The pathogenesis of experimentally induced amebic liver abscess in the gerbil (Meriones unguiculatus).
Sequential development and pathology of experimentally induced amebic liver abscess in the gerbil (Meriones unguiculatus) were studied from 1 to 60 days after inoculation. Early lesions were characterized by an acute inflammatory response, which became granulomatous at 5 days. Early granulomas were discrete, with well-defined fibrohistiocytic walls. Trophozoite dissemination as a result of fibrolysis of granuloma wall was confined to the liver parenchyma. The granulomatous cellular infiltrate (less than 20 days) was characterized by granulocytes and histiocytes; older granulomas (greater than 30 days) were composed of lymphocytic infiltrate, plasma cells, and a few granulocytes, and were characterized by the absence of epithelioid histiocytes. The degree of pathologic change adjacent to liver granulomas followed the sequential development of the amebic liver abscess. Severe changes observed were portal canal lymphocytic infiltration, the presence of foreign body giant cells, periportal fibrosis, proliferation of bile duct epithelium, and hepatocyte anisonucleosis and ballooning degeneration. The pathogenesis of the infection and the usefulness of the gerbil model for the study of human amebiasis are discussed.
D000818:Animals; D005549:Foreign-Body Reaction / Q000473:pathology; D005849:Gerbillinae; D006098:Granulocytes / Q000473:pathology; D006099:Granuloma / Q000473:pathology; D006644:Histiocytes / Q000473:pathology; D008099:Liver / Q000473:pathology*; D008101:Liver Abscess, Amebic / Q000209:etiology / Q000473:pathology*; D008297:Male; D010950:Plasma Cells / Q000473:pathology; D013997:Time Factors