If genetically resistant and susceptible rabbits inhale a certain number of human type tubercle bacilli, no tuberculosis in the lungs of the resistant animals is seen, as a rule several months after infection, while there is a variable and often extensive disease in the susceptible rabbits. The analogy to the presence or absence of active tuberculosis in man infected with the tubercle bacillus is evident. The inhaled tubercle bacilli multiply for but a short time in the resistant rabbits and are usually rapidly and completely destroyed. In the susceptible rabbits, the bacilli multiply profusely for a much longer time and persist in large numbers even months after inhalation. Whatever be the cause of the more rapid destruction of tubercle bacilli in the resistant animal, the resulting more rapid release of the contained antigens enhances the development of allergic sensitivity and antibodies in these animals. The development of an acquired resistance against tubercle bacilli of the human type is sufficiently rapid to affect the genesis of the initial gross primary pulmonary foci that result from the inhalation of a given number of bacilli. The greater the genetic resistance, the fewer the initial primary foci. Variations in genetic resistance are essentially variations in the rate of development of acquired resistance. It is suggested that variations in genetic resistance to inhaled human type tubercle bacilli may affect the prevalence of alveolar phagocytes capable of acquiring adequate resistance to the growth of the bacilli in their cytoplasm. The prevalence of such cells is subject to hormonal and immunological influences.

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In this study the attempt has been made to follow the fate of tubercle bacilli in the lung, liver, spleen, kidney and bone marrow of rabbits infected intravenously with large and small doses of human and bovine tubercle bacilli by determining the number of colonies recoverable from similar quantities of tissue on egg media at varying intervals during the course of infection. This method offers certain possibili-ties for the elucidation of this problem precluded by the modes of attack used hitherto. Histological methods, while giving precise data in regard to tissue changes produced by the tubercle bacilli, are poor instruments for determining the fate of the bacilli in a given organ. Without stressing the notorious difficulties in staining the organism at all times, histological technique can give no definite answer to the question whether certain stained bacilli are living or dead, and it is the number of living bacilli that is of importance. Again animal inoculation, while an excellent index of the presence of living virulent bacilli, is a very inaccurate index of the number of living bacilli in a given specimen of tissue, for it is possible to infect guinea pigs with even a very few bacilli.