Abstract

Sporocysts developing in the heart of the snail host from irradiated Echinostoma paraensei miracidia are unable to form rediae and can survive for only a brief time. However, they still were able to reduce temporarily the strong natural resistance to Schistosoma mansoni in juveniles of a strain of Biomphalaria glabrata selected for genetic resistance to this parasite. S. mansoni primary sporocysts, unable to survive in single (control) infections in this host strain, developed successfully in most snails in which irradiated E. paraensei sporocysts were present. After the echinostome sporocysts were destroyed by host amebocytes, the snails regained their natural resistance against a new infection by miracadia of S. mansoni. Successful initiation of an infection with S. mansoni was achieved only in the presence of living irradiated echinostomes. Once the schistosome infection had become well established, however, developing primary and secondary sporocysts could survive and produce cercariae, although the protecting echinostomes had by then been destroyed. Early growth stages of the primary sporocysts apparently are more vulnerable to the snail's defensive reaction and generally do not survive unless protected by irradiated E. paraensei sporocysts. After the S. mansoni sporocysts grow older, they develop their own capacity to interfere with the snail's natural resistance and continue to survive and produce progeny without further protection by the echinostomes. Irradiated sporocysts have a lower capacity to interfere with the snail's natural resistance than do nonirradiated sporocysts. Suitability, as distinguished in this paper from susceptibility, can be separated from resistance of the snail to trematodes by employing double infections.

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