Biology subjects

Walsman, J. C.

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

10 recordsLinked to original sources

bioRxiv2026

Thermal variability interacts with infection load and the evolution of host-parasite defense

Rising temperatures and unpredictable weather patterns are directly linked to emerging infectious diseases that threaten global biodiversity. Thermal variability affects host-parasite interactions, and understanding how animal hosts respond to temperature variability and parasite infection is paramount for conservation and for predicting zoonotic spillover. Hosts employ two strategies to defend against parasites: resistance (inhibiting or limiting infection) and tolerance (limiting the negative effects of infection). This observation raises a fundamental question: How does thermal variability affect the expression and evolution of resistance versus tolerance? Subsequently, how does the evolution of resistance versus tolerance influence parasite load dynamics? Here, we first review why temperature may differentially affect resistance and tolerance mechanisms, thereby altering host selection and eco-evolutionary disease outcomes. Second, to highlight the importance of these interactions, we present a model that illustrates key potential effects of temperature variability on host defense mechanisms. Our model demonstrates that temperature variability alone could drive lower infection prevalence and loads, but it also selects for host tolerance, ultimately leading to higher net prevalence and loads. We also find widely divergent outcomes depending on how temperature impacts defense strategies. These results highlight key areas for future empirical and theoretical work on the interactions among temperature variability, infection load, and host defense evolution.

ecology↗

bioRxiv2025

A continuous-time microparasite model incorporating infection intensity and parasite aggregation

Disease outcomes depend heavily on infection intensity which is often heterogeneous across and within host populations. Most individuals carry low pathogen loads and a few carry high loads, a pattern known as aggregation. While well-characterized in macroparasite systems, aggregation and infection intensity are rarely incorporated into microparasite models. This raises key questions: Do similar mechanisms underlie aggregation in macro- and microparasite systems? And how do aggregation and load-dependent effects shape outcomes such as host suppression and virulence-transmission trade-offs? To address these questions, we developed a novel continuous time microparasite model that allows the pathogen load distribution across hosts to evolve dynamically, shaped by within- and between-host processes. We applied this framework to the amphibian chytrid fungus system involving Batrachochytrium den-drobatidis (Bd), a fungal pathogen threatening amphibian populations worldwide. Our results show that load-dependent mortality reduces aggregation, while faster within-host replication increases it. Aggregation, in turn, weakens host suppression and flat-tens virulence-transmission trade-off, shifting peak transmission to higher replication rates. Overall, our continuous-time microparasite model provides new insights into how infection intensity and aggregation influence host-pathogen dynamics and offers a valuable framework for advancing theoretical and data-driven understanding of how within-host processes scale to population-level disease dynamics for microparasites.

ecology↗

bioRxiv2024

The mean and variance of infection load reveal unseen host evolution

Heterogeneity among individuals, in number of parasites, body size, etc., can have critical interactions with population dynamics. We tease these out with a relatively simple model of such interactions in a case study of microparasite load with empirically supported assumptions to ask a key question. How does variance in microparasite load interact with population-level dynamics? We show how the mean and variance of infection load vary throughout an epidemic. Further, we show how mean and variance have mutual negative feedbacks on each other mediated by high disease-induced death rates at high loads. Helpfully, we find that mean and variance provide information into underlying processes as well. Population-level trends in the mean and variance reveal underlying trends in within-host processes, e.g., differentiating host evolution of defence that manifests as tolerance, constitutive resistance, inducible resistance, or acquired resistance. Such inference may be critical for managing endangered Mountain Yellow Legged Frog populations recovering from Batrachochytrium dendrobatidis epidemics. Lastly, we demonstrate the impact of pathogen load variance on host fitness, pathogen fitness, and host population depression by pathogens. Our results demonstrate the importance of trait heterogeneity and the insights available from relatively simple models, both for microparasite infection load and possibly other traits.

ecology↗

bioRxiv2024

Wildlife provisioning selects for higher pathogen virulence in hosts with incomplete immunity

Anthropogenic food provisioning provides massive inputs of food to wildlife, with profound ecological and evolutionary consequences. By altering wildlife condition, density, and behavior, provisioning can influence transmission of infectious diseases and thus may impose strong selection pressure on wildlife pathogens. But surprisingly, we lack theory on the eco-evolutionary consequences of provisioning for host-pathogen dynamics. Here we develop a mathematical model of the eco-evolutionary dynamics of a wildlife pathogen under provisioning, motivated by Mycoplasma gallisepticum, a bacterial pathogen that emerged, spread, and changed its virulence in provisioned house finches. We model how provisioning influences the evolution of pathogen virulence, defined here as mortality associated with infection. Consistent with past empirical work, house finches recover from infection and acquire incomplete immunity; this incomplete immunity is stronger if their initial infection was with a more virulent pathogen strain. We find that, even though provisioning improves body condition, it should still select for higher virulence, and thus may actually lead to declines in host populations. These negative effects arise because provisioning magnifies the impact of incomplete immunity, selecting for higher virulence and driving host populations down. Our results highlight that food provisioning can select for more virulent pathogens, with potentially far-reaching implications for conservation.

ecology↗

bioRxiv2024

Do fungi look like macroparasites? Quantifying the patterns and mechanisms of aggregation for host-fungal parasite relationships

Most hosts contain few parasites, whereas few hosts contain many. This pattern, known as aggregation, is well-documented in macroparasites where parasite intensity distribution among hosts affects host-parasite dynamics. Infection intensity also drives fungal disease dynamics, but we lack a basic understanding of host-fungal aggregation patterns, how they compare to macroparasites, and if they reflect biological processes. To address these gaps, we characterized aggregation of the fungal pathogen Batrachochytrium dendrobatidis (Bd) in amphibian hosts. Utilizing the slope of Taylors Power Law, we found Bd intensity distributions were more aggregated than macroparasites, conforming closely to lognormal distributions. We observed that Bd aggregation patterns are strongly correlated with known biological processes operating in amphibian populations, such as epizoological phase--invasion, post-invasion, and enzootic--and intensity-dependent disease mortality. Using intensity-dependent mathematical models, we found evidence of evolution of host resistance based on aggregation shifts in systems persisting with Bd following disease-induced declines. Our results show that Bd aggregation is highly conserved across disparate systems and is distinct from aggregation patterns in macroparasites, and contains signatures of potential biological processes of amphibian-Bd systems. Our work lays a foundation to unite host-fungal dynamics under a common theoretical framework and inform future modeling approaches that may elucidate host-fungus interactions.

ecology↗

bioRxiv2023

Associating with kin selects against disease tolerance

Behavioural and physiological immunity are key to slowing epidemic spread. Here, we explore the evolutionary and epidemic consequences of their different costs for the evolution of tolerance vs. resistance: behavioural resistance affects social cohesion, with associated group-level costs, while physiological resistance costs should accrue to the individual. Further, the transmission-reduction benefits of resistance accrue differently to susceptible hosts and those already infected; infected hosts only benefit indirectly, by reducing transmission to kin. We therefore model the coevolution of transmission-reducing defences expressed in susceptible hosts with those expressed in infected hosts, as a function of kin association, and analyse the effect on population-level outcomes. Using parameter values for guppies, Poecilia reticulata, and their gyrodactylid parasites, we find that: 1) either susceptible or infected hosts should invest heavily in preventing infection, but not both; 2) kin association drives investment in physiological resistance more strongly than in behavioural resistance; 3) even weak levels of kin association can favour altruistic infected hosts that invest heavily in resistance (vs. selfish tolerance), eliminating the disease. Overall, our finding that weak kin association affects the coevolution of infected and susceptible investment in both behavioural and physiological immunity suggests that kin selection may affect disease dynamics across systems.

evolutionary biology↗

bioRxiv2021

A paradox of parasite resistance: Disease-driven trophic cascades increase the cost of resistance, selecting for lower resistance with parasites than without them

Most evolutionary theory predicts that, during epidemics, hosts will evolve higher resistance to parasites that kill them. Here, we provide an alternative to that typical expectation, with an explanation centered on resource feedbacks. When resistance is costly, hosts evolve decreasing resistance without parasites, as expected. But with parasites, hosts can evolve lower resistance than they would in the absence of parasites. This outcome arises in an eco-evolutionary model when four conditions are met: first, resistance has a fecundity cost (here, via decreased foraging/exposure rate); second, resources increase during epidemics via trophic cascades; third, increased resources magnify the benefit of maintaining a fast foraging rate, thereby magnifying the cost of evolving a slower foraging/exposure rate (i.e., resistance); fourth, that amplification of the cost outweighs the benefit of resistance. When these conditions are met, hosts evolve lower resistance than without parasites. This phenomenon was previously observed in a mesocosm experiment with fungal parasites, zooplankton hosts, and algal resources. Re-analyzing this experiment produced evidence for our models mechanism. Thus, both model and experiment indicate that, via resource feedbacks, parasites can counterintuitively select against resistance.

ecology↗

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↗