Biology subjects

Walsman, J. C.

Publications and source records attributed to Walsman, J. C..

3 recordsLinked to original sources

bioRxiv2021

Social hosts evade predation but have deadlier parasites

Parasites exploit hosts to replicate and transmit, but overexploitation kills host and parasite (1): predators may shift this cost-benefit balance by consuming hosts (2-4) or changing host behavior, but the strength of these effects remains unclear. Modeling both, we find a primary, strong effect: hosts group to defend against predators (5), increasing parasite transmission, thus multiple infections, and therefore favoring more exploitative, virulent, parasites (6). Indeed, among 18 Trinidadian Gyrodactyus spp. parasite lines, those collected from high predation guppy populations were more virulent in common garden than those from low predation populations. Our model accurately predicted this result when parametrized with our experimentally demonstrated virulence-transmission trade-off, implicating the behavioral effects of predation. Broadly, our results indicate that reduced social contact selects against parasite virulence. One-Sentence SummaryOur theory and data show predators cause increased host social grouping; the resulting transmission favors parasite virulence.

ecology↗

bioRxiv2021

Parasite-driven cascades or hydra effects: susceptibility and foraging depression shape parasite-host-resource interactions

O_LIWhen epidemics kill hosts and increase their resources, should the density of hosts decrease (with a resource increase, this constitutes a trophic cascade) or increase (a hydra effect)? Seeking answers, we integrate trait measurements, a resource-host-parasite model, and experimental epidemics with plankton. This combination reveals how a spectrum from cascades to hydra effects can arise. It reflects tension between parasite-driven mortality (a density-mediated effect) and foraging depression upon contact with parasite propagules (a trait-mediated one). C_LIO_LIIn the model, mortality rises when higher susceptibility to infection increases infection prevalence. Epidemics release resources while suppressing hosts (creating a cascade). In contrast, when hosts are less susceptible and parasites depress their foraging, a resource feedback can elevate host density during epidemics (creating a hydra effect), particularly at higher carrying capacity of resources. This combination elevates primary production relative to per-host consumption of resources (two key determinants of host density). C_LIO_LIWe test these predictions of the qualitative effects of host traits and resource carrying capacity with trait measurements and a mesocosm experiment. Trait measurements show clonal lines of zooplankton hosts differ in their foraging depression and susceptibility. We seeded resource-host-parasite mesocosms with different host genotypes and provided different nutrient supplies to test model predictions. Hydra effects and trophic cascades arose under different conditions, as predicted by the model. C_LIO_LIHence, tension between trait-mediated and density-mediated effects of parasites governs the fate of host density during epidemics - from cascades to hydra effects - via feedbacks with resources. C_LI

ecology↗

bioRxiv2021

'Resistance is futile': Weaker selection for resistance during larger epidemics further increases prevalence and depresses host density

What determines how much resistance hosts evolve? One might intuit that hosts evolve higher resistance when parasites are more abundant. However, the opposite pattern can arise due to costs of resistance. Here we illustrate with mathematical, experimental, and field approaches how ecological context can increase parasite abundance and select for lower resistance. Resistance is futile when all host genotypes become sufficiently infected. To make this argument, we first analyzed an eco-evolutionary model of parasites, hosts, and hosts resources. We determined eco-evolutionary outcomes for resistance (mathematically, transmission rate) and densities along gradients that drive epidemic size. When epidemic drivers are high, hosts evolve lower resistance, amplifying epidemics and decreasing host density. Experimental mesocosms qualitatively agreed. In the experiment, higher supply of nutrients drove larger epidemics of survival-reducing fungal parasites. Evolving zooplankton hosts were less resistant at high nutrients than at low. Less resistance, in turn, was associated with higher infection prevalence and lower host density. We also analyzed the size of naturally occurring epidemics, finding a broad, bimodal distribution of epidemic sizes consistent with the eco-evolutionary model. Together, our three approaches supported predictions that high epidemic drivers lead to evolution of lower resistance which drives higher prevalence and lower host density.

evolutionary biology↗