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It has been recognized that Schistosoma mansoni infection causes depression of T-cell responsiveness. In this study we have evaluated whether immunodepression associated to schistosomiasis could be reverted by specific treatment. T-cell immune response was assessed by means of intradermal tests using recall antigens in a group of 22 patients with hepatosplenic schistosomiasis, one year after treatment with oxamniquine and compared with a group of untreated hepatosplenic patients. Only 27% of treated patients presented complete anergy to all tested antigens, in marked contrast to 80% unresponsiveness showed by hepatosplenic patients without treatment. Although most of the treated individuals showed some response to the tested antigens, in some individuals this unresponsiveness still persisted after treatment. Anergy was not found in any normal individual of the control group. It was concluded that Schistosoma mansoni infected patients may recover their normal immune responsiveness after the elimination of the worm by treatment.

Of 1,125 individuals, residents in an area where mansonic schistosomiasis is hyperendemic, were studied regarding the clinical forms correlated to the racial groups (indian mestizo, white, light mullato, medium mullato, dark mullato and negro) and to their socio-economic level according to a set of 16 variables. The white individuals (10.5%) showed a significantly higher incidence of the hepatosplenic forms; in the other racial groups there were similar frequencies, altogether 3.6%. Those with hepatosplenomegaly had a higher socio-economic level and when they also belonged to the white race the relative risk (2.78) was significantly higher.

The coefficient of inbreeding (for Wright) was studied in Catolândia, in the state of Bahia, Brazil, an area considered hyperendemic for manson schistosomiasis in a population of 1,130 inhabitants. The coefficient of inbreeding was estimated for 1,123 individuals it was classified as f greater than 0 in 13.2% (n = 148). In the hepatosplenic group the frequency of f greater than 0 was 26.8%, and in the hepatointestinal group the frequency was 12.5%. The frequency of the hepatosplenic diagnosis in whites who were f = 0 did not differ from that which was observed in the negroid group. These verifications were confirmed by the Woolf's test; the relative risk of the whites, f greater than 0 in acquiring hepatosplenic schistosomiasis was 14.1. These observations reinforce the influence of the genetic component in the development of the hepatosplenic form of the mansons schistosomiasis.