THE PATHOGENESIS AND PATHOLOGY OF EXPERIMENTAL TYPE I PNEUMOCOCCIC PNEUMONIA IN THE MONKEY.

The pathogenesis of lobar consolidation and microscopic pathology of induced Type I pneumococcic pneumonia in a series of fourteen monkeys, killed at close intervals of time after infection, have been studied. The inflammatory process which resulted in consolidation was primarily intraalveolar and intrabronchial. The pneumococci spread within the air spaces as a result of the dissemination of the infected edema fluid directly from alveolus to alveolus through the pores of Kohn and from bronchiole to bronchiole as a result of repeated aspiration during breathing. The pneumonic process within the air spaces developed and progressed independently of the reaction in the interstitial tissues. The organisms spread to the interstitial tissue secondarily from the alveolar spaces. Once in the interstitial tissues they appeared to be the important source of infection producing bacteremia but not important in the mechanism by which consolidation was produced. The exudate cells came chiefly from the blood. The large mononuclear cells which replaced the polymorphonuclear leucocytes were derived principally from the hypertrophy and transformation of lymphocytes and monocytes into macrophages after they entered the exudate in the early stages of the disease. The part the local septal cells played as the source of the macrophages could not be accurately determined. The reaction of the septal cells appeared to be chiefly one of swelling without detachment and occasional proliferation to form binucleated attached cells. To follow the transformation of the hematogenous mononuclear cells into macrophages in the exudate, the inflammatory reaction must be examined at frequent intervals during the first 36 hours of the disease. The similarity of the pathogenesis of lobar consolidation in human pneumonia to that observed in the experimentally induced disease in monkeys and dogs was discussed.