02/14/2012
Deer Farming Bill Advances Chris Lawrence Charleston
Jack Oliver -- Marion Co. Deer Farmer
Legislation backed by the deer farming industry in West Virginia is advancing in the state Senate. A bill which would move the supervision of deer farm operations away from the DNR and under the umbrella of the Department of Agriculture passed the Senate Finance Committee this week and is due to be voted on by the full Senate.
"The biggest thing we're trying to accomplish is the slaughter and sale of our animals for venison product on the open market," said Jack Oliver the owner of a deer farming operation in Marion County.
Oliver told committee members this week the deer farms are a lucrative business for a number of different products.
"Last year alone I sold $12,000 worth of semen out of my bucks," Oliver said. "We sell breeding stock. We sell antlers. We sell semen out of our animals, we sell urine out of our animals. There are endless amounts of ways to make money."
The one thing they cannot do under the present rules is sell the meat to restaurants as a venison product.
The DNR issued a crackdown on the sale of venison meat after the discovery of Chronic Wasting Disease in Hampshire County. The emergency rule drove a number of deer farming facilities out of business. Oliver says the numbers are starting to rebuild. Presently there are 37 such facilities in the state.
The DNR raises concerns about the potential for disease spread and the mingling of artificially raised animals from pens with the wild whitetail population. The issue of escape from those captive facilities is a concern.
"We have pedigrees and we have DNA on our animals," Oliver told lawmakers. "We can differentiate our animals from wild live stock using the DNA."
Oliver compared the raising of captive deer to the breeding process for rodeo bulls in Texas. He said rodeo bulls are bred with specific skills in mind, twisting and turning and a rough disposition to wow a rodeo audience. He says those bulls which don't meet the criteria are shipped to the slaughter house. He and his fellow deer farmers want the opportunity to do the same with captive whitetails which don't meet the parameters set aside for a quality captive whitetail.
"The Department of Agriculture hasn't gone to lobby for the takeover of deer population in this state," said Deputy Ag Commissioner Bob Tabb. "What this is about is health issues and regulation. If it's behind the fence and game being raised in a captive manner, pretty much everything from that deer can be sold except for the meat."
WHY is the department of agriculture taking over the DNR’s job about deer game farming and CWD there from, and the bigger question is, WHY IS THE GAME FARM INDUSTRY SO FIRED UP ABOUT THIS, AND WANTING IT TO HAPPEN $$$
I could not find the bill, so as I could post it, and what the reasons were ???
bbbut, let’s look at some past history of these game farms and CWD there from, shall we.
FIRST, this one sentence here takes the cake ;
"Last year alone I sold $12,000 worth of semen out of my bucks," Oliver said. "We sell breeding stock. We sell antlers. We sell semen out of our animals, we sell urine out of our animals. There are endless amounts of ways to make money."
what Oliver failed to tell you was, everything his industry stands for, stands for the spread of Chronic Wasting Disease CWD. God, the ignorance is profound. the greed has brought us to where we are today. these deer farms will be the demise to the wild. you can thank the almighty dollar for that. I don’t know where to start with this ignorance$ now I am sure the game farm industry failed to tell you all this ;
well, let’s just start with the first part of that sentence, the $12,000 worth of semen full of CWD maybe ???
price of poker goes up for those Boone-Crocket type straw bred bucks. see ;
PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep
now, what about those antlers and the velvet there from ;
see the CDC warning about antler velvet and the risk of cwd and cjd there from ;
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
see full text and more ;
now the third stupid thing Oliver said in that one sentence was about the third product, that spreads CWD, in which he sells, of which is NOT tested for CWD, URINE. the use of URINE, 100% deer or elk urine, untested for CWD, is as about as stupid as one could do for the deer and elk herds. but you do it, because ;
A. IT MAKES MONEY !
B. the myth that it makes you a better hunter
however, C. is what OLIVER et al do not tell you ;
C. URINE PRODUCTS HAVE THE HIGH LIKELIHOOD, BASED ON SCIENCE, TO SPREAD CWD.
THAT ONE SENTENCE OLIVER SAID, AND RAMIFICATIONS THERE FROM, COULD HAVE THE POTENTIAL TO SPREAD CWD TO HELL AND BACK ;
"Last year alone I sold $12,000 worth of semen out of my bucks," Oliver said. "We sell breeding stock. We sell antlers. We sell semen out of our animals, we sell urine out of our animals. There are endless amounts of ways to make money."
please, give me the chance to show you the science, please read on, I am vested in nothing but the truth, you should be too. your deer herds depend on it. you hunters are the stewards of the forest and the hunt, NOT these game farm industry, AND OR whom every THEY want to regulate them. the department of agriculture does not have a good record when it comes to TSE Prion surveillance and or eradication.
look, the DNR et al are not out to get anyone, when it comes to CWD and TSE prion disease. they are trying to protect your deer and elk herds. the DNR is not your enemy here, the game farm industry is. please I urge all of you to look at the science. I have no dog in this hunt. however, CWD, and friendly fire there from, that my friends involves all of us. you, me, our children, family, friends. I assure you of that. ...
all you folks screaming for less government in your life. well, be careful what you wish for ;
TSE prion disease such as Chronic Wasting Disease, knows no borders, they know no country, and the know no age groups. red or blue, right or left, republican or democrat, it is 100% fatal once clinical in man and animal. I lost my mother to the Heidenhain Variant of Creutzfedlt Jakob Disease December 14, 1997, and have been trying to validate her death, and warn others of the science, that does not reach the public domain. I am PRO-hunter, I am a meat eater. I am ANTI-stupid. take this information with how ever many grains of salt you wish, but please be warned, the science is there, but politics has trumped science in the world of TSE prion disease since day one $$$
it’s all about money folks $$$
Greetings West Virginia Deer hunters et al,
please be sure, if you allow these slimy, slime ball lobbyist type come in and allow the deer farming industry to police themselves, then God help you all. these game farms are nothing more than a petri dish for infectious disease such as, and especially Chronic Wasting Disease, if nothing else. I urge you all to ban all game farms. here is why ;
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.
Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.
However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.
Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <
SNIP...SEE FULL TEXT ;
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
Thursday, February 09, 2012
Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
Monday, February 13, 2012
Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164
Tuesday, February 14, 2012
Oppose Indiana House Bill 1265 game farming cervids
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
Thursday, January 26, 2012
The Risk of Prion Zoonoses
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167
Thursday, January 26, 2012
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659
now, a few things to ponder about those said double fences that will supposedly stop those deer from escaping.
what about water that drains from any of these game farms. surrounding water tables etc., are the double fences going to stop the water from becoming contaminated? where does it drain? who's drinking it?
Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area
65
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- tracy.a.nichols@aphis.usda.gov
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.
snip...
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.
snip...end...full text at ;
what about rodents there from? 4 American rodents are susceptible to CWD to date. are those double fences going to stop these rodents from escaping these game farms once becoming exposed to CWD?
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation perio d of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these spec ies as potential hosts, bridge species, and reservoirs of CWD is required.
please see ;
SOURCE REFERENCE
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§ * Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France Contributed by D. Carleton Gajdusek, December 22, 1999
see full text:
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Cathrin E. Bruederle,1* Robert M. Hnasko,1 Thomas Kraemer,2 Rafael A. Garcia,3 Michael J. Haas,3 William N. Marmer,3 and John Mark Carter1 1USDA-ARS WRRC, Foodborne Contaminants Research Unit, Albany, California, United States of America 2Forensic Toxicology, Institute of Legal Medicine, Saarland University, Homburg/Saar, Germany 3USDA-ARS ERRC, Fats, Oils and Animal Coproducts Research Unit, Wyndmoor, Pennsylvania, United States of America Neil Mabbott, EditorUniversity of Edinburgh, United Kingdom *
OLD BSE TSE PRION HISTORY
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed.
89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence.
90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.
91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.
snip...
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)
PAUL BROWN SCRAPIE SOIL TEST
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)
INCINERATION TEMPS
Requirements include:
a. after burning to the range of 800 to 1000*C to eliminate smell; well heck, this is just typical public relations fear factor control. do you actually think they would spend the extra costs for fuel, for such extreme heat, just to eliminate smell, when they spread manure all over your veg's. i think not. what they really meant were any _TSE agents_.
b. Gas scrubbing to eliminate smoke -- though steam may be omitted; c. Stacks to be fitted with grit arreaters;
snip...
1.2 Visual Imact
It is considered that the requirement for any carcase incinerator disign would be to ensure that the operations relating to the reception, storage and decepitation of diseased carcasses must not be publicly visible and that any part of a carcase could not be removed or interfered with by animals or birds.
full text;
18. The EA’s assertion at the Thruxted planning inquiry that the precautionary principle does not apply in the case of Thruxted Mill in view of the low risk entailed by its effluent discharge is entirely unfounded. The source data presented by the EA at the Thruxted Inquiry derive in part from its assumptions concerning the segregation of infectivity to the various products of rendering. The EA also stipulates a minimum particle size of 1013 molecules for human infection and assumes there is a 2500-fold reduction of infectivity by rendering, filtration and biological treatment prior to discharge. In fact, the minimum particle size may be at least 1012 times lower. The reduction in the input levels of BSE infectivity prior to discharge will also be very substantially less than implied in the EA source data, and may indeed be minimal. The EA assumes that biological treatment of the rendering effluent will reduce or eliminate BSE infectivity. This is probably the exact opposite of what is actually likely to happen.
19. In his proof of evidence at the Thruxted Inquiry, Mr Young asserted that "effective filtering of clumps of material is likely". As already mentioned, infectious prions are known to pass
[PDF]BSE INQUIRY Statement of behalf of the Environment Agency ...
File Format: PDF/Adobe Acrobat - View as HTML
... his Statement of March 1998 to the BSE Inquiry ... systems subject to regular or intermittent
contamination by rapid movement of recharge water ...
BSE INQUIRY
Statement of behalf of the Environment Agency
Concerning Thruxted Mill
By
Mr C. P. Young
Principal Hydrogeologist, Soil Waste and Groundwater Group
WRc plc; Medmenham, Bucks
Friday, February 25, 2011
Soil clay content underlies prion infection odds
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.
www.landesbioscience.com Prion
see more about soil content and CWD here ;
URINE AND TSE PRIONS
In August 2010
NEW RULES CAME INTO EFFECT FOR:
1) hunters using natural attractants (e.g., deer urine used for hunting)
Use of Natural Attractants Prohibited
Ontario Hunters – if you possess and use products that contain, or purport to contain, any body part of a member of the deer family, you must be aware of this regulation.
The Amended Regulation
Ontario has passed an amendment to O. Reg 665/98 (Hunting) under the Fish and Wildlife Conservation Act, 1997. This amendment prohibits possession and use of products that contain, or purport to contain, body parts of any member of the deer family including blood, urine, gland oils and other fluids, for the purposes of hunting. This prohibition applies to body parts and fluids from hunter-harvested deer or moose and applies to all hunting in Ontario.
One potential pathway for the spread of CWD is from possession and use of hunting attractants that contain body parts of members of the deer family. These products contain urine, blood, gland oil or other bodily fluids obtained from captive/farmed deer, elk or other cervids. This regulation also prohibits hunters from possessing or using these types of materials (i.e., body fluids and parts) obtained from wild and farmed cervids for the purposes of hunting in Ontario. These products may contain infectious material and may be capable of introducing CWD to Ontario.
Important Information
Hunters in Ontario may still possess and use artificial or plant-based products that can attract or lure deer and moose but do not contain any body parts of a member of the deer family. These alternative products are commonly available from merchants selling hunting equipment as well as through the Internet.
Why is this Amendment Required?
CWD is not thought to be present in Ontario at this time. However, these products may contain infectious material and may be capable of introducing CWD to Ontario. As the source of these products is often of an unknown origin and from animals of unknown health status, and as CWD continues to be detected in some captive/farmed deer and elk, these actions must be taken to minimize risks.
Possession of High Risk Carcass Parts Originating from Outside the Province Now Prohibited. This applies to all members of the deer family.
Ontario Hunters - if you hunt outside Ontario and bring the carcasses or parts of any member of the deer family (e.g. white-tailed, mule, black tailed or other deer and elk, etc.) into Ontario, you need to be aware that the ban on possessing high risk animal parts now applies to moose and caribou.
The Amended Regulation
Ontario has amended an existing regulation to prohibit the possession in Ontario of high risk body parts and fluids of members of the deer family harvested in other jurisdictions to also include moose and caribou.
High risk parts include the head, spinal column, unprocessed antlers or hide, hoofs, lymph nodes, eyes, spleen, mammary glands, entrails and internal organs. These animal parts are considered high risk because in sick or infected animals they contain prions that may transmit CWD.
The regulation applies to all members of the deer family (referred to as "cervids" and comprising more that 37 species) including all species of deer, elk, moose and caribou that are harvested outside Ontario and transported back or possessed in Ontario.
At the time of the initial regulation proposal, moose and caribou were generally not considered a risk of contracting or transfer of CWD. However, since that time, wild moose in two U.S. states have tested positive for CWD and recent scientific evidence indicates that caribou may be susceptible to infection by CWD. As a result, an amendment under the Fish & Wildlife Conservation Act, 1997 in now in effect. This amendment expands the definition of "cervid" in the regulation to include moose and caribou, so that these species are now also included under the regulation.
Items in the regulation include:
1. It is now illegal in Ontario to possess any part of the antlers, head, brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary glands, entrails, internal organs or spinal column of any member of the deer family that has been killed outside Ontario.
2. The prohibition above (#1) does not apply to finished taxidermy mounts, tanned skin, canine teeth with no tissue attached.
3. Antlers or antlers with skull cap attached may be legally possessed as long as there is no tissue or skin attached to them and they are separate from the remainder of the skull.
4. It is also legal to possess a hide or skin of the head of any member of the deer family including that part of the hide commonly referred to as the "cape" only if:
• all other tissue is removed, AND • it is kept in a container from which nothing can escape, (e.g., cooler taped shut, enclosing the animal in plastic or a tarp), AND • it is delivered to a tanner or taxidermist within five days of coming into Ontario.
5. If all or portion of the hide or skin of the head identified above (#4) is disposed of, it must be done at a waste disposal site authorized under the Environmental Protection Act such as a municipal landfill.
6. None of these rules (#1 to #5) apply to the prohibited parts (the antlers, head, brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary glands, entrails, internal organs or spinal column) of any member of the deer family if they are transported through Ontario to another jurisdiction in a container from which nothing can escape, (e.g., cooler taped shut, enclosing the animal in plastic or a tarp).
7. If you are transporting the antlers, head, brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary glands, entrails, internal organs or spinal column of any member of the deer family in a container as described above, it must be labelled to show the species of cervid, the place where it was acquired and the name and address of the person who owns the parts in the container.
8. If you have transported a member of the deer family into Ontario that was harvested or killed in another jurisdiction, but later find out that it has tested positive for CWD, you must immediately notify a Ministry of Natural Resources Office and provide information as requested.
Important Information
Hunters will still be allowed to bring in meat and other parts such as antlers and hides, if those antlers and hides are properly treated to reduce risk of CWD transfer (see Items #3 and #4 above).
The regulation applies to all members of the deer family from all states, provinces or other jurisdictions whether CWD has been detected in that jurisdiction or not. The regulation does not affect hunters who have harvested an animal in Ontario. However, persons who wish to export Ontario deer, moose, elk or caribou should check with applicable jurisdictions should they wish to possess these Ontario cervids out of province.
Why is this Amendment Required?
CWD is not thought to be present in Ontario at this time. However, it's possible that by transporting out-of-province infected parts of carcasses into Ontario, disease-causing prions could be spread into the environment. These prions may live for years, increasing the risk that Ontario deer, moose, elk or caribou could become infected with CWD. This regulation will minimize that risk.
Most North American jurisdictions, whether CWD is present or not, are taking steps to minimize the spread of CWD. Manitoba and more than 20 states in the United States have already taken action to address the spread of CWD through high risk carcass parts.
Transport of Live White-tailed Deer, American Elk, Moose or Woodland Caribou into Ontario Now Restricted Unless Accompanied by a Provincial Permit
Transporting live white-tailed deer, American elk, moose, woodland caribou and their hybrids into Ontario now requires a permit under a new regulation under the Fish & Wildlife Conservation Act, 1997. This applies to the transport of live white-tailed deer, American elk, moose and woodland caribou into Ontario for any purpose, including farming, slaughter, and display in zoos.
Anyone wishing to transport live white-tailed deer, American elk, moose or woodland caribou into Ontario is required to meet new conditions to minimize the risk of spreading Chronic Wasting Disease. MNR now requires written notice regarding health status and documentation of a premise assessment from the Ontario Ministry of Agriculture, Food and Rural Affairs (OMAFRA) before issuing a permit to transport these species into Ontario. Information from OMAFRA on the permit system.
For information about these new requirements and about the process for applying for a permit please contact:
•the Animal Health Coordinator with Ontario Ministry of Agriculture, Food and Rural Affairs (OMAFRA) at (519) 826-7612, or •the Wildlife Health Policy Advisor with the Ministry of Natural Resources (MNR) at (705) 755-1573.
Why is this Regulation Required?
Chronic Wasting Disease (CWD) is a degenerative, fatal brain disease that affects certain members of the deer family, including white-tailed deer, elk, and moose. The disease is believed to be caused by abnormal proteins called prions. CWD is in the same family of diseases as bovine spongiform encephalopathy (BSE or Mad Cow Disease).
There is no evidence to date that CWD can be transmitted to humans or to domestic livestock such as cattle. However, CWD has been detected in wild and/or captive/farmed deer, elk or moose in 18 U.S. states and two Canadian provinces. There is a significant risk to wild Ontario deer, elk, caribou and moose if CWD enters Ontario as the disease is fatal in these species and there is no cure.
CWD is not believed to be present in the wild in Ontario. One potential pathway for the spread of CWD is the movement of infected cervids and/or their hybrids from other jurisdictions that could spread infective prions to other wild or captive animals in Ontario.
Thursday, June 09, 2011
Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission
Tuesday, September 02, 2008
Detection of infectious prions in urine (Soto et al Available online 13 August 2008.)
2011 AND WE STILL HAVE HUNTERS POURING 100% UNTESTED (potentially CWD infected) URINE ALL OVER THEMSELVES FOR A KILL. ...TSS
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...
Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.
www.gamecalls.net/hunting...lures.html
ELK SCENT/SPRAY BOTTLE
Works anytime of the year *
100 % Cow Elk-in-Heat urine (2oz.) *
Economical - mix with water in spray mist bottle *
Use wind to your advantage
Product Code WP-ESB $9.95
www.elkinc.com/Scent.asp
prions in urine?
DEER & ELK URINE, LURES & SCENT CONTROL DEPARTMENT by MRS.DOE PEE'S Main Index
The Turkey Pro Sez... "Premium, fresh, top-quality, pure 100% undiluted deer lures from Mrs. Doe Pee really work. I won't trust anything else when I'm after big bucks. Sam Collora, owner of the company, proved how well his products work when he bagged this monster buck in 1996.............snip......end........CWD
snip...end
######## Bovine Spongiform Encephalopathy #########
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
Saturday, May 14, 2011
Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion Persistence Promotes Deer Population Decline and Extinction
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
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transg enic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient tra nsmission of a natural sheep classical scrapie isolate to primates.
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas
Comment from Terry Singeltary
Document ID: APHIS-2011-0032-0002Document Type: Public Submission
This is comment on Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program
Docket ID: APHIS-2011-0032RIN:
Topics: No Topics associated with this document
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Show Details
Document Subtype: Public Comment
Status: Posted
Received Date: January 24 2012, at 12:00 AM Eastern Standard Time
Date Posted: January 25 2012, at 12:00 AM Eastern Standard Time
Comment Start Date: January 24 2012, at 12:00 AM Eastern Standard Time
Comment Due Date: March 26 2012, at 11:59 PM Eastern Daylight Time
Tracking Number: xxxxxxxx
First Name: Terry
Middle Name: S.
Last Name: Singeltary
City: Bacliff
Country: United States
State or Province: TX
Organization Name: LAYPERSON
Submitter's Representative: CJD TSE PRION VICTIMS
Comment:
Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001) I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban. Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate. I believe that all game farms should be SHUT DOWN PERMANENTLY. CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the CWD TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
Tuesday, December 20, 2011 CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
additional data submission ;
Name: Terry S. Singeltary
Address:
Bacliff, TX,
Submitter's Representative: CJD TSE PRION VICTIMS
Organization: LAYPERSON
--------------------------------------------------------------------------------
General Comment
Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)
I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban.
Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate.
I believe that all game farms should be SHUT DOWN PERMANENTLY.
CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the CWD TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
Does CWD exist in Virginia?
Yes. To date, two positive cases of CWD have been confirmed in Virginia. The first case of CWD was discovered in a female deer killed by a hunter in November 2009 on private land in Frederick County. The second confirmed case was found during the 2010 hunting season, from a male deer harvested less than two miles away form the first positive. Both cases are within a few miles of where CWD has been detected in Hampshire County, West Virginia every year since 2005. For more information about CWD in West Virginia, see WVDNR's website.
To establish whether CWD occurs in Virginia, the Virginia Department of Game and Inland Fisheries (VDGIF) initiated a CWD surveillance program in fall 2002. From 2002 to 2010, approximately 5,300 samples have been collected across Virginia. This program has included testing deer using three different surveillance approaches: (a) active random sampling of hunter-killed and road-killed deer, (b) targeted surveillance of clinical suspect (sick-looking) and high-risk animals, and (c) testing of all deer that die in captivity (a DGIF permit is required to possess any member of the deer family in Virginia, and most are held in zoos). Except for statewide sampling in 2002 and 2007, active sampling has been confined to an area in Frederick and Shenandoah Counties nearest the CWD cases in West Virginia.
Surveillance and Management Plan for Chronic Wasting Disease 2011-2012
layperson
Terry S. Singeltary Sr.
