Interaction of Pneumocystis carinii with Host Lungs: an Ultrastructural Study

Pneumocystis carinii pneumonia was produced in rats by the administration of corticosteroids, low (8%) protein diet, and tetracycline in the drinking water. The rats were sacrificed at weekly intervals, and their lungs were examined by electron microscopy. For the first 6 weeks, few alterations were noted in host pulmonary tissue, except a close attachment of P. carinii trophozoites to the type I pneumocytes. At 7 to 8 weeks, when the infection reached the peak intensity on light microscopy, degenerative changes occurred in the type I pneumocyte, beginning with subepithelial bleb formation and followed by denudation of the basement membrane. This denuded surface appeared to be the site both of exudation of serum and tissue fluid into the alveolar space and of spread of P. carinii into the interstitium. There was hypertrophy of type II pneumocytes, which also occurred in uninfected control rats ingesting tetracyclines. With tapering of the corticosteroid dose, P. carinii was slowly cleared from the lungs, but latent infection persisted for at least 21 weeks. The host response to the corticosteroid dose tapering included increased prominence of alveolar macrophages and progressive interstitial lymphocytic infiltrate and fibrosis. Thus, P. carinii interacts with, and is associated with damage to, specific host cells. This interaction is important in the host-parasite relationship in this infection.