Twelve young adult captivity-born tamarin monkeys (Saguinus fuscicollis) were each exposed to 150 cercariae of Schistosoma mansoni (KEB strain): 6 by the percutaneous (pc) and 6 by the subcutaneous (sc) route. The prepatent period, as determined by eggs in the feces, was 34-39 days for both groups. Weekly quantitative fecal examinations revealed that although both groups actively passed eggs for as long as the duration of the experiment (18 months), the sc group excreted a significantly higher number of eggs/gram/day in the feces than did the pc group. Eggs recovered from the feces of both groups were viable: they hatched and the miracidia invaded snails which subsequently yielded infective cercariae. A significantly greater number of worms was recovered from tamarins infected by the sc route as compared to those with pc infections, and large numbers of eggs were found in affected organs of the sc group. Chronically infected tamarins with high tissue egg loads developed focal granulomatous nodules along the serosal walls of the small intestines, which in some cases, apparently had budded off to lie free in the abdominal cavity. Hepatic granulomas from animals with acute infections were significantly larger than those from chronically infected monkeys. Our results strongly suggest the presence of a skin barrier to infection in the tamarin monkey, and that if this barrier is bypassed, the tamarin can serve as a permissive host for S. mansoni. The small body size of this monkey (less than 400 g) is an obvious reason for the establishment of the tamarin monkey as a laboratory nonhuman primate model for human schistosomiasis mansoni.