For nearly two decades, scientists have watched white-nose syndrome tear through North American bat colonies while trying to explain how a dusting of fungus could be so deadly. Recent work now outlines a clear chain of events: a cold-loving pathogen attacks bat wings, disrupts basic body chemistry, and pushes vital organs toward failure.
The story is no longer just about a strange fungus in caves. It is about skin as a life-support system, about dehydration and electrolytes, and about how a small mammal built for hibernation can be tipped into lethal trouble by damage measured in millimeters. With that biology mapped in more detail, the central question has shifted from “what is killing bats?” to “can the process be interrupted in time?”
From mysterious fungus to named killer
White-nose syndrome first appeared as a baffling affliction in northeastern hibernation sites, with bats found dead or flying in midwinter, their muzzles coated in white growth. Since its discovery in 2006, the disease has killed millions of bats across North America, according to an official USGS strategy on bat health that describes WNS as a defining threat to bat conservation.
The early years were marked by shock and guesswork, but the picture sharpened once a newly described fungus was consistently found on affected animals. A 2009 fact sheet from the USGS, covering the winter of 2006–2007, tied this fungus directly to WNS and reported that hundreds of thousands of bats had already died in that first wave, based on counts from at least 82 affected hibernacula in the northeastern United States. That document framed the pathogen as the central suspect and captured the moment when a strange cave phenomenon became a continent-scale wildlife disease with a named microbial driver.
Wing lesions as a lethal organ failure
For years, the white fuzz on bat noses drew the most attention, but the real damage turned out to be on their wings. Peer-reviewed research in BMC Biology showed that the characteristic lesions of WNS are caused by fungal infection that eats into the thin wing membranes, not just the fur or muzzle. In that study, pathologists argued that bat wings behave like an organ, handling gas exchange, circulation, and temperature control, and that the fungal lesions could disrupt all of those functions at once.
This idea reframes the disease: the fungus is not merely cosmetic, it is punching holes in a vital surface that helps keep the animal’s internal chemistry steady. A peer-reviewed article archived by the USGS in the Journal of Wildlife went further, linking this wing damage to dehydration-related electrolyte depletion. As the fungus destroys wing tissue, bats lose water and dissolved salts through the damaged skin, in a way that resembles fluid and electrolyte loss through burn injuries in people.
Electrolytes, arousals, and failing hearts
Once scientists started measuring blood chemistry in infected bats, the mystery of sudden winter deaths began to make more sense. The electrolyte study in the USGS record linked WNS to severe losses of key ions in the bloodstream, showing that affected animals had patterns consistent with dehydration-related electrolyte depletion. These findings support the idea that the fungus drives a slow leak of water and salts that the hibernating body is poorly equipped to correct.
A national news release from USGS scientists pulled the physiological story together. The researchers reported that the effects of WNS began before there was severe damage to the wings and before the disease caused death, and that these early changes could inhibit normal heart function. In their summary of how WNS kills bats, the scientists described how electrolyte imbalances and repeated arousals from hibernation sap fat reserves and stress the cardiovascular system long before an animal is found on the cave floor.
Reconstructing the early outbreak
With the mechanism clearer, researchers have gone back to the beginning to confirm when and where this process first took hold. A peer-reviewed analysis of archival specimens, cataloged by the USGS in the Journal of Wildlife, confirmed a definitive case of WNS in little brown bats (Myotis lucifugus) from New York in spring 2007. By re-examining stored carcasses with modern diagnostics, the authors showed that these animals had the characteristic fungal lesions and pathology that define the syndrome.
This retrospective work matters because it sets a firm baseline for how quickly the disease expanded. The 2009 USGS fact sheet noted that since the winter of 2006–2007, hundreds of thousands of bats had died from WNS in the Northeast. When that early mortality estimate is lined up with the New York archival confirmation from spring 2007, it indicates that the fungus was well established and lethal before managers had a name for it or a plan to contain it.
A continental spread, mapped in real time
What began in northeastern caves is now a continental phenomenon. An official year-in-review page on bat health reports that as of December 2025, bats with WNS were confirmed in 41 states and five Canadian provinces. That same USGS program summary notes that by late 2025, the fungus or the disease had been detected at 698 sites in the United States and Canada, with confirmed disease in at least 596 counties, showing how thoroughly it has moved through suitable hibernation habitat despite cave closures, decontamination campaigns, and years of public warnings.
The westward march has been tracked one detection at a time. An official press release from the U.S. Fish and Wildlife Service documented the first detection of the WNS-causing fungus in Oregon, describing how wildlife staff identified the pathogen on a bat and linking it to the same agent behind the eastern outbreak. That announcement illustrates how, even with better science, managers are often reacting to new positives at the edge of the map rather than staying ahead of the spread.
More from Morning Overview
*This article was researched with the help of AI, with human editors creating the final content.
