Characterization of the long-distance dispersal kernel of white-tailed deer and evaluating its impact on chronic wasting disease spread in Wisconsin
Chronic wasting disease (CWD) is a fatal neurodegenerative disease infecting cervids. It is highly contagious and caused by misfolded prions that propagate via templated conformational conversion of the cervid’s normal prion protein. Prevalence of CWD in free-ranging deer in North America is mostly low, but in some regions local prevalence has reached 80%. CWD prions can be transmitted via direct contact with infected individuals or indirectly through the environment. Infected individuals shed prions through feces, urine, saliva or carcasses, and prions have long environmental persistence. Long-distance dispersal of infected deer poses a significant risk for CWD spread. We propose an integrodifference equation (IDE) model to capture CWD dynamics and the consequences of long-distance dispersal behavior in white-tailed deer (WTD, Odocoileus virginianus ). A diffusion-settling model characterizes long-distance dispersal kernels, accommodating hypothetical dispersal behaviors through time-dependent settling rate functions. Three new closed-form dispersal kernels are approximated using Laplace’s method and parameterized with GPS location data collected from WTD in Wisconsin, USA. Settling rates reflecting ongoing sensitivity to stimuli which prompt deer to disperse from their natal home range give the most supported long-distance dispersal kernel. Impact of long-distance dispersal on CWD spread is quantified using the IDE model. At high population densities, long-distance dispersal can magnify CWD spread by a factor of four. At lower population densities single infected individuals cannot initiate an outbreak, but CWD may still spread due to the accumulation of environmental hazard from prions behind the wave of invasion, possibly presenting substantial management challenges.