PATHOGENESIS OF EXPERIMENTAL PULMONARY PARAGONIMIASIS IN CATS

  • 1 January 1978
    • journal article
    • research article
    • Vol. 39  (11) , 1827-1832
Abstract
Specific-pathogen-free cats (n = 20) were inoculated orally with metacercariae of Paragonimus kellicotti and necropsied 1-263 days later. The immature 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 5-23 days postinoculation (PID). 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 eosinohphilic 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 55-263, 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 P. kellicotti ova in the alveolar tissue adjacent to cysts. The interior surface of the fluke-containing cysts became partially epithelialized by cells from communicating bronchioles.