The Classification of Pulmonary Tuberculosis

and

An Outline of Standardised Principles of

Management

By
MILOSH SEKULICH

“
In

all science progress is the result only of a series of continuous efforts, often
ignored or unknown, and the pretended discoveries are only the continuation
or the consequence of facts acquired, but insufficiently known or wrongly
interpreted; the scientific prospectors are generally isolated, often repulsed,
even at the moment when the ensemble of workers follows them
and of ten forgets them.” Th. Tuffier, Paris, trans. Lawrason Brown, 1941.

Ever since the time of Hippocrates attempts have been made to classify tuber-
culosis. Not until the 19th century was a clear clinical division made between acute
and chronic forms (Fournet, 1839); later there was a tendency to describe these forms
as ‘galloping consumption’ and ‘consumption’; to-day they can be accurately described,
not only on clinical grounds, but pathologically, radiologically and pathogenetically
as ‘malig nant primary’ and ‘advance secondary’.

The first clinico-pathological classification was by Bard (1898, 1927). He
described four forms: parenchymatous, interestitial, bronchial, and post-pleuritic.
Bard postulated the still valid principle that every form must have ‘per son evolution,


It is pointless even to mention any of the other numerous classifications which
have been suggested. They are all deficient in some respect. I have tried many of them
during the past 35 years, and fail to give satisfaction.

What is wanted is an international classification with standardised terminology,
and one which would bring order into the present confused picture. This is one of the
pre-requisites for the compilation of comparable statistics from diverse areas. Is this
possible? I believe that with the vastly increased knowledge of tuberculosis available
to-day it can be done. It can now be based on the pathogenetic types of the disease,
its clinico-pathological forms, and the extent and degree of activity of the disease.
Such a global classification includes all those mentioned above, except Ranke’s which
is based on an erroneous hypothesis. It has been fully described in my books (Sekulich,
1953, 1955, 1956).

The Classification

My classification consists essentially of the following two types and four forms,
the latter of which can be subdivided into numerous subforms for clinical purposes;
only five subforms are required for epidemiological purposes; various particulars of
extent and activity are added according to the purpose in view.

1
. Primary Type

1. Inflammatory Form (Benign Primary)

2. Caseous Form (Malignant Primary)

2. Secondary Type


It is only after primary disease, in one or other of these forms, has become
quiescent that secondary disease can arise, either by a new exogenous infection (in appro-
ximately 70 per cent) or by autogenous reactivation (in about 30 per cent).

Ind. J. Tub., Vol. IV, No. 4.

MILOSH SEKULICH 157

II. Secondary Disease

1. (a)
Active Fibro-caseous Form—
This includes unilateral and bilateral
minimal, moderately advanced and advanced disease, as well as abortive tuberculosis;
(b)
Quiescent Fibro-caseous Form—
including residual lesions, calcified or round foci,
and no visible residual lesion (complete absorption).

2. (a)
Active Fibrous Form—
including localised and disseminated chronic
miliary disease, localised and diffuse fibrous tuberculosis with emphysema, fibrocavi-
taria, fibrous tuberculosis of all these forms with dissemination (usually a terminal
event);—including localised or disseminated calcified nodules, hard fibrosis, round
focus, and residual sclerosis.

The extent of the lesion
should be defined by zones, that is upper, middle, or

complete absensce of fibrosis. Similar findings were observed also in autopsies of young
adults who had recently come to the town from the mountains.

An apparently similar but pathologically different autopsy picture, however,
was commonly encountered in other adults but never in infants. In this latter picture,
caseous hilar nodes were absent and fibrosis was conspicuously present, especially in
the form of cavities with a thick fibrotic wall. These two superficially similar, but
essentially different, findings in autopsies always corresponded to two quite different
clinical histories, especially as regards the duration of the disease. The first was invari-
ably fatal within a few months and always in less than a year, while the second was
usually of several years’ duration, ending in an acute phase lasting several months.
Accordingly, on the basis of the duration of the disease in life, I began to classify these
two clinico-pathological syndroms as ‘acute’ and ‘chronic’ types of the disease respecti-
vely. Later, when it was found that the second form often exhibited a calcified primary
complex, the conception of ‘primary’ and ‘secondary’ tuberculosis as two distinct types
corresponding to ‘acute’ and ‘chronic’ came into my mind.

Ind. J. Tub., Vol. IV, No. 4.

158 THE CLASSIFICATION OF PULMONARY TUBERCULOSIS
Since the acutely fatal primary type above mentioned was obviously very differ-
ent clinically and pathologically from the naturally healing benign primary complex,
the idea arose of two contrasted forms of the primary type, which were termed ‘benign’
and ‘malignant’ respectively.

The conception of the two forms of secondary disease (fibro-caseous and fibrous)
was only reached after several years’ pointed study of serial radiographs. At this time
the Assman focus (1925, 1930) and Simon foci (1930) had already been described, but
the evolution of the secondary type of the disease was not clear. Collapse therapy
and improved rest treatment were now resulting in numerous cases of healing and healed

lesion of the disease. When we compare serial radiographs showing regression towards
complete absorption with serial radiographs showing progression, we see exactly the
same picture in reverse. In cases, however, which in the process of regression leave
residual lesions, we have to ignore the scarring of the associated foci and, when this is
done, we see again exactly the same picture in reverse.

The crucial clinical demonstration of the truth of this law is to be found in the
study of a large series of cases (I have personally observed several hundreds) in which
the course of the primary type of the disease was observed from activity to quiescence,
and in which, after a varying interval of months or years, the secondary type of tuber-
culosis appeared, developed and regressed to quiescence. After this study I was at
last convinced that the natural history of pulmonary tuberculosis was indeed governed
by this law, and the outline of my classification logically followed. It appears to be the
key to the solution of most problems of diagnosis, management and epidemiology
in tuberculosis. It also provides the only yardstick which I have found reliable for
comparative measurements in all branches of tuberculosis.

Ind. J. Tub Vol. IV, No. 4.

MILOSH SEKULICH 159
Pathogenetic Basis of the Classification

My classification was primarily based on clinical and pathological study of many
cases over long periods of years. It has now been found that the deductions then
made, purely from clinical and pathological data, are neatly supported by a
reasoned consideration of the complex operation of Rich’s five fundamental factors
of influence in the pathogenesis at each and every stage of the disease.
The five fundamental pathogenetic factors are:

I. Quantity of pathogenic tubercle bacilli

the various degree of natural and acquired resistance will exercise their influence in
the opposite sense, thus restricting the multiplication of the bacilli and the progression
of the lesion.

Mechanism of the Primary Disease

When tuberculous infection is first established in the previously uninfected
body the tissues react at the beginning as they would against many kinds of implanted
foreign material, namely with hyperaemia, infiltration of polymorphonuclear leuco-
cytes and exudation of fluid, and later with mononuclear cell emigration; if this process
extends to tubercle formation or an area of infiltration a ‘lesion’ may be said to have
began. During this early period the host factor opposing the growth of the bacillus
is natural resistance only, and this is insufficient to prevent the tubercle bacilli from
multiplying and spreading to the regional lymphatic node and blood stream, thus produ-
cing hilar node infection in the case of the lungs, and
pre-clinical bacillaemia.
It is
only when acquired resistance appears that a significant change occurs, the lesion taking
on the characteristics of primary tuberculous disease. From this point the ‘original
lesion’ develops in one of two ways, depending on the relative potency of the infecting
dose on the one hand and the degree and rapidity of development of acquired resistance
on the other.

The dose of bacilli implanted by inhalation is usually small, having been esti-
mated to be between 1 and 400 bacilli per droplet. This dose may multiply, however,

Ind. J. Tub., Vol IV, No. 4.

160 THE CLASSIFICATION OF PULMONARY TUBERCULOSIS
into a large quantity of bacilli before the appearance of acquired resistance if the latter

malignant primary complex.

The benign primary form, being characterised by a perifocal inflammatory
reaction is, with its subforms, termed the
inflammatory form
although there may be
some caseation in the focus or lymph node. The malignant primary complex, being
characterised predominantly by caseation, is, with its subforms, termed the
caseous
form.

The evidence in favour of these developments is partly derived from animal
experiments and partly from numerous clinical observations in man. In animals the
influence of the factors ‘quantity of bacilli’ and hypersensitivity are easily demonstrable,
but laboratory animals do not exhibit acquired resistance to such a degree as man.
These animals succumb in about six months to the smallest dose of tuberculous infec-
tion, while in man most of the infected survive with primary disease which becomes
quiescent in six to twelve months. There is no other obvious explanation of this
difference than the ability of the human being to develop and maintain acquired resis-
tance. In not more than 5 per cent of children under two years seen at Chest Clinics
in England does acquired resistance fail; in these cases the malignant primary complex
develops, although there is no reason to suppose that the infective dose inhaled is
usually different from that inhaled by children with the benign primary complex.

Benign primary tuberculosis
consists of the benign primary complex with its
associated lesions. The benign primary complex consists of a primary focus and its
tuberculous regional lymphatic node. It may be associated with a small or large perifo-
cal inflammation and it is nearly always unilateral, the bilateral primary complex being


treatment. The residual lesions include multiple fibrous scars or multiple calcified
nodules or multiple encapsulated foci, and rarely a single quiescent focus,

Mechanism of Secondary Disease

In the previously infected body in which the primary disease has become quies-
cent or healed, established infection may again take place in exactly the same way as in
primary disease, or may occur by reactivation of the primary disease. But here the
established infection is usually initiated in the presence of hypersensitivity and of slight
residual acquired resistance. This has an immense influence on the development of the
‘initial lesion of secondary disease’ after the stage of established infection; and this
lesion at once begins to show quite different characteristics from those of the ‘original
lesion of primary disease’. The initial tissue reactions of hyperaemia, infiltration,
exudation and tubercle formation (area of inflammation) are more rapid and acute,
but checked at an earlier stage than in primary disease under the influence of acquired
resistance (Koch’s phenomenon). Spread to the regional lymphatic nodes is almost
completely prevented and bacillaemia is neutralised or immediately checked by the
acquired resistance rapidly recalled and present at an earlier stage. For the same
reason fibrosis is rapidly developed in the lesion, and is present side by side with some
degree of caseation, which develops under the influence of the hypersensitivity. From
this point the initial lesion of secondary disease develops in one of two directions;
(1) that of unilateral fibro-caseous disease, with characteristic bronchial spread if
progressing, or (2) that of bilateral symmetrical fibrous disease, spread through the
blood stream. The unilateral fibro-caseous form is characterised by a mixture of case-
ous and fibrous elements, frequently associated with inflammatory reactions, and steadily
progressing without significant involvement of the regional lymph nodes (‘minimal’,
‘moderately advanced’ and ‘advanced’ fibro-caseous disease with or without caseous
dissemination). The bilateral fibrous form is characterised mainly by fibrous nodules
(caseation being very slight) or by patches of infiltration. These are situated bilaterally
in the apices, and extend slowly downwards (localised chronic miliary tuberculosis

miliary tuberculosis, (2) localised fibrous tuberculosis with emphysema, (3) diffuse
tuberculosis with emphysema, and (4) fibrocavitaria—the form in which cavitation
occurs typically within a caseous focus (such as a ‘round focus’) and not by caseous
extension. An occasional development, usually terminal, is fibrous tuberculosis with
caseous dissemination. When the fibrous form heals it ends in localised calcified nodules
(mostly in the upper zones), disseminated calcified nodules, or residual fibro-sclerosis,
and occasionally by absorption. Their initial localisation is symmetrical and, in nearly
100 per cent, in both upper zones. This applies both to the active and quiescent stages.

In its symmetrical distribution from onset, its development symmetrically
downwards, its prolonged course, relative absence of bronchial spread, generally small
element of caseation and prominent fibrosis, it has a natural history quite different from
that of the fibro-caseous form, although it produces occasionally localised reactivation
and cavitation. It differs even more from primary disease. (It should be noted that
mere cavitation is not in itself sufficient to assign a case to the fibro-caseous form).

Localisation

A marked difference is demonstrated by clinical observation between the localisa-
tion of the
original
lesion of primary disease and that of the
initial
lesion of secondary
disease. In primary disease, both benign and malignant, the original lesion was establi-
shed in the middle and lower zones taken together in approximately 80 per cent
of my series cases; while in secondary disease the initial was established
in the upper zone in over 80 per cent (Sekulich, 1955). Here is an outstanding difference
between the respective localisations of the first lesion of primary and that of secondary
disease.

of differential diagnosis of the primary from the secondary type of the disease.

Primary Disease
1. Recent tuberculin conversion (3 to 8 weeks previously).

2. Radiological evidence of the primary complex or enlarged hilar lymphatic
node.

3. Localisation of the original lesion. It is in the middle zone in about
50 per cent of cases, and in the lower and upper zones in about 25 per cent each.

4. Recent normal radiograph prior to the development of the lesions.

5. Characteristic evolution and involution of primary disease, including
especially the tendency to caseous dissemination in malignant primary tuberculosis.

Secondary Disease

1. Radiological evidence of a healed primary lesion prior to the appearance
of the new lesion or concurrent with it.

2. History of tuberculin conversion and clear lungs of at least a year’s duration.

3. Absence of fresh macroscopic involvement of regional lymphatic nodes.

4. In the fibro-caseous form, the typical unilateral minimal lesion usually in
an upper zone (about 90 per cent), and in the fibrous form, localised chronic miliary
foci in both upper zones (about 100%).

5. Relatively slow progression and only occasional dissemination in compari-

the world, into which
M. tuberculosis
has never penetrated, and on the other extreme
there are certain areas in the Middle West and North West of the United States, where
tuberculosis has almost disappeared, tuberculin positives in young adults being less
than 10 per cent. Between these two extremes there are numerous degrees. For
instance, whilst in South Africa malignant primary disease is on the increase, in England
this form is becoming rare. Any change that occurs is not in the character of the disease,
but in the epidemiological picture, arid this varies according to the prevalence of the
factor of infection on one hand and the factor of resistance on the other. These two
factors are the essential elements in an epidemiological classification. They must be
clearly distinguished, and this can only be accomplished when the cases concerned
are classified to primary and secondary types and the four main forms of the disease.
In the management and rehabilitation of a case, and especially in epidemiological work
physiological and accidental factors play a very important part in resistance.

In all forms of pulmonary tuberculosis the essential approach to management
is to distinguish the original primary or the initial secondary lesion (which are the first
to start and the last to heal) from their associated foci. By rest treatment and chemo-
therapy we firstly attack ‘and heal the associated lesions. Sometimes all the lesions,
the original or initial and associated foci, are controlled by short or prolonged chemo-
therapy. When, however, the original or initial lession is not brought to quiescence,
mechanical or surgical means of dealing with it are needed.

When considering collapse therapy or resection at least four factors are of
importance: (a) pleural thickening or obliteration, (b) bronchial involvement, (c) the
age of the patient, and (d) the social and environmental factors.

There is clear evidence that benign primary tuberculosis with or without rest
treatment heals naturally either by complete absorption or calcification. This also is


2. The only complications for which chemotherapy is indicated, are tubercu-
lous meningitis, tuberculous endobronchitis, and non-pulmonary tuberculosis.

3. Benign primary tuberculosis complicated with pleural effusion occasionally
requires aspiration of the fluid for mechanical reasons in addition to rest treatment.

4. Quiescent benign primary disease complicated with a round focus or with
bronchiectasis requires preventive or therapeutic resection, in particular cases.

Building up of the body’s resistance and life immunity are here the main aim
of rest treatment.

II. Malignant Primary Tuberculosis

1. Early diagnosis and prompt treatment is particularly indicated in these
forms owing to their rapidly progressive character.

2. Rest treatment alone is insufficient in contrast with the management of the
benign primary complex.

3. Rest treatment and prompt chemotherapy are the immediate indication,
and these should be carried on for several months or years until the lesions are rendered
quiescent. In early diagnosed and some advanced cases the original and associated
lesions may be healed by chemotherapy alone. In far advanced cases, however, the
associated lesions may be ‘cooled’ or rendered regressive. When this has been accom-
plished a suitable form of collapse therapy is usually required. Treatment in this order
greatly reduces the need for bilateral collapse therapy, other than PP. The most suit-
able initial form of collapse therapy is usually PP. even when the visible lesions are
unilateral, since associated foci on the other side may be present but invisible. All

require prolonged rest treatment and prompt chemotherapy which may last for months
and even for a year or two. Frequent routine examinations should follow in every
case for many years. Its non-pulmonary complications should be treated as in other
forms.

III. Fibro-caseous Form

Minimal Lesion:
Every case of minimal lesion should be treated. It seems that
the most rapid method of treatment is rest and chemotherapy which may or may not
be followed by collapse therapy. If collapse therapy becomes indicated it should follow
rest and chemotherapy. Major surgery is even less justifiable.

Moderately Advanced Disease:
Moderately advanced disease should be treated
actively in every case. The most rapid and successful management in general is rest
combined with chemotherapy which may be followed by collapse therapy, and even
major surgery in particular cases. Untreated moderately advanced disease is liable to
progress into advanced or bilateral fibro-caseous forms.

Advanced Disease:
Advanced disease should be treated actively in every
case. The most rapid and successful management in general is rest treatment together
with chemotherapy which may be frequently followed by collapse therapy if possible
or major surgery. The latter is more frequently required than in other forms of fibro-
caseous disease.

Bilateral Fibro-caseous Disease:
In bilateral fibro-caseous disease the most
rapid and successful management in general is by rest combined with chemotherapy in


1. The active fibrous form should be treated by rest, and this may be sufficient
provided that it can be prolonged for two years or more.

2. The period of activity is shortened by combining chemotherapy with rest
treatment.

3. A considerable number of cases of the fibrous form can become quiescent
without collapse therapy.

4. Collapse therapy following rest and chemotherapy does, however, further
shorten the period of activity. It must, however, always be applied bilaterally, even in
fibrocavitaria when a visible cavity is present only on one side.

5. In the fibrocavitaria form, collapse therapy is nearly always indicated follow-
ing rest and chemotherapy.

6. The presence of pulmonary emphysema is characteristic of certain of these
forms, and does not contraindicate collapse therapy in the form of pneumoperitoneum.
On the contrary PP is beneficial in these cases, providing that over-exertion is avoided.

In conclusion it should be emphasised that the control or eradication of tuber-
culosis in any country depends mainly upon the maintenance of a good standard of liv-
living, in other words controlling what is called here the ‘physiological and accidental
factors’.

Bibliography and References

ALBHECHT
, E. (1907). ‘Zur klinischen Einteilung der Tuberculoseprocesse in den

path. Ges., 19, 143.

Kuss, G. (1898). ‘De L’ eredite parasitaire de la tuberculose humanie; ParisNational
Tuberculosis Association (1955). ‘Diagnosic Standards and Classification of
Tuberculosis., New York 19, N.Y.

Parrot (1876). Cpt. rend. Sec. biol., 28, 308.

RANKE
, K.E. (1916). ‘Primaraffect, Sekundare and Tertiare Stadien der Lungentuber-
kulose.’ Dtsch. Arch. Klin. Med., 119, 201.

” (1919) Ibid., 129, 224.

RICH
, A.R. (1951) The Pathogenesis of Tuberculosis. Second Edition, Blackwell
Scientific Publications, Oxford.

SEKULICH
, M. (1949). ‘A Key to the Classification of Pulmonary Tuberculosis.
Brit. I. Tuberc. and Drs. Chest, January 1949

” (1953). The Classification of Pulmonary Tuberculosis, William Heinemann,
London.

” (1954). ‘Congenital Tuberculosis after Pleural Effusion in the Mother.’
Brit. Med. Journ., May 8, p. 1093.

” (1954). ‘Pleural Effusion in Young People.’ Brit. Med. Journ., June 12,