Submitted to: Journal of Wildlife Diseases
Publication Type: Peer reviewed journal
Publication Acceptance Date: 10/14/2009
Publication Date: N/A
Citation: Interpretive Summary: Chronic wasting disease or CWD is a fatal brain disorder of deer and elk in some areas of North America. Although the disease is transmitting among deer, relative susceptibility and incubation time may be associated with genetic changes in the gene for the prion protein, the disease marker. Mule deer congregate in matrilineal groups, with female offspring often remaining with their dams. Genetic markers can be used to identify related deer, providing information on relatednesss among wild deer. In this study, we examined the prion genotypes and maternal genetic markers in samples from 250 mule deer from 3 discrete sites in the Rocky Mountains of Colorado. There were fewer CWD positive deer than expected in one genetic group, confirming the observation that deer with this genotype may be at lower risk of CWD or may have a longer incubation period. There was no evidence that male deer related to a positive buck were at increased risk of CWD. However, CWD-positive females tended to be more closely related to each other than expected. This finding supports the model that once a member of a female group becomes infected with CWD, the disease is passed to other females within the group. The use of molecular markers in CWD epidemiology studies provides useful data on transmission of this disease among free ranging deer.
Technical Abstract: Chronic wasting disease is a transmissible spongiform encephalopathy or prion disease of farmed and free ranging mule deer, white tailed deer, Rocky Mountain elk, and moose in some areas of the United States. The disease is enzootic in herds of free ranging mule deer in the Rocky Mountain National Park and contiguous areas. The mode of transmission is not known but models based on surveillance of hunter killed deer suggest that males transmit disease when traveling among groups of females during the breeding season. Deer in matrilineal groups, once infected, spread disease to related members of the group sharing foraging ranges. Within infected groups, homozygosity for the PRNP allele encoding serine at codon 225 appears to be associated with higher infection rates. In this study, the models were tested on 3 populations of mule deer with non-contiguous ranges. Mitochondrial markers were used to estimated kinship and PRNP genotype was determined by sequencing of the open reading frame of PRNP. Chronic wasting disease positive deer were not genetically distinct from negative deer when evaluated by multilocus microsatellite genotypes. PRNP genotyping results supported the earlier observation that codon 225 serine homozygosity was associated with higher disease rates than codon 225 serine/phenylalanine heterozygotes but only among male deer. CWD-positive female deer tended to be more closely related to each other than expected; the trend was not found in male deer. Because male mule deer do not form kin groups and do not tend to breed in groups of does to which they are related, it was not surprising that there was no increased relatedness among CWD-positive males. Addition of molecular genetic tools to classical epidemiology studies should be useful in understanding the patterns of spread of CWD in mule deer in North Central Colorado.