Hibernation, the use of prolonged torpor to depress metabolism, is employed by mammals to conserve resources during extended periods of extreme temperatures and/or resource limitation. Mammalian hibernators arouse to euthermy periodically during torpor for reasons that are not well understood, and these arousals may facilitate immune processes. To determine whether arousals enable host responses to pathogens, we used dual RNA-Seq and a paired sampling approach to examine gene expression in a hibernating bat, the little brown myotis (Myotis lucifugus). During torpor, transcript levels differed in only a few genes between uninfected wing tissue and adjacent tissue infected with Pseudogymnoascus destructans, the fungal pathogen that causes white-nose syndrome. Within 70-80 min after emergence from torpor, large changes in gene expression were observed due to local infection, particularly in genes involved in pro-inflammatory host responses to fungal pathogens, but also in many genes involved in immune responses and metabolism. These results support the hypothesis that torpor is a period of relative immune dormancy and arousals allow for local immune responses in infected tissues during hibernation. Host-pathogen interactions were also found to regulate gene expression in the pathogen differently depending on the torpor state of the host. Hibernating species must balance the benefits of energy and water conservation achieved during torpor with the costs of decreased immune competence. Interbout arousals allow hibernators to optimize these, and other, trade-offs during prolonged hibernation by enabling host responses to pathogens within brief, periodic episodes of euthermy.

Infectious diseases caused by invasive, environmentally persistent fungal pathogens have increasingly endangered global biodiversity, yet disease management remains a major conservation challenge. A prominent example is white‐nose syndrome (WNS), a disease caused by the invasive fungal pathogen Pseudogymnoascus destructans (Pd) that has devastated populations of multiple North American bat species, but for which few effective management tools exist. Here, we propose that strategies to delay environmental transmission of Pd during early winter could limit WNS disease effects across winter, benefitting bats. We used a small captive experiment and a multi‐year field trial on wild, free‐ranging bats to assess an environmental control strategy to manage Pd within its environmental reservoir in Pennsylvania, USA, where the pathogen has become endemic. The strategy centers on the application of Polyethylene Glycol 8000 (PEG) to roost substrates in summer, prior to bat hibernation, as a means to disrupt environmental transmission to bats in early winter. In the captive experiment, environmental transmission of Pd to immunologically naïve little brown myotis (Myotis lucifugus) occurred from roost substrates inoculated with Pd, but the application of PEG to these substrates effectively blocked this transmission. In the field trial, Pd load and infection extent both declined substantially in free‐ranging M. lucifugus after treatment relative to controls, with declines exceeding effects of inter‐site and inter‐annual variation. Pathogen prevalence and load also declined substantially after PEG treatment in big brown bats (Eptesicus fuscus). No negative effects of PEG treatment were observed in body condition or colony counts of bats or in the microbial community. Together, these results are consistent with effective environmental control of Pd and reduced WNS disease effects in bats within contaminated hibernacula. The results also highlight the potential of carefully designed environmental control strategies for managing environmentally persistent pathogens.

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