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Background  White-nose Syndrome (WNS) is a mycosis caused by a cutaneous infection with the fungus  Pseudogymnoascus destructans  ( Pd ). It produces hibernation mortality rates of 75–98% in 4 bats:  Myotis lucifugus ,  M. septentrionalis ,  M. sodalis , and  Perimyotis subflavus . These high mortality rates were observed during the first several years after the arrival of  P. destructans  at a hibernation site. Mortality is caused by a 60% decrease in torpor bout duration, which results in a premature depletion of depot fat prior to spring.    Results  Little is known about the long-term effects of  Pd  on torpor and mortality, thus we conducted a 9-year study on  M. lucifugus  at 5 of the hibernation sites where  Pd  first appeared in North America during the winter of 2007–08. The  M. lucifugus  hibernating at one of these sites one year after the arrival of  Pd  (2008–09) had: a) a mean torpor bout duration of 7.6 d, b) no depot fat reserves by March, and c) an apparent over-winter mortality rate of 88%. The  M. lucifugus  hibernating at this same site 6–9 years after the arrival of  Pd , in contrast, had: a) a mean torpor bout duration of 14.7 d, b) depot fat remaining in March, and c) an apparent mortality rate of 50%. The number of  M. lucifugus  hibernating at 2 of these sites has consistently increased since 2010 and is now more than 3.0-fold higher than the number remaining after the winter of 2008–09.    Conclusions  These findings indicate that this population of  M. lucifugus  has evolved mechanisms to hibernate well in the presence of  Pd , thus reducing over-winter mortality.

The evolution of a bat population with white-nose syndrome (WNS) reveals a shift from an epizootic to an enzootic phase