Abstract
Chytridiomycosis, a disease caused by Batrachochytrium dendrobatidis, has contributed to worldwide amphibian population declines; however, the pathogenesis of this disease is still somewhat unclear. Previous studies suggest that infection disrupts cutaneous sodium transport, which leads to hyponatremia and cardiac failure. However, infection is also correlated with unexplained effects on appetite, skin shedding, and white blood cell profiles. Glucocorticoid hormones may be the biochemical connection between these disparate effects, because they regulate ion homeostasis and can also influence appetite, skin shedding, and white blood cells. During a laboratory outbreak of B. dendrobatidis in Australian Green Tree Frogs, Litoria caerulea, we compared frogs showing clinical signs of chytridiomycosis to infected frogs showing no signs of disease and determined that diseased frogs had elevated baseline corticosterone, decreased plasma sodium and potassium, and altered WBC profiles. Diseased frogs also showed evidence of poorer body condition and elevated metabolic rates compared with frogs showing no signs of disease. Prior to displaying signs of disease, we also observed changes in appetite, body mass, and the presence of shed skin associated with infected but not yet diseased frogs. Collectively, these results suggest that elevated baseline corticosterone is associated with chytridiomycosis and correlates with some of the deleterious effects observed during disease development.
Highlights
Emerging infectious diseases (EIDs) of wildlife can have profound effects on animal biodiversity [1,2]; little is known about the pathogenesis of most wildlife EIDs [3]
Individuals that displayed clinical signs of chytridiomycosis had significantly elevated baseline CORT, decreased plasma sodium and potassium, altered white blood cell (WBC) profiles, increased resting metabolic rate (RMR), and decreased body condition compared with non-diseased individuals
It is important to note that non-diseased individuals were infected, but released thousands of Batrachochytrium dendrobatidis (Bd) zoospores while diseased individuals released millions of zoospores, on average
Summary
Emerging infectious diseases (EIDs) of wildlife can have profound effects on animal biodiversity [1,2]; little is known about the pathogenesis of most wildlife EIDs [3]. Since wildlife EIDs are often associated with anthropogenic and environmental stressors, pathogenesis is likely influenced by the host’s response to stressors [3,4,5,6]. The stress response is of interest in a disease context, because it is mediated by glucocorticoid (GC) hormones that are known to affect susceptibility to infection [8]. GCs influence a suite of physiological functions in vertebrates, including reproduction, development, blood ion homeostasis, metabolism, appetite, growth, and, importantly in the context of disease, immunity [9]. Warne et al [10] exposed Rana sylvatica to ranaviruses and observed an increase in corticosterone (CORT; the most abundant amphibian GC) concentration and accelerated developmental changes consistent with the effects of endogenous and exogenous elevations of CORT in non-diseased amphibians
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