Biology subjects

Freedman, A. S.

Publications and source records attributed to Freedman, A. S..

3 recordsLinked to original sources

bioRxiv2024

A unifying theoretical framework for tick-borne disease risk to explain conflicting results of exclosure experiments across scales

Disease ecology has focused greatly on determining how changes to biodiversity may drive infectious disease risk for humans. Fencing off experimental areas (exclosures) has been a common experimental approach to assess how removing large-bodied hosts may affect disease risk, especially with tick-borne pathogens (TBPs). However, exclosure experiments have found conflicting results based on the experiments scale, with smaller exclosures tending to increase tick densities inside the exclosure and larger exclosures tending to decrease tick densities inside. Previously, we have lacked a unifying theoretical framework able to reconcile the results of exclosure experiments across spatial scales. We present a spatially explicit model of TBP risk incorporating tick dispersal by small competent mammal hosts which can enter the exclosure and by large incompetent mammal hosts excluded from the exclosure. Our model reproduces the scale-dependence and spatial patterning observed in past exclosure experiments while elucidating their causal mechanisms. Specifically, the modeled exclosures produce high densities of infected ticks near their boundaries, with the densities decreasing towards the exclosures center. Empirical results have found lower tick densities at the exclosures edge than its center, a pattern we demonstrate can also be produced if we additionally allow ticks in their free-living questing stage to disperse.

ecology↗

bioRxiv2024

Effects of Host-Tree Foliage on Polymorphism in an Insect Pathogen

The theory of host-pathogen interactions has successfully shown that persistent pathogen virulence may be explained through tradeoffs between different pathogen fitness components, but classical theory cannot explain pathogen coexistence. More recent theory invokes both tradeoffs and environmental heterogeneity, but resembles classical theory in focusing on a limited range of possible tradeoffs, and therefore has seen few applications. To better understand the usefulness of tradeoff theory for explaining pathogen coexistence in nature, we measured components of pathogen fitness in two distantly related morphotypes of a baculovirus that infects larvae of the Douglas-fir tussock moth (Orgyia pseudotsugata). We show that the two morphotypes vary in multiple components of fitness, including the probability of infection given exposure to the pathogen, the incubation time of the pathogen, variability in the incubation time of the pathogen, and the detectability of the pathogen. Moreover, because the baculovirus is transmitted when host larvae accidentally consume infectious virus particles while feeding on foliage of the insects host trees, the strength and direction of the differences in fitness components of the two morphotypes depends on the host-tree species on which host larvae consume the virus. Through simulations of a model parameterized using our experimental data, we demonstrate how several varying fitness components can work in concert to promote strain coexistence, particularly highlighting the role of variability in incubation time. Our results suggest that the two morphotypes may coexist because of variation in forest tree-species composition, providing important empirical evidence that tradeoffs and environmental heterogeneity can together modulate pathogen competition.

ecology↗

bioRxiv2020

Stony coral populations are more sensitive tochanges in vital rates in disturbed environments

Reef-building corals, like many long-lived organisms, experience environmental change as a combination of separate but concurrent processes, some of which are gradual yet long-lasting, while others are more acute but short-lived. For corals, some chronic environmental stressors, such as rising temperature and ocean acidification, are thought to induce gradual changes in colonies vital rates. Meanwhile, other environmental changes, such as the intensification of tropical cyclones, change the disturbance regime that corals experience. Here, we use a physiologically structured population model to explore how chronic environmental stressors that impact the vital rates of individual coral colonies interact with the intensity and magnitude of disturbance to affect coral population dynamics and cover. We find that when disturbances are relatively benign, intraspecific density dependence driven by space competition partially buffers coral populations against gradual changes in vital rates. However, the impact of chronic stressors is amplified in more highly disturbed environments, because disturbance weakens the buffering effect of space competition. We also show that coral cover is more sensitive to changes in colony growth and mortality than to external recruitment, at least in non-self-seeding populations, and that space competition and size structure mediate the extent and pace of coral-population recovery following a large-scale mortality event. Understanding the complex interplay among chronic environmental stressors, mass-mortality events, and population size structure sharpens our ability to project coral dynamics in an increasingly disturbed future.

ecology↗