scholarly journals Getting in Front of Chronic Wasting Disease: Model-Informed Proactive Approach for Managing an Emerging Wildlife Disease

2021 ◽  
Vol 7 ◽  
Author(s):  
Aniruddha V. Belsare ◽  
Joshua J. Millspaugh ◽  
J. R. Mason ◽  
Jason Sumners ◽  
Hildegunn Viljugrein ◽  
...  

Continuing geographic spread of chronic wasting disease (CWD) poses a serious threat to the sustainable future of cervids and hunting in North America. Moreover, CWD has been detected in captive cervids in South Korea and, in recent years, in free-ranging reindeer in Europe (Norway). Management of this disease is limited by logistical, financial, and sociopolitical considerations, and current strategies primarily focus on reducing host densities through hunter harvest and targeted culling. The success of such strategies in mitigating the spread and prevalence of CWD only upon detection is questionable. Here, we propose a proactive approach that emphasizes pre-emptive management through purposeful integration of virtual experiments (simulating alternate interventions as model scenarios) with the aim of evaluating their effectiveness. Here, we have used a published agent-based model that links white-tailed deer demography and behavior with CWD transmission dynamics to first derive a CWD outbreak trajectory and then use the trajectory to highlight issues associated with different phases of the CWD outbreak (pre-establishment/transition/endemic). Specifically, we highlight the practical constraints on surveillance in the pre-establishment phase and recommend that agencies use a realistic detection threshold for their CWD surveillance programs. We further demonstrate that many disease introductions are “dead ends” not leading to a full epidemic due to high stochasticity and harvesting in the pre-establishment phase of CWD. Model evaluated pre-emptive (pre-detection) harvest strategies could increase the resilience of the deer population to CWD spread and establishment. We conclude it is important to adaptively position CWD management ahead of, rather than behind, the CWD front.

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

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.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Edoardo Bistaffa ◽  
Tram Thu Vuong ◽  
Federico Angelo Cazzaniga ◽  
Linh Tran ◽  
Giulia Salzano ◽  
...  

AbstractChronic wasting disease (CWD) is a highly contagious prion disease affecting captive and free-ranging cervid populations. CWD has been detected in United States, Canada, South Korea and, most recently, in Europe (Norway, Finland and Sweden). Animals with CWD release infectious prions in the environment through saliva, urine and feces sustaining disease spreading between cervids but also potentially to other non-cervids ruminants (e.g. sheep, goats and cattle). In the light of these considerations and due to CWD unknown zoonotic potential, it is of utmost importance to follow specific surveillance programs useful to minimize disease spreading and transmission. The European community has already in place specific surveillance measures, but the traditional diagnostic tests performed on nervous or lymphoid tissues lack sensitivity. We have optimized a Real-Time Quaking-Induced Conversion (RT-QuIC) assay for detecting CWD prions with high sensitivity and specificity to try to overcome this problem. In this work, we show that bank vole prion protein (PrP) is an excellent substrate for RT-QuIC reactions, enabling the detection of trace-amounts of CWD prions, regardless of prion strain and cervid species. Beside supporting the traditional diagnostic tests, this technology could be exploited for detecting prions in peripheral tissues from live animals, possibly even at preclinical stages of the disease.


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.


2016 ◽  
Vol 47 (1) ◽  
Author(s):  
Sylvie L. Benestad ◽  
Gordon Mitchell ◽  
Marion Simmons ◽  
Bjørnar Ytrehus ◽  
Turid Vikøren

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