Plastic products are increasingly a source of pollution found in aquatic systems. These products degrade, releasing microplastic leachates such as Bisphenol A (BPA). BPA is a xenoestrogen that imitates estrogen and disrupts the endocrine system. It has been shown to impact both vertebrate and invertebrate organisms, including freshwater mollusks that serve as intermediate hosts to trematode parasites. While the effects on these hosts have been described, the influence of BPA on the parasites within these hosts, and any subsequent influence on parasite transmission, has not been examined. The purpose of this research was to determine whether BPA influences the reproduction and transmission in the human trematode parasite, Schistosoma mansoni, throughout its complex life cycle. We exposed snail intermediate hosts infected with the parasite to either no, low, or high concentrations of BPA and recorded parasite reproduction, longevity, and transmission to definitive hosts, as well as parasite reproductive success within the definitive host.
Results/Conclusions
We found that BPA exposure does impact parasite reproduction and longevity, but only at low concentrations. Parasites in the low exposure treatment had higher reproduction and longevity than those exposed to high concentrations, or no amount, of BPA. This suggests that there is a threshold of BPA exposure, above which parasites cannot respond. Interestingly, this increase in reproduction at the intermediate host stage did not translate to an increase in parasite transmission, as there were no significant differences between any treatment in terms of infectivity to, or parasite reproduction in, the definitive host. This indicates that an increase in parasite reproduction at one stage in a life cycle does not translate to impacts across the life cycle, and that changes at the intermediate host level cannot be used to predict changes in disease and parasite prevalence in definitive host populations. More specifically, any impact of BPA on snail intermediate hosts in the field should not be expected to increase in the transmission or virulence of S. mansoni in human populations.