Interactions between two digenean parasites, Diplostomum spathaceum and Schistosoma mansoni , and their respective intermediate snail hosts, Lymnaea stagnalis and Biomphalaria glabrata , were investigated. D.spathaceum infections in juvenile L.stagnalis became patent 9 to 10 weeks post-infection and inhibited initiation of host oviposition. Adult L.stagnalis resisted infection with D.spathaceum . Both juvenile and adult B.glabrata were susceptible to S.mansoni and the infections become patent 5 weeks after infection. B.glabrata infected as juveniles failed to begin egg-laying whilst those infected as adults showed a dramatic reduction of oviposition 4 weeks post-infection, i.e before the onset of patency. Infection with D.spathaceum , but not S.mansoni , resulted in the appearance of three polypeptides (68.3, 40.8 &'38 34.5 kDa) in snail serum. The additional peptides were not directly related to failure of snail reproduction and are probably of parasite origin. Reproductive failure of infected snails was linked to the later stages of cercarial development by a method developed to manipulate infections using the anthelmintic, praziquantel. D.spathaceum and S.mansoni infections were suppressed in their snail hosts following oral treatment with praziquantel. Praziquantel was selective for cercariae and inhibited cercarial shedding of both digenean species for approximately 5 to 6 weeks before recovery. In mature B.glabrata , harbouring 7 week-old infections of S.mansoni , suppression of cercarial shedding was accompanied by temporary recovery of reproduction. Snail fecundity was halted once more 2 weeks prior to resumption of cercarial shedding. Reproductive recovery depended upon the state of infection and maturity of the host at infection. Failure of D.spathaceum to infect adult L.stagnalis was attributed to the more developed and therefore more competent internal defence system of adult snails. Infection of juvenile, immunologically immature, L.stagnalis with D.spathaceum resulted in several changes in the snail immune system and infection seemed to prevent normal development of several facets of snail immunity.