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Snail host parental investment throughout a Schistosoma mansoni infection

Parental investment theory describes the ability of organisms to respond to an environmental challenge by increasing the fitness of future offspring. Utilizing life history changes, organisms can maximize fitness by increasing their total reproductive output or by investing more into the success of fewer offspring. In cases where parasitic infections result in castration of their host, increased reproductive effort known as fecundity compensation has been demonstrated in a variety of organisms. This response appears predictive of expected future reproductive losses. Organisms struggling with an environmental pathogen, may attempt to better prepare their offspring for the environment they are experiencing through transgenerational immune priming (TGIP). In immune priming, primary infection lowers the prevalence and intensity of a subsequent infection by the same pathogen. Transgenerational immune priming carries pathogen resistance into further generations without genotypic changes. The focus of this study was to determine whether invertebrate parental investment into offspring parasite resistance varies over the course of an infection. Utilizing the snail host Biomphalaria glabrata and its trematode parasite Schistosoma mansoni, offspring were reared from specific time intervals in the parent’s infection and subsequently exposed to the same pathogen when each cohort reached the same age- 12 weeks. Differences in infection prevalence and intensity were expected based on when the offspring were born during their parent’s infection. A trade-off was predicted between the number of offspring produced in a cohort and offspring resistance to future infections. Offspring born during the period of fecundity compensation were predicted to exhibit lower resistance due to a dilution of individual investment by parents into a larger offspring pool. While our results did not support TGIP, there were differences in offspring prevalence, as well as an indication that parent health may interact with genetics in offspring resistance. Results suggest that parental condition can influence resistance of B. glabrata offspring to S. mansoni but that TGIP may not be operating in this system.