ORCID Profile
0000-0003-0615-6578
Current Organisation
University of Oxford
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Publisher: The Royal Society
Date: 06-2021
Abstract: 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 h er 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.
Publisher: Wiley
Date: 14-07-2021
DOI: 10.1111/GCB.15761
Abstract: 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.
Publisher: Wiley
Date: 28-03-2019
DOI: 10.1111/EVO.13724
Abstract: Research predicting the impact and spread of infectious disease has been heavily influenced by the idea of an evolutionary trade-off between a pathogen's virulence and its transmission rate. In a meta-analysis of the key underlying relationships, Acevedo et al. (2019) highlight the surprising lack of empirical evidence for this influential hypothesis.
Publisher: Cold Spring Harbor Laboratory
Date: 04-05-2022
DOI: 10.1101/2022.05.04.488533
Abstract: Phenotypic plasticity in response to shifts in temperature, known as thermal acclimation, is an essential component of the ability of a species to cope with environmental change. Not only does this process potentially improve an in idual’s thermal tolerance, it will also act simultaneously on various fitness related traits that determine whether a population increases or decreases in size. In light of global change, thermal acclimation therefore has consequences for population persistence that extend beyond simply coping with heat stress. This particularly important when we consider the additional threat of parasitism associated with global change, as the ability of a pathogen to invade a host population depends on both its capacity to proliferate within a host and spread between hosts, and thus the supply of new susceptible hosts in a population. Here, we use the host Daphnia magna and its bacterial pathogen Pasteuria ramosa to investigate how thermal acclimation may impact various aspects of host and pathogen performance at the scale of both an in idual and the population. We independently test the effect of maternal thermal acclimation and direct thermal acclimation on host thermal tolerance, measured as knockdown times, as well as host fecundity and lifespan, and pathogen infection success and spore production. We find that direct thermal acclimation enhances host thermal tolerance and intrinsic rates of population growth, despite a decline observed for host fecundity and lifespan. Pathogens, on the other hand, faired consistently worse at warmer temperatures at the within-host scale, and also in their potential to invade a host population. Our results suggest that hosts could benefit more from warming than their pathogens, but highlight that considering both within- and between-host thermal performance, including thermal tolerance and fitness traits, is needed to fully appreciate how increasing thermal variability will impact host and pathogen populations.
Publisher: Wiley
Date: 06-11-2020
DOI: 10.1002/ECE3.6828
Publisher: Wiley
Date: 26-06-2020
DOI: 10.1111/JEB.13663
Publisher: Wiley
Date: 26-06-2019
DOI: 10.1111/GCB.14713
Abstract: 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 in idual'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 r ing) 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 r ing rate slowed, upper thermal limits of both healthy and infected in iduals 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.
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Tobias Hector.