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Abstract Disease results from interactions among the host, pathogen, and environment. Inoculation trials can quantify interactions among these players and explain aspects of disease ecology to inform management in variable and dynamic natural environments. White-nose Syndrome, a disease caused by the fungal pathogen, Pseudogymnoascus destructans ( Pd ), has caused severe population declines of several bat species in North America. We conducted the first experimental infection trial on the tri-colored bat, Perimyotis subflavus , to test the effect of temperature and humidity on disease severity. We also tested the effects of temperature and humidity on fungal growth and persistence on substrates. Unexpectedly, only 37% (35/95) of bats experimentally inoculated with Pd at the start of the experiment showed any infection response or disease symptoms after 83 days of captive hibernation. There was no evidence that temperature or humidity influenced infection response. Temperature had a strong effect on fungal growth on media plates, but the influence of humidity was more variable and uncertain. Designing laboratory studies to maximize research outcomes would be beneficial given the high costs of such efforts and potential for unexpected outcomes. Understanding the influence of microclimates on host–pathogen interactions remains an important consideration for managing wildlife diseases, particularly in variable environments. 

The persistence of populations declining from novel stressors depends, in part, on their ability to respond by trait change via evolution or plasticity. White‐nose syndrome (WNS) has caused rapid declines in several North America bat species by disrupting hibernation behaviour, leading to body fat depletion and starvation. However, some populations ofMyotis lucifugusnow persist withWNSby unknown mechanisms.

We examined whether persistence ofM. lucifiguswithWNScould be explained by increased body fat in early winter, which would allow bats to tolerate the increased energetic costs associated withWNS. We also investigated whether bats were escaping infection or resistant to infection as an alternative mechanism explaining persistence.

We measured body fat in early and late winter during initialWNSinvasion and 8 years later at six sites where bats are now persisting. We also measured infection prevalence and intensity in persisting populations.

Infection prevalence was not significantly lower than observed in declining populations. However, at two sites, infection loads were lower than observed in declining populations. Body fat in early winter was significantly higher in four of the six persisting populations than duringWNSinvasion.

Physiological models of energy use indicated that these higher fat stores could reduceWNSmortality by 58%–70%. These results suggest that differences in fat storage and infection dynamics have reduced the impacts ofWNSin many populations. Increases in body fat provide a potential mechanism for management intervention to help conserve bat populations.