Format

Send to

Choose Destination
BMC Physiol. 2014 Dec 9;14:10. doi: 10.1186/s12899-014-0010-4.

White-nose syndrome initiates a cascade of physiologic disturbances in the hibernating bat host.

Author information

1
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Dr., Madison, Wisconsin, USA. mverant@usgs.gov.
2
US Geological Survey - National Wildlife Health Center, 6006 Schroeder Rd., Madison, Wisconsin, USA. cmeteyer@usgs.gov.
3
US Geological Survey - National Center, Environmental Health, 12201 Sunrise Valley Dr., Reston, Virginia, USA. cmeteyer@usgs.gov.
4
Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen, Scotland, UK. j.speakman@abdn.ac.uk.
5
US Geological Survey - Fort Collins Science Center, 2150 Centre Ave. Building C, Fort Collins, Colorado, USA. cryanp@usgs.gov.
6
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Dr., Madison, Wisconsin, USA. jmlorch@wisc.edu.
7
US Geological Survey - National Wildlife Health Center, 6006 Schroeder Rd., Madison, Wisconsin, USA. dblehert@usgs.gov.

Abstract

BACKGROUND:

The physiological effects of white-nose syndrome (WNS) in hibernating bats and ultimate causes of mortality from infection with Pseudogymnoascus (formerly Geomyces) destructans are not fully understood. Increased frequency of arousal from torpor described among hibernating bats with late-stage WNS is thought to accelerate depletion of fat reserves, but the physiological mechanisms that lead to these alterations in hibernation behavior have not been elucidated. We used the doubly labeled water (DLW) method and clinical chemistry to evaluate energy use, body composition changes, and blood chemistry perturbations in hibernating little brown bats (Myotis lucifugus) experimentally infected with P. destructans to better understand the physiological processes that underlie mortality from WNS.

RESULTS:

These data indicated that fat energy utilization, as demonstrated by changes in body composition, was two-fold higher for bats with WNS compared to negative controls. These differences were apparent in early stages of infection when torpor-arousal patterns were equivalent between infected and non-infected animals, suggesting that P. destructans has complex physiological impacts on its host prior to onset of clinical signs indicative of late-stage infections. Additionally, bats with mild to moderate skin lesions associated with early-stage WNS demonstrated a chronic respiratory acidosis characterized by significantly elevated dissolved carbon dioxide, acidemia, and elevated bicarbonate. Potassium concentrations were also significantly higher among infected bats, but sodium, chloride, and other hydration parameters were equivalent to controls.

CONCLUSIONS:

Integrating these novel findings on the physiological changes that occur in early-stage WNS with those previously documented in late-stage infections, we propose a multi-stage disease progression model that mechanistically describes the pathologic and physiologic effects underlying mortality of WNS in hibernating bats. This model identifies testable hypotheses for better understanding this disease, knowledge that will be critical for defining effective disease mitigation strategies aimed at reducing morbidity and mortality that results from WNS.

PMID:
25487871
PMCID:
PMC4278231
DOI:
10.1186/s12899-014-0010-4
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center