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

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 disturban

White-Nose Syndrome Disease Severity and a Comparison of Diagnostic Methods

White-nose syndrome is caused by the fungus Pseudogymnoascus destructans and has killed millions of hibernating bats in North America but the pathophysiology of the disease remains poorly understood. Our objectives were to (1) assess non-destructive diagnostic methods for P. destructans infection compared to histopathology, the current gold-standard, and (2) to evaluate potential metrics of disease severity. We used data from three captive inoculation experiments involving 181 little brown bats (Myotis lucifugus) to compare histopathology, quantitative PCR (qPCR), and ultraviolet fluorescence as diagnostic methods of P. destructans infection. To assess disease severity, we considered two histology metrics (wing area with fungal hyphae, area of dermal necrosis), P. destructans fungal load (qPCR), ultraviolet fluorescence, and blood chemistry (hematocrit, sodium, glucose, pCO2, and bicarbonate). Quantitative PCR was most effective for early detection of P. destructans, while all three methods were comparable in severe infections. Correlations among hyphae and necrosis scores, qPCR, ultraviolet fluorescence, blood chemistry, and hibernation duration indicate a multi-stage pattern of disease. Disruptions of homeostasis occurred rapidly in late hibernation. Our results provide valuable information about the use of non-destructive techniques for monitoring, and provide novel insight into the pathophysiology of white-nose syndrome, with implications for developing and implementing potential mitigation strategies