Article impact statement: Data sharing and coordinated monitoring are needed to assess species' response to threats to inform conservation planning at relevant scales.

Rapid evolution of advantageous traits following abrupt environmental change can help populations recover from demographic decline. However, for many introduced diseases affecting longer‐lived, slower reproducing hosts, mortality is likely to outpace the acquisition of adaptive de novo mutations. Adaptive alleles must therefore be selected from standing genetic variation, a process that leaves few detectable genomic signatures. Here, we present whole genome evidence for selection in bat populations that are recovering from white‐nose syndrome (WNS). We collected samples both during and after a WNS‐induced mass mortality event in two little brown bat populations that are beginning to show signs of recovery and found signatures of soft sweeps from standing genetic variation at multiple loci throughout the genome. We identified one locus putatively under selection in a gene associated with the immune system. Multiple loci putatively under selection were located within genes previously linked to host response to WNS as well as to changes in metabolism during hibernation. Results from two additional populations suggested that loci under selection may differ somewhat among populations. Through these findings, we suggest that WNS‐induced selection may contribute to genetic resistance in this slowly reproducing species threatened with extinction.

Rapid evolution of advantageous traits following abrupt environmental change can help populations grow and avoid extinction through evolutionary rescue. Here, we provide the first genetic evidence for rapid evolution in bat populations affected by white-nose syndrome (WNS). By comparing genetic samples from before and after little brown bat populations were decimated by WNS, we identified signatures of soft selection on standing genetic variation. This selection occurred at multiple loci in genes linked to hibernation behavior rather than immune function, suggesting that differences in hibernation strategy have allowed these bats to survive infection with WNS. Through these findings, we suggest that evolutionary rescue can be a conservationrelevant process even in slowly reproducing taxa threatened with extinction.

Emerging infectious diseases have resulted in severe population declines across diverse taxa. In some instances, despite attributes associated with high extinction risk, disease emergence and host declines are followed by host stabilisation for unknown reasons. While host, pathogen, and the environment are recognised as important factors that interact to determine host–pathogen coexistence, they are often considered independently. Here, we use a translocation experiment to disentangle the role of host traits and environmental conditions in driving the persistence of remnant bat populations a decade after they declined 70–99% due to white‐nose syndrome and subsequently stabilised. While survival was significantly higher than during the initial epidemic within all sites, protection from severe disease only existed within a narrow environmental space, suggesting host traits conducive to surviving disease are highly environmentally dependent. Ultimately, population persistence following pathogen invasion is the product of host–pathogen interactions that vary across a patchwork of environments.

Reduced populations of Myotis lucifugus (Little Brown Myotis) devastated by white-nose syndrome (WNS) persist in eastern North America. Between 2009 and 2013, we recaptured 113 marked individuals that survived between 1 and 6 winters in New England since the arrival of WNS. We also observed signs of reproductive success in 57 recaptured bats.