PERI-PORTAL FIBROSIS OF THE LIVER DUE TO NATURAL OR EXPERIMENTAL-INFECTION WITH SCHISTOSOMA-MANSONI OCCURS IN THE KENYAN BABOON

The chronic granulomatous inflammation that occurs during schistosomia sis mansoni and its reparative healing lead to hepatic fibrosis, with subsequent portal hypertension (a life-threatening sequela). In the mu rine model, granuloma modulation invariably leads to formation of fibr ous tissue and deposition of extracellular matrix. Typically, < 10% of patients infected with Schistosoma mansoni progress to clay-pipe stem fibrosis. Similar fibrosis occurs in chimpanzees during experimental infections. Although previous studies of schistosomiasis mansoni in Ke nyan baboons have failed to demonstrate appreciable liver fibrosis, cl assical peri-portal fibrosis has now been observed in the livers of th ree yellow baboons (Papio cynocephalus cynocephalus) with natural S. m ansoni infections and three olive baboons (P. c. anubis) with experime ntal infections after each was challenged with 1000 S. mansoni cercari ae. The peri-portal fibrosis was indicated by marked fibroblast accumu lation, increased collagen deposition, bile-duct hyperplasia and blood -vessel proliferation. The lesions were more severe in the naturally i nfected baboons than in those experimentally infected. No accompanying portal hypertension, ascites or portocaval anastomosis was noted in a ny of the animals. The development of the baboon as a model for chroni c human schistosomiasis mansoni map be feasible.