ARMI conducts original research on various amphibian diseases in the lab and field. Our research has included estimating the impacts of diseases on the growth of populations, developing and testing potential treatments, affects of stressors on susceptibility to disease, how diseases are transmitted in the wild, and how to model disease distributions and spread.

ARMI disease research is conducted throughout the country, but disease ecologist Daniel Grear is based at the National Wildlife Health Center in Madison, Wisconsin, and coordinates the health screenings and investigations of amphibian mortalities (e.g., identification, pathology) in addition to collaborating on many disease research projects.

Amphibians at our long-term monitoring sites are periodically screened for diseases and we investigate mass mortality events.


National Wildlife Health Center - ARMI

Cave Bd sampling.
Left to Right: Tabby Cavendish (Great Smoky Mountains NP), Brian Gregory (USGS), and Jamie Barichivich (ARMI) swabbing salamanders for Batrachochytrium dendrobatidis (Bd) in Rockhouse Cave, Wheeler NWR, Alabama. Photo by: Alan Cressler.

Disease - ARMI Papers & Reports

Data Release complex ecological relationships-boreal toads-disease
Authors: Erin L Muths; Brittany A Mosher; Kathryn P Huyvaert; Larissa L Bailey
Outlet: Dryad
Data used in manuscript that examines several potential factors influencing disease dynamics in the boreal toad–disease system: geographic isolation of populations, amphibian community richness, elevational differences, and habitat permanence.
Data Release Effects of Snowpack, Temperature, and Disease on Demography in a Wild Population of Amphibians
Authors: Erin L Muths
Outlet: USGS
Data used in an assessment of the effects of snowpack, temperature and disease on demography in boreal toads in Wyoming.
Papers & Reports Context-dependent variation in persistence of host populations in the face of disease
Authors: Bennett Hardy; Erin L Muths; David N Koons
Date: 2021-12 | Outlet: Journal of Animal Ecology
In Focus: Valenzuela-Sanchez, A., Azat, C., Cunningham, A. A., Delgado, S., Bacigalupe, L. D., Beltrand, J., Serrano, J. M., Sentenac, H., Haddow, N., Toledo, V., Schmidt, B. R., & Cayuela, H. (2022). Interpopulation differences in male reproductive effort drive the population dynamics of a host exposed to an emerging fungal pathogen. Journal of Animal Ecology, XX, XXXX-XXXX. Understanding the nuances of population persistence in the face of a stressor can help predict extinction risk and guide conservation actions. However, the exact mechanisms driving population stability may not always be known. In this paper, Valenzuela-Sanchez et al. (2022) integrate long-term mark-recapture data, focal measurements of reproductive effort, a population matrix model, and inferences on life history variation to reveal differences in demographic response to disease in a susceptible frog species (Rhinoderma darwinii). Valenzuela-Sanchez et al. found that demographic compensation via compensatory recruitment explained the positive population growth rate in their high disease prevalence population whereas the low disease prevalence population did not compensate and thus had decreasing population growth. Compensatory recruitment was likely due to the high probability of males brooding, and the high number of brooded larvae in the high prevalence population compared to low prevalence and disease-free populations. Valenzuela-Sanchez et al. also document faster generation times in the high prevalence population, which may indicate a faster life history that may be contributing to the population’s ability to compensate for reduced survival. Lastly, the authors find a positive relationship between disease prevalence and the number of juveniles in a given population that suggest a possible prevalence threshold when increased reproductive effort may occur. Altogether, their study provides novel support for increased reproductive effort as the pathway for compensatory recruitment leading to increasing population growth despite strong negative effects of disease on adult survival. Their results also caution the overgeneralization of the effects of stressors (e.g., disease) on population dynamics, where context-dependent responses may differ among host populations of a given species.
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