Exposure to Corticosterone Affects Host Resistance, but Not Tolerance, to an Emerging Fungal Pathogen

Abstract

Host responses to pathogens include defenses that reduce infection burden (i.e., resistance) and traits that reduce the fitness consequences of an infection (i.e., tolerance). Resistance and tolerance are affected by an organism's physiological status. Corticosterone (“CORT”) is a hormone that is associated with the regulation of many physiological processes, including metabolism and reproduction. Because of its role in the stress response, CORT is also considered the primary vertebrate stress hormone. When secreted at high levels, CORT is generally thought to be immunosuppressive. Despite the known association between stress and disease resistance in domesticated organisms, it is unclear whether these associations are ecologically and evolutionary relevant in wildlife species. We conducted a 3x3 fully crossed experiment in which we exposed American toads (Anaxyrus [Bufo] americanus) to one of three levels of exogenous CORT (no CORT, low CORT, or high CORT) and then to either low or high doses of the pathogenic chytrid fungus Batrachochytrium dendrobatidis (“Bd”) or a sham exposure treatment. We assessed Bd infection levels and tested how CORT and Bd affected toad resistance, tolerance, and mortality. Exposure to the high CORT treatment significantly elevated CORT release in toads; however, there was no difference between toads given no CORT or low CORT. Exposure to CORT and Bd each increased toad mortality, but they did not interact to affect mortality. Toads that were exposed to CORT had higher Bd resistance than toads exposed to ethanol controls/low CORT, a pattern opposite that of most studies on domesticated animals. Exposure to CORT did not affect toad tolerance to Bd. Collectively, these results show that physiological stressors can alter a host’s response to a pathogen, but that the outcome might not be straightforward. Future studies that inhibit CORT secretion are needed to better our understanding of the relationship between stress physiology and disease resistance and tolerance in wild vertebrates.

Extreme Competence: Keystone Hosts of Infections

“…One of the best known involves responses to stressors [48]. Variation in stress responses affect multiple aspects of competence in most taxa, but few studies have yet considered whether EC can arise via stress [18,19,49]. Symbionts that live on and within hosts might also affect EC [50], as these organisms sculpt host immune functions and behavior [51,52].…”

Glucocorticoids modulate gastrointestinal microbiome in a wild bird

“…The activation of the HPA axis may, therefore, be beneficial in the short term if, for instance, increased glucocorticoids reduce the load of the opportunistic pathogenic bacteria commonly found in the gut. Indeed, some recent studies suggest that glucocorticoids might reduce the proportion of some microbial taxa [ 12 ], and improve host resistance to some fungal, viral and bacterial pathogens [ 13 , 14 ].…”

Exogenous glucocorticoids amplify the costs of infection by reducing resistance and tolerance, but effects are mitigated by co-infection

“…We found no evidence that corticosterone increased tolerance by elevating red blood cell production rates [13], but corticosterone could suppress pro-inflammatory Th1 activity and thereby reduce the number of cells destroyed by the host's immune system [11,14]. Experimental elevation of corticosterone in other host -parasite systems have been shown to decrease [8] or have no effect [15] on tolerance. However, to our knowledge, these laboratory-based experiments are not associated with similar field-based observational or experimental studies.…”