Identifying the sources of ongoing and novel disease outbreaks is critical for understanding the diffusion of epizootic diseases. Identifying infection sources is difficult when few physical differences separate individuals with different origins. Genetic assignment procedures show great promise for assessing transmission dynamics in such situations. Here, we use genetic assignment tests to determine the source of chronic wasting disease infections in free-ranging white-tailed deer (Odocoileus virginianus) populations. Natural dispersal is thought to facilitate the geographic diffusion of chronic wasting disease, but egression from captive cervid populations represents an alternative source of infection that is difficult to detect due to physical similarities with wild deer. Simulated reference populations were created based on allele frequencies from 1,912 empirical microsatellite genotypes collected in four sampling subregions and five captive facilities. These reference populations were used to assess the likelihood of ancestry and assignment of 1,861 free-ranging deer (1,834 noninfected and 27 infected) and 51 captive individuals to captive or wild populations. The ancestry (Q) and assignment scores (A) for free-ranging deer to wild populations were high (average Q_wild = 0.913 and average A_wild = 0.951, respectively), but varied among subregions (Q_wild = 0.800–0.947, A_wild = 0.857–0.976). These findings suggest that captive egression and admixture are rare, but risk may not be spatially uniform. Ancestry and assignment scores for two free-ranging deer with chronic wasting disease sampled in an area where chronic wasting disease was previously unobserved in free-ranging herds indicated a higher likelihood of assignment and proportion of ancestry attributable to captive populations. While we cannot directly assign these individuals to infected facilities, these findings suggest that rare egression events may influence the epizootiology of chronic wasting disease in free-ranging populations. Continued disease surveillance and genetic analyses may further elucidate the relative disease risk attributable to captive and wild sources.