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Title:Persistence of ranavirus in an East-Central Illinois amphibian community
Author(s):Low, Kelsey Megan
Director of Research:Allender, Matthew C; Phillips, Christopher A
Doctoral Committee Chair(s):Allender, Matthew C; Phillips, Christopher A
Doctoral Committee Member(s):Allan, Brian F; Roca, Alfred L
Department / Program:School of Integrative Biology
Discipline:Ecol, Evol, Conservation Biol
Degree Granting Institution:University of Illinois at Urbana-Champaign
Abstract:Amphibians are declining globally, and infectious disease is one of their primary threats. Ranaviruses infect cold-blooded vertebrates, with FV3-like ranaviruses being associated with amphibian mortality events across much of North America. The frequency of these mortality events is unknown, due to difficulties in establishing and maintaining longitudinal surveillance programs. Experimental studies have suggested environmental covariates such as temperature affect viral replication, host immune function, or both to exacerbate disease and induce outbreaks. However, field-based investigations have found inconclusive results concerning environmental effects on disease prevalence or the probability of mortality events. Studies investigating interspecies variation in susceptibility or transmission dynamics have concluded that host species identities strongly influence disease dynamics, however this has not been incorporated into field-based studies which focus on a handful of species to test for the presence of FV3. In this dissertation, I investigated how ranaviral disease is affected by environmental covariates, amphibian community composition, host identity, and host genetics. First, I used surveillance data from three consecutive years, and more intensive amphibian surveillance over two years to characterize temporal variation in infection prevalence between amphibian species, to identify host roles in disease dynamics, and to evaluate how infection prevalence and intensity responded to environmental covariates. I identified Green frogs (R. clamitans) as the reservoir host, which maintain pathogens longitudinally, and Wood frogs (R. sylvatica) as the amplification host, which increase transmissions and disease risk within the community. I found that transmission dynamics between these hosts explain the intensity and sporadic nature of mortality events. Additionally, I found that increasing amphibian species richness was negatively related to the probability of a mortality event due to decreased density of R. sylvatica. Next, I evaluated whether environmental DNA could be used to detect ranavirus outbreaks, and to provide insight to host infections and rates of viral amplification and decay in wetland water. I found that environmental titer closely tracked the viral load of all amphibian hosts standardized by their relative abundances. However, timing of the peak in mortalities was not consistent with peak in environmental titer, and environmental titer decayed within two weeks of a mortality event requiring monitoring at least every two weeks to confirm the presence of an outbreak event. Then, I examined how infection with ranavirus influences growth rates in larval amphibians, and if surviving an outbreak has any sub-lethal effects on amphibians after metamorphoses. Surprisingly, I found that survivors benefitted from reduced competition, emerging larger or more abundant at metamorphoses. Additionally, I found that ranavirus mediates competition between R. sylvatica and chorus frog (Pseudacris spp.) tadpoles because within created wetlands, Pseudacris tadpoles only survived to metamorphoses after an outbreak removed 100% of R. sylvatica tadpoles. Growth and development rates were similar in wetlands that experienced ranavirus outbreaks, thus I did not detect sublethal effects of infection or exposure on fitness within surviving metamorphs. Finally, I investigated how genomic contribution from a sexually reproductive species (small-mouthed salamander, A. texanum) influenced disease outcomes and pathogenesis in tetraploid hybrids (A. texanum x A. platineum). I found that tetraploid hybrids developed all clinical signs and had mortality rates, intermediate to the genetically contributing species. I concluded that this resulted from beneficial effects of alleles inherited from A. texanum. This was the first study finding strong evidence of genomic factors influencing disease outcomes in Ambystoma salamanders and highlights the need to describe and understand immune responses to FV3 in larval amphibians. Together, these studies provide evidence that outbreaks of ranaviral disease are predominantly driven by processes occurring within the community of larval amphibians, and that outbreaks benefit species that are less susceptible which may change community composition in the long term. Outbreaks can be studied with eDNA, provided sampling frequency is adequate, and genomic composition influences patterns of host susceptibility.
Issue Date:2019-11-21
Rights Information:Copyright 2019 Kelsey Low
Date Available in IDEALS:2020-03-02
Date Deposited:2019-12

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