Date of Award
Master of Science
This thesis represents two lines of investigation that as a whole integrate physiology and ecology of infectious diseases. While each chapter is a distinct body of work, these studies are linked in that both focus on extrinsic or intrinsic factors influencing hosts’ susceptibility to infection, as well as hosts’ potential to transmit disease. In chapter one, I used a meta-analysis as a tool to review what is known about the stress-linked susceptibility hypothesis, which poses that persistent activation of the stress axis might result in increased disease susceptibility in wild animals, mainly as a result of allostatic overload and the immunosuppressive actions of stress hormones. My goal in evaluating the strength of association between distinct stressors and health indices in wildlife populations was manifold. First, I wanted to investigate which specific stressors are more likely to increase disease susceptibility in wild animals. Second, I was interested in the reliability of stress biomarkers as indicators of stress-induced immunosuppression or disease susceptibility. Finally, I used this chapter as a bridge for my second chapter by addressing how “fast-paced” and “slow-paced” phenotypes within wild populations cope differently with stressors, thus also differentially altering epizootic risk. My meta-analysis indicated that the highly variable outcomes of ecological studies can be attributed to several factors, ranging from possible erroneous classification of stimuli as physiological stressors to a lack of consensus on the endocrine profiles of stressed animals. The second chapter of this work consists of an empirical investigation of the pace-of-life (POL) hypothesis in the context of host disease susceptibility and transmissibility. Individuals with a fast-paced life history often exhibit relatively high metabolic rates and investment in growth, development, and reproduction. To support these faster rates, they often exhibit decreased investment in immunity, as well as associated bold behaviors for increased foraging and competiveness to ensure access to resources. These associated functional physiological and behavioral traits likely also influence exposure and susceptibility to pathogens, and infectiousness; factors central to disease dynamics. Through transmission trials using ranavirus and larval amphibians as a model system, I found that repeatable latency-to-food profiles of larval hosts, which characterize a POL axis associated with development and metabolic rates, were predictive of individual susceptibility and infectiousness. Faster-paced larval amphibians had greater exposure to pathogens (contacts), higher risk of infection (susceptibility), and shed greater pathogen populations when infected. Through these findings, I argue that The POL framework can allow for a priori identification of individual hosts that are more likely to spread infectious disease and may provide insight into understanding and potentially managing disease outbreaks that threaten wildlife and humans alike.
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