Linking anthropogenic resources to wildlife–pathogen dynamics:
Becker, Daniel Joseph
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For many wildlife, consumer–resource interactions are altered by human activities that provide supplemental food. As anthropogenic resources are often more abundant and predictable than natural foods, subsidized populations can be larger, aggregated, and better-fed than wild animals. A growing literature suggests anthropogenic resources can have profound impacts on host–pathogen interactions, in some cases increasing cross-species transmission. However, predicting when and where anthropogenic resources will increase such risks is complicated, as supplemental resources can simultaneously affect hosts and pathogens through multiple and opposing mechanisms. Factors enhancing transmission, such as increased aggregation, could be offset by improved immunity due to lower starvation stress. The aim of this dissertation is to develop and test an integrative framework for understanding how anthropogenic resources affect wildlife disease. I first built supplemental resources into mechanistic models to explore the overall effect of provisioning on epidemiological outcomes; this work demonstrated that how resources affect host immunity is critical for understanding if supplemental feeding increases or decreases transmission. I next synthesized the literature on how host–pathogen interactions respond to supplemental feeding to test support for these theoretical mechanisms; this meta-analysis demonstrated strong support for higher contact rates in supplemented populations increasing infection but variable effects of provisioning on host condition and weak effects on demography. I next extended models to a metapopulation scale to predict how the landscape-level deployment of supplemental food affects infection dynamics; these studies improved existing theory on pathogen dynamics in metapopulations and showed that host occupancy can be maximized and infection can be minimized if landscapes contain heterogeneous mixtures of unprovisioned and provisioned habitats. Lastly, I examined these processes in the context of a natural system by asking how anthropogenic resources interact with immunity, demography, and bacterial infection for vampire bats in Latin America. Results suggested that livestock expansion could stimulate bat demography and innate immunity, in turn having strong negative effects on prevalence of a vector-borne pathogen but no relationship with a directly transmitted pathogen. Collectively, this dissertation provides theoretically informed and testable predictions for how anthropogenic resources affect wildlife disease across taxa and in an important applied system.