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.
Summary The management of infectious diseases is an important conservation concern for a growing number of wildlife species. However, effective disease control in wildlife is challenging because feasible management options are often lacking. White‐nose syndrome (WNS) is an infectious disease of hibernating bats that currently threatens several North American species with extinction. Currently, no effective treatments exist for WNS. We conducted a laboratory experiment to test the efficacy of probiotic treatment with Pseudomonas fluorescens, a bacterium that naturally occurs on bats, to reduce disease severity and improve survival of little brown bats Myotis lucifugus exposed to Pseudogymnoascus destructans, the fungal pathogen that causes WNS. We found that application of the probiotic bacteria at the time of fungal infection reduced several measures of disease severity and increased survival, whereas bacterial treatment prior to pathogen exposure had no effect on survival and worsened disease severity. Synthesis and applications. Our results suggest that probiotic treatment with Ps. fluorescens has potential for white‐nose syndrome disease management, but the timing of application is critical and should coincide with natural exposure of bats to P. destructans. These results add to the growing knowledge of how natural host microbiota can be implemented as a biocontrol treatment to influence disease outcomes.
Processes associated with recovery of survivors are understudied components of wildlife infectious diseases. White-nose syndrome (WNS) in bats provides an opportunity to study recovery of disease survivors, understand implications of recovery for individual energetics, and assess the role of survivors in pathogen transmission. We documented temporal patterns of recovery from WNS in little brown bats (Myotis lucifugus) following hibernation to test the hypotheses that: (1) recovery of wing structure from WNS matches a rapid time scale (i.e. approximately 30 days) suggested by data from free-ranging bats; (2) torpor expression plays a role in recovery; (3) wing physiological function returns to normal alongside structural recovery; and (4) pathogen loads decline quickly during recovery. We collected naturally infected bats at the end of hibernation, brought them into captivity, and quantified recovery over 40 days by monitoring body mass, wing damage, thermoregulation, histopathology of wing biopsies, skin surface lipids and fungal load. Most metrics returned to normal within 30 days, although wing damage was still detectable at the end of the study. Torpor expression declined overall throughout the study, but bats expressed relatively shallow torpor boutswith a plateau in minimum skin temperatureduring intensive healing between approximately days 8 and 15. Pathogen loads were nearly undetectable after the first week of the study, but some bats were still detectably infected at day 40. Our results suggest that healing bats face a severe energetic imbalance during early recovery from direct costs of healing and reduced foraging efficiency. Management of WNS should not rely solely on actions during winter, but should also aim to support energy balance of recovering bats during spring and summer.
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