 ± 0.27 in controls. The difference was
highly significant (t= 12.14, df= 138, P < 0.001).
80 out of 94 patients showed abnormalities
of either plasma copper level or of plasma zinc
level or both. 14 patients had normal plasma
copper as well as zinc level. 20 patients had
normal plasma copper and low plasma zinc
level (value less than 70 ug%). There were 6
patients who had high plasma copper level
(value exceeding 145 ug%) and normal zinc
TABLE 1
Correlation Between Plasma (Cu) and Zine, (Zn) in Relation to Normal Values at the time of admission to the study
Ind. J, Tub., Vol. XXIX, No. 3

PLASMA COPPER AND ZINC LEVELS IN PULMONARY TUBERCULOSIS 181
level, while 54 patients had high plasma copper As there was no statistical difference in
level and as well as low plasma zinc level, plasma copper and zinc concentration between
treated and untreated groups (vide table 1),
C. Correlation between plasma copper con a11 the Patients (94) were clubbed together for
centration and zinc concentration with sputum analysis.
status of tuberculosis patients:
TABLE 2
Correlation between Plasma Copper and Zinc Levels with Sputum Status
Sputum for A.F.B. No. of Ps. Plasma Copper Plasma Zinc
Meam (ug%) ± S.D. % rise Meantug%) ± S.D. % fall
Positive 46. 175.4 ± 19.3 38.5 54.6 ± 16.5 38.8
Negative 48 139.8 ± 39.4 10.4 71.7 ± 22.5 19.7
Normal Value: 126.6ug% ±20.6 89.3 ug% ± 9. 5
It is apparent from table 2 that plasma
copper concentration was significantly higher
in sputum positive cases (t=5.61 df=92,
P

182 B.K. KHANNA, et at.,
tically significant (between I & II—1 = 1.77, patients who had improved with the therapy,
df=75, P > 0.05; II & III—1=3.52, df=64, irrespective of the therapy administered. Con-
P < 0.001; and I & III—t==3.86, df=43, P < sequently, the values obtained in these patients
0.001). Plasma zinc changes were manifest even are being presented below as a single group,
in patients with one or two zones involvement
as compared to serum copper level which In the patients, who showed improvement
showed no change from normal in these patients due to chemotherapy, plasma copper level
(i.e. those with less than 3 zones involvement). declined from mean value of 152.4 ug% to
TABLE 4
Table showing the levels of Plasma Copper and Zinc in Relation to Predominant Nature of the Lesion
Nature of predominant lesion No. of patients Plasma Copper Plasma Zinc
Mean (ug%) ± S.D. % rise Mean (ug%) ± S.D. % fall
Exudative 26 149.6 ± 30.4 18 68.9 ± 16.6 21.7
Productive 10 141.9 ± 15.8 12 73.9 ±14.5 17
Cavitary 44 171.9 ± 30 35.8 56.5 ±13.1 37
Fibrotic 12 131 3.5 79.5 ±17.6 11
Miliary 2 192 51.6 61 31
Normal Value : 126.6 ug% ±20.6 89.3 ug% ±9.8
Plasma copper concentration was highest in
cases suffering from miliary tuberculosis. It
showed a rise of 51.6% from normal value.
Plasma zinc level was lowest in cavitary cases
and registered a fall of 37 % from the normal.
We were unable to find any correlation of
plasma copper and zinc level with duration of
disease as reported by the patient (which, no
doubt, was highly subjective), mean temperature
of the patients, and the average size of the
cavities seen in our cases.
E. Follow up group:
Out of a total 94 patients, only 30 patients
stayed in the wards for a period of 3 months to
permit us a follow up of these patients. They
were administered (S+P+H in 6 cases, S+Tf-H
in 21 cases, S+H+E in 2 cases and S-j-H
in 1 case) four different regimen. 25 of them
improved clinically, radiographically and
bacteriologically. On the other hand, 5 of them
had remained stationary.
There was no different in plasma copper and
zinc levels between the various sub-groups of
149.2 ug%, but the difference was not statistically
significant (t=0.43, df=48, P > 0.05).
The level of plasma zinc rose with effective
chemotherapy. The rise was found to be significant
(t== 3.10, df=48, P < 0.01). On the other
hand, cases showing no improvement did not
have any significant effect on the plasma zinc
level.
Discussion
Pulmonary tuberculosis affects metabolism
of trace elements like any other infectious
disease. High plasma copper and low plasma
zinc concentrations obtained in our cases reflect
only one aspect of these disturbances. Similar
observations have been recorded by other
workers too (Tani 1965, Halsted and Smith
1970, Underwood 1971, Beisel, Pekarek,
Wannemacher 1974, Bogden et al 1977), though
some of them have highlighted the alterations
in plasma copper level (Tani 1965) while others
have focused attention on the plasma zinc level
(Halsted and Smith 1970). Bogden et al (1977)
have attempted to study both the trace metals
at the same time in proved cases of pulmonary
tuberculosis and have come to similar con-
Ind. J. Tub., Vol. XXIX, No. 3

PLASMA COPPER AND ZINC LEVELS IN PULMONARY TUBERCULOSIS
183
TABLE 5
Correlation of Plasma Copper ami Zinc Level with Response to Therapy in Follow-up group
(30 Patients)
No. of Patients Before treatment Alter 3 months’ treatment
Plasma Cu Plasma Zn Plasma Cu Plasma Zn
Mean
(ug%) ±
S.D.
% Mean rise
(ug %)
± S.D.
% Mean %
fall (ug%) change
±S.D.
Mean
(ug%) ±
S.D.
%
change
Improvement
25 152.4
±25
No Improvement
5 172.4
±8.7
20.3 65.6
±15.7
24 64.6
±36.8
26.5 149.2 2.3
±23 (fall)
27.6 176.5 5.5
±8.8 (rise)
78
±12.3
62
±34
13
(rise)
2.9
(fain
elusions. However, they have raised and left
many questions unanswered, which no doubt,
will have serious bearing on the trace element
metabolism in pulmonary tuberculosis. In this
study we have attempted to answer some of
these.
Plasma Copper and Zinc
Tuberculosis
levels in Pulmonary
Rise in plasma copper and fall in plasma
zinc level was recorded in our cases. Both of
these alterations were found to be statistically
significant. Fall in plasma zinc level was more
pronounced compared to rise in plasma copper
level. Lowering of plasma zinc has been considered
to be a more sensitive index of tuberculous
infection compared to rise in plasma
copper level (Beisel, Pekarek and Wannemacher
1974). Consequently, Bogden et al
(1977) concluded that low plasma zinc level
with normal plasma copper may mean that
infection is in early stages.
Patients of pulmonary tuberculosis, who had
demonstrable acid fast bacilli (A.F.B.) in
sputum smear examination had higher plasma
copper level and lower plasma zinc level compared
to those who did not have A.F.B. in
their sputum smear. This again shows that the
activity of the lesion has a direct bearing on
the plasma level of these trace elements. The
same was found to be true for patients who had
lesions extending beyond two zones of the
lung. Lesionwise, patients with miliary tuberculosis
had highest rise in plasma copper level
and maximum depression of plasma zinc level.
These cases were closely followed by patients
having cavities in the lungs. The patients having
predominantly productive lesions had minimal
alterations in plasma level of these trace
elements. Those having predominantly
fibrotic lesion did not have any alteration in
their plasma copper level, though slight depression
in their zinc level was seen.
It might, therefore, seem that alterations
in the plasma level of these trace elements can
be directly associated with evidence of activity
of tuberculous lesions which may be direct, for
example, sputum containing acid fast bacilli
or indirect such as nature and extent of pulmonary
radiographic lesion. Understandably,
because of the highly subjective and variable
factors, no clear cut correlation could be
obtained between plasma level of these trace
elements and age and sex of patients, duration
of illness, temperature of patients and size of
the cavities as observed radiographically.
Alterations noted after 3 months of effective
chemotherapy
The patients who had improved following
therapy revealed elevation of plasma zinc level
which was more pronounced and more rapid
Ind. J. Tub., Vol. XXIX, No. 3

184 B.K. KHANNA, et al.,
compared to depression in plasma copper level.
Rise in plasma zinc level was found to be
significant though decline in plasma copper
level was not statistically significant. Plasma
zinc level, therefore, appears to be a more
sensitive indicator of activity of the tuberculous
lesion as compared to plasma copper level.
In patients who did not improve with
chemotherapy, the process of rise in the plasma
copper and decline in plasma zinc continued
unabated.
Four schedules of chemotherapy were administered
in our patients. Alterations in the
level of these trace elements did not appear to
be influenced by the chemotherapy employed.
Indeed it was the improvement in clinical
condition of the patients which appeared to be
the only influencing factor.
The more gradual change in the plasma
copper level is consistent with the concept that
a period of time is required to allow the liver
to synthesize and release the copper binding
protein, ceruloplasmin (Beisel, Pekarek and
Wannemacker 1974). The persistence of high
copper concentrations in contrast to more
rapid return of zinc concentration to base line
value could be because of relatively long half
life of ceruloplasmin (Beisel, Pekarek and
Wannemacker 1974). Tani (1965) has demonstrated
that serial measurements of both serum
iron and copper concentrations could not only
serve as an indicator of a favourable host
response to chemotherapy but also as an early
sign of relapse. Our study has confirmed that
serial measurements of plasma copper and,
more importantly, plasma zinc level may serve
as an indirect pointer to the diagnosis of tuberculosis,
to the degree of tuberculo-toxaemia,
to the extent and nature of the pulmonary
involvement and to the favourable response of
the host to the specific anti tuberculosis therapy.
The role of kidneys in retention of copper
and increased excretion of zinc leading to
alterations in the serum level of those trace
elements has not yet been defined.
REFERENCES
1. Beisel W.R., Pekarek R.S., Wannemacker R.W., :
The impact of infections disease on trace element
metabolism of the host. Trace element metabolism
in animals. Volume 2. Edited by Hoekstra W.G.,
Suttie, J.W., Ganther, H.E. et al. Baltimore,
University Park Press, 1974, pp. 217-240.
2. Bogden, J.D., Lintz, D.I., Joselow, M.M., Charles,
J., and Salaki, J.S. Effect of pulmonary tuber
culosis on blood concentrations of copper and
zinc, Am. J. Clin. Path.; 1977, 67, 251-256.
3. Halsted, J.A., and Smith J.C. Plasma zinc in health
and diseases, Lancet; 1970, 322-324.
4. Tani P. Serum iron, copper, iron-binding capacity
and marrow hemosiderin in pulmonary tuberculosis,
Ann. Med. Intern. Fenn.; 1965, 54 Suppl. 44, 1.
5. Underwood, F.J. (1971) Trace elements in human
and animal nutrition, New York Academic Press,
1971, pp. 68-73, pp. 214-216.
Ind. J. Tub., Vol. XXIX, No. 3

PLASMA ERYTHOCYTE AND LEUCOCYTE FREE ALPHA AMINO NITROGEN
ALTERATIONS IN PULMONARY TUBERCULOSIS AND EFFECT OF A
GLUCOSE LOAD ON THESE PARAMETERS
S.C. SETH, HARBANS LAL, A.S. SAINI AND M.S. PARMAR
Summary : Plasma, erythrocyte and leucocyte free amino nitrogen (FαAN) levels were estimated
in bacteriologically proved active cases of pulmonary tuberculosis, arrested cases and controls
(15 subjects in each ,group). The effect of a glucose load on these parameters was also studied. In
active pulmonary tuberculosis, plasma and leucocyte FαAN levels were decreased while erythrocyte
FαAN concentration remained unaltered when compared with the controls and with the group of
arrested cases. The glucose load led to fall in the levels of plasma FαAN in all the three groups. The
possible mechanism (s) for the low levels of plasma and leucocyte FαAN in patients with pulmonary
tuberculosis is discussed.
Introduction
In protein calorie malnutrition which is a
condition associated with reduced protein
anabolism, both plasma and leucocyte free a-
amino nitrogen (FαAN) levels are reduced as
compared to normals (Gupta and Agarwal,
1973; Lai ct al 1975). Further, a variety of
infections are known to alter free amino acid
levels in plasma, the pattern of change may
depend upon the type of microorganism responsible
for infection (George et al, 1974;
Wannemacher et al, 1975). Serum amino acid
concentration has been shown to be decreased
in pulmonary tuberculosis (Kibrik and Khautina,
1973X However, leucocyte free amino acid
concentration in pulmonary tuberculosis has
not been studied, as yet. It will therefore be
interesting to study both plasma and leucocyte
FαAN concentrations in pulmonary tuberculosis.
It is further planned to see the effect
of a glucose load on these parameters since
Jaya Rao and Raghuramulu (1972) found that
after a glucose load, plasma FαAN concentration
is reduced in normal children and that the
reduction is delayed in malnourished subjects.
Material and Methods
Fifteen patients (13 males and 2 females)
in the age group of 23 to 40 years except 3 who
were between 50-65 years, having active
pulmonary tuberculosis were selected for the
study. The activity of the disease was proved by
positive sputum for acid fast bacilli (AFB) and
by the presence of pulmonary lesion radiologically.
All the patients had cough expectoration,
mild to moderate evening rise of fever, complaint
of generalised weakness and malaise.
The mean hemoglobin concentration of the
patients was 10.5il.87g/dl. These patients
also had 15-20% weight loss when compared
with the normal weight for their age and height.
They were not receiving any therapy for at
least 2 weeks prior to study. Another group
included 15 subjects who had earlier taken
antitubercular treatment for at least 18 months
and were not getting medication for two weeks
prior to study. Disease was considered quiescent
after clinical, radiological and repeated
sputum examination which did not reveal any
activity. The mean hemoglobin concentration
of this group was 12.4±1.23g/dl which was
comparable with the controls (12.8rtO.95g/dl).
Fifteen apparently normal persons within the
same age group not having any illness or infection
for at least two weeks prior to the study
served as controls.
Fasting venous blood (3-5 ml) was collected
for the estimation of free L-amino nitrogen
(FαAN) in plasma, erythrocyte and leucocyte,
in tubes containing heparin as anticoagulant.
Each subject was then orally administered 100 g
of D-glucose in 2-3 dl of water. Thereafter three
blood samples were collected at 45, 90 and 135
min, respectively. Blood was allowed to sediment
at 4° for 30 min for the seperation of
plasma, erythrocytes and leucocytes. The
blood was centrifuged at 500g for 5 minutes and
plasma was removed. From the remaining
aliquot erythrocytes and leucocytes were separated
as reported by Gupta and Agarwal (1973).
Plasma, erythrocyte and leucocyte FαAN
concentrations were estimated according to the
principle of Goodwin (1968), as reported by
Lai and Agarwal (1974).
Results
Plasma erythrocyte and leucocyte free a-amino
nitrogen (FαAN) concentrations in different
groups :
Fasting plasma FαAN concentration was
49.3±12.38mg/l in normal controls and 50.4±
Departments of Tuberculosis & Chest Diseases and Biochemistry, Medical College, Rohtak-124 001.
Ind. J. Tub., Vol. XXIX, No 3

186 S.C. SETH, HARBANS LAL, A.S. SAINI AND M.S. PARMAR
TABLE 1
Fasting plasma, erythrocyte and leucocyte free α.-amino nitrogen concentrations in normal subjects, patients and arrested
cases of pulmonary tuberculosis
(Values are means ± S.D. for 15 subjects in each group.)
Subjects
Free a-amino nitrogen
Plasma (mg/1)
(mg/l)
Erythrocyle
Leucocyte
(µ.g/10 8 colls)
Controls 49.3 ± 12.38 105.2 ± 38.33 4.40 ± 1.10
Patients 37.6 ± 4.48* 97.3 ± 28.84 2.93 ± 0.56**
Arrested 50.4 ± 7.18 109.7 ± 32.14 3.70 ± 0.82
* P < 0.001 when patients compared with the controls and treated cases. ** P < 0.001 when patients compared
with the controls and < 0.01 when compared with the group of treated
subjects.
The erythrocyte FαAN concentrations at
7.18 mg/1 in a group of treated cases.-The
various times remained unaltered in the different
levels in the two groups were comparable with each groups studied (P>0.05; fig 2).
other. In patients with pulmonary tuberculosis the
value was lowered to 37.6±4.48 mg/1, the decrease
being statistically significant when compared with
the other two groups (P

PLASMA ERYTHROCYTE ALTERATIONS 187
reduced when compared with the controls
(P

188 S.C. SETH, HARBANS LAL, A.S. SAINI AND M.S. PARMAR
condition with enhanced protein catabolism
and neoglucogensesis. The findings of low
FαAN in leucocyte in a protein catabolic
process like tuberculosis would mean that
leucocyte like muscle may also participate in
transferring amino acids to liver for neoglucjjenesis.
Similar observations have been made
in protein calorie malnutrition where again
low FαAN levels in leucoyte have been explained
because of the protein catabolic state
resulting in transfer of amino acids from
leucocyte to liver (Lai et al, 1979). Beisal (1972
and 1975) reported that infection is associated
with low insulin/glucagon ratio which is likely
to promote neoglucogenesis and it may also
be a reason for increased neoglucogenesis
observed in tuberculosis. The erythrocyte did
not show any change in FαAN levels meaning
thereby that unlike leucocytes, erythrocytes
do not participate in protein catabolic response,
since erythrocyte is insulin insensitive cell.
Erythrocyte amino acid levels were not found
to be significantly altered with the food intake
whereas plasma amino acid levels were reduced
(Elwyn, 1966).
As shown in Table II, glucose load in different
groups led to reduction in the levels of
plasma FαAN. However, FαAN levels in
erythrocytes and leucocytes were not affected
(figs 2 and 3). It was also interesting that the
response was slightly delayed in patients. Reduction
in plasma amino acid levels in healthy
individual after a glucose load has been reported
by several workers (Munro and Thompson,
1953; Swendseid et al, 1967; Adibi et al, 1975).
Potter et al (1972) suggested that glucose depletes
plasma free amino acids by promoting the
cellular uptake of amino acids with or without
protein synthesis. The delayed response in
plasma FαAN in patients with tuberculosis
may be a result of delayed insulin response in
these patients.
REFERENCES
1. Adibi, S.A., Morse, E.L. and Amin. P.M. : Role of
insulin and glucose in the induction of hypoaminoacidemia
in man: Studies in normal juvenile diabetic
and insuloma patients. J. Lab, Clin. Med. 1975,
85, 395.
2. Beisel, W.R. : Interrelated changes in host metabolism
during generalised infectious illness. Am. J.
Clin. Nutr. 1972, 25, 1254.
3. Beisel, W.R. : Metabolic response to infection.
Am. Rev. Med. 1975, 26, 9.
4. Elwyn, D.H. : Distribution of amino acids between
plasma and red blood cells in the dog. Fe.i. Prar.
1965, 25, 854.
Ind, J. Tub., Vol. XXIX, No. 3
5. George, D.T., Rayfield, R.J. and Wannamacher,
R.W.. Jr. : Altered glucoregulatory hormones
during acute pneumococcal sepsis in Rhesus
monkey. Diabetes 1974, 15, 544.
6. Goodwin, J.F. : The calorimetric estimation of
plasma amino nitrogen with DNFB. Clit,. Chem.
1968, 14. 1080.
7. Gupta, M. and Agarwal, K.N. : Free amino acid
patterns of plasma erythrocyte and leucocyte
in hypoproteinemia. Br. J. Nutr. 1973, 29, 151.
8. Java Rao, K.S. and Raghuramulu, N.: Insulin
secretion in Kwashiorkor. ,7. Clin. Entiocrinol.
Met’,b. 1972, 35, 62.
9. Kibrik, D.S. and Khautina, F.S. : Fiee amino acid
contents in blood during pulmonary tuberculosis.
Sov. Med. Rnssian (Eng. Tranf.) 1973, 36, 146.
10. Lai, H. and Agarwal, K.N. : Influence of hormones
on free alpha amino nitrogen alterations in plasma
erythrocyte and leucocyte in rats. Nutr. Metab.
1974, 17, 148.
11. Lai, H., Agarwal, K.N. And Shanker, R. : Changes
in free alpha amino nitrogen and nucleic acid
patterns in protein deficient rats. Indian J. Expt.
Biol 1975, 13, 19.
12. Lai, H., Saini, A.S., Yadav, N.S. and Dhatt, P.S. :
Free alpha amino nitrogen levels in protein calorie
malnutrition Proc. Nutr. So.. India 1979, 23, 39.
13. Munro, H.N. and Thompson, W.S.T. : Influence
of glucose on amino acid metabolism. Metabolism
1953, 2, J54.
14. Potter, E.L., Purser, D.B. and Bergen. G.W.: Plasma
reference index for predicting limiting amino
acids of sheep and rats. J. Anim. Sci. 1972, 34, 650.
15. Swendseid, M.E., Juttle, S.G., Drenick, G.J., Joven,
C.B. and Massay, F.J. : Plasma amino acid response
to glucose administration in various nutritive
states. Am. J. Cliv. Nutr. 1967, 20, 243.
16. Wannemacher, R.W., Jr., Pekerck, R.S., Bertalloni,
P.J., Vollmer, R.J. and Beisel, R.W. . Changes
in plasma amino acids following experimentally
induced sandfly fever virus infection. Metabolism
1972, 21,67.
17. Wannemachsr, R.W., Jr., Dinterman, R.E., Perkerck,
R.S., Bertalloni, P.J. and Beisel, W.R. :
Urinary amino acid excretion during experimentally
induced sandfly fever in map. Am. J. Clw.
Nutr. 1975, 28, 110.
-

SERUM MUCOPROTEIN (TYROSINE) LEVEL AND LACTIC DEHYDROGENASE
ACTIVITY IN CHILDHOOD TUBERCULOSIS*
S.D. SINGH** AND N.M. JAIN***
Summary : Mucoprotein (tyrosine) levels and lactic dehydrogenase activity were estimated in the
serum of fifty children suffering from tuberculosis and 10 healthy controls. It was observed that various
types of childhood tuberculosis showed raised values of serum mucoprotein ranging from 9.5 to
139 mgm% with maximum rise incases of tuberculous pleural effusion. Lactic dehydrogenase
activity was also increased ranging from 132 to 560 I.U., with maximum rise in cases of tuberculous
meningitis.
Introduction and Review
The prevalence of childhood tuberculosis is
still high in India. Various authors have reported
14 to 17 % of total admissions in hospital
being due to tuberculosis. However, the prevalance
of the disease is much more than can
be presumed from hospital admissions. Early
detection of cases and their proper management
is necessary to prevent serious complications of
the disease which otherwise may endanger
life of these children. The authors in their
study of measles cases found that those cases
of measles which were associated with tuberculosis
had significantly higher levels of serum
mucoprotein (tyrosine). It was therefore planned
to study the changes in serum mucoprotein
(Tyrosine) in childhood tuberculosis, since
authentic information about it is lacking so
far.
Mucoproteins are polypeptides of high
molecular weight and are an important constituent
of the ground substance of connective
tissue. Tyrosine constitutes 4-2% fraction of
mucoproteins. The exact physiological significance
of this fraction is not known. Variations
in serum mucoprotein level have been reported
in various disorders. According to Greenspan
(1965) total mucoprotein levels are lowered in
impaired hepatic function and endocrine functions,
while inflammatory, neoplasic and traumatic
changes tend to increase the mucoprotein
levels. The number of cases studied were Malnutrition
19, Diabetes 18, Rheumatism 13, renal
disorders 16, Indian childhood Cirrhosis 14 and
Measles 17. Elevated levels of total serum
mucoprotein in tuberculosis in adults have
been reported by Pilheu et al (1962). They
have also described changes in various types
of tuberculosis which revert to normal
with regression of disease, in these cases. However,
studies in childhood are lacking.
Lactic dehydrogenase (LDH) was first discovered
by Meyerh of in 1979. Lactic dehydrogenase
is an intracellular glycolytic enzyme
which catalyses the reversible reduction of
alpha keto and alpha and gamma di keto acids
to their corresponding hydroxy acids in the
presence of reduced nicotinamide adenine
dinucleotide. Normal value of serum lactic
dehydrogenase varies from 50-150 L.U. in older
children and 300 to 1500 in newborn (Nelson,
1975 and Pohowala, 1973) L.D.H. is very
widely distributed in body tissues like brain,
liver, lymph nodes, kidney, heart, lung, erythrocytes,
leucocytes and is also present in cerebrospinal
fluid and serum (Abderhalden, 1961).
Lactic dehydrogenase activity in serum is
markedly elevated in patients with megaloblastic
anaemia, acute leukemia, urinary tract
infection, pulmonary embolism, pulmonary
tuberculosis in adults, tubercular meningitis
(Amader and Pochen, 1966; Agrawal, 1968;
Zimmermann and Henry, 1969: Brijkishore and
Nagrath, 1970).
Material and Methods
* Paper presented at 3rd Asian Congress of Paediatrics at Bangkok.; 1979.
** Prof. & Head, Department of Paediatrics
*** Asstt. Surgeon, Distt. Narsinghpur, M.P.
(From the Department of Paediatrics, M.G.M. Medical College, Indore).
50 children suffering from childhood tuberculosis
were taken up for this study. 15 cases
had uncomplicated primary tuberculosis, 10
cases had bronchogenic tuberculosis, 5 cases
were of plural effusion, 10 cases of collapse
with consolidation and 10 were of tuberculous
meningitis. 10 healthy controls in the same age
groups were concurrently taken.
Routine investigations like total and differential
count, blood E.S.R. tuberculin test and
X-ray chest were done. Total serum proteins
and its fractions were also analysed. Serum
mucoprotein (tyrosine) was estimated by modified
Winzler method (Winzler et al 1948). Estimation
of serum lactic dehydrogenase activity
Ind. J. Tub., Vol. XXIX, No. 3

190 S.D. SINGH AND N.M. JAIN
was made by calorimetric method of Cabaud
and Wroblewski (King, 1959).
There was no case below the age of one year,
(Table 1).
Observations
The total proteins in controls ranged between
TABLE 1
Showing Age & Sex Distribution of Cases in Various Types of Childhood Tuberculosis
*
No. Types of tuberculosis Total No. Sex Distribution Age-Wise Distribution of
cases Male Female 0-1 yr. 1-5 yrs. about 5
1. Primary tuberculosis 15 8 7 1 14
2. Tuberculosis Broncho-Phenomena 10 7 3 1 6 3
3. Tuberculous pleural effusion 5 3 2 2 3
4. Tuberculous collapse consolidation 10 5 5 2 5 3
5. Tuberculous meningitis 10 6 4 8 2
Total 50 29 21 4 35 11
TABLE 2
Showing Mean Levels of Serum Proteins in Various Types of Childhood Tuberculosis
SI.
No.
Types of cases
Total proteins
(In gms%)
Albumin
(In gms%)
Globulin
(In gms%)
A/G Ratio
1. Controls 6.12 3.05 2.80 1.04
2. Primary tuberculosis 5.80 2.71 3.27 0.77
3. Tubercular Broncho pneumonia 6.10 2.40 3.60 0.73
4. Tubercular Pleural effusion 6.90 2.30 4.60 0.53
5. Tubercular collapse consolidation 5.80 2.20 3.50 0.64
6. Tuberculous meningitis 5.70 2.10 3.60 0.59
Discussion 6-6.5 gms. %, with an average of 6.12 gms %.
In tuberculosis cases it ranged between 4-7.8
Out of the 50 children included in this study, gms%. The albumin fraction had lower values
35 were in the age group of 1 to 5 years and in all types of cases. The globulin fraction
only four were, below the age of one year, showed elevated levels as compared to controls.
29 of these children were males and 21 were This type of change in total proteins and its
females. There were 8 cases of tuberculous fractions was also described by Seibett and
meningitis between the age of one to five years. Nelson (1947).
Ind. J. Tub., Vol. XXIX, No. 3

SERUM MUCOPROTEIN (TYROSINE) LEVEL AND LACTIC -DEHYDROGENASE
TABLE 3
Showing Mean Levels of Serum Mucoprotein (Tyrosine) and Lactic Dehydrogenase Activity in various types
of Childhood Tuberculosis.
SI.
No.
Types of cases
Serum Mucoprotein (Tyrosine)
(in mgm %)
Serum lactic Dehydrogenase
(in I.U.)
1. Control 5.02 130.8
2. Primary Tuberculosis 17.52 170.0
3. Tubercular Broncho-pneumonia 83.20 359.0
4. Tubercular pleural effusion 126.00 297.5
5. Tubercular collapse consolidation 46.70 260.6
6. Tubercular meningitis 55.70 367.4
Mucoprotein (tyrosine) values in normal
cases ranged between 2.4-7.6 mgms. % with an
average of 5.02 rag. % and lactic dehydrogenase
activity in serum in normal persons ranged
between 102 to 216 I.U., with a mean level of
130.8 I.U.
Mucoprotein (tyrosine) fraction was increased
in all clinical types of childhood tuberculosis,
but the increase was not uniform in
all types. In cases of uncomplicated primary
tuberculosis values ranged between 9.5-26.5
mgms. % with an average of 17.52 mgms. % ±
5.5. In the other forms of tuberculosis, Mucoprotein
values were substantially raised as
follows:
Tuberculous
Broncho-pneumonia —71-96mgm%, average
83, 20mgm% ± 9.(
Pleural Effusion
Collapse
consolidation
— lll-139mgms%, averagel26%mgm
; ± 12.:
—31-58 mgm%, average
46.70mgm% ± 10.95
TB Meningitis —42-69mgm%, average
55.70 mgm% ± 9.40
It would be seen that the values were highest
in cases of pleural effusion. Table 2 will show
that the serum globlin level was also highest
(4.60 gm%) in pleural effusion. In other words,
mucoprotein level follows the level of serum
globlin since mucoprotein (tyrosine) goes with
a 2 globlin fraction of the serum. Mucoprotein
levels are increased usually following infection,
destruction of collagen tissue and involvement
of the liver. Factors which may be responsible
for the maximum increase in cases of pleural
effusion are not known.
There is also a suggestion of a possible
correlation between mucoprotein level and
severity of tuberculous disease, since the mucoprotein
level is lowest in uncomplicated primary
tuberculosis as compared to the other more
severe forms of tuberculosis.
Serum lactic dehydrogenase levels were also
increased in tuberculous cases. The values in
different manifestations were as follows (Table 3):
Primary Tuberculosis
(uncomplicated)
—132-236 IU, average
170 ± 32.6
Tuberculous
Broncho-pneumonia —280-492 IU, average
359 IU ± 74.3
Pleural Effusion
Collapse
Consolidation
TB Meningitis
—272-336 IU. average
297.5 IU ± 27.7.
—148-396 IU, average
260.6 IU ± 66.4
—272-460 IU. average
367.4 IU ± 56
Lactic dehydrogenase values depend on its
Ind. J. Tub., Vol. XXIX, No.3

192 S.D. SINGH AND N.M. JAIN
release from damaged tissue because of changes
in cellular permeability. In 63 to 100% cases
of post-primary tuberculosis, liver is involved.
This being a source of LDH activity, increased
values are seen in pulmonary disease. Since
brain is the richest source of LDH, maximum
LDH activity in cases of TB Meningitis may
be due to its increase in the CSF. This view is
supported by Aronson (1966) and Jain (1976).
REFERENCES
1. Abderhalden, R. : Clinical Enzymalogy, B.K.
Onmort and Company, INC, 1961.
2. Agrawal, R.K. : Observations on pleural effusion
with special reference to enzyme study and pleural
biopsy. Thesis for M.D. (Medicine) University
of Indore, 1968.
3. Amader, E., Pochen, E.J. Serum Lactic dehydrogenase
activity and radio active scanning in diagnosis
of pulmonary embolism. Ann. Intern. Med.
1966, 65, 1247.
4. Aronson, M.B. : Enzyme determination in neurological
and neuromuscular disorders of infancy
and childhood. Paed. Clin. North. America. 1966,
7:527.
5. Brijidshore, Nagrath, S.P.: Serum and pleural fluid
lactic dehydrogenase activity in tuberculous pleural
effusion. The J. of Ase. Phy. Ind. 1970, 18:15.
6. Greenspan, E.M. ; Clinical significance of serum
mucoprotein. Adv. Int. Med., 19o5, 7:101.
7. Jain, N.N. : Serum L.D.H. activity in childhood
tuberculosis thesis for M.D. (Paed.) University
of Indore, 1976.
8. King, E.L. : Routine methods for estimation of
L.D.H. Activity. J.M. Lab. Tach. 1959, 16:26.
9. Nelson : Text book of Paediatrics, 1975. W.B.
Saunders and Co.
10. Pilheu, K.A. Lannello, J.A. Wilson, J. : Serum
proteins in Pulmonary tuberculosis. Dis. of Chest
1962, 41:173.
11. Pohowalax, P. : Serum L.D.H. activity in newborn,
Thesis for M.D. (Paed.) University of Indore,
1973.
12. Seibett, F.B. Nelson, J.M. : Serum proteins in
tuberculosis. Am. Rev. Tub. 1974, 47:66.
13. Singh, S.D. Chhaparwal, B.C. Deshpande, J. : Serum
Mucoprotein (Tyrosine) in rheumatism, Ind. Jour,
of Paed., 1971, 38:32.3.
14. Sineh, S.D. Khan, M.A. Dabke, A.T. Chhaparwal,
B.C. : Serum Mucoprotein (tyrosine) in Indian
Childhood Cirrhosis, Paed. Clin. Ind., 1973. Jan, 51.
15. Singh, S.D. Bhagwat, C. Kutumbale, A, : Serum
Mucoprotein (tyrosine) in protein calories
Malnutrition. Paed. Clin. Ind., 1975, 10:117
16. Singh, S.D. Mehta, S. Chhaparwal, B.C. Khan.
M.A. : Serum mucoprotein levels in acute
glomerulonephritis and nephrotic syndromes in
children. The Indian Practitioner, 1975, Sept., 564.
17. Singh, S.D. Parekh, P. Jain N.N. : Serum Mucoprotein
(tyrosine) in meagles. Paed. Clin. India,
1976, Oct. 205.
18. Singh, S.D. Pathak, R. Kutumbale, A. Ramnani,
R.O. : Serum mucoprotein (tyrosine) in diabetes
mellitus. Jour. Diab. Asso. Ind., 1977, 17:27.
19. Winzler, R.J. Devom, A.N. Mehli, J.W. Smythe,
I.M. : Studies in mucoprotein in human plasma,
its determination and isolation. Clin. Invast, 1948,
27:609.
20. Zimmermann, M.G. Henry, J.B. : Serum enzyme
estimation as an aid to diagnosis. Clinical Diagnosis,
W.B. Saunders Co. Philadelphia. P.p. 558,
1969.
Ind. J. Tub., Vol. XXIX, No. 3

Introduction
POSTERIOR FOSSA CYSTIC ARACHNOIDITIS : AN UNCOMMON
PRESENTATION OF NEURO-TUBERCULOSIS
V.K. SRIVASTAVA and G.N.N. REDDY
Summary : Thirty cases of posterior fossa cystic arachnoiditis were studied over a period of three
years. Out of these, nine cases showed evidence of tuberculous pathology. It is these nine cases, where
neurotuberculosis presented in form of a pseudocyst, which form the basis of this presentation. Their
clinical profile and clinico-radio-pathological correlation is being presented.
In literature, various presentations of neurotuberculosis
have been described. We are presenting
nine cases, where the patients presented
with symptoms and signs of raised intracranial
pressure with localisation to posterior fossa.
At surgery, arachnoid at cisterna magna was
found to be thickened and ballooned. For the
present communication, posterior fossa cystic
arachnoiditis is defined as a pseudocyst, formed
by adhesions around cisterna magna. In literature,
various terms like posterior fossa meningitis
and arachnoiditis with cerebellar syndrome, have
been used. In earlier part of the century, Horrax
(1924) and Craig (1932) described similar cases.
In recent literature, there has been a dearth of
such reports.
female patients (Table IV). Six patients presented
with less than six months’ duration,
whereas the rest presented with a history of
one year or more. Most of the patients presented
with symptoms of headache, vomiting
and seizures. Of the six patients who presented
with seizures, three had focal and three had
generalised seizures. Four patients had history
of fever in the present illness (Table 1). Only
one patient gave a past history, suggestive of
pulmonary tuberculosis.
Symptom
TABIH 1
Symptomatology
Number of
Cases
Material and Method
Arachnoid was studied from thirty cases of
posterior fossa cystic arachnoiditis. Tissue
culture or staining of tissue section for demonstration
of acid fast bacilli was not done in
any of the cases. The diagnosis of tuberculous
arachnoid was made on presence of all or any
of the following histological criteria.
(a) Presence of caseation necrosis.
(b) Presence of typical Langhans giant cells.
(c) Presence of follicles made up of epitheloid
cells and mononuclear cellular
aggregation.
On histological grounds, nine cases were
found to be tuberculous. These nine cases
were analysed in retrospect. A clinicoradiopathological
correlation was attempted.
Findings
Clinical features
Headache 8
Vomiting 7
Seizures f.
Fever 4
Unsteadiness of gait 4
Giddiness 3
Double vision 2
Blurring of vision 1
Diminished vision 2
Deafness 1
Excessive sleep 1
Altered sensorium 5
Four out of nine cases were in the paediatric
age group. Seven were males and two were
General Physical Examination did not reveal
any significant findings. Objectively, five cases
*Department of Neurosurgery, National Institute of Mental Health and Neuro Sciences (NIMHANS)
Bangalore-560 029.
Ind. J. Tub., Vol. XXIX, No. 3

194 V.K. SRIVASTAVA AND G.N.N. REDDY
presented with altered sensorium, out of which
one was unconscious and decerebrating at the
time of admission. Of the seven patients with
fundal changes, six had bilateral florid papilloedema,
whereas one presented with Foster-
Kennedy syndrome. Three patients out of nine
were nearly blind. Gait disorders in five patients
were in form of a broad-based gait with difficulty
in tandem walking (Table II). All the
nine cases had symptoms and signs of raised
intracranial pressure. Five out of these nine
cases presented with symptoms and signs of
raised intracranial pressure alone without any
localisation. Two cases had a definite localisation
to posterior fossa. One case suggested a
diffuse lesion and one had a false localisation to
supratentorial compartment (Table IV).
Erythrocytic sedimentation rate was high
in five cases. Other blood investigations were
well within normal limits. Ventricular CSF
obtained at the time of ventriculography was
subjected to biochemical analysis (Table 111).
Cellular reaction was found in seven cases,
which was predominantly lymphocytic. C.S.F.
was not examined for acid fast bacilli as there
was no clue to tuberculous etiology before
operation.
Physical signs
TABLE II
Physical Signs
Number of Cases
Altered sensorium at the time of admission 5
Neck* stiffness 4
Fundal changes 7
Changes in visual acuity 3
Other cranial nerve deficits 3
Pyramidal involvement 1
Nystagmus
Truncal ataxia 3
Hypotonia 2
Inco ordination 3
Gait disorders 5
C
TABLE III
Analysis of Ventricular C.S.F.
SI. No. Cell Count Types of cells Protein mg% Chloride mg% Glucose ing% Globulin
1 16
*100
°L
L
40
190
720
QNS
40
QNS
+
2 18 L 7 680 42 Absent
3 41
*333
L L 20
350
760
QNS
44
QNS
Absent
4 0 — 20 760 46 Absent
5 45 L 8 720 40 +
6 45 L 7 700 20 +
7 0 — 20 700 43 Absent
8 12 L 38 QNS 32 Absent
9 2 *8 L L 9
250
720
700
40
34
Absent
Ind. J. Tub., Vol. XXIX, No. 3

POSTERIOR FOSSA CYSTIC ARACHNOIDITIS 195

196 V.K. SRIVASTAVA AND G.N.N. REDDY
Fig. 1 (a and b)
Conray Ventriculogram showing symmetrical dilatation of whole ventricular system, including the fourth ventricle.
Radiological features
X-ray skull showed evidence of raised
intracranial pressure in only one case. X-ray
chest showed evidence of primary complex in
only one case. Carotid angiography showed
ventricular dilatation in seven cases.
Ventriculography showed aqueductal block
in two cases. Total fourth ventricular exit
block was found in six cases. In one case, the
block was partial (Table IV). Symmetrical
dilatation of whole ventricular system including
fourth ventricle was found in six cases (Fig. 1).
In three cases, an irregular filling defect was
found (Fig. 2). In one case, no pattern seemed
to emerge.
Operative findings
Posterior fossa craniectomy was done in all
cases. At surgery, the dura was found to be
tense. After opening dura, cisterna magna area
was found to be ballooned. The pseudocyst
was found to be indenting the inferior vermis
and in some cases, adjacent cerebellar hemi-
Ind. J. Tub., Vol. XXIX, No. 3
spheres. Arachnoid in the region of cisterna
magna was found to be thickened and opaque.
It was adherent to the underlying cerebellum.
After excising arachnoid, cerebellum became
lax and pulsatile. C.S.F. flow could be established
in all the cases.
Histopathology
Histopathology showed thickened arachnoid
with varying degree of cellular reaction (Fig. 3).
Frank caseation necrosis was found in three
cases (Fig. 4) (Table IV).
Prognosis
Four out of nine patients died. Of five
surviving patients, three are normal after a
follow up of ten, eleven and nineteen months
respectively. One patient looked sick one month
after discharge and was found to have jaundice.
One patient, two months later, was found to
have residual deficits, in the form of ataxia.
left facial (L.M.N) palsy and left conjugate
gaze palsy.

POSTERIOR FOSSA CYSTIC ARACHNOIDITIS 197
\
>*•
Fig 2 (a and b)
Conray ventriculogram showing irregular filling defect in fourth ventricle.
Fig. 3
Photomicrograph showing presence of follicles
tuberculous arachnoid (H and E x 25).
Autopsy findings
Out of four deaths, autopsy was available
in two cases (cases 8 and 9). Brain in both the
cases showed evidence of basal exudates.
in
Photomicrograph showing evidence of caseation necrosis
in tuberculous arachnoid (H x B x 25).
Adhesions were found at the foremen magendie
area, blocking the fourth ventricular exit.
Both the cases showed evidence of ventricular
dilatation. In one case basilar artery showed
Ind. J. Tub., Vol. XXIX, No. 3

198 V.K. SRIVASTAVA AND G.N.N. REDDY
Since lumbar puncture could not be done
in any of these cases in view of raised intracranial
pressure, it is interesting to note the
ventricular C.S.F. findings. Predominently
lymphocytic reaction suggests a chronic inflammatory
pathology. C.S.F. analysis from the
pseudocyst, though available only in three
cases, suggests that the pathology is more
active in that area. It is clearly evidenced by
higher cellular count and protein values as
compared to their corresponding ventricular
C.S.F. analysis (Table III).
Ventriculographic rinding of obstructive
hydrocephalus due to tuberculous etiology has
been well-documented. Sifontes, Sabeti and
Sorvidillo (1957) showed pneumoencephalographic
evidence of 4th ventricular exit block
in one of their cases. Dastur and Pandya
(1972) while describing cases of tuberculous
meningitis, showed 22 cases with 4th ventricular
exit block and 10 cases with aqueductal
block. Tandon, P.N. (1978) has also described
cases of obstructive hydrocephalus in tuberculous
meningitis.
Fig. 5
Autopsy specimen to demonstrate basal exudative
reaction.
an almost total occlusion of lumen due to
endarteritis. Some of the cranial nerves were
found to be trapped in the mesh of exudate
(Fig. 5). Microscopy confirmed the tuberculous
pathology in both cases.
Discussion
In earlier part of the century, Horrax (1924)
and Craig (1932) described cases of cystic
arachnoiditis. They considered an infective
aetiology for their cases. The exact nature of
infection was not specified in their cases. Udani,
Parekh and Dastur (1972) while describing
various manifestations of neuro-tuberculosis,
mentioned two cases of posterior fossa meningitis.
Our cases appear to similate these cases.
All nine cases clinically and radiologically
presented like a posterior fossa tumour. Only
in one case, where there were meningeal signs
with diffuse involvement associated with fever,
tuberculous etiology was suspected preoperatively.
None of the other cases gave a preoperative
clue to tuberculous etiology.
We fail to understand at the moment as to
why these cases differ from cases of typical
tuberculous meningitis. We feel inclined to
attribute the difference to immunological
reasons.
It is suggested that these cases represent
rarer cases of obstructive hydrocephalus of
tuberculous etiology and it is the conversion
of cisterna magna into a pseudocyst due to
arachnoiditis (slightly different for immunological
reasons) in the posterior fossa, that
forms the basis of this anatomo-clinical syndrome.
REFERENCE
1. Craig, W.M., Chronic cystic arachnoiditis, Amer.
J. Surg.; 1932, 17, ?84.
2. Dastur, H.M., Pandya, and Rao, V.C. Aetiology
of hydrocephalus in tuberculous meningitis, Neurol
(Bombay) Suppl. 1972, 1, 73.
3. Horrax, G., Generalised cisternal arachnoiditis
simulating brain tumour: its surgical treatment
and results. Arch. Surg.; 1924, 9, 95.
4. Reddy, G.N.N., Srivastava, V.K., Sagar, C.V.
and Murthy V.S., Infratentorial arachnoid cyst,
an enigma, Paper presented at 27th Annual Conference
of Neurological Society of India held at
Poona; 1977.
Ind. J. Tub., Vol. XXIX, No. 3

POSTERIOR FOSSA CYSTIC ARACHNOIDITIS 199
5. Sifoutes, J.E., Sordillo, S.V.R. and Lincoln, E.M.
P.E.G. in tuberculous meningitis, J. Paediatr.;
1957, 50, 695.
6. Tandon, P.N., Tuberculous meningitis. In Infections
of the Nervous System, part 1 Edited by
Vinken, P.J. and Bruyn G.W.; 1978, 195.
7. Udani, P.M., Parekh, Usha, Bhat, C. and Dastur,
D.K.. Neurological tuberculosis in children with
further observations: Tuberculosis of the Nervous
system: Monograph on the proceedings of
the symposium, held in Bombay on 2nd to 5th
February, 1972: 1972, 37.
8. Udani, P.M., Parekh, Usha, C. and Dastur, D.K.:
Neurological and related syndromes in CNS
tuberculosis—Clinical features and pathogenesis,
J. Neurol. Sci.; 1971, 14, 341.
Ind. J. Tub., Vol. XXIX, No.3

LUPUS VULGARIS (VERRUCOSUS) ASSOCIATED WITH PULMONARY
TUBERCULOSIS
T.R. KAPUR*
Summary : An unusual case of Lupus Vulgaris ^Verrucosus) associated with Pulmonary Tuberculosis
in a young man is presented. He had asymptomatic pulmonary tuberculosis and developed
a cold abscess in the perineum, leading to two bilateral, symmetrical Verrucosus plaques in the Ischiorectal
areas. Chemotherapy gave excellent results.
Introduction
That the human skin may react in many
different ways to a single infective organism
is nowhere better illustrated then in Tuberculosis.
It can produce nodules, papillomatous
tumours, vegetative verrucosus and cicatricial
lesions. A classification based on morphology
is not possible because Lupus Vulgaris may
produce all the above types of lesions; hence a
classification based on immunologic pattern is
made (Augustine, 1973). In Tuberculosis Lupus
Vulgaris (LV) and Tuberculosis Verrucosa
Cutis (TVC) immunity is good. On the other
hand immunity is variable i.e. moderate in
Scrofuloderma and Gumma but poor in tuberculosis
cutis orificials. Tuberculoids are allergic
in nature with high degree of immunity.
Clinical data from different geographic
regions suggest a marked variation in the
incidence of various forms of cutaneous tuberculosis.
While skin tuberculosis appears to
be rare in the U.S.A., incidence in Europe is
reported to be around 1 % of all skin diseases
(Wolff, 1971). Kagoj (1949) observed in 0.2%
cases in Yugoslavia. Some investigators (Fasal
and Rhodes, 1952 and Zoon, 1957) report
that cutaneous tuberculosis is rare in tropics
but studies from East, South and North of
India do not suggest this to be of such an uncommon
occurrence. Incidence was 0.5%
(Banerjee, 1956), 0.24% (Satyanarayan. 1962)
and 0.11 % (Mammen, 1973) and 0.59% (Singh,
1974) and 0.28% (Pandhi, Bedi, Kanwar and
Bhutani, 1977) respectively.
pain in abdomen, diminished appetite or fever.
General examination did not reveal anaemia
or lymphadenitis. Weight was 72 kgs.
Lungs were clear clinically. Abdomen was
not doughy. No lump was felt. Liver and
spleen were not palpable. No Ischio-rectal sinus
could be demonstrated. Cutaneous examination
revealed two erythematous verrucosus, well
demarcated plaques starting 1 cm from the
anal margin and extending over Ischio-rectal
region. Both the plaques were almost symmetrical
and equal in size (5 cm x 6 cm). The
surfaces were slightly wet with pus discharge
from adjoining abscess (Fig. 1). There was one
indurated abscess with discharging pus in the
left perineum 2 cms away at 7 O’clock of the
anal margin. There was hypoaesthesia over the
plaques without any thickened cutaneous nerve
twigs to the plaques. The clinical features
were not suggestive of L.V. (Verrucosus).
Presenting Features
A twenty-six years old, well-built man
reported without any history of fever, cough,
pain in the chest or haemoptysis. He developed
an abscess in the left perineum in July 1977
which burst in due course. The pus discharge
was contaminating the perianal area and he
felt small plaques on either side of the perianal
areas in September 1977. The plaques enlarged
gradually and he got admitted on 1st December
1977. He denied history of recurrent diarrhoea,
Fig. 1
Two erythematous, verrucosus, well-demarcated
Plaques, seen between anal and Ischiorectal regions.
Both are almost symmetrical and equal in size.
Investigations
DGI for treponema pallidum was negative.
Scrappings for fungus in 10% KOH were also
negative. Skin clippings were stained for mycobacteria
tuberculosis and leprae and were
*Lt.-Colonel; Classified Specialist (Derm & Yen), Military Hospital, Bareilly-243 001.
Ind. J. Tub,, Vol. XXIX, No. 3

LUPUS VULGARIS (VERRUCOSUS) ASSOCIATED WITH PULMONARY TUBERCULOSIS 201
negative for both. Sputum was negative for
tubercle bacilli repeatedly. Pus from discharging
abscess was negative for tubercle bacilli by
direct smear and culture. Saprophytic staphylococci
were grown from pus on blood agar
media. Blood counts & ESR were within normal
limits. Tuberculin reaction was 11 mm. X-ray
chest revealed streaky-cum mottled opacities
in the left apex and slight pulling up of the left
hilum. Plain X-ray abdomen did not reveal
any abnormal calcificarion or radio-opaque
calculi. Skin biopsy showed hyperkeratosis and
acanthosis of epidermis which in areas was
appearing as pseudoepitheliomatous hyperplasia.
There was also scattered atrophy of
epidermis. The dermis showing granulomatous
infiltration by lymphocytes, histiocytes, a few
epithelioid cells and Langhans type of gaint
cells. Caseation was absent. Tubercles were
seen in the upper corium. Tubercle bacilli
could not be demonstrated on staining the
specimen. Guinea pig inoculation of pus or
biopsy material was not done due to lack of
facilities.
Treatment
The lesions were diagnosed as L.V. (Verrucosus)
on histopathological evidence, associated
with cold abscess and pulmonary tuberculosis
in the left upper zone. He was placed on antitubercular
treatment consisting of Streptomycin.
Isoniazid and Ethionamide daily in the 2nd
week of December 1977. The surface of the
plaques started drying up along with regression
of the borders by the end of 2nd week of the
therapy. The plaques almost subsided with nonindurated
residual erythema with a slight
indurated lower border on the right side and the
abscess healed after 90 days of therapy. He was
put on Streptomycin with Isoniazid biweekly
for another 15 months (total treatment 18
months). X-ray chest revealed healed foci with
a light scaring in Ischio-rectal areas on the
completion of 18 months’ therapy.
Discussion
A well built individual with asymptomatic
pulmonary tuberculosis of the left lung of unknown
duration, developed a cold abscess in
the perineum which is one of the possibilities
in Lupus Vulgaris (Mammen, 1973 and Singh
1974). Acute tuberculous ulcers (Orificial tuberculosis)
also occur around anus but only in
individuals suffering from advanced pulmonary
or intestinal tuberculosis (Wilkinson, 1969).
There was nothing to suggest abdominal tuberculosis.
In lupus vulgaris, face is reported to be the
commonest site in the European countries
(Wolff, 1971 and Horwitz 1959). In India,
lower extremities especially the buttocks seem
to be affected most often, most probably due
to accidental inoculation of the crawling children
on the ground where Mycobacterium tuberculosis
may have been deposited in the sputum
(Singh, 1974 and Pandhi et al, 1977). The
patient developed two identical verrucosus
lesions in the Ischio-rectal areas due to exogenons
inoculation with the pus discharge from the
cold abscess. As the suppurative material,
rich in bacilli, comes to the surface of the skin
through sinuses, it reinfects skin and produces
lupus vulgaris lesions (Singh, 1974). There is
usually a single lesion but dissemination may
occur through endogeous spread if the cellular
immunity is depressed (Pandhi et al, 1977 and
Wilkinson 1969).
Lesion of the L.V. appear to be more
common as compared to T.V.C. in Indian
studies (Mammen, 1973 and Pandhi et al,
1977). Both the lesions developed in an individual
with good immunity (Augustine,
1973; Mammen, 1973; Wilkinson, 1969 and
Moschella 1975). Singh (1974) observed cases
with histological evidence of L.V. at sites where
T.V.C. is commonly found i.e. exposed
areas. He postulated the interplay of several
factors like immunity of the host, dose of
inoculum and virulence of bacilli, being responsible
for the difference. On the other hand
Pandhi et al (1977) and Kumar and Bhutani
(1959) are of the opinion that L.V. and T.V.C.
should be categorized together because they
feel there are no immunological or bacteriological
differences between the two conditions.
Clinico-pathological differences are only quantitative
and morphological differences are not
adequate to justify two different terms. Epidermal
changes are helpful in differentiating
between L.V. and T.V.C. (Mammen 1973).
In L.V. a combination of achanthosis and
atrophy of the epidermis is very common
whereas in T.V.C. acanthosis and hyperkaratosis
are constant features. The granuloma
appears in upper corium in L.V. but it is in middermis
in T.V.C. (Wilkinson, 1969 and
Moschella, 1975). The author feels that L.V.
and T.V.C. are two separate entities morphologically
as well as histopathologically. appearing
in an individual having good cellular immunity.
The clinico-histopathology in the case reported
here was suggestive of Lupus Vulgaris
(Verrucosus).
Tubercle bacilli could not be demonstrated in
this case. Pandhi et al (1977) failed to demonstrate
bacilli in all the 23 cases of L.V. and 11
cases of T.V.C. on staining the smear as well
Ind. J. Tub., Vol. XXIX, No. 3

202 T.R. KAPUR
as by culture and guinea pig inoculation in
all the four cases where it was carried out.
Bacilli were cultured in 6% out of 4000 cases
in L.V. (Wilkinson, 1969). It is postulated that
the bacilli are destroyed or walled off by local
tissue reaction.
Tuberculosis of the other organs may be
associated with the Lupus Vulgaris. Glandular
involvement is the most frequent but pulmonary
tuberculosis is also common (Mammen, 1973;
Singh 1974 and Wilkinson 1969).
There are different schedules of antitubercular
therapy for pulmonary and cutaneous
tuberculosis (Mammen, 1973; Pandhi et al
1977; Wilkinson, 1969 and Citron, 1973). As
a routine three drugs are prescribed for the
first 90 days. Later, the therapy is continued
with two drugs for another 15 months as
per schedule of the Tuberculosis Chemotherapy
Centre, Madras (Tuberculosis Chemotherapy
Centre, 1964 and Ramakrishna, et al 1969).
Pandhi et al (1977) treated cases with streptomycin
and isoniazid daily for one year.
There was complete recovery in 12, good
response in another 12 but no response in
one case. In Lupus Vulgaris, scars may break
down and active lumps may frequently reappear
in scar tissue. Therefore it is suggested
that a full course of anti-tubercular therapy
for 18 months should be given instead of 6 to
12 months (Augustine, 1973: Mammen, 1973;
Pandhi et al, 1977 and Wilkinson, 1969), even
in the absence of associated tuberculosis of the
other organs to prevent a relapse in the scars.
Use of calciferol (Vitamin D2) is discouraged
these days due to its toxicity.
REFERENCES
1. Augustine S.M. : Tuberculosis of the skin; Antiseptic;
1973, 70, 791.
2 Banerjee, B.M. : Common clinical manifestations
of Tuberculosis of skin in the tropics; Indian
J. Derm., 1956; 1,11.
3. Citron, K.M. : Tuberculosis; Brit. Med. ].; 1973,
2, 296.
4. Fasal P. and Rhodes B. : Cutaneous tuberculosis
and Sarcoidosis in the American Negro and Inhabitants
of Tropical Countries, In hand book of
Tropical Dermatology and Medical Mycology,
Ed., Simons R.G., Vol. 1, Elsevier Pub. Co.,
Amsterdam, 1952.
5. Horwitz O. : The localization of lupus vulgaris
of the skin, Acta Tuber Scand, supp; 1959, 47,
175.
6. Kagoj, F. : The Luposa Tuberculose, 1: 292, 1949
(quoted by Singh, 1974).
7. Kumar A.S., Bhutani L.K. : Self Assessment
programme, Ind. J. Derm. Vener Leprol; 1979,
45, 67.
8. Lahiri, K.D. : Etiology and patholoey of skin
tuberculosis in the tropics, Ind. J. Derm.; 1956,
2, 3.
9. Mammen, A., Thambiah, A.S. : Tuberculosis of
the skin, Ind. .1. Derm. Vener; 1973, 39, 15’.
10. Moschella, S.L. : Benign Reticulo-endothelial
diseases, Dermatology, Vol. 1, 1st Ed. Edited by
Moschella, S.L., Pillsbury D.M. and Burley H.J.,
W.B. Saunders Coy, Philadelphia, 1975; Paee
795.
11. Pandhi, R.K., Bedi, T.R., Kanwar AJ. & Bhutani,
I.K., Cutaneous tuberculosis—A clinical and
investigative study, Ind. J. Derm.; 1977, 22,99.
12. Ramakrishna C.V., Devadatta, S., Evans C,
Fox W., Menon N.K., Nazarath O. and Velu
S., et al : A four year follow up of patients with
quiescent pulmonary tuberculosis at the end of
a year of chemotherapy with twice weekly isoniazid
plus streptomycin or daily isoniazid plus PAS;
Tubercle; 1969, 50, 115.
13. Satyanarayan B.V. : Tuberculoma—A brief review
together with statistical analysis and observations,
Ind. J. Derm. Vener.; 1962, 28, 25.
14. Singh, C. : Lupus Vulgaris in India, Ind. J. Derm.
Vener.; 1974, 40, 257.
15. Tuberculosis Chemotherapy Centre, of
the WHO; 1964, 31, 247.
Bulletin
16. Wilkinson, D.S. : Tuberculosis of the skin, Text
Book of Dermatology, 1st Ed., Editors Rook A,
Wilkinson D.S. and Ebling F.I.D., Blackwell
Scientific Publications, Oxford 1969; Page 655.
17. Wolff, K. : Tuberculosis in Dermatology in general
medicine, Mycobacterial diseases, 1st Ed., Edited
by Thomas B. Fitzpatrick et al, McGraw Hill
Book Co. New York, 1971; Page 1743.
18. Zoon J.J. : Tuberculosis of the skin in consideration
about Pathogenesis; Arch Derm.; 1957; 75,
161.
Ind. J. Tub., Vol. XXIX, No. 3

BOOK REVIEW
Clinical Investigation of Respiratory Disease:
Edited by T.J.H. Clark; Chapman & Hall
Ltd., London. 1981, pp. 526. Price £22.50.
There have been tremendous advances in the
science and art of medicine in recent years.
As a result of these, there is better understanding
of the structure and functioning of
the various systems of the human body. New
investigative procedures based on this knowledge
are being evolved for assessment as well
as diagnosis of various conditions some of
which used to be obscure. This comprehensive
book deals with procedures pertaining to the
respiratory system.
Non-respiratory functions of the lung have
not attracted sufficient attention till recently.
There is better understanding of the metabolic
and biochemical functions of the lung as well
as mechanism of host defence. Similarly,
advances in the field of immunology have helped
to devise some sophisticated diagnostic pro
cedures, which are being increasingly deployed
in routine clinical practice. Chapters dealing
with these aspects are a »very welcome and
important feature of this book.
The Editor has presented in one volume
all that is worth knowing and applying in the
investigation of chest diseases. The timehonoured
diagnostic procedures like history
taking, physical signs, symptoms and pulmonary
function tests have not been neglected.
New knowledge about radiological procedures
such as radio-isotope imaging and computerised
tomographic scanning have also been included.
Screening procedures for asymptomatic diseases
and their cost-effectiveness have been dealt
with in a proper perspective. References have
also been made to tumour markers and ectopic
hormones. New light has been thrown on
susceptibility to smoking-induced lung cancer
in relation to the subjects’ capacity to metabolise
the carcinogens in cigarettes and accumulation
of drugs in the lungs as an important
factor in causing local drug toxicity leading to
pulmonary fibrosis following prolonged administration
of drugs like Busulphan and Bleomycin.
The Editor is conscious of the investigations
tending to become more and more complex.
The object of the book appears to be to make
the clinician conversant with all possible investigations
and yet to be selective and critical in
the choice of investigations based on their corelation
with signs and symptoms etc.
Tendency to resort to every conceivable investigation
in every situation as a substitute for
history and orderly physical examination has
been rightly deprecated.
All the contributors are specialists in their
own field. The book is well-written, wellproduced
and amply illustrated. It would be
extremely useful for the post-graduate students
as well as a reference book for the clinician.
Ind. J. Tub., Vol. XXIX, No. 3

Citation read on the occasion of the presentation of the TAI Gold Medal
to Dr. R.N. Tandon, former Professor and Head of the Department of TB
and Chest Diseases, Lucknow University, on 2.11.1981
The Tuberculosis
Association of India
awards a “Gold
Medal” every year to a
person who has rendered
outstanding
service to promote the
cause of Tuberculosis
in India. For the year
1981, the Association
has selected Prof. R.N.
Tandon, former Professor
and Head of the
Department of Tuberculosis
and Chest Diseases,
Lucknow University,
for this Award.
Born in November 1899 at Agra (Uttar
Pradesh) Dr. R.N. Tandon graduated from
St. John’s College, Agra in 1921, took his
M.B.B.S degree from the King George Medical
College. Lucknow in 1926 and joined the K.G.
Hospital (now known as the Gandhi Memorial
Hospital) as Senior House Surgeon. During
the years 1927 to 1929, he visited U.K. and
Europe for further studies and obtained
D.M.R.E. (Cambridge) and TDD (Wales). He
joined the Bhowali Sanatorium in 1930 as its
Assistant Superintendent and in 1934 he was
awarded an International Scholarship at the
Carlo Forlanini Institute for six months. Later,
he undertook a study tour abroad for two
years during which period he passed the
Membership Examination of the Royal College
of Physicians at Edinburg with Tuberculosis
as his special subject and also worked in several
institutions in Paris, Switzerland and Berlin.
On his return to India in 1936 he was deputed
by the Uttar Pradesh Government to establish
a TB Clinic at Allahabad, in 1945 he was
appointed as the Head of the newly started
Tuberculosis Department of the Lucknow University,
with clinic and nearly 100 beds in the
Kasturba TB Hospital, and subsequently as
Professor and Head of the Department of
Tuberculosis and Chest Disease?. Dr. Tandon
is a renowned teacher and his students are now
manning Tuberculosis services throughout the
country.
Apart from his professional distinction and
fame as a renowned teacher and an eminent
clinician, Dr. Tandon was closely associated
with the Uttar Pradesh Tuberculosis Association
for several years as its founder-member, Vice-
President and Organising Secretary for TB
Seal Sale. He has also been the Vice-President
of the Anti-TB League, Lucknow. for a long
time.
Dr. Tandon was a member of the Technical
Committee of the Tuberculosis Association of
India from 1958-65, its Chairman in 1961-62
and President of the 18th National Conference
on TB & Chest Diseases held in Bangalore in
1962. He attended practically all the National
Conferences held from its inception till his
retirement. He was also a member of the Central
Committee of the Tuberculosis Association of
India during the years 1966-75. He was the
recipient of the first Wander-TAT Oration in
1973 which he delivered at the 28th National
Conference on Tuberculosis and Chest Diseases
held in Madras in January 1974.
In recognition of the meritorious services
rendered in the field of tuberculosis, the Tuberculosis
Association of India decided to award
its Gold Medal to him.
Ind. J. Tub., Vol. XXIX, No. 3

Obituary
DR. R. VISWANATHAN
The grand old man of tuberculosis and chest diseases discipline is no more. Dr. R. Viswanathan,
doyen of the discipline, and a renowned scientist died, literally, in harness on 14th July, 1982. In the
83rd year of life, he was exceptionally agile both physically and mentally. Even on the last day preceding
his fatal illness of about a month, he fulfilled the daily routine of his work.
Dr. Viswanathan was a muifi-splendoured personality.
Few have achieved such excellence in so many spheres. He
was brilliant academician, a talented clinician, a gifted teacher, a
prolific writer and a research worker of the highest calibre.
Having obtained M.D. in general medicine from Madras
and M.R.C.P. from London, he joined the Madras Medical
College as an Assistant Professor of Medicine and later
joined the Visakhapatnam Medical College as Professor.
During the second World War, he served as a medical
specialist to the Indian Army from 1942 to 1946. After release
from the Army, he Joined the Directorate-Genera! of Health
Services as first Tube! culosis Adviser to the Government of
India and Deputy Director-General. He took over as founder
Director of the Vallabhbhai Pate! Chest Institute and after
retirement from this post in 1969, he had been working as
Emeritus Scientist CS1R and Honorary Professor, V.P.
Chest Institute, Delhi University. He was the Dean of the
Faculty of Medical Sciences of Delhi University from 1946 to 1964.
Apart from guiding hundreds of students in their research
studies during his long professorial career, he had to his credit original and outstanding research in
several fields, especially pulmonary eosinophilia, pulmonary oedema of high altitude, acute massive
collapse of the lung, bronchiectasis, etc. He contributed to the discovery of a new species of candide
which, in recognition of his contribution, was named after him.
He was closely associated with the Tuberculosis Association of India for several years and was
a member of all its important committees, viz. Central Committee, Executive Committee, Technical
Committee, Research Committee and the Local Advisory Committee. He was also a founder fellow of
the National Academy of Medical Sciences. He was the President of the Indian Association for Chest
Physicians from its inception till last year when it transformed itself into the National College of Chest
Physicians. He was Founder President of the Asthma and Chronic Bronchitis Foundation of India.
He presided at the 8th National Congress of Diseases of Chest in 1963; Conference of Association of
Physicians of India in 1968: National Tuberculosis Conference in 1968 and World Congress on Asthma,
Bronchitis and Allied Conditions in 1974.
He published over 150 scientific papers in reputed National and International Journals, apart
from numerous Orations and Guest Lectures in Conferences in India and abroad. He was the author
of seven books, one of which dealt with his personal reminiscences, and contributed chapters in text
and reference books. He was probably the best known medical scientist of this country in the International
circles.
Honours and awards came to him galore. He was a Padtna Bhushan and Honorary Physician to
the President of India. The Tuberculosis Association of India awarded its Gold Medal for outstanding
achievements to him in 1972. He was also the recipient of Dhanwantri Prize of the National Science
Academy, Eugino Morelli Prize and Forlanini Medal from Italy.
His demise is a great loss to the country, its medical profession, the Tuberculosis Association of
India and many other organisations. The void left by him will be extremely difficult, if not impossible,
to fill. May God grant eternal peace to the departed soul and may his achievements continue to inspire
the coming generations!
Ind. J. Tub., Vol. XXIX, No. 3

NEWS AND NOTES
KOCH CENTENARY CELEBRATIONS
The Tuberculosis Association of India
celebrated the Centenary of the Discovery of
Tubercle Bacillus by Robert Koch by organising
a special function in Delhi on 24th March,
1982. Brief details about this function appeared
in the “News & Notes” section of the April
1982 issue of this Journal. The following are
brief details of the various functions held in
the States to celebrate the Centenary:
Andhra Pradesh: In Andhra Pradesh the
State TB Association designated its Xth State
TB Workers’ Conference held in Hyderabad
from the 12th to 15th March, 1982 as “Robert
Koch’s Discovery of TB Centenary Conference”.
Details of this Conference were given
in the previous issue of the Journal. The
Prakasam District TB Association conducted
an intensive BCG Vaccination programme in
the slum areas of Ongole, Addanki, Giddalur,
Markapur Chirala. Kandukur and Kanigiri
covering 3207 children. The Association also
conducted two anti-TB Shibirs in Rajupalem
and Gundayapalem and intensified its health
education and case-finding activities. The District
Association of Nizamabad organised a few
health camps in some villages and slum areas.
In cooperation with the Public Relations Office,
lectures were arranged in the Beedi Factories
with the help of Flip Charts, slides, cinema
shows, display of posters, etc. The Adilabad
District TB Association also carried out an
intensive health education programme and
offered incentives to indigent patients for regularity
in taking drugs. The West Godavari
District Association organised an anti-TB
Shibir in Prathikollanka which was attended
by about 400 people. An intensive BCG vaccination
programme in the slum areas of Eluru,
Narsapur, Kovvur, Bhimavaram, T.P. Gudem
and Nidadavolu Municipalities was undertaken
and a total of 3027 BCG vaccinations were
given. A valedictory function was held in the
Red Cross Hall at Government Headquarters
Hospital, Eluru. The Visakhapatnam District
Association arranged a Tuberculosis and Chest
Diseases Camp at Peda Gantyada, which was
attended by 769 patients.
Assam: The Assam TB Association, which
had become inactive after bifurcation of the
State into Assam and Meghalaya, has now
revived its activities with headquarters at
Gauhati. The Executive and other Committees
of the Association are being reconstituted and
the newly constituted General Body is expected
Ind. J. Tub., Vol. XXIX, No. 3
to meet towards the end of July 1982. As part
of the Centenary Celebrations of the Discovery
of the Tubercle Bacillus the Association organised
public meetings at different places to educate
the people about the various aspects of tuberculosis
and pamphlets and leaflets were also
widely distributed throughout the State. The
Association has also taken steps to intensify
the case-finding and health education activities.
An article on ‘Fight TB’ in English by Dr. J.N.
Bhuyan, Honorary Secretary, State TB Association
and another article on Tuberculosis in
Assamese by Dr. A.K. Adhikary, were published
in the local dailies. A radio talk on Tuberculosis
was broadcast from the AIR Station at Gauhati
on 19.7.1982. The State Association proposes
to organise a refresher course in tuberculosis for
private medical practitioners. The first State
Tuberculosis Workers Conference is also proposed
to be held towards the end of the current
year after revitalisation of the District TB
Association.
Bengal: The Bengal TB Association organised
a special function to celebrate the hundredth
anniversary of the discovery of Tubercle Bacillus
by Robert Koch and also the 5th State TB &
Chest Diseases Workers Conference in Calcutta
on the 22nd and 23rd May, 1982. Shri B.D.
Pande. Governor of West Bengal and President
of the Bengal TB Association inaugurated the
centenary function by unveiling the Portrait of
Robert Koch and by switching on 100 Coloured
bulbs. Dr. Werner Handke, Consul-General
of the Federal German Republic was the Guestin-Chief.
Dr. P.K. Sen, Chairman of the Association,
proposed the Vote of thanks Dr. P.K-
Chatterjee presided over the Conference while
Dr. B.B. Manna delivered the Guest Lecture.
The subjects discussed at the conference included
Pathology, Control of Tuberculosis, Air
Pollution, Pediatric Tuberculosis and Bronchial
Asthma. About 300 delegates attended the
Conference. A souvenir was also brought out
on this occasion.
Bihar: The Bihar Tuberculosis Association
celebrated the Centenary by organising a special
function on the 18th April, 1982 at the I.M.A.
Hall, Patna. The First State Conference of
TB & Chest Diseases workers was also combined
with this function. Dr. Umeshwar Prasad
Verma, Minister for Health & Family Welfare,
Bihar, inaugurated the celebrations while Shri
Shamaele Bani, State Minister for P.R.D. and
Higher Education, Bihar was the Chief Guest.
Dr. M. Pathak, Chairman of the Association
welcomed the guests and Prof. R. Viswanathan,

NEWS & NOTES 207
Professor Emeritus, V.P. Chest Institute, University
of Delhi and Prof. U.N. Shahi, Retd.
Head of the Department of Surgery. Patna
Medical College were the Guest Speakers. The
function was attended by a large number of
TB Workers from all over the State including
District TB Officers, teachers of Patna and
Nalanda Medical Colleges, general practitioners,
High Court Judges and a cross-section of the
population.
In the afternoon the Scientific Session was
inaugurated by Dr. A.K.N. Sinha, Presidentelect,
World Medical Association. The subjects
discussed included all aspects of tuberculosis.
Dr. R. Viswanathan delivered a Guest Lecture
on “Chronic Bronchitis”. The function concluded
with a Vote of Thanks by Dr. B.K. Prasad,
Organising Secretary. A Souvenir was released
on the occasion by Shri Shamaele Bani, State
Minister for P.R.D. and Higher Education and
the film ‘Your Enemy—TB’ was shown to the
audience which was very much appreciated.
Goa: The Government and the State TB
Association of Goa, Daman & Diu jointly
arranged a function to celebrate the Centenary
of the Discovery of Tubercle Bacillus by Robert
Koch in the Auditorium of Hotel Mandovi in
Panjim on 15th May, 1982. The function was
inaugurated by the Lt.-Governor of Goa and
it was presided over by the Chief Minister of
the State. Dr. Jacinto Estibeiro, Director of
Health Services and Chairman, TB Association
of Goa, Daman & Diu gave the welcome address
and Dr. Ananda Helecar, Deputy Director
of Health Services, introduced the Chief Guests.
Dr. S.P. Pamra, Honorary Technical Adviser,
Tuberculosis Association of India, delivered
the Key Note Address. The function came to
a close with a Vote of Thanks by Dr. Damodar
Bhounsule, Honorary Secretary of the State
TB Association.
The Centenary function was followed by a
Symposium on Tuberculosis on 16.5.1982 which
was attended by over 100 General Practitioners.
Dr. Pamra delivered three lectures at the
Symposium on the various aspects of tuberculosis
and its management. The other lecturers
were Dr. K.C. Mohanty. Hony. Professor and
Head of the Dept. of TB, Grant Medical
College and J.J. Group of Hospitals, Bombay
and Dr. A.S. Bagga, Prof, of Tuberculosis,
Medical College, Goa. The subjects discussed
included Epidemiology, Pathology and Differential
Diagnosis of Tuberculosis, Chemotherapy
of Tuberculosis and Role of General
Practitioners in Tuberculosis Control Programme.
There was also a Panel Discussion with
Dr. S.P. Pamra as the Moderator.
Gujarat: The Gujarat TB Association celebrated
the Centenary along with their Xth
State TB & Chest Diseases Workers Conference
held at Ahmedabad on the 14th March,
1982. The Conference was inaugurated by
Shri N. Vittal, Health Secretary to the Government
of Gujarat and it was presided over by
Dr. A.G. Patel, Vice-Chairman, State TB
Association and Medical Superintendent, S.P.
Sanatorium, Baroda. Dr. S.H. Patel, Honorary
Secretary of the State Association presented a
brief report on the working of the State Association
while Dr. A.S. Shah, the Treasurer
read out the messages. A booklet on Tuberculosis,
brought out in cooperation with the
local branch of the I.M.A., was presented by
Dr. P.K. Pandya, Honorary Secretary, Scientific
Committee of the Gujarat State IMA Branch
and it was formally released by Dr. O.P. Gupta,
Director, Medical & Health, Gujarat State.
The Scientific sessions included two panel
discussions, one on “Recent Trends and
Advances in the management of Tuberculosis”
chaired by Dr. S.B. Trivedi and the other on
“Present Status of Tuberculosis situation in
Gujarat” chaired by Shri Bhogibhai Lalani.
The Conference came to a close with a Vote of
Thanks proposed by Dr. I.G. Bhatt, Honorary
Secretary. TB Relief Organisation, Ahmedabad.
The State Association, in cooperation with
its District and Taluk Associations, arranged
for special radio talks, T.V. programmes,
screening of film on T.B., etc. with a view to
educate the public on various aspects of tuberculosis.
The Association also organised a press
conference and distributed a hand-out on
Robert Koch and other literature on tuberculosis
for publication in the lay press. They
also put up banners and posters at public
places and organised public meetings in cooperation
with the local branches of the I.M.A.,
Lions and Rotary Clubs, etc.
Jammu & Kashmir: The Centenary was
celebrated in Jammu & Kashmir State on the
24th March, 1982, by organising public
meetings in all the Districts under the Chairmanship
of the Divisional Commissioner.
Special efforts were made to create better
awareness among the public about tuberculosis
and the facilities available for its diagnosis and
treatment and also to motivate patients to
take treatment regularly and as long as advised.
A special function was organised at the TB
Demonstration Centre, Srinagar, and it was
addressed by the District Tuberculosis Officer,
and the Director of the Centre. The function
was covered by Radio Kashmir. The feature
film “Fight against TB” in Kashmiri language
was also screened.
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208 NEWS & NOTES
Karnataka: The Karnataka Government
constituted a special Committee, with Dr. K.
Nagappa Alva as Chairman, to celebrate the
Centenary of the Discovery of Tubercle Bacillus
and also the Silver Jubilee of the S.D.S. TB
Hospital, Bangalore in a befitting manner.
The Centenary celebration, presided over by
Shri A.K.A. Samad, Minister for Health &
Family Welfare, Government of Karnataka,
was inaugurated by Shri Govind Narain, the
State Governor and the Silver Jubilee Celebrations
of the S.D.S. TB Hospital by Shri R.
Gundu Rao, Chief Minister of Karnataka, at
a special function held on the 28th May, 1982
at the Auditorium of the Bangalore Medical
College, Bangalore. The Health Exhibition on
Tuberculosis, arranged in connection with the
Centenary Celebrations, was inaugurated by
Smt. Chandra Govind Narain while the Special
Souvenir brought out on the occasion was
released by Shri Dharam Singh, Minister for
Housing & Urban Development, Government
of Karnataka. The function came to a close
with a Vote of Thanks proposed by Dr. B.
Krishnacharya, Joint Director (TB), Government
of Karnataka. The Scientific Sessions
were held on the 29th and 30th of May at the
National Tuberculosis Institute and the S.D.S.
TB Hospital, Bangalore, and these were chaired
by Dr. V. Parameswara, President, I.M.A.,
Karnataka and Dr. Y. Rajasekhara, ex-
Superintendent, S.D.S. TB Hospital, respectively.
The subjects discussed included Tuberculosis
in Children, Recent Developments in
the Studies of Mycobacteria, case-finding in
Tuberculosis, Chemotherapy, of Tuberculosis,
Review of National Tuberculosis Programme,
Role of Survey in Tuberculosis, Respiratory
Allergy, Tubercular Meningitis, Role of Voluntary
Organisation, etc. The celebrations concluded
with a Valedictory function presided
over by Shri K. Nagappa Alva and with Shri
A.K.A. Samad, Minister for Health & Family
Welfare, Government of India, as the Chief
Guest.
Kerala: The Kerala TB Association inaugurated
the Centenary Celebrations by organising a public
meeting at the Primary Health Centre, Kesavapuram,
Trivandrum on 24.3.1982. The meeting
was attended by prominent public leaders and
members of the profession. Dr. A. Ananthaswamy,
Supervising Medical Officer, BCG
Campaign, gave a talk on infection and preventive
measures of tuberculosis and the District
Medical Officer of Health, Trivandrum, inaugurated
a BCG Camp where about 2000
children were vaccinated. An exhibition highlighting
the magnitude of the tuberculosis
problem, mode of infection, symptoms treatment,
prevention, etc. was inaugurated in the
Conference Hall of the Association by Dr. P.U.
Abubacker, Additional Director of Health
Services, Kerala. The exhibition is being moved
from place to place and shown throughout the
State with a view to educate the people and
create better awareness among them about
tuberculosis. Another public meeting was held
in the IMA Hall, Trivandrum, on the same day
under the joint auspices of the State TB Association
and IMA branch, Trivandrum with
Prof. R. Ananthanarayan in the Chair. Dr. B.N.
Kudubi, Superintendent, Sanatorium for Chest
Diseases, Pulayanarcottah and Dr. M. Habeeb,
District TB Officer, Trivandrum, spoke on
“The life of Dr. Robert Koch” and “Recent
trends in the Management of Tuberculosis”
respectively. The District TB Association,
Ernakulam, organised tuberculosis detection
medical camps and BCG vaccination camps
while seminars and panel discussions were held
under the joint auspices of the district TB
Associations and I.M.A. Branches of Kottayam,
Trichur, Shornur. Palghat and Manjeri. Special
articles on Dr. Robert Koch and on the various
aspects of tuberculosis were published both in
the English and Malayalam dailies and magazines
and talks by leading TB Specialists over the
All India Radio, Trivandrum, Trichur and
Calicut, in the form of questions and answers,
group discussions, etc., were also arranged.
Essay competitions among Arts and Science
students and Medical College Students were
held and prizes were awarded for the best
essay from each category. The Anti-TB Week
was celebrated in all the districts and the film
on tuberculosis was shown on these occasions.
Madhya Pradesh: The Madhya Pradesh
Association celebrated the Centenary by
organising its First Madhya Pradesh TB and
Chest Diseases Workers’ Conference in Bhopal
on the 8th and 9th of May, 1982. Dr. M.N.
Nagu, Director, Medical and Health Services,
Madhya Pradesh, presided over the Scientific
Sessions. H.E. the Governor of Madhya
Pradesh addressed the afternoon session and
distributed the various medals, prizes, etc. to
distinguished TB workers and for highest
collections by sale of TB Seals. Dr. S.P. Pamra,
Honorary Technical Adviser, T.A.T. delivered
the Dr. N.L. Bordia Memorial Oration on
“Tuberculosis an Enigma”. About 50 delegates
attended the Scientific Sessions.
The Anti-TB Association of Indore in collaboration
with the Indore Chest Society and the
Indian Medical Association organised a function
to celebrate the Centenary of the Discovery
of Tubercle Bacillus by Robert Koch at the
Maharaja Yeshwant Rao Hospital. Dr. S.M.
Jain spoke on the achievements of Robert Koch,
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NEWS & NOTES 209
Dr. S. Mandovra about the treatment of tuberculosis
and Dr. K.C. Sharma about the control
of Intestinal Tuberculosis. The function was
followed by organising special health education
programmes in the Maharaja Yeshwant Rao
Hospital, TB Clinic. Malharganj, Cloth Market
Hospital, Manorama Raje TB Hospital and
E.S.I. Hospital.
Maharashtra: The Maharashtra State Anti-
TB Association advised its District Associations
and I.M.A. branches all over the State to celebrate
the Centenary in a befitting manner by
organising reorientation courses for general
practitioners intensifying their health education
activities and carry out mass immunisation and
case-finding programmes in urban and rural
areas. The State TB Association and the
Bombay branch of the I.M.A jointly organised
a Conference on the 26th, 27th and 28th March,
1982 of which one morning and an afternoon
were devoted for discussing the various aspects
of tuberculosis and its management. The Association
also organised jointly with the Lions
Club of Mazgaon, a special meeting presided
over by His Excellency Shri Homi J.H. Taleyarkhan,
Governor of Sikkim, whe.re workers in
tuberculosis in the State were honoured. Special
functions were also held at Pune, Nasik and
Nanded where a symposium, a panel discussion
and some Guest Lectures on tuberculosis were
arranged. The Association arranged publication
of special articles on different aspects of tuberculosis
in English and Marathi dailies. Mass
immunisation and case-finding programmes
were held at Sudhagad, Pali Taluka in Raigad
district and Dindori Taluka in Nasik District.
The main aspects of the project were multiple
vaccination for all the children of eligible group
in the Taluka, door-to-door enumeration of TB
symptomatics and their sputum examination
and a series of diagnostic shibirs following
BCG vaccination programme. The Bombay
City programme for enumeration of the symptomatics
with the help of N.S.S. students will
commence shortly. The Bombay Municipal
Corporation has released Rifamycin for all
cases which would be discovered in the intensive
drive.
Meghalaya: The State TB Association celebrated
the Centenary of the Discovery of
Tubercle Bacillus by organising’a Special function
at Shillong on 17th July, 1982. The function
presided over by Shri D.D. Lapang, Minister
for Health & Family Welfare and President,
Meghalaya TB Association, was inaugurated
by Shri Prakash Mehrotra, Governor of Assam
and Meghalaya by unveiling the portrait of
Robert Koch. Dr. L.N. Chintey, Honorary
Secretary of the State Association welcomed the
distinguished invitees and Dr. (Mrs.) F.N.
Kharkongor, Deputy Director, Pasteur Institute,
proposed the Vote of Thanks. This was
followed by a Scientific Session which was
chaired by Dr. O. Lyngdoh and a panel
discussion with Drs. E. Lyngdoh and C.M.
Brahma as moderators. The session was well
attended and the subjects discussed covered
all aspects of tuberculosis. The function
came to a close with the screening of the film
‘Your Enemy—TB’.
Orissa: The Orissa State TB Association
organised its 3rd State TB & Chest Diseases
Workers’ Conference and also a special function
to celebrate the Centenary of the Discovery of
the Tubercle Bacillus by Robert Koch at the
Medical College, Burla on the 13th and 14th
March, 1982. The Minister of State for Health
and Family Welfare, Orissa, inaugurated the
function. On the 14th a Seminar on TB Control
Programme was organised which was chaired
by the Director of Health Services. The Scientific
Sessions were presided over by the Director
of Medical Education and Training.
The State Association also organised a
Symposium on Tuberculosis at the S.C.B.
Medical College, Cuttack on 26.4.1982 which
was attended by a large number of students
from the Medical Colleges of Cuttack, Berhampur
and Burla.
Sikkim: The Sikkim Anti-TB Association,
organised a special function to celebrate the
Centenary on 25th May, 1982, in the Secretariat
Hall at Raj Bhavan, Gangtok. The function
was inaugurated by the Hon’ble Shri S.
Shankaranand, Union Minister for Health and
Family Welfare in the presence of Shri Homi
J.H. Taleyarkhan, Governor of Sikkim, Kumari
Kumud Ben Joshi, Union Deputy Minister for
Health, Shri N.B. Bhandari, Chief Minister of
Sikkim, Shri S.M. Limboo, State Health Minister
and delegates from Sikkim and North-Eastern
States. In his inaugural address Shri Shankaranand
urged the need for community involvement
in the fight against tuberculosis and
assured the State Government of adequate
Central assistance in their efforts to control
tuberculosis in the State. Shri Homi J.H.
Taleyarkhan stressed the need for expansion
of the domiciliary treatment services coupled
with an army of devoted health visitors to
monitor the health of the patients and to see
that they take medicines regularly at home and
visit the treatment centres at regular intervals
for check-up. The Chief Minister, Shri N.B.
Bhandari and the State Health Minister Shri S.
M. Limboo paid rich tributes to Robert Koch
for his epoch-making discovery which brought
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210 NEWS & NOTES
tuberculosis control within the realm of possibility.
The function came to a close with a
Vote of Thanks by Dr. A. Pazo, Joint Secretary
of the State Association.
Tamil Nadu: The Tamil Nadu Tuberculosis
Association organised an Anti-TB Week in
Madras from 15.4.1982. His Excellency the
Governor of Tamil Nadu, Thiru Sadiq Ali,
unveiled the Portrait of Robert Koch and delivered
the valedictory address. TheHon’ble Dr. H.V.
Hande, Minister for Health presided and Smt.
Tara Cherian, M.L.C. Chairman, State Social
Welfare Board distributed prizes to the winners
in the Essay Competition conducted by the
Association both in English and Tamil for the
students of City Colleges and Higher Secondary
Schools. The Health Education activities were
also intensified during the week. A series of
lectures and film shows were arranged with the
help of the Lions Club and certain Primary
Health Centres. Articles of topical interest on
Tuberculosis, its prevention and control were
published in “The Hindu” in English and
“Dinamani” in Tamil. Radio and Television
authorities arranged suitable programmes on
Tuberculosis in which Dr. K.V. Krishnaswami,
Dr. Santosham and others participated. As
part of effective delivery of Primary Health
Care at the peripheral level, some of the District
Associations organised case-finding programmes
in selected villages and intensified their health
education activities by holding public meetings,
organising cultural programmes, film shows,
etc. The Medical Colleges at Coimbatore,
Tirunelveli. Madurai and Chingleput conducted
symposia on the History of TB and at Tirupathur
in North Arcot District, the local Indian
Medical Association Branch organised a
Refresher Course for General Medical Practitioners
and also a training programme rfo paramedical
personnel.
Tripura: The TB Association of Tripura
proposes to celebrate the Koch Centenary Year
by launching a special case-finding drive in certain
groups of workers, viz. tea garden, jute mill,
beedi sramik etc. phase by phase. It has chosen
the Kalashara Tea Garden workers to start
with, and the programme will be carried out in
cooperation with the Department of TB,
Government of Tripura. The Tripura Jute Mill
has agreed for a similar check up drive among
its workers which will be taken up shortly.
Beedi workers of Bishalgarh Block area will
be taken up later.
Uttar Pradesh: The Uttar Pradesh TB Association
organised its 5th State TB and Chest
Diseases Workers’ Conference in Dehra Dun
from 8th to 10th January, 1982. The Conference
was inaugurated by the State Finance
Minister and the Scientific Sessions were
presided over by Dr. O.P. Mital. Dr. S.P.
Pamra Honorary Technical Adviser of the
Tuberculosis Association of India delivered the
Key Note Address on “Case-finding”. The
subjects discussed at the Scientific Sessions
included National TB Programme, Chemotherapy
and recent advances, Extra-pulmonary
Tuberculosis, Childhood Tuberculosis, Allergic
and other Respiratory Diseases, etc.
Ind. J. Tub,, Vol. XXIX, No. 3