Wednesday, August 4, 2010: 9:50 AM
408, David L Lawrence Convention Center
Nathan A. Haislip1, Jason T. Hoverman2, Debra L. Miller3 and Matthew J. Gray1, (1)Center for Wildlife Health, University of Tennessee, Knoxville, TN, (2)Department of Forestry and Natural Resources, Purdue University, West Lafayette, IN, (3)Center for Wildlife Health, Dept of Forestry, Wildlife, and Fisheries, Univ Knoxville, TN
Background/Question/Methods The emergence of infectious diseases has sparked concern throughout the scientific community because they threaten global biodiversity, and consequently can impact the structure and function of ecological communities. Ecological stressors may be important components contributing to the emergence of infectious diseases. While organisms are surrounded by a diversity of ecological stressors, predation risk is one of the common stressors in nature. In response to predators, prey can adaptively alter their behavior, morphology, and life history traits. Although enhancing survival, the stress of predators can suppress immune function, which may increase susceptibility to pathogens. Thus, predator-rich communities may be hotspots for disease emergence. For over three decades, amphibian populations have been declining across the globe. While there are many hypothesized causes of these declines, the emergence of infectious diseases is receiving increased attention. More specifically, ranaviruses have been reported as the etiologic agent in amphibian die-offs on five continents, in four Canadian provinces, and in over thirty U.S. states, infecting dozens of species. Other than the association with amphibian die-off events, little is known about the ecology of the amphibian-ranavirus system. Our goal was to determine if the risk of predation increases the susceptibility of tadpoles from four amphibian species (
Hyla chrysoscelis,
Lithobates clamitans,
Lithobates sylvaticus, and
Pseudacris feriarum) to ranaviral infection and disease. Our experimental design was a factorial combination of two virus treatments and three predator treatments. The virus treatments consisted of a no-virus control and a virus exposure of 10
3 plaque-forming units mL
-1. The predator treatments were a no-predator control and predator cues from either larval dragonflies (
Anax sp.) or adult water bugs (
Belostoma flumineum). Each of the six treatments was replicated five times for a total of thirty experimental units.
Results/Conclusions We found that tadpoles of the four species reduced activity by 22-48% following continuous exposure to invertebrate predator cues. In addition, virus exposure resulted in reduced activity for Hyla chrysoscelis and Lithobates clamitans, and significantly reduced survival by 17-100% across all species. Exposure to predator cues did not affect survival or infection rates, and did not interact with the virus treatments. Together, our results suggest that the expression of adaptive inducible defenses in anuran larvae does not increase ranaviral disease risk. However, additional studies are needed that test other natural (e.g., competition) and anthropogenic (e.g., pesticide) stressors to understand disease risk within natural communities.