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Over the past three decades, intensive studies of murine schistosomiasis have provided important clues to the understanding of the human disease, but growing evidence suggests that these results derived from highly inbred strains of mice might not have direct applicability to the human infection. Recent data based on the baboon indicate that infection in this non-human primate might mirror the human situation. In this review, Mramba Nyindo and Idle Farah demonstrate that baboons provide an excellent non-human primate model that produces pathology and disease closely resembling that observed in humans, and address how studies in baboons can provide insights into mechanisms regulating schistosomiasis mansoni pathology and immunity. They also address, in a general way, issues related to the use of non-human primates in biomedical research.

The chronic granulomatous inflammation that occurs during schistosomiasis mansoni and its reparative healing lead to hepatic fibrosis, with subsequent portal hypertension (a life-threatening sequela). In the murine model, granuloma modulation invariably leads to formation of fibrous tissue and disposition 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 Kenyan baboons have failed to demonstrate appreciable liver fibrosis, classical peri-portal fibrosis has now been observed in the livers of three yellow baboons (Papio cynocephalus cynocephalus) with natural S. mansoni infections and three olive baboons (P. c. anubis) with experimental infections after each was challenged with 1000 S mansoni cercariae. The peri-portal fibrosis was indicated by marked fibroblast accumulation, increased collagen deposition, bile-duct hyperplasia and blood-vessel proliferation. The lesions were more severe in the naturally infected baboons than in those experimentally infected. No accompanying portal hypertension, ascites or portocaval anastomosis was noted in any of the animals. The development of the baboon as a model for chronic human schistosomiasis mansoni may be feasible.

Light and scanning electron microscopic study of intestines of 5 baboons (Papio anubis) in a state of acute schistosomiasis mansoni after exposure to 800 cercariae was made. In addition to overt granulomatous inflammation in the mucosa of the colon and ileum, more subtle microscopic lesions consisting of smooth muscle hypertrophy and villous atrophy were present. The intensity and distribution of these lesions were less marked in 5 baboons previously vaccinated with 40,000 30-krad-attenuated cercariae and presenting a 39% mean protection level measured as a percent reduction in adult worms recovered from mesenteric vasculature at perfusion. No similar lesions were observed in 2 normal uninfected and nonvaccinated baboons. These results are comparable to what has been reported in mice infected by Schistosoma mansoni. The data indicate that villous atrophy, hypertrophy of muscularis mucosa, nd goblet cell hyperplasia are important pathological changes to be included in the evaluation of the efficacy of schistosomiasis vaccines in the baboon model, together with the routine adult worm recovery from mesenteric blood vessels and the overt liver and bowel pathology.

Acute gastric dilatation in two black and white colobus monkeys is described. The subfamily colobini have a ruminant-like stomach and a pregastric fermentation, of important for the observations described.