As a result of global climate change, species are experiencing an escalation in the severity and regularity of extreme thermal events. With patterns of disease distribution and transmission predicted to undergo considerable shifts in the coming years,...
As a result of global climate change, species are experiencing an escalation in the severity and regularity of extreme thermal events. With patterns of disease distribution and transmission predicted to undergo considerable shifts in the coming years, the interplay between temperature and pathogen exposure will likely determine the capacity of a population to persist under the dual threat of global change and infectious disease. In this study, we investigated how exposure to a pathogen affects an individual's ability to cope with extreme temperatures. Using experimental infections of Daphnia magna with its obligate bacterial pathogen Pasteuria ramosa, we measured upper thermal limits of multiple host and pathogen genotype combinations across the dynamic process of infection and under various forms (static and ramping) of thermal stress. We find that pathogens substantially limit the thermal tolerance of their host, with the reduction in upper thermal limits on par with the breadth of variation seen across similar species entire geographical ranges. The precise magnitude of any reduction, however, was specific to the host and pathogen genotype combination. In addition, as thermal ramping rate slowed, upper thermal limits of both healthy and infected individuals were reduced. Our results suggest that the capacity of a population to evolve new thermal limits, when also faced with the threat of infection, will depend not only on a host's genetic variability in warmer environments, but also on the frequency of host and pathogen genotypes. We suggest that pathogen‐induced alterations of host thermal performance should be taken into account when assessing the resilience of any population and its potential for adaptation to global change.
Upper thermal limits were reduced by exposure to infectious disease; and depended on the severity of infection, the type of thermal stress encountered and the specific genotype of both the host and pathogen. We observed that pathogens could reduce thermal limits at a magnitude equivalent in scale to the natural variation in thermal limits seen within species over large geographic and ecological ranges.