SCHISTOSOMA-MANSONI - SUSCEPTIBILITY DIFFERENCES BETWEEN MALE AND FEMALE MICE CAN BE MEDIATED BY TESTOSTERONE DURING EARLY INFECTION

In murine Schistosoma mansoni infections, fewer adult worms develop in male than in female mice infected with the same number of cercariae. To evaluate a potential role for testosterone in this phenomenon, test osterone levels were manipulated in groups of CBA/J mice that were the n infected and monitored for survival rates, worm burdens, organomegal y, and egg production. By 16 weeks of infection, more than 80% of mice in groups with low levels of testosterone (untreated females, castrat ed males, or carrier-treated castrates) were dead, while less than 40% of those in groups with high levels of testosterone (sham-castrated m ales, testosterone-treated castrates, or testosterone-treated female m ice) succumbed to infection. The mean number of worms recovered from m ice in the low testosterone level groups was comparable among groups, and significantly greater than that from those in high-testosterone-le vel groups. The degree of organomegaly observed correlated strongly wi th worm burden, but the number of hepatic eggs per female worm did not differ significantly between groups. When male mice were castrated or sham-castrated 5 weeks after S. mansoni infection, no significant dif ferences in host survival occurred. Furthermore, female mice treated w ith testosterone demonstrated reduced worm burdens if the testosterone was given 10 days prior to infection but not if the testosterone was given 10 days or 5 weeks after infection. Thus, the host sex bias obse rved in parallel-infected male and female mice appears to be related t o the presence of male gonadal tissue or testosterone early in infecti on, during the development of immature schistosomules.