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Population genetic structure of a common host predictsthe spread of white-nose syndrome, an emerginginfectious disease in batsARYN P. WILDER, THOMAS H. KUNZ and MICHAEL D. SORENSONDepartment of Biology, Boston University, 5 Cummington Mall, Boston, MA 02215, USAAbstractLandscape complexity influences patterns of animal dispersal, which in turn may affectboth gene flow and the spread of pathogens. White-nose syndrome (WNS) is an intro-duced fungal disease that has spread rapidly throughout eastern North America, caus-ing massive mortality in bat populations. We tested for a relationship between thepopulation genetic structure of the most common host, the little brown myotis (Myotislucifugus), and the geographic spread of WNS to date by evaluating logistic regressionmodels of WNS risk among hibernating colonies in eastern North America. Wehypothesized that risk of WNS to susceptible host colonies should increase with bothgeographic proximity and genetic similarity, reflecting historical connectivity, toinfected colonies. Consistent with this hypothesis, inclusion of genetic distancebetween infected and susceptible colonies significantly improved models of diseasespread, capturing heterogeneity in the spatial expansion of WNS despite low levels ofgenetic differentiation among eastern populations. Expanding our genetic analysis tothe continental range of little brown myotis reveals strongly contrasting patterns ofpopulation structure between eastern and western North America. Genetic structureincreases markedly moving westward into the northern Great Plains, beyond the cur-rent distribution of WNS. In western North America, genetic differentiation of geo-graphically proximate populations often exceeds levels observed across the entireeastern region, suggesting infrequent and/or locally restricted dispersal, and thus rela-tively limited opportunities for pathogen introduction in western North America.Taken together, our analyses suggest a possibly slower future rate of spread of theWNS pathogen, at least as mediated by little brown myotis.Keywords: emerging infectious disease, fungal pathogen, population genetic structure,RAD-seq, white-nose syndromeReceived 18 February 2015; revision received 18 September 2015; accepted 21 September 2015IntroductionThe spatial spread of emerging infectious diseases isshaped in part by complex landscapes, which influencehost dispersal and in turn the genetic structure of hostpopulations. The geographic structure of genetic varia-tion in hosts and pathogens can thus shed light on dis-ease dynamics across space and time (Archieet al.2009;Biek & Real 2010). Genetic variation in pathogens hasbeen used to reveal sources of infection, reservoir hostsor refugia (Girardet al.2004; Rambautet al.2008), aswell as invasion and spatial diffusion dynamics(Holmes 2004; Bieket al.2007; Tianet al.2015). Lesscommonly, population genetics has been used to mea-sure the connectivity of host populations over heteroge-neous landscapes to understand rates and routes ofhost-mediated pathogen dispersal (Blanchonget al.2008; Rioux Paquetteet al.2014). We assessed host pop-ulation genetic structure to test whether historical pat-terns of connectivity and gene flow are correlated withthe spatial spread to date of white-nose syndromeCorrespondence: Aryn P. Wilder, Fax: +1 (617) 353 6340;E-mail: apw@bu.edu©2015 John Wiley & Sons LtdMolecular Ecology (2015)24, 5495–5506doi: 10.1111/mec.13396