Abstract
Summary Mice, multimammate rats, hamsters and gerbils, all highly susceptible to Schistosoma mansoni infection, showed considerable differences in anatomic and physiologic responses to acute and chronic infection. Functional portal obstruction was greater in mice than in other species, as evidenced by greater portal hypertension relative to hepatic egg burden. Significant portasystemic collateral veins were seen only in mice. Hepatic granulomas were considerably larger in mice than in other species. In very early (40-day) massive or very late (84-week) light infections in mice, portal hypertension was slight, granulomas were small and portasystemic collaterals were rare. The intensity of infection in these acute and chronic experiments was such that liver egg burdens in both these groups were similar to those of mice with marked portal hypertension and collateral circulation 9 to 12 weeks after infection. The data suggest that the greater portal hypertension in mice is related to the larger size of granulomas in this species. Histologic findings did not reveal other factors of probable importance in the genesis of portal hypertension, though pylephlebitis and segmental portal fibrosis were present. Total hepatic blood flow, measured in lightly infected mice between 12 and 60 weeks after exposure, remained normal. The size of granulomas around recently deposited eggs in the mouse liver decreased slightly with increasing duration of infection.