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Pneumocystis carinii pneumonia was produced in two groups of rats by the administration of corticosteroids, a low-protein (8%) diet, and tetracycline in the drinking water. A third group not on corticosteroids or a low-protein diet served as controls. Members of the first group were sacrificed weekly for 8 weeks, and lungs were examined. A highly significant correlation was found between the histopathological assessment of the intensity of P. carinii infection and the number of cysts counted in enzyme-digested lungs. P. carinii progressively filled alveoli, and cyst counts increased from -104 to 109 cysts/g of lung at peak intensity of infection at 7 to 8 weeks. The second group of rats was placed on a regular diet and tapering doses of corticosteroids after week 4, and they were sacrificed at varying intervals for up to 21 weeks. P. carinii was not cleared from the lungs until after week 13 (more than 6 weeks after discontinuation of all steroids). Histologically, there was an increased prominence of alveolar macrophages and the progressive development of interstitial mononuclear cell infiltrate and fibrosis. Thus, P. carinii grows slowly in vivo and interacts with specific host cells. The resulting changes may be important in the pathogenesis of the infection and in the clearance of the organism from the lung after immunocompetence has been restored.

We compared histological and immunological techniques in the early diagnosis of Pneumocystis carinii pneumonia in bronchial lavage fluid of steroid-treated rats. The rats were sacrificed weekly and lavage fluids were: (i) examined with cresyl echt violet and Giemsa stains; (ii) examined for P. carinii antigens by indirect fluorescent-antibody, counterimmunoelectrophoresis, and double-diffusion techniques, using high-titer specific antisera to P. carinii raised in rabbits. P. carinii was detected in lavage fluid by cresyl echt violet at 2 weeks of steroids and persisted even with steroid tapering; the intensity of the infection in lavage fluid closely paralleled that in the lungs. P. carinii was not detected in lavage by Giemsa stain until 4 weeks and disappeared from the fluids with steroid tapering. P. carinii was detected by indirect fluorescent antibody as early as 1 week of steroids, and the results correlated well with those of cresyl echt violet. P. carinii antigens were not detected in lavage fluids or serum by counterimmunoelectrophoresis or double-diffusion techniques. Although precipitin lines sometimes occurred, they were nonspecific. In this model, cresyl echt violet and indirect fluorescent antibody were the preferred techniques for the early diagnosis of P. carinii infection in bronchial lavage fluid.

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