Endemic chronic wasting disease causes mule deer population decline in Wyoming
''Our findings support CWD as a population-limiting disease of mule deer with the potential to cause dramatic declines that resemble local population extinction.''
''Other studies have found a negative association between CWD prevalence and λ [11,12,40,42], but none have documented λ estimates resulting from endemic CWD as low as those reported here.''
Endemic chronic wasting disease causes mule deer population decline in Wyoming
Melia T. DeVivo , David R. Edmunds, Matthew J. Kauffman, Brant A. Schumaker, Justin Binfet, Terry J. Kreeger , Bryan J. Richards, Hermann M. Schätzl, Todd E. Cornish
Published: October 19, 2017https://doi.org/10.1371/journal.pone.0186512
Abstract
Chronic wasting disease (CWD) is a fatal transmissible spongiform encephalopathy affecting white-tailed deer (Odocoileus virginianus), mule deer (Odocoileus hemionus), Rocky Mountain elk (Cervus elaphus nelsoni), and moose (Alces alces shirasi) in North America. In southeastern Wyoming average annual CWD prevalence in mule deer exceeds 20% and appears to contribute to regional population declines. We determined the effect of CWD on mule deer demography using age-specific, female-only, CWD transition matrix models to estimate the population growth rate (λ). Mule deer were captured from 2010–2014 in southern Converse County Wyoming, USA. Captured adult (≥ 1.5 years old) deer were tested ante-mortem for CWD using tonsil biopsies and monitored using radio telemetry. Mean annual survival rates of CWD-negative and CWD-positive deer were 0.76 and 0.32, respectively. Pregnancy and fawn recruitment were not observed to be influenced by CWD. We estimated λ = 0.79, indicating an annual population decline of 21% under current CWD prevalence levels. A model derived from the demography of only CWD-negative individuals yielded; λ = 1.00, indicating a stable population if CWD were absent. These findings support CWD as a significant contributor to mule deer population decline. Chronic wasting disease is difficult or impossible to eradicate with current tools, given significant environmental contamination, and at present our best recommendation for control of this disease is to minimize spread to new areas and naïve cervid populations.
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Discussion
Our findings support CWD as a population-limiting disease of mule deer with the potential to cause dramatic declines that resemble local population extinction. Other studies have found a negative association between CWD prevalence and λ [11,12,40,42], but none have documented λ estimates resulting from endemic CWD as low as those reported here. The only scenario in which population growth rate was stable (λ = 1) was in the absence of CWD. Even without CWD mortality, we predicted that this population would not grow under current conditions. This finding was unremarkable considering mule deer populations throughout North America are underperforming in the absence of CWD [43]. Chronic wasting disease may exacerbate population declines in herds that are currently considered CWD-free. From 2010–2014, we predicted the southern Converse County herd would decline by >50% using our estimated λ = 0.79 and a starting population size of ~6,100 deer. Earlier models of CWD epidemics in mule deer using prevalence observed in our study herd forecasted similar dramatic outcomes [44,45]. This population has experienced population declines of approximately 50% based on WGFD population estimates prior to the start of our study [19]. However, this population did not appear to decline as dramatically during the study as our estimate of λ would suggest based on WGFD population estimates (approximately a 4% decline from 2010 to 2014) [19]. While the 2010 and 2014 population size estimates were not strikingly different, the general trend over time suggests a declining population. From 2011 to 2012, WGFD estimated a 19% decline in mule deer numbers and a 15% decline the following year [19]. These declines observed during our study fall within our 95% CI for λ (0.72, 0.87). In 2013, greater spring precipitation ended a year-long drought and moderate winter conditions resulted in a 5% increase of the population estimate in 2014 [19]. Therefore, while the population experienced productive years and deer numbers increased; these increases were marginal compared to the larger declines observed over multiple years.
We did not find disease-associated declines in reproduction for mule deer, nor have they been observed in sympatric white-tailed deer [40]. Females were pregnant regardless of CWD status during captures when they were approximately 75 days bred. Despite evidence that suggests CWD-positive mule deer recruit fewer fawns than CWD-negative deer [11], we did not detect a difference in fawn recruitment based on CWD status. Even with a reduction in fawn recruitment of CWD-positive mule deer in Colorado, inclusion of this vital rate in models did not significantly influence λ [11]. While CWD did not have a detectable impact on annual pregnancy and recruitment, lifetime reproduction of prime-aged females was likely reduced due to increased annual mortality of CWD-infected individuals. Prion-infected Table Mesa mule deer in Colorado survived an additional 1.6 years on average compared to 5.2 years for uninfected deer [16]. Furthermore, fawns produced by CWD-negative deer, which more likely possessed the more resistant genotype compared to CWD-positive deer in our study, potentially contributed to the increase of the F allele in the population.
Prion protein genotype was important in determining CWD infection and influenced λ for Prnp-specific segments of the population. As was expected, mule deer that possessed the 225SS Prnp genotype were more likely to be CWD-positive compared to 225SF and 225FF deer in our study. We only detected one 225SF CWD-positive deer even though 225*F deer comprised 22% of the study population. Two radio-collared 225FF deer were captured in 2013 and survived to study termination in 2014 with negative tonsil biopsy IHC results. However, evidence suggests current IHC techniques may have lower sensitivity in detecting CWD-positive tissues of 225FF mule deer [46]. Both 225FF deer were estimated to be 3.5 years old during their initial capture, both were pregnant in 2013 and 2014, and during 2013 recruitment surveys, one had a single fawn at heel. The other 225FF deer was not observed during 2013 fawn recruitment surveys. During 2014 captures, ultrasound revealed that one 225FF deer was pregnant with twins and the other was pregnant with a single fetus. Based on a small sample size, free-ranging 225FF mule deer appeared to be as ecologically fit as 225SS deer. The few 225FF mule deer observed in captivity were characterized as atypical in behavior, body condition, and reproductive performance [46]. Formal investigations looking at the effects of Prnp genotype on fitness are necessary to determine how populations with greater numbers of 225FF mule deer will persist despite their reduced susceptibility to CWD.
Estimates of λ for 225SS and 225*F segments of the population were mediated by varying CWD incidence rates. Using 225SS CWD incidence in our matrix model, we estimated an annual population decline of 33% of 225SS deer. A model incorporating 225*F CWD incidence estimated an annual population decline of 1%. These results suggest the 225*F segment of the population was nearly stable while the 225SS segment of the population was declining rapidly. Using previously published data of mule deer genotyped in the early 2000s from the same geographic area [15], we estimated a 10% population increase in the F allele frequency in less than 10 years [47]. Other factors were not identified that may potentially increase F allele frequency in the absence of CWD as it was outside of the scope of our study. Adaptation to CWD has previously been demonstrated in elk [48] and white-tailed deer [49] using empirical data and statistical models.
Natural selection in favor of less susceptible Prnp genotypes may be assisted with selective predation by mountain lions and harvest by hunters of prion-infected deer. While CWD-positive deer were more likely to be killed by mountain lions compared to uninfected deer, it is not clear if this source of mortality regulated or influenced the observed CWD epidemic. Selective predation of CWD-positive deer in Table Mesa, Colorado did not appear to control CWD transmission [16] and it also did not appear to curtail CWD prevalence in the current study herd. Theoretic modeling incorporating 15% predation rate and four times greater risk of predation of prion-infected deer resulted in the eradication of CWD in a closed population [50]. While we observed one year of 15% predation of marked deer in 2010, 3–4% predation rate was typical for most years of the study and it never exceeded 15%. While direct mortality could decrease the subset of infected animals in a population, predators may also act as mechanical vectors that spread prions across the landscape. Infectious prions were demonstrated to pass through the digestive system of coyotes (Canis latrans) three days post ingestion suggesting the potential role of carnivores in prion transport and spread [51]. At this time, empirical evidence that supports a predator influence on CWD epidemics does not exist. However, with the expected spread of CWD into areas such as the Greater Yellowstone Area that is occupied by several large predators (i.e. wolves (Canis lupus), grizzly bears (Ursus arctos), and mountain lions), the role of predators in prion transmission dynamics may soon become more relevant [50]. A multi-predator system may have a greater impact on an emerging CWD epidemic, especially before significant prion contamination occurs in the environment.
Hunting mortality was minimal in our study, although it appeared that sympatric CWD-positive mule deer and white-tailed deer were selectively harvested [13]. It is unclear why others have found no difference in hunting risk between infected and uninfected deer [52], but it is logical that CWD-positive individuals are more vulnerable to harvest due to behavioral changes associated with the disease. The precipitous decline in survival of CWD-positive males increased predictably during the short hunting season around day 250. However, unpredictably there was an observed accelerated decline in the survival curve of CWD-positive females after day 275. Multiple factors may have contributed to greater mortality of CWD-positive females on winter range including increased risk of predation and stressors associated with the rut, hunting season, recruitment of fawns, and winter conditions. Regardless of the cause, CWD-positive deer were more likely to die on winter ranges. This has important implications for the spread and translocation of CWD across the landscape. Congregating deer on winter range may act as a source for CWD-infection to disparate populations when deer migrate in the spring to different summer ranges. These temporal behaviors could explain some of the spatial heterogeneity of CWD prevalence across the landscape [53].
Without an effective CWD vaccine or treatment, management of this disease is limited to focusing on those individuals that are not yet prion-infected. According to our sensitivity analysis, changes in CWD-negative adult survival would cause the greatest changes in λ. Improving survival of uninfected mule deer may partially mitigate the impact of CWD. However, to achieve close to stable population growth rates required an unrealistic scenario of 100% survival of CWD-negative deer under high CWD prevalence conditions. We observed low fawn recruitment (0.51 fawns) during the study regardless of disease status compared to an adjacent herd (0.68 fawns) located north of SCMDH [54] and populations throughout the species range (> 0.75 fawns) [11,55]. Management strategies that focus on improving both adult survival of CWD-negative deer and fawn recruitment may increase λ. Mule deer populations that currently experience low adult and fawn survival should be closely monitored for CWD because our models predicted less than ideal outcomes once CWD was established.
Lastly, we predicted stable population growth only when CWD prevalence was reduced to 0% in our model. Eradication of CWD is an improbable goal in endemic areas, especially where CWD has been detected for over a decade and potentially present for over 50 years [45]. However, these findings highlight the importance of preventing or slowing the spread of CWD to naïve populations. Mule deer populations currently undergoing declines in the absence of CWD, such as in Nevada and South-central British Columbia [56,57] and in western Wyoming, should be routinely surveyed for detection of CWD. Intensive surveillance that could detect the first few positive CWD cases and rapid removal of prion-infected individuals may be the difference between an established epidemic and local CWD eradication as apparently accomplished in New York and Minnesota [58,59]. While most state agencies focus efforts on collecting hunter harvested and road-killed deer for CWD testing, we recommend incorporating predator-killed deer to the repertoire based on our finding of greater susceptibility of CWD-positive deer to predation [16,17]. Many other non-disease-associated factors contribute to declining mule deer populations and CWD could be the fatal consequence for many herds. Due to the lack of effective management tools to eliminate CWD once established, we suggest management focus efforts and research on how to slow or potentially prevent the movement of CWD across the landscape into uninfected populations.
Conclusions
With this study, we have demonstrated the long-term consequences of endemic CWD on a free-ranging mule deer population. Chronic wasting disease caused significant declines in the study mule deer herd as well as in sympatric white-tailed deer [13]. Unlike sympatric white-tailed deer, where removal of female harvest may permit λ to increase to stable levels based on model estimates [13], elimination of the mule deer doe/fawn hunting season prior to the onset of our study did not result in λ ≥ 1. A limited antlered-only harvest in this herd provides a reliable source for monitoring short-term CWD prevalence trends [53]. Additionally, improving and conserving critical mule deer habitats may diminish the negative impacts of CWD, but will not completely mitigate the undesirable population effect of CWD based on our model outcomes. Lastly, without the use of effective vaccines, treatments, and sustainable techniques to reduce CWD incidence, management can currently only focus on slowing the spread of CWD to CWD-free populations.
Acknowledgments
We thank the personnel of the University of Wyoming and the Wyoming Game and Fish Department for technical assistance in the field and laboratory, including G. Andrews, K. Andrews, K. Bardsley, J. Berg, A. Boerger-Fields, B. Bonner, G. Boyd, R. Burton, J. Cavender, W. Cook, A. Dadelahi, S. Dwinnell, S. Edberg, H. Edwards, K. Fambrough, R. Grogan, C. Hansen, C. Havlik, J. Henningsen, B. Howell, M. Huizenga, N. Hull, M. Jaeger, P. Jaeger, J. Jennings-Gaines, T. Jones, M. Kauffman, A. Kerr, A. Kesterson, H. Killion, K. Latta, R. Lebert, D. Lutz, D. Manore, M. Miller, K. Monteith, M. Nelson, H. O’Brien, B. Saeed, K. Speiser, W. Steen, M. Stuart, F. Sunshine Packard, S. Talbott, T. Tobiasson, M. Vasquez, A. Williams, B. Wise, and M. Wood. We are very grateful to many private landowners that granted us access to their properties for this research. This manuscript was greatly improved by the comments of P. Cross, three reviewers, and our Associate Editor, and figure editing by P. Whelan. Any use of trade, firm, or product names is for descriptive purposes only and does not imply endorsement by the U.S. Government.
''Our findings support CWD as a population-limiting disease of mule deer with the potential to cause dramatic declines that resemble local population extinction.''
''Other studies have found a negative association between CWD prevalence and λ [11,12,40,42], but none have documented λ estimates resulting from endemic CWD as low as those reported here.''
WEDNESDAY, JULY 26, 2017
Wyoming CWD found in new elk hunt area in Southeast Washakie County CWD found in new elk hunt area in Southeast Washakie County
The Wyoming Game and Fish Department has diagnosed chronic wasting disease (CWD) in a cow elk that was found dead in southeast Washakie County.
7/26/2017 11:10:05 AM
CHEYENNE -
The Wyoming Game and Fish Department has diagnosed chronic wasting disease (CWD) in a cow elk that was found dead in southeast Washakie County. The elk was found about 30 miles southwest of Kaycee. The dead elk was part of the Bighorns elk movement study. This study is evaluating the migrations and behaviors of elk in the Bighorn Mountains. CWD is less common in elk than it is in deer, and CWD has been documented in this part of the state in deer, for elk it has previously been detected to the northeast of Elk Hunt Area 48, where this recent cow elk was found, in Elk Hunt Area 34. “We have many means of monitoring for CWD and following its movement across the state. The disease moves very slowly, especially in elk, but this research and data is necessary as it will guide our future management decisions,” said Scott Edberg, deputy division chief of the Wildlife Division. “We will continue our increased level of monitoring and ask for those who hunt to help by submitting harvested animals for testing. We also ask that those who see a sick animal to report it to Game and Fish.” Last year, Game and Fish personnel collected and analyzed more than 3,350 CWD samples throughout the state, a significant increase from past years. This year Game and Fish will sample a similar number.
Please visit the Game and Fish website for more information on chronic wasting disease transmission and regulations on transportation and disposal of carcasses. (renny.mackay1@wyo.gov)
- WGFD -
MONDAY, MARCH 27, 2017
Wyoming CWD Postive Mule Deer Doe Near Pinedale
WEDNESDAY, MARCH 01, 2017
Wyoming mule deer test positive for CWD in Cody
WEDNESDAY, JULY 26, 2017
Chronic wasting disease continues to spread Disease of cervids causing local population declines
TUESDAY, NOVEMBER 29, 2016
Wyoming CWD Report monitoring efforts increase with focus on improving herd health
FRIDAY, OCTOBER 20, 2017
USAHA CWD TSE PRION Laboratory Approval, Testing, for Regulatory Diseases
FRIDAY, OCTOBER 20, 2017
USAHA Live Animal Testing for Chronic Wasting Disease CWD TSE Prion
FRIDAY, OCTOBER 20, 2017
USAHA SCRAPIE TSE PRION RESOLUTIONS
WEDNESDAY, OCTOBER 4, 2017
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA) a review 2017
TUESDAY, OCTOBER 17, 2017
EFSA asked to review risk from processed animal proteins in feed PIG PAP and CWD TSE Prion Oral Transmission
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.
Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.
Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.
To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.
Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
11:19 AM
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