Host–parasite coevolution may result in life-history changes in hosts that can limit the detrimental effects of parasitism. Fecundity compensation is one such life-history response, occurring when hosts increase their current reproductive output to make up for expected losses in future reproduction due to parasitic infection. However, the potential trade-offs between this increase in quantity and the quality of offspring have been relatively unexplored. This study uses the trematode, Schistosoma mansoni, and its snail intermediate host, Biomphalaria glabrata, to better understand how this host life-history response, fecundity compensation, impacts host reproduction. Measures of host reproductive output as well as offspring hatching success and survival were collected to assess the reproductive consequences of infection. Infected snails exhibited fecundity compensation by increasing the number of eggs laid and the overall probability of laying eggs compared to uninfected snails. Parental infection status did not play a significant role in hatching or offspring survival to maturity. Offspring from a later reproductive bout demonstrated a higher hatching success rate. Overall, the lack of an apparent trade-off between quantity and quality of offspring suggests that infected parental snails invest more resources towards reproduction not only to increase reproductive output, but also to maintain the fitness of their offspring, possibly at the expense of their own longevity.

Colonial hosts offer unique opportunities for exploitation by endoparasites resulting from extensive clonal propagation, but these interactions are poorly understood. The freshwater bryozoan, Fredericella sultana, and the myxozoan, Tetracapsuloides bryosalmonae, present an appropriate model system for examining such interactions. F. sultana propagates mainly asexually, through colony fragmentation and dormant propagules (statoblasts). Our study examines how T. bryosalmonae exploits the multiple transmission routes offered by the propagation of F. sultana, evaluates the effects of such transmission on its bryozoan host, and tests the hypothesis that poor host condition provokes T. bryosalmonae to bail out of a resource that may soon be unsustainable, demonstrating terminal investment. We show that infections are present in substantial proportions of colony fragments and statoblasts over space and time and that moderate infection levels promote statoblast hatching and hence effective fecundity. We also found evidence for terminal investment, with host starvation inducing the development of transmission stages. Our results contribute to a growing picture that interactions of T. bryosalmonae and F. sultana are generally characterized by parasite persistence, facilitated by multiple transmission pathways and host condition-dependent developmental cycling, and host tolerance, promoted by effective fecundity effects and an inherent capacity for renewed growth and clonal replication.

In the production of the infective cercariae of trematodes, the terminal investment hypothesis of life-history theory predicts that the rate of host exploitation and cercarial production should increase during the period of cercarial shedding since the reproductive value of the parasite decreases during this period. In contrast, a bet hedging hypothesis that focuses on the success of transmission when host contact rate is variable predicts that cercarial production should decrease in an attempt to keep the host alive for longer and thus would increase the probability of successful transmission. We examined these two hypotheses under laboratory conditions and recorded the production of Diplostomum spathaceum cercariae from naturally infected snail hosts, Lymnaea stagnalis. The average number of cercariae produced per day decreased as the snail host approached death counter to the terminal investment hypothesis. The finding supports the prediction of the bet hedging hypothesis and implies that the pattern of cercarial production may be explained by reduced virulence of the parasite within the snails to ensure extended total production time of cercariae. Nevertheless, survival of infected snails was still lower than uninfected snails suggesting that ultimately the infection still increased snail mortality rate. Cercarial production varied between days but was not cyclic, probably because of the physiology of the sporocysts within snails. Fewer cercariae were released at night, which may increase transmission efficiency to diurnally-active fish hosts. The mechanisms associated with daily cercarial production are discussed.