IS DISRUPTION TO PASSIVE GAS-EXCHANGE A MECHANISM OF DEHYDRATION FOR WNS-INFECTED HIBERNATING BATS?

Author

Charleve Carey, Southern Illinois University CarbondaleFollow

Date of Award

8-1-2014

Degree Name

Master of Science

Department

Zoology

First Advisor

Boyles, Justin

Abstract

Emergent epizootics are responsible for dramatic declines in wildlife populations over the past few years. An emerging fungal-borne epizootic, called white-nose syndrome (WNS), is responsible for a catastrophic decline of hibernating bats in North America The fungus, Pseudogymnoascus destructans (Pd), is the causative agent of WNS, but to date, we have limited understanding of how an infection with Pd can lead to mortality in hibernating bats. Evidence suggests dehydration is an important part of the pathogenesis of WNS. Cryan et al. (2010) proposed four possible mechanisms by which infection could lead to dehydration. In this study, I tested one of these hypotheses - Pd infection could cause disruption to passive gas-exchange pathways across the wing membranes, thereby causing a compensatory increase in water-intensive pulmonary respiration. I hypothesized total evaporative water loss would be greater when passive gas-exchange was inhibited, especially at low ambient temperatures. I found that bats did not lose more water when passive gas-exchange was retarded (at least within the resolution of my equipment). This study provides evidence against the proposed proximal mechanism that disruption to passive gas-exchange causes dehydration and ultimately death to WNS-infected bats.