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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