Pathogenesis of experimental pulmonary paragonimiasis in cats.

Specific-pathogen-free cats (n = 20) were inoculated orally with metacercariae of Paragonimus kellicotti and necropsied between 1 and 263 days later. The immature Paragonimus flukes excysted in the intestine, penetrated the intestinal wall, and migrated from the peritoneal cavity through the diaphragm to the pleural surface of lungs by postinoculation days (PID) 5 to 23. This migration resulted in multifocal eosinophilic peritonitis and myositis. The flukes entered the lung by penetration of the pleura, which resulted in multifocal pleural hemorrhage and eosinophilic pleuritis. Immature flukes developed in the subpleural alveolar tissue surrounded by intense eosinophilic and neutrophilic inflammation. Communications developed between the fluke-containing subpleural cavities and adjacent bronchioles by PID 39, and ova from the sexually mature flukes entered the bronchioles. From PID 55 to 263, other prominent pulmonary lesions were peribronchiolar infiltration of lymphocytes and plasma cells, hyperplasia of bronchioles and peribronchiolar glands, and chronic active eosinophilic granulomatous pneumonia associated with degenerating Paragonimus ova in the alveolar tissue adjacent to cysts. The interior surface of the fluke-containing cysts became partially epithelialized by cells from communicating bronchioles.