Friday, September 28, 2012

Stray elk renews concerns about deer farm security Minnesota

Local News


Stray elk renews concerns about farm security


Posted: Sep 28, 2012, 6:26 am By John Weiss The Post-Bulletin, Rochester MN


The Department of Natural Resources is investigating how a mature bull elk ended up on U.S. 52 near Zumbrota, where it was struck and killed by a truck on Sept. 20.


DNR officials are also investigating whether a mature whitetail deer shot by a bow hunter on Sunday near Marion, escaped from a game farm.


A truck driver hit the elk about 9 p.m., destroying the truck but not injuring the driver, said Don Nelson, area DNR wildlife supervisor.


Where the elk came from is puzzling, Nelson said. It had a slit on its ear that might have been from a game farm ear tag, but the slit had healed over, he said. The Minnesota Board of Animal Health had no reports of bull elks missing from game farms, he said.


To complicate the investigation, a bull elk was recorded on a trail camera several days before in Waseca County about 45 miles away, and a Goodhue County deputy saw a bull elk that morning near Wanamingo, a few miles from where it was struck.


Those two clues hint that the elk was moving into the area from the west, but that would be very unusual, Nelson said. Wild elk are found a few hundred miles west of here, and there's a small herd in northwestern Minnesota, but mature bulls rarely roam far from home, he said.


The antlers were damaged in the collision, so it's hard to compare them with the photos from the trail camera, he said.


"I don't have a good sense of where this animal came from," he said.


The carcass was taken to be tested for chronic wasting disease and other things that might help identify where it came from, he said.


The DNR has a better handle on where the whitetail doe originated. A blue tag on the doe strongly indicates it came from a game farm, Nelson said.


The animal was shot outside the zone where all deer shot have to be tested for CWD, which was found nearly two years ago in a deer shot near Pine Island. The tagged doe is still being tested, he said.


Again, the DNR is working with the Board of Animal Health on that case.


Seeing a mature elk in southeastern Minnesota is extremely rare, Nelson said, but seeing a deer from a game farm "is more common than we would like to see," he said.












Last year, only one deer was removed from the airport. It was unclear how the deer got past the wildlife fence — there might have been a small opening in the fence, or the deer might have simply jumped the 10 feet. Scherschligt said wildlife studies indicate that deer can sometimes jump 12-foot-tall obstructions, and the U.S. Department of Agriculture rates some whitetail deer as capable of jumping 15 feet.












Jumping to a vertical height of at least eight feet, deer can scale over barriers you may think are impossible. Watching a deer confronted with a vertical, eight-foot tall, hight-tensile wire fence then


watching it leap over from a standing position makes a startling impression. A frightened deer mhurdle a fence as high as 12 feet if given a running start and enough adrenalin. Horizontally, a deer may leap 15 to 30 feet, the longer distance only when frightened. In general, a deer may jump high or long, but not both at the same time. Deer have also been known to crawl under fences and through openings as small as 7.5 inches. The will of a deer to penetrate a fence is dependent on the force of the motivation behind it.














Sauer (1984) reported white-tailed deer could jump a 2.1-m fence from a standing start and could jump a 2.4-m fence from a running start. In contradiction, Fitzwater (1972) indicates that a 2.4-m fence is sufficient to prevent deer from jumping. Ludwig and Bremicker (1981) concluded that 2.4-m fencing was effective at keeping deer out of roadways as long as the length of the fence is extended well beyond the high-risk area for deer-vehicle collisions.

















Saturday, March 17, 2012


Minnesota CWD DNR, Can chronic wasting disease jump from deer to humans? yes, maybe some day YOUTUBE







Friday, January 21, 2011


MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND








Tuesday, January 25, 2011


Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island






MINNESOTA has had a problem with deer and elk escapees for some time, see ;





Deer, elk continue to escape from state farms

 
 
 

Article by: DOUG SMITH , Star Tribune Updated: March 14, 2011 - 12:08 PM




Curbing chronic wasting disease remains a concern; officials are increasing enforcement.



Almost 500 captive deer and elk have escaped from Minnesota farms over the past five years, and 134 were never recaptured or killed.


So far this year, 17 deer have escaped, and officials are still searching for many of those.


The escapes fuel concern that a captive animal infected with a disease such as chronic wasting disease (CWD) could spread it to the state's wild deer herd. There are 583 deer and elk farms in Minnesota, holding about 15,000 animals. Since 2002, CWD has been confirmed on four farms, and herds there were killed. This year, the first confirmed case of the fatal brain disease in a Minnesota wild deer was found near Pine Island – where a captive elk farm was found in 2009 to be infected with CWD.


State officials with the Board of Animal Health, which oversees the deer and elk farms, and the Department of Natural Resources say there is no firm evidence the elk herd, since destroyed, is responsible for infecting that deer.


But given the proximity of the cases, suspicion remains high. And others say the continued escape of captive animals is problematic.


"It's a loose cannon, and unfortunately it has the potential of threatening our entire wild deer herd," said Mark Johnson, executive director of the Minnesota Deer Hunters Association. He only recently learned that 109 deer and elk escaped in 32 incidents in 2010, and 24 of those animals never were recovered.


"The escapes themselves are startling and worrisome, but the two dozen not accounted for are a real concern," he said.


Dr. Paul Anderson, an assistant director at the Board of Animal Health, said the escapes are unacceptable.


"We've talked to the industry people and we all agree those numbers are too high," Anderson said. "We and the producers need to do a better job. We're going to increase our enforcement in 2011."


But he said the risk to the wild deer herd is minimal. Deer and elk generally die within three years of exposure to CWD, and 551 of the 583 Minnesota farms have had CWD surveillance for three or more years.


"We're very confident those farms don't have CWD," he said. As for the other 32 farms, "we don't think they have CWD either, but our confidence levels are not as good. We're pushing them."


The law requires farmers to maintain 8-foot fences, but most of the escapes are caused by human error, Anderson said. "They didn't close a gate or didn't get it shut right," he said.


Captive deer and elk brought into the state must come from herds that have been CWD-monitored for at least three years. Anderson said 184 animals were shipped here in the past year, and farmers exported 1,200 outstate.


The DNR is hoping the lone wild deer that tested positive for CWD is an aberration. Officials have long said CWD is potentially devastating to the state's wild deer herd. The DNR is killing 900 deer near Pine Island to determine if other deer might have the disease. So far, all have tested negative. Since 2002, the agency has tested more than 32,000 hunter-harvested deer, elk and moose.


While the Board of Animal Health licenses and oversees the deer and elk farms, the DNR is responsible for animals that have escaped for more than 24 hours. Escaped deer and elk can keep both DNR conservation officers and wildlife managers busy.


Tim Marion, an assistant area wildlife manager in Cambridge, has 38 deer and elk farms in his four-county work area, which includes Isanti, Chisago, Mille Lacs and Kanabec counties. Since last August, he's had 21 animals escape from four farms. Dogs broke into two pens, a tree fell on a fence in a third and another owner said someone opened a gate while he was away.


Four of those deer were shot and seven recaptured. Ten remain unaccounted for. Finding them can be difficult. Of nine deer that escaped from a farm near Mora, officials shot one two miles away, another four miles away and a third 8.5 miles from the farm. All were reported by people who spotted the animals at recreational deer feeders because they had tags in one ear, as required by law.


"There's no way we would have gotten any of these deer without the landowners helping us," Marion said.


But he has another problem.


"Three of those deer out there have no tags in the ear," he said. Will he find them?


"All I can say is we're trying," he said.


DNR conservation officer Jim Guida of Nisswa knows firsthand about escaped deer. He was bow hunting last fall near home when he shot a 10-point buck. Later, he was stunned to find a tag in its left ear.


"I thought it might be a [wild] research deer tagged at Camp Ripley," Guida said.


Wrong. It had escaped from a farm a year earlier.



 
 
 



Friday, August 31, 2012


COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review







Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting







Saturday, February 04, 2012


Wisconsin 16 MONTH 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







Saturday, June 09, 2012


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







Friday, August 24, 2012


Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America







Saturday, September 01, 2012


Resistance of Soil-Bound Prions to Rumen Digestion







Monday, September 17, 2012


Rapid Transepithelial Transport of Prions Following Inhalation












TSS

Thursday, September 27, 2012

TAHC Proposes Modifications to Chronic Wasting Disease (CWD) Rules September 27, 2012

NEWS RELEASE


Texas Animal Health Commission


“Serving Texas Animal Agriculture Since 1893”


Dee Ellis, DVM, MPA ● Executive Director


P.O. Box l2966 ● Austin, Texas 78711 ● (800) 550-8242 http://www.tahc.state.tx.us


For more information contact the Communication & PR Dept. at 1-800-550-0710 or at bonnie.ramirez@tahc.state.tx.us


_____________________________________________________________________________________________



FOR IMMEDIATE RELEASE


September 27, 2012


TAHC Proposes Modifications to Chronic Wasting Disease (CWD) Rules


AUSTIN – The Texas Animal Health Commission (TAHC) will soon be accepting public comments on rules proposed at its September 18 meeting to amend Chapter 40, entitled “Chronic Wasting Disease (CWD)”. Publication of the proposed rules is expected to be in mid-October with a 45 day comment period to follow.


The proposed rules revise numerous current requirements in an effort to address recent developments involving CWD. This includes the diagnosis of CWD in two mule deer near the New Mexico border and the addition of red deer and Sika deer to the list of species susceptible to CWD. The amendments would also bring Texas rules into alignment with the recently released Federal CWD interim final rule, which sets the minimum standards for interstate movement of cervid species.


The proposed TAHC rules apply to the non-indigenous cervid species of Texas under its jurisdiction. The Texas Parks and Wildlife Department (TPWD) is also in the process of evaluating its rules for the cervid species it regulates (indigenous to Texas), including white-tailed deer and mule deer.


Below are key points of the proposed rules to Chapter 40:


• Require additional cervid species such as North American Elk or Wapiti, red deer and Sika deer to participate in surveillance for CWD if they are being moved or transported within the state.


• Provide enrollment requirements for the TAHC Complete Monitored Herd Program for CWD, based in large part on the USDA interim final rule on CWD.


o Complete physical inventory of the herd every three years


o Fences must be 8 feet in height for herds enrolling after the rule is effective


o Require 30 feet of separation between herds, with no shared working facilities


o Requires reporting of all CWD suspicious animals and testing of all death losses in animals 12 months of age or older (changed from 16 months).


• Delegates authority to the Executive Director to issue an order to declare a CWD high risk area or county based on sound epidemiological principles for disease detection, control and eradication.


“The rule proposals are written to meet the federal standards but they can be adapted to recognize comments received,” Dr. Andy Schwartz, Assistant Executive Director, said. “The TAHC is committed to hosting as many meetings as necessary with the cervid industry and stakeholder groups to ensure that a successful Texas specific program is created that matches the USDA interim final rule. The TAHC’s ultimate goal is to enhance marketability.” CWD has never been shown to affect people or domestic livestock. The progressively fatal disease causes chronic weight loss and abnormal behavior such as disorientation. Prions (the infectious agent of CWD), are present in the body fluids of infected animals, and can be shed onto the soil where they may remain infectious to other susceptible animals for many years. For this reason the proposed TAHC rules apply to land, as well as cervids where CWD has been found or is likely to be found.


At its September 18 meeting, the Commission also passed a rule proposed at their previous meeting, establishing movement restriction zones in the Trans-Pecos Region of far West Texas. This will allow a coordinated effort between the TAHC and TPWD to control and contain CWD in the Hueco Mountains where it was recently discovered. The two agencies are currently working on plans for enhanced hunter kill surveillance and movement control enforcement for the coming hunting season.


“The TAHC will continue to work closely with Texas Parks and Wildlife and the CWD Task Force to ensure alignment of our rules and cooperation to protect the health of the entire cervid population of Texas,” said Dr. Dee Ellis, State Veterinarian and TAHC Executive Director.


A detailed explanation of the rule proposals will be available soon on the TAHC web site at http://www.tahc.state.tx.us/regs/proposals.html .


The TAHC rule proposals have a comment period of 45 days once they have been published. The TAHC encourages and appreciates all comments.


Comments on the TAHC’s proposed regulations must be submitted in writing to Carol Pivonka, Texas Animal Health Commission, 2105 Kramer Lane, Austin, Texas 78758, by fax at (512) 719-0721 or by e-mail to comments@tahc.state.tx.us . Founded in 1893, the Texas Animal Health Commission works to protect the health of all Texas livestock, including: cattle, swine, poultry, sheep, goats, equine animals, and exotic livestock.




###









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).










see full text ;





Saturday, February 04, 2012



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









Last year, only one deer was removed from the airport. It was unclear how the deer got past the wildlife fence — there might have been a small opening in the fence, or the deer might have simply jumped the 10 feet. Scherschligt said wildlife studies indicate that deer can sometimes jump 12-foot-tall obstructions, and the U.S. Department of Agriculture rates some whitetail deer as capable of jumping 15 feet.








Jumping to a vertical height of at least eight feet, deer can scale over barriers you may think are impossible. Watching a deer confronted with a vertical, eight-foot tall, hight-tensile wire fence then

watching it leap over from a standing position makes a startling impression. A frightened deer mhurdle a fence as high as 12 feet if given a running start and enough adrenalin. Horizontally, a deer may leap 15 to 30 feet, the longer distance only when frightened. In general, a deer may jump high or long, but not both at the same time. Deer have also been known to crawl under fences and through openings as small as 7.5 inches. The will of a deer to penetrate a fence is dependent on the force of the motivation behind it.










Sauer (1984) reported white-tailed deer could jump a 2.1-m fence from a standing start and could jump a 2.4-m fence from a running start. In contradiction, Fitzwater (1972) indicates that a 2.4-m fence is sufficient to prevent deer from jumping. Ludwig and Bremicker (1981) concluded that 2.4-m fencing was effective at keeping deer out of roadways as long as the length of the fence is extended well beyond the high-risk area for deer-vehicle collisions.











Monday, June 11, 2012



OHIO Captive deer escapees and non-reporting








Wednesday, September 26, 2012



TPWD Gearing Up for CWD Response during Deer Season








Monday, September 17, 2012



New Mexico DGF EXPANDS CHRONIC WASTING DISEASE CONTROL AREAS, while Texas flounders








Monday, March 26, 2012



Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas








Monday, March 26, 2012



3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER








Saturday, June 09, 2012



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








Wednesday, June 13, 2012



TAHC Modifies Entry Requirements Effective Immediately for Cervids DUE TO CWD



FOR IMMEDIATE RELEASE








Saturday, July 07, 2012



TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal



Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time.








Tuesday, July 10, 2012



Chronic Wasting Disease Detected in Far West Texas








key word here is _considering_. so consider this, CWD still spreading in Texas. ...TSS




Friday, September 07, 2012



Texas Wildlife Officials Considering New Deer Movement Rules in Response to CWD








Friday, August 31, 2012



COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review








Friday, June 01, 2012



TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS








Friday, August 24, 2012



Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America








Saturday, September 01, 2012



Resistance of Soil-Bound Prions to Rumen Digestion









Monday, September 17, 2012



Rapid Transepithelial Transport of Prions Following Inhalation








Thursday, September 27, 2012



Genetic Depletion of Complement Receptors CD21/35 Prevents Terminal Prion Disease in a Mouse Model of Chronic Wasting Disease




http://chronic-wasting-disease.blogspot.com/2012/09/genetic-depletion-of-complement.html






CDC



October 2012



Synopsis Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease



Controlling the spread of CWD, especially by human action, is a more attainable goal than eradication. Human movement of cervids has likely led to spread of CWD in facilities for captive animals, which has most likely contributed to establishment of new disease foci in free-ranging populations (Figure 1, panel A). Thus, restrictions on human movement of cervids from disease-endemic areas or herds continue to be warranted. Anthropogenic factors that increase cervid congregation such as baiting and feeding should also be restricted to reduce CWD transmission. Appropriate disposal of carcasses of animals with suspected CWD is necessary to limit environmental contamination (20), and attractive onsite disposal options such as composting and burial require further investigation to determine contamination risks. The best options for lowering the risk for recurrence in facilities for captive animals with outbreaks are complete depopulation, stringent exclusion of free-ranging cervids, and disinfection of all exposed surfaces. However, even the most extensive decontamination measures may not be sufficient to eliminate the risk for disease recurrence (20; S.E. Saunders et al. unpub. data)








Wednesday, June 01, 2011



Management of CWD in Canada: Past Practices, Current Conditions, Current Science, Future Risks and Options








Thursday, June 09, 2011



Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission








Thursday, February 17, 2011



Environmental Sources of Scrapie Prions








CWD, GAME FARMS, BAITING, AND POLITICS


















TSS

Genetic Depletion of Complement Receptors CD21/35 Prevents Terminal Prion Disease in a Mouse Model of Chronic Wasting Disease

Genetic Depletion of Complement Receptors CD21/35 Prevents Terminal Prion Disease in a Mouse Model of Chronic Wasting Disease



Brady Michel*, Adam Ferguson*, Theodore Johnson*, Heather Bender*, Crystal Meyerett-Reid*, Bruce Pulford*, Adriana von Teichman†, Davis Seelig*, John H. Weis‡, Glenn C. Telling*, Adriano Aguzzi† and Mark D. Zabel*



+ Author Affiliations



*Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University Prion Research Center, Fort Collins, CO 80523; †Institute for Neuropathology, University Hospital of Zürich, CH-8091 Zürich, Switzerland; and ‡Department of Pathology, University of Utah, Salt Lake City, UT 84132



Address correspondence and reprint requests to Prof. Mark Zabel, Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University Prion Research Center, 1619 Campus Delivery, Fort Collins, CO 80523-1619. E-mail address: mark.zabel@colostate.edu



Abstract



The complement system has been shown to facilitate peripheral prion pathogenesis. Mice lacking complement receptors CD21/35 partially resist terminal prion disease when infected i.p. with mouse-adapted scrapie prions. Chronic wasting disease (CWD) is an emerging prion disease of captive and free-ranging cervid populations that, similar to scrapie, has been shown to involve the immune system, which probably contributes to their relatively facile horizontal and environmental transmission. In this study, we show that mice overexpressing the cervid prion protein and susceptible to CWD (Tg(cerPrP)5037 mice) but lack CD21/35 expression completely resist clinical CWD upon peripheral infection. CD21/35-deficient Tg5037 mice exhibit greatly impaired splenic prion accumulation and replication throughout disease, similar to CD21/35-deficient murine prion protein mice infected with mouse scrapie. TgA5037;CD21/35−/− mice exhibited little or no neuropathology and deposition of misfolded, protease-resistant prion protein associated with CWD. CD21/35 translocate to lipid rafts and mediates a strong germinal center response to prion infection that we propose provides the optimal environment for prion accumulation and replication. We further propose a potential role for CD21/35 in selecting prion quasi-species present in prion strains that may exhibit differential zoonotic potential compared with the parental strains.



Footnotes



This work was supported by National Institute of Neurological Disorders and Stroke Grant R01 NS56379. Received June 8, 2012. Accepted August 22, 2012. Copyright © 2012 by The American Association of Immunologists, Inc.



snip...




Discussion




We investigated the role of the complement receptors CD21/35 in CWD prion accumulation, replication, and disease progression.We observed a complete rescue from terminal CWD of Tg5037 mice lacking CD21/35. Only 3 of 11 nonclinical Tg5037;CD21/352/2 mice displayed detectable, yet reduced, prion neuropathology and PrPRES deposition in their brains. These results reveal a more dramatic outcome than earlier studies showing only a partial rescue of CD21/35-deficient mice from scrapie infection, despite those mice expressing only WT (i.e., 5-fold less) PrPC levels. This could reflect differences between mouse and cervid CD21 expression, as are apparent between mouse and human CD21. However, little is known about cervid CD21. The gene has yet to be cloned, so comparative analyses with murine CD21/35 are impossible at present. We can, however, compare CD21 sequence homology and phylogeny among other species that are susceptible to TSEs. For example, sheep, which are susceptible to scrapie, a TSE that closely resembles CWD in transmission efficiency, and lymphotropism, express a CD21 molecule that shares 65% sequence identity with murine CD21/35, including their ligand binding domains (Fig. 5A). This may explain the similar lymphotropic characteristics of murine and ovine scrapie. Ovine CD21 also shares 65% identity with human CD21/35. Overall, CD21/35 from these three species share 52% identity and 64% similarity. In contrast, bovine CD21, which is 40% larger than the other three CD21/35 molecules (∼1400 compared with ∼1000 aa, respectively), shares ,20% similarity to the other three CD21/35 molecules. Phylogenetic analysis reveals a clustering of murine, ovine, and human CD21/35 proteins, with bovine CD21 much more distantly related (Fig. 5B). Interestingly, bovine spongiform encephalopathy has been shown to have little or no lymphotropic characteristics (44–47), perhaps owing to the vastly different CD21 molecule that bovids express.



These results indicate a significant role in prion pathogenesis for CD21/35, the importance of which may vary by prion strain. Complement components C1q and C3 have recently been shown to exhibit similar strain preferences in vitro and in vivo (48). We are currently investigating other prion strains to determine the contribution of CD21/35 to prion pathogenesis in those infection models. Interestingly, cross-species prion transmission was recently shown to result in a higher infection rate of the lymphoreticular system than the CNS in the xenohost (49). This crossspecies infection resulted in distinct lymphotropic and neurotropic strains with differential host ranges. These strains may result from tissue-specific strain selection or mutation. The higher efficiency of prion infection in the spleen (which harbors CD21/35- expressing FDCs and B cells) compared with the brain (which lacks them) alludes to a critical role for CD21/35 in prion retention, replication, and possibly strain selection in trans-species prion infection. The lack of CD21/35 that delays peripheral prion accumulation might further limit the lymphoid replication of neurotropic prion strains, resulting in delayed or abrogated disease progression. If so, this would have profound implications for prion xenotransmission and possible therapeutic approaches aimed at CD21/35. For example, targeting CD21/35 to slow the spread of neurotropic prions could be an attractive alternative to most prion disease therapeutics developed to date that target the CNS, which can complicate drug delivery. Interfering with CD21/35-mediated prion strain selection could also mitigate emergence of new prion strains with expanded host ranges and prevent a breach of the species barrier similar to the one that likely caused the bovine spongiform encephalopathy and subsequent new-variant Creutzfeldt- Jakob disease outbreak 15 y ago in the United Kingdom.



To study the kinetics of extraneural CWD prion accumulation, we amplified PrPRES from spleens of CWD prion-infected Tg5037 and Tg5037;CD21/352/2 mice at various time points throughout infection. At 15, 70, and 140 dpi and at terminal disease, prion accumulation was significantly lower in CD21/35-deficient mice. The extremely high prion load detected at 15 dpi most likely reflects increased retention of prion inocula early after infection. This delay in extraneural prion accumulation strongly correlates with abrogation of prion neuropathology and terminal disease. These results coincide with our previous data from scrapie mouse models (17), further strengthening evidence that CD21/35 play an integral part in prion accumulation in peripheral lymphoid organs that ultimately facilitates neuroinvasion.



Furthermore, we show that CD21/35 are present in prion preparations enriched from spleen homogenates by NaPTA precipitation. We also demonstrate GC formation in spleens during prion infection primarily dependent on CD21/35 and PrPC expression on FDCs. It may seem surprising that CD21/35 expression on FDCs, rather than B cells, correlates with prion-induced GC formation, because CD21/CD19/CD81 B cell coreceptor ligation helps activate B cells to form GCs. However, maximal B cell activation and GC formation require signaling from both the BCR and B cell coreceptor (32, 33). In this study, we show that although prion infection stimulates CD21/35 translocation to lipid rafts on B cells, signaling appears to be suboptimal for GC formation in the absence of concomitant BCR translocation. We observed a strong dependence on both PrP and CD21/35 expression on FDCs for a strong GC response. Paradoxically, CD21/35 translocation did not occur on FDCs, which are the major prion trappers and replicators but lack other B cell coreceptor components required for CD21/35 movement. One could therefore argue that GC formation represents an artifact, rather than being a driver of splenic prion replication. Elimination of GCs had no effect on peripheral prion replication and disease progression in mice infected i.p. with RML5 (50), supporting this interpretation. However, GC-deficient mice infected intracranially with 139A mouse-adapted scrapie prions exhibited a significant delay to terminal disease (51). Thus, distinct prion strains may differentially influence GC formation and subsequent prion pathogenesis. Additionally, this discrepancy further highlights potential preferences of distinct tissues for different prion strains. CD21/35- expressing cells within GCs may facilitate this selection process in the lymphoid system. Increased retention of prions on FDCs could induce a persistent state of prion presentation to adjacent B cells sufficient to cause an atypical GC response (40). FDCs may coax B cells to linger there, providing increased lymphotoxin signaling to FDCs that may promote formation of hypertrophic dendrites that efficiently retain and replicate prions. Consistent with their role as long-lived, long-term APCs, FDCs may also present prions to neighboring PrPC-expressing B cells that could induce CD21/35 translocation and move prions proximal to PrpC in lipid rafts and promote further prion replication and GC formation.



Taken together, these data support a principal role of CD21/35 in peripheral prion pathogenesis by trapping PrPRES on both B cells and FDCs. CD21/35 expression on FDCs remains of paramount importance in this process, with B cells playing a lesser, but still important, role. We have recently shown that few prion-bearing B cells transport prions from infection sites to draining lymph nodes, but their presence increased dramatically within lymph nodes, indicating a prominent role for B cells in intranodal prion trafficking (52). We propose that CD21/35 mediate this and other crucial processes in lymph node prion trapping and replication and we are currently testing this hypothesis.



Acknowledgments



We thank Ed Hoover and Steve Dow for helpful advice and discussion of the project and data.



snip...end







full text ;
















TSS

Wednesday, September 26, 2012

TPWD Gearing Up for CWD Response during Deer Season

Media Contact: Shawn Gray 432-837-2051, shawn.gray@tpwd.state.tx.us


Sept. 25, 2012


TPWD Gearing Up for CWD Response during Deer Season


Public hearings to include workshops for hunters, landowners


AUSTIN – Wildlife officials are asking mule deer hunters and landowners in far West Texas to familiarize themselves with new protocols developed as part of Texas Parks and Wildlife Department’s (TPWD) Chronic Wasting Disease response plan. The plan includes mandatory check stations for harvested mule deer taken inside the CWD Containment Zone, which covers portions of Hudspeth and El Paso counties. See map of CWD zones at http://www.tpwd.state.tx.us/cwd .


The response plan is being implemented after tissue samples from two mule deer in far West Texas this past summer tested positive for CWD. These are the first cases of CWD detected in Texas deer.


CWD workshops will be held in conjunction with upcoming public hearings to inform landowners, hunters, and outfitters about CWD, care of meat, appropriate management actions, and check station requirements. TPWD will present proposed amendments to deer movement rules, answer questions and take public comment during the public hearing segment of the meetings.


Meetings are set for Oct. 2 in Fort Stockton at the Pecos County Civic Center; Oct. 3 in Alpine at the Alpine Independent School District Auditorium; and Oct. 4 in Van Horn at the Van Horn Convention Center. The workshops will start at 6 p.m. and the public hearing will begin at 7:30 p.m.


CWD is a member of the group of diseases called transmissible spongiform encephalopathies (TSEs). Other diseases in this group include scrapie in sheep, bovine spongiform encephalopathy (BSE or mad cow disease) in cattle, and Cruetzfeldt-Jakob disease in humans. CWD among cervids is a progressive, fatal disease that commonly results in altered behavior as a result of microscopic changes made to the brain of affected animals. An animal may carry the disease for years without outward indication, but in the latter stages, signs may include listlessness, lowering of the head, weight loss, repetitive walking in set patterns, and a lack of responsiveness. CWD is not known to affect humans.


There is no vaccine or cure for CWD, but steps have been taken to minimize the risk of the disease spreading from beyond the area where it currently exists. For example, within the CWD Containment Zone, human-induced movements of wild or captive deer, elk, or other susceptible species will be restricted and mandatory hunter check stations will be established.


Hunters taking mule deer inside the Containment Zone during the general season, Nov. 23 – Dec. 9, are required to submit their harvest (unfrozen head) for CWD sampling at mandatory check stations within 24 hours of harvest.


“We recommend hunters in the Containment Zone and High Risk Zone quarter deer in the field and leave all but the quarters, backstraps and head at the site of harvest if it is not possible to bury the inedible carcass parts at least 6 feet deep on the ranch or take them to a landfill,” said Shawn Gray, mule deer program leader for TPWD.


Hunters that harvest deer in the Containment Zone during the archery-only season or outside the general season under the authority of MLDP (Managed Lands Deer Permits) will need to call TPWD at (512) 221-8491 the day the deer is harvested to make arrangements to have the deer sampled for CWD.


Mandatory check stations will be open from 9 a.m. to 9 p.m. Nov. 23 – Dec. 10. Stations will be located in Cornudas at May’s Café (on US 62-180) and in Van Horn at Van Horn Convention Center (1801 West Broadway).


In addition to protocols within the Containment Zone, TPWD has created a High Risk Zone for voluntary CWD sampling during the hunting season. Biologists have been collecting voluntary mule deer harvest data in the region since 1980 and this year CWD sampling will be offered in addition to age and weight measurements.


Voluntary check stations will be set up at the following locations during the first three weekends of the general season, Saturday through Monday (Nov. 24–26, Dec. 1–3 and Dec. 8–10), from 9 a.m. – 5 p.m. Saturday and Sunday and 9 a.m. – 1 p.m. Monday:


Midland at Naturally Fresh (Deer Processor) (1501 Elwyn)


Bakersfield at Chevron Station (south of I10; Exit 294)


Sanderson at Slim’s Auto Repair (823 West Oak; Intersection of US 90 and 285)


Alpine at Hip-O Taxidermy (east side of town on US 90, across from Dairy Queen)


“All deer brought to the check stations this season will be aged as part of our CWD surveillance,” said Gray. “We also intend to collect other biological information such as antler measurements and field dressed weights as time allows.”


Although wildlife officials cannot say how long the disease has been present in Texas or if it occurs in other areas of the state, they have had an active CWD surveillance program for more than a decade.


“We have tested more than 26,500 wild deer in Texas since 2002, and the captive-deer industry has submitted more than 7,400 CWD test results as well,” said Mitch Lockwood, Big Game Program Director with TPWD. “But that part of West Texas is the toughest place to conduct an adequate CWD surveillance program because so few deer are harvested out there each hunting season. Thanks to the cooperation and active participation of several landowners, we were able to begin getting an idea of the prevalence and geographic distribution of the disease without needing to remove many deer.”


More information on CWD can be found on TPWD’s website, http://www.tpwd.state.tx.us/cwd or at the Chronic Wasting Disease Alliance website, http://www.cwd-info.org


2012-09-25









> TPWD Gearing Up for CWD Response during Deer Season




I’m not holding my breath. ...TSS




Monday, September 17, 2012



New Mexico DGF EXPANDS CHRONIC WASTING DISEASE CONTROL AREAS, while Texas flounders








Monday, March 26, 2012



Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas









Monday, March 26, 2012



3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER









Saturday, June 09, 2012



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









Wednesday, June 13, 2012


TAHC Modifies Entry Requirements Effective Immediately for Cervids DUE TO CWD


FOR IMMEDIATE RELEASE









Saturday, July 07, 2012


TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal


Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time.









Tuesday, July 10, 2012


Chronic Wasting Disease Detected in Far West Texas









key word here is _considering_. so consider this, CWD still spreading in Texas. ...TSS




Friday, September 07, 2012


Texas Wildlife Officials Considering New Deer Movement Rules in Response to CWD









Friday, August 31, 2012


COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review









Friday, June 01, 2012


TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS










Friday, August 24, 2012


Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America










Saturday, September 01, 2012


Resistance of Soil-Bound Prions to Rumen Digestion










Monday, September 17, 2012


Rapid Transepithelial Transport of Prions Following Inhalation













TSS

Friday, September 21, 2012

Chronic Wasting Disease CWD raises concerns about deer farms in Iowa

Updated: 21 September 2012 | 6:30 am



Disease raises concerns about deer farms in Iowa




Most cases found so far in state tied to confined animals






Iowa’s first seven cases of chronic wasting disease — all directly related to confined whitetail deer — have put a bull’s eye on the backs of the state’s deer breeders and the pay-to-shoot facilities they supply.



Critics of penned deer operations — mainly hunters and game managers — say captive deer are more likely than wild deer to spread the always fatal brain disease and that killing penned deer violates the “fair chase” premise that underlies ethical hunting.



“I’ve been crucified and demonized,” said Tom Brakke, a deer breeder and hunting preserve proprietor whose deer have been implicated in five of the state’s seven positive CWD tests.



Tim Powers, field director for the Iowa chapter of Whitetails Unlimited, said many Iowa deer hunters fear that wild deer will soon be infected and resent the role of game farms in the spread of the disease.



Confined deer operations are the “Typhoid Mary of the ungulates,” said Sen. Dick Dearden, D-Des Moines, chairman of the Senate Natural Resources Committee.



Like many other Iowa hunters, Dearden said he thinks the shooting preserves, where people pay to shoot deer in an enclosure, are more trouble and expense than they are worth.



“I don’t understand how people who shoot confined deer would call themselves hunters,” said Dearden, who observed that opposition to hunting penned animals is “probably the only issue that PETA (People for the Ethical Treatment of Animals) and I agree on.”



Iowa recorded its first CWD case in July at the Pine Ridge Hunting Lodge near Bloomfield in Davis County.



The Department of Natural Resources, which regulates hunting preserves, and the Department of Agriculture and Land Stewardship, which regulates breeding facilities, have since confirmed six more positive tests — all but two related to the Davis County hunting preserve and to a Cerro Gordo County deer breeding facility, both owned by Tom and Rhonda Brakke of Clear Lake.



The Clear Lake facility has recorded a positive test, as have three deer raised at that facility and shipped to a combination shooting and breeding facility in Pottawattamie County, according to State Veterinarian David Schmitt.



The other two positive tests at the Pottawattamie facility involved a deer acquired from another Iowa breeder and a deer that was a natural addition to the herd, Schmitt said.



Tom Brakke said no deer have entered his breeding facility in the past 10 years and that his herd — about 500 deer at Clear Lake and more than 150 at the Bloomfield preserve — have been enrolled for the past nine years in a CWD monitoring program under which every deer that dies or is killed is tested for the disease. (story continues below map)











“Nothing comes in 10 years. Every deer that died in the past nine years has been tested. The incubation period for CWD is 48 months. How did I get CWD? That’s what I want to know,” said Brakke, who sees his investment of 20 years and $2.5 million rapidly disappearing.



While hunters worry that Brakke’s deer have already infected or will soon infect wild Iowa deer, it is “most definitely” possible that his deer could have been infected by wild Iowa deer, Brakke said.



Whitetail expert Willie Suchy, leader of the DNR’s wildlife research unit, said CWD is “more likely to show up among captive animals” because they are often moved from one facility to another, increasing their exposure.



Bryan Richards, a disease investigator for the U.S. Geological Survey National Wildlife Health Center in Madison, Wis., said captive and wild deer are equally susceptible to CWD.



Nevertheless, he said, disease outbreaks accelerate in a captive environment.



“You are forcing contact in a pen. A sick animal will soon have contact with every animal in the pen,” he said.



Richards said “there is ample evidence right there in Iowa that CWD moves through game farm enclosures.”



Both Suchy and Richards said managing deer in the CWD era would be greatly simplified and rendered more effective if there were an economical diagnostic test. Today’s standard test is performed post-mortem on brain cells, which can be extracted only from dead animals.



That penned deer are more susceptible than wild deer to chronic wasting disease is a “common misconception,” according to Wayne Johnson of Farley, a member of the Iowa Whitetail Deer Association board of directors.



With CWD confirmed in all of Iowa’s neighboring states, “it was bound to show up in Iowa,” he said.



One reason the disease showed up first among confined deer is that all confined deer in Iowa over the age of 1 are tested for CWD when they die, which compares with a small percent of the wild deer herd, about 1 percent in any given year, according to Iowa Whitetail Deer Association spokesman Scott Kent, who is raising about 250 whitetails on a combined hunting and breeding facility near Osceola.



Johnson, who keeps 13 deer in a 2-acre pen, said he raises whitetails for both fun and profit.



The few that he sells each year go to hunting preserves and bring anywhere from $500 to $5,000 each, depending on the size of their antlers, Johnson said.



Pine Ridge Lodge’s 2011 price list includes whitetail bucks from $3,500 for antlers in the 160 to 169-inch range all the way up to $30,000 for monster bucks with antlers measuring more than 300 inches.



Another common misconception, according to both Brakke and Johnson, is that deer within hunting preserves are easy to shoot.



“They are still a wild animal, and they have a lot of room to run and hide” within a 320-acre enclosure, the minimum size allowed under Iowa law, Johnson said.



“I love to hunt myself, and if it wasn’t a real hunt I wouldn’t do it,” Brakke said.



DNR spokesman Kevin Baskins confirmed that the state’s first CWD-positive deer was shot just two hours after it stepped off the truck, which would not have given the animal much time to acclimate to its new surroundings.



Randy Taylor, chairman of the legislative committee of the Iowa Bowhunters Association, said the organization is concerned that commercial deer operations are threatening the health of Iowa’s wild deer. “We will recommend that the Legislature pass stricter rules governing the operation of deer breeding and shooting facilities,” Taylor said.



Dearden said he is “really looking at” revisiting state rules governing commercial deer operations in the upcoming session of the Legislature.



Although Department of Agriculture and the DNR appear to be working well together, the split jurisdiction is an area of concern, Dearden said.



Brakke’s 330-acre hunting preserve will be depopulated under an agreement with the DNR. The agreement allows Brakke to honor commitments for hunts previously scheduled between Sept. 8 and Dec. 25, said Dale Garner, chief of the DNR’s Wildlife Bureau. Any deer killed during those hunts will be tested for CWD and any remaining after those hunts will be killed and tested for the fatal brain disease, Garner said.





http://thegazette.com/2012/09/21/disease-raises-concerns-about-deer-farms-in-iowa/





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.






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








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.













snip...please see full text ;





Saturday, February 04, 2012



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









Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting








Tuesday, September 11, 2012


Agreement Reached with Owner to De-Populate CWD Deer at Davis County Hunting Preserve Iowa







Wednesday, September 05, 2012


Additional Facility in Pottawatamie County Iowa Under Quarantine for CWD after 5 deer test positive








Friday, July 20, 2012


CWD found for first time in Iowa at hunting preserve








Tuesday, June 05, 2012


Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session








Saturday, September 01, 2012


Resistance of Soil-Bound Prions to Rumen Digestion








Friday, August 31, 2012


COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review









Saturday, June 09, 2012


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








*** 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)







Wednesday, February 16, 2011


IN CONFIDENCE


SCRAPIE TRANSMISSION TO CHIMPANZEES


IN CONFIDENCE







PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer


Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA







PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)










Thursday, May 31, 2012


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







Monday, September 17, 2012


Rapid Transepithelial Transport of Prions Following Inhalation







GAME FARMERS, CWD, AND THEIR COMMENTS...disturbing...frightening even. it seems they are oblivious to their own demise. ...


see comments ;








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).







Friday, August 24, 2012


Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America


The overall diagnostic specificity was 99.8%. Selective use of antemortem rectal biopsy sample testing would provide valuable information during disease investigations of CWD-suspect deer herds.










TSS