Winter Hibernation Energy Drain: How White-Nose Syndrome Kills Bats

Researchers have developed a detailed explanation of how white-nose syndrome is killing bats in parts of North America - the fungus Pseudogymnoascus destructans makes bats die by increasing the amount of energy they use during winter hibernation. Researchers from the U.S. Geological Survey and the University of Wisconsin created a model for how the disease progresses from initial infection to death in bats during hibernation. Since bats must carefully ration their energy supply during this time to survive without eating until spring, they tested the energy depletion hypothesis by measuring the amounts of energy used by infected and healthy bats hibernating under similar conditions.

Researchers have developed a detailed explanation of how white-nose syndrome is killing bats in parts of North America - the fungus Pseudogymnoascus destructans makes bats die by increasing the amount of energy they use during winter hibernation.

Researchers from the U.S. Geological Survey and the University of Wisconsin created a model for how the disease progresses from initial infection to death in bats during hibernation. Since bats must carefully ration their energy supply during this time to survive without eating until spring, they tested the energy depletion hypothesis by measuring the amounts of energy used by infected and healthy bats hibernating under similar conditions.

They found that bats with white-nose syndrome (WNS) used twice as much energy as healthy bats during hibernation and had potentially life-threatening physiologic imbalances that could inhibit normal body functions.


A northern long-eared bat affected by white-nose syndrome. Credit: J.R. Hoyt

Scientists also found that these effects started before there was severe damage to the wings of the bats and before the disease caused increased activity levels in the hibernating bats.

"This model is exciting for us, because we now have a framework for understanding how the disease functions within a bat," said University of Wisconsin and USGS National Wildlife Health Center scientist Michelle Verant, the lead author of the study. "The mechanisms detailed in this model will be critical for properly timed and effective disease mitigation strategies."

"Clinical signs are not the start of the disease -- they likely reflect more advanced disease stages," Verant said. "This finding is important because much of our attention previously was directed toward what we now know to be bats in later stages of the disease, when we observe visible fungal infections and behavioral changes."

Key findings of the study include:

Bats infected with P. destructans had higher proportions of lean tissue to fat mass at the end of the experiment compared to the non-infected bats. This finding means that bats with WNS used twice as much fat as healthy control bats over the same hibernation period. The amount of energy they used was also higher than what is expected for normal healthy hibernating little brown bats.

Bats with mild wing damage had elevated levels of dissolved carbon dioxide in their blood resulting in acidification and pH imbalances throughout their bodies. They also had high potassium levels, which can inhibit normal heart function.

Citation: Michelle L Verant, Carol U Meteyer, John R Speakman, Paul M Cryan, Jeffrey M Lorch,  David S Blehert, "White-nose syndrome initiates a cascade of physiologic disturbances in the hibernating bat host," BMC Physiology 2014, 14:10 doi:10.1186/s12899-014-0010-4

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