Photo of biologists meeting outside Greeley Mine, Vermont

White-nose syndrome was first observed in four caves centered roughly 30 km west of Albany, New York, in the winter of 2006/2007. Photographs subsequently emerged of apparently affected bats in nearby Howes Cave, New York, taken during the previous winter, providing the earliest evidence of the disease. Counts at winter colonies of all 6 hibernating bat species in New York revealed that populations had been stable or increasing in recent decades, prior to the arrival of WNS. Whereas the effects of WNS appear to vary between species and winter hibernation sites (“hibernacula”), overall colony losses at the most closely monitored sites have reached 95 percent within 2 to 3 years of initial detection. As of April 2011, WNS has been detected in 6 of the 9 species of hibernating bats that occur in the affected region (Connecticut, Delaware, Indiana, Kentucky, Maryland, Massachusetts, New Hampshire, New Jersey, New York, North Carolina, Ohio, Pennsylvania, Tennessee, Vermont, Virginia, West Virginia, and the Canadian provinces: New Brunswick, Nova Scotia, Ontario, and Quebec). Species known to be susceptible to WNS thus far are the little brown bat (Myotis lucifugus), Indiana bat (M. sodalis), northern long-eared bat (M. septentrionalis), eastern small-footed bat (M. leibii), tricolored bat (Perimyotis subflavus), and big brown bat (Eptesicus fuscus). Three additional bat species were found in 2010 that tested positive for the presence of Geomyces destructans, the fungus associated with WNS, but not with the pathological invasion of the skin that is characteristic of the disease. These bats, the gray bat (M. grisescens), the cave myotis (M. velifer), and the southeastern myotis (M. austroriparius), were found in Missouri, Oklahoma, and Virginia, respectively, and their discovery could portend the spread of WNS into new regions of the southeastern and western U.S., and beyond, in the near future. The disease appears to affect bats most during long torpor bouts characteristic of winter hibernation. Therefore, bat species that use hibernation as a strategy for surviving the winter months, collectively called the “cave bats,” are most notably affected. It is currently not known if WNS is causing mortality in bats that use torpor during winter but do not regularly occur in caves and mines, such as the so-called migratory “tree bats” (for example, silver-haired bats [Lasionycteris noctivagans], hoary bats [Lasiurus cinereus], eastern red bats [Lasiurus borealis]).

The rapid and widespread mortality associated with WNS is unprecedented in hibernating bats; moreover, epizootic disease outbreaks such as WNS have not previously been documented in bats. Like other top mammalian predators, such as polar bear (Ursus marinus), sea otter (Enhydra lutris), and gray wolf (Canis lupus), most of the affected bat species are long lived (~5 to 15 years or more); hibernating bats typically only have one offspring per year, and population growth depends on high rates of adult survival. Therefore, naturally low reproductive rates combined with the high mortality observed in populations with WNS will likely prevent affected bat populations from recovering quickly.

White-nose syndrome was named for the visible presence of a white fungus around the muzzles, ears, and wing membranes of affected bats. Scientists recently identified a previously unknown species of cold-loving fungus (G. destructans) as a consistent pathogen causing skin infection in bats at affected sites. This fungus thrives in low temperatures (5-14º C; 40-55º F) and high levels of humidity (>90 %), conditions characteristic of many bat hibernacula. Pathologic findings thus far indicate that such fungal infections can be detected as early as October, and it is hypothesized that bats affected by WNS arouse from hibernation more frequently, and/or for longer periods than normal, and are prematurely expending the fat reserves they rely on for winter survival. Chronic disturbance of hibernating bats has been known to cause high rates of winter mortality through fat loss, and aberrant behaviors associated with WNS may cause bats to consume critical fat reserves prematurely during winter. Aberrant behaviors observed at sites affected by WNS include shifts of large numbers of bats in hibernacula to locations near the entrances or unusually cold areas; large numbers of bats dispersing during the day from hibernacula, even during mid-winter; a general unresponsiveness to human disturbance; and, on occasion, large numbers of fatalities, either inside the hibernacula, near the entrance, or in the immediate vicinity of the entrance. Additionally, recent hypotheses suggest that the characteristic wing pathology associated with WNS may cause death by disruption of important wing-dependent physiological functions, such as water balance, thermoregulation and mechanical function of the wing leading to dehydration, increased thirst-mediated arousals, increased heat loss, and inhibition of flight. Although evidence indicates that skin infection by G. destructans is the plausible primary cause of mortality associated with WNS, the exact processes by which skin infection leads to death remain undetermined, and it is unclear the extent to which other conditions may contribute to susceptibility of species or individuals to fungal infection and/or mortality.

For the purpose of implementing elements of this plan, WNS will be defined as Suspect when G. destructans DNA or characteristic conidia morphology is detected on bats in the absence of histopathologic evidence, or when field signs associated with WNS are observed in winter bat populations within a previously confirmed WNS affected state but diagnostic tests were either negative or not performed. WNS will be defined as Confirmed Positive upon histopathological characterization of skin invasion typical of G. destructans infection. Furthermore, a hibernaculum or area will be considered to be Infected if it is associated with bats that are either suspect or confirmed positive for WNS.