Hosts can avoid parasites (and pathogens) by reducing social contact, but such isolation may carry costs, e.g. increased vulnerability to predators. Thus, many predator–host–parasite systems confront hosts with a trade-off between predation and parasitism. Parasites, meanwhile, evolve higher virulence in response to increased host sociality and consequently, increased multiple infections. How does predation shift coevolution of host behaviour and parasite virulence? What if predators are selective, i.e. predators disproportionately capture the sickest hosts? We answer these questions with an eco-coevolutionary model parametrized for a Trinidadian guppy–
- NSF-PAR ID:
- 10472039
- Publisher / Repository:
- Nature Ecology and Evolution
- Date Published:
- Journal Name:
- Nature Ecology & Evolution
- Volume:
- 6
- Issue:
- 7
- ISSN:
- 2397-334X
- Page Range / eLocation ID:
- 945 to 954
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Gyrodactylus spp. system. Here, increased predation drives host coevolution of higher grouping, which selects for higher virulence. Additionally, higher predator selectivity drives the contact rate higher and virulence lower. Finally, we show how predation and selectivity can have very different impacts on host density and prevalence depending on whether hosts or parasites evolve, or both. For example, higher predator selectivity led to lower prevalence with no evolution or only parasite evolution but higher prevalence with host evolution or coevolution. These findings inform our understanding of diverse systems in which host behavioural responses to predation may lead to increased prevalence and virulence of parasites. -
Abstract Virulence, the degree to which a pathogen harms its host, is an important but poorly understood aspect of host-pathogen interactions. Virulence is not static, instead depending on ecological context and potentially evolving rapidly. For instance, at the start of an epidemic, when susceptible hosts are plentiful, pathogens may evolve increased virulence if this maximizes their intrinsic growth rate. However, if host density declines during an epidemic, theory predicts evolution of reduced virulence. Although well-studied theoretically, there is still little empirical evidence for virulence evolution in epidemics, especially in natural settings with native host and pathogen species. Here, we used a combination of field observations and lab assays in the
Daphnia -Pasteuria model system to look for evidence of virulence evolution in nature. We monitored a large, naturally occurring outbreak ofPasteuria ramosa inDaphnia dentifera , where infection prevalence peaked at ~ 40% of the population infected and host density declined precipitously during the outbreak. In controlled infections in the lab, lifespan and reproduction of infected hosts was lower than that of unexposed control hosts and of hosts that were exposed but not infected. We did not detect any significant changes in host resistance or parasite infectivity, nor did we find evidence for shifts in parasite virulence (quantified by host lifespan and number of clutches produced by hosts). However, over the epidemic, the parasite evolved to produce significantly fewer spores in infected hosts. While this finding was unexpected, it might reflect previously quantified tradeoffs: parasites in high mortality (e.g., high predation) environments shift from vegetative growth to spore production sooner in infections, reducing spore yield. Future studies that track evolution of parasite spore yield in more populations, and that link those changes with genetic changes and with predation rates, will yield better insight into the drivers of parasite evolution in the wild. -
Abstract Theory on the evolution of niche width argues that resource heterogeneity selects for niche breadth. For parasites, this theory predicts that parasite populations will evolve, or maintain, broader host ranges when selected in genetically diverse host populations relative to homogeneous host populations. To test this prediction, we selected the bacterial parasite
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Predators and parasites are critical, interconnected members of the community and have the potential to shape host populations. Predators, in particular, can have direct and indirect impacts on disease dynamics. By removing hosts and their parasites, predators alter both host and parasite populations and ultimately shape disease transmission. Selective predation of infected hosts has received considerable attention as it is recognized to have important ecological implications. The occurrence and consequences of preferential consumption of uninfected hosts, however, has rarely been considered. Here, we synthesize current evidence suggesting this strategy of selectively predating uninfected individuals is likely more common than previously anticipated and address how including this predation strategy can change our understanding of the ecology and evolution of disease dynamics. Selective predation strategies are expected to differentially impact ecological dynamics and therefore, consideration of both strategies is required to fully understand the impact of predation on prey and host densities. In addition, given that different strategies of prey selectivity by predators change the fitness payoffs both for hosts and their parasites, we predict amplified coevolutionary rates under selective predation of infected hosts compared to uninfected hosts. Using recent work highlighting the critical role that predators play in disease dynamics, we provide insights into the potential mechanisms by which selective predation on healthy individuals can directly affect ecological outcomes and impact long‐term host–parasite coevolution. We contrast the consequences of both scenarios of selective predation while identifying current gaps in the literature and future research directions.more » « less