Friday, September 02, 2016

Chronic Wasting Disease Drives Population Decline of White-Tailed Deer

Research Article
Chronic Wasting Disease Drives Population Decline of White-Tailed Deer
David R. Edmunds, Matthew J. Kauffman, Brant A. Schumaker, Frederick G. Lindzey, Walter E. Cook, Terry J. Kreeger, Ronald G. Grogan, Todd E. Cornish
Chronic Wasting Disease Drives Population Decline of White-Tailed Deer
PLOS x Published: August 30, 2016 •
Chronic wasting disease (CWD) is an invariably fatal transmissible spongiform encephalopathy of white-tailed deer, mule deer, elk, and moose. Despite a 100% fatality rate, areas of high prevalence, and increasingly expanding geographic endemic areas, little is known about the population-level effects of CWD in deer. To investigate these effects, we tested the null hypothesis that high prevalence CWD did not negatively impact white-tailed deer population sustainability. The specific objectives of the study were to monitor CWD-positive and CWD-negative white-tailed deer in a high-prevalence CWD area longitudinally via radio-telemetry and global positioning system (GPS) collars. For the two populations, we determined the following: a) demographic and disease indices, b) annual survival, and c) finite rate of population growth (λ). The CWD prevalence was higher in females (42%) than males (28.8%) and hunter harvest and clinical CWD were the most frequent causes of mortality, with CWD-positive deer over-represented in harvest and total mortalities. Survival was significantly lower for CWD-positive deer and separately by sex; CWD-positive deer were 4.5 times more likely to die annually than CWD-negative deer while bucks were 1.7 times more likely to die than does. Population λ was 0.896 (0.859–0.980), which indicated a 10.4% annual decline. We show that a chronic disease that becomes endemic in wildlife populations has the potential to be population-limiting and the strong population-level effects of CWD suggest affected populations are not sustainable at high disease prevalence under current harvest levels.
Chronic wasting disease (CWD) is a uniformly fatal, progressive neurodegenerative transmissible spongiform encephalopathy (TSE) that occurs in wild cervid populations in 21 U.S. states and two Canadian provinces [9]. The TSEs are caused by proteinase-resistant, abnormal isoforms (PrPres) of normal host cellular proteins (PrPC) known as prions. The causative agent of CWD is known as PrPCWD.
There are few studies on population-level effects of CWD on cervid populations. One such study was conducted on a mule deer population near Boulder, Colorado, USA [10]. Deer abundance declined 45% during 1988–2006. It was believed CWD had been endemic since 1985 and was highly prevalent (males = 41%; females = 20%). The decline was attributed to high prevalence of CWD resulting in low overall adult survival (0.72).
Information suggests CWD has potential to cause population declines and possibly localized extinctions at high prevalence; however, this has not been definitively proven or observed. To address if and how CWD negatively impacts deer population dynamics, we intensively monitored a white-tailed deer population in southeastern Wyoming over a protracted time-period (2003–2010) to estimate population vital rates and model the influence of disease on population performance. We hypothesized that demographic rates are altered by CWD to an extent large enough to lower the population growth rate. The specific objectives were to monitor CWD-positive and CWD-negative white-tailed deer in a high-prevalence CWD endemic area throughout their lifespan via radio-telemetry and global positioning system (GPS) collars. We sought to determine the following for the two segments of the population: a) demographic and disease indices including CWD prevalence, causes of mortality, pregnancy and recruitment rates, b) annual survival, and c) finite rate of population growth (λ). These indicators allowed us to determine the magnitude of the effect of CWD on a free-ranging white-tailed deer population.
The difference in survival by CWD-status and the high proportion of CWD-positive deer in this population help explain the declining population trend (λ1 = 0.896). The CWD-positive deer were 4.5 times more likely to die annually than CWD-negative deer. These results support concerns of wildlife managers, wildlife disease experts, and conservationists that this endemic (chronic) disease can negatively impact deer population sustainability at high disease prevalence. The sensitivity analysis and LTRE indicated survival of fawns, yearlings, and 2.5 year-old CWD-negative deer were primarily responsible for the reduction in λ1 caused by CWD. It is likely that CWD and hunter harvest, the main causes of mortality, have produced the young age structure observed in this population. ***At the current λ1, this population is not sustainable with possible extinction in 48 years at current levels of mortality and fecundity given the worst-case scenario of frequency dependent transmission [39] and no immigration or genetic selection for less susceptible genotypes for CWD [40].
Our estimate of λ is the lowest reported for a free-ranging cervid population with endemic CWD. Dulberger et al. [41] reported a λ of 0.97 (95% credible interval = 0.82–1.09) in a CWD-endemic mule deer population in Colorado, and λ = 1.0 has been reported for CWD-endemic elk populations in South Dakota and Colorado [42, 43]. These values were not particularly worrisome as λ either overlapped 1.0 given the credible interval or was equal to 1.0, indicating stable populations. It is particularly concerning how low our λ1 value was given that the study species was white-tailed deer, which have a higher lifetime reproductive potential than the other three CWD susceptible species.
Hunter harvest often is a major cause of mortality in white-tailed deer, which are the most common and wide-spread big game species in North America. We demonstrated that CWD-positive adults were over-represented in hunter harvest, and others [44] have suggested CWD-positive mule deer also are more vulnerable to hunter harvest. The behavioral shifts, including movement patterns, changes in breeding behavior during harvest, decreased reaction time to stimuli, and changes in habitat type used by CWD-positive mule deer may have caused biased harvest proportions. Conversely, Grear et al. [45] found no difference in harvest susceptibility between CWD-negative and CWD-positive white-tailed deer in Wisconsin, perhaps due to relatively low CWD prevalence (6.3% in adults). It is probable that the behavioral changes suggested by Conner et al. [44] affect CWD-positive deer susceptibility to harvest. Captive CWD-positive deer often show altered response to human activity [4], including an apparent lack of recognition of human presence. Activity analysis suggested CWD-positive bucks did not participate in the rut at the same level as CWD-negative bucks; the rut coincided with the hunting season [11]. Our data support the notion that CWD-positive bucks were less aware of the rut and the hunting season and were more susceptible to being shot by a hunter.
Over-representation of CWD-positive deer in the hunter harvest suggests behavior is altered by CWD prior to clinically recognizable CWD infection. Rather than thinking of CWD as a strictly pre-clinical disease followed by a short, obvious clinical stage of disease, we believe CWD infection should be envisioned as a slow, progressive decline in health and alteration of normal behavior, which ends with clinically recognizable disease. Given the relatively short clinical stage of CWD and the limited hunting season, it is hard to believe CWD-positive deer would be more susceptible to harvest if this slow alteration in health and behavior does not occur. Further, the majority of hunters do not intentionally harvest emaciated or sick animals.
There was a discrepancy in sex ratio of deer that died of clinical CWD (female: male = 12: 5). The high proportion of bucks in the harvest (76%) and over-representation of CWD-positive deer compared to CWD-negative deer may explain why females comprised 71% of clinical CWD cases. Data suggest CWD-positive bucks were harvested at a higher rate than expected and prior to reaching terminal stages of disease while the low harvest rate of does facilitated disease progression to clinical CWD. Females lived longer (137.2 weeks) after testing positive for CWD than bucks (107.4 weeks), which supports this argument. Also, the matriarchal social structure of females may explain why CWD incidence was higher in females and a more steady progression than males. Males were removed earlier in disease progression and had less time to spread disease directly to susceptible bucks in their bachelor herds throughout most of the year. Meanwhile, females progressed to clinical CWD, presumably shedding infectious prions into the environment and transmitting prions directly to susceptible females in their familial groups early in infection [46] and throughout most of the year. It is known that CWD prevalence is not spatially homogenous [47–50]. White-tailed deer are highly faithful to small home ranges in the Rocky Mountain West [11]. Prolonged prion shedding by CWD-positive does within their home range, including favored bedding locations, accompanied by communal grooming and shared home ranges with females provided opportunity for disease transmission through time.
Our study finding of higher incidence in does than bucks contradicts other reported studies that documented higher incidence in bucks than does (e.g., [45, 50, 51]). Presumably in hunted populations, bucks were the favored hunted sex as well. We believe that this discrepancy may be a function of the riparian habitat concentrating white-tailed deer and thus environmental contamination and allowing for the proposed role of does in the transmission of CWD in our study system. It is possible that in the future, when other habitats, such as winter lots in Wisconsin (where CWD has not been endemic for as long as Wyoming) have had similar time to become equivalently contaminated, does may become similarly important to transmission and incidence may increase in does in these population. In other words, perhaps our study population is an indicator of things to come, where initially bucks experience higher incidence until a threshold is met when does experience higher CWD incidence. This scenario assumes concentrated environmental contamination, however. For wide-ranging and dispersed populations, bucks may always experience higher incidence than females.
It is important to note that hunters may have had a bias in regards to harvesting collared deer. It is possible that hunters avoided shooting collared does in lieu of harvesting an uncollared doe to avoid altering the study results and to not have to deal with the hassle of returning a collar. Hunters targeting bucks may not have had such concerns if the antler size was large enough. If this was the case, then we may have over-emphasized the ratio of bucks to does in the harvest ratio. We believe this bias was relatively minor, at least within the main study site that encompassed the majority of the winter range, because hunters were forced to use one hunting outfitter on the VR Ranch and after conversations with this outfitter, they at least claimed to not be biased for or against harvesting collared animals.
Pregnancy and recruitment results indicate CWD does not compromise reproduction in female white-tailed deer. Blanchong et al. [52] also determined pre-clinical CWD did not negatively impact female reproduction in Wisconsin white-tailed deer. No difference in pregnancy indicates does participate in the rut regardless of CWD infection-status. It was not possible to determine if there was a difference in pregnancy and recruitment between pre-clinical and clinical CWD-positive does. However, it was common during the study to find one or two near-term fetuses in clinical-CWD female carcasses during the third trimester (Cornish and Edmunds, unpublished data). It is likely that fetuses exacerbate emaciation and hasten the death of does with terminal CWD. Our findings suggest does in pre-clinical disease give birth to fawns and are as successful at raising fawns to early September as CWD-negative does. Equal reproduction by CWD-positive does should dampen somewhat the negative effects of CWD on deer populations. Future research on neonate and young fawn survival is warranted, specifically to address the ability of CWD-positive white-tailed deer does to raise young to the age of population recruitment.
Pregnancy-specific protein B (PSPB) is not 100% accurate; Duquette et al. [53] documented 5 cases where white-tailed deer were found to be pregnant by trans-abdominal ultrasound but were deemed nonpregnant by PSPB. However, overall they found strong agreement between the two methods and recommended using either depending on the study objectives. We feel comfortable that the PSPB was an appropriate test, but it is possible that we underestimated pregnancy rates and therefore overestimated λ1, which already is extremely low for a white-tailed deer population. Considering the high pregnancy rates reported in this study, the impact on λ1 from inaccurate tests likely was minimal.
The modeling exercise that determined λ1 can be expected to be less than 1.0 (assuming other vital rates remain constant) at a prevalence of 27% suggests that as CWD in a population approaches these values, wildlife managers may choose to switch their objectives from lowering CWD prevalence by decreasing deer density to one of maintaining a sustainable population. The hunting-free Leslie matrix indicated removing additive hunting mortality in female deer resulted in a sustainable population. Therefore, it is recommended that at high CWD prevalence, hunting of does should be limited or ceased if the objective is to maintain population numbers. Currently this is a rare situation in most CWD endemic areas due to the relatively short period of time CWD has been present in most locations; this population should serve as an indication of what can happen at high prevalence when CWD has been endemic for an extended time period. Through time as prevalence rises in other endemic populations, more managers will be forced to make these choices if more effective management strategies or treatments are not developed. This recommendation is contingent on continued surveillance and monitoring of CWD in deer and elk populations in endemic areas as well as few or only minor public health concerns regarding CWD transmission to humans or livestock. Furthermore, if it becomes possible to accurately target and remove CWD-positive deer in a cost-effective manner, this management approach should be implemented in these populations where non-targeted culling is likely to be detrimental to population sustainability.
This population highlights the potential long-term negative outcome of endemic CWD to population sustainability and stresses the importance of preventing CWD from becoming endemic in a population, rather than attempting to manage it after the fact. Therefore, as previously suggested [43], the best management strategy remains minimizing movement of CWD to new areas.
see full text ;
***At the current λ1, this population is not sustainable with possible extinction in 48 years at current levels of mortality and fecundity given the worst-case scenario of frequency dependent transmission [39] and no immigration or genetic selection for less susceptible genotypes for CWD [40]. ***

UW Research Finds First-Ever Evidence of White-Tailed Deer Declines from CWD


man working with blindfolded deer David Edmunds, recent UW Ph.D. graduate, performs a tonsil biopsy on a white-tailed deer to test for chronic wasting disease. He and other UW researchers have documented the first conclusive evidence that CWD found at high prevalence leads directly to population declines in free-ranging deer populations. (Todd Cornish Photo)


September 2, 2016 — Chronic wasting disease has caused significant declines in east-central Wyoming white-tailed deer populations, according to new research published this week by University of Wyoming scientists.


Chronic wasting disease (CWD) is a prion disease of deer, elk and moose found in 24 states and two Canadian provinces.


The research, led by recent UW Ph.D. graduate David Edmunds, under the direction of Associate Professor Todd Cornish in the Department of Veterinary Sciences, is the first conclusive evidence that CWD found at high prevalence leads directly to population declines in free-ranging deer populations.


The findings, published in the scientific journal PLOS ONE this week, provide new information that could influence management of this continually expanding disease.


“Chronic wasting disease has likely been present in southeast Wyoming deer and elk populations for approximately 50 years,” Edmunds says. “It has been steadily increasing to the point that some hunt areas are seeing populations with as many as 30 percent to almost 50 percent of harvested deer testing positive for this disease.”


For eight years, he and his colleagues tracked white-tailed deer east of Casper to determine if CWD itself can cause population numbers to decline by increasing mortality of deer annually.


“We found that CWD drastically reduced annual survival rates in the deer population, especially in females,” Edmunds says.


Working as a graduate student under Cornish in the Wyoming Wildlife/Livestock Health Center in the Department of Veterinary Sciences, Edmunds and colleagues captured both female and male fawns on their winter ranges to test whether they had CWD; pregnancy tested females; and marked all deer with radio transmitters attached to collars for tracking purposes.


two men and a woman in wooded area with binoculars, gps tracking gear and papers


From left, Associate Professor Todd Cornish, graduate student David Edmunds and graduate student Melia DeVivo use telemetry to find radio-collared deer in a chronic wasting disease study. (Todd Cornish Photo)


Deer were tracked throughout the year and captured annually to retest for CWD. A variety of data were collected, including survival and pregnancy rates, number of fawns seen alongside does in late summer, and CWD prevalence. All of these were used to determine the population growth rate -- which is by how much the population size varies from one year to the next.


The researchers found that over the study period from 2003-10, the population declined 10 percent annually, which they say could lead to localized extinctions in less than 50 years.


“The decline was caused directly by CWD lowering annual survival of female deer, which have the biggest impact on population growth rates,” Edmunds says. “This was because CWD-positive deer died both directly from the disease and were more likely to be killed by hunters than CWD-negative deer.”


Cornish says the findings highlight the importance of preventing CWD from spreading into new deer and elk populations.


“We really do not have any effective strategies currently to manage CWD once it becomes established in landscapes and in populations,” he says. “Now that we know CWD causes populations to decline once the disease reaches significant levels in deer, this is a disease to be taken very seriously, with more research on control and prevention strategies warranted.”


Edmunds and Cornish are two of the co-authors of the report published Tuesday -- along with a collaborative team of researchers from the Wyoming Cooperative Fish and Wildlife Research Unit, the Wyoming Game and Fish Department, UW’s College of Agriculture and Natural Resources, and Texas A&M University.


To read the article summarizing the research in PLOS ONE, go to


Prions efficiently cross the intestinal barrier after oral administration: Study of the bioavailability, and cellular and tissue distribution in vivo
Wednesday, August 31, 2016
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***
What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
The previous assessment concentrated on the incursion of disease from North America through the imports of animal feed or the movement of contaminated clothing, footwear and equipment. The results suggested that import of pet feed was a non-negligible risk, but given the unlikely contact of resident deer in GB with such non-ruminant feed, this was considered overall a negligible to very low risk. The movement of contaminated clothing, footwear or equipment (particularly hunting equipment) could pose a very low risk, although the volume of contaminated soil which would need to be ingested to give rise to an infection is likely to be higher than would be present. There is a variable level uncertainty in all these assessments.
The new assessment focuses on an additional potential route of entry: the importation of natural deer urine lures. The main conclusions from this assessment are:
In areas of North America where CWD has been reported, given that CWD is excreted in faeces, saliva, urine and blood, and survives in the environment for several years there is a medium probability that the deer urine in North America contains CWD (high uncertainty; depends on the source of deer used for production).
The risk of a deer in GB being infected per 30 ml bottle of urine imported from the USA is very low, albeit with high uncertainty. Overall it is concluded that the risk of at least one infection of deer in the UK with CWD per year from deer urine lures imported from the USA is medium. This assumes a high number of 30 ml bottles imported per year from all areas of the USA.
None of the species affected by CWD in North America are present in GB. For a British species to become infected with CWD following exposure, the dose and inherent susceptibility of the species will be important. Based on current scientific evidence Red deer (Cervus elaphus elaphus) are susceptible to CWD, Fallow deer (Dama dama) are likely to be less susceptible and Roe deer (Capreolus capreolus) have a gene conferring susceptibility. Therefore, it is likely that given exposure to an infectious dose of CWD, deer in GB could become infected with CWD.
Overall, the probability of importing CWD into GB from North America and causing infection in British deer is uncertain but likely to be negligible to very low via movement of deer hunters, other tourists and British servicemen and very low via imported (non-
ruminant) animal feed and medium for the use of lures. However, if it was imported and (a) deer did become infected with CWD, the consequences would be severe as eradication of the disease is impossible, it is clinically indistinguishable from BSE infection in deer (Dalgleish et al., 2008) and populations of wild and farmed deer would be under threat.
The USA has implemented a Herd Certification Programme for farmed and captive cervids. So far, 29 States are approved for HCP status (APHIS, 2015). The list includes States such as Colorado, where CWD is present, therefore it is recommended that any sourcing of such natural urine lures should be not only from States with an HCP programme, but also from a herd which is registered as being regularly tested free of CWD.
Animal urine is not considered a commodity which is subject to animal by-products legislation for imports. Internet sales are common and although a license would be required, there are no conditions for the safe sourcing of such products. Deer urine lures are also available in Europe and may be produced from carcases of hunted deer. The use of deer urine produced from a species not present in Europe (such as white tailed deer) is questioned for its value with native GB deer according to the British Deer Society survey.
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
What is the risk of chronic wasting disease being introduced into Great Britain? A Qualitative Risk Assessment October 2012
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids, as well as non-ruminants such as cats and dogs as well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Terry Singeltary Sr. comment ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
Thursday, August 25, 2016
FSIS Green Bay Dressed Beef Recalls Beef Products Due To Possible Specified Risk Materials Contamination the most high risk materials for BSE TSE PRION AKA MAD COW TYPE DISEASE
In the USA, USDA et al sometimes serves SRM’s up as appetizers or horderves.
Monday, June 20, 2016
*** Specified Risk Materials SRMs BSE TSE Prion Program
Saturday, January 31, 2015
RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings in countries with a “negligible risk status for BSE” and on the risk of modification of the list of specified risk materials (SRM) with regard to BSE
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Sunday, August 28, 2016
Transmissible Spongiform Encephalopathy TSE Prion and how Politics and Greed by the Industry spread madcow type diseases from species to species and around the globe
Monday, August 29, 2016
kind regards, terry


Post a Comment

Subscribe to Post Comments [Atom]

<< Home