Subject: Feedgrounds in WY spawn disease FYI
Elk Feedgrounds: Heading in the right direction
What began as a noble effort — feeding snowbound elk in 1912 at what is now the National Elk Refuge in Jackson Hole — has become a ticking disease time bomb. More than 22,000 elk are now unnaturally fed during the winter at the refuge and on 22 other disease-plagued, state-run feedgrounds.
Yet in August 2011, the future of healthy wildlife at the National Elk Refuge in Jackson Hole took a startling turn for the better when a circuit court in Washington, D.C., said that the artificial feeding of elk and bison must be phased out.
In strong language, the judges said the U.S. Fish & Wildlife Service was not adhering to its mandate to protect wildlife in natural surroundings. They also pointed out what we've said all along — that feedgrounds are petri dishes for devastating diseases. Finally, the court ruled that the state of Wyoming, which has been a proponent of unnatural feeding, would have no veto power over the ruling. Read our press release about the ruling here . ( Send a message right now to the federal officials who are in charge of the of phasing out feeding on the National Elk Refuge. Tell them you support natural feeding, not artifical feeding.)
This ruling supersedes a 2010 decision in which a judge ruled against our lawsuit asking that artificial feeding be phased out over five years; the circuit court also made the same ruling, but unlike the previous court, which allowed feeding to continue "indefinitely". This time a phaseout has been ordered.
Ironically, the 2010 decision took place at about the same time that the U.S. Geological Survey released a study showing that elk-to-elk brucellosis transmission is increasing in Greater Yellowstone, in large part due to dense concentrations of elk at feedgrounds.
The country's foremost expert on prions, Dr. Stanley Prusiner at the University of California-San Francisco, told the Jackson Hole News & Guide that feedgrounds likely will be the primary mover of Chronic Wasting Disease once it arrives in the ecosystem. In response, U.S. Fish & Wildlife Service health chief Tom Roffe said it's time to close the feedgrounds. Ultimately, it would be best to phase out all feeding in Wyoming so that elk return to foraging on their natural winter range, which will sustain healthy, free-ranging herds forever.
With all this good news, there are still 22 operating feedgrounds that the 2011 phase-out request does not apply to. On feedgrounds, elk congregate unnaturally and create Petri dishes for brucellosis, scabies, hoof rot and, potentially, chronic wasting disease. Conversely, on native winter ranges, elk are far healthier so we will continue to push for the ultimate phase-out of all feeding throughout the state.
Our Mission: To carefully phase out artificial feeding at the National Elk Refuge and other feed grounds to allow for naturally sustaining populations and the regeneration of native plant communities and diverse wildlife in Jackson Hole.
IF Yellowstone the most famous elk herd — the Jackson Hole collection that congregates in already unnatural and unhealthy numbers at the National Elk Refuge, if they are not already exposed, and some infected with CWD, it will be a miracle. IF and when it is documented, it will be terrible. this artificial feeding should have been stopped long ago. once CWD arrives, it will be a killing field for the elk there. please help stop this. ...tss
A Better Plan for Healthy, Free-roaming Elk and Bison
Unnaturally dense winter concentrations of too many
elk have contributed to a dramatically higher incidence
in wildlife disease and renders the National Elk Refuge
highly susceptible to the devastating effects of Chronic
Wasting Disease, which has moved westward to the edge
of Greater Yellowstone and Jackson Hole.
Disease petri dish? (Top).
Higher incidents of disease are one result of unnaturally
dense winter concentrations of elk at the refuge in Jackson Hole.
Elk await a handout of alfalfa pellets.
Case Number # 9857
The state of Wyoming operates 23 winter feedgrounds for elk, many of them on federal lands. These feedgrounds artificially concentrate elk populations, which fuels the spread of diseases such as brucellosis and creates the prospect of a major chronic wasting disease epidemic. Conservationists sued to compel long overdue environmental analysis of alternatives to elk-feeding in Wyoming.
In July 2009 the 10th Circuit Court of Appeal ruled that the four elk feed grounds on land managed by the Bureau of Land Management are exempt from a new environmental impacts analysis, due to an old memorandum of understanding agreed to by the BLM and the state of Wyoming. However, as a result of this lawsuit, the U.S. Forest Service prepared an environmental impact statement examining the impacts of feed grounds within the Bridger-Teton National Forest.
Harmful practice of winter feeding leads to overcrowding and diseases
August 4, 2011
Jackson, WY —
A federal appeals court confirmed yesterday the U.S. Fish and Wildlife Service's obligation to phase out artificial winter feeding of elk and bison at the National Elk Refuge in Jackson Hole, Wyoming. The court's ruling responds to a lawsuit brought by the Greater Yellowstone Coalition, Jackson Hole Conservation Alliance, Wyoming Outdoor Council, National Wildlife Refuge Association and Defenders of Wildlife challenging a 2007 refuge management plan that allowed the indefinite continuation of winter feeding on the refuge despite overcrowding and the threat of diseases.
It has become apparent that crowding of elk and bison on winter feed lines—like crowding of children in a kindergarten class room—exposes the animals to a high danger of disease transmission.
Although the court did not order the Fish and Wildlife Service to set a firm deadline for ending the feeding program as the conservationists had requested, the ruling made it clear that the harmful practice must stop to protect the refuge and the elk.
"With this decision, the courts have confirmed that ending feedlots on the National Elk Refuge is critical to protect the long-term health and viability of elk and bison populations," said Evan Hirsche, President of the National Wildlife Refuge Association. "The U.S. Fish and Wildlife Service should quickly develop a timeline for elimination of supplemental feeding.
"The management of the Elk Refuge must now move forward in accordance with their legal mandates," the panel of three judges said, “all the while preparing the animals for the eventual cessation of supplemental feeding …” (Page 6)
“The science is clear: Artificial feeding on the Elk Refuge creates a breeding ground for disease. The court confirmed the serious danger this well-intentioned but harmful practice poses to the health of elk throughout the Greater Yellowstone region,” said Mike Leahy, Northern Rockies program director for Defenders of Wildlife. “While we were hoping the court would ask the Fish and Wildlife Service to set a firm timeline for phasing out supplemental feeding, the important thing about the ruling is that it reaffirms Fish and Wildlife Service’s jurisdiction over managing the refuge and its obligation to end the feeding.”
The decision further states, “The whole point of a National Elk Refuge is to provide a sanctuary in which populations of healthy, reproducing elk can be sustained … The Refuge can hardly provide such a sanctuary if, every winter, elk and bison are drawn by the siren song of human-provided food to what becomes, through the act of gathering, a miasmic zone of life-threatening diseases.” (page 9) “There is no doubt that unmitigated continuation of supplemental feeding would undermine the conservation purpose of the National Wildlife Refuge System.” (page 10)
The panel of three appellate judges also said, “Wyoming has no veto over the Secretary’s duty to end a practice that is concededly at odds with the long-term health of the elk and bison in the Refuge.” (page 12)
“Science and the law are clear that ending feeding at the earliest opportunity will best protect wildlife. The leadership of the Fish and Wildlife Service should now act expeditiously to avoid the catastrophic effects of Chronic Wasting Disease, which has been detected as close as 45 miles from the Refuge,” said Lloyd Dorsey of the Greater Yellowstone Coalition. “The sooner supplemental feeding is phased out, the better for all wildlife and for all those who treasure wildlife.”
Earthjustice represented the conservationists in the lawsuit.
Read the ruling.
Contact: Tim Preso, Earthjustice, (406) 586-9699 Lloyd Dorsey, Greater Yellowstone Coalition, (307) 734-6004 Louise Lasley, Jackson Hole Conservation Alliance, (307) 733-9417 James Navarro, Defenders of Wildlife, (202) 772-0247 Evan Hirsche, National Wildlife Refuge Association, (202) 292-2421
USCA Case #10-5144 Document #1322265 Filed: 08/03/2011 Page 1 of 12
United States Court of Appeals FOR THE DISTRICT OF COLUMBIA CIRCUIT Argued May 12, 2011 Decided August 3, 2011 No. 10-5144
Around the turn of the last century, a series of severe winters in Wyoming strained the elk populations and spurred the good people of Jackson to save the elk by feeding them. When Congress created the Refuge in 1912, the federal government continued this practice, which the parties refer to as supplemental feeding. For roughly seventy days each winter, approximately 7000 elk and 1000 bison are drawn daily to the federal trough.
In recent years, it has become apparent that this practice, though born of benevolence, causes significant problems. According to the Department of the Interior, supplemental feeding leads to a seasonal concentration of elk and bison that is “an unnatural situation that has contributed to . . . an increased risk of potentially major outbreaks of exotic diseases . . . [and] damage to and loss of habitat.” Final Bison and Elk Management Plan and Environmental Impact Statement for the National Elk Refuge / Grand Teton National Park / John D. Rockefeller, Jr., Memorial Parkway 9 (Feb. 1, 2007) [hereinafter February 2007 Management Plan and EIS]. This risk poses an existential threat to the elk and bison and puts the very purpose of the Refuge at jeopardy.
See id.USCA Case #10-5144 Document #1322265 Filed: 08/03/2011 Page 3 of 12
(noting that the risk of diseases posed by increased concentrations of the animals has “the greatest potential to hinder . . . [the] purposes . . . [of] the National Elk Refuge”).
One major problem is brucellosis—also known as “Bangs disease, undulant fever, and contagious abortion,” id. at 564—which causes an infected female to abort her first calf, leaving behind contaminated fetal tissue on the ground capable of transmitting the disease to other animals, id. at 129. Brucellosis rates within normal Wyoming elk herds are approximately two percent, but rates among elk that frequent the Refuge feeding lines have averaged around seventeen percent in recent years. Id. at 130. Another major problem, chronic wasting disease (CWD), is the elk version of mad cow disease: Like its bovine counterpart, CWD assaults the central nervous system, causing brain lesions, behavioral changes, a loss of body condition, and ultimately death. CWD is caused by abnormal, non-living proteins known as prions that persist in the soil where infected animals graze, even after intensive efforts to remove them. Id. at 136-40. Statistical sampling suggests that in open, elk-hunt areas in Wyoming, the prevalence of CWD in elk averages around four percent. Id. at 137. But in confined areas—like those created by the feed lines—the prevalence can exceed ninety percent. Id. CWD is not yet prevalent in the Refuge, but if that changes, “environmental contamination will become a major concern due to the disease’s ability to persist in the environment for a long period of time.” Id.
All agree that supplemental feeding increases the risk of such diseases. Without supplemental feeding, the elk would gather in smaller groups, meaning that one sick elk would infect only the handful of others around it. But because the feeding lines bring so many together, the disease of one can quickly become that of many, if not all.
The Defenders also argue that the plan unlawfully gives the Wyoming Fish and Game Department a veto over whether supplemental feeding will end. They point to language in the plan stating that the agencies will seek to “decrease reliance on intensive supplemental winter feeding, including complete transition to free-standing forage if and when several established criteria are met, including support from the Wyoming Game and Fish Department and the public.” April 2007 Management Plan 137 (emphasis added).
Regardless of how we might have read this language in the first instance, the Secretary has assured us in his briefs and at oral argument that the language confers no veto. See Appellees’ Br. 34 (characterizing the disputed provision as “aspirational” rather than a grant of any power to Wyoming); Wyoming's Br. 28 n.6 (also agreeing that Wyoming does not have a veto); cf. Wyoming v. United States, 279 F.3d 1214, 1234 (10th Cir. 2002) (“[F]ederal management and regulation of federal wildlife refuges preempts state management and regulation of such refuges . . . where state management and regulation stand as an obstacle to the accomplishment of the full purposes and objectives of the Federal Government.”). We take the Secretary at his word that Wyoming has no veto over the Secretary’s duty to end a practice that is concededly at odds with the long-term health of the elk and bison in the Refuge.
For the foregoing reasons, the district court’s judgment is
Quarterly Newsletter from the Animal Health Division of the Mar 2010 Montana Department of Livestock Volume 4, Issue 1
From my chair, I see the three greatest contributors to elk disease, not necessarily in the order of importance as; Yellowstone National Park bison, elk feed grounds in Wyoming, and elk congregation/ distribution issues in the state of Montana. Ultimately, it is not in the best interest of the livestock industry or wildlife health to promote large congregations of elk to assemble during the abortion/calving season.
Harmful practice of winter feeding leads to overcrowding and diseases
Groups Seek to Protect Elk From Disease
Monday, May 10, 2010
Appeal earlier ruling allowing artificial winter feeding
Appeals Court Rules in Case Challenging Elk Feed Grounds
Friday, July 10, 2009
Phasing out annual winter feedings needed to protect elk, other wildlife
Elk Herds in Wyoming Harmed by Feedings
Tuesday, June 3, 2008
Conservation organizations argue that artificial winter feedings are detrimental to elk and their habitat
Conservationists Call for Wyoming Elk Feeding Reforms
Monday, November 21, 2005
Action requested to prevent chronic wasting disease epidemic
From a small nexus in southeast Wyoming and northeast Colorado three decades ago, CWD has already spread to Canada and 20 states, including half of Wyoming. So far, it has not reached Wyoming’s feed-ground elk. Where animals are dispersed across winter ranges in Wyoming and Colorado, less than 10 percent of elk have become infected. But on game farms and in research facilities, the nearest surrogates to Wyoming’s feed grounds, the disease has proven devastating.
If the worst should happen, feed grounds will create 23 hotspots for the spread of CWD throughout the Greater Yellowstone Ecosystem, where some 200,000 elk, moose, and deer — plus adjacent herds in Idaho and Montana — are at risk.
Yet the state of Wyoming and federal resource agencies have shown little interest in acting to reduce this risk, even though science and logic advocate returning Jackson Hole’s treasured elk to a free-ranging herd that can withstand the assault of CWD or the next emerging disease, whatever it might be.
Of the alternatives for safeguarding the elk and all the ecological, economic, and social benefits they provide, the most realistic choice is allowing an unfed, free-ranging herd to sustain itself on range that is 98 percent in public ownership. While a smaller elk herd may be unacceptable to some people, I’ve concluded that this is far preferable to an overstocked range riddled with diseased and dying animals.
Embarking on this path will not only diminish disease threats, but remedy other problems that are the consequences of an overstocked range, including damaged wildlife habitats, declining biodiversity, controversial elk hunts and citizen-financed feeding programs.
Besides science and logic, a federal court decision now backs a change in elk management policy. In a case brought by five conservation organizations, a District of Columbia appellate court ruled August 2011 that winter-feeding on the National Elk Refuge is inconsistent with law. Without more delay, it is time for the state and federal agencies charged with stewarding the public’s wildlife and wildlands to make this change happen.
Dr. Bruce Smith tells truth about feeding elk that Wyoming politicians need to heed, but refuse By Ralph Maughan On December 19, 2011
After 22 years as the chief biologist at the National Elk Refuge, Bruce Smith pens an easy-to-read, but stark warning about continuing elk feeding- Prions are bit like tiny pieces of radioactive material in that they are very dangerous promoters of illness and for practical purposes never really go away, resting in the dust and grass ready to kill far into the future. On the other hand, they are not radioactive. They are just proteins, but proteins that are deformed and infectious like viruses, brain eaters that are not even alive.
Wyoming’s politicians are a strange breed when it comes to elk and many other animals. They worry greatly about a couple hundred wolves that are arguably making the elk herds there stronger by culling out disease, but they can’t bring themselves to deal with a nightmarish microscopic killer protein, the prion that causes a transmissible spongiform encephalopathy, more commonly called chronic wasting disease or just plain “mad elk disease” among elk, deer, moose, and many more animals.
Dr. Bruce Smith has spent his career studying and managing elk on the Wind River Indian Reservation and the famed National Elk Refuge at Jackson, Wyoming. Recently retired from federal public service, he has written Where Elk Roam: Conservation and Biopolitics of Our National Elk Herd. (see also at amazon.com). It is beautifully written and it is also a last ditch warning to Wyoming where business interests can’t wean themselves from the tourists who want to see them feed elk and the hunters who think winter feeding of elk keeps the herds big and strong.
Todd Wilkinson has an excellent interview of Dr. Smith in the latest Wildlife Art Journal. “An Interview With Biologist Bruce Smith About Mad Elk Disease*. Author of ‘Where Elk Roam’ Tackles Threats To America’s Most Famous Wapiti Herd.” Written By Todd Wilkinson.
Unfortunately we have already heard from Wyoming’s state game vet on the issue. Can anyone guess what they are going to do
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8 Responses to Dr. Bruce Smith tells truth about feeding elk that Wyoming politicians need to heed, but refuse
Terry S. Singeltary Sr. says:
December 19, 2011 at 9:13 am
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Sunday, November 13, 2011
COLORADO CWD CJD TSE PRION REPORTING 2011
Close elk feeding grounds, make elk migrate, avoid disease disaster
By Ken Cole On November 3, 2011 ·
In Bison, brucellosis, Disease, Elk, Wildlife Disease, Wildlife News, WyomingChronic Wasting Disease (CWD) has been found in elk, deer, and moose in several areas of Wyoming and has been moving ever closer to the already brucellosis infected elk herds that use feeding grounds in northwest Wyoming. The feeding grounds long ago caused the elk to stop migrating to a unique area along the Continental Divide called the Red Desert far to the south.
A retired biologist who worked at the National Elk Refuge near Jackson is calling for an end to the feeding program and putting forth an idea to train the elk their former migration route south. He is hoping to avoid the oncoming CWD outbreak which will undoubtably infect entire herds and soon enter Yellowstone National Park causing a wildlife disaster. The feeding grounds are like petri dishes for disease because of the high density of elk. Brucellosis thrives on the feeding grounds and continues to have wide ranging repercussions for elk and bison in places far removed from the feeding grounds. Also, CWD has a nasty habit of infecting soils for the long term leaving an area capable of infecting elk for years and years.
CWD is a prion, or a virus made of protein rather than RNA or DNA like most viruses. It is related to mad cow disease, scrapie in sheep, and Creutzfeldt-Jakob disease in humans and is deadly. CWD results in a condition called spongiform encephalopathy, meaning that the brain of its victims has spongelike holes in it. It is unknown whether CWD infects humans but it is recommended that people avoid coming into contact with the nerve tissue of the animals such as the brain or spinal column.
Retired biologist: Stop feeding, make elk migrate By By Angus M. Thuermer Jr. – Jackson Hole News & Guide
Wednesday, October 24, 2012
WYOMING Deer Hunt Area 132 Near Green River Added to CWD List
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.
In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters. If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2 .
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal . ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233 .
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514 .
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102 .
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121 .
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
Friday, November 09, 2012
Chronic Wasting Disease CWD in cervidae and transmission to other species
Saturday, September 01, 2012
Resistance of Soil-Bound Prions to Rumen Digestion
Friday, October 26, 2012
CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT PRODUCTS, BAITING, AND MINERAL LICKS
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: firstname.lastname@example.org
North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents.
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
Monday, September 17, 2012
Rapid Transepithelial Transport of Prions Following Inhalation
Thursday, December 29, 2011
Aerosols An underestimated vehicle for transmission of prion diseases?
please see more on Aerosols and TSE prion disease here ;
Soil clay content underlies prion infection odds
W. David Walter 1 , * , Daniel P. Walsh 2 , * , Matthew L. Farnsworth 3 , Dana L. Winkelman 1 & Michael W. Miller 2
1 United States Department of the Interior, United States Geological Survey, Colorado Cooperative Fish and Wildlife Research Unit , Fort Collins , Colorado
80523-1484, USA. 2 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, Colorado 80526-2097, USA. 3 United States Department
of Agriculture, Animal and Plant Health Inspection Services, Veterinary Services, Centers for Epidemiology and Animal Health , Fort Collins , Colorado
80526-8117 , USA . * These authors contributed equally to this work. Correspondence and requests for materials should be addressed to M.W.M.
(email: email@example.com ) .
Received 6 Sep 2010 | Accepted 19 Jan 2011 | Published 15 Feb 2011 DOI: 10.1038/ncomms1203
Environmental factors — especially soil properties — have been suggested as potentially important in the transmission of infectious prion diseases. Because binding to montmorillonite (an aluminosilicate clay mineral) or clay-enriched soils had been shown to enhance experimental prion transmissibility, we hypothesized that prion transmission among mule deer might also be enhanced in ranges with relatively high soil clay content. In this study, we report apparent influences of soil clay content on the odds of prion infection in free-ranging deer. Analysis of data from prion-infected deer herds in northern Colorado, USA, revealed that a 1 % increase in the clay-sized particle content in soils within the approximate home range of an individual deer increased its odds of infection by up to 8.9 % . Our findings suggest that soil clay content and related environmental properties deserve greater attention in assessing risks of prion disease outbreaks and prospects for their control in both natural and production settings.
The capacity of clay minerals and clay-laden soils to capture and enhance infectivity of shed or deposited prions 19,20,25 – 27 and the common tendency of ruminants to ingest soil both deliberately and incidentally in the course of foraging and grooming 12,44,45 provide an elegantly simple hypothetical mechanism for indirect prion transmission, as follows: infected individuals propagate infectious prions in mucosa-associated lymphoid tissues and shed prions into ingesta and saliva; ingested and environmental soil microparticles with a high phyllosilicate (especially smectite) content bind to, sequester and enhance infectivity of prions both before and after leaving the host; microparticle-bound prions are incorporated into surface soil; susceptible individuals consume contaminated soil and some become infected. (Also see Supplementary Figure S1 .) This mechanism may underlie the apparent importance of indirect transmission in explaining observed patterns of prion infection among captive mule deer 10,11 , and perhaps among sheep 3,4,6,7 . In light of these and others ’ findings, soil clay content and related environmental properties deserve greater attention in assessing local and regional risks of prion disease outbreaks and prospects for their control in natural and production settings.
Friday, February 25, 2011
Soil clay content underlies prion infection odds
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
2009 CWD SYMPOSIUM UTAH
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area
Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- firstname.lastname@example.org
Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.
The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
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Tuesday, January 10, 2012
ESHRE position statement concerning prion detection in urinary gonadotropin formulations
Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Sheep Naturally/Experimentally Infected with Scrapie and Deer with Preclinical/Clinical Chronic Wasting Disease
▿Richard Rubenstein1,*, Binggong Chang1, Perry Gray2, Martin Piltch2, Marie S. Bulgin3, Sharon Sorensen-Melson3 and Michael W. Miller4 + Author Affiliations
1Departments of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, New York 11203 2Los Alamos National Laboratory, Los Alamos, New Mexico 87545 3University of Idaho, Caine Veterinary Teaching and Research Center, 1020 E. Homedale Road, Caldwell, Idaho 83607 4Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, Colorado 80526-2097
Prion diseases, also known as transmissible spongiform encephalopathies, are fatal neurodegenerative disorders. Low levels of infectious agent and limited, infrequent success of disease transmissibility and PrPSc detection have been reported with urine from experimentally infected clinical cervids and rodents. We report the detection of prion disease-associated seeding activity (PASA) in urine from naturally and orally infected sheep with clinical scrapie agent and orally infected preclinical and infected white-tailed deer with clinical chronic wasting disease (CWD). This is the first report on PASA detection of PrPSc from the urine of naturally or preclinical prion-diseased ovine or cervids. Detection was achieved by using the surround optical fiber immunoassay (SOFIA) to measure the products of limited serial protein misfolding cyclic amplification (sPMCA). Conversion of PrPC to PrPSc was not influenced by the presence of poly(A) during sPMCA or by the homogeneity of the PrP genotypes between the PrPC source and urine donor animals. Analysis of the sPMCA-SOFIA data resembled a linear, rather than an exponential, course. Compared to uninfected animals, there was a 2- to 4-log increase of proteinase K-sensitive, light chain immunoglobulin G (IgG) fragments in scrapie-infected sheep but not in infected CWD-infected deer. The higher-than-normal range of IgG levels found in the naturally and experimentally infected clinical scrapie-infected sheep were independent of their genotypes. Although analysis of urine samples throughout the course of infection would be necessary to determine the usefulness of altered IgG levels as a disease biomarker, detection of PrPSc from PASA in urine points to its potential value for antemortem diagnosis of prion diseases.
Received 13 May 2011. Accepted 14 June 2011. ↵*Corresponding author. Mailing address: Downstate Medical Center, Departments of Neurology and Physiology/Pharmacology, Box 1213, 450 Clarkson Avenue, Brooklyn, NY 11203. Phone: (718) 270-2019. Fax: (718) 270-2459. E-mail: email@example.com. ↵▿ Published ahead of print on 29 June 2011.
Copyright © 2011, American Society for Microbiology. All Rights Reserved.
Sunday, July 03, 2011
Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD Deer
Thursday, June 09, 2011
Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission
CHRONIC WASTING DISEASE: A MODEL FOR PRION TRANSMISSION VIA SALIVA AND URINE
Sunday, December 06, 2009
Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer
Wednesday, March 18, 2009
Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay
*** Tuesday, September 02, 2008
Detection of infectious prions in urine (Soto et al Available online 13 August 2008.)
THE states are going to have to regulate how many farms that are allowed, or every state in the USA will wind up being just one big private fenced in game farm.
kind of like they did with the shrimping industry in the bays, when there got to be too many shrimp boats, you stop issuing permits, and then lower the exist number of permits, by not renewing them, due to reduced permits issued.
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ??
11,000 game farms X $465,000., do all these game farms have insurance to pay for this risk of infected the wild cervid herds, in each state ??
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)
Friday, October 12, 2012
Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule Proposals for “Chronic Wasting Disease (CWD)”
Texas Animal Health Commission (TAHC)
Tuesday, November 13, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD
Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail firstname.lastname@example.org
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.
These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed Analysis Ingredients / Products Feeding Directions
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS 22.6 KG.
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products 15%, Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Pyosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement, Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game Pellets A RATION FOR DEER F3153
GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat (Min) 2.0% Crude Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca) (Max) 1.75% Phosphorus (P) (Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products, 15% Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Phosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement, Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
FEEDING DIRECTIONS Feed as Creep Feed with Normal Diet
Grain Products, Roughage Products (not more than 35%), Processed Grain By-Products, Plant Protein Products, Forage Products, __Animal Protein Products__, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite, Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide, Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid, Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
DIRECTIONS FOR USE
Deer Builder Pellets is designed to be fed to deer under range conditions or deer that require higher levels of protein. Feed to deer during gestation, fawning, lactation, antler growth and pre-rut, all phases which require a higher level of nutrition. Provide adequate amounts of good quality roughage and fresh water at all times.
full text ;
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
Monday, June 18, 2012
natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds captive Korea and Experimental oral transmission to red deer (Cervus elaphus elaphus)
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
----- Original Message -----
From: David Colby To: email@example.com
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware
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UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit
*** Saturday, October 6, 2012 ***
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report