title: Hibernating little brown myotis (Myotis lucifugus) show variable immunological responses to white-nose syndrome.
abstract: 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.
authors.affiliation: Department of Biology, Center for Ecology and Conservation Biology, Boston University, Boston, Massachusetts, United States of America. msm035@bucknell.edu
authors.forename: Marianne S
authors.initials: MS
authors.lastname: Moore
authors.forename: Jonathan D
authors.initials: JD
authors.lastname: Reichard
authors.forename: Timothy D
authors.initials: TD
authors.lastname: Murtha
authors.forename: Morgan L
authors.initials: ML
authors.lastname: Nabhan
authors.forename: Rachel E
authors.initials: RE
authors.lastname: Pian
authors.forename: Jennifer S
authors.initials: JS
authors.lastname: Ferreira
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Kunz
mesh_terms: D000820:Animal Diseases / Q000276:immunology* / Q000382:microbiology*; D000818:Animals; D001203:Ascomycota / Q000276:immunology*; D002685:Chiroptera / Q000276:immunology* / Q000382:microbiology*; D016207:Cytokines / Q000097:blood / Q000276:immunology; D005260:Female; D006605:Hibernation / Q000276:immunology*; D007136:Immunoglobulins / Q000097:blood / Q000276:immunology; D007958:Leukocyte Count; D009181:Mycoses / Q000662:veterinary*; D012621:Seasons; D014481:United States
chemical_list: D016207:Cytokines; D007136:Immunoglobulins