Abstract

Laboratory studies indicate that miracidia of Fasciola hepatica can penetrate several species of lymnaeids in Europe, other than the natural host lymnaea truncatula. However, the production of cercariae from infections in abnormal hosts is unlimited to a small percentage of juvenile snails infected before a species-specific age. Juvenile Lymnaea palustris, of known ages, were exposed individually to F. hepatica miracidia and killed at 24 h intervals up to 14 days post exposure, and then processed for histological examination to ascertain reasons for the failure of F. hepatica infections to develop successfully in this abnormal host. The results indicate that the course of infection is rapidly halted by a cellular encapsulation response against the sporocyst. The response may be divided into two stages: first, the development of a cellular capsule and the concomitant degeneration of the sporocyst; second, the removal of the remains of the parasite and dispersal of the capsule. The efficiency of the response appears to increase with increasing age of the snail; statistical manipulation of the data obtained from histological investigations suggest that the defence mechanisms develop quickly in the first 6 days post hatching with little subsequent development during the experimental period. However, as sporocysts were encapsulated and killed regardless of age of the snail at exposure to infection, it is unlikely that in the host-parasite system used any of the infections would have survived.

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