For questions/concerns about this disease in humans, please call your doctor or the Montana Department of Public Health and Human Services (DPHHS).
For questions about this disease/parasite in wildlife, please call the FWP Wildlife Health Lab at (406) 577-7882.
White-nose Syndrome (WNS), a disease caused by the cold-adapted fungus, Pseudogymnoascus destructans (Pd), has killed millions of North American bats since its detection in New York in 2006 (Blehert et al. 2008, Lorch et al. 2011, Frick et al. 2015). The disease is characterized by visible white fungal growth on the nose, ears, and wings of susceptible species of bats during the over-winter period of hibernation. The onset and severity of disease is related to fungal load, which typically builds in the environment over a period of years after the fungus is introduced, and is influenced by hibernacula temperature and humidity, bat colony size and species composition. Pd, which causes damage to wing, tail, and ear membranes on hibernating bats, causes bats to repeatedly rouse from torpor and burn through fat reserves needed to survive winter (Reeder et al. 2012). Some individuals that survive until spring mount an extreme inflammatory immune response to Pd which further contributes to mortality (Lilley et al. 2017, Davy et al. 2020). Individuals that survive through hibernation and spring emergence typically recover and clear infections to the point that spores and disease lesions are no longer detectable on bats by mid to late summer. Severity of disease differs among bat species, and appears to be related to variation in susceptibility, the immune response to infection, and hibernation behavior and ecology (Hoyt et al. 2021).
WNS has driven significant and sustained population declines among numerous bat species across the eastern half of North America (Frick et al. 2010, Frick et al. 2015, Langwig et al. 2012, Nocera et al. 2019), and as a result, several bat species have been listed or petitioned for listing under the United States Endangered Species Act.
Pd is believed to have been introduced from Eurasia through the accidental transport of an infected bat or fungal spores (Hoyt et al. 2021). Among Eurasian bat species, Pd causes much less severe disease and is not known to cause mass-mortality events. Since its initial detection in New York in 2006, national surveillance efforts have tracked the spread of Pd and WNS westward across North America (see updated map at whitenosesyndrome.org). In 2016, Pd was detected in Washington state, and 2019 detections in California indicate pathogen and disease spread from a western front. As of 2021, the Rocky Mountains remains the last large area where Pd has yet to be detected, although models predict the pathogen’s imminent arrival (National Wildlife Health Center, unpublished data).
Montana has been conducting Pd surveillance since 2012, with annual surveillance in at least 4-5 sites across the state since 2017. In 2019, FWP began collaborating with the National Wildlife Health Center to implement Pd surveillance informed by a west-wide spatial spread model. In 2021, FWP expanded surveillance efforts to include annual sampling across a 36-cell state-wide grid to gather the information needed to relate local Pd/WNS status with trends in state-wide bat acoustic data. This design will facilitate an assessment of the impacts of Pd/WNS on Montana bat species’ occupancy and activity.
Pd was detected for the first time in Montana during surveillance efforts in the spring of 2020, followed by our first detection of WNS in the spring of 2021 in eastern Montana.
Pd has been detected in 62 species of hibernating bats across the northern hemisphere (Hoyt et al. 2021). In North America, WNS has been documented in 12 bat species, and Pd is known to infect, but not cause disease, in another 9 species. Pd is known to be capable of causing WNS in seven of Montana’s 15 bat species, it has been detected in four other species that may serve as local or regional vectors, and seems likely to affect at least two other Montana species due to the close relatedness of species that have been impacted to date (Maxell 2015). While observations of WNS across the eastern US have informed our predictions of what to expect in the West, important questions remain about how the disease will play out among bat populations that have very different roosting ecologies than their counterparts back east. In 2019, FWP developed a plan to document the arrival and spread of Pd/WNS in Montana and to understand the disease’s impacts on our bat populations. Information from this program will be used to inform the scale of Montana’s conservation efforts needed to maintain healthy bat populations well into the future.
Because of the devastating impacts of WNS on North American bat populations, considerable efforts are underway to identify and test management tools to prevent infection, reduce disease severity and impacts, and boost overall bat survival to offset disease costs. Approaches include experimental tools aimed at directly controlling Pd through microbial, chemical, physical, or vaccine treatments of bats or hibernacula (e.g. Hoyt et al. 2019, Cheng et al. 2017, Cornelison et al. 2014, Turner et al. 2021, Palmer et al. 2018, Rocke et al. 2019), ecological approaches towards bolstering bat health and survival in the face of WNS (Cheng et al. 2019, Wilcox et al. 2016), or attempts to conserve habitat (Johnson & King 2018, White-nose Syndrome Conservation and Recovery Working Group 2018) and mitigate other sources of mortality such as that from wind development (Baerwald et al. 2009, Arnett et al. 2011) and anthropogenic structure loss (White‐nose Syndrome Conservation and Recovery Working Group 2015).
Pd thrives in cool and humid subterranean conditions (Verant et al. 2012, Langwig et al. 2012). Transmission occurs during fall and winter seasons via direct contact between bats and through contact with Pd-contaminated environments. Much of the transmission revolves around winter hibernacula, where infected bats shed spores that infect neighboring bats, contaminate cave environments, persist throughout the year, and can reinfect bats returning to hibernate (Langwig et al. 2015). The onset and severity of disease is related to fungal load, which typically builds in the environment over a period of years after the fungus is introduced, and is influenced by hibernacula temperature and humidity, bat colony size and species composition.
The onset and severity of WNS is related to the fungal load of Pd, which typically builds in hibernacula environments over a period of years after the fungus is introduced, and is influenced by hibernacula temperature and humidity, bat colony size and species composition. Pd causes damage to wing, tail, and ear membranes on hibernating bats, and causes them to repeatedly rouse from torpor and burn through fat reserves needed to survive winter (Reeder et al. 2012). Some individuals that survive until spring mount an extreme inflammatory immune response to Pd which further contributes to mortality (Lilley et al. 2017, Davy et al. 2020). Pd has caused mass-mortality events in hibernacula across the eastern US, in some cases causing declines of >95% of hibernating bat populations. Individuals that survive through hibernation and spring emergence typically recover and clear infections to the point that spores and disease lesions are no longer detectable on bats by mid to late summer. Severity of disease differs among species, and appears to be related to variation in susceptibility, the immune response to infection, and hibernation behavior and ecology (Hoyt et al. 2021).
There are no public health concerns associated with Pd and WNS in bats.
Arnett, E.B., Huso, M.M., Schirmacher, M.R. and Hayes, J.P., 2011. Altering turbine speed reduces bat mortality at wind‐energy facilities. Frontiers in Ecology and the Environment, 9(4), pp.209-214.
Baerwald, E.F., Edworthy, J., Holder, M. and Barclay, R.M., 2009. A large‐scale mitigation experiment to reduce bat fatalities at wind energy facilities. The Journal of Wildlife Management, 73(7), pp.1077-1081.
Blehert, D.S., Hicks, A.C., Behr, M., Meteyer, C.U., Berlowski-Zier, B.M., Buckles, E.L., Coleman, J.T., Darling, S.R., Gargas, A., Niver, R. and Okoniewski, J.C., 2009. Bat white-nose syndrome: an emerging fungal pathogen?. Science, 323(5911), pp.227-227.
Cheng, T.L., Mayberry, H., McGuire, L.P., Hoyt, J.R., Langwig, K.E., Nguyen, H., Parise, K.L., Foster, J.T., Willis, C.K., Kilpatrick, A.M. and Frick, W.F., 2017. Efficacy of a probiotic bacterium to treat bats affected by the disease white‐nose syndrome. Journal of Applied Ecology, 54(3), pp.701-708.
Cheng, T.L., Gerson, A., Moore, M.S., Reichard, J.D., DeSimone, J., Willis, C.K., Frick, W.F. and Kilpatrick, A.M., 2019. Higher fat stores contribute to persistence of little brown bat populations with white‐nose syndrome. Journal of Animal Ecology, 88(4), pp.591-600.
Cornelison, C.T., Gabriel, K.T., Barlament, C. and Crow, S.A., 2014. Inhibition of Pseudogymnoascus destructans growth from conidia and mycelial extension by bacterially produced volatile organic compounds. Mycopathologia, 177(1-2), pp.1-10.
Davy, C.M., Donaldson, M.E., Bandouchova, H., Breit, A.M., Dorville, N.A., Dzal, Y.A., Kovacova, V., Kunkel, E.L., Martínková, N., Norquay, K.J. and Paterson, J.E., 2020. Transcriptional host–pathogen responses of Pseudogymnoascus destructans and three species of bats with white-nose syndrome. Virulence, 11(1), pp.781-794.
Frick, W.F., Pollock, J.F., Hicks, A.C., Langwig, K.E., Reynolds, D.S., Turner, G.G., Butchkoski, C.M. and Kunz, T.H., 2010. An emerging disease causes regional population collapse of a common North American bat species. Science, 329(5992), pp.679-682.
Frick, W.F., Puechmaille, S.J., Hoyt, J.R., Nickel, B.A., Langwig, K.E., Foster, J.T., Barlow, K.E., Bartonička, T., Feller, D., Haarsma, A.J. and Herzog, C., 2015. Disease alters macroecological patterns of North American bats. Global Ecology and Biogeography, 24(7), pp.741-749.
Hoyt, J.R., Langwig, K.E., White, J.P., Kaarakka, H.M., Redell, J.A., Parise, K.L., Frick, W.F., Foster, J.T. and Kilpatrick, A.M., 2019. Field trial of a probiotic bacteria to protect bats from white-nose syndrome. Scientific reports, 9(1), pp.1-9.
Hoyt, J.R., Kilpatrick, A.M. and Langwig, K.E., 2021. Ecology and impacts of white-nose syndrome on bats. Nature Reviews Microbiology, 19(3), pp.196-210.
Johnson, C.M. and R.A. King, eds. 2018. Beneficial Forest Management Practices for WNS-affected Bats: Voluntary Guidance for Land Managers and Woodland Owners in the Eastern United States. A product of the White-nose Syndrome Conservation and Recovery Working Group established by the White-nose Syndrome National Plan (www.whitenosesyndrome.org). 39 pp.
Langwig, K.E., Frick, W.F., Bried, J.T., Hicks, A.C., Kunz, T.H. and Marm Kilpatrick, A., 2012. Sociality, density‐dependence and microclimates determine the persistence of populations suffering from a novel fungal disease, white‐nose syndrome. Ecology letters, 15(9), pp.1050-1057.
Langwig, K.E., Frick, W.F., Reynolds, R., Parise, K.L., Drees, K.P., Hoyt, J.R., Cheng, T.L., Kunz, T.H., Foster, J.T. and Kilpatrick, A.M., 2015. Host and pathogen ecology drive the seasonal dynamics of a fungal disease, white-nose syndrome. Proceedings of the Royal Society B: Biological Sciences, 282(1799), p.20142335.
Lilley, T.M., Prokkola, J.M., Johnson, J.S., Rogers, E.J., Gronsky, S., Kurta, A., Reeder, D.M. and Field, K.A., 2017. Immune responses in hibernating little brown myotis (Myotis lucifugus) with white-nose syndrome. Proceedings of the Royal Society B: Biological Sciences, 284(1848), p.20162232.
Lorch, J.M., Meteyer, C.U., Behr, M.J., Boyles, J.G., Cryan, P.M., Hicks, A.C., Ballmann, A.E., Coleman, J.T., Redell, D.N., Reeder, D.M. and Blehert, D.S., 2011. Experimental infection of bats with Geomyces destructans causes white-nose syndrome. Nature, 480(7377), pp.376-378.
Maxell, B.A. 2015. Montana Bat and White‐Nose Syndrome Surveillance Plan and Protocols 2012‐2016, Montana Natural Heritage Program, Helena, MT, pp. 1-210.
Nocera, T., Ford, W.M., Silvis, A. and Dobony, C.A., 2019. Patterns of acoustical activity of bats prior to and 10 years after WNS on Fort Drum Army Installation, New York. Global Ecology and Conservation, 18, p.e00633.
Palmer, J.M., Drees, K.P., Foster, J.T. and Lindner, D.L., 2018. Extreme sensitivity to ultraviolet light in the fungal pathogen causing white-nose syndrome of bats. Nature communications, 9(1), pp.1-10.
Reeder, D. M. et al. Frequent arousal from hibernation linked to severity of infection and mortality in bats with white-nose syndrome. PLoS ONE 7, e38920 (2012).
Rocke, T.E., Kingstad-Bakke, B., Wüthrich, M., Stading, B., Abbott, R.C., Isidoro-Ayza, M., Dobson, H.E., dos Santos Dias, L., Galles, K., Lankton, J.S. and Falendysz, E.A., 2019. Virally-vectored vaccine candidates against white-nose syndrome induce anti-fungal immune response in little brown bats (Myotis lucifugus). Scientific reports, 9(1), p.6788.
Turner, G.G., Sewall, B.J., Scafini, M.R., Lilley, T.M., Bitz, D. and Johnson, J.S., 2021. Cooling of bat hibernacula to mitigate white‐nose syndrome. Conservation Biology.
Verant ML, Boyles JG, Waldrep W Jr, Wibbelt G, Blehert DS (2012) Temperature-Dependent Growth of Geomyces destructans, the Fungus That Causes Bat White-Nose Syndrome. PLOS ONE 7(9): e46280. https://doi.org/10.1371/journal.pone.0046280
White‐nose Syndrome Conservation and Recovery Working Group. 2015. Acceptable Management Practices for Bat Control Activities in Structures ‐ A Guide for Nuisance Wildlife Control Operators. U.S. Fish and Wildlife Service, Hadley, MA.
White-nose Syndrome Conservation and Recovery Working Group, 2018. Acceptable Management Practices for Bat Species Inhabiting Transportation Infrastructure. A product of the White-nose Syndrome National Plan (www.whitenosesyndrome.org). 49 pp.
Wilcox, A. and Willis, C.K., 2016. Energetic benefits of enhanced summer roosting habitat for little brown bats (Myotis lucifugus) recovering from white-nose syndrome. Conservation physiology, 4(1).