Greetings Wisconsin Hunters and DNR et al,
I believe that the Wisconsin Game Farm CWD testing protocol is flawed, by having the age limit on testing i.e. deer that are 16 months of age or older. it’s well documented that fawns are very susceptible to CWD at a early age, and the logic behind the 16 months of age or older for the testing of any dead deer will only lead to more CWD. it’s like the old flawed surveillance for Creutzfeldt Jakob Disease in the USA, and the threat of proven Iatrogenic spread there from, and then putting a age limit on CJD surveillance of anyone > or equal to 55 years and over, do not have to be reported, however, in the 55 year and older, the CJD infection rate jumps from 1 per 1,000,000 to 1 in 9,000, and the only folks to have been proven to pass the Iatrogenic CJD via tissues and organs are sporadic CJD victims. another example of industry regulations, i.e. BSE testing of cattle only 30 month and older. cattle have been documented with BSE as young as 20 months.
ALSO, some states have ;
“ Samples will not be collected from fawns. “
they problem is, you cannot half way do something, and these TSE prion disease regulations have all been set up to half way do something, i.e. industry friendly regulations $$$
by the time of any confirmation of any fawn with CWD, by these Wisconsin CWD testing protocols i.e. 16 months of age or older of any deer found dead on a deer farm, by the time one is detected, the majority of the herd would be infected with CWD, and the surrounding environment of that game farm totally contaminated for years, if not decades. simply put, any game farm threatens the wild herds with CWD.
WITH over 500 documented game farms in Wisconsin alone, in my opinion, the whole state of Wisconsin should be quarantined, not just those 9 documented CWD game farms, and there are a few other states I would call for the same thing to be done.
Wisconsin farms testing dead deer that are 16 months of age or older, only ???
Wisconsin
You are required to have all farm-raised deer that are 16 months of age or older that die for any reason sampled for CWD within seven (7) days of being killed (or discovered dead) by a private veterinarian certified to take the samples. If the deer was killed by a hunter, the hunter must be informed of the test results.
http://docs.legis.wisconsin.gov/code/admin_code/atcp/10.pdf
Research Article
Demographic Patterns and Harvest Vulnerability of Chronic Wasting Disease Infected White-Tailed Deer in Wisconsin
DANIEL A. GREAR,1 Department of Wildlife Ecology, University of Wisconsin, Madison, WI 53706, USA MICHAEL D. SAMUEL, U.S. Geological Survey—Wisconsin Cooperative Wildlife Research Unit, University of Wisconsin, Madison, WI 53706, USA JULIE A. LANGENBERG, Wisconsin Department of Natural Resources, Madison, WI 53707, USA DELWYN KEANE, Wisconsin Veterinary Diagnostic Laboratory, Madison, WI 53705, USA
Abstract
Chronic wasting disease (CWD) is a fatal disease of white-tailed deer (Odocoileus virginianus) caused by transmissible protease-resistant prions. Since the discovery of CWD in southern Wisconsin in 2001, more than 20,000 deer have been removed from a .2,500-km2 disease eradication zone surrounding the three initial cases. Nearly all deer removed were tested for CWD infection and sex, age, and harvest location were recorded. Our analysis used data from a 310-km2 core study area where disease prevalence was higher than surrounding areas. We found no difference in harvest rates between CWD infected and noninfected deer. Our results show that the probability of infection increased with age and that adult males were more likely to be infected than adult females. Six fawns tested positive for CWD, five fawns from the core study area, including the youngest (5 months) free-ranging cervid to test positive. The increase in male prevalence with age is nearly twice the increase found in females. We concluded that CWD is not randomly distributed among deer and that differential transmission among sex and age classes is likely driving the observed patterns in disease prevalence. We discuss alternative hypotheses for CWD transmission and spread and, in addition, discuss several possible nonlinear relationships between prevalence and age. Understanding CWD transmission in free-ranging cervid populations will be essential to the development of strategies to manage this disease in areas where CWD is found, as well as for surveillance strategies in areas where CWD threatens to spread. (JOURNAL OF WILDLIFE MANAGEMENT 70(2):546–553; 2006)
Key words
Chronic wasting disease (CWD), disease prevalence, epidemiology, harvest vulnerability, Odocoileus virginianus, prion, transmissible spongiform encephalopathy (TSE), white-tailed deer, Wisconsin.
http://forestandwildlifeecology.wisc.edu/facstaff/samuel/2006_grear_et_al_demographic_patterns.pdf
Wisconsin : Six White-Tailed Deer Fawns Test Positive for CWD
Date: May 13, 2003 Source: Wisconsin Department of Natural Resources
Contacts: Julie Langenberg Wildlife Veterinarian 608-266-3143 Tom Hauge Director, Bureau of Wildlife Management 608-266-2193
MADISON -- Six fawns in the area of south central Wisconsin where chronic wasting disease has been found in white-tailed deer have tested positive for the disease, according to Department of Natural Resources wildlife health officials. These are the youngest wild white-tailed deer detected with chronic wasting disease (CWD) to date.
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
"This is the first intensive sampling for CWD in fawns anywhere," said Dr. Julie Langenberg, Department of Natural Resources wildlife veterinarian, "and we are trying to learn as much as we can from these data".
"One noteworthy finding is simply the fact that we found positive fawns," Dr. Langenberg said. "These results do show us that CWD transmission can happen at a very young age in wild white-tailed deer populations. However, we found that the percentage of fawns infected with CWD is very low, in the area of 0.14 percent. If there was a higher rate of infection in fawns, then fawns dispersing in the spring could be much more worrisome for disease spread."
Dr. Langenberg noted that while the youngest CWD-positive fawns had evidence of disease-causing prions only in lymph node tissue, several of the older CWD-positive fawns had evidence of CWD prions in both lymph node and brain tissues -- suggesting further progression of the disease.
"Finding CWD prions in both lymph and brain tissues of deer this young is slightly surprising," said Langenberg, "and provides information that CWD infection and illness may progress more rapidly in a white-tailed deer than previously suspected. Published literature suggests that CWD doesn't cause illness in a deer until approximately 16 months of age. Our fawn data shows that a few wild white-tailed deer may become sick from CWD or may transmit the disease before they reach that age of 16 months."
One of the positive fawns was shot with a doe that was also CWD positive. Information about these fawn cases combined with will help researchers who are studying the age and routes of CWD transmission in wild deer populations. "More data analysis and ongoing deer movement studies should give us an even better understanding of how this disease moves across the landscape", said Langenberg.
"Thanks to eradication zone hunters who submitted deer of all ages for sampling, we have a valuable set of fawn data that is contributing to our state's and the nation's understanding about CWD," Langenberg said.
> > > Two of the six fawns with CWD detected were 5 to 6 months old. < < <
Why doesn't the Wisconsin DNR want to routinely test fawns ?
The DNR highly discourages the testing of any fawns regardless of where they were harvested. Of the more than 15,000 fawns from the CWD-MZ that have been tested, only 23 were test positive, and most of those were nearly one year old. It is exceedingly unlikely that a deer less than one year old would test positive for CWD, even in the higher CWD prevalence areas of southern Wisconsin. Few fawns will have been exposed to CWD, and because this disease spreads through the deer's body very slowly, it is very rare in a fawn that the disease has progressed to a level that is detectable. This means that testing a fawn provides almost no information valuable to understanding CWD in Wisconsin's deer herd and does not provide information of great value to the hunter in making a decision about venison consumption.
> > > It is exceedingly unlikely that a deer less than one year old would test positive for CWD < < < ???
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm
and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.
specific susceptibility? 194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000).
198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).
SCWDS BRIEFS
Volume 17 January 2002 Number 4
CWD News from Nebraska and Kansas
Infection with the chronic wasting disease (CWD) agent recently was found in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent to a pen containing CWDaffected captive elk in northern Sioux County, Nebraska.
Four of the positive deer were fawns approximately 8 months old, which is unusually young for animals testing positive for CWD.
A January survey of 39 free-ranging deer collected within 15 miles of the positive elk and deer pens detected 8 (20%) infected animals. Test results are pending for additional deer collected inside and outside of the enclosure, and additional surveillance is planned for free-ranging deer in northwestern Nebraska. Previously, CWD had been documented in Nebraska in only two wild mule deer, both of which came from Kimball County in the southwestern panhandle adjacent to the endemic area of northeastern Colorado and southwestern Wyoming.
CWD in adult deer and fawns
A hundred and thirty-three white-tailed deer in the study were killed after CWD was diagnosed in the deer within the fenced area. Paired samples of formalin-fixed tissue for CWD diagnosis and frozen tissue for DNA sequence analysis were collected. Fifty per cent (67/133) of deer were diagnosed with CWD (Table 2) using an immunohistochemical assay for PrPd in formalin-fixed, paraffinembedded brain and lymphoid tissues.
Five of the CWD-positive deer were fawns, less than 1 year of age.
Early CWD (PrPd detected in the tonsil or retropharyngeal node but not brain) was diagnosed in 14 deer (12 adults ranging from 1?5 to more than 5 years of age and two fawns). Late CWD (PrPd detectable in brain as well as lymphoid tissues) was diagnosed in 53 deer (50 adults ranging in age from 1?5 to 7 years of age and three fawns). None of the CWD-positive deer showed clinical signs of the disease (weight loss, hypersalivation, disorientation) or gross changes consistent with CWD (serous atrophy of fat) at necropsy.
Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had CWD i.e. 1 positive out of 51 samples.
2003
Boone-Winnebago Unit Fawn 51 1 2.0%
2011 FAWN CWD POSITIVE ILLINOIS
1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING
2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING
3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTING
For example, in 2008 a fawn tested positive and in 2010 an infected yearling buck was detected in Smith County
PPo3-40:
Mother to Offspring Transmission of Chronic Wasting Disease
Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley and Edward A. Hoover Colorado State University, Department of Microbiology, Immunology and Pathology, Fort Collins, CO USA
Key words: Chronic wasting disease, vertical transmission, muntjac deer
We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Six fawns were born to these CWD-infected doe. Six fawns were born to 6 CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age. In addition, sPMCA assays have also demonstrated amplifiable prions in maternal placental (caruncule) and mammary tissue of the dam. Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.
"PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age"
Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus)
The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species. Introduction
http://vir.sgmjournals.org/content/80/10/2757.full.pdf
Wisconsin is home to about 500 deer farmers, and there are more than 8,000 farms in the U.S., according to Laurie Seale of Gilman, who's president of Whitetails of Wisconsin.
http://www.deerfarms.com/wi.shtml
http://www.wisconsinoutdoor.com/gamefarm.htm
http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html
NOW, if you look at the map that shows these game farms in relations to surround CWD infection rate in the wild, you will see the close proximity from one to the other i.e. CWD infected game farms, to CWD infection in the wild.
please see map here, and you will see that this phenomenon is NOT only unique to Wisconsin, but with most all other game farms in other states. see map here ;
http://www.nwhc.usgs.gov/disease_information/chronic_wasting_disease/index.jsp
and that’s just the documented farms. ...
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
http://chronic-wasting-disease.blogspot.com/2012/01/9-game-farms-in-wisconsin-test-positive.html
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf
SNIP...SEE FULL TEXT ;
http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html
Friday, February 03, 2012
Long kills controversial fenced hunting bill INDIANA
http://chronic-wasting-disease.blogspot.com/2012/02/long-kills-controversial-fenced-hunting.html
http://www.prpsc.proboards.com/index.cgi?board=prpsccwd&action=display&thread=2
http://www.prpsc.proboards.com/index.cgi
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 ;
http://www.landesbioscience.com/
http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf
http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html
http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html
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 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.
http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html
please see ;
http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf
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
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html
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
http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html
see full text study below ;
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
http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html
Tuesday, January 24, 2012
CWD found in two free-ranging deer from Macon County Missouri
http://chronic-wasting-disease.blogspot.com/2012/01/cwd-found-in-two-free-ranging-deer-from.html
Saturday, December 31, 2011
Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation
http://chronic-wasting-disease.blogspot.com/2011/12/depopulation-plan-being-developed-for.html
Saturday, December 31, 2011
Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation
http://chronic-wasting-disease.blogspot.com/2011/12/depopulation-plan-being-developed-for.html
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html
Sunday, November 13, 2011
COLORADO CWD CJD TSE PRION REPORTING 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/colorado-cwd-cjd-tse-prion-reporting.html
Wednesday, December 21, 2011
CWD UTAH San Juan deer hunting unit
http://chronic-wasting-disease.blogspot.com/2011/12/cwd-utah-san-juan-deer-hunting-unit.html
Wednesday, January 04, 2012
CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT
http://chronic-wasting-disease.blogspot.com/2012/01/cwd-nebraska-ngpc-26-deer-carcasses.html
TSS
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