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New studies solve some mysteries about the plague that's killing our bats

REUTERS
A bat suffering from white-nose syndrome

Two recent studies of white-nose syndrome (WNS) have turned up intriguing new details of how the disease seems to progress, not only within individual bats but also across bat populations.

Neither points directly to a cure for the fungal plague of WNS, which has killed nearly 6 million American bats in the last eight years and continues to push some species toward extinction.

But if effective cures are developed – along the lines, say, of bacterial agents that hold some promise of killing the fungus/spores, without unacceptable side effects – each set of findings points toward possible deployment strategies, and thus toward reversing the catastrophic losses of these key contributors to ecosystem health.

WNS attacks hibernating bats during the cool months of winter. Scientists have suspected that it kills by rousing the bats from rest, or torpor, sending them out and about for flights in wintry weather when they should be resting. (Thus the public-service announcements encouraging winter recreationists to report sightings of bats on the wing to conservation agencies.)

But a study from the University of Wisconsin at Madison suggests that it’s not quite so simple.

Researchers there gathered 60 little brown bats from a Wisconsin hibernaculum, placed them in tube socks and then in coolers, and took them to the lab for a series of measurements, including a test to establish that they were WNS-free.

Thirty-nine were then treated with spores of the Pseudogymnoascus destructans fungus, while 21 were assigned to a control group.

Fat metabolism increases

At first there was little difference in torpor arousal patterns between the two groups. However, the infected bats burned away their fat reserves at twice the rate of the control bats, and this pattern established itself before the bats displayed any visible signs of the disease, such as lesions on the non-furry skin of their muzzles, wings and ears.

As the disease progressed and the lesions appeared, the bats developed signs of dehydration and of decreased ability to clear carbon dioxide from their lungs, resulting in a buildup of CO2 in the bloodstream; the researchers speculate that once the CO2 levels reach a certain point, the bats’ bodies respond with hyperventilation, which makes torpor impossible.

Diseased bats also had higher concentrations of potassium in their blood; that interferes with heart function. But both groups lost body mass at about the same rate.

Good news on one point: The diseased bats also recovered at a much better rate than is often seen in the wild; only four of the 39 died in the end, compared with five of the 21 control bats.

These findings would seem to support observations that if infected bats can be kept alive until springtime, they can bounce back from WNS.

As lead researcher Michelle Verant put it in last week’s announcement of her findings by the U.S. Geological Survey, which partnered in the project:

This model is exciting for us, because we now have a framework for understanding how the disease functions within a bat. The mechanisms detailed in this model will be critical for properly timed and effective disease mitigation strategies.

Seasonal patterns of spread

Timing of WNS spread and intervention was the focus of the second study, published last month by a team of researchers who studied 30 bat colonies from Illinois to New Hampshire.

Twenty of these were assessed at hibernacula, and 10 at maternity sites where bats were raising new pups. Protection of woodland maternity sites, of course, is the focus of growing controversy as federal officials prepare habitat-protection rules that could restrict summertime logging in Minnesota and other states.

This team focused on whether such typical, seasonal factors as social and sexual contact seemed to shape the trends in WNS infection. They looked at five additional species besides the little brown bat: northern long-eared, eastern small-footed, tri-colored, big brown and Indiana bats.

It has long been known that fungal infection spreads intensively in the bats’ winter hibernacula, in part because WNS needs cool temperatures to thrive and can’t survive once the hosts’ reawakened bodies warm beyond a certain point.

The new findings suggest that disease transmission may occur only in the hibernacula, because infected individuals were found only between early autumn – when bats begin to swarm at the sites of their upcoming hibernation – and late spring, when they’ve remerged for the warm months.

Disease prevalence peaked in late winter, as hibernation began to wind down, and the overall rates seemed unaffected by population size, birth rates, migration behavior or any other factors besides exposure to spores during hibernation.

Strategic implications

And this has potential implications for the use of any disease-fighting agents or strategies that may be developed:

The seasonal patterns of transmission we have documented can be used to more effectively guide management interventions. When bats first become infected with P. destructans, loads, and therefore tissue invasion and damage, are relatively low. Therefore, applying treatments that reduce or clear infection during the autumn and early would be most effective for reducing transmission, impacts and spread to new sites.

However, if treatments offer only short-term protection, our data suggest that treated bats will probably be rapidly re-infected upon return to natural environments owing to exceedingly high infection prevalence in other hosts. Our results also suggest that another management strategy, culling bats to remove infected individuals, would be ineffective during the winter, because nearly 100% of individuals are already infected by early hibernation.

Finally, while rearing temperate bats in captivity is exceedingly challenging, if this strategy were attempted, capturing bats during late summer would maximize the fraction of uninfected bats that could be brought into captivity.

On the bright side, the paper points out that the apparently minimal summertime spread of WNS via long-distance traveling bats may mean that relatively disease-free regions like Minnesota – where the fungus has been detected at two sites, but no diseased bats have emerged – can expect  their good luck to perhaps continue.

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