Infectious diseases are a growing concern for both humans and wildlife. The negative effects of infectious disease have been exemplified by the recent global amphibian population declines associated with disease outbreaks. Although multiple pathogens and factors play a role in these declines, the aquatic fungal pathogen, Batrachochytrium dendrobatidis (Bd), has received considerable attention due to its substantial contribution to amphibian population declines around the world. Bd prevalence and severity appears to be increasing worldwide, either from recent anthropogenic spread of the pathogen or from changes in the environment that have altered host-pathogen dynamics. This dissertation explores the factors that affect host susceptibility to Bd.
I first tested the effects of hormonal stress on susceptibility to Bd (Chapter 2). Using corticosterone, the major chronic stress hormone in amphibians, I was able to mimic the physiological effects of stress without altering other factors that may affect the host-pathogen relationship. I exposed three species of larval amphibians to corticosterone for two weeks to induce chronic stress before challenging them with exposure to Bd. I found that exposure to corticosterone did not alter infection prevalence or severity in any species, indicating that chronically elevated levels of corticosterone do not affect susceptibility to Bd.
I next examined the interactive effects of the ubiquitous stressor, ultraviolet-B radiation (UVB), and host infection by Bd (Chapter 3). UVB can cause lethal and sublethal effects in amphibians, including increased susceptibility to pathogens. In outdoor mesocosms, I used ambient levels of UVB to stress larval amphibians while simultaneously exposing them to Bd. Although exposure to UVB increased mortality, it did not alter infection.
To investigate the effects of community structure on infection prevalence and severity, I studied how six anuran species (frogs and toads) differed in susceptibility to Bd (Chapter 4). I experimentally exposed post-metamorphic amphibians native to North America to Bd under identical laboratory conditions. All species tested had higher rates of mortality when exposed to Bd compared to unexposed controls. However, the species differed widely in their rates of Bd-associated mortality, even though there was no difference in infection levels among species. I also found that within species, the relationship between body size and infection varied, indicating physiological differences in the way that amphibian species respond to pathogen infection.
Finally, I studied the effects of the amphibian host community on infection. I experimentally exposed larval amphibians to Bd after manipulating host density and species richness in the laboratory (Chapter 5). I recorded five measures of disease risk and found a dilution effect where greater species richness decreased disease risk, even after taking into account changes in density. Together with Chapter 4, this study emphasizes the need to understand the effects of the community on host-pathogen dynamics.
This dissertation provides insight into the effects of stress and community structure on disease dynamics. Although there has been a great effort to understand Bd since it was discovered, the ecology of Bd remains relatively unknown. My research represents an important step in understanding the host-pathogen relationship in a changing environment.