Data from: Temperature drives epidemics in a zooplankton-fungus disease system: a trait-driven approach points to transmission via host foraging

Climatic warming will likely have idiosyncratic impacts on infectious
diseases, causing some to increase while others decrease or shift
geographically. A mechanistic framework could better predict these
different temperature-disease outcomes. However, such a framework remains
challenging to develop, due to the non-linear and (sometimes) opposing
thermal responses of different host and parasite traits, and due to the
difficulty of validating model predictions with observations and
experiments. We address these challenges in a zooplankton-fungus (Daphnia
dentifera-Metschnikowia bicuspidata) system. We test the hypothesis that
warmer temperatures promote disease spread and produce larger epidemics.
In lakes, epidemics that start earlier and warmer in autumn grow much
larger. In a mesocosm experiment, warmer temperatures produced larger
epidemics. A mechanistic model parameterized with trait assays revealed
that this pattern arose primarily from the temperature-dependence of
transmission rate (β), governed by the increasing foraging (and hence
parasite exposure) rate of hosts (f). In the trait assays, parasite
production seemed sufficiently responsive to shape epidemics as well;
however, this trait proved too thermally insensitive in the mesocosm
experiment and lake survey to matter much. Thus, in warmer environments,
increased foraging of hosts raised transmission rate, yielding bigger
epidemics through a potentially general, exposure-based mechanism for
ectotherms. This mechanistic approach highlights how a trait-based
framework will enhance predictive insight into responses of infectious
disease to a warmer world.