Two University professors search for cure to fungus decimating bat population

Beth Rogers and Sophia Reeder

Contributing Writers

On Aug. 30, 120 little brown bats from Montana arrived on campus. They join the 80 bats currently residing in the Robert L. Rooke Science Center.

Currently, two biology labs are working on a joint research project studying the effects of white-nose syndrome (WNS) in little brown bats. The Reeder lab, led by Associate Professor of Biology DeeAnn Reeder, focuses primarily on the physiology and behavior of afflicted bats. The Field lab, led by Associate Professor of Biology Ken Field, is studying their immune response on the cellular level.

WNS is a devastating condition that has been linked to widespread mortality among multiple bat species in the northeastern United States. Since its discovery in New York during the winter of 2006-2007, WNS has spread as far south as Alabama and as far west as Missouri. It is almost always a fatal affliction, and nearly six million bats in North America have already been killed.

The disease is caused by Pseudogymnoascus destructans, a cold-loving white fungus that colonizes on the skin of bats while they hibernate. The fungus has been shown to invade the tissues and cause lesions on the wings and muzzles of infected bats. During hibernation, the fungus growth stimulates little brown bats to arouse more frequently, causing them to deplete their stored energy reserves to the point of death. The fatality rate for little browns with white-nose syndrome is almost 90 percent. Big brown bats have a WNS mortality rate of only 40 percent.

The most destructive characteristic of P. destructans is its tendency to be highly transmissible from bat to bat. Many of the bat species most commonly affected by white-nose syndrome form tight clumps when they hibernate, facilitating the spread of the fungus between both individuals and species. Currently there are no known means of preventing transmission.

Nine North American bat species have been affected by white-nose syndrome, although they don’t all seem to be affected to the same extent. Bat populations in Europe seem to be relatively unaffected by WNS. Researchers believe that P. destructans was present across the Atlantic long before it was transmitted to the United States, and that European bats possess an immunity to the fungus that North American bats lack.

Bats are known for being reservoirs for more than 60 zoonotic (human-infecting) viruses, such as rabies, Ebola, and a predecessor to the human severe acute respiratory syndrome (SARS) virus. But despite the deadly infections they host, the bat immune system remains largely misunderstood. What researchers are trying to discern is why, of all the pathogens that bats encounter, P. destructans is their Achilles’ heel.

The Field lab is working to develop an assay to detect anti-P. destructans antibodies, which will show if bats are mounting an adaptive immune response to the fungus. They are also studying the immune cells of both exposed and unexposed bats to get a better picture of how the different components of the bat immune system fit together.

“By understanding the immune responses of bats, we hope to discover a way to slow the progress of this disease,” Field said.

The Reeder lab is focusing on the physiological and behavioral consequences of white-nose syndrome in survivors.

This research project will result in increased understanding of the bat immune system and help to explain why different bat species respond differently to the same pathogens. In addition, it will lead to future investigation of why certain bat species are so vulnerable to P. destructans and ways that bats can defend themselves against white-nose syndrome.

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