Year of Award


Document Type


Degree Type

Doctor of Philosophy (PhD)

Degree Name

Fish and Wildlife Biology

Department or School/College

Division of Biological Sciences

Committee Chair

Angela D. Luis

Commitee Members

Amy J. Kuenzi, Creagh W. Breuner, Dean E. Pearson, Mike F. Minnick


amplification effect, density-dependent transmission, dilution effect, epidemiological models, orthohantaviruses, species-specific parasites


University of Montana


Globally, biodiversity is declining while emerging infectious diseases are on the rise. To explain this pattern, the “dilution effect” hypothesis predicts that with lower diversity, disease increases, because diversity “dilutes” disease. Although there is strong support for this hypothesis, there is evidence to support the “amplification effect” hypothesis, which predicts lower disease with lower diversity. Recently, there has been a push to investigate underlying mechanisms than general patterns to create a more mechanistic framework across disease systems. However, mechanisms have been mostly examined with indirectly-transmitted disease systems (e.g., Lyme disease), while less attention has been directed towards directly-transmitted systems, such as rodent-hantavirus systems.

For my dissertation, I investigated mechanisms behind diversity-disease patterns in directly-transmitted disease systems, using the North American deermouse (Peromyscus maniculatus)-Sin Nombre hantavirus (SNV) system as a model. SNV is an emerging zoonosis with high human fatality. A dilution effect has been primarily reported for this well-studied system, which exhibits density-dependent transmission. Because community composition than diversity pe se, is most likely responsible for a dilution effect, in this dissertation I primarily considered heterospecific competitors as the component of the community responsible for affecting disease.

In Chapter 1, I briefly introduce my dissertation. In Chapter 2, I discuss theory and empirical evidence of mechanisms that underlie patterns between disease and diversity (or community composition) across rodent-hantavirus systems through a systematic literature review. I conclude that host density is most likely the primary mechanistic driver, with density-independent mechanisms (i.e. contact rates, probability of transmission given contact and infectious period) requiring further investigation. In Chapter 3, I experimentally validate the use of two enzyme immunoassays for measuring fecal corticosterone metabolites in deermice, as a measure of stress. In Chapter 4, I present observational data that voles and shrews have negative impacts on deermouse stress physiology but differentially influence scar numbers (a proxy for contact rates). In Chapter 5, I use a mathematical model with interspecific competition and a deconstructed transmission rate (i.e. contact rates and probability of transmission) to show that non-monotonic patterns (increase then decrease) between competitor density and disease prevalence represent most of the realistic parameter space examined.



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