A study has been made of repeated attacks of experimental lobar pneumonia in the dog produced by the intrabronchial injection of Pneumococcus Type I. Twenty-five individual dogs were given 78 infections in all at intervals of 3 days to 19 months. The number of attacks to which a single animal was subjected varied from two to eleven. It was found that recovery from this experimental disease conferred on the animal increased resistance against subsequent infections as shown by the fact that such animals regularly survived doses of culture which in the dog infected for the first time produced a fatal outcome. The recurrent attacks of pneumonia were uniformly mild in character; the febrile course was brief; the pulmonary lesion was usually confined to a single lobe, and bacteremia seldom occurred. There was no detectable difference between the second and the subsequent infections, which could be produced whenever desired, nor did the time intervals between attacks appear to bear any relationship to the severity of the experimental disease. Tests for acquired antipneumococcal immune substances in the blood after recovery showed their presence in some animals and not in others, yet dogs without demonstrable humoral immunity appeared to be just as resistant to reinfection as those possessing it.
A comparison of the pathogenesis of these secondarily induced lesions with those of the initial infection revealed certain striking differences between the two. Secondary lesions produced in the lobe previously affected tended to evolve much more rapidly than did the primary ones. They were characterized by the early appearance of a generalized macrophage reaction and a marked diminution in the numbers of pneumococci in the tissues or their complete absence. These changes occurred more slowly in secondary lesions initiated in hitherto uninvolved lobes. The macrophage reaction, which consists of a swelling of the fixed tissue cells (histiocytes) and a subsequent liberation of macrophages into the alveolar exudate, is regarded as a significant evidence of increased antipneumococcal resistance, since it has been observed to occur regularly at the time of recovery from the first infection and is accompanied by the local disappearance of the invading microorganisms.