Disentangling the Biotic and Abiotic Drivers of the Amphibian Disease Chytridiomycosis Public Deposited



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  • The ongoing worldwide loss of biodiversity has been described as a "biodiversity crisis," "the Anthropocene defaunation," and alternatively "an extinction spasm." More recently, many scientists have come to the conclusion that we are witnesses to Earth's sixth major mass extinction event, which has the potential to fundamentally alter basic ecological functions on global scale. One of the many causes of population declines, species extirpations, and extinctions contributing to this profound loss of biodiversity are emerging infectious diseases. The occurrence and spread of infectious diseases can be assisted by numerous anthropogenic causes. For example, habitat fragmentation and access to formerly undeveloped areas can increase the rate and the risk of interaction between domestic and wild animals, leading to "spill-over" of pathogens from unaffected reservoir hosts to susceptible hosts. Alternatively, global trade can lead to "pathogen pollution" caused by the translocation of pathogens or parasites directly or via the translocation of invasive species that often act as reservoir hosts in invaded ranges. Moreover, an overall increase in animal stress associated with habitat degradation, invasive species, or climate change can negatively affect the immune responses of an otherwise healthy host, which can transform benign infections into pathogenic infections. One emerging infectious disease that is in part responsible for this great loss of biodiversity is chytridiomycosis, which has been associated with numerous amphibian population declines and extinctions. Chytridiomycosis is caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd), which has been found on every continent where amphibians exist. Whereas Bd can infect a wide range of amphibians, there is also a wide range of heterogeneity of responses to infection. This heterogeneity exists at the species-level where some species can act as unaffected reservoirs of the disease; while at the other end of the spectrum, some species will die within days of exposure. This heterogeneity can exist at the population-level within a species; some populations survive with a persistent infection, while simultaneously mass mortality events can eliminate nearby populations of the same species. Furthermore, heterogeneity can exist within one population, where some amphibian life stages, or some individuals of the same life stage, survive after Bd-exposure while other life stages or individuals will not survive. Understanding the biotic and abiotic causes, of different responses to Bd is paramount to limiting further losses of amphibian biodiversity as well cascade effects of the loss of amphibians in ecosystems. This thesis elucidates some of the potential causes of these differences, specifically addressing heterogeneity among host species, host populations, host ages, and environmental temperature, a key environmental component that influences the biology of Bd. Previous studies have investigated the relationship between climate and chytridiomycosis by comparing differences susceptibility or sensitivity as a function of mean temperature over time. However, in addition to the predicted general warming trends associated with anthropogenic climate change, many models also predict increases in both the magnitude and frequency of extreme weather events, which can result in unusual temperature shifts for a given habitat. In Chapter 2, I describe an experiment in which I investigated how temperature shifts may influence Bd infection intensity and survival in amphibian larvae. Consistent with the "lag effect" hypothesis, Bd abundance was higher in larval red legged frogs (Rana aurora) that experienced a shift in temperature from cold to warm compared to frogs exposed to a constant temperature. Similarly, Bd abundance was lower in larval western toads (Anaxyrus boreas) that experienced a shift in temperature from warm to cold, compared to larval toads exposed to a constant temperature. In Chapter 3, I discuss the ontogeny of susceptibility to Bd infection and report on an experiment I performed in two species of frog over the first nine months post-metamorphosis. The youngest frogs of both species were the least susceptible to chytridiomycosis. Increasing age was associated with an increase in likelihood of Bd infection, increased infection intensity, and increased risk of mortality after infection. In Chapter 4, I examine differences in response to Bd infection among 10 distinct populations, using wood frogs (Lithobates sylvaticus) collected as eggs and raised in a common garden environment through metamorphosis. I observed differences in survival after Bd-exposure among the populations, but did not observe differences in infection intensity among populations. These results suggest that populations of wood frog share a similar level of resistance to Bd infection, but differ in levels of tolerance to infection of a given intensity. This thesis describes and helps disentangle the biotic drivers (the ontogeny of susceptibility and population-level variation in susceptibly) and a key abiotic parameter (temperature) of chytridiomycosis in amphibians. The information provided may assist conservationists and population managers to focus conservation efforts and mitigate the losses of these ecologically important creatures caused by this disease.
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