Deer Farming News Investigation

[Larry]

I found this on the CDC web site

 

 

Fatal Degenerative Neurologic Illnesses in Men Who Participated in Wild Game Feasts --- Wisconsin, 2002

Creutzfeldt-Jakob disease (CJD) is a fatal neurologic disorder in humans. CJD is one of a group of conditions known as transmissible spongiform encephalopathies (TSEs), or prion diseases, that are believed to be caused by abnormally configured, host-encoded prion proteins that accumulate in the central nervous tissue (1). CJD has an annual incidence of approximately 1 case per million population in the United States (1) and occurs in three forms: sporadic, genetically determined, and acquired by infection. In the latter form, the incubation period is measured typically in years. Recent evidence that prion infection can cross the species barrier between humans and cattle has raised increasing public health concerns about the possible transmission to humans of a TSE among deer and elk known as chronic wasting disease (CWD) (2). During 1993--1999, three men who participated in wild game feasts in northern Wisconsin died of degenerative neurologic illnesses. This report documents the investigation of these deaths, which was initiated in August 2002 and which confirmed the death of only one person from CJD. Although no association between CWD and CJD was found, continued surveillance of both diseases remains important to assess the possible risk for CWD transmission to humans.

Case Reports

Case 1. In December 1992, a Wisconsin man aged 66 years with a history of seizures since 1969 sought treatment for recurring seizures, increasing forgetfulness, and worsening hand tremors. Electroencephalographic (EEG) examination demonstrated focal epileptiform activity and nonspecific diffuse abnormalities, but no specific diagnosis was made. In February 1993, he was hospitalized for increasing confusion, ataxia, and movement tremors of his extremities. A magnetic resonance image (MRI) demonstrated mild, nonspecific enhancement along the inferior parasagittal occipital lobe. A repeat EEG showed bifrontal intermittent, short-interval, periodic sharp waves, suggesting a progressive encephalopathy; a diagnosis of CJD was suspected. The man died later that month; neuropathologic examination of brain tissue during autopsy indicated subacute spongiform encephalopathy, compatible with CJD.

The man was a lifelong hunter who ate venison frequently. He hunted primarily in northern Wisconsin but also at least once in Montana. He hosted wild game feasts at his cabin in northern Wisconsin from 1976 until shortly before his death. Fixed brain tissue obtained during the autopsy was sent for analysis to the National Prion Disease Pathology Surveillance Center (NPDPSC) and reexamined at the institution where the autopsy was conducted. Histopathologic examination did not substantiate the diagnosis of prion disease. In addition, 27 brain tissue sections were negative for prions by immunostaining despite positive antibody reactions against other proteins (controls), which indicated that other epitopes in the tissue samples were preserved.

Case 2. In May 1999, a Minnesota man aged 55 years with no previous history of a neurologic disease sought evaluation and treatment following a 3-month history of progressive difficulty in writing and unsteadiness of gait. A computerized tomography (CT) scan and MRI examination of his head did not indicate any abnormality. In June 1999, he was hospitalized following onset of dementia, speech abnormalities, and myoclonic jerking. An EEG indicated left-hemispheric periodic sharp waves and moderate generalized background slowing; CJD was diagnosed clinically. In July 1999, following worsening symptoms and development of right upper extremity dystonia, the patient died. Neuropathologic evaluation of brain tissue during autopsy demonstrated widespread subcortical spongiform lesions, consistent with CJD.

The man was not a hunter but had a history of eating venison. He made an estimated 12 visits to the cabin where the wild game feasts were held, but he participated in only one feast during the mid-1980s. Sections of fixed and frozen brain tissue obtained during autopsy were analyzed at NPDPSC, and prion disease was confirmed by immunohistochemical and Western blot testing. The Western blot characteristics and prion disease phenotype in this patient were consistent with the most common form of sporadic CJD, classified as M/M (M/V) 1 (3). Subsequent genetic typing confirmed the presence of methionine homozygosity (M/M) at codon 129 of the patient's prion protein gene.

Case 3. In June 1992, a Wisconsin man aged 65 years sought treatment for progressive slowing of speech, worsening memory, and personality changes. By January 1993, his speech was reduced to one-word utterances. Neurologic examination showed a flat affect, decreased reflexes, and apraxia. A CT head scan showed mild atrophy, and an EEG was normal. Pick's disease was diagnosed. By May, he was unable to perform any daily living activities; he died in August 1993. Neuropathologic evaluation of brain tissue during autopsy showed symmetrical frontal lobe cerebral cortical atrophy and mild temporal lobe atrophy. No Pick's bodies or spongiform lesions were observed.

The man had a history of eating venison and participated regularly in wild game feasts held at the cabin owned by patient 1. He was a lifelong hunter and hunted mostly in Wisconsin but also in Wyoming and British Columbia. No game was brought to the wild game feasts from his hunting trips outside of Wisconsin. Examination of fixed brain tissue sent to NPDPSC demonstrated no lesions indicative of CJD, and immunohistochemical testing with antibody to the prion protein did not demonstrate the granular deposits seen in prion diseases.

Epidemiologic Investigation

Wild game feasts consisting of elk, deer, antelope, and other game that occurred at a cabin in northern Wisconsin owned by patient 1 began in 1976 and continued through 2002. These feasts typically involved 10--15 participants and usually occurred on weekends before or during hunting seasons in the fall and occasionally in the spring. Wild game brought to these feasts usually were harvested in Wisconsin, but three men who attended these feasts reported hunting in the western United States and bringing game back to Wisconsin. These activities took place in Colorado (near the towns of Cortez, Trinidad, Collbran, Durango, and Meeker), Wyoming (near the towns of Gilette and Cody), and Montana (near the town of Malta). CWD was not known to be endemic in these areas at the time that these hunting activities took place.

Information was obtained for 45 (85%) of 53 persons who were identified as possibly participating in the wild game feasts; all were male. Information was obtained by direct interview or from family members of decedents. Of the 45 persons, for whom information was obtained, 34 were reported to have attended wild game feasts. Seven of the 34 feast attendees were deceased, including the three patients. None of the four other decedents had a cause of death attributed to or associated with a degenerative neurologic disorder. None of the living participants had any signs or symptoms consistent with a degenerative neurologic disorder.

Reported by: JP Davis, MD, J Kazmierczak, DVM, M Wegner, MD, R Wierzba, Div of Public Health, State of Wisconsin Dept of Health and Family Svcs. P Gambetti, National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, Ohio. L Schonberger, MD, R Maddox, MPH, E Belay, MD, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; V Hsu, MD, EIS Officer, CDC.

Editorial Note:

CWD was first described in the United States in the 1960s and classified as a TSE in 1978. Previously localized to a contiguous endemic area in northeastern Colorado and southeast Wyoming, since 2000, CWD has been found in free-ranging deer or elk in Illinois, Nebraska, New Mexico, South Dakota, Wisconsin, and outside the previously known endemic areas of Colorado and Wyoming. CWD has been identified also in captive deer or elk in Colorado, Kansas, Minnesota, Montana, Nebraska, Oklahoma, South Dakota, and Wisconsin (4). Because a variant form of CJD, with specific neuropathologic and molecular characteristics that distinguish it from sporadic CJD, has been associated with eating cattle products infected with a prion that causes bovine spongiform encephalopathy (5), concern has been raised about the possibility that the prion associated with CWD might be transmitted to humans in a similar way.

In this investigation, because only one of the three cases in Wisconsin had neuropathologic confirmation of a prion disease, no association could be made between case participation in the wild game feasts and the development of CJD. Although patient 2 had confirmed CJD, he was unlikely to have eaten CWD-infected venison at these feasts because venison and other game from outside Wisconsin that was served at these feasts did not originate from known CWD-endemic areas, and the man participated in the feasts only once. In addition, the prion disease in this case was consistent with the most common form of sporadic CJD, without apparent unusual neuropathologic or molecular characteristics that might occur if the prion related to CWD had been responsible for the disease.

The findings in this report are subject to at least two limitations. First, not all members participating in wild game feasts could be identified, and not all persons listed as participating could be contacted for interviews. Second, interviews that were conducted required recall of events that occurred up to 25 years ago, limiting the detail or accuracy of events. However, the similar responses obtained from different sources support the accuracy of the investigation findings.

A previous investigation of unusually young CJD patients in whom the transmission of CWD was suspected also did not provide convincing evidence for a causal relationship between CWD and CJD (2). However, limited epidemiologic investigations cannot rule out the possibility that CWD might play a role in causing human illness. Ongoing surveillance of CJD, particularly in states with CWD, is important to assess the risk, if any, for CWD transmission to humans. Because the confirmation of CJD and the detection of a new prion disease require neuropathologic study of brain tissue, physicians are encouraged to contact NPDPSC (http://www.cjdsurveillance.com; telephone, 216-368-0587) to confirm diagnoses of CJD and to distinguish its various subtypes. Because of the known severity of TSEs in humans and the possibility that the CWD prion can affect humans, animals with evidence of CWD should be excluded from the human food or animal feed chains. Hunters and wild venison consumers should follow precautionary guidelines available from the Wisconsin Department of Agriculture, Trade, and Consumer Protection (http://datcp.state.wi.us/core/consumerinfo) to prevent potential exposures to the CWD agent.

 

 

[Four Season Whitetail's]

^{you might want to check this out}

 

 

 

^{Wisconsin : Mysterious Marathon County case underscores lack of knowledge of CWD}

^{Date: March 10, 2014}

Source: Marshfield News Herald

^Contacts:

Marshfield News Herald

^{ELAND — It’s been almost five months since a prize buck on a game farm in eastern Marathon County tested positive for chronic wasting disease, and investigators are as befuddled about the case today as they were in November.}

^{The game farm, Wilderness Whitetails, and its affiliated breeding farm in Portage County have followed all of the protocols set forth by the Wisconsin Department of Agriculture, Trade and Consumer Protection intended to prevent the spread of the deadly disease. Wilderness Whitetails is a 351-acre, family-run hunting ranch that started business 37 years ago, owner Greg Flees said in December. The disease was found in a routine test after a hunter killed the animal.}

^{The herd had been “closed” for more than a decade, Flees said, meaning that no deer had been brought into the operations from the outside. The breeding farm is double-fenced, which keeps wild deer from getting close to the captive animals to prevent the spread of chronic wasting disease, but the hunting preserve is not, in accordance with state regulations.}

^{No deer had tested positive on the preserve before; it was the first new CWD-infected deer tested on any Wisconsin farm since October 2008, and the farthest north a captive deer had been found to have the disease. The infected buck was one of the preserve’s 270 deer, game for people who pay for the right to hunt them.}

^{Flees cooperated fully with the investigation of how the buck got sick, said Paul McGraw, state veterinarian. But even with Flees’ help and subsequent investigative efforts, McGraw said he doesn’t think there ever will be an answer as to how that buck got sick — which leaves hunters in eastern Marathon County nervous.}

^{“This guy has got a real good record,” McGraw said. “This particular farm has done a lot (to prevent CWD exposure). There’s a low risk that CWD is in the breeding herd.”}

^{The case underscores just how little is known about CWD, and the knowledge gap makes it difficult to manage the disease.}

^{“There’s not been a lot of research done on it,” McGraw said. “And there are not a lot of good answers.”}

^{CWD upswing}

^{The Wilderness Whitetails case comes at a time when the disease continues to run rampant among wild deer in Iowa County and western Dane County, where the state Department of Natural Resources says that one in four adult male deer has the fatal disease. The prevalence rate of 25 percent is based on 2013 test results from that deer management zone. The rate has more than doubled since 2002, when 8 percent to 10 percent of bucks had the disease.}

^{The CWD stakes are high in a state that places a premium on hunting socially, culturally and economically. In 2010, deer hunting licenses and permits generated $22.7 million for the DNR, according to PolitiFact Wisconsin. Estimates of the overall economic impact to the state as a whole exceed $1 billion.}

^{CWD affects elk and moose as well as deer, according to the U.S. Department of Agriculture. It was first recognized in 1967 and belongs to a family of diseases called transmissible spongiform encephalopathies. Other TSEs include bovine spongiform encephalopathy in cattle, scrapie in sheep and goats and Creutzfeldt-Jacob disease in humans. CWD, though, is distinct from those other diseases, the USDA said.}

^{The growth of CWD in southern Wisconsin, coupled with the Wilderness Whitetails case, is troubling, said Marcell Wieloch, 71, of Mosinee, a longtime deer hunter with gun and bow.}

^{“The elephant in the room, the fear that some people have, is if they shoot that deer, and eat that deer, sooner or later it’s going to transfer to Creutzfeldt-Jacob disease,” Wieloch said. “You start bringing those threads together.”}

^{No one understands specific causes of CWD. Most scientists believe, however, that TSE diseases are caused by proteins called prions. And scientists agree that CWD often is transmitted directly from one animal to another through saliva, feces and urine containing abnormal prions, according to the USDA.}

^{Records show the buck killed at Wilderness Whitetails never came in contact with another infected deer, so it’s a mystery as to how it contracted CWD. Three possibilities include that the buck got the disease spontaneously; that it came from exposure in the herd of the hunting preserve or breeding farm; or that it picked up the disease in the environment, McGraw said.}

^{“We don’t know if there are prions in the soil, whether it can survive a while in the environment,” McGraw said. “We don’t see any scientific way of naming any one of these possibilities as the reason (the Wilderness Whitetails buck had the disease.)”}

^{Unknown future}

^{The state DNR, which oversees CWD policy among wild deer, uses one main tool to quash the disease. It prohibits deer baiting and feeding in areas where CWD has been found in deer. Marathon County already was under the restriction because farm deer in Portage County had been tested as CWD positive. The Wilderness Whitetail case extended the region to Shawano and Waupaca counties, said Tami Ryan, chief of the DNR’s wildlife health program.}

^{The DNR also will step up its surveillance for CWD in the area to get a better idea how prevalent the disease is.}

^{“There is no CWD in the wild deer in Marathon County, as far as we know,” Ryan said.}

^{Did finding CWD in a captive herd increase the potential for the disease to spread to wild deer? It’s a concern, Ryan said, but there is no way to know.}

^{Wieloch would like to see the DNR take a more aggressive stance against CWD. Other states, such as Colorado, he said, have helped limit its spread by using sharpshooters to kill deer in CWD zones.}

^{Ryan said one reason the DNR hasn’t taken more drastic steps is because of the public and hunters as a whole, have opposed those measures.}

^{“We respond by social influence and outlook, attitude and opinion,” Ryan said. “The tide is shifting a little bit. Based on our past experience, we’re seeing more public sentiment that wishes we were doing more, taking a stronger stance.”} 

 

© Chronic Wasting Disease Alliance

 ^{http://www.nwhc.usgs.gov/images/cwd/cwd_map.jpg}

CWD detected in Washburn County in northwest Wisconsin

Baiting and feeding ban

Deer baiting and feeding is banned in Washburn, Burnett, Barron and Polk counties. For more information on the ban, please see the baiting and feeding regulations.

During the 2011 gun deer season, a 3.5-year-old doe exhibiting symptoms associated with Chronic Wasting Disease (CWD) was sampled by Spooner DNR wildlife staff. Testing confirmed that this deer was positive for CWD. Genetic testing was also done, confirming that the 3.5-year-old doe was a wild deer from northwest Wisconsin. Since discovering CWD, the DNR has been actively testing deer found within a 10-mile radius of the initial positive deer's location, just west of Shell Lake. The DNR has a goal to sample 500 adult deer within the 10-mile intensive monitoring area. To reach this goal we need a lot of help from all deer hunters hunting within the 10-mile intensive monitoring area [PDF]. Hunters can help by providing the head or lymph nodes from their adult deer at one of the sampling stations [PDF]. It is important to test every adult deer that is harvested or dies within the 2-mile area for CWD.

Northwest Wisconsin CWD sampling update

During the 2012-13 CWD sampling season 1,074 samples were collected. No additional CWD positive deer were detected, which strongly indicates that CWD was detected early in its infection of the deer herd of northwest Wisconsin. We would like to thank everyone who submitted a deer for testing in the past year. Without your help we would not have reached our sampling goal.

For the 2013 season local wildlife staff in Washburn County sampled approximately 500 deer during the 9 day deer gun season. The table will be updated as results come back and the data is entered into the database system.

CWD results from deer killed during 2013 CWD year (April 1, 2013 - March 31, 2014). Surveillance Area Negative Positive Inconclusive Results* Results Pending Totals 2 mile radius 49** 0 0 0 49 2-10 mile radius 450*** 0 4 0 454 Disease suspect deer from Barron, Burnett, Polk or Washburn 5 0 0 0 5 Totals 504 0 4 0 508

 

[Four Season Whitetail's]

Prevalence & surveillance

Since 2002, chronic wasting disease (CWD) prevalence within our western monitoring area has shown an overall increasing trend in all sex and age classes. During the past 12 years, the trend in prevalence in adult males has risen from 8-10 percent to nearly 25 percent, and in adult females from about 3-4 percent to more than 10 percent. During that same time, the prevalence trend in yearling males has increased from about 2 percent to about 7 percent and in yearling females from roughly 2 percent to about 6 percent.

We continue to find that disease prevalence is higher in males than females and higher in adults than yearlings. It is important to keep in mind that annual prevalence estimates are subject to sampling variation, and that trends over time give us better information. These annual monitoring data are important for Wisconsin's understanding of CWD distribution and prevalence.

The graphs in the links below show estimates of trend in prevalence of CWD in the western monitoring area for yearling and adult males and females during 2002-2013. Illustrated in the graphs are trend curves that are based on all 12 years of test results

[Four Season Whitetail's]

I found this on the CDC web site

 

 

Fatal Degenerative Neurologic Illnesses in Men Who Participated in Wild Game Feasts --- Wisconsin, 2002

Creutzfeldt-Jakob disease (CJD) is a fatal neurologic disorder in humans. CJD is one of a group of conditions known as transmissible spongiform encephalopathies (TSEs), or prion diseases, that are believed to be caused by abnormally configured, host-encoded prion proteins that accumulate in the central nervous tissue (1). CJD has an annual incidence of approximately 1 case per million population in the United States (1) and occurs in three forms: sporadic, genetically determined, and acquired by infection. In the latter form, the incubation period is measured typically in years. Recent evidence that prion infection can cross the species barrier between humans and cattle has raised increasing public health concerns about the possible transmission to humans of a TSE among deer and elk known as chronic wasting disease (CWD) (2). During 1993--1999, three men who participated in wild game feasts in northern Wisconsin died of degenerative neurologic illnesses. This report documents the investigation of these deaths, which was initiated in August 2002 and which confirmed the death of only one person from CJD. Although no association between CWD and CJD was found, continued surveillance of both diseases remains important to assess the possible risk for CWD transmission to humans.

Case Reports

Case 1. In December 1992, a Wisconsin man aged 66 years with a history of seizures since 1969 sought treatment for recurring seizures, increasing forgetfulness, and worsening hand tremors. Electroencephalographic (EEG) examination demonstrated focal epileptiform activity and nonspecific diffuse abnormalities, but no specific diagnosis was made. In February 1993, he was hospitalized for increasing confusion, ataxia, and movement tremors of his extremities. A magnetic resonance image (MRI) demonstrated mild, nonspecific enhancement along the inferior parasagittal occipital lobe. A repeat EEG showed bifrontal intermittent, short-interval, periodic sharp waves, suggesting a progressive encephalopathy; a diagnosis of CJD was suspected. The man died later that month; neuropathologic examination of brain tissue during autopsy indicated subacute spongiform encephalopathy, compatible with CJD.

The man was a lifelong hunter who ate venison frequently. He hunted primarily in northern Wisconsin but also at least once in Montana. He hosted wild game feasts at his cabin in northern Wisconsin from 1976 until shortly before his death. Fixed brain tissue obtained during the autopsy was sent for analysis to the National Prion Disease Pathology Surveillance Center (NPDPSC) and reexamined at the institution where the autopsy was conducted. Histopathologic examination did not substantiate the diagnosis of prion disease. In addition, 27 brain tissue sections were negative for prions by immunostaining despite positive antibody reactions against other proteins (controls), which indicated that other epitopes in the tissue samples were preserved.

Case 2. In May 1999, a Minnesota man aged 55 years with no previous history of a neurologic disease sought evaluation and treatment following a 3-month history of progressive difficulty in writing and unsteadiness of gait. A computerized tomography (CT) scan and MRI examination of his head did not indicate any abnormality. In June 1999, he was hospitalized following onset of dementia, speech abnormalities, and myoclonic jerking. An EEG indicated left-hemispheric periodic sharp waves and moderate generalized background slowing; CJD was diagnosed clinically. In July 1999, following worsening symptoms and development of right upper extremity dystonia, the patient died. Neuropathologic evaluation of brain tissue during autopsy demonstrated widespread subcortical spongiform lesions, consistent with CJD.

The man was not a hunter but had a history of eating venison. He made an estimated 12 visits to the cabin where the wild game feasts were held, but he participated in only one feast during the mid-1980s. Sections of fixed and frozen brain tissue obtained during autopsy were analyzed at NPDPSC, and prion disease was confirmed by immunohistochemical and Western blot testing. The Western blot characteristics and prion disease phenotype in this patient were consistent with the most common form of sporadic CJD, classified as M/M (M/V) 1 (3). Subsequent genetic typing confirmed the presence of methionine homozygosity (M/M) at codon 129 of the patient's prion protein gene.

Case 3. In June 1992, a Wisconsin man aged 65 years sought treatment for progressive slowing of speech, worsening memory, and personality changes. By January 1993, his speech was reduced to one-word utterances. Neurologic examination showed a flat affect, decreased reflexes, and apraxia. A CT head scan showed mild atrophy, and an EEG was normal. Pick's disease was diagnosed. By May, he was unable to perform any daily living activities; he died in August 1993. Neuropathologic evaluation of brain tissue during autopsy showed symmetrical frontal lobe cerebral cortical atrophy and mild temporal lobe atrophy. No Pick's bodies or spongiform lesions were observed.

The man had a history of eating venison and participated regularly in wild game feasts held at the cabin owned by patient 1. He was a lifelong hunter and hunted mostly in Wisconsin but also in Wyoming and British Columbia. No game was brought to the wild game feasts from his hunting trips outside of Wisconsin. Examination of fixed brain tissue sent to NPDPSC demonstrated no lesions indicative of CJD, and immunohistochemical testing with antibody to the prion protein did not demonstrate the granular deposits seen in prion diseases.

Epidemiologic Investigation

Wild game feasts consisting of elk, deer, antelope, and other game that occurred at a cabin in northern Wisconsin owned by patient 1 began in 1976 and continued through 2002. These feasts typically involved 10--15 participants and usually occurred on weekends before or during hunting seasons in the fall and occasionally in the spring. Wild game brought to these feasts usually were harvested in Wisconsin, but three men who attended these feasts reported hunting in the western United States and bringing game back to Wisconsin. These activities took place in Colorado (near the towns of Cortez, Trinidad, Collbran, Durango, and Meeker), Wyoming (near the towns of Gilette and Cody), and Montana (near the town of Malta). CWD was not known to be endemic in these areas at the time that these hunting activities took place.

Information was obtained for 45 (85%) of 53 persons who were identified as possibly participating in the wild game feasts; all were male. Information was obtained by direct interview or from family members of decedents. Of the 45 persons, for whom information was obtained, 34 were reported to have attended wild game feasts. Seven of the 34 feast attendees were deceased, including the three patients. None of the four other decedents had a cause of death attributed to or associated with a degenerative neurologic disorder. None of the living participants had any signs or symptoms consistent with a degenerative neurologic disorder.

Reported by: JP Davis, MD, J Kazmierczak, DVM, M Wegner, MD, R Wierzba, Div of Public Health, State of Wisconsin Dept of Health and Family Svcs. P Gambetti, National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, Ohio. L Schonberger, MD, R Maddox, MPH, E Belay, MD, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; V Hsu, MD, EIS Officer, CDC.

Editorial Note:

CWD was first described in the United States in the 1960s and classified as a TSE in 1978. Previously localized to a contiguous endemic area in northeastern Colorado and southeast Wyoming, since 2000, CWD has been found in free-ranging deer or elk in Illinois, Nebraska, New Mexico, South Dakota, Wisconsin, and outside the previously known endemic areas of Colorado and Wyoming. CWD has been identified also in captive deer or elk in Colorado, Kansas, Minnesota, Montana, Nebraska, Oklahoma, South Dakota, and Wisconsin (4). Because a variant form of CJD, with specific neuropathologic and molecular characteristics that distinguish it from sporadic CJD, has been associated with eating cattle products infected with a prion that causes bovine spongiform encephalopathy (5), concern has been raised about the possibility that the prion associated with CWD might be transmitted to humans in a similar way.

In this investigation, because only one of the three cases in Wisconsin had neuropathologic confirmation of a prion disease, no association could be made between case participation in the wild game feasts and the development of CJD. Although patient 2 had confirmed CJD, he was unlikely to have eaten CWD-infected venison at these feasts because venison and other game from outside Wisconsin that was served at these feasts did not originate from known CWD-endemic areas, and the man participated in the feasts only once. In addition, the prion disease in this case was consistent with the most common form of sporadic CJD, without apparent unusual neuropathologic or molecular characteristics that might occur if the prion related to CWD had been responsible for the disease.

The findings in this report are subject to at least two limitations. First, not all members participating in wild game feasts could be identified, and not all persons listed as participating could be contacted for interviews. Second, interviews that were conducted required recall of events that occurred up to 25 years ago, limiting the detail or accuracy of events. However, the similar responses obtained from different sources support the accuracy of the investigation findings.

A previous investigation of unusually young CJD patients in whom the transmission of CWD was suspected also did not provide convincing evidence for a causal relationship between CWD and CJD (2). However, limited epidemiologic investigations cannot rule out the possibility that CWD might play a role in causing human illness. Ongoing surveillance of CJD, particularly in states with CWD, is important to assess the risk, if any, for CWD transmission to humans. Because the confirmation of CJD and the detection of a new prion disease require neuropathologic study of brain tissue, physicians are encouraged to contact NPDPSC (http://www.cjdsurveillance.com; telephone, 216-368-0587) to confirm diagnoses of CJD and to distinguish its various subtypes. Because of the known severity of TSEs in humans and the possibility that the CWD prion can affect humans, animals with evidence of CWD should be excluded from the human food or animal feed chains. Hunters and wild venison consumers should follow precautionary guidelines available from the Wisconsin Department of Agriculture, Trade, and Consumer Protection (http://datcp.state.wi.us/core/consumerinfo) to prevent potential exposures to the CWD agent.

 

Scary if ever found to be true. I can tell you where there are over 100 people that ate a CWD positive deer in Ny State and to date there has never been an health issue with any of them.  Good News!

[Terry]

Where?

[Four Season Whitetail's]

As we have all heard, CWD was found in Oneida County, New York. CWD was confirmed on 2 different farms, the 1st farm owned by John Palmer and the 2nd by Martin Proper.

 

The 1st positive was a 6-year-old doe that was harvested for a fireman's benefit dinner. In talking to John, he said, "I picked out the fattest, healthiest looking doe I had."

 

Most people have been led to believe that CWD-positive deer exhibit signs of poor health, but the deer farming industry has found this to be untrue. The vast majority of those animals that have tested positive have shown little, if any signs of sickness.

 

The herd was depopulated only days after the 1st positive was found. On a Tuesday morning, sharpshooters came in and after 6 hours had put down the remaining 18 deer. Samples were collected and sent in for analysis. Friday the results were back; 3 more positives were found for CWD. These 3 deer all came from New York State's Rehabilitation Program. John Palmer acquired these deer from New York's wild population through conservation officers.

 

John Palmer's herd started when he purchased a few deer from Ohio in 1994. Later, he added other deer from a New York source. 7 years ago John started rehabilitating fawns. John said he took in 1-14 fawns per year from all over New York. John had the responsibility of determining whether the fawn could be released back into the wild or had to stay forever in a pen in his privately owned herd. He also relocated some of these fawns to other producers. This is how Martin Proper came into the picture.

 

Martin Proper is the owner of the 2nd positive herd. The animal that tested positive for CWD on his farm was a 4- or 5-year-old buck that died from pneumonia, another rehabilitated wild deer from New York. Martin received 2 deer from John Palmer's herd; one doe that was blind and one doe born with only 3 feet. They had bred and had produced some offspring. The aforementioned buck killed one of these does during last year's rut, and was not tested because it happened before their CWD Program was up and running. The rest of Martin's herd was put down and samples analyzed. No other positives were found.

 

There were 5 positives found in these 2 herds; 4 were deer taken from the wild [as rehabilitated fawns]. It is unclear to John where the very first doe originated, but he felt it could have originated from the wild as well.

 

Taking deer from the wild is not condoned by the cervid industry and is strongly discouraged; nonetheless, it did happen with the deer in this situation.

 

A statement released by the New York State Department of Environmental Conservation (DEC) on 5 Apr 2005 announced plans to conduct intensive monitoring of the wild deer population surrounding both farms to determine whether CWD has spread to the wild herds.

 

The NYS DEC has already directed blame towards the farmed deer industry for bringing CWD into New York, even though there is a clear history of the DEC taking deer out of the wild and placing them into John Palmer's herd for rehabilitation. The question should be, "Where did the wild deer of New York get CWD?"

 

Adding to the questions, without any answers, John is a taxidermist and has taken work from all over North America. He mentioned receiving work from the following states and Canadian province: Saskatchewan, Montana, Idaho, Illinois, Kansas, Colorado and Wyoming. When looking at where CWD has been found in the wild, many of these locations appear on that list.

 

In a study released by Beth Williams and Mike Miller, they noted that [a deer] was just as likely to contract CWD from a live infected deer as it was to be housed in a pen with a dead positive carcass.

 

Did one or more of the many dead animals brought into John's taxidermy studio have CWD? John stated that he kept the rehabilitation fawns in the same garage where he did much of his taxidermy work. It was common practice for John to sweep up his shop and deposit the salt and chemicals along the deer fence as a weed retardant.

 

The industry has always said that movement of CWD-positive carcasses would move CWD much faster and farther than moving live animals. Is the New York situation just that? Is there a need to regulate movement of CWD-positive carcasses?

 

There are many points that come to the forefront from the situation in New York:

 

* The detection of CWD in New York clearly shows that the monitoring system is working. These programs are set up to identify herds at risk.

 

* This event highlights the need for surveillance. Without the state monitoring/surveillance programs, these positive deer would not be detected. The more herds on these programs, the lower the risk.

 

* In the face of CWD, the best defense is herd monitoring/surveillance. What better way to get participation than to recognize those who have already participated in these programs and allow for continued movement for their herds that have met the needed criteria? The event in New York has _in no way_ compromised the health status of any herd that has been enrolled in a CWD monitoring/surveillance program.

 

* CWD conjures up many questions that remain unanswered. There is a continued need for the government agencies involved and the industry to work together to resolve some of those questions.

 

* As previously seen, in discoveries of CWD, including this New York case, all too often the producer is portrayed as a villain. There is no one who wants this "disease" to be found on their property. When CWD is found, the industry expects the producers to be treated fairly and with respect. The finger-pointing and intimidation tactics are _not_ needed to resolve the issues involved with CWD and private ownership of deer in the United States.

 

Deer farmers are fathers, mothers, sons, and daughters. They have served this country in the armed forces. Deer farmers come from all walks of life; doctors, lawyers, carpenters, plumbers, and housekeepers. The one thing they all have in common is the passion they have for their deer. Let us work together to resolve the issues that CWD brings to the forefront across this great country of ours.

 

 

Gary Nelson, President

NADeFA

[email protected]

 

[it has been reported in other newspaper sources that the owner of index herd in NY not only put the salt and other products from cleaning up his taxidermy work along his fence lines -- thus exposing his captive herd -- but also that the fawns in the taxidermy garage area may have licked, mouthed, or chewed on entrails from some deer.

 

It is stated in this NADeFA release that the owner of the index herd was to decide whether the rehabilitated deer could return to the wild or were not capable of survival on their own, presumably because of serious injury, such as 3 legs, or imprinting on people. However, he was instructed to turn some loose in the wild.

 

If the fawn or fawns in question consumed -- or otherwise contacted -- infected tissues in the taxidermy shop and then were released to the wild, then it could be speculated that NYS DEC would likely find exposed wild animals. If the fawn was originally wild, exposed through taxidermy work on other wild animals, and then released back to the wild, it would be difficult to say that captive animals brought disease to wild animals. It would be more acceptable to say the wild animals have introduced this disease to captive animals

 

If you read the words of the case of CWD in Michigan you will read a story that plays out much like Ny's cases. Found at a deer/Taxidermist shop and never to be found again.  Just the true facts!

[Culvercreek hunt club]

You dont keep up much huh.  Ny did that...Against the law and now are being sued in a lawsuit filed by the Ny deer farmers.  Should be hitting the headlines soon.   You think the safe act is against your right... Same idea when you start pushing land owner rights and free trade.  Money does talk.

What is the section of the law that restricts export?

[Larry]

check this map out its from usgs shows where cwd is along with game farms.

http://www.nwhc.usgs...cwd/cwd_map.jpg

[bowaholic]

I am from Westmoreland in Oneida County, and as I'm sure many of you know, this is where CWD was found in penned deer.  Some a-hole, not naming names (cough Palmer cough) had whitetail deer in captivity behind his house about a mile from my house.  because of him over 3000 deer in my county and Madison county were killed by the DEC.  The purpose of the kill was to look from contaminated wild deer as the genius decided to let some of his "rehabilitated" deer go.  One was found in the wild (one he had let go).  But due to him thinking it was a good idea my area was nothing like it was before.  You can't argue that he could have tested the deer to see if they had the disease because the only way to test for CWD is to take a sample of the spinal cord and glands at the base of the skull.  (watched this done as we had to for years take every deer we harvester to a check station for testing)  High fenced hunts and deer farming CAN hurt the wild population.    

[bowaholic]

I've spoken to Palmer before as he is a taxidermist and I have an animal there now being mounted(wont say the animal incase he is on here and does a bad job on purpose and has had it for over a year now....should have been done well before now), I've been behind his house and saw the pens where he kept the deer,  he now has exotic goats and other animals in the same pen as the deer were in.  CWD can be spread through fecal matter in the soil, the un-infected deer comes along eats the grass and then contracts the disease.  He is a MORON and shouldn't even have a cat...

[nyantler]

I've spoken to Palmer before as he is a taxidermist and I have an animal there now being mounted(wont say the animal incase he is on here and does a bad job on purpose and has had it for over a year now....should have been done well before now), I've been behind his house and saw the pens where he kept the deer,  he now has exotic goats and other animals in the same pen as the deer were in.  CWD can be spread through fecal matter in the soil, the un-infected deer comes along eats the grass and then contracts the disease.  He is a MORON and shouldn't even have a cat...

I know him as well... all I can say is that he is a bit shady and it didn't surprise me to find out the CWD was found at his place. I wouldn't have him stuff a pillow for me.

[Four Season Whitetail's]

I am from Westmoreland in Oneida County, and as I'm sure many of you know, this is where CWD was found in penned deer.  Some a-hole, not naming names (cough Palmer cough) had whitetail deer in captivity behind his house about a mile from my house.  because of him over 3000 deer in my county and Madison county were killed by the DEC.  The purpose of the kill was to look from contaminated wild deer as the genius decided to let some of his "rehabilitated" deer go.  One was found in the wild (one he had let go).  But due to him thinking it was a good idea my area was nothing like it was before.  You can't argue that he could have tested the deer to see if they had the disease because the only way to test for CWD is to take a sample of the spinal cord and glands at the base of the skull.  (watched this done as we had to for years take every deer we harvester to a check station for testing)  High fenced hunts and deer farming CAN hurt the wild population.    

Oh how many holes can be found in this post.   First off, you must be young and very clueless of the life of a person who did deer rehab. Years ago we had no choice but to take fawns. Back then it was common practice for the DEC to drop off any found fawn. Could be found in hay fields or on the side of the road with dead moms.  If you were a farmer they told you to keep them. If you did rehab they said YOU HAD TO RELEASE THEM. So your little rant there holds no water.

 

The 3000 deer killed to find 1 deer with CWD was the bright moves of your DEC. There has been more deer killed looking for something that may kill deer than the disease would ever kill.  Wisconsin thought they would do the same.  What did that get them?  A stronger herd with twice the numbers than before they shot thousands. CWD is doing no damadge to any herds in any states. Period!!!

 

Your thoughts about deer fecal,CWD and eating grass?  Shows you dont pay much attention to the very disease you complain about!

[mike rossi]

link wont work, never mind

Edited April 4, 2014 by mike rossi

[mike rossi]

http://news.wildlife.org/featured/a-growing-threat/

 

[Four Season Whitetail's]

http://news.wildlife.org/featured/a-growing-threat/

Do you realize how foolish you look by posting crap that is over a year plus old.  What makes you even more foolish is that you post something from a state that was fighting for its life in the middle of a multi million dollar lawsuit filled by the Brakke farm against them for killing their livestock and shutting them down.

 Maybe you should now put up the link to the court hearing i that shows the state of Iowa LOST the court case and are now costing the Iowa taxpayers 2.5 million dollars for the replacement of the animals and another 1.2 million for the lost income from their high fence operation sales. Thats the real news and what happens when you play with a persons 2nd.... 

 

You may really want stick to the wings and feather posts on this site. At least some of your posts have some kind of meaning with them. 

[Doc]

Do you realize how foolish you look by posting crap that is over a year plus old.  What makes you even more foolish is that you post something from a state that was fighting for its life in the middle of a multi million dollar lawsuit filled by the Brakke farm against them for killing their livestock and shutting them down.

 Maybe you should now put up the link to the court hearing i that shows the state of Iowa LOST the court case and are now costing the Iowa taxpayers 2.5 million dollars for the replacement of the animals and another 1.2 million for the lost income from their high fence operation sales. Thats the real news and what happens when you play with a persons 2nd.... 

 

You may really want stick to the wings and feather posts on this site. At least some of your posts have some kind of meaning with them. 

Nice argument against the article, and peripheral things around the article, but none of that really is an argument against the content.

[Four Season Whitetail's]

Nice argument against the article, and peripheral things around the article, but none of that really is an argument against the content.

I guess it does. They were shut down because of a so called disease and then to hear their ow state white coats try and save rheir a$$ by saying tey now feel that CWD is not a threat to Iowa,s herd or the citizens of Iowa.  They lost the whole battle to the tune of almost 4 million because of the false content of the article. Why do you think the USDA no loner eradicates a positive herd anywhere any longer?  Now its management of CWD and whitetails can still be moved to hunting ranches.  

 

Even for CWD positive herds!!!  Start losing millions and it dont take long for states to start thinking...Well maybe this CWD stuff is not as bad as we first thought it may be.  Funny what the loss of money does for some!!