TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: THE ROLE OF GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL CONTAMINATION IN DISEASE CONTROL
Location: Animal Diseases Research
Title: Molecular genealogy tools for white-tailed deer with chronic wasting disease
| Ernest, H - UC DAVIS |
| Hoar, B - UC DAVIS |
| Well, J - UC DAVIS |
| O'Rourke, Katherine |
Submitted to: Canadian Journal of Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 14, 2009
Publication Date: May 4, 2010
Citation: Ernest, H., Hoar, B.R., Well, J.A., Orourke, K.I. 2010. Molecular genealogy tools for white-tailed deer with chronic wasting disease. Canadian Journal of Veterinary Research. 74(2):152-156.
Interpretive Summary: Chronic wasting disease (CWD) is a fatal degenerative brain disorder of deer, elk, and moose. The disease appears to be caused by prions, which are abnormally folded proteins formed in the lymph nodes and brain of infected deer after contact with an infected animal. The amount of time needed for transmission of disease is not known. White tailed deer live in family groups, with adult females and their female offspring spending much of the year together. Males leave the family group at adolescence and travel among groups during the breeding season. This social pattern supports a model in which disease is spread among females by repeated contact during the year and among groups by males visiting many groups during each breeding season. In this study, we developed a set of genetic tools to examine the family groups in a herd of white tailed deer in a fenced area in Nebraska. The density of deer was unusually high (more than 200 deer in 1.2 square miles, compared to less than 30 deer per square mile in forested areas of Wisconsin. Also, the rate of CWD was 50%, much higher than the 5% to 20% found in free ranging deer. We also tested a sample of deer ranging within 20 km of the fenced area. We tested the hypothesis that female deer within a family unit with a CWD-positive animal would have higher disease rates than male deer and that pairs of related animals would be more likely to have disease than unrelated deer. We used a large set of DNA markers to identify parents, siblings, aunts, and grandparents of the infected deer. Under these conditions, we did not see an increased rate of CWD among related deer. This finding may be due to the high density of deer or to the practice of providing food and water for the deer at various times of the year, encouraging the tight grouping of multiple families at the common feed and water areas. The DNA markers will be useful in examining herds of wild deer in more typical social groups.
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy or prion disease of deer, elk, and moose. CWD is a fatal neurologic disease with a long preclinical incubation period, during which the disease is probably transmitted to healthy animals through direct exposure or environmental contamination by the causative agent. Although the routes of infection are not known, the saliva and blood of deer contain the agent. Deer live in matrilineal groups as fawns, with males leaving the group at adolescence. The does and female progeny remain together much of the year. Adult males travel among groups during the breeding season, visiting as many groups as possible. This spatial grouping supports a model in which disease is spread by repeated exposure among females in a matrilineal group and transmitted among groups by males during the breeding season. In this study, we applied molecular genetic tools to reconstruct family relationship for a fenced herd of deer with a high CWD prevalence and for nearby free-ranging herds. We tested the hypotheses that females within first order (full sibs or parent-offspring) kin groups containing a CWD-positive adult female were more likely than males to test CWD positive and that dyads of CWD-positive individuals related in first order occurred at a higher frequency than predicted by chance alone. WE used a panel of 39 microsatellite markers and a set of mitochondrial sequences to provide kinship data for all deer in the fenced facility (n=200) and a sample of deer generally ranging within 20 km of the facility. In this system, we found no association between kinship and CWD status, although it is likely that the results were impacted by the high population density (200 deer in 1.2 square miles), the concentrated sources of feed and water during some times of the year, and the high disease prevalence. However, the study identifies a panel of genetic markers suitable for identifying first degree and second degree relatives. This panel will be useful in examining the disease patterns in the more typical settings of free ranging deer in areas with a density of fewer than 30 deer per square mile and disease prevalence of 15% to 30%.