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US Department of Agriculture ends funding for chronic wasting disease CWD

Posted Jun 25 2012 12:10pm
for all those game farmers that thought the USDA was the save all to the cervid game farming and ranching with CWD, instead of the DNR. please see ;




US Department of Agriculture ends funding for chronic wasting disease



Friday, June 22, 2012 | 6:00 a.m. CDT; updated 9:02 p.m. CDT, Sunday, June 24, 2012



Chronic wasting disease has been discovered in the wild deer population in Macon County, and residents are concerned about how it will affect the hunting industry in the region. ¦ Carrie Durkee



BY Hannah Wiese, John McLaughlin



COLUMBIA — When Missouri confirmed its first case of chronic wasting disease in a captive white-tailed buck at the Linn County Heartland Wildlife Ranch in February 2010, state and federal officials soon agreed on the need to kill all of the deer in an infected 800-acre pasture on the property.


Yet it took nearly a year from the time the disease was confirmed at the commercial hunting operation for officials to move in and start killing all the game, according to a 2011 Animal and Plant Health Inspection Service report.


A gunner and two spotters, one using an infrared scope, aboard a Missouri Conservation Department helicopter swept the 800-acre pasture in April 2011 looking for the final few deer but saw none. An inspection of the pasture the following month affirmed that the captive deer were dead — 100 in all.


The 100 dead deer were buried in the infected 800-acre pasture with no additional positives found, said Jason Sumners, deer biologist for the Missouri Conservation Department.


Jay Brasher of Utah, who owns the Linn County ranch where the disease was detected, told the Missourian in November that the U.S. Department of Agriculture reimbursed him more than $100,000 for the captive deer killed on the 800 acres at his fenced hunting operation in Linn County.


“It wasn’t nearly what the animals were worth,” he said.


Captive game at the commercial hunting ranch include red deer, white-tailed deer, Rocky Mountain elk, American bison and sheep, according to the ranch's website.


Before depopulating the infected pasture, ranch staff killed 46 white-tailed deer and four red deer from the enclosed 800 acres to test for the disease. The staff also killed 20 elk cows and an additional 10 red deer from separate enclosures at the facility for testing. No positive results for chronic wasting disease were found.


For a three-day, three-night hunt at a Heartland Wildlife Ranch, prices range from $1,800 to kill a cow elk to upwards of $18,500 for a trophy red stag, according to Heartland's 2011 pricing guide.


Bagging a trophy white-tailed buck can cost $15,500 or more, according to the guide.


After depopulating the infected Linn County pasture, testing 10 miles away at a separate commercial hunting facility owned by Brasher in Macon County found the disease in one white-tailed deer in October, another in December and two cases in March.


The discoveries in Macon County came as the federal government was cutting $17 million in nationwide assistance used for compensating owners of infected captive deer herds killed in an effort to control the disease, according to the U.S. Department of Agriculture's 2012 budget.


The funding cut also eliminated federal assistance in monitoring for the disease in wild and captive deer, leaving Missouri and other states on their own in the fiscal battle to keep the disease in check.


Now that the disease has jumped into the wild population, the Missouri Conservation Department plans to step up testing in counties around the two ranches and is pushing new measures designed to contain the disease.


While the state quarantined the Macon County ranch and ordered it depopulated, there's no federal money to help, Sumners said.


Without federal compensation, Brasher said in November that he had considered not killing off deer at his Macon County facility. If he were not to do so, the Missouri Agriculture Department would slap a permanent quarantine on the facility designed to keep the captive deer from leaving the fenced enclosure, according to the department.


Healthy deer, including those in the wild population, can get the disease from nose-to-nose contact with an infected deer, contact with an infected deer's excrement, mere contact with disease-laced soil or other contact with an infected deer, Sumners said.


The Missouri Conservation Department's Wildlife Code calls for the fencing of captive game such as deer to be 8 feet high and "constructed with material of sufficient strength to prevent escape."


Matt Dunfee, coordinator for the nongovernmental Chronic Wasting Disease Alliance, said "it is highly probable, if not a certainty" that captive deer stick their noses through fencing to make contact with wild deer, particularly during mating season.


Sumners said the fencing at the Linn and Macon County Heartland Wildlife Ranches meets Missouri standards, and the fencing material is woven wire with 4 square-inches of space between the wires. He said confined deer are capable of sticking their noses through the gaps.


In January, a Linn County landowner wrote to the Missouri Conservation Department noting he had seen a white-tailed doe inside a Heartland Wildlife Ranch enclosure jump and clear the 8-foot fencing, according to documents provided by the Missouri Department of Agriculture.


In a return email, Christine Tew, spokeswoman for the Missouri Agriculture Department, told the landowner that a depopulation of the facility was under way and a quarantine was in place to prevent live deer from exiting the commercial hunting operation's property without testing.


The Missouri Agriculture Department announced on May 7 that the depopulation of the infected Macon County commercial hunting facility was complete, with the ranch's staff handling the killing of 366 total cervids, or any of various hoofed animals such as deer and elk, at the 3,000-acre facility since October 2011 — when the disease was first confirmed at the property.


Ten total slaughtered cervids from the Macon County facility tested positive for the disease, and the operation remains under quarantine. State and federal officials will conduct a final inspection of the facility to ensure the depopulation is finished, according to the Missouri Agriculture Department.


Officials from the Conservation, Agriculture, and Health and Senior Services departments plan to work with Brasher and his staff in developing a five-year management plan, according to the department.


Linda Hickam, state veterinarian for the Missouri Agriculture Department, could not be reached in previous attempts for an interview, and Dane Henry — a veterinary medical officer at the Animal and Plant Health Inspection Service — said department policy prohibited him from speaking directly with journalists.


Dunfee said delays in depopulating all of the deer from the two ranches could have compromised efforts in Missouri to keep the disease in check.


If Missouri had killed off deer at the commercial hunting operations right away, the state might have been able to stop the disease from spreading into the wild population, he said.


Billion-dollar deer


The loss in federal funds couldn't have come at a worse time for Missouri, which is moving from detecting the disease to trying to contain it.


Soon after the federal cuts, the state's first wild white-tailed deer tested positive for the disease within two miles of the infected Macon County commercial hunting operation, which would have made Missouri eligible for an increase in federal funding.


Five total diseased wild deer have been found to date, all of which were killed within two miles of each other outside of the Macon County ranch.


Missouri would have been in the same tier of funding as Wisconsin — which lost about $2 million to fight its outbreak, according to the Wisconsin Department of Natural Resources.


The U.S. Department of Agriculture issued funding in three tiers:


■ Tier 1 funding, the greatest amount provided, went to states with wild deer infected with the disease.


■Tier 2 funding went to states with neighboring states having wild infections.


■Tier 3 funding went to states with neither wild infections nor neighboring states with wild infections, which received no money.


The Missouri Conservation Department began testing for chronic wasting disease in 2002 and paid for it in-house until 2006, when the federal government pitched in the first time with $90,000.


By 2007, the U.S. Department of Agriculture had cut its share of Missouri assistance to $75,000, and in 2010 the amount declined to $70,000, according to the Conservation Department.


The $70,000 covered statewide testing prior to finding the disease in Missouri, Sumners said. Now that money will have to come from elsewhere in the Conservation Department budget.


“Seventy thousand dollars is no small amount of money,” he said. "While it probably won’t affect chronic wasting disease testing, it could impact something else getting done. We’re still going to do testing, absolutely.”


From where in the department the money will come has yet to be determined, he said. “At this point, I don’t see the cut impacting how we do business.”


The Conservation Department plans to step up its testing of hunter-killed deer during hunting season and has established a six-county perimeter around where the diseased wild deer were detected — outside the infected Macon County commercial hunting facility, Sumners said.


The counties include: Sullivan, Adair, Macon, Linn, Sheridan and Randolph counties.


The department will also sample random deer provided by area taxidermists in northern Missouri, Sumners said. The samples will be mostly bucks, which are more likely to carry the disease, he said. Last year, the department focused on southern Missouri for random taxidermist testing.


Pending approval of control measures for wild deer, Missouri conservation officials will begin taking additional steps by the fall, Sumners said.


As reported previously by the Missourian, the measures being considered include:


■Targeted culling, or selectively shooting deer from within a site known to be infected to slim out the population.


In May, the department approved a ban on recreational deer feeders in a six county perimeter of the infected Macon County ranch, which includes: Adair, Chariton, Linn, Macon, Randolph and Sullivan counties.


The department also approved removing antler-size restrictions in the six-county area to allow for more killing of bucks, which are more likely to carry the disease.


Within the six-county area, the department recommends that hunters not remove whole carcasses or carcass parts, especially the head or spinal column.


Processed and wrapped meat, meat that has had bones removed, other portions of the deer lacking head and spinal cord parts, hides or capes, with all the excess tissue removed, antlers, antlers attached to scull plats or sculls lacking brain and muscle tissue, upper canine teeth, and finished taxidermy products make the exceptions to this recommendation.



“Deer are worth $1.1 billion to Missouri,” Sumners said, and efforts to protect them will continue.



Risky syndrome


Chronic wasting disease kills cervids — such as elk, moose and deer — and has not yet been proven to affect livestock, house pets or humans, according to the Missouri Agriculture, and Health and Senior Services departments.


Nonetheless, health officials advise against the consumption of diseased deer, especially certain deer parts where the mutated prions — the infectious agent of the disease — accumulate: the brain, eyes, lymph nodes, spinal cord and spleen.


Symptoms of the syndrome are extreme weight loss, tremors, stumbling and excessive salivation, and deer might carry the disease without displaying any symptoms for three or more years, according to the Missouri Conservation Department.


The department recommends that hunters concerned about possible disease transmission wear rubber or latex gloves when field dressing and processing deer.


At the Linn County Heartland Wildlife Ranch, exposed carcass remains were found at five locations during depopulation efforts, according to the Animal and Plant Health Inspection Service report.


One location was an above-ground enclosure made of hay bales — which might have been leaching carcass runoff into nearby private land — that shared a fenced enclosure with captive red deer, the report stated. The other sites were uncovered carcass pits.


"Depending on when the infection was introduced," these carcass disposal sites might have been a source of disease exposure, according to the report.


Dunfee said infective prions can remain in the soil for at least three years, and every previous effort to clean an infected environment has failed.


Brasher said he was allowed to place non-native red deer back in the infected 800-acre enclosure and continue his hunting operation. He said in November that the Macon County Heartland Wildlife Ranch was for sale, but that he intended to repopulate the ranch and reopen it to hunting if it doesn't sell.


The ranch carries a price tag of $16.5 million after the listing was reduced by $5 million, according to Open Fences and other land broker websites.


The lack of federal assistance crippled national surveillance for the disease, Dunfee said. “Most states will likely reduce or stop active surveillance" for chronic wasting disease, he said. "We can’t stop it.”


Supervising editor is John Schneller.








>>> Chronic wasting disease kills cervids — such as elk, moose and deer — and has not yet been proven to affect livestock, house pets or humans, according to the Missouri Agriculture, and Health and Senior Services departments.




CWD HAS PROVEN to infect, cattle, cats, 4 North American rodents and a new prion disease has been found in dogs. ...please see ;




see what CWD did with first and second passage of testing in the lab to cattle ;


first passage ;


These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.






second passage


Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie.






Chronic Wasting Disease CWD cervids interspecies transmission


Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions


David W. Colby1,* and Stanley B. Prusiner1,2


+ Author Affiliations


1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu


SNIP...




Greetings,


I believe the statement and quote below is incorrect ;


"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."


Please see ;


Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.






"although the infection rate was low (4 of 13 animals [Hamir et al. 2001])."


shouldn't this be corrected, 86% is NOT a low rate. ...




kindest regards,


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518




MARCH 1, 2011


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: flounder9@verizon.net


Cc: stanley@XXXXXXXX


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 ProfessorDepartment of Chemical EngineeringUniversity of Delaware




====================END...TSS==============


SNIP...SEE FULL TEXT ;









PO-041: Susceptibility of domestic cats to CWD infection


Amy Nalls, Jeanette Hayes-Klug, Kelly Anderson, Davis Seelig, Kevin Carnes, Susan Kraft, Edward Hoover, Candace Mathiason


Colorado State University; Fort Collins, CO USA


Domestic and non-domestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE); very likely due to consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), 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-infected deer brain homogenate.


Between 40 and 43 months two IC-inoculated cats developed slowly progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors, and ataxia”’ultimately mandating euthanasia. PrPCWD was detected in the brains of these animals by western blot, immunohistochemistry (IHC), and quaking-induced conversion (RT-QuIC) assays. No clinical signs of TSE were detected in the remaining primary passage cats at 86 months pi. Feline-adapted CWD (FelCWD) was sub-passaged into groups (n = 4 or 5) of cats by IC, PO, and IP/SQ routes.


All 5 IC inoculated cats developed symptoms of disease 20–24 months pi (approximately half the incubation period of primary passage). Additional symptoms in these animals included increasing aggressiveness and hyper responsiveness. FelCWD was demonstrated in the brains of all the affected cats by western blot and IHC. Currently, 3 of 4 IP/SQ, and 1 of 4 PO inoculated cats have developed abnormal behavior patterns consistent with the early stage of feline CWD. Magnetic resonance imaging (MRI) has been performed on 11 cats (6 clinically ill, 2 asymptomatic, and 3 age-matched negative controls). Abnormalities were detected in 4 of 6 clinically ill cats and included multifocal signal changes consistent with inflammation, ventricular size increases, more prominent sulci, and white matter tract cavitation.


These results demonstrate that CWD can be transmitted and adapted to the domestic cat, and raise the potential for cervid-to-feline transmission in nature.



========================



OR-12: Chronic wasting disease transmission and pathogenesis in cervid and non-cervid Species


Edward A. Hoover, Candace K. Mathiason, Nicholas J. Haley, Timothy D. Kurt, Davis M. Seelig, Nathaniel D. Denkers, Amy V. Nalls, Mark D. Zabel, and Glenn C. Telling


Prion Research Program, Department of Microbiology, Immunology, and Pathology; Colorado State University; Fort Collins, CO USA


Since its recognition as a TSE in the late 1970s, chronic wasting disease (CWD) of cervids has been distinguished by its facile spread and is now recognized in 18 states, 2 Canadian provinces, and South Korea. The efficient horizontal spread of CWD reflects a prion/host relationship that facilitates efficient mucosal uptake, peripheral lymphoid amplification, and dissemination by exploiting excretory tissues and their products, helping to establish indirect/environmental and well as direct (e.g., salivary) transmission. Recent studies from our group also support the likelihood of early life mother to offspring and aerosol CWD prion transmission. Studies of cervid CWD exposure by natural routes indicate that incubation period for detection of overt infection, while still uncertain, may be much longer than originally thought.


Several non-cervid species can be infected by CWD experimentally (e.g., ferrets, voles, cats) with consequent species-specific disease phenotypes. The species-adapted prions so generated can be transmitted by mucosal, i.e., more natural, routes. Whether non-cervid species sympatric with deer/elk can be infected in nature, however, remains unknown. In vitro CWD prion amplification studies, in particular sPMCA, can foreshadow in vivo susceptibility and suggest the importance of the PrPC rigid loop region in species barrier permissiveness. Trans-species CWD amplification appears to broaden the host range/strain characteristics of the resultant prions. The origins of CWD remain unknown, however, the existence of multiple CWD prion strains/ quasi-species, the mechanisms of prion shedding/dissemination, and the relationship between sheep scrapie and CWD merit further investigation.







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 period 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 species as potential hosts, bridge species, and reservoirs of CWD is required.






please see ;







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 . http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf




see history of MAD DOGS AND ENGLISHMAN



Monday, March 26, 2012


CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE







what about water running through an infected game farm ??





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 ;

















Thursday, May 31, 2012


CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more








Saturday, June 09, 2012


USDA Establishes a Herd Certification Program for Chronic Wasting Disease in the United States







Thursday, May 31, 2012


Missouri MDC staff will provide information on five recently found cases of CWD in free-ranging deer in northwest Macon County June 2, 2012







Tuesday, January 24, 2012


CWD found in two free-ranging deer from Macon County Missouri








Friday, October 21, 2011


Chronic Wasting Disease Found in Captive Deer Missouri








Friday, February 26, 2010


Chronic wasting disease found in Missouri deer







CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).


SNIP...


Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).


PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS






Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012


CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B).







Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE







Saturday, February 04, 2012


Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised







Tuesday, June 05, 2012


Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session







Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission







Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey



Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD



Accepted 15 November 2010. Abstract Full Text PDF References .




Abstract




The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.








"These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent."




Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007




Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov




The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.








now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ??




“Our conclusion stating that we found no strong evidence of CWD transmission to humans”




From: TSS (216-119-163-189.ipset45.wt.net)




Subject: CWD aka MAD DEER/ELK TO HUMANS ??




Date: September 30, 2002 at 7:06 am PST




From: "Belay, Ermias"




To:




Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"




Sent: Monday, September 30, 2002 9:22 AM




Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS




Dear Sir/Madam,




In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.




That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.




Ermias Belay, M.D. Centers for Disease Control and Prevention




-----Original Message-----




From:




Sent: Sunday, September 29, 2002 10:15 AM




To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV




Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS




Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS




Thursday, April 03, 2008




A prion disease of cervids: Chronic wasting disease




2008 1: Vet Res. 2008 Apr 3;39(4):41




A prion disease of cervids: Chronic wasting disease




Sigurdson CJ.




snip...




*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,




snip...




full text ;








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







Monday, May 23, 2011 CDC



Assesses Potential Human Exposure to Prion Diseases Travel Warning



Public release date: 23-May-2011



Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences




CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.




"While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases," commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta."But it's also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents."




Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.




CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.




Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.




The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.




The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.




According to Abrams, "The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health."




###




The article is "Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.




In an accompanying podcast CDC's Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast .









Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.






NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;



Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II






Monday, June 27, 2011


Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates





Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.


snip...


*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip...


full text ;






CJD9/10022


October 1994


Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ


Dear Mr Elmhirst,


CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT


Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.


The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.


The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.


The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.


I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.












Tuesday, June 19, 2012

Experimental Oral Transmission of Chronic Wasting Disease to Reindeer (Rangifer tarandus tarandus)
http://chronic-wasting-disease.blogspot.com/2012/06/experimental-oral-transmission-of.html





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)
http://chronic-wasting-disease.blogspot.com/2012/06/natural-cases-of-cwd-in-eight-sika-deer.html




***again I bring this study to your attention***





White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection




Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS




Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.




see full text ;












and again, here’s why I brought it to your attention ;






*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.





(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)




















Saturday, March 5, 2011





MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
 
 


 
 
 
 




Sunday, February 12, 2012





National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas
 
 








TSS
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