Acquired immunity and epidemiology of Schistosoma haematobium

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Abstract
HUMAN immune responses to schistosome infection have been characterized in detail1–5. But there has been controversy6 over the relative importance of ecological factors (variation in exposure to infection) and immunological factors (acquired immunity) in determining the relationships between levels of infection and age typically found in areas where infection is endemic7,8. Independent effects of exposure and age on the rates of reinfection with Schistosoma haematobium after chemotherapy have been demonstrated in the Gambia9 and Zimbabwe8. This age effect could be the result of acquired immunity to infection. Indeed, allowing for variation in exposure and age, low rates of reinfection in the Gambia are correlated with high amounts of specific IgE antibodies10—human IgE can kill S. mansoni schistosomulae in vitro11. Further, animals can acquire immunologically mediated resistance to S. mansoni infection12–14, although nonimmunological factors could also be involved15. Acquisition of this immunity seems to be related to the cumulative effects of repeated infection and provides only partial protection12,13,16. These characteristics are consistent with immuno-epidemiological data for both S. mansoni and S. haematobium infections of humans4,17. We have now analysed age–prevalence data for human infection with S. haematobium, and find patterns of variation that are indeed consistent with the epidemiological effects of acquired immunity predicted by mathematical models.

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