Document Type



Doctor of Philosophy


Biology, Ecology

Date of Defense


Graduate Advisor

Robert E. Ricklefs, Ph.D.


Robert E. Ricklefs

Jonathan M. Chase

Sharon L. Deem

Patricia G. Parker


This dissertation examines the role of mammalian biodiversity in maintaining overall ecosystem health in the Greater Yellowstone Ecosystem (GYE). The study explores the pathways by which anthropogenic disturbance prevents or promotes the emergence of human infectious diseases. I studied two paramount research questions: Question 1: What are the direct effects of anthropogenic disturbance on rodent community assemblages and the consequent indirect effects on public health? I first surveyed the GYE rodent community and their pathogens by using land use as a measure of anthropogenic disturbance (e.g., human settlements, horseback ranches, pastures, undisturbed). I identified pathogens in rodent blood samples by Reverse Line Blotting. I screened for 41 pathogens belonging to 8 pathogen genera. Next, I used a variety of methods to elucidate the general pattern of host-pathogen association in the system, to tease apart the effect of land use change on infection patterns in the rodent assembly, and to study reservoir population density change among treatments. Question 2: Thriving key focal species — What are the determinants of disease coinfection, host community competence, and host immunity? Here, I used a community competence modelling approach to assess how community assemblage influences disease prevalence across treatments. Then, I explored the pathogen co-infection patterns in individual rodent hosts. Lastly, I addressed the role of rodent life-history strategies in determining community disease prevalence by measuring innate and acquired immune responses across land use change. To conclude, I show that anthropogenic disturbance increased overall disease risk for rodents, not because a particular hyper-reservoir species became more abundant, but rather because the abundance of other hosts, albeit less competent reservoirs, increased significantly. My results reveal that the direct effect of anthropogenic disturbance on the occurrence and density of infectious diseases reflects a complex array of numerous interacting factors that determine the risk components of a given zoonosis.

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