Exogenous reinfection and pulmonary tuberculosis a study of the pathology

Abstract

Summary o (1) Three arguments are usually invoked against exogenous reinfection in the pathogenesis of pulmonary tuberculosis: permanent virulence of the primary lesions, thus responsible even for disease arising very many years later; acquired tuberculous immunity, preventing the production of new foci by reinfection; finally a brief interval-less than five years-between primary infection and phthisis in the great majority of cases. The present study is a critique of these arguments, on the basis of work in the field of pathology. (2) The sum total of published studies shows that primary calcified foci, both glandular and pulmonary, are sterile in over 80 per cent of cases-sterility proven by guinea-pigs inoculation. The average period taken for calcification being five years, the primary complex cannot, save in exceptional cases, be the source of pulmonary tuberculosis appearing much later. (3) Study of the pathology shows that reinfection does produce pulmonary foci. At necropsy of subjects dying of non-tuberculous causes, reinfection foci have been found in 24 to 60 per cent of cases. These foci are similar to the pulmonary component of the primary complex, and since primary foci can result in phthisis, there is little reason to believe that reinfection foci may not pursue the same course. The number of reinfection foci increases with age, this fact is in favour of an exogenous origin. (4) The theory of a brief interval between primary infection and phthisis in nearly all cases cannot be considered rigorously proved for the countries where it was formulated. For other countries it is definitely disproved. At necropsy of 301 adults who had died of pulmonary tuberculosis, in Paris, the primary glandular focus was ‘stony’ (completely calcified or ossified) in 67.7 per cent of cases, chalky in 6 per cent, caseous in 10.3 per cent; in 16 per cent of caes, no glandular focus was found. Even in the 15–20 age-group, half had completely calcified primary glandular sequelae. In the great majority of the subjects in this study, therefore, the primary infection had occurred long ago, and the disease must have been due to reinfection, in view of the demonstrated sterility of calcified lesions. (5) In reinfection tuberculosis the source of reinfection must be much more often exogenous than endogenous. In the cases discussed, there is no sign of reactivation in the calcified primary foci; it is not conceivable that bacilli would be liberated and disseminated without any evidence in the original focus. To the claim that endogenous reinfection nevertheless occurs, from foci of post-primary dissemination, one must oppose the extreme improbability that, many years after the primary infection such foci are any less sterile than the primary focus. The conclusion is that, in the epidemiological conditions of this study, many more cases from exogenous reinfection than from primary infection or endogenous reinfection. (6) It is probable that in the future the respective proportion of cases of pulmonary tuberculosis due to primary infection and to reinfection will be modified, the first increasing at the expense of the second, in relation to improvement in epidemiological conditions.