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.

Global change is shifting both temperature patterns and the geographic distribution of pathogens, and infection has already been shown to substantially reduce host thermal performance, potentially placing populations at greater risk that previously thought. But what about individuals that are able to successfully clear an infection? Whilst the direct damage a pathogen causes will likely lead to reductions in host's thermal tolerance, the response to infection often shares many underlying pathways with the general stress response, potentially acting as a buffer against subsequent thermal stress. Here, by exposing Drosophila melanogaster to heat‐killed bacterial pathogens, we investigate how activation of a host's immune system can modify any response to both heat and cold temperature stress. In a single focal population, we find that immune activation can improve a host's knockdown times during heat shock, potentially offsetting some of the damage that would subsequently arise as an infection progresses. Conversely, immune activation had a detrimental effect on CTmax and did not influence lower thermal tolerance as measured by chill‐coma recovery time. However, we also find that the influence of immune activation on heat knockdown times is not generalizable across an entire cline of locally adapted populations. Instead, immune activation led to signals of local adaptation to temperature being lost, erasing the previous advantage that populations in warmer regions had when challenged with heat stress. Our results suggest that activation of the immune system may help buffer individuals against the detrimental impact of infection on thermal tolerance; however, any response will be population specific and potentially not easily predicted across larger geographic scales, and dependent on the form of thermal stress faced by a host.

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Global climate change has led to more extreme thermal events. Plants and animals harbour diverse microbial communities, which may be vital for their physiological performance and help them survive stressful climatic conditions. The extent to which microbiome communities change in response to warming or cooling may be important for predicting host performance under global change. Using a meta-analysis of 1377 microbiomes from 43 terrestrial and aquatic species, we found a decrease in the

The frequency and severity of both extreme thermal events and disease outbreaks are predicted to continue to shift as a consequence of global change. As a result, species persistence will likely be increasingly dependent on the interaction between thermal stress and pathogen exposure. Missing from the intersection between studies of infectious disease and thermal ecology, however, is the capacity for pathogen exposure to directly disrupt a host's ability to cope with thermal stress. Common sources of variation in host thermal performance, which are likely to interact with infection, are also often unaccounted for when assessing either the vulnerability of species or the potential for disease spread during extreme thermal events. Here, we describe how infection can directly alter host thermal limits, to a degree that exceeds the level of variation commonly seen across species large geographic distributions and that equals the detrimental impact of other ecologically relevant stressors. We then discuss various sources of heterogeneity within and between populations that are likely to be important in mediating the impact that infection has on variation in host thermal limits. In doing so we highlight how infection is a widespread and important source of variation in host thermal performance, which will have implications for both the persistence and vulnerability of species and the dynamics and transmission of disease in a more thermally extreme world.

The climate is warming at an unprecedented rate, pushing many species toward and beyond the upper temperatures at which they can survive. Global change is also leading to dramatic shifts in the distribution of pathogens. As a result, upper thermal limits and susceptibility to infection should be key determinants of whether populations continue to persist, or instead go extinct. Within a population, however, individuals vary in both their resistance to both heat stress and infection, and their contributions to vital growth rates. No more so is this true than for males and females. Each sex often varies in their response to pathogen exposure, thermal tolerances, and particularly their influence on population growth, owing to the higher parental investment that females typically make in their offspring. To date, the interplay between host sex, infection, and upper thermal limits has been neglected. Here, we explore the response of male and female Daphnia to bacterial infection and static heat stress. We find that female Daphnia, when uninfected, are much more resistant to static heat stress than males, but that infection negates any advantage that females are afforded. We discuss how the capacity of a population to cope with multiple stressors may be underestimated unless both sexes are considered simultaneously.

Natural populations are experiencing an increase in the occurrence of both thermal stress and disease outbreaks. How these two common stressors interact to determine host phenotypic shifts will be important for population persistence, yet a myriad of different traits and pathways are a target of both stressors, making generalizable predictions difficult to obtain. Here, using the host Daphnia magna and its bacterial pathogen Pasteuria ramosa , we tested how temperature and pathogen exposure interact to drive shifts in multivariate host phenotypes. We found that these two stressors acted mostly independently to shape host phenotypic trajectories, with temperature driving a faster pace of life by favouring early development and increased intrinsic population growth rates, while pathogen exposure impacted reproductive potential through reductions in lifetime fecundity. Studies focussed on extreme thermal stress are increasingly showing how pathogen exposure can severely hamper the thermal tolerance of a host. However, our results suggest that under milder thermal stress, and in terms of life-history traits, increases in temperature might not exacerbate the impact of pathogen exposure on host performance, and vice versa.

As a result of global change, hosts and parasites (including pathogens) are experiencing shifts in their thermal environment. Despite the importance of heat stress tolerance for host population persistence, infection by parasites can impair a host's ability to cope with heat. Host–parasite eco-evolutionary dynamics will be affected if infection reduces host performance during heating. Theory predicts that within-host parasite burden (replication rate or number of infecting parasites per host), a key component of parasite fitness, should correlate positively with virulence—the harm caused to hosts during infection. Surprisingly, however, the relationship between within-host parasite burden and virulence during heating is often weak. Here, we describe the current evidence for the link between within-host parasite burden and host heat stress tolerance. We consider the biology of host–parasite systems that may explain the weak or absent link between these two important host and parasite traits during hot conditions. The processes that mediate the relationship between parasite burden and host fitness will be fundamental in ecological and evolutionary responses of host and parasites in a warming world. This article is part of the theme issue ‘Infectious disease ecology and evolution in a changing world’.