Conspecific disturbance contributes to altered hibernation patterns in bats with white-nose syndrome

Abstract The emerging wildlife disease white-nose syndrome (WNS) affects both physiology and behaviour of hibernating bats. Infection with the fungal pathogen Pseudogymnoascus destructans ( Pd ), the first pathogen known to target torpid animals, causes an increase in arousal frequency during hibern...

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Bibliographic Details
Published in:Physiology & behavior 2015-03, Vol.140, p.71-78
Main Authors: Turner, James M, Warnecke, Lisa, Wilcox, Alana, Baloun, Dylan, Bollinger, Trent K, Misra, Vikram, Willis, Craig K.R
Format: Article
Language:English
Subjects:
Animals
Arousal - physiology
Behaviour
Body Temperature - physiology
Chi-Square Distribution
Chiroptera - physiology
Communicable Diseases, Emerging - microbiology
Communicable Diseases, Emerging - physiopathology
Communicable Diseases, Emerging - veterinary
Hibernation
Hibernation - physiology
Mycoses - microbiology
Mycoses - physiopathology
Mycoses - veterinary
Myotis lucifugus
Nose - microbiology
Psychiatry
Rewarming rate
Skin
Time Factors
Torpor
Torpor - physiology
White-nose syndrome
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Summary:Abstract The emerging wildlife disease white-nose syndrome (WNS) affects both physiology and behaviour of hibernating bats. Infection with the fungal pathogen Pseudogymnoascus destructans ( Pd ), the first pathogen known to target torpid animals, causes an increase in arousal frequency during hibernation, and therefore premature depletion of energy stores. Infected bats also show a dramatic decrease in clustering behaviour over the winter. To investigate the interaction between disease progression and torpor expression we quantified physiological (i.e., timing of arousal, rewarming rate) and behavioural (i.e., arousal synchronisation, clustering) aspects of rewarming events over four months in little brown bats ( Myotis lucifugus ) experimentally inoculated with Pd . We tested two competing hypotheses: 1) Bats adjust arousal physiology adaptively to help compensate for an increase in energetically expensive arousals. This hypothesis predicts that infected bats should increase synchronisation of arousals with colony mates to benefit from social thermoregulation and/or that solitary bats will exhibit faster rewarming rates than clustered individuals because rewarming costs fall as rewarming rate increases. 2) As for the increase in arousal frequency, changes in arousal physiology and clustering behaviour are maladaptive consequences of infection. This hypothesis predicts no effect of infection or clustering behaviour on rewarming rate and that disturbance by normothermic bats contributes to the overall increase in arousal frequency. We found that arousals of infected bats became more synchronised than those of controls as hibernation progressed but the pattern was not consistent with social thermoregulation. When a bat rewarmed from torpor, it was often followed in sequence by up to seven other bats in an arousal “cascade”. Moreover, rewarming rate did not differ between infected and uninfected bats, was not affected by clustering and did not change over time. Our results support our second hypothesis and suggest that disturbance, not social thermoregulation, explains the increased synchronisation of arousals. Negative pathophysiological effects of WNS on energy conservation may therefore be compounded by maladaptive changes in behaviour of the bats, accelerating fat depletion and starvation.
ISSN:0031-9384
1873-507X
DOI:10.1016/j.physbeh.2014.12.013