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1 June 2014 Genetic assignment tests reveal dispersal of white-tailed deer: implications for chronic wasting disease
Michelle L. Green, Mary Beth Manjerovic, Nohra Mateus-Pinilla, Jan Novakofski
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Investigating sources of infection for new disease cases is critical to effective disease management. Chronic wasting disease (CWD) was first detected among white-tailed deer (Odocoileus virginianus) in Illinois in 2002. Although CWD was focused in northern Illinois, 4 infected deer were sampled in 2011 from locations greater than 100 km south of the disease focus. We used assignment tests (Geneclass2 and Oncor) to determine a likely genetic source location for infected deer. Our baseline data set consisted of 310 deer sampled from 10 locations. From the baseline data set, we determined the most likely genetic source location of 15 CWD-positive and 15 CWD-negative deer. A total of 17–20% back-assigned to their sample location as their most likely genetic source location and the remainder of the animals cross-assigned to another location. The average distance between locations was 41.4 km for Geneclass2 and 43.4 km for Oncor (range 0.0–90.8 km). Distances between source and sampling locations were similar for positive and negative animals. Distances for males were greater than those for females using Oncor, but there was no difference in distance based on age. Because there are few barriers to gene flow for white-tailed deer, managers should reduce movement of deer in CWD-infected areas in an effort to reduce direct and indirect transmission of CWD.

The movement of individual animals, particularly dispersal and migration of infected hosts (Hosseini et al. 2006), influences the spatial spread of directly transmitted diseases (Grenfell et al. 2001; Russell et al. 2004; Hosseini et al. 2006). Directly transmitted diseases move through populations of free-ranging animals by waves (Russell et al. 2004). These waves travel away from the original site of infection and have been explained by the spread of infective “spark” individuals that move from core disease areas to new locations (Grenfell et al. 2001).

Chronic wasting disease (CWD—Williams and Young 1980) is a fatal neurological disease of North American cervids. CWD is a transmissible spongiform encephalopathy that causes the accumulation of abnormally folded cellular prion proteins that ultimately lead to lesions in the brain. As evidenced by the emergence of the disease in recent years, CWD is considered the most contagious member of the prion family (Gilch et al. 2011). Although transmission mechanisms are still not completely understood, infection primarily occurs by horizontal transmission through direct contact (Miller et al. 1998, 2000; Miller and Williams 2003) and indirect exposure to prions in the environment (Miller and Williams 2003; Mathiason et al. 2006; Angers et al. 2009; Haley et al. 2009; Tamgüney et al. 2009). Vertical transmission from mother to fetus also may occur in white-tailed deer (Odocoileus virginianusNalls et al. 2013), but this transmission route is thought to be rare (Miller and Williams 2003). Clinical signs are not detectable until at least a year following exposure (Williams and Miller 2002). As animals advance through the disease, their infectivity increases and they shed more infectious prions into their environment (Williams and Miller 2002). Because CWD is contagious and invariably fatal, wildlife managers are concerned with limiting prevalence and geographic spread.

Prevalence of CWD has been attributed at least partially to animal movement (Conner and Miller 2004). Deer exhibit a variety of movement behaviors (see review in Stewart et al. 2011) that contribute to disease transmission and spread. Long-distance and frequent movements are of obvious concern to disease management, but resident deer exhibiting minimal movement within a home range have the potential to severely contaminate their environment through prion shedding (Williams and Miller 2002; Sigurdson and Miller 2003; Mathiason et al. 2006; Angers et al. 2009; Tamgüney et al. 2009; Haley et al. 2011). In areas where infected deer have shed prions into the environment, other deer will be at risk of CWD infection from environmental contamination (Miller et al. 1998). Given the fact that prions persist in the environment for years after initial contamination, infection risk also persists over time (Miller et al. 2004). If infected home ranges have a steady occupancy rate, new occupants are at risk of becoming infected and shedding additional prions into the environment, effectively producing a continuous contribution of prions. Such a state of prion load in the environment not only has the potential to infect animals that move into the area and stay for an extended period of time, but also those that visit the site for a short time and carry the infection to a new location after migration or dispersal events.

In Illinois, wildlife managers have been working to control the spread of CWD since it was first detected in November 2002 (Mateus-Pinilla et al. 2013; Manjerovic et al. 2014). The 1st case, an adult female white-tailed deer, was culled in Boone County (Fig. 1). Since the 1st detection, a disease focus has established along the border of Boone and Winnebago counties. Many of the CWD-infected animals sampled since 2002 were collected in the disease focus but the geographic range of CWD has spread. As of May 2013, CWD-infected deer have been detected in 12 counties (Fig. 1). Wildlife managers in Illinois employ a 2-part management program for disease surveillance and control (Manjerovic et al. 2014). Much of the disease detection and surveillance is accomplished by testing deer culled by recreational hunters. Sampling hunter-harvested deer allows for testing over a large geographic range and increases the chance of identifying infected animals as the disease spreads. In 2011, recreational hunters culled a small number of potential CWD-positive spark cases in La Salle and Grundy counties, far south of the disease focus (approximately 100–125 km [Fig. 1]).

Fig. 1.