Host Sex Modulates the Energetics of Pathogen Proliferation and Its Dependence on Environmental Resources

Gipson, Stephen A. Y.; Pettersen, Amanda K.; Heffernan, Lindsey M.; Hall, Matthew D.

doi:10.1086/718717

Cited by 7 publications

(14 citation statements)

References 54 publications

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“…The resources available to a parasite are directly linked to the pool of resources available to its host. How much host resource is given to the parasite can vary, depending on a range of factors, including the stage of infection, population density, host sex and manipulation of host physiology [97][98][99][100][101][102]. A host could increase its resource intake to accommodate the additional stress of infection (e.g.…”

Section: Host Heat Tolerance During Infection: What Mechanisms Could ...mentioning

confidence: 99%

“…The impact of infection on host metabolic rate will be a key determinant of host thermal performance. However, the relationship between within-host parasite burden and host metabolic rate may not always be linear [ 98 , 112 , 113 ], which could blur the link between parasite burden and host heat tolerance.…”

Section: Host Heat Tolerance During Infection: What Mechanisms Could ...mentioning

confidence: 99%

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Infection burdens and virulence under heat stress: ecological and evolutionary considerations

Hector

Gehman

King

2023

Phil. Trans. R. Soc. B

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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’.

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Section: Host Heat Tolerance During Infection: What Mechanisms Could ...mentioning

confidence: 99%

Section: Host Heat Tolerance During Infection: What Mechanisms Could ...mentioning

confidence: 99%

Infection burdens and virulence under heat stress: ecological and evolutionary considerations

Hector

Gehman

King

2023

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

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“…shown to correlate positively with pathogen load in this study system (Gipson et al, 2022;Nørgaard et al, 2021). Clearing infection, however, is instead expected to occur more rapidly.…”

Section: Discussionmentioning

confidence: 58%

“…Measures of host activity and feeding rates are currently not available for hosts that were exposed to a pathogen and successfully resisted infection in this system. However, infection has been shown to reduce activity (Nørgaard et al, 2019a(Nørgaard et al, , 2019b and slightly reduce feeding rates (albeit in a genotype-specific manner, Gipson et al, 2022;Nørgaard et al, 2021), hinting that resistant hosts are most likely behaving differently. However, regardless of the mechanism, our results suggest that the physiological (i.e.…”

Section: Discussionmentioning

confidence: 99%

“…Using the crustacean Daphnia magna and its obligate bacterial pathogen Pasteuria ramosa , we estimated metabolic rate, via oxygen consumption rates (Gipson et al., 2022; Nørgaard et al., 2021), for 10 compatible host–pathogen genotypic combinations, plus controls. Disease progresses swiftly in this system, with immune activation expected shortly after exposure (Auld et al., 2010; Labbé & Little, 2009), followed by the rapid loss of fecundity and an increase in mortality (Clerc et al., 2015; Gipson & Hall, 2018; Hall et al., 2019).…”

Section: Introductionmentioning

confidence: 99%

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The hidden costs of resistance: Contrasting the energetics of successfully and unsuccessfully fighting infection

Hall,

Phillips,

White

et al. 2024

Functional Ecology

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Exposure to a pathogen is predicted to lead to increased energy use as hosts attempt to activate a costly immune system and repair damaged tissue. To meet this demand, metabolic rates, which capture the rate at which a host can use, transform and expend energy, are expected to increase. Yet for many host–pathogen systems, metabolic rates after encountering a pathogen are just as likely to decrease as increase, suggesting that increased energy expenditure may not always be best for fighting infection. Diverging metabolic trajectories have been previously attributed to the different pathways that specific pathogen classes, such as bacteria or viruses, induce in a host. Here, we test how the magnitude and direction of metabolic change following pathogen exposure might also depend on whether a host has cleared infection or is instead fighting to reduce pathogen burden, as well as interactions between host and pathogen genotypes of a single host–pathogen system. Using a model system, Daphnia magna and its bacterial pathogen, we quantified changes in mass‐independent metabolic rates over a 30‐day period for multiple host and pathogen genotypes. We found that the metabolic trajectory of an exposed host diverged quickly during the infection process. For hosts that were exposed to a pathogen and resisted infection, their mass‐independent metabolic rates remained suppressed long after exposure, leading to a sustained reduction in total energy use compared to unexposed animals. The reverse was true for hosts in which the pathogen was able to establish an infection. Underlying these changes were differences in the energetic burden that each pathogen genotype imposed on its host, as well as changes in the way host genotype and the outcome of infection shaped underlying scaling relationships between host body mass and metabolic rates. Our results demonstrate how variation in an organism's metabolic rate and overall energy use can arise from within a single host–pathogen encounter and depend on the likelihood of pathogen clearance, as well as the within‐species genetic variability of both hosts and pathogens. Read the free Plain Language Summary for this article on the Journal blog.

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

Butterworth,

Heffernan,

Hall

2024

Proc. R. Soc. B.

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Throughout the animal kingdom, there are striking differences in the propensity of one sex or the other to become infected. However, precisely when we should expect males or females to be the sicker sex remains unclear. A major barrier to answering this question is that very few studies have considered how the susceptibility of males and females changes across the full range of pathogen doses encountered in nature. Without quantifying this ‘dose–susceptibility’ relationship, we have likely underestimated the scope for sex differences to arise. Here, we use the Daphnia magnia – Pasteuria ramosa system to reveal that sex differences in susceptibility are entirely dose-dependent, with pathogens having a higher probability of successfully establishing an infection in mature males at low doses, but mature females at high doses. The scope for male–female differences to emerge is therefore much greater than previously appreciated—extending to sex differences in the upper limits to infection success, per-propagule infectivity risks and density-dependent pathogen behaviour. Applying this expanded scope across the animal kingdom will help us understand when and why a sicker sex emerges, and the implications for diseases in nature—where sex ratios, age structure and pathogen densities vary drastically.

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Host Sex Modulates the Energetics of Pathogen Proliferation and Its Dependence on Environmental Resources

Cited by 7 publications

References 54 publications

Infection burdens and virulence under heat stress: ecological and evolutionary considerations

Infection burdens and virulence under heat stress: ecological and evolutionary considerations

The hidden costs of resistance: Contrasting the energetics of successfully and unsuccessfully fighting infection

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

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