Carey Charleve S, Boyles Justin G
Cooperative Wildlife Research Laboratory, Department of Zoology, Center for Ecology, Southern Illinois University, Carbondale, IL 62901, USA.
Cooperative Wildlife Research Laboratory, Department of Zoology, Center for Ecology, Southern Illinois University, Carbondale, IL 62901, USA
J Exp Biol. 2015 Jul;218(Pt 13):1986-9. doi: 10.1242/jeb.118950. Epub 2015 May 5.
Pseudogymnoascus destructans is the causative fungal agent of white-nose syndrome (WNS), an emerging fungal-borne epizootic. WNS is responsible for a catastrophic decline of hibernating bats in North America, yet we have limited understanding of the physiological interactions between pathogen and host. Pseudogymnoascus destructans severely damages wings and tail membranes, by causing dryness that leads to whole sections crumbling off. Four possible mechanisms have been proposed by which infection could lead to dehydration; in this study, we tested one: P. destructans infection could cause disruption to passive gas-exchange pathways across the wing membranes, thereby causing a compensatory increase in water-intensive pulmonary respiration. We hypothesized that total evaporative water loss would be greater when passive gas exchange was inhibited. We found that bats did not lose more water when passive pathways were blocked. This study provides evidence against the proposed proximal mechanism that disruption to passive gas exchange causes dehydration and death to WNS-infected bats.
毁灭隐球菌是白鼻综合征（WNS）的致病真菌病原体，这是一种新出现的真菌传播的 epizootic。WNS 导致了北美冬眠蝙蝠的灾难性减少，但我们对病原体与宿主之间的生理相互作用了解有限。毁灭隐球菌严重损害翅膀和尾膜，导致干燥，进而使整个部分脱落。已经提出了四种感染可能导致脱水的机制；在本研究中，我们测试了其中一种：毁灭隐球菌感染可能会破坏翅膀膜上的被动气体交换途径，从而导致耗水量大的肺呼吸代偿性增加。我们假设当被动气体交换受到抑制时，总蒸发失水量会更大。我们发现，当被动途径被阻断时，蝙蝠并没有失去更多的水分。这项研究提供了证据，反对所提出的近端机制，即被动气体交换的破坏会导致感染 WNS 的蝙蝠脱水和死亡。
