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Effects of chytrid fungus and a glyphosate-based herbicide on survival and growth of wood frogs (Lithobates sylvaticus)

Megan K. Gahl, Bruce D. Pauli and Jeff E. Houlahan
Ecological Applications
Vol. 21, No. 7 (October 2011), pp. 2521-2529
Published by: Wiley
Stable URL: http://www.jstor.org/stable/41416676
Page Count: 9
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Effects of chytrid fungus and a glyphosate-based herbicide on survival and growth of wood frogs (Lithobates sylvaticus)
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Abstract

Anthropogenic-derived Stressors in the environment, such as contaminants, are increasingly considered important cofactors that may decrease the immune response of amphibians to pathogens. Few studies, however, have integrated amphibian disease and contaminants to test this multiple-stressor hypothesis for amphibian declines. We examined whether exposure to sublethal concentrations of a glyphosate-based herbicide and two strains of the pathogenic chytrid fungus, Batrachochytrium dendrobatidis (Bd) could: (1) sublethally affect wood frogs (Lithobates sylvaticus) by altering the time to and size at metamorphosis, and (2) directly affect survivability of wood frogs after metamorphosis. Neither Bd strain nor herbicide exposure alone significantly altered growth or time to metamorphosis. The two Bd strains did not differ in their pathogenicity, and both caused mortality in post-metamorphic wood frogs. There was no evidence of an interaction between treatments, indicating a lack of herbicide-induced susceptibility to Bd. However, the trends in our data suggest that exposure of wood frogs to a high concentration of glyphosate-based herbicide may reduce Bd-caused mortality compared to animals exposed to Bd alone. These results exemplify the complexities inherent when populations are coping with multiple Stressors. In this case, the perceived Stressor, glyphosate-based herbicide, appeared to affect the pathogen more than the host's immune system, relieving the host from disease 1 caused effects. This suggests caution when invoking multiple Stressors as a cause for increased disease susceptibility and indicates that the effects of multiple Stressors on disease outcome depend on the interrelationships of Stressors to both the pathogen and the host.

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