PS 40-111
Tadpole resistance to trematode infection under varying temperatures

Wednesday, August 13, 2014
Exhibit Hall, Sacramento Convention Center
Karie A. Altman, Biological Sciences, Oakland University, Rochester, MI
Michelle N. Golembieski, Biological Sciences, Oakland University, Rochester, MI
Eric T. Fetzner, Biological Sciences, Oakland University, Rochester, MI
Elizabeth L. Scott, Biological Sciences, Oakland University, Rochester, MI
Jeffrey P. Stephens, Biological Sciences, Oakland University, Rochester, MI
Thomas R. Raffel, Biological Sciences, Oakland University, Rochester, MI
Background/Question/Methods

Temperature variability is expected to increase in amplitude and frequency as the climate changes, which could influence parasite-host interactions. The “temperature variability hypothesis” proposes that increased temperature variability will increase parasitic infection, because the relatively small body size of parasites should allow them to acclimate to new temperatures more rapidly than their larger hosts. This hypothesis is based in part on the “beneficial acclimation hypothesis” of thermal biology, which posits that fully-acclimated organisms will have improved physiological performance (e.g., parasite infectivity or host resistance) relative to unacclimated organisms. We tested predictions of this hypothesis with controlled-temperature experiments using trematode parasite (Ribeiroia ondatrae) infection in green frog tadpoles (Lithobates clamitans) as a model system. We acclimated tadpoles to six “acclimation temperatures” and switched them to six new “exposure temperatures” prior to parasite exposure. Parasites were always acclimated to their respective exposure temperatures to isolate acclimation effects on host resistance. Host resistance to parasitism was measured by quantifying the proportion of parasites that encysted in hosts and the rate of parasite clearance using fluorescently-labeled parasites.

Results/Conclusions

We found that warm-acclimated tadpoles were more resistant to parasite encystment at warmer exposure temperatures, and cold-acclimated tadpoles were more resistant at colder temperatures, as predicted by the beneficial acclimation hypothesis. This result suggests that future increases in temperature variability might cause a general increase in tadpole infection with trematode parasites, as predicted by the temperature variability hypothesis. However, there was a nonlinear effect of host acclimation temperature on parasite clearance rates, with tadpoles acclimated to the middle temperatures performing better than tadpoles acclimated to more extreme temperatures. Thus the effects of temperature variability on host resistance overall are more complex than predicted by beneficial acclimation alone. Temperature-explicit physiological models will likely be necessary to predict effects of future changes in temperature variability on this parasite-host system.