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The devastating bat fungal disease, white-nose syndrome (WNS), does not appear to affect all species equally. To experimentally determine susceptibility differences between species, we exposed hibernating naïve little brown myotis (Myotis lucifugus) and big brown bats (Eptesicus fuscus) to the fungus that causes WNS, Pseudogymnoascus destructans (Pd). After hibernating under identical conditions, Pd lesions were significantly more prevalent and more severe in little brown myotis. This species difference in pathology correlates with susceptibility to WNS in the wild and suggests that survival is related to different host physiological responses. We observed another fungal infection, associated with neutrophilic inflammation, that was equally present in all bats. This suggests that both species are capable of generating a response to cold tolerant fungi and that Pd may have evolved mechanisms for evading host responses that are effective in at least some bat species. These host-pathogen interactions are likely mediated not just by host physiological responses, but also by host behavior. Pd-exposed big brown bats, the less affected species, spent more time in torpor than did control animals, while little brown myotis did not exhibit this change. This differential thermoregulatory response to Pd infection by big brown bat hosts may allow for a more effective (or less pathological) immune response to tissue invasion.

The persistence of populations declining from novel stressors depends, in part, on their ability to respond by trait change via evolution or plasticity. White-nose syndrome (WNS) has caused rapid declines in several North America bat species by disrupting hibernation behaviour, leading to body fat depletion and starvation. However, some populations of Myotis lucifugus now persist with WNS by unknown mechanisms. We examined whether persistence of M. lucifigus with WNS could be explained by increased body fat in early winter, which would allow bats to tolerate the increased energetic costs associated with WNS. We also investigated whether bats were escaping infection or resistant to infection as an alternative mechanism explaining persistence. We measured body fat in early and late winter during initial WNS invasion and 8 years later at six sites where bats are now persisting. We also measured infection prevalence and intensity in persisting populations. Infection prevalence was not significantly lower than observed in declining populations. However, at two sites, infection loads were lower than observed in declining populations. Body fat in early winter was significantly higher in four of the six persisting populations than during WNS invasion. Physiological models of energy use indicated that these higher fat stores could reduce WNS mortality by 58%-70%. These results suggest that differences in fat storage and infection dynamics have reduced the impacts of WNS in many populations. Increases in body fat provide a potential mechanism for management intervention to help conserve bat populations.

Reduced populations of Myotis lucifugus (Little Brown Myotis) devastated by white-nose syndrome (WNS) persist in eastern North America. Between 2009 and 2013, we recaptured 113 marked individuals that survived between 1 and 6 winters in New England since the arrival of WNS. We also observed signs of reproductive success in 57 recaptured bats.

Environmental pollutants may negatively affect the immune system of animals. Yet, this phenomenon has not been studied thoroughly in terrestrial animals that use polluted water for drinking and/or foraging. We experimentally tested the hypothesis that exposure to sewage water would affect the activation of the immune response in the bat Pipistrellus kuhlii that drinks from bodies of open water. We selected two water sources where bats forage in the Negev desert, Israel: natural springs and a sewage-polluted man-made reservoir. We captured 13 non-reproductive female bats in the vicinity of the natural springs and offered seven of them water from the sewage-polluted source for 30 days (treatment) and the remaining six bats were offered water from the natural spring (control). Consumption of contaminated water did not alter the bactericidal ability of blood plasma or the proportions of monocytes circulating in the blood. However, our data provided evidence that the 30-day treatment can cause a decrease in the relative levels of neutrophils and an increase in the levels of lymphocytes. Our study provides a first account for the effect of sewage pollution on bat immune response which may be important in desert environments, where water sources are scarce. We suggest hypotheses for future, more focused studies.

White-nose syndrome (WNS) is an emerging infectious disease devastating hibernating North American bat populations that is caused by the psychrophilic fungus Geomyces destructans. Previous histopathological analysis demonstrated little evidence of inflammatory responses in infected bats, however few studies have compared other aspects of immune function between WNS-affected and unaffected bats. We collected bats from confirmed WNS-affected and unaffected sites during the winter of 2008–2009 and compared estimates of their circulating levels of total leukocytes, total immunoglobulins, cytokines and total antioxidants. Bats from affected and unaffected sites did not differ in their total circulating immunoglobulin levels, but significantly higher leukocyte counts were observed in bats from affected sites and particularly in affected bats with elevated body temperatures (above 20°C). Bats from WNS-affected sites exhibited significantly lower antioxidant activity and levels of interleukin-4 (IL-4), a cytokine that induces T cell differentiation. Within affected sites only, bats exhibiting visible fungal infections had significantly lower antioxidant activity and levels of IL-4 compared to bats without visible fungal infections. Overall, bats hibernating in WNS-affected sites showed immunological changes that may be evident of attempted defense against G. destructans. Observed changes, specifically elevated circulating leukocytes, may also be related to the documented changes in thermoregulatory behaviors of affected bats (i.e. increased frequencies in arousal from torpor). Alterations in immune function may reflect expensive energetic costs associated with these processes and intrinsic qualities of the immunocapability of hibernating bats to clear fungal infections. Additionally, lowered antioxidant activity indicates a possible imbalance in the pro- versus antioxidant system, may reflect oxidative tissue damage, and should be investigated as a contributor to WNS-associated morbidity and mortality.

White-nose syndrome (WNS) is an emerging infectious disease affecting several species of hibernating bats in North America and threatening at least one species with regional extinction. The syndrome is associated with a cutaneous fungal infection caused by the newly described fungus, Geomyces destructans (Gd) , reduced fat reserves, atypical behavior, severe wing damage, and high mortality. Six North American bat species are currently affected by WNS, but Gd has been reported from three other hibernating species. Given the rapid geographic spread of Gd , several other species are at risk of infection. G. destructans has also been isolated from nine European bat species. However, no other symptoms of WNS or associated mass mortality of bats associated with this fungus has been observed in Europe. The postulated pathogenic role of Gd is not fully understood, although it appears to disrupt the physiology and alter the behavior of hibernating bats. Given the unique life-history traits of hibernating bats, decimated populations will recover very slowly, if at all, unless the syndrome can be effectively managed. Without implementation of effective management practices ( e.g. , mitigation and recovery), lasting ecological and economic impacts at both regional and national scales can be expected.

White-nose syndrome (WNS) is the most devastating condition ever reported for hibernating bats, causing widespread mortality in the northeastern United States. The syndrome is characterized by cutaneous lesions caused by a recently identified psychrophilic and keratinophylic fungus (Geomyces destructans), depleted fat reserves, atypical behavior, and damage to wings; however, the proximate cause of mortality is still uncertain. To assess relative levels of immunocompetence in bats hibernating in WNS-affected sites compared with levels in unaffected bats, we describe blood plasma complement protein activity in hibernating little brown myotis (Myotis lucifugus) based on microbicidal competence assays using Escherichia coli, Staphylococcus aureus and Candida albicans. Blood plasma from bats collected during mid-hibernation at WNS-affected sites had higher bactericidal ability against E. coli and S. aureus, but lower fungicidal ability against C. albicans when compared with blood plasma from bats collected at unaffected sites. Within affected sites during mid-hibernation, we observed no difference in microbicidal ability between bats displaying obvious fungal infections compared to those without. Bactericidal ability against E. coli decreased significantly as hibernation progressed in bats collected from an affected site. Bactericidal ability against E. coli and fungicidal ability against C. albicans were positively correlated with body mass index (BMI) during late hibernation. We also compared complement activity against the three microbes within individuals and found that the ability of blood plasma from hibernating M. lucifugus to lyse microbial cells differed as follows: E. coli>S. aureus>C. albicans. Overall, bats affected by WNS experience both relatively elevated and reduced innate immune responses depending on the microbe tested, although the cause of observed immunological changes remains unknown. Additionally, considerable trade-offs may exist between energy conservation and immunological responses. Relationships between immune activity and torpor, including associated energy expenditure, are likely critical components in the development of WNS.