White-nose syndrome increases torpid metabolic rate and evaporative water loss in hibernating bats

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2017-12, Vol.313 (6), p.R680-R686
• Main Authors: McGuire, Liam P, Mayberry, Heather W, Willis, Craig K R
• Format: Article
• Language: English
• Subjects: Animal diseases; Animals; Arousal; Ascomycota - classification; Ascomycota - pathogenicity; Bats; Body Temperature Regulation; Chiroptera; Chiroptera - metabolism; Chiroptera - microbiology; Correlation analysis; Dermatomycoses - metabolism; Dermatomycoses - microbiology; Dermatomycoses - physiopathology; Dermatomycoses - veterinary; Disease control; Energy expenditure; Energy Metabolism; Environment; Fluorescence; Fungal diseases; Fungi; Hibernation; Humidity; Infections; Male; Mathematical models; Medical treatment; Metabolic rate; Nose; Respirometry; Severity of Illness Index; Skin diseases; Therapeutic applications; Time Factors; Torpor; Up-Regulation; Water loss; Water Loss, Insensible; White-nose syndrome; Wildlife
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00058.2017

Fungal diseases of wildlife typically manifest as superficial skin infections but can have devastating consequences for host physiology and survival. White-nose syndrome (WNS) is a fungal skin disease that has killed millions of hibernating bats in North America since 2007. Infection with the fungus causes bats to rewarm too often during hibernation, but the cause of increased arousal rates remains unknown. On the basis of data from studies of captive and free-living bats, two mechanistic models have been proposed to explain disease processes in WNS. Key predictions of both models are that WNS-affected bats will show ) higher metabolic rates during torpor (TMR) and ) higher rates of evaporative water loss (EWL). We collected bats from a WNS-negative hibernaculum, inoculated one group with , and sham-inoculated a second group as controls. After 4 mo of hibernation, TMR and EWL were measured using respirometry. Both predictions were supported, and our data suggest that infected bats were more affected by variation in ambient humidity than controls. Furthermore, disease severity, as indicated by the area of the wing with UV fluorescence, was positively correlated with EWL, but not TMR. Our results provide the first direct evidence that heightened energy expenditure during torpor and higher EWL independently contribute to WNS pathophysiology, with implications for the design of potential treatments for the disease.