scholarly journals Control and Surveillance Operations to Prevent Chronic Wasting Disease Establishment in Free-Ranging White-Tailed Deer in Québec, Canada

Animals ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 283 ◽  
Author(s):  
Marianne Gagnier ◽  
Isabelle Laurion ◽  
Anthony J. DeNicola

Chronic wasting disease (CWD), a degenerative and fatal prion disease affecting cervids, was detected for the first time in the province of Québec, Canada, in a red deer (Cervus elaphus) farm in the Laurentides region on 10 September 2018. To assess CWD prevalence and control the disease in the free-ranging white-tailed deer (Odocoileus virginianus) population, a response plan including enhanced surveillance, population control, regulatory measures, and public outreach was deployed by the Ministry of Forests, Wildlife, and Parks (MFFP). In the 401 km2 white-tailed deer control area, a total of 750 free-ranging white-tailed deer were culled over 70 days, from 22 September to 15 December 2018. Of the culled deer, 534 were tested for CWD. We also tested for CWD a total of 447 white-tailed deer hunted from the enhanced surveillance zone and 2584 free-ranging white-tailed deer harvested outside this zone. Regulations were applied to prevent the spread of the disease through movements of infected animals harvested by hunters. Although no case of CWD was detected in free-ranging cervids in Québec in 2018, this does not confirm the absence of the disease in these populations. However, the results suggest that if CWD is present, few free-ranging cervids are infected, making it possible to prevent its establishment in the province of Québec.

2013 ◽  
Vol 49 (2) ◽  
pp. 270-278 ◽  
Author(s):  
Ryan J. Monello ◽  
Jenny G. Powers ◽  
N. Thompson Hobbs ◽  
Terry R. Spraker ◽  
Katherine I. O’Rourke ◽  
...  

2008 ◽  
Vol 89 (5) ◽  
pp. 1324-1328 ◽  
Author(s):  
Matteo Perucchini ◽  
Karen Griffin ◽  
Michael W. Miller ◽  
Wilfred Goldmann

Variation in PrP prion gene sequence appears to modulate susceptibility to chronic wasting disease (CWD), a naturally occurring prion disease affecting four North American species of the family Cervidae. Wapiti (Cervus elaphus nelsoni) PrP is polymorphic at codon 132 [methionine (M) or leucine (L)]. We genotyped 171 samples, collected between 2002 and 2005 from CWD-infected and uninfected wapiti from three free-ranging populations in Colorado, USA, to study influences of PrP polymorphisms on CWD susceptibility further. Overall genotype frequencies for 124 apparently uninfected animals were 65.3 % MM132, 32.3 % ML132 and 2.4 % LL132; for 47 CWD-infected animals, these frequencies were 70.2 % MM132, 27.7 % ML132 and 2.1 % LL132. Surprisingly, our data revealed that, among recent (approx. 2002–2005) CWD cases detected in free-ranging Colorado wapiti, the three PrP codon 132 genotypes were represented in proportion to their abundance in sampled populations (P≥0.24) and all three genotypes showed equivalent susceptibility to infection.


1999 ◽  
Vol 80 (10) ◽  
pp. 2765-2679 ◽  
Author(s):  
K. I. O’Rourke ◽  
T. E. Besser ◽  
M. W. Miller ◽  
T. F. Cline ◽  
T. R. Spraker ◽  
...  

The PrP gene encodes the putative causative agent of the transmissible spongiform encephalopathies (TSEs), a heterogeneous group of fatal, neurodegenerative disorders including human Creutzfeldt–Jakob disease, bovine spongiform encephalopathy, ovine scrapie and chronic wasting disease (CWD) of North American deer and elk. Polymorphisms in the PrP gene are associated with variations in relative susceptibility, pathological lesion patterns, incubation times and clinical course of TSEs of humans, mice and sheep. Sequence analysis of the PrP gene from Rocky Mountain elk showed only one amino acid change (Met to Leu at cervid codon 132). Homozygosity for Met at the corresponding polymorphic site (Met to Val) in humans (human codon 129) predisposes exposed individuals to some forms of Creutzfeldt–Jakob disease. In this study, Rocky Mountain elk homozygous for PrP codon 132 Met were over-represented in both free- ranging and farm-raised CWD-affected elk when compared to unaffected control groups.


2017 ◽  
Vol 114 (46) ◽  
pp. 12208-12212 ◽  
Author(s):  
Ryan J. Monello ◽  
Nathan L. Galloway ◽  
Jenny G. Powers ◽  
Sally A. Madsen-Bouterse ◽  
William H. Edwards ◽  
...  

Pathogens can exert a large influence on the evolution of hosts via selection for alleles or genotypes that moderate pathogen virulence. Inconsistent interactions between parasites and the host genome, such as those resulting from genetic linkages and environmental stochasticity, have largely prevented observation of this process in wildlife species. We examined the prion protein gene (PRNP) in North American elk (Cervus elaphus nelsoni) populations that have been infected with chronic wasting disease (CWD), a contagious, fatal prion disease, and compared allele frequency to populations with no history of exposure to CWD. The PRNP in elk is highly conserved and a single polymorphism at codon 132 can markedly extend CWD latency when the minor leucine allele (132L) is present. We determined population exposure to CWD, genotyped 1,018 elk from five populations, and developed a hierarchical Bayesian model to examine the relationship between CWD prevalence and PRNP 132L allele frequency. Populations infected with CWD for at least 30–50 y exhibited 132L allele frequencies that were on average twice as great (range = 0.23–0.29) as those from uninfected populations (range = 0.04–0.17). Despite numerous differences between the elk populations in this study, the consistency of increase in 132L allele frequency suggests pathogen-mediated selection has occurred due to CWD. Although prior modeling work predicted that selection will continue, the potential for fitness costs of the 132L allele or new prion protein strains to arise suggest that it is prudent to assume balancing selection may prevent fixation of the 132L allele in populations with CWD.


2000 ◽  
Vol 36 (4) ◽  
pp. 676-690 ◽  
Author(s):  
Michael W. Miller ◽  
Elizabeth S. Williams ◽  
Craig W. McCarty ◽  
Terry R. Spraker ◽  
Terry J. Kreeger ◽  
...  

2014 ◽  
Vol 52 (9) ◽  
pp. 3237-3243 ◽  
Author(s):  
Nicholas J. Haley ◽  
Scott Carver ◽  
Laura L. Hoon-Hanks ◽  
Davin M. Henderson ◽  
Kristen A. Davenport ◽  
...  

2006 ◽  
Vol 87 (7) ◽  
pp. 2109-2114 ◽  
Author(s):  
Chad Johnson ◽  
Jody Johnson ◽  
Joshua P. Vanderloo ◽  
Delwyn Keane ◽  
Judd M. Aiken ◽  
...  

The primary sequence of the prion protein affects susceptibility to transmissible spongiform encephalopathies, or prion diseases, in mice, sheep and humans. The Prnp gene sequence of free-ranging, Wisconsin white-tailed deer was determined and the Prnp genotypes of chronic wasting disease (CWD)-positive and CWD-negative deer were compared. Six amino acid changes were identified, two of which were located in pseudogenes. Two alleles, a Q→K polymorphism at codon 226 and a single octapeptide repeat insertion into the pseudogene, have not been reported previously. The predominant alleles – wild-type (Q95, G96 and Q226) and a G96S polymorphism – comprised almost 98 % of the Prnp alleles in the Wisconsin white-tailed deer population. Comparison of the allelic frequencies in the CWD-positive and CWD-negative deer suggested that G96S and a Q95H polymorphism were linked to a reduced susceptibility to CWD. The G96S allele did not, however, provide complete resistance, as a CWD-positive G96S/G96S deer was identified. The G96S allele was also linked to slower progression of the disease in CWD-positive deer based on the deposition of PrPCWD in the obex region of the medulla oblongata. Although the reduced susceptibility of deer with at least one copy of the Q95H or G96S allele is insufficient to serve as a genetic barrier, the presence of these alleles may modulate the impact of CWD on white-tailed deer populations.


2006 ◽  
Vol 18 (6) ◽  
pp. 553-557 ◽  
Author(s):  
Terry R. Spraker ◽  
Thomas L. Gidlewski ◽  
Aru Balachandran ◽  
Kurt C. VerCauteren ◽  
Lynn Creekmore ◽  
...  

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