DAO 123:159-171 (2017)  -  DOI: https://doi.org/10.3354/dao03089

ABSTRACT: Although it is well established that glucocorticoid hormones (GCs) alter immune function and disease resistance in humans and laboratory animal models, fewer studies have linked elevated GCs to altered immune function and disease resistance in wild animals. The chytrid fungal pathogen Batrachochytrium dendrobatidis (Bd) infects amphibians and can cause the disease chytridiomycosis, which is responsible for worldwide amphibian declines. It is hypothesized that long-term exposure to environmental stressors reduces host resistance to Bd by suppressing host immunity via stress-induced release of GCs such as corticosterone (CORT). We tested whether elevation of CORT would reduce resistance to Bd and chytridiomycosis development in the red-legged salamander Plethodon shermani. Plasma CORT was elevated daily in animals for 9 d, after which animals were inoculated with Bd and subsequently tested for infection loads and clinical signs of disease. On average, Bd-inoculated animals treated with CORT had higher infection abundance compared to Bd-inoculated animals not treated with CORT. However, salamanders that received CORT prior to Bd did not experience any increase in clinical signs of chytridiomycosis compared to salamanders not treated with CORT. The lack of congruence between CORT effects on infection abundance versus disease may be due to threshold effects. Nonetheless, our results show that elevation of plasma CORT prior to Bd inoculation decreases resistance to infection by Bd. More studies are needed to better understand the effects of CORT on animals exposed to Bd and whether CORT variation contributes to differential responses to Bd observed across amphibian species and populations.

KEY WORDS: Behavior · Chytridiomycosis · Disease · Plethodon shermani · Glucocorticoid · Stress hormone · Immunity