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Testing the Population-Level Effects of Stress-Induced Susceptibility in the Ranavirus-Wood Frog System
Jesse L Brunner1, Nicole C Dahrouge2, Erica J Crespi1
1School of Biological Sciences Washington State University Pullman Washington USA.
Stressful conditions did not increase the likelihood or severity of ranavirus epidemics in wood frogs. While higher temperatures accelerated disease spread, individual susceptibility did not directly scale to population-level epidemic outcomes.
Area of Science:
- Ecology
- Environmental Science
- Disease Ecology
Background:
- Chronic stressors (physical, chemical, biotic) increase individual animal susceptibility to infections.
- This increased susceptibility is often assumed to lead to more likely and severe disease epidemics at the population level.
Purpose of the Study:
- To investigate whether individual-level stress-induced susceptibility to ranavirus scales up to population-level epidemic outcomes.
- To test the impact of environmental stressors (salinity and temperature) on ranavirus epidemic dynamics in larval wood frogs.
Main Methods:
- Ranavirus epidemics were initiated in mesocosm populations of larval wood frogs (Lithobates sylvaticus).
- Populations were exposed to a factorial combination of low and high salinity with ambient or elevated temperatures.
- Epidemic likelihood, severity, and progression rate were monitored.
Main Results:
- Contrary to expectations, ranavirus epidemics were not more likely or severe under stressful conditions (low/high salinity, elevated temperature).
- Elevated temperatures significantly increased the speed of epidemic progression.
- Individual susceptibility to stressors did not directly translate to population-level epidemic severity.
Conclusions:
- The scaling of individual-level stressor impacts to population-level disease outcomes is not always straightforward.
- Environmental stressors may influence disease dynamics in complex ways that do not simply amplify epidemic risk.
- Further research is needed to understand the mechanisms behind the decoupling of individual susceptibility and population-level epidemic severity.
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