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Experimental Infection with Schistosoma Japonicum in Chimpanzees

Parasitologic, Clinical, Serologic, and Pathological Observations^*

Franz von Lichtenberg, Elvio H. Sadun, Allen W. Cheever, Duane G. Erickson, Anthony J. Johnson AND H. Worth Boyce

Parasitologic, serologic, pathologic, biochemical, and clinical studies were conducted in 15 chimpanzees exposed to Schistosoma japonicum cercariae. Numerous viable eggs were passed in the feces after a prepatent period of 5 to 8 weeks. Worm recoveries at autopsy varied considerably, but not evidence was found of a reduction in worm burdens with infections up to 17 months' duration. No consistent difference was observed in the percent recovery and location of worms in animals exposed only once or in those exposed repeatedly. Most eggs in tissues were found in the liver and large intestine, but numerous eggs were also present in the small intestine and lungs of heavily infected animals. Nearly normal hepatic blood flow was maintained via the hepatic artery even in animals with completely obstructed intrahepatic portal branches. Well-developed portasystemic collateral venous channels effectively decompressed the portal system. Hepatomegaly and severe portal fibrosis were common gross findings; variable degrees of pipe-stem fibrosis consistent with infection intensity were found. The development of pipe-stem fibrosis was particularly rapid and destructive, and hepatic lesions were more inflammatory and polymorphous with S. japonicum than has been reported with Schistosoma mansoni. Marked intestinal lesions were present in a variable and patchy segmental distribution. Glomerular lesions occurred in most chimpanzees with pipe-stem fibrosis, and the prothrombin time was abnormal in several of the more severely diseased animals. Marked hypoalbuminemia and hypergammaglobulinemia were frequent. Hypoglycemia and uremia appeared to be important factors in some infected animals. The chimpanzee was a particularly valuable model for studies on the pathogenesis of schistosomiasis japonica.

Accepted for publication June 8, 1971.

^* This work was partially supported by Grant No. AI-02631, of the National Institute of Allergy and Infectious Diseases, National Institutes of Health, and by contract No. DA 49-193-MD-2253 of the U. S. Army Research and Development Command, Armed Forces Epidemiological Board.

Present address: Peter Bent Brigham Hospital, Boston, Massachusetts 02115.

Present address: National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.