The Classification of Pulmonary Tuberculosis and An Outline of Standardised Principles of Management pot

a Active Malignant Primary—this has serious subforms, lobar caseous pneumonia, bronchopneumonia, or acute miliary tuberculosis; b Quiescent Malignant Primary—characterised by calcified

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, son pronostic, sa marche generate, une veritable unite lui conferant la possession d’une certain autonomic’ This system has survived until the present day, but owing to the

introduction of numerous morphological sub-forms, has become over-elaborated It remains confusing because it takes no account of pathogenesis

The first pathological classification, based on a description of the pathological lesions, was by Albrecht (1907) The lesions were divided into three groups: (1)

indurating, cirrhotic, healing, (2) nodular (productive), and (3) caseous-pneumonic (exudative).

Another widely-adopted clinico-pathological classification was that of Turban (1907) Here the basis was the quantitative extent of the lung lesions: three stages were differentiated by physical signs This system was supplemented by the radiologi- cal findings to form the basis of the official British and American classifications Two further factors, the degree of activity, and sputum findings were introduced into the British classification; in America many changes in emphasis and other details have been made in the last 50 years, some of them being admittedly retrograde

The first pathogenetic classification was that of Ranke (1916, 1919) He believed that in its evolution tuberculosis, like syphilis, passes through three well-defined stages

Recently, Dufourt (1953) like New man (1930) has attempted to combine the classification of Bard and Ranke He believes that the ‘cycle of the infection’ can

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156 THE CLASSIFICATION OF PULMONARY TUBERCULOSIS

thus be expressed, but the fallacies of the Ranke classification make this attempt confusing and unsatisfactory Pathogenesis has been greatly advanced by Rich (1951) and others since Ranke’s day

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

1 Fibro-caseous Form (Bronchogenic)

2 Fibrous Form (Haematogenous)

For clinical purposes the categories required are briefly outlined below:

I Primary Disease :

1 (a) Active Benign Primary—This includes persons with a radiologically

invisible lesion but with a positive tuberculin reaction, and also those with a radiologi- cally visible lesion, complicated sometimes by resolving pneumonia, atelectasis, or pleural effusion;

(b) Quiescent Benign Primary—including those with a calcified nodule or

round focus or no residual lesion, absorption having been completed

2 (a) Active Malignant Primary—this has serious subforms, lobar caseous

pneumonia, bronchopneumonia, or acute miliary tuberculosis;

(b) Quiescent Malignant Primary—characterised by calcified nodules or round

foci or again, no residual lesion

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)

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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

lower zone or a combination of these

The degree of activity should be described in the following terms active, pro-

gressive, stationary, regressive or inactive, quiescent, arrested, recovered

For epidemiological purposes only 9 categories are needed:

I.—Active forms: (1) benign primary; (2) malignant primary; (3) minimal

secondary; (4) moderately advanced secondary; (5) advanced secondary; (6) fibrous secondary; (7) fibrocavtaria secondary; (8) non-pulmonary

II.—Quiescent forms: residual lesions of any of the above.

History of the Classification

When I commenced work on tuberculosis in the year 1923 active and healed primary tuberculosis had already been described by Parrot (1876) , Kuss (1898), Ghon (1912, 1916, 1923) and others The calcified primary complex (Ranke 1916, 1919) was often observed in autopsies of persons dying from other causes than tuberculosis, and the active stage of benign primary disease ending with a calcified primary complex was diagnosable by serial radiographs In autopsies in children we frequently saw active progressive forms (acute miliary tuberculosis, lobar caseous pneumonia and case- ous pneumonia and caseous bronchopneumonia) It was gradually realised that these were always associated with unilateral caseous hilar lymphatic nodes and with almost 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

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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 secondary disease Serial radiographs in such regressive cases often showed, after some years, lesions somewhat similar either to a unilateral Assman focus or to bilateral Simon foci This observation of the course of regression led me in many instances to imagine that a similar but reversed course must have been followed during the evolution

or progressive stage of the disease I therefore gradually acquired the habit of placing serial radiographs in reverse order, from the healed lesion back to the advanced stage The course of evolution and involution of the active lesions, as radiographically always appeared to follow the same route but in opposite directions It gradually became apparent that regression in secondary disease, ended in two different ways, (1) with a unilateral lesion similar to the Assman focus and (2) with a bilateral apical lesion some what similar to Simon foci At this stage it was becoming fairly clear to me that in the secondary type of the disease there were two distinct forms, which could be correctly described as ‘fibro-caseous’ and ‘fibrous’ disease respectively

The late results of collapse therapy and early results of chemotherapy contribut-

ed new facts regarding the process of regression of the disease, and regarding arrest of the process of progression at an earlier stage than had previously been seen From the facts thus collected, it became clear that all four forms of the disease exhibited a similar but reversed course during these two phases It then seemed reasonable to

described this process as a general ‘law’ This principle was formulated as ‘the law

of evolution and involution in tuberculosis’ The pathological processes involved in the

two phases, progression and regression, are of course, different In the developing lesion there is perifocal reaction, exudation, caseation, liquefaction and destruction of tissue In the regressing lesion (apart from that ending in complete absorption) the reparatory forces of fibrosis, calcification, sclerosis, cellular regeneration, compensatory emphysema, etc., all help to close the gap partially or completely But it is regularly observed both pathologically and radiologically that the most recent active associated lesions are absorbed or healed first in the process of regression and the ‘original’ (pri- mary) or ‘initial’ (secondary) lesions last; and by observation of the process of regres- sion in uncomplicated cases we are finally led back to what was the original or initial 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

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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

II Virulence of the infecting bacilli

III Natural resistance

IV Acquired resistance

V Hypersenisitivity

These factors determine the pathogenetic type and form of the disease Certain

physiological and accidental factors may greatly influence the establishment and develop-

ment of the disease Such physiological factors include heredity, sex and age; the acci-

dental factors include malnutrition, physical and mental overstrain, intercurrent infec-

tions, trauma, occupational risks, endosrine disturbances, alcoholism, etc These

factors cannot determine or change the type of the disease, although they may modify

its form and influence its extent and activity

The extent and activity of the lesions vary directly with three of the funda-

mental factors of pathogenesis, quantity of bacilli, virulence of bacilli, and hypersensiti-

vity; and they vary inversely with the two fundamental factors, natural and acquired

resistance The greater the quantity and virulence of the bacilli and the higher the

degree of hypresensitivity the larger and more destructive will the lesions be; while

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,

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160 THE CLASSIFICATION OF PULMONARY TUBERCULOSIS

into a large quantity of bacilli before the appearance of acquired resistance if the latter

is delayed In contrast, when acquired resistance develops rapidly and strongly, the multiplication of bacilli is suddenly stopped, reparative changes of fibrosis limit the spread of the lesion, and encapsulation begins This is the characteristic lesion of the benign primary complex, which is much the most common of the two primary forms of the disease If acquired resistance, however, is delayed and weak, the bacilli in the infecting dose multiply geometrically during the preliminary period of natural resistance only, and by the time that the spreading inflammatory lesion begins to be checked by acquired resistance it already occupies a relatively large area From this time ‘the origi- nal lesion of primary disease’ takes on the characteristics of the malignant primary complex, which is the second and much rarer form of primary tuberculous disease in man

The appearance of acquired resistance is closely followed by the appearance

of hypersensitivity in both forms This is at first more a liability than an asset In the benign primary form where the original lesion is small and is being rapidly localised by fibrosis, the reaction produced by hypersensitivity is mainly a perifocal inflammation of very variable degree In fact this perifocal inflammation of the benign primary complex varies from almost nothing to a large pulmonary inflammation of the lung, with or without pleural effusion In the case of the malignant primary complex the effect of hypersensitivity is exerted on the lesion itself which is unprotected by significant fibrosis Here hypersensitivity actually destroys such fibrosis as is present and encourages necrosis and caseation, and consequently further extension of the original lesion and dissemina- tion Hence the malignant primary form is characterised predominantly by caseation

in the original lesion and in its regional node as well as in their associated foci

Occasionally malignant primary disease showing bronchopneumonia or acute disseminated and generalised miliary tuberculosis may arise by an accident from a benign primary complex so located as to allow discharge of a caseous mass into a bron- chus or a blood vessel Here the factor of ‘quantity of bacilli’ effectively overbalances the acquired resistance present and produces similar effects to that of a natural exending 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

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an exceptional finding (some 2 per cent) It may be complicated by resolving tuber- culous pneumonia or atelectasis, or a combination of these, or by pleural effusion, or occasionally by meningitis or other non-pulmonary metastases When this disease heals it is either completely absorbed or leaves a residual encapsulated caseous focus,

or a calcified nodule, or a scar, or a round focus (about 2 cm diameter), and a healed

or calcified lymphatic node; sometimes there are also a few neighbouring or distant calcified foci and more frequently a few symmetrical bilateral, apical foci After a period of quiescence, reactivation may occur, rarely, giving rise to the minimal lesion

of secondary tuberculosis (about 5 per cent of minimal lesions), but more frequently

to the localised chronic miliary form (about 25 per cent of the fibrous forms) and to non-

pulmonary forms of secondary disease Exogenous secondary infections, however,

follow much more commonly after a short or sometimes a long, period of quiescence, giving rise to the unilateral minimal lesion (in about 70 per cent of these cases) The remainder proceed to complete healing and immunity which is permanent in the vast majority of benign primary cases

Malignant primary tuberculosis consists of the malignant primary complex,

namely that expanding type of primary complex in which the original caseous pneumo- nic focus progresses, sometimes cavitates (primary cavity), and exhibits no tendency towards encapsulation It is always associated with multiple caseous lymphatic nodes

In its evolution it may be complicated by lobar caseous pneumonia, caseous broncho- pneumonia and disseminated or generalised miliary tuberculosis When these lesions heal, complete absorption is possible only if they have had early chemotherapy and other 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 and other subforms including fibrocavitaria)

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Fibro-caseons Form

The minimal lesion is the initial lesion of this form It is a small asymmetrical unilateral secondary lesion commencing with a few tubercles or small area of inflamma- tion or both In its course it has a strong tendency to develop caseation and fibrosis concomitantly (in contrast with untreated malignant primary disease) It is of relatively chronic destructive type, spreading and disseminating mainly by the bronchial route, and may progress through three stages from ‘minimal’ to ‘moderately advanced’ and

‘advanced’ phthisis At any of these stages it may be complicated occasionally by sudden limited or widespread caseous dissemination, although far less regularly than in malignant primary disease The reverse process of regression and healing over a period of time can regularly be observed in treated cases by means of serial radiographs, and it is then constantly found that a similar but opposite course to that of progression,

is followed from ‘advanced’ through ‘moderately advanced’ to ‘minimal’ and finally to the residual lesion or lesions The residual lesions of the fibro-caseous form are scars, calcified nodules or one of more round foci

Fibrous Form

The initial lesion of the fibrous form, localised chronic miliary tuberculosis,

is characterised by symmetrical multiple small tubercles or small discrete areas of inflammation usually situated in both upper zones They may sometimes be radiologi-

cally invisible until they have healed They arise not by inhalation but by reactivation

and haemic spread to produce the following types of lesions: (1) disseminated chronic 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

In explanation of the localisation of the first lesion of primary disease in the absence of acquired resistance and hypersensitivity, we have to search for mechanical factors As the predominant localisation of the original lesion of primary disease in man is in the midzone (in 50 per cent of cases) it would seem that the larger infected

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droplets gain access to this area for mechanical reasons more readily than to other parts

of the lung

The apical localisation of the initial lesion of secondary disease seems to be strikingly associated with the presence of a lower degree of acquired resistance (or possi- bly a different degree of hypersensitivity) in the apex than in other parts of the lung The real issue is, however, still undetermined, namely what is the mechanism by which acquir-

ed resistance (or hypersensitivity) so influences localisation that it becomes predomina- ntly apical in secondary disease

Summary and Conclusions

Primary and secondary tuberculosis are two distinct types of the disease, with

an entirely different natural history, onset, character and localisation of the lesions, course and termination In their progression and regression they are, however, govern-

ed by the same law—’law of evolution and evolution in tuberculosis’ There are two distinct original lesions in primary tuberculosis, the benign and the malignant, and two distinct initial lesions in secondary tuberculosis, the unilateral minimal lesion and the bilateral localised chronic miliary tuberculosis, and these lead respectively to the fibro- caseous and fibrous forms of secondary disesase The following are the chief criteria

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- son with malignant primary disease; progression more rapid and bacillaemic metasta- ses almost absent in the fibro-caseous form as compared with the fibrous form

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6 Characteristic different course and termination of secondary tuberculosis,

as compared with primary; regression ultimately to the minimal lesion in the fibro- caseous form and localised chronic miliary foci in the fibrous form, finally ending in residual lesions in both forms with their characteristic localisation

The Principles of Management

Management of tuberculosis, as employed to-day, is largely empirical, and a physician is greatly handicapped by the absence of standardised methods of approach, based logically on fundamental principles If the fundamental principles of pathogene- sis are understood and a ‘complete diagnosis’ is made on the basis of type and form of the disease as well as extent and activity, then management can be prescribed with a feeling of satisfaction by any practitioner It should be clearly reconginsed, however, that a correct classification is the key to correct and standardised principles of management; and that only with standardised principles of management can results

in various series and in various countries be compared to best advantage and the knowledge derived therefrom adapted to general use

There is ample evidence that M tuberculosis has not changed its virulence and

pathogencity for centuries; that there is no change in the natural history of the two types and four forms of pulmonary tuberculosis What is persistently changeable,

is the distribution of cases of the two types and four forms There are certain parts in

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 the case, although much less frequently, in minimal and localised chronic miliary second- ary tuberculosis For the former approximately a year is needed for quiescence; for the latter at least two years When the primary disease is healed, secondary disease develops in a small minority of cases, but true relapse of healed secondary disease is very rare

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