Infectious Agents Trigger Trophic Cascades

Buck, Julia C.; Ripple, William J.

doi:10.1016/j.tree.2017.06.009

Cited by 78 publications

(97 citation statements)

References 95 publications

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“…Alongside direct effects on host condition and fitness, alterations of GCs could represent a critical route by which parasites have trait-mediated indirect effects, similar to those of predators (Buck & Ripple, 2017;Raffel, Martin, & Rohr, 2008). Such effects of predators are thought to have a greater influence on prey than direct consumption (Peacor, Peckarsky, Trussell, & Vonesh, 2013) and can be mediated by predator-induced alterations of prey GCs (reviewed by Hawlena & Schmitz, 2010).…”

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confidence: 99%

Parasite infection leads to widespread glucocorticoid hormone increases in vertebrate hosts: A meta‐analysis

O’Dwyer

Dargent

Forbes

et al. 2019

Journal of Animal Ecology

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Parasites and pathogens (hereafter parasites) commonly challenge organisms, but the extent to which their infections are physiologically stressful to hosts remains unclear. Importantly, vertebrate hormones, glucocorticoids (GCs), have been reported to increase, decrease or show no alterations stemming from infections, challenging the generality of parasite‐associated GC responses and motivating a search for important moderator variables. We undertook the first meta‐analysis of changes in vertebrate GCs following experimental infection with parasites, extracting 146 effect sizes from 42 studies involving 32 host and 32 parasite species to test for general patterns of GC following infection, as well as the influence of moderators. Overall, infection increased GCs relative to preliminary or control levels when the single largest effect sizes from repeated measures studies were examined, suggesting that parasites of vertebrate hosts can be thought of generally as physiological stressors by elevating GCs. When all effect sizes were included along with the moderator of sampling time post‐infection (tPI), parasite infection still had a positive effect on host GCs. However, the strength of that effect did not relate consistently to tPI, illustrating temporal differences in GC changes during the course of infection among parasite taxa (e.g. arthropod vs. bacterial infections). Other moderator variables examined did not influence GC responses. Studies broadening the range of host and parasite taxa, and sampling during critical time windows, would aid in our understanding of variation in the host stress response and its consequences for fitness of both vertebrate hosts and their parasites.

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confidence: 99%

Parasite infection leads to widespread glucocorticoid hormone increases in vertebrate hosts: A meta‐analysis

O’Dwyer

Dargent

Forbes

et al. 2019

Journal of Animal Ecology

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“…Fecal avoidance can alter vegetation structure (Ödberg and Francis‐Smith ) and at Coal Oil Point, latrine avoidance likely reduces vertebrate seed predation, potentially increasing plant recruitment. Such pre‐infection trait‐mediated parasite cascades are rarely documented (Buck and Ripple ), but might be widespread for virulent parasites, like raccoon roundworms, that occur at detectable focal sites. Animals likely face far more exposure to parasites than to predators, yet the extent to which other parasites elicit avoidance and how this behavior impacts disease transmission, population dynamics, and ecosystem structure remains hidden in most ecosystems.…”

Section: Discussionmentioning

confidence: 99%

Fear of feces? Tradeoffs between disease risk and foraging drive animal activity around raccoon latrines

Weinstein

Moura

Mendez

et al. 2018

Oikos

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Fear of predation alters prey behavior, which can indirectly alter entire landscapes. A parasite‐induced ecology of fear might also exist if animals avoid parasite‐contaminated resources when infection costs outweigh foraging benefits. To investigate whether animals avoid parasite contaminated sites, and if such avoidance balances disease costs and foraging gains, we monitored animal behavior at raccoon latrines – sites that concentrate both seeds and pathogenic parasite eggs. Using wildlife cameras, we documented over 40 potentially susceptible vertebrate species in latrines and adjacent habitat. Latrine contact rates reflected background activity, diet preferences and disease risk. Disease‐tolerant raccoons and rats displayed significant site attraction, while susceptible birds and small mammals avoided these high‐risk sites. This suggests that parasites, like predators, might create a landscape of fear for vulnerable hosts. Such non‐consumptive parasite effects could alter disease transmission, population dynamics, and even ecosystem structure.

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“…The consequences of parasitism on food webs regarding trophic cascades (Buck and Ripple 2017) or in terms of stabilisation (Hilker and Schmitz 2008;Prosnier et al 2018) or destabilisation (Hudson et al 1998;Prosnier et al 2018) are most often investigated through the lens of ecology. On the other hand, parasite evolution is frequently addressed through the evolution of virulence or transmission, sometimes in a context of trophic interactions (Cressler et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Evolution of predator foraging in response to prey infection favors species coexistence

Prosnier

Médoc

Loeuille³

2020

Preprint

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Article Keyword: Adaptive foraging, virulence, vulnerability, predator diet, profitability, parasitism Running title: Prey-infection induce diet evolution Number of words: 4 470 List of elements: Article (23p) with 1 table and 5 figures. Appendix (4p) with 2 figures. AbstractAs acknowledged by Optimal Foraging theories, predator diets depend on prey profitability.Parasites, ubiquitous in food webs, are known to affect simultaneously host vulnerability to predation and host energy contents, thereby affecting profitabilities. In this work, we study the eco-evolutionary consequences of prey infection on predator diet. We also analyze the consequences for coexistence between prey, predators and parasites. We model a trophic module with one predator and two prey species, one of these prey being infected by a parasite, and distinguish between two effects of infection: a decrease in host fecundity (virulence effect) and an increase in vulnerability to predation (interaction effect). Predator foraging may evolve toward specialist or generalist strategies, the latter being less efficient on a given resource. We show that the virulence effect leads to specialisation on the non-infected prey while the interaction effect, by increasing prey profitability, favors specialisation on the infected prey.Combining the two effects at intermediate intensities promotes either generalist predators or the diversification of foraging strategies (coexistence of specialists), depending of trade-off shape. We then investigate how the evolution of predator diet affects the niche overlap between predator and parasite. We show that interaction effects systematically lead to a high niche overlap, ultimately resulting in the loss of the parasite. Virulence effects conversely favor coexistence by allowing a separation of the predator and parasite niches.

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Infectious Agents Trigger Trophic Cascades

Cited by 78 publications

References 95 publications

Parasite infection leads to widespread glucocorticoid hormone increases in vertebrate hosts: A meta‐analysis

Parasite infection leads to widespread glucocorticoid hormone increases in vertebrate hosts: A meta‐analysis

Fear of feces? Tradeoffs between disease risk and foraging drive animal activity around raccoon latrines

Evolution of predator foraging in response to prey infection favors species coexistence

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