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      Wing pathology of white-nose syndrome in bats suggests life-threatening disruption of physiology

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      Author(s): 1 , 2 , , 3 , , 2
      Publication date (Electronic):
      Journal: BMC Biology
      Publisher: BioMed Central

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          Abstract

          White-nose syndrome (WNS) is causing unprecedented declines in several species of North American bats. The characteristic lesions of WNS are caused by the fungus Geomyces destructans, which erodes and replaces the living skin of bats while they hibernate. It is unknown how this infection kills the bats. We review here the unique physiological importance of wings to hibernating bats in relation to the damage caused by G. destructans and propose that mortality is caused by catastrophic disruption of wing-dependent physiological functions. Mechanisms of disease associated with G. destructans seem specific to hibernating bats and are most analogous to disease caused by chytrid fungus in amphibians.

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          Metabolic rate and body temperature reduction during hibernation and daily torpor.

          Fritz Geiser (2003)
          Although it is well established that during periods of torpor heterothermic mammals and birds can reduce metabolic rates (MR) substantially, the mechanisms causing the reduction of MR remain a controversial subject. The comparative analysis provided here suggests that MR reduction depends on patterns of torpor used, the state of torpor, and body mass. Daily heterotherms, which are species that enter daily torpor exclusively, appear to rely mostly on the fall of body temperature (Tb) for MR reduction, perhaps with the exception of very small species and at high torpor Tb, where some metabolic inhibition may be used. In contrast, hibernators (species capable of prolonged torpor bouts) rely extensively on metabolic inhibition, in addition to Tb effects, to reduce MR to a fraction of that observed in daily heterotherms. In small hibernators, metabolic inhibition and the large fall of Tb are employed to maximize energy conservation, whereas in large hibernators, metabolic inhibition appears to be employed to facilitate MR and Tb reduction at torpor onset. Over the ambient temperature (Ta) range where torpid heterotherms are thermo-conforming, the Tb-Ta differential is more or less constant despite a decline of MR with Ta; however, in thermo-regulating torpid individuals, the Tb-Ta differential is maintained by a proportional increase of MR as during normothermia, albeit at a lower Tb. Thermal conductance in most torpid thermo-regulating individuals is similar to that in normothermic individuals despite the substantially lower MR in the former. However, conductance is low when deeply torpid animals are thermo-conforming probably because of peripheral vasoconstriction.
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            Mammalian hibernation: cellular and molecular responses to depressed metabolism and low temperature.

            Corinne S. Martin, T. Andrews, Hannah V Carey (2003)
            Mammalian hibernators undergo a remarkable phenotypic switch that involves profound changes in physiology, morphology, and behavior in response to periods of unfavorable environmental conditions. The ability to hibernate is found throughout the class Mammalia and appears to involve differential expression of genes common to all mammals, rather than the induction of novel gene products unique to the hibernating state. The hibernation season is characterized by extended bouts of torpor, during which minimal body temperature (Tb) can fall as low as -2.9 degrees C and metabolism can be reduced to 1% of euthermic rates. Many global biochemical and physiological processes exploit low temperatures to lower reaction rates but retain the ability to resume full activity upon rewarming. Other critical functions must continue at physiologically relevant levels during torpor and be precisely regulated even at Tb values near 0 degrees C. Research using new tools of molecular and cellular biology is beginning to reveal how hibernators survive repeated cycles of torpor and arousal during the hibernation season. Comprehensive approaches that exploit advances in genomic and proteomic technologies are needed to further define the differentially expressed genes that distinguish the summer euthermic from winter hibernating states. Detailed understanding of hibernation from the molecular to organismal levels should enable the translation of this information to the development of a variety of hypothermic and hypometabolic strategies to improve outcomes for human and animal health.
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              Hibernation: the immune system at rest?

              Hannah V Carey, Hjalmar Bouma, F G Kroese (2010)
              Mammalian hibernation consists of torpor phases when metabolism is severely depressed, and T(b) can reach as low as approximately -2°C, interrupted by euthermic arousal phases. Hibernation affects the function of the innate and the adaptive immune systems. Torpor drastically reduces numbers of all types of circulating leukocytes. In addition, other changes have been noted, such as lower complement levels, diminished response to LPS, phagocytotic capacity, cytokine production, lymphocyte proliferation, and antibody production. Hibernation may therefore increase infection risk, as illustrated by the currently emerging WNS in hibernating bats. Unraveling the pathways that result in reduced immune function during hibernation will enhance our understanding of immunologic responses during extreme physiological changes in mammals.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMC Biol
                Title: BMC Biology
                Publisher: BioMed Central
                ISSN (Electronic): 1741-7007
                Publication date Collection: 2010
                Publication date (Electronic): 11 November 2010
                Volume: 8
                Page: 135
                Affiliations
                [1 ]United States Geological Survey, Fort Collins Science Center, Fort Collins, CO 80526, USA
                [2 ]United States Geological Survey, National Wildlife Health Center, Madison, WI 53711, USA
                [3 ]University of Pretoria, Department of Zoology and Entomology, Pretoria 0002, South Africa
                Article
                Publisher ID: 1741-7007-8-135
                DOI: 10.1186/1741-7007-8-135
                PMC ID: 2984388
                PubMed ID: 21070683
                SO-VID: 1a02469f-d17c-4d10-9782-6d96d9c78bfd
                Copyright © Copyright ©2010 Cryan et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 19 August 2010
                Date accepted : 3 November 2010
                Categories
                Subject: Opinion

                ScienceOpen disciplines: Life sciences
                Data availability:
                ScienceOpen disciplines: Life sciences

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