Is there a sicker sex? Dose relationships modify male–female differences in infection prevalence

Butterworth, Nathan J.; Heffernan, Lindsey; Hall, Matthew D.

doi:10.1098/rspb.2023.2575

Cited by 2 publications

(1 citation statement)

References 86 publications

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“…Due to differences in early survival, handling errors, and male individuals set up unintentionally, sample sizes for the different treatment combinations and disease traits varied between 17 and 26. All exposed individuals were included in the analysis of host traits in order to capture the changes in a host's phenotype that can manifest even when infection isn't ultimately "successful" for the pathogen in producing mature transmission spores (Butterworth et al, 2024;Hall et al, 2024).…”

Section: Analysis Of Individual-based Metricsmentioning

confidence: 99%

Acclimation to warmer temperatures can protect host populations from both further heat stress and the potential invasion of pathogens

Hector,

Shocket,

Sgrò

et al. 2024

Global Change Biology

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Thermal acclimation can provide an essential buffer against heat stress for host populations, while acting simultaneously on various life‐history traits that determine population growth. In turn, the ability of a pathogen to invade a host population is intimately linked to these changes via the supply of new susceptible hosts, as well as the impact of warming on its immediate infection dynamics. Acclimation therefore has consequences for hosts and pathogens that extend beyond simply coping with heat stress—governing both population growth trajectories and, as a result, an inherent propensity for a disease outbreak to occur. The impact of thermal acclimation on heat tolerances, however, is rarely considered simultaneously with metrics of both host and pathogen population growth, and ultimately fitness. Using the host Daphnia magna and its bacterial pathogen, we investigated how thermal acclimation impacts host and pathogen performance at both the individual and population scales. We first tested the effect of maternal and direct thermal acclimation on the life‐history traits of infected and uninfected individuals, such as heat tolerance, fecundity, and lifespan, as well as pathogen infection success and spore production. We then predicted the effects of each acclimation treatment on rates of host and pathogen population increase by deriving a host's intrinsic growth rate (rm) and a pathogen's basic reproductive number (R0). We found that direct acclimation to warming enhanced a host's heat tolerance and rate of population growth, despite a decline in life‐history traits such as lifetime fecundity and lifespan. In contrast, pathogen performance was consistently worse under warming, with within‐host pathogen success, and ultimately the potential for disease spread, severely hampered at higher temperatures. Our results suggest that hosts could benefit more from warming than their pathogens, but only by linking multiple individual traits to population processes can the full impact of higher temperatures on host and pathogen population dynamics be realised.

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Section: Analysis Of Individual-based Metricsmentioning

confidence: 99%

Acclimation to warmer temperatures can protect host populations from both further heat stress and the potential invasion of pathogens

Hector,

Shocket,

Sgrò

et al. 2024

Global Change Biology

Self Cite

View full text Add to dashboard Cite

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The sicker sex is plastic: Thermal plasticity determines sex biases in pathogen transmission

Butterworth,

Lush,

Moore

et al. 2024

Preprint

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Sex differences are predicted to play an important role in the spread and evolution of pathogens. However, attempts to generalize the sicker sex have been challenged by intraspecific variability of sex biases across the infection process. Sex specific plasticity provides a framework to resolve this by elucidating how infection is shaped at the sex pathogen environment interface. Using the Daphnia magna and Pasteuria ramosa system, we measure infection outcomes for males and females across three temperatures and seven pathogen densities to quantify how sex specific plasticity shapes susceptibility, pathogen loads, and ultimately transmission. We find unique forms of plasticity at each stage of infection, including equivalent, sex specific, and divergent plasticity. Integrating these into a single estimate of transmission reveals a clear pattern, male-biased transmission at cold temperatures, and female-biased transmission at warm temperatures. Sex specific thermal plasticity thus determines the sicker sex, with implications for pathogen spread and evolution in a warming world.

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Is there a sicker sex? Dose relationships modify male–female differences in infection prevalence

Cited by 2 publications

References 86 publications

Acclimation to warmer temperatures can protect host populations from both further heat stress and the potential invasion of pathogens

Acclimation to warmer temperatures can protect host populations from both further heat stress and the potential invasion of pathogens

The sicker sex is plastic: Thermal plasticity determines sex biases in pathogen transmission

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