Prelude to a panzootic: Gene flow and immunogenetic variation in northern little brown myotis vulnerable to bat white-nose syndrome

The fungus that causes bat white-nose syndrome (WNS) recently leaped from eastern North America to the Pacific Coast. The pathogen's spread is associated with the genetic population structure of a host (Myotis lucifugus). To understand the fine-scale neutral and immunogenetic variation among northern populations of M. lucifugus, we sampled 1142 individuals across the species' northern range. We used genotypes at 11 microsatellite loci to reveal the genetic structure of, and directional gene flow among, populations to predict the likely future spread of the pathogen in the northwest and to estimate effective population size (Ne). We also pyrosequenced the DRB1-like exon 2 of the class II major histocompatibility complex (MHC) in 160 individuals to explore immunogenetic selection by WNS. We identified three major neutral genetic clusters: Eastern, Montane Cordillera (and adjacent sampling areas), and Haida Gwaii, with admixture at intermediate areas and significant substructure west of the prairies. Estimates of Ne were unexpectedly low (289-16 000). Haida Gwaii may provide temporary refuge from WNS, but the western mountain ranges are not barriers to its dispersal in M. lucifugus and are unlikely to slow its spread. Our major histocompatibility complex (MHC) data suggest potential selection by WNS on the MHC, but gene duplication limited the immunogenetic analyses.