Genetic assessment of environmental features that influence deer dispersal: implications for prion‐infected populations

Abstract

The landscape can influence host dispersal and density, which in turn, affect infectious disease transmission, spread, and persistence. Understanding how the landscape influences wildlife dispersal and pathogen epidemiology can enhance the efficacy of disease management in natural populations. We applied landscape genetics to examine relationships among landscape variables, dispersal of white-tailed deer hosts and transmission/spread of chronic wasting disease (CWD), a fatal prion encephalopathy. Our focus was on quantifying movements and population structure of host deer in infected areas as a means of predicting the spread of this pathology and promoting its adaptive management. We analyzed microsatellite genotypes of CWD-infected and uninfected deer from two disease foci (Southern Wisconsin, Northern Illinois). We quantified gene flow and population structure using F ST , assignment tests, and spatial autocorrelation analyses. Gene flow estimates were then contrasted against a suite of landscape variables that potentially mediate deer dispersal. Forest fragmentation and grassland connectivity promoted deer movements while rivers, agricultural fields and large urbanized areas impeded movement. Landscape variables, deer dispersal, and disease transmission covaried significantly and positively in our analyses. Habitats with elevated host gene flow supported the concept of dispersalmediated CWD transmission by reflecting a concomitant, rapid CWD expansion. Large, interrelated social groups isolated by movement barriers overlapped disease foci, suggesting that philopatry exacerbated CWD transmission. Our results promote adaptive management of CWD by predicting patterns of its spread and identifying habitats at risk for invasion. Further, our landscape genetics approach underscores the significance of topography and host behavior in wildlife disease transmission.Electronic supplementary material The online version of this article (

Enhancement of Risk for Lyme Disease by Landscape Connectivity, New York, New York, USA

“…Furthermore, the amount of water surrounding the park negatively affected I. scapularis tick density, suggesting that water might also serve as a barrier for deer movement into particular parks and could limit tick population persistence. Our findings are consistent with studies that have found agricultural fields, large urbanized areas ( 27 ), and a combination of landscape features with low permeability, such as waterways and roads, to impede deer movement ( 29 ), potentially slowing tick expansion.…”

Fine‐scale spatial genetic structure of deer in a suburban landscape

“…Our results are consistent with the expectation that deer populations are spatially structured, and echo the findings of other genetics studies of deer populations at broader spatial scales (Blanchong et al , Kelly et al ). In populations with sex‐biased dispersal and female philopatry, high levels of genetic diversity are maintained by partitioning variation among social groups (Blanchong et al ).…”

Influence of the geographic distribution of prion protein gene sequence variation on patterns of chronic wasting disease spread in white-tailed deer (Odocoileus virginianus)

“…Previous studies with a population genetics approach have utilized neutral markers (i.e. microsatellites) to correlate patterns of genetic ancestry with potential for disease spread [51,52]. In areas such as northern Illinois, there are few barriers to dispersal and population genetic studies have found the deer population to be relatively homogenous [52].…”

“…Though neutral markers suggest that white-tailed deer in northern Illinois are fairly homogeneous in their genetic structure [52], comparisons of the proportion of protective haplotypes at various geographic scales demonstrated that they are not evenly distributed throughout the population. It is possible that the geographic distribution of PRNP haplotypes may vary due to stochastic factors such as genetic drift.…”