Chronic Wasting Disease Transmission Risk Assessment for Farmed Cervids in Minnesota and Wisconsin
Chronic Wasting Disease Transmission Risk Assessment for Farmed Cervids in Minnesota and Wisconsin
Viruses. 2021 Aug; 13(8): 1586. Published online 2021 Aug 11. doi: 10.3390/v13081586 PMCID: PMC8402894 PMID: 34452450
Chronic Wasting Disease Transmission Risk Assessment for Farmed Cervids in Minnesota and Wisconsin
James M. Kincheloe,1,2,* Amy R. Horn-Delzer,3 Dennis N. Makau,2 and Scott J. Wells2 Holger Wille, Academic Editor and Debbie McKenzie, Academic Editor
Author information Article notes Copyright and License information Disclaimer
Associated Data
Data Availability Statement
Abstract
CWD (chronic wasting disease) has emerged as one of the most important diseases of cervids and continues to adversely affect farmed and wild cervid populations, despite control and preventive measures. This study aims to use the current scientific understanding of CWD transmission and knowledge of farmed cervid operations to conduct a qualitative risk assessment for CWD transmission to cervid farms and, applying this risk assessment, systematically describe the CWD transmission risks experienced by CWD-positive farmed cervid operations in Minnesota and Wisconsin. A systematic review of literature related to CWD transmission informed our criteria to stratify CWD transmission risks to cervid operations into high-risk low uncertainty, moderate-risk high uncertainty, and negligible-risk low uncertainty categories. Case data from 34 CWD-positive farmed cervid operations in Minnesota and Wisconsin from 2002 to January 2019 were categorized by transmission risks exposure and evaluated for trends. The majority of case farms recorded high transmission risks (56%), which were likely sources of CWD, but many (44%) had only moderate or negligible transmission risks, including most of the herds (62%) detected since 2012. The presence of CWD-positive cervid farms with only moderate or low CWD transmission risks necessitates further investigation of these risks to inform effective control measures.
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5. Conclusions
This qualitative CWD risk assessment identified several moderate transmission risks with associated high uncertainty along with the well-understood high and negligible transmission risks. For the CWD-positive farms detected in Minnesota and Wisconsin, high transmission risks were the likely source of CWD in the majority of cases, but cervids on many other farms (including a higher proportion of recent cases) likely acquired CWD through moderate transmission risks. This category of moderate transmission risks presents opportunities for further research to provide the scientific basis to inform improved CWD mitigation strategies. Additionally, for more robust surveillance and monitoring systems, industry stakeholders should be encouraged to adopt recently developed higher sensitivity diagnostic techniques, such as RT-QuIC and sPCMA.
Keywords: chronic wasting disease, transmissible spongiform encephalopathy, transmission, cervid, prion, risk analysis
Acknowledgments The authors acknowledge the Minnesota Board of Animal Health for funding this project and the Minnesota Board of Animal Health and the Wisconsin Department of Agriculture, Trade, and Consumer Protection for providing CWD case investigation information. The authors also acknowledge the contributions of Cara Cherry for her review of early Minnesota farmed cervid CWD cases and Linda Glaser and Mackenzie Reberg for assisting in obtaining Minnesota case data and their reviews of the analysis.
Voluntary Chronic Wasting Disease Herd Certification Program Annual Update, FY2020
Last Modified: Feb 9, 2021
U.S. Department of Agriculture
Animal and Plant Health Inspection Service (APHIS) Veterinary Services
Annual Update from the Cervid Health Team
Voluntary Chronic Wasting Disease Herd Certification Program (HCP)
The APHIS National CWD Herd Certification Program (HCP) was implemented in 2014. It is a voluntary Federal-State-industry cooperative program administered by APHIS and implemented by participating States. The program provides uniform national herd certification standards that minimize the risk of spreading CWD in farmed cervid populations. Participating States and herd owners must comply with requirements for animal identification, fencing, recordkeeping, inspections/inventories, as well as animal mortality testing and response to any CWD-exposed, suspect, and positive herds. APHIS monitors the Approved State HCPs to ensure consistency with Federal standards through annual reporting by the States.
With each year of successful surveillance, herds participating in the HCP will advance in status until reaching five years with no evidence of CWD, at which time herds are certified as being low risk for CWD. Only farmed cervids from enrolled herds certified as low risk for CWD may move interstate. FY 2020 marks the eighth year that Approved States have submitted their CWD HCP annual reports to APHIS.
The current Cervid Health Program staff officers are as follows: Dr. Mark Lyons, Dr. Jennifer Siembieda, and Dr. Tracy Nichols
Voluntary Herd Certification Participation Summary
Currently, 28 States participate in the voluntary CWD Herd Certification Program encompassing 2,145 enrolled herds, of which, 1,723 had the certified status in the program.
1,616 enrolled deer herds, of which, 1,297 were certified
371 enrolled elk herds, of which, 328 were certified
147 enrolled mixed species herds, of which, 98 were certified
CWD in Farmed Cervids Summary of CW Detections
There were 22 newly identified CWD positive herds in FY20
13 of these herds were not participants in the Federal HCP
2 herds were considered enrolled in the HCP
7 herds were certified in the HCP
Half of the herds were located within 20 miles of identified CWD in the wild, half were not CWD Herds by State
Pennsylvania: Eight new CWD positive herds
Breeding herd of 33 WTD, HCP certified, depopulated with Federal indemnity
Breeding herd of 6 WTD, not in HCP, depopulated with Federal indemnity
Breeding herd of 15 WTD, not in HCP, depopulated by owner\
Hunt preserve of 58 WTD, not in HCP, populated and under quarantine
Breeding herd of 75 WTD, not in HCP, populated and under quarantine
Breeding herd of WTD, not in HCP, populated and under quarantine
Breeding herd of 90 WTD, not in HCP, populated and under quarantine
Breeding herd of 4 WTD, not in HCP, populated and under quarantine
Iowa: Two new CWD positive herds
Breeding herd of 23 WTD, HCP certified, depopulated with Federal indemnity
Breeding herd of 13 WTD, HCP certified, depopulated with Federal indemnity
Minnesota: Two new CWD positive herds
Breeding herd of 3 WTD, enrolled in HCP, not certified, depopulated by owner
Breeding herd of 6 WTD, enrolled in HCP, not certified, depopulated with Federal indemnity
Colorado: Two new CWD positive herds
Breeding herd/hunt preserve of 9 elk, HCP certified, depopulated by owner
Breeding herd of 8 elk, HCP certified, populated and under quarantine
Utah: Two new CWD positive herds
Breeding herd of 465 elk, not in HCP, partial depopulation with Federal indemnity- removed purchased animals, populated-quarantine
Breeding herd of 103 elk, not in HCP, partial depopulation with Federal indemnity- removed purchased animals, populated-quarantine
Michigan: One new CWD positive herd
Hunt preserve of >600 WTD, not in HCP, populated and under quarantine
Montana: One new CWD positive herd
Breeding herd of 3 elk, not in HCP, populated and under quarantine
Texas: one new CWD positive herd
Breeding herd of 59 WTD, not in HCP, depopulated with Federal indemnity
Kansas: One new CWD positive herd
Breeding herd of 20 elk, HCP certified, depopulated with Federal indemnity
Ohio: Eight new CWD positive herd
Breeding herd of 138 WTD, HCP certified, depopulated with Federal indemnity
Research
Whole genome study investigating the association of genetics with CWD susceptibility has been published.
Blinded validation of the genetic predicative model is almost complete
A standardized protocol has been developed, in partnership with ARS, USGS, University of WI, and NIH for tissue sample testing using RT-QuIC
A study is starting shortly to determine the sensitivity and specify of RT-QuIC utilizing the standardized protocol
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Voluntary Chronic Wasting Disease Herd Certification Program Annual Update, FY2020
Cervids: CWD Voluntary Herd Certification Program
Last Modified: Jun 29, 2021
CWD status of captive herds
Title: Chronic wasting disease in a Wisconsin white-tailed deer farm
Author item KEANE, DELWYN item BARR, DANIEL item BOCHSLER, PHILIP item HALL, S item GIDLEWSKI, THOMAS item O'Rourke, Katherine item SPRAKER, TERRY item SAMUEL, MICHAEL Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: 5/5/2008 Publication Date: 9/2/2008
Citation: Keane, D.P., Barr, D.J., Bochsler, P.N., Hall, S.M., Gidlewski, T.E., O'Rourke, K.I., Spraker, T.R., Samuel, M.D. 2008. Chronic wasting disease in a Wisconsin white-tailed deer farm. Journal of Veterinary Diagnostic Investigation. 20(5):698-703.
Interpretive Summary: Chronic wasting disease is a fatal disease of deer and elk. Clinical signs, including weight loss, frequent urination, excessive thirst, and changes in behavior and gait, have been reported in mule deer and elk with this disorder. Clinical signs in captive white tailed deer are less well understood. In a previous study, a captive facility housed 200 deer, of which half were positive for the disease with no clinical signs reported. In this study, we examined 78 white tailed deer from a captive facility with a history of chronic wasting disease and no animals with clinical signs. Examination of the brain and lymph nodes demonstrated that the abnormal prion protein, a marker for disease, was observed in 60 of the deer. Biopsy of the rectal mucosa, a test that can be performed on live deer, detected 83% of the infected animals. The prion genetics of the deer was strongly linked to the rate of infection and to disease progression. The results demonstrate that clinical signs are a poor indicator of the disease in captive white tailed deer and that routine testing of live deer and comprehensive necropsy surveillance may be needed to identify infected herds.
Technical Abstract: Chronic wasting disease CWD is a transmissible spongiform encephalopathy or prion disease of deer and elk in North America. All diseases in this family are characterized by long preclinical incubation periods following by a relatively short clinical course. Endpoint disease is characterized by extensive deposits of aggregates of the abnormal prion protein in the central nervous system,. In deer, the abnormal prion proteins accumulate in some peripheral lymphoid tissues early in disease and are therefore suitable for antemortem and preclinical postmortem diagnostics and for determining disease progression in infected deer. In this study, a herd of deer with previous CWD diagnoses was depopulated. No clinical suspects were identified at that time. Examination of the brain and nodes demonstrated that 79% of the deer were infected. Of the deer with abnormal prion in the peripheral lymphoid system, the retropharyngeal lymph node was the most reliable diagnostic tissue. Biopsy of the rectal mucosal tissue, a site readily sampled in the restrained or chemically immobilized deer, provided an accurate diagnosis in 83% of the infected deer. The retina in the eye of the deer was positive only in late stage cases. This study demonstrated that clinical signs are a poor indicator of disease, supports the use of the retropharyngeal lymph node as the most appropriate postmortem sample, and supports a further evaluation of the rectal mucosal tissue biopsy as an antemortem test on a herd basis.
Chronic wasting disease in a Wisconsin white-tailed deer farm
WISCONSIN DNR CONFIRMS CWD IN WILD DEER HARVESTED IN VILAS COUNTY WITH A TOTAL OF 9,040 POSITIVE WILD CASES TO DATE
FOR IMMEDIATE RELEASE: 2021-12-17
Contact: DNR Office of Communications
DNR CONFIRMS CWD IN WILD DEER HARVESTED IN VILAS COUNTY
BAITING AND FEEDING BANS RENEWED FOR VILAS AND FOREST COUNTIES AND REMAIN IN EFFECT FOR ONEIDA COUNTY
The Wisconsin DNR confirms CWD in wild deer harvested in Vilas County. Baiting and feeding bans renewed for Vilas and Forest Counties and remain in effect for Oneida County. MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) confirms a wild deer tested positive for chronic wasting disease (CWD) in the Town of Lincoln in Vilas County. This is the first confirmed wild positive case of CWD in Vilas County.
As required by state law, the DNR enacts three-year baiting and feeding bans in counties where CWD has been detected and two-year bans in adjoining counties that lie within 10 miles of a CWD detection.
Following state law, the DNR will renew a three-year baiting and feeding ban in Vilas County as well as a two-year ban in Forest county, as the deer was harvested within 10 miles of the county line. Oneida County is also within 10 miles of the Vilas positive’s harvest location but is already under a longer three-year baiting and feeding ban due to a positive CWD detection at a game farm earlier this year.
Baiting or feeding deer encourages them to congregate unnaturally around a shared food source where sick deer can spread CWD through direct contact with healthy deer or by leaving behind infectious prions in their bodily secretions.
More information regarding baiting and feeding regulations and CWD in Wisconsin is available here.
The DNR asks deer hunters in Vilas, Forest and Oneida counties to assist with efforts to identify where CWD occurs. Those harvesting deer within 10 miles of the newly detected positive case are especially encouraged to have their harvested adult deer tested for CWD. Collecting CWD samples is essential for assessing where and to what extent CWD occurs in deer across the state.
The DNR will work with Vilas County Deer Advisory Council members to schedule a meeting in January to discuss response actions. Members of the public will be invited to attend this meeting and will have the opportunity to provide input.
CWD is a fatal, infectious nervous system disease of deer, moose, elk and reindeer/caribou. It belongs to the family of diseases known as transmissible spongiform encephalopathies (TSEs) or prion diseases. The Wisconsin DNR began monitoring the state's wild white-tailed deer population for CWD in 1999. The first positives were found in 2002.
Information on how to have deer tested during the 2020-21 hunting seasons is available here.
Wisconsin Portage County Deer Farm Tests Positive for CWD
Portage County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: December 17, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wisconsin.gov
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that two white-tailed deer at a Portage County hunt ranch have tested positive for chronic wasting disease (CWD). Positive samples were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
The 200-acre farm and its herd of approximately 370 deer are under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal’s death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement, and permit requirements.
More information
About CWD:
DATCP’s farm-raised deer program:
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This table shows available CWD test results for the selected year for each of DNR's four zones statewide. Results for an individual year are for the CWD year, which runs from April 1st through March 31st. For example, the results for the 2021 CWD year would be April 1st, 2021 through March 31st, 2022. Deer will not have full data until the datasheet is entered.
DNR Zone # Sampled # Analyzed Positive for CWD
Central Farmland Zone 5669 3231 19
Central Forest Zone 509 284 3
Northern Forest Zone 1977 1024 0
Southern Farmland Zone 6864 4919 849
Unknown Zone 162 54 2
Totals: 15181 9512 873
This table shows available CWD test results for each of DNR's four zones statewide. It includes data released through December 16, 2021. Deer will not have full data until the datasheet is entered.
DNR Zone # Sampled # Analyzed Positive for CWD
Central Farmland Zone 54182 51724 78
Central Forest Zone 7028 6801 47
Northern Forest Zone 29498 28539 6
Southern Farmland Zone 186740 184763 8904
Unknown Zone 3049 2933 5
Statewide Totals: 280497 274760 9040
Wisconsin Eau Claire County Deer Farm Tests Positive for CWD
Eau Claire County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: November 9, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005,
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that a white-tailed deer from an Eau Claire County hunt ranch has tested positive for chronic wasting disease (CWD). Positive samples from a 3-year-old buck were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
The herd of approximately 15 deer is under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff. The ranch was confirmed to have received the deer from a Waukesha County deer farm, which also has been placed under quarantine.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal’s death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement, and permit requirements.
More information
About CWD:
DATCP’s farm-raised deer program:
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Wisconsin Outagamie County Deer Farm Tests Positive for CWD
Outagamie County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: September 2, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wisconsin.gov
Download PDF
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that a deer farm in Outagamie County has tested positive for chronic wasting disease (CWD). Positive samples were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
The farm was already under quarantine after receiving animals from a CWD affected farm. The herd of approximately 30 deer will remain under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal's death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement and permit requirements.
More information
DATCP's farm-raised deer program: https://datcp.wi.gov/Pages/Programs_Services/FarmRaisedDeer.aspx
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CARCASS MOVEMENT, PROCESSING AND DISPOSAL
The movement of dead or alive CWD positive deer, moose, elk or reindeer/caribou (natural or human-assisted) is a key pathway in the spread of CWD. The infectious nature of the CWD prion contributes to an increased risk of introduction and spread of CWD if dead carcasses are brought to new areas and not disposed of properly.
FIND CWD SAMPLING AND CARCASS DISPOSAL LOCATIONS NEAR YOU
Wisconsin Langlade County Deer Farm Tests Positive for CWD
Langlade County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: September 1, 2021
Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wisconsin.gov
Download PDF
MADISON, Wis. – The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that a deer farm in Langlade County has tested positive for chronic wasting disease (CWD).
A positive sample from a 1-year-old doe was confirmed by the National Veterinary Services Laboratory in Ames, Iowa. All 57 deer at the 6-acre farm were already under quarantine after receiving animals from a CWD-affected farm. The herd will remain under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal's death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement and permit requirements.
More information
DATCP's farm-raised deer program: https://datcp.wi.gov/Pages/Programs_Services/FarmRaisedDeer.aspx
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Deer Farms in Sauk, Taylor Counties Test Positive for CWD
Release Date: August 11, 2021
Media Contact: Kevin Hoffman, Public Information Officer, (608) 224-5005, kevin.hoffman@wi.gov
MADISON — The Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that deer farms in Sauk and Taylor counties have tested positive for chronic wasting disease (CWD). Results were confirmed by the National Veterinary Services Laboratory in Ames, Iowa.
Positive samples were taken from a 6-year-old doe in Taylor County and a 9-year-old buck in Sauk County. There is no connection between the two locations. The 227 whitetail deer at the 22-acre double-fenced Taylor County farm and the two whitetail deer at the 1-acre singlefenced Sauk County farm have been quarantined, meaning no live animals or whole carcasses are permitted to leave the property. The herds will remain under quarantine while an epidemiological investigation is conducted by DATCP and U.S. Department of Agriculture (USDA) veterinarians and staff.
CWD is a fatal, neurological disease of deer, elk and moose caused by an infectious protein called a prion that affects the animal's brain, and testing for CWD is typically only performed after the animal’s death. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement and permit requirements.
More information
About CWD:
DATCP’s farm-raised deer program:
Title: Chronic wasting disease in a Wisconsin white-tailed deer farm
Author item KEANE, DELWYN item BARR, DANIEL item BOCHSLER, PHILIP item HALL, S item GIDLEWSKI, THOMAS item O'Rourke, Katherine item SPRAKER, TERRY item SAMUEL, MICHAEL
Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: 5/5/2008 Publication Date: 9/2/2008
Citation: Keane, D.P., Barr, D.J., Bochsler, P.N., Hall, S.M., Gidlewski, T.E., O'Rourke, K.I., Spraker, T.R., Samuel, M.D. 2008. Chronic wasting disease in a Wisconsin white-tailed deer farm. Journal of Veterinary Diagnostic Investigation. 20(5):698-703. Interpretive Summary: Chronic wasting disease is a fatal disease of deer and elk. Clinical signs, including weight loss, frequent urination, excessive thirst, and changes in behavior and gait, have been reported in mule deer and elk with this disorder. Clinical signs in captive white tailed deer are less well understood. In a previous study, a captive facility housed 200 deer, of which half were positive for the disease with no clinical signs reported. In this study, we examined 78 white tailed deer from a captive facility with a history of chronic wasting disease and no animals with clinical signs. Examination of the brain and lymph nodes demonstrated that the abnormal prion protein, a marker for disease, was observed in 60 of the deer. Biopsy of the rectal mucosa, a test that can be performed on live deer, detected 83% of the infected animals. The prion genetics of the deer was strongly linked to the rate of infection and to disease progression. The results demonstrate that clinical signs are a poor indicator of the disease in captive white tailed deer and that routine testing of live deer and comprehensive necropsy surveillance may be needed to identify infected herds.
Technical Abstract: Chronic wasting disease CWD is a transmissible spongiform encephalopathy or prion disease of deer and elk in North America. All diseases in this family are characterized by long preclinical incubation periods following by a relatively short clinical course. Endpoint disease is characterized by extensive deposits of aggregates of the abnormal prion protein in the central nervous system,. In deer, the abnormal prion proteins accumulate in some peripheral lymphoid tissues early in disease and are therefore suitable for antemortem and preclinical postmortem diagnostics and for determining disease progression in infected deer. In this study, a herd of deer with previous CWD diagnoses was depopulated. No clinical suspects were identified at that time. Examination of the brain and nodes demonstrated that 79% of the deer were infected. Of the deer with abnormal prion in the peripheral lymphoid system, the retropharyngeal lymph node was the most reliable diagnostic tissue. Biopsy of the rectal mucosal tissue, a site readily sampled in the restrained or chemically immobilized deer, provided an accurate diagnosis in 83% of the infected deer. The retina in the eye of the deer was positive only in late stage cases. This study demonstrated that clinical signs are a poor indicator of disease, supports the use of the retropharyngeal lymph node as the most appropriate postmortem sample, and supports a further evaluation of the rectal mucosal tissue biopsy as an antemortem test on a herd basis.
Chronic Wasting Disease Positives in Farm-raised Deer
Revised: 3/1/2021
County (Premises #) Sample Collection Date of First CWD Positive in Farmraised Deer Sample Collection Date of Last CWD Positive in Farmraised Deer Total CWD Positive in Farm-raised Deer
Portage(1) 9/4/2002 1/18/2006 82
Walworth(1) 9/20/2002 12/13/2002 6
Manitowoc 3/5/2003 3/5/2003 1
Sauk(1) 10/3/2003 10/3/2003 1
Racine 5/1/2004 5/1/2004 1
Walworth(2) 7/28/2004 11/3/2004 3
Crawford 1/19/2005 1/25/2007 2
Portage(2) 9/22/2008 11/18/2008 2
Jefferson 12/1/2008 12/1/2008 1
Marathon 11/7/2013 11/9/2020 113
Richland(1) 9/13/2014 11/19/2014 8
Eau Claire 6/8/2015 11/24/2015 34
Oneida 11/4/2015 12/8/2020 23
Iowa(1) 1/22/2016 11/19/2020 5
Oconto 9/4/2016 1/15/2021 215
Shawano 9/18/2017 1/10/2021 63
Waupaca 9/21/2017 12/7/2017 12
Washington 2/18/2018 11/15/2018 12
Richland(2) 5/11/2018 5/11/2018 1
Dane 5/16/2018 5/16/2018 1
Iowa(2) 5/18/2018 5/18/2018 21
Marinette 5/19/2018 12/4/2020 2
Sauk(2) 6/4/2018 11/28/2018 2
Portage(3) 10/23/2018 10/23/2018 1
Portage(4) 11/16/2018 5/1/2019 8
Forest 1/8/2019 12/7/2020 8
Burnett(1) 7/30/2019 7/30/2019 1
Trempealeau 11/7/2019 11/4/2020 3
Burnett(2) 9/3/2020 9/3/2020 1
Registered Deer Farms and Past/Current CWD Farms
^_ Hunting Ranches Infected with CWD Currently in Operation
^_ Deer Farm Infected with CWD Currently in Operation
!( Past Positive CWD Farms, Depopulated
!( Currently Registered Farm-Raised Deer Farms
CWD Affected Counties March 2021
Wisconsin Buckhorn Flats CWD
The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82.
The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.
see;
Title, Baiting and Feeding
Baiting and feeding deer brings a greater number of deer into close contact with each other. This increases the chances of Chronic Wasting Disease (CWD) being transmitted from deer to deer. One of the ways this can be done is nose to nose contact. Deer droppings and urine are also concentrated at bait sites or feeding station. That also increases the chances for a healthy deer to pick up the prions that cause CWD.
Outdoor News, Feb. 23, 2018 Pg. 9
The state's worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for CWD from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70 acer pen in January 2006, 60 of the remaining deer 76 deer carried CWD, a nearly 80 percent infection rate.
This proves that concentrating deer increases the spread of CWD.
Solution, ban baiting and feeding
BE IT RESOLVED, that the Conservation Congress, DNR and Legislative Bodies work together to write a law that puts a moratorium on baiting and feeding until a cure is found for wild deer in Wisconsin.
Harold Halverson
Private Citizen W12431 820th Ave. River Falls, Wi. 54022 PH 715-781-6804
THURSDAY, JANUARY 20, 2022
Wisconsin this month fortified its standing as the capital of the world for Chronic Wasting Disease CWD TSE PrP
FRIDAY, FEBRUARY 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
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FRIDAY, FEBRUARY 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
Greetings Wisconsin hunters et al,
With CWD spreading, and CJD rising in the USA and Canada, with rise in pcsCJD i.e. pending classification sporadic CJD i.e. they don’t know what or where in the world this strain came from, and refuse to investigate further, ignoring updated science that not only has CWD mutated into a second strain i.e. Wisconsin Strain of CWD, and the fact that many scientist around the globe are very concerned for the potential of CWD being a zoonosis disease. Also ignoring recent updated science that shows a link between atypical BSE and atypical Scrapie with sporadic CJD. All this moved me to dig a bit deeper into these game farms that raise deer and or elk to enhance their natural size and antler spread and circumference i.e. farmed ‘straw’ bred bucks. in my opinion, there is no ethics in hunter farmed 'straw' bred bucks. I wanted to find out just how dangerous these game farms are to the wild, considering for the captives, most are nothing more than a petri dish for disease i.e. CWD.
What I found was interested, and concerning. the close proximity from cwd infected game farm to cwd infected game farm, and the CWD infection in the wild surrounding those said game farms.
I wrote the Wisconsin DNR and division of animal health asking ;
‘‘Could you please tell me where I can locate the information on each CWD infected game farm in Wisconsin (all nine to date), dates they became infected, infection rate, etc. ???’’
They were very kind in replying and supplied the following information ;
Farm CWD first Detected Incidence
Hall 09-04-2002 82 1 hunted in 2002, 6 hunted in 2003, 10 hunted in 2004, 4 in breeding herd 2005, 61 in breeding herd 2006 (60 of 76 at depop)
Hirschboeck 09-20-2002 6 2 in 2002 & 4 of 122 at depopulation
Sperber 03-05-2003 1 197 remaining depoped
Hetzel 10-03-2003 1 2 remaining depoped
Breber 05-01-2004 1 15 remaining depoped
Kuhnke 07-28-2004 3 1 in July, 1 in Aug, 1 of 23 at depop
Christensen 01-07-2005 2 1 in 2007, owner killed and buried remaining 33
Landwer 09-22-2008 2 1 of 66 at depop
Hookstead 10-01-2008 1 2 remaining depoped
---------
99 total positives
Dr Bourie
CWD Program Manager
Div of Animal Health
======================
From: Ryan, Tamara M - DNR
Sent: Wednesday, February 01, 2012 4:11 PM
To: Terry S. Singeltary Sr. ; Bourie, Richard D - DATCP Cc: Thiede, Kurt A - DNR ; Ross, Laurie J - DNR ; Hauge, Tom M - DNR Subject: RE: Singeltary request re cwd game farms Wisconsin
Hello Terry –
Thanks for checking in. Please know that attempts have been made to respond to your request. Dr. Bourie of DATCP responded on Monday which was the same date your email was forwarded to him. However, I received an email from him advising that his email communications to your email address were bouncing back & he requested additional contact information. I looked into this and determined we only had your email address. I’m certain that he will be getting in contact with you once he sees this email chain. In the interim, please respond to all with your phone number & address just in case.
Thank you.
P Tami Ryan
Wildlife Health Section Chief Bureau of Wildlife Management Wisconsin Department of Natural Resources Phone: 608-266-3143 Fax: 608-267-7857 Email: tamara.ryan@wi.gov
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, February 01, 2012 3:52 PM
To: Ryan, Tamara M - DNR; Bourie, Richard D - DATCP Cc: Thiede, Kurt A - DNR; Ross, Laurie J - DNR; Hauge, Tom M - DNR
Subject: Re: Singeltary request re cwd game farms Wisconsin
Greetings again WDNR et al,
I have still yet to get any answer about my questions below.
‘‘Could you please tell me where I can locate the information on each CWD infected game farm in Wisconsin (all nine to date), dates they became infected, infection rate, etc. ???’’
this is important information, and the public should be able to acquire this information, you would think ?
thank you,
kind regards,
terry
From: Ryan, Tamara M - DNR
Sent: Monday, January 30, 2012 8:10 AM
To: Bourie, Richard D - DATCP
Cc: Thiede, Kurt A - DNR ; Ross, Laurie J - DNR ; Hauge, Tom M - DNR ; flounder9@verizon.net
Subject: FW: Singeltary request re cwd game farms Wisconsin
Mr. Singeltary – This information can be obtained from the Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP). I’ve copied Dr. Bourie from DATCP who is the best person to respond to your request.
Dr. Bourie – Please respond to Mr. Singeltary on the email request below. Thank you.
Tami
P Tami Ryan Wildlife Health Section Chief Bureau of Wildlife Management Wisconsin Department of Natural Resources Phone: 608-266-3143 Fax: 608-267-7857 Email: tamara.ryan@wi.gov
--------------------------------------------------------------------------------
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, January 25, 2012 02:15 PM
To: Ross, Laurie J - DNR Subject: cwd game farms Wisconsin
Greetings WDNR et al,
Could you please tell me where I can locate the information on each CWD infected game farm in Wisconsin (all nine to date), dates they became infected, infection rate, etc. ???
many thanks,
kind regards,
terry
===============end...TSS===============
strange this comes out after two weeks of me asking questions ???
Bourie and Deer Farmers Weather the CWD Storm
By lsiekmann | Published: February 2, 2012
http://wfbf.com/ag-newswire/bourie-and-deer-farmers-weather-the-cwd-storm/
HOW could one call 9 infected CWD game farms, weathering the storm ???
MOST disturbing about the 9 CWD infected game farms in Wisconsin in report above, was the ‘Christensen’ farm, where the ‘owner killed and buried remaining 33’ deer. what’s disturbing to me is not the fact that 33 potentially CWD infected deer were buried, apparently before any CWD testing was done on those remaining 33 suspect CWD exposed deer. that could be one heck of a hot spot for years, decades to come. seems the officials could have dug those deer up, incinerated the remains, then dug up the soil around that pit where all those dead, suspect deer were buried at, and then treat all that soil some how. seems the ‘Christensen’ farm was trying to hide something. ...just my take...tss
A review of those 9 CWD infected game farms in Wisconsin ;
Hirschboeck 09-20-2002 6 2 in 2002 & 4 of 122 at depopulation
Wisconsin : DNR Hunting Deer That Escaped From Farm Now Under Quarantine
Date: October 24, 2002 Source: Milwaukee Journal Sentinel
Contacts: Lee Bergquist lbergquist@journalsentinel.com
State officials said Wednesday they recently learned that several deer escaped in March from a northern Walworth County deer farm that is known to have harbored at least one deer with chronic wasting disease.
The DNR has dispatched wardens to a game farm owned by James Hirschboeck of the Town of Troy in the hope of finding and killing the deer, which are believed to be roaming in the wild.
Hirschboeck is also under investigation, accused of trying to sell deer that had been quarantined and could not be moved, an affidavit filed for a search warrant in Dane County says.
The affidavit also says Hirschboeck is suspected in the past four weeks of trying to entice another deer farm operator with whom he had done business to falsify records.
In an interview, Hirschboeck denied any wrongdoing. "None of that is true," he said.
Warden Karl Brooks said the escapes of "several" deer took place in March - shortly after the fatal deer disease was first reported in the wild deer population near Mount Horeb in Dane County.
This is the first admission by state officials that deer have escaped from a game farm tainted by the disease.
The escaped deer are believed to have tags in their ears. Neighbors have reported seeing deer with ear tags near Hirschboeck's 80-acre farm, Brooks said.
In addition to efforts to kill the tagged deer, Brooks said, an estimated 500 deer that will be killed and tested this hunting season in Walworth County will help determine whether the fatal brain disease has moved to a new part of the state.
Officials Monitor Farm
Hirschboeck's farm came under scrutiny by the DNR after it was discovered that he bought deer from another Walworth County deer farm that is suspected to have sold a deer to a third farm in Portage County that later tested positive for the disease. That buck, sold to deer farmer Stan Hall, tested positive for the disease in September.
The buck was the first of two captive deer in Wisconsin to have tested positive. So far, 40 wild deer from a 411-square-mile region of Dane, Iowa and Sauk counties have been found with the disease.
The first finding in captive deer last month prompted the state agriculture department to quarantine the two farms in Walworth County and a third farm in Portage County. A fourth game farm in Dane County has been quarantined, as well.
On Oct. 16, it was learned that a deer on the Hirschboeck farm also tested positive after state investigators found deer there appearing to be in poor health.
As the DNR began investigating Hirschboeck's business dealings, they recently learned that some of his deer had escaped. Brooks said the DNR believes the deer that tested positive on his farm was there long enough to have intermingled with the escaped deer.
"This is extremely significant because it confirms our fears that CWD might not be as easily contained as we initially had hoped," Brooks said.
Source Uncertain
Wisconsin officials are not sure how the disease showed up in Wisconsin, but one theory points to the possibility of an infected game farm. Game farms routinely moved deer in and out of the state until the agriculture department effectively banned such shipments in March.
When the presence of chronic wasting disease was reported Feb. 28, it was the first time deer with chronic wasting disease - captive or wild - had been found east of the Mississippi River.
The finding has thrust deer hunting in Wisconsin into tumult as hunters wonder how widely the disease has spread and whether venison is safe to eat. One effect: License sales are down about 23% from the same time last year.
The DNR has said it believed the disease is contained in and around the 411-square-mile region, where it wants to kill as many as 25,000 deer this hunting season.
Experts also have indicated that venison should be safe to eat, and as recently as last week, Dennis Maki, an infectious disease expert at the University of Wisconsin-Madison, said finding the abnormal protein that is believed to cause the disease in meat was remote.
The World Health Organization advises people not to eat any part of a deer suspected of having the disease or the brain, eyes, spleen, tonsils, lymph nodes or spinal cord of any deer.
As part of its investigation, the DNR said that Hirschboeck:
* Asked Hall to alter his deer farm records twice in the past four weeks. * Tried to convince another game farm operator, Michael E. Bischel of Helenville in Jefferson County, to subvert the quarantine. Bischel told the DNR that Hirschboeck suggested that he buy a large buck from Hirschboeck, kill it, bind its front and back hooves, and then saw off its antlers so wardens would not recognize it.
Hirschboeck denied both allegations and said he has cooperated fully with the DNR and the agriculture department.
* Sold six does to Bischel in January but did not provide any receipts. Hirschboeck said he sold deer to Bischel but was never paid. Bischel could not be reached for comment. * Was not registered to operate a game farm in 2001 and faces forfeitures totaling $1,033. * Was issued five citations totaling $1,002.50 for feeding wild game and failing to cleaning up the feed after being ordered to do so.
=====================
436 deer have escaped from farms to wild; State finds violations, lax record keeping at many sites, report says
March 19, 2003 Milwaukee Journal-Sentinel (Wisconsin) by Lee Bergquist lbergquist@journalsentinel.com
A state inspection of private deer farms, prompted by the discovery of chronic wasting disease, found that 436 white-tailed deer escaped into the wild, officials said Tuesday. The Department of Natural Resources found that captive deer have escaped from one-third of the state's 550 deer farms over the lifetime of the operations. The agency also uncovered hundreds of violations and has sought a total of 60 citations or charges against deer farm operators.
These and other findings come as state officials say they are still no closer to understanding how the fatal deer disease got to Wisconsin.
Since the discovery a little more than a year ago, chronic wasting disease has thrown both deer hunting and management of Wisconsin's 1.4 million deer herd into tumult. Fewer hunters went into the woods last year, and a booming deer population has the DNR worried that the number of whitetails could grow out of control.
Tuesday's findings were presented to the state Department of Agriculture, Trade and Consumer Protection. The DNR had regulated deer farms, but the authority was transferred to the Agriculture Department on Jan. 1. Now agriculture regulators oversee elk, deer and other captive cervids.
Stricter regulations -- and closer attention to the operations of game farms -- should cut down on future violations, officials from the two agencies said. Tougher reporting requirements also will help authorities keep better track of the movement of animals, they said.
Permanent rules take effect in June, and include tighter controls on moving animals and requiring the reporting of escaped animals within 48 hours. There will be mandatory testing of every deer age 16 months or older that dies.
Almost from the start of the state's battle against chronic wasting disease, game farm operators came under scrutiny because their business involves the buying and selling of captive deer and elk across state lines. When the disease was first discovered here Feb. 28, 2002, Wisconsin became the first state to have the disease east of the Mississippi River.
A representative of the deer industry said Tuesday that the DNR is trying to shift blame for chronic wasting disease to his industry.
"The state of Wisconsin has spent a year chasing chronic wasting disease, and they have made zero progress," said Gary Nelson, president of Whitetails of Wisconsin. "In the past, they have essentially collected our fees and ignored us. Now that they have discovered CWD, they are looking for someone to blame."
A DNR representative agreed that the agency could have done a better job keeping tabs on deer farms.
"We're not pointing fingers," said Karl Brooks, a conservation warden with the DNR. "But two things that we know for sure is that there is CWD in the wild deer population, and we have found CWD on game farms."
CWD found on 2 farms
Seven deer have tested positive for the disease on game farms -- one on a Portage County farm and six on a Walworth County farm -- since the disease was discovered in three wild deer killed near Mount Horeb in western Dane County. One deer that tested positive on the Walworth County farm escaped and roamed free for six months.
Regulations have only begun to catch up to the captive deer industry, and "unfortunately, it took CWD to get us there," said agriculture secretary Rod Nilsestuen at a news briefing in Madison.
As the DNR prepared to hand over authority for overseeing game farms to the agriculture department, it sent 209 conservation wardens to 550 farms to collect information, attempt to pinpoint the source of the disease and to learn whether other deer had been exposed to it.
The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling.
At least 227 farms conducted part of their business on a cash basis, making it hard to track animal movement with financial records.
For example, both the Internal Revenue Service and the state Department of Revenue have been contacted about a deer farm near Wild Rose in Waushara County that is suspected of selling six large bucks for $45,000 in cash and not using live deer shipping tags as required.
The DNR found that game farm operators have more deer in captivity than their records show, which is "due in part because the owners of a number of large deer farm operations were unable to accurately count the number of deer within their fences," the audit found.
Hundreds of deer escape
The DNR found a total of 671 deer that escaped farms -- 436 of which were never found -- because of storm-damaged fences, gates being left open or the animals jumping over or through fences.
In one example in Kewaunee County, a deer farmer's fence was knocked down in a summer storm. Ten deer escaped, and the farmer told the DNR he had no intention of trying to reclaim them. The DNR found five of the deer, killed them and cited the farmer for violation of a regulation related to fencing.
Another deer farmer near Mishicot, in Manitowoc County, released all nine of his whitetails last summer after he believed the discovery of chronic wasting disease was going to drive down the market for captive deer.
The DNR found 24 instances of unlicensed deer farms and issued 19 citations.
===============end...tss===============
Sperber 03-05-2003 1 197 remaining depoped
Wisconsin : Diseased Elk Found in Manitowoc County
Date: March 25, 2003 Source: Milwaukee Journal Sentinel
Contacts: Dennis Chaptman dchaptman@journalsentinel.com
Game-farm animal is first ill non-deer discovered here
Madison - Chronic wasting disease has been found in a farm-raised elk in Manitowoc County, marking the first time in Wisconsin that the ailment has been found in an animal other than a deer, state officials said Tuesday.
A 6-year-old female elk, one of 20 imported by Valders elk farmer Eugene Sperber from Stearns County, Minn., tested positive for the the fatal brain disease after dying in a fight with another elk.
Sperber's herd was quarantined by state agriculture officials in September, when state animal health officials discovered that it may have been exposed to the disease, which has been found in the state's white-tailed deer population.
The Minnesota Board of Animal Health reported in August that an elk from an Aitkin County farm in northern Minnesota tested positive for the disease. That animal had also spent time on two other farms, including the one in Stearns County.
That prompted Wisconsin officials to track other animals from those farms that may have entered Wisconsin game farms. They found 32 animals on six farms, and all were quarantined, including those on Sperber's farm.
Sperber, who could not be reached for comment Tuesday, imported the 20 elk in December 2000 and January 2001.
One of the imported elk died earlier and was not tested for the disease, and all of the remaining 18 imported elk were killed for testing Friday, before the National Veterinary Services Laboratory in Ames, Iowa, reported Monday that one elk tested positive for the disease.
Test results on the other animals are pending, said Donna Gilson, a spokeswoman for the state agriculture department.
The fate of Stearns' other 180 elk, which did not come from Minnesota but are under quarantine, has not been decided.
"We're concerned for the deer and elk industry, and for this particular farmer," Gilson said. "It's a really tough situation to be in after a year that's been difficult for deer and elk farmers in general. It's been hard for them economically and emotionally."
First in the region
Tuesday's news marked the first time that chronic wasting disease has been discovered in the northeastern part of the state. A total of 80 diseased deer have been found in Dane, Iowa, Sauk and Richland counties; and seven infected deer were discovered on game farms in Walworth and Portage counties.
Sarah Shapiro Hurley, a Department of Natural Resources veterinarian, said wildlife officials are monitoring the situation in Manitowoc County closely, but don't believe it poses a threat to the deer population there.
"Free-ranging and captive animals do have areas of interface, but we don't have any reason to believe that we have anything going on in the wild herd that is connected with that situation in the captive herd," she said.
DNR and state agriculture officials will continue to evaluate the case and monitor information from Manitowoc County, Hurley added. There were no immediate plans to shoot and test any more wild deer in response to the latest finding, she said.
"We took a very adequate sample in Manitowoc County this fall," she said, referring to the more than 200 samples - none of them showing infection - taken during the annual hunt.
Game farms under scrutiny
Wisconsin imposed emergency restrictions on moving animals to and from game farms in April 2002 to curb the spread of the disease. Chronic wasting disease attacks the brains of the animals, causing them to become emaciated, act abnormally and eventually die.
Dan Gunderson, spokesman for the Wisconsin Commercial Elk and Deer Farmers Association, said the discovery is a difficult one for the Sperbers.
"This is not only a financial loss, but it's almost like losing part of your family, and the loss is taken personally," said Gunderson, in a telephone interview after he visited the farm.
Gunderson said the discovery also shows that farmers, working in tandem with state agriculture officials, have established an effective monitoring plan.
"It's a bad-news, good-news story," he said. "All of their elk, even though they didn't all come from Minnesota, are quarantined until 2006. It's a business tragedy, but the good news is the system under which the department of agriculture is regulating it works."
Gilson said agency officials were not surprised that the disease turned up in a farm-raised elk here, especially considering the animal's history in Minnesota.
"It's been primarily a disease of elk out west and, in the wild, in mule deer, but on farms it's been an elk disease there," she said. "We weren't as surprised as we were disappointed."
Gunderson said the finding means that farmers need to be watchful and keep working with state officials.
Gilson added that animal health investigators now will attempt to trace the movements of elk from the Valders farm to other locations, she added.
"The DNR found chronic wasting disease because it went looking for it," she said.
==============================end...tss==========================
Hetzel 10-03-2003 1 2 remaining depoped
Wisconsin : Whitetail On Sauk County Farm Tests Positive For CWD
Date: October 21, 2003 Source: Wisconsin Department of Agriculture, Trade and Consumer Protection
Contacts: Donna Gilson 608-224-5130
MADISON -- A whitetail deer from a Sauk County farm has tested positive for chronic wasting disease, State Veterinarian Dr. Robert Ehlenfeldt said today.
The 2-year-old buck, owned by William Hetzel, Hillpoint in Bear Creek Township, died of digestive problems Oct. 1 and was tested routinely as the law requires. The National Veterinary Services Laboratory in Ames, Iowa, reported Monday, Oct. 20, that the test was positive.
The buck was one of only four deer on the farm. The others are a doe and her two fawns. The farm has been quarantined, which prohibits any live animals from being moved off the property. The herd is enrolled in the CWD monitoring program.
Agriculture officials are checking herd records to find out where the infected animal originated.
The Wisconsin Department of Agriculture, Trade and Consumer Protection's policy is to kill and test herds where CWD is found, as well as herds where infected animals originated. There is no approved CWD test for live animals.
This is the 10th farm-raised animal in Wisconsin to test positive for CWD and the fourth farm where the disease has been found. One of the infected animals was an elk; the rest have been whitetail deer. Currently 13 herds are under quarantine: four connected with on-farm CWD cases in Portage and Walworth counties; two that received animals from a herd in Minnesota later found to be infected; and seven that are within the Department of Natural Resources CWD eradication zone.
=====================end...tss=======================
Breber 05-01-2004 1 15 remaining depoped
Wisconsin : CWD-Positive Deer Found on Racine County Farm
Date: May 25, 2004 Source: Wisconsin Department of Agriculture, Trade, and Consumer Protection
Contacts: Donna Gilson 608-224-5130
MADISON -- A whitetail deer that died on a Racine County farm has tested positive for chronic wasting disease, State Veterinarian Dr. Robert Ehlenfeldt announced today.
The National Veterinary Services Laboratory in Ames, Iowa, reported the test results Friday, May 21. According to the farm's records on file with the Wisconsin Department of Agriculture, Trade and Consumer Protection, the doe was 9 years old. She had died of natural causes and a sample for CWD testing was collected May 1. Department rules require that all farm-raised deer and elk 16 months or older must be tested when they die, go to slaughter or are killed.
The deer was owned by Colin Breber, of Raymond, and was one of a small herd of about 10 whitetails. The herd is enrolled in the state's CWD monitoring program.
Breber's farm was quarantined Saturday, May 22, because the remaining animals have been exposed to CWD. The quarantine stops movement of live deer off the farm. Department staff are tracing movements of deer onto and from the farm, to find the source of the CWD-positive deer as well as other herds that may have been exposed.
Department policy calls for destroying herds in which CWD has been found, as well as source herds where CWD positive animals originated.
In all, 15 herds in Wisconsin are under quarantines related to CWD. Only two of those herds actually have had animals test positive. The rest are herds that may have been exposed to CWD, either because of contact with infected animals or because they are within the Department of Natural Resources disease eradication zone.
To date, 16 farm-raised animals in Wisconsin have tested positive for CWD on five farms. One of the infected animals was an elk; the rest have been whitetail deer.
==============end...tss========================
Kuhnke 07-28-2004 3 1 in July, 1 in Aug, 1 of 23 at depop
Wisconsin : CWD-Infected Herd Destroyed On Walworth County Farm
Date: November 04, 2004 Source: Wisconsin Department of Agriculture, Trade and Consumer Protection
Contacts: Contact: Donna Gilson 608-224-5130
MADISON -- A Walworth County herd of farm-raised deer and elk was destroyed Wednesday, Nov. 3, because it was infected with chronic wasting disease.
The herd of 12 white-tailed deer and 9 elk owned by Wayne Kuhnke, Delavan, was killed by gunshot by wildlife specialists from the U.S. Department of Agriculture Wildlife Services. They worked under contract with the Department of Agriculture, Trade and Consumer Protection, which regulates farm-raised deer in Wisconsin.
The Kuhnke herd had been under quarantine since September 2002 because Wisconsin animal health officials linked it to animals in two CWD-infected herds. Recently two animals from the Kuhnke herd also tested positive for CWD.
Brain stem samples were removed from each animal and shipped to the National Veterinary Services Laboratory in Ames, Iowa, for testing. Test results are expected within three weeks. Carcasses were sent to the Wisconsin Veterinary Diagnostic Laboratory for chemical digestion.
Kuhnke will be required to burn or bury all feed, bedding, manure and wooden feed troughs used by the deer. He also must clean all organic material from metal, concrete or plastic items that came in contact with the animals. DATCP staff will then disinfect those articles with a strong chlorine bleach solution. In areas of heavy animal traffic, the owner will need to scrape off and bury 2 inches of topsoil and replace it.
Kuhnke may not re-introduce farm-raised deer or elk to the property for five years. He may use the property for other species.
Kuhnke will receive federal and state indemnity payments for the animals. The indemnity amounts have not been determined yet. The U.S. Department of Agriculture will pay disposal costs.
To date, 19 CWD-positive animals have been found on six Wisconsin farms. All have been white-tailed deer except for one elk imported from a Minnesota herd later found to be infected. More than 8,000 farm-raised deer and elk have been tested in Wisconsin, and about 540 herds are enrolled in the CWD monitoring program.
Currently 17 herds are under quarantine because there has been at least one CWD-positive animal found in them, because they are linked to infected herds, or because they are inside the Department of Natural Resources CWD eradication zones.
===================end...tss=================
Christensen 01-07-2005 2 1 in 2007, owner killed and buried remaining 33
Wisconsin : CWD-Positive Whitetail Found On Crawford County Farm
Date: January 26, 2005 Source: Wisconsin Department of Agriculture, Trade and Consumer Protection
Contacts: Donna Gilson 608-224-5130
MADISON -- A white-tailed deer that died on a Crawford County farm has tested positive for chronic wasting disease, State Veterinarian Dr. Robert Ehlenfeldt announced today.
The National Veterinary Services Laboratory in Ames, Iowa, reported the test results Friday, Jan. 21. The 19-month-old buck died from respiratory causes, according to the laboratory report, and was sampled for CWD testing Jan. 12. Wisconsin Department of Agriculture, Trade and Consumer Protection rules require that all farm-raised deer and elk 16 months or older must be tested when they die, go to slaughter or are killed.
The deer was owned by Curtis Christenson, Eastman, and was one of a herd of about 40 animals. The herd is enrolled in the state’s CWD monitoring program.
Christenson’s herd was quarantined Jan. 21, because the remaining animals have been exposed to CWD. The quarantine stops movement of live deer off the farm. Department staff are tracing movements of deer onto and from the farm, to find out if other herds may have been exposed.
In an unrelated case, Ehlenfeldt announced he has quarantined a deer herd owned by Don Schnell, Rosholt. The Portage County deer herd was quarantined because a deer sold from it to an Almond hunting preserve tested positive after being shot on the preserve. No other animals on Schnell's farm have tested positive.
In all, 20 herds in Wisconsin are under quarantines related to CWD. Ten of those herds are related to on-farm CWD cases. The rest are herds that may have been exposed to CWD, because they are within the Department of Natural Resources disease eradication zone.
To date, 28 farm-raised animals in Wisconsin have tested positive for CWD on seven farms, out of more than 10,000 tested. One of the infected animals was an elk; the rest have been white-tailed deer.
================end...tss===================
Landwer 09-22-2008 2 1 of 66 at depop
PUBLIC HEARINGS
Robert Landwer, Owner, and Kathy Landwer, Agent (R10-06) – Request to Amend the Portage County Zoning Ordinance by Changing the Zoning Classification of an Area Approximately 8.59 Acres From A4, General Agricultural Zoning District to C4, Highway Commercial Zoning District – Part of Parcel #016-25-0718-06.01 – Town of Eau Pleine.
Piesik read the public hearing notice. Lucht provided a report stating the requested change is to locate a wood chipping and asphalt grinding facility. The Land Conservation Division (LCD) and Wisconsin Department of Natural Resources (DNR) will be working with the site on stormwater issues.
The site is on the location of a former deer farm. Approximately one year ago, the deer tested positive for chronic wasting disease (CWD) and had to be destroyed. Department of Agriculture, Trade, and Consumer Protection (DATCP) ordered the fence surrounding the property to remain for five years in order to keep wild deer, elk, and other animals out of the area to prevent the spreading of CWD. The site will be accessed by a new driveway built through the wooded portion of the site; a gate will be opened and closed as the site is accessed. Petitioner states there will be approximately 8-10 trucks per day traveling on and off the site during the peak season. Portage County Planning and Zoning Department staff recommends approval of the request.
http://www.co.portage.wi.us:8080/APPS/committees/committees.nsf/a31acf8e580f5f9186257475006d61cf/335c85b6575f2d458625774b005430eb?OpenDocument
====================end...tss==========================
Hookstead 10-01-2008 1 2 remaining depoped
Buck at Jefferson County preserve had chronic wasting disease e-mail print By Lee Bergquist of the Journal Sentinel Dec. 19, 2008 |(0) Comments
A 7-year-old buck from a Jefferson County hunting preserve has tested positive for chronic wasting disease, state agriculture officials reported Friday.
The white-tailed deer was killed Dec. 1 as part of an effort by the owner of the 53-acre preserve to cull his herd and repopulate it with new stock, said Donna Gilson, a spokeswoman for the Department of Agriculture, Trade and Consumer Protection.
Two deer remain on the preserve and will be killed. They have been quarantined by State Veterinarian Robert Ehlenfeldt.
Gilson said the agriculture department will trace any possible movement of deer from the preserve to other captive facilities.
The hunting preserve, Maple Hill Whitetails, is owned by Steve Hookstead of Helenville. According to the preserve's Web site, the business offers hunts, and breeding and genetics services. Hookstead was unavailable for comment.
Hookstead's breeding herd will not be killed because the deer are separated from the hunting preserve by a fence, Gilson said.
Chronic wasting disease was discovered in wild deer in Wisconsin in 2002. Since then, 98 deer and one elk have tested positive from nine captive facilities. More than 22,500 farm-raised deer and elk have been tested.
Chronic wasting disease is always fatal and affects deer, elk and moose.
The disease is a transmissible spongiform encephalopathy, a class of diseases that includes mad cow disease in cattle, scrapie in sheep and Creutzfeldt-Jakob disease in humans.
According to the World Health Organization, any tissue that may have come from deer with CWD should not be eaten, but there is no evidence the disease can be transmitted to humans.
http://www.jsonline.com/news/wisconsin/36473349.html
=================end...tss===============
NOW, if you look at the map that shows these game farms in relations to surround CWD infection rate in the wild, you will see the close proximity from one to the other i.e. CWD infected game farms, to CWD infection in the wild.
please see map here, and you will see that this phenominum is NOT only unique to Wisconsin, but with most all other game farms in other states. see map here ;
http://www.nwhc.usgs.gov/disease_information/chronic_wasting_disease/index.jsp
MORE INFORMATION ON FARMED DEER IN WISCONSIN ;
Information for Farm-Raised Deer Keepers in Wisconsin
Wisconsin Administrative Rules for Farm-Raised Deer Keepers (see sections 10.45 to 10.58)
http://docs.legis.wisconsin.gov/code/admin_code/atcp/10.pdf
General Requirements
General Requirements Summary Brochure (2 page PDF)
New Farm-Raised Deer Keeper Application (4 page PDF)
CWD Sampling Reimbursement (1 page Word doc)
General Fencing Requirements
Herds With White-tailed Deer (see section 90.21)
Herds With No White-tailed Deer (see section 90.20)
Premises Within 5 Miles of Multiple CWD Positive
http://docs.legis.wisconsin.gov/code/admin_code/atcp/10.pdf
CWD Herd Status Program
CWD Herd Status Program Summary Brochure (2 page PDF)
CWD Herd Status Program Application Packet (5 page PDF)
Census Documents (for CWD Herd Status Program)
Census Instructions (1 page Word doc)
Inventory Census Form (3 page PDF)
Purchased Additions (1 page PDF)
Live Subtractions (1 page PDF)
Deaths (1 page PDF)
Newborn Summary (1 page PDF)
Request for Electronic Census Form (1 page Word doc)
Hunting Preserves
Hunting Preserves in Wisconsin Summary Brochure (2 page PDF)
Hunting Preserve Certificate Application (2 page PDF)
Moving Requirements
In-State Movement Requirements (1 page Word doc)
In-State Shipping Permit (2 page Word doc)
Importing Into Wisconsin
Exporting to Other States
Useful Information
To Purchase a CD List of Registered Farm-Raised Deer Keepers
Wisconsin Department of Natural Resources - Wild deer testing positive for CWD
United States Geological Survey - Chronic Wasting Disease in North America
Laboratories that are certified by the United States Department of Agriculture
Deer Keeper Organizations
Whitetails of Wisconsin
Wisconsin Commercial Deer and Elk Farmer’s Association
Reindeer Owners and Breeders Association
North American Elk Breeder Association
For more information or to sign up for updates contact:
Dr. Richard Bourie, Program Manager
(608) 224-4886
Richard.Bourie@wisconsin.gov
Karen Torvell, Program Associate
(608) 224-4896
Karen.Torvell@wisconsin.gov
http://datcp.wi.gov/Farms/Deer_Farming/index.aspx
Additionally, the last day for APHIS funding for CWD testing of farmed cervids would be December 31, 2011. After that day, APHIS-approved laboratories and the National Veterinary Services Laboratories (NVSL) would be using established user fees, and producers would be charged directly for routine CWD testing...
see full text letter here ;
http://www.wcdefa.org/ECM_USDA_CWD_letter_101411.pdf
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
Greetings Wisconsin Hunters outdoorsman/woman et al ,
I will quote something from another deer hunting forum in another state, that was well said ;
“Ironic that one can operate a game farm to pose such a threat to wildlife and not only avoid responsibility for mitigating the danger (maintaining fences) but also get the state to buy your failed business.”
kind regards,
terry
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm
Delwyn P. Keane1⇓ Daniel J. Barr1 Philip N. Bochsler1 S. Mark Hall2 Thomas Gidlewski3 Katherine I. O'Rourke4 Terry R. Spraker5 Michael D. Samuel6 1University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory, Madison, WI 2The U.S. Department of Agriculture, Animal Plant Health Inspection Service, National Veterinary Services Laboratories, Pathobiology Laboratory, Ames, IA 3The U.S. Department of Agriculture, Animal Plant Health Inspection Service, Veterinary Services, Fort Collins, CO 4The U.S. Department of Agriculture, Agricultural Research Service, Animal Disease Research Unit, Pullman, WA 5The Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 6The U.S. Geological Survey, Wisconsin Cooperative Wildlife Research Unit, University of Wisconsin, Madison, WI. ↵University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory, 445 Easterday Lane, Madison, WI 53706. Delwyn.Keane@wvdl.wisc.edu Next Section
Abstract In September 2002, chronic wasting disease (CWD), a prion disorder of captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus virginianus) from a captive farm in Wisconsin. The facility was subsequently quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty animals (79%) were found to be positive by immunohistochemical staining for the abnormal prion protein (PrPCWD)in at least one tissue; the prevalence of positive staining was high even in young deer. Although none of the deer displayed clinical signs suggestive of CWD at depopulation, 49 deer had considerable accumulation of the abnormal prion in the medulla at the level of the obex. Extraneural accumulation of the abnormal protein was observed in 59 deer, with accumulation in the retropharyngeal lymph node in 58of 59 (98%), in the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of 58 (83%). The retina was positive in 4 deer, all with marked accumulation of prion in the obex. One deer was considered positive for PrPCWD in the brain but not in the extraneural tissue, a novel observation in white-tailed deer. The infection rate in captive deer was 20-fold higher than in wild deer. Although weakly related to infection rates in extraneural tissues, prion genotype was strongly linked to progression of prion accumulation in the obex. Antemortem testing by biopsy of rectoanal mucosal-associated lymphoid tissue (or other peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for surveillance in captive herds at risk for CWD infection.
http://vdi.sagepub.com/content/20/5/698.long
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf
SNIP...SEE FULL TEXT ;
FRIDAY, FEBRUARY 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
*** 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, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Saturday, December 31, 2011
Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation
MONDAY, OCTOBER 11, 2021
Minnesota DNR temporarily bans farmed deer movement into and within state to protect state’s wild white-tailed deer
MINNESOTA CWD TSE PRION
Minnesota DNR learns of 2 Minnesota deer farms that received deer from a CWD-positive farm in Wisconsin
Minnesota
DNR Statement
For Immediate Release:
Sept. 28, 2021
For more information:
Contact DNR Information Center
by email or call 888-646-6367.
DNR learns of 2 Minnesota deer farms that received deer from a CWD-positive farm in Wisconsin
On Monday, Sept. 27, 2021, the Minnesota Department of Natural Resources learned that deer farms in Minnesota were among those that received deer from a Wisconsin farm where chronic wasting disease (CWD) was discovered in August 2021.
According to a report in the Milwaukee Journal Sentinel, the farm where CWD was detected sold nearly 400 deer to 40 farms in seven states during the past five years.
The DNR contacted the Minnesota Board of Animal Health (BAH) the same day (Sept. 27) to verify the authenticity of the report. The BAH confirmed that two Minnesota deer farms had received a total of five deer from the Wisconsin farm between 2016 and 2017. It is unknown if the deer were infected when they were transferred to Minnesota.
“The news that Minnesota deer farms imported deer from a Wisconsin farm infected with CWD is extremely concerning,” said DNR Commissioner Sarah Strommen. “The DNR is actively considering management responses to this latest threat to Minnesota’s wild deer.”
A Stillwater, Minn. farm (now out of business) initially received two deer in 2016. The deer were transferred to a farm (now out of business) in Grand Meadow, Minn. in early 2019. The two deer were then transferred to a Wisconsin farm in late 2019. The DNR is working to determine whether those animals are still alive, or have died and were tested.
A Clear Lake, Minn. farm received three deer from the Wisconsin farm in the fall of 2017. Two of those deer were killed in early 2021; CWD was not detected in them. The third deer is still alive. The owner is awaiting payment prior to making the animal available for testing. At this time, the entire Clear Lake herd is quarantined.
Protecting Minnesota’s wild deer herd from CWD, an always-fatal disease, is a top priority for the DNR. The DNR will continue working aggressively on this issue.
Sept. 28, 2021
Minnesota DNR learns of 2 Minnesota deer farms that received deer from a CWD-positive farm in Wisconsin
WEDNESDAY, SEPTEMBER 29, 2021
Minnesota DNR learns of 2 Minnesota deer farms that received deer from a CWD-positive farm in Wisconsin
FRIDAY, JUNE 25, 2021
Minnesota Legislature a Threat For Wild Cervid, Fumbles Football Again With Farmed CWD TSE Prion
FRIDAY, JUNE 11, 2021
Minnesota Deer farming drives predicament over CWD-infested dump site on public land
TUESDAY, JUNE 01, 2021
Minnesota DNR to protect wild deer health through temporary ban on movement of farmed deer
TUESDAY, MAY 25, 2021
Minnesota Twelve additional white-tailed deer tested positive for Chronic Wasting Disease (CWD) in the infected Beltrami County farmed deer herd
MONDAY, FEBRUARY 22, 2021
Minnesota Nine more deer added to tally of CWD positive whitetails at Houston County farm
WEDNESDAY, APRIL 07, 2021
Minnesota 3-year-old white-tailed doe at a Beltrami County farm has been confirmed CWD positive
MONDAY, FEBRUARY 01, 2021
Minnesota 2020 hunting season and early 2021 special hunts confirmed CWD TSE Prion in 22 wild deer
TUESDAY, JANUARY 21, 2020
Minnesota CWD update test results from deer harvested in the 2019 hunting season and the special hunts have returned 27 wild deer tested positive for CWD all from the southeast DMZ
THURSDAY, NOVEMBER 19, 2020
Minnesota Deer testing finds additional cases of chronic wasting disease, to date, 95 wild deer have tested positive for CWD in Minnesota
SUNDAY, AUGUST 20, 2017
Minnesota Fearing spread of CWD, agency pushing animal health board to suspend farmer's license
FRIDAY, JANUARY 20, 2017
Minnesota Chronic Wasting Disease investigation traces exposure to Meeker County farm
FRIDAY, JANUARY 20, 2017
Minnesota Chronic Wasting Disease investigation traces exposure to Meeker County farm News Release For immediate release: January 20, 2017
Contact: Michael Crusan
Chronic Wasting Disease investigation traces exposure to Meeker County farm White-tailed deer tests positive for the disease near Dassel, Minnesota
The Minnesota Board of Animal Health confirms CWD on a Meeker County farm near Dassel. Positive CWD samples came from a two-year-old female white-tailed deer that died on the farm. In accordance with state law, tissue samples were collected from the carcass and submitted for CWD testing. Farmed deer, 12 months of age and older, are required to be tested for CWD if they die or are slaughtered.
Samples are tested at the University of Minnesota Veterinary Diagnostic Laboratory and forwarded to the National Veterinary Services Laboratory in Ames, Iowa, which officially confirms CWD. The Board shares information with the Minnesota Department of Natural Resources and works with the USDA as it investigates CWD cases in farmed deer. The DNR responds to and manages CWD in wild deer, while the Board of Animal Health regulates farmed deer.
The Board’s records show this positive deer was born on the CWD positive Crow Wing County farm and moved to the Meeker County farm in December 2014. As of December 30, 2016, there are three confirmed CWD positive farmed deer in Minnesota. Two are associated with the previously reported case in Crow Wing County. The third, and most recent case in Meeker County, was part of a herd of 14 white-tailed deer, which remain quarantined on the farm.
“This is why it’s important for the Board to maintain accurate animal identification and herd inventories,” said Dr. Paul Anderson, assistant director at the Board of Animal Health. “We were able to look back at five years of recorded deer movements out of the infected Crow Wing County herd, locate herds that received deer from it, and investigate those farms for a CWD infection. This tracing led to the discovery in Meeker County.”
Update on Crow Wing County case: The original quarantine remains in place on the Crow Wing County herd after two female deer tested positive for CWD. The Board is reviewing animal movement records into and out of the herd during the past five years.
Movement records out of the herd show deer were moved to four other Minnesota farms during the five year trace-back period. One of those herds is the Dassel farm in Meeker County. All associated herds remain under movement restrictions.
Movement records into the herd show one of the two CWD infected deer was moved into the herd in 2014 from a deer farm that is no longer in business. The other positive deer was born on the farm.
CWD is a disease of deer and elk caused by an abnormally shaped protein, a prion, which can damage brain and nerve tissue. There is no danger to other animal species. The disease is most likely transmitted when infected deer and elk shed prions in saliva, feces, urine, and other fluids or tissues. The disease is always fatal and there are no known treatments or vaccines. CWD is not known to affect humans, though consuming infected meat is not advised.
Information about Minnesota’s farmed deer and elk herds can be found on the Board of Animal Health website: https://www.bah.state.mn.us/deer-elk/.
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Wednesday, January 11, 2017
Minnesota DNR CWD found in 2 more deer; 5-county feeding ban now in place
TUESDAY, NOVEMBER 22, 2016
Minnesota Tests confirm 2 CWD-positive deer near Lanesboro
TESTS CONFIRM 2 CWD-POSITIVE DEER NEAR LANESBORO
November 22, 2016
DNR initiates disease response plan; offers hunters information on field dressing
Test results show two deer harvested by hunters in southeastern Minnesota were infected with Chronic Wasting Disease, according to the Department of Natural Resources.
One deer has been confirmed as CWD-positive. Confirmation of the second is expected later this week. The deer, both male, were killed near Lanesboro in Fillmore County during the first firearms deer season.
The two deer were harvested approximately 1 mile apart. These are the only deer to test positive from 2,493 samples collected Nov. 5-13. Results are still pending from 373 additional test samples collected during the opening three days of the second firearms season, Nov. 19-21.
CWD is a fatal brain disease to deer, elk and moose but is not known to affect human health. While it is found in deer in states bordering southeastern Minnesota, it was only found in a single other wild deer in Minnesota in 2010.
The DNR discovered the disease when sampling hunter-killed deer this fall in southeastern Minnesota as part of its CWD surveillance program. Dr. Lou Cornicelli, DNR wildlife research manager, said hunter and landowner cooperation on disease surveillance is the key to keeping the state’s deer herd healthy.
“We were proactively looking for the disease, a proven strategy that allows us to manage CWD by finding it early, reacting quickly and aggressively to control it and hopefully eliminating its spread,” he said.
It is unknown how the two CWD-positive deer, which were harvested 4 miles west of Lanesboro in deer permit area 348, contracted the disease, Cornicelli said.
“We want to thank hunters who have brought their deer to our check stations for sampling,” he said. “While finding CWD-positive deer is disappointing, we plan to work with hunters, landowners and other organizations to protect the state’s deer herd and provide hunters the opportunity to pass on their deer hunting traditions.”
These are the first wild deer found to have CWD since a deer harvested in fall 2010 near Pine Island tested positive. It was found during a successful disease control effort prompted by the detection in 2009 of CWD on a domestic elk farm. The DNR, landowners and hunters worked together to sample more than 4,000 deer in the Pine Island area from 2011 to 2013, and no additional infected deer were found.
The National Centers for Disease Control and Prevention as well as the World Health Organization have found no scientific evidence that the disease presents a health risk to humans who come in contact with infected animals or eat infected meat. Still, the CDC advises against eating meat from animals known to have CWD...
snip...see more here;
TUESDAY, NOVEMBER 22, 2016
Minnesota Tests confirm 2 CWD-positive deer near Lanesboro
Friday, August 05, 2016
MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION UPDATE
Thursday, September 19, 2013
Chronic Wasting Disease CWD surveillance, deer feeding ban continues in southeastern Minnesota
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Friday, May 25, 2012
Chronic Wasting Disease CWD found in a farmed red deer from Ramsey County Minnesota
SATURDAY, MARCH 17, 2012
Minnesota CWD DNR, Can chronic wasting disease jump from deer to humans? yes, maybe some day YOUTUBE
Tuesday, January 25, 2011
Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island
Friday, January 21, 2011
MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND
Saturday, October 31, 2009
Elk from Olmsted County herd depopulated to control CWD Three additional elk from the 558-head herd tested positive
Tuesday, January 27, 2009
Chronic Wasting Disease found in a farmed elk from Olmsted County ST. PAUL, Minn.
CHRONIC WASTING DISEASE UPDATE September 6, 2002
Minnesota has announced the finding of CWD in a captive elk in Aitkin County. The animal was a five-year-old male. It had been purchased from a captive facility in Stearns County in August of 2000. The herd where the elk was found has been placed under quarantine as has two additional facilities where the infected elk had resided prior to it coming to the farm in Aitkin County. Minnesota DNR officials will test wild deer in the area to determine if there is any sign of CWD in the free-ranging population. This is the first case of CWD in either captive or freeranging cervids in Minnesota. Several more states have passed bans on the importation of deer and elk carcasses from states where CWD has been found in wild animals. Previously the states of Colorado, Illinois and Iowa and the province of Manitoba had passed such bans. The states of Vermont, Oregon and Missouri have enacted similar bans. Numerous states have issue voluntary advisories to their out-of-state hunters encouraging them not to bring the carcass or carcass parts of deer and elk into their state. The bans do permit the importation of boned out meat, hides or cape with no meat attached, clean skull cap with antler attached, finished taxidermy heads or the ivories of elk. The state of Georgia has recently banned the importation of live cervids into that state also. Some citizens of Colorado have formed a new political action group called Colorado Wildlife Defense (just happens that the acronym is CWD). The stated goal of this group are; Elimination of big game diseases, especially CWD; promotion of healthy wildlife habitat; promotion of scientifically sound wildlife research; promotion of a discussion of the ethics of hunting and wildlife management; education of the hunting and non hunting public. Their action plan calls for; requiring double fencing of all game farms at owners expense; all game farmers provide annual proof of bonding; prohibit new licenses for deer and elk farms; prohibit expansion in acreage of existing game farms; prohibit the transfer of game farm licenses; prohibit charging for hunting behind high wire; prohibit blocking of traditional migratory paths by high fences; requiring game farms to maintain environmental controls and prohibit the escape of contaminated water or soil; requiring immediate reporting of missing deer or elk from game farms; and requiring all game farm deer and elk to be tested for brucellosis and TB. Wisconsin has announced that 7 more free-ranging deer have tested positive for CWD. They have expanded their eradication zone by an additional 15 square miles to cover these findings. The total number of free-ranging CWD positive in Wisconsin is now 31 white-tail deer.
In 2000, a elk farmer in Wisconsin received elk from a CWD exposed herd in Colorado. At that time, the farmer advised the Wisconsin Department of Agriculture that both animals from the exposed herd in Colorado were dead. He has now advised Wisconsin Ag. that he was mistaken and that one of the animals is still alive in his herd. The second draft of the implementation documents for the National CWD Plan was distributed to committee members and others on Friday, August 30. The final documents are due to APHIS and USFWS on Friday, September 13. The herd of captive elk in Oklahoma that had been exposed to CWD will be destroyed this week. This herd had an elk test positive for CWD in 1997 but the depopulation of the herd was not agreed to by the owners and federal representatives until this week. Since the discovery of CWD in the herd, the remaining animals have been under quarantine, however, in the meantime the herd has dropped from 150 animals to 74. Due to a lack of communication, not all of the 76 animals that died in the interim were tested for CWD. All remaining animals will be tested but the true degree of infection rate of the herd will never be known.
The owners of the facility will not be permitted to restock the area with cervids for a period of five years. A New York based organization, BioTech Research Fund I LLC has committed a $1 million line of credit to fund commercialization of tests for brain-wasting disorders and production of various vaccines to Gene-Thera of Wheat Ridge, Colorado. Gene-Thera has spent three years developing new ways not only to diagnose CWD, but create vaccines for mad cow disease, E. coli contaminants and foot-and-mouth disease. Its tests for CWD have been successful in more than 100 samples from Colorado and Wisconsin according to company officials. Gene-Thera plans to license and market some o fits disease test kits by the end of the year, then begin volume distribution by mid-2003. The abstracts of the presentations from the CWD Conference in Denver August 6 and 7 have been posted on the Colorado Division of Wildlife web site. You will need adobe acrobat reader to read them.
The Division web site is: http://wildlife.state.co.us/CWD/Symposium_booklet.pdf
Minnesota: Second case in a game farmed elk discovered in Stearns Co.
This is a trace forward from the previously affected game farm in Aitkins Co. An additional game farm in Benton Co is under quarantine.
snip...
Supporting Documents: Colorado: CWD-Exposed Elk Used in 1990 Study- Wildlife officials call W. Slope move a mistake
Date: January 17, 2003 Source: Denver Post Contacts: Theo Stein Environment Writer
The Colorado Division of Wildlife knowingly used a herd of captive elk exposed to chronic wasting disease in a grazing study on the Western Slope in January 1990, possibly introducing the disease to the elk-rich area. "It was a bad call," said Jeff Ver Steeg, the division's top game manager. "I can't deny it." About 150 wild elk were allowed to graze in the same pens near Maybell after the research herd was removed and may have picked up the abnormal protein that causes the disease from the feces and urine left by the captive elk. While the Division of Wildlife has expressed concern before that its animals might have helped spread CWD, this is the first time the agency has acknowledged it knowingly moved elk exposed to CWD deep into an area where the disease was not known to already exist. Studies that could help determine the source of CWD on the Western Slope are incomplete, and officials say what data that do exist are so new and so spotty they may not provide all the answers. So far, it appears that less than 1 percent of deer and elk in the area are infected, compared with as much as 15 to 20 percent in hotspots in northeastern Colorado. But as wildlife officials grapple with CWD's appearance in northwestern Colorado, officials now admit the decision to continue the grazing study over the objections of some biologists was an error. At the time, biologists wanted to see whether elk grazing on winter range depleted forage that ranchers wanted for fattening cattle in spring. "I think in hindsight a lot of good people probably did some dumb things, myself included," said Bruce Gill, a retired wildlife manager who oversaw research efforts and remembers the debate over the project. "Had we known CWD would explode into such a potentially volatile ecologic and economic issue, we wouldn't have done it." Elk ranchers, who have been blamed for exporting the disease from its stronghold on the Colorado and Wyoming plains to seven states and two Canadian provinces, say the agency's belated disclosure smacks of a coverup. "It's pure negligence," said Jerry Perkins, a Delta banker and rancher who is now demanding a legislative inquiry. "If I'd have moved animals I knew to be infected around like that, I'd be in jail." Grand Junction veterinarian and sportsman Dick Steele said he faults the agency for not disclosing information about CWD-exposed research animals before October, when information was posted on the Division of Wildlife website. "This went way beyond poor judgment," he said. "My main concern is that this has been hidden for the last 12 years. It would have been real important to our decision-making process on how to deal with CWD." While the Maybell information is new, Perkins and other ranchers have long suspected Division of Wildlife research facilities near Meeker and Kremmling, which temporarily housed mule deer kept in heavily infected pens at the Fort Collins facility, have leaked CWD to the wild. Fear of an outbreak led the agency to sample 450 deer around the Meeker and Kremmling facilities. None tested positive, but the sample size was only large enough to detect cases if the infection rate was greater than 1 percent. This fall, tests on 23,000 deer and elk submitted by hunters statewide have revealed 48 CWD cases north of Interstate 70 and west of the Continental Divide. Biologists believe the infection rate in that area, which includes the Maybell, Meeker and Kremmling sites, is still well below 1 percent. But CWD has never been contained in a wild population, so experts fear the problem will grow worse.
The Division of Wildlife says it will be months before a statistical analysis of the fall's sampling results can be completed, an exercise that may shed light on the disease's origin on the Western Slope. "We're just not going to speculate at this point," said Ver Steeg of the possible Maybell connection. "This is one possibility, but certainly not the only possibility." Some biologists think a defunct elk ranch near Pagoda, which had dozens of unexplained deaths in the mid-'90s, is another, a suggestion Perkins rejects. "It may be inconclusive to them," said Perkins. "It isn't inconclusive to us."
To date, 19 CWD-positive animals have been found on six Wisconsin farms.
*** All have been white-tailed deer except for one elk imported from a Minnesota herd later found to be infected.
More than 8,000 farm-raised deer and elk have been tested in Wisconsin, and about 540 herds are enrolled in the CWD monitoring program.
CWD disease detected on Lac qui Parle County cervid farm southwestern Minnesota (2006-03-15)
Date: March 15, 2006 at 12:36 pm PST
Chronic wasting disease detected on Lac qui Parle County cervid farm (2006-03-15) The Board of Animal Health announced today that chronic wasting disease (CWD) has been detected in one domestic white-tailed deer on a cervid farm in Lac qui Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine the number of wild deer in the area. It is expected that not many deer will be found because the area is highly agricultural, with little deer habitat surrounding the farm. DNR will conduct opportunistic sampling of deer, like road kills, in the immediate area now and will conduct intensive hunter-harvested surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted surveillance for CWD in wild deer in the area. The farm is located near the northern boundary of deer permit area 447, where wild deer surveillance for CWD last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447. In total, we collected 392 samples from those permit areas during the regular firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent confidence of detecting a 1 percent infection rate, according to Mike DonCarlos, DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in Stearns County in 2003, which followed the first discovery of CWD in an Aitkin County elk farm," DonCarlos said. “The DNR response will be similar to the Stearns County action and will include an initial assessment of wild deer populations in the area and development of a surveillance program for next fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not present in wild deer," Cornicelli said. “In addition, all indications are that this positive captive deer has not contacted any wild deer, but we will conduct additional surveillance this fall to be sure."
Minnesota Chronic Wasting Disease CWD TSE Prion
Minnesota Department of Natural Resources Chronic Wasting Disease Response Plan
WHAT ABOUT THOSE OUTBREAKS OF TRANSMISSIBLE MINK ENCEPHALOPATHY TME PrP IN WISCONSIN AND MINNESOTA???
Epidemiology Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old. The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In Factsheet Veterinary Services February 2002 APHIS 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.
snip...
The 1985 Stetsonville Outbreak The most recent TME outbreak occurred on one mink ranch in Stetsonville, WI, in 1985. In the herd of 7,300 adult mink, 60 percent of the animals died. Clinical signs included tail arching, incoordination, and hyperexcitability. At the most advanced stages of the disease, the animals were in trancelike states and eventually died. The outbreak lasted 5 months. Microscopic examination of sections of the brain confirmed the spongelike changes characteristic of TME. Diagnostic tests identified the prion protein. The following year, mink born during the outbreak showed no signs of TME. The late Richard Marsh, a veterinary virologist at the University of Wisconsin who studied the transmission of TME and other TSE’s, investigated this outbreak. Marsh learned that the mink were fed a diet composed of fresh meat products from “downer cattle” and commercial sources of fish, poultry, and cereal. Downer cattle are nonambulatory and cannot rise because they are affected with a condition such as a metabolic disease, broken limbs, or a central nervous system disorder. Marsh theorized that the meat from these downer cattle introduced a TSE agent to the mink in which TME resulted. Although Marsh’s hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of more than 20,141 cattle have been examined at APHIS’ National Veterinary Services Laboratories and other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another TSE in cattle.
http://www.aphis.usda.gov/publications/animal_health/content/printable_version/fs_ahtme.pdf
AND as everyone knows, the rest is history, those dead-stock downers, the most high risk cattle, were NOT tested, and in FACT, was a major source of YOUR CHILDRENS SCHOOL LUNCH PROGRAM, all across the Nation. sorry, these are the most high risk cattle for TSE aka mad cow disease, and i am a bit touchy about this topic. ...sorry. ...terry
DOWNER COW SCHOOL LUNCH PROGRAM
http://downercattle.blogspot.com/
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.
We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.
snip...
PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf
1985
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
NOW, back to those mad mink i.e. TME. let me throw a curve ball here ;
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* and Richard A. Bessen† Emerging Infectious
Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine- passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, Htype BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profi les, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME. The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE. Transmissible mink encephalopathy (TME) is a rare prion disease in ranch-raised mink (Mustela vison) in North America and Europe (1–4). Six outbreaks have been reported from 1947 through 1985 in North America, and several have been linked to contaminated commercial feed (1). Although contamination of feed with scrapie-infected sheep parts has been proposed as the cause of TME, the origin of the disease remains elusive. The idea that scrapie in sheep may be a source of TME infection is supported by fi ndings that scrapie-infected mink have a similar distribution of vacuolar pathologic features in the brain and the same clinical signs as mink with natural and experimental TME (5). However, mink are not susceptible to scrapie infection following oral exposure for up to 4 years postinoculation, which suggests that either the scrapie agent may not be the source of natural TME infection or that only specifi c strains of the scrapie agent are able to induce TME (6,7). Epidemiologic investigations in the Stetsonville, Wisconsin, outbreak of TME in 1985 suggested a possible cattle origin, since mink were primarily fed downer or dead dairy cattle but not sheep products (8). Experimental transmission of Stetsonville TME into cattle resulted in transmissible spongiform encephalopathy (TSE) disease with an incubation period of 18.5 months. Back passage of bovine TME into mink resulted in incubation periods of 4 and 7 months after oral or intracerebral inoculation, respectively, which was similar to that found following inoculation of Stetsonville TME into mink by these same routes (8). These fi ndings indicated that cattle are susceptible to TME, and that bovine-passaged TME did not result in a reduced pathogenicity for mink. These studies raised the question as to whether an unknown TSE in cattle was the source of TME infection in the Stetsonville outbreak. Several additional TME outbreaks in the United States have been associated with mink diet that contained downer or dead cattle (9). ...
snip...full text ;
CWD, is but a small piece, of a very big puzzle. ...TSS
*** PLEASE NOTE, before i forget ;
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS
WEDNESDAY, JANUARY 12, 2022
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA, what if?
TEXAS CHRONIC WASTING DISEASE CWD TSE PrP
“Regarding the current situation involving CWD in permitted deer breeding facilities, TPWD records indicate that within the last five years, the seven CWD-positive facilities transferred a total of 2,530 deer to 270 locations in 102 counties and eight locations in Mexico (the destinations included 139 deer breeding facilities, 118 release sites, five Deer Management Permit sites, and three nursing facilities).'' ...
It is apparent that prior to the recent emergency rules, the CWD detection rules were ineffective at detecting CWD earlier in the deer breeding facilities where it was eventually discovered and had been present for some time; this creates additional concern regarding adequate mitigation of the risk of transferring CWD-positive breeder deer to release sites where released breeder deer come into contact with free-ranging deer...
Commission Agenda Item No. 5 Exhibit B
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
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A third issue is the accuracy of mortality reporting. Department records indicate that for each of the last five years an average of 26 deer breeders have reported a shared total of 159 escapes. Department records for the same time period indicate an average of 31 breeding facilities reported a shared total of 825 missing deer (deer that department records indicate should be present in the facility, but cannot be located or verified).
Listen here;
Nov 3, 2021
Nov 4, 2021
Counties where CWD Exposed Deer were Released, September 2021
Number of CWD Exposed Deer Released by County, September 2021
TPWD CWD TSE PRION TRACKER UPDATE TEXAS 270 CONFIRMED TO DATE POSTIVE CAPTIVE AND WILD
2021-11-18 Free Range Medina N/A White-tailed Deer M 3.5
2021-11-04 Free Range El Paso N/A Mule Deer F 4.5
2021-10-18 Breeder Deer Medina Facility #4 White-tailed Deer M 4
2021-10-12 Breeder Deer Hunt Facility #9 White-tailed Deer F 8.189041096
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 1.208219178
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 1.21369863
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 1.205479452
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 2.208219178
2021-10-12 Breeder Deer Uvalde Facility #8 White-tailed Deer M 2.117808219
2021-10-08 Breeder Deer Duval Facility #13 White-tailed Deer F 3.238356164
2021-10-08 Breeder Deer Medina Facility #4 White-tailed Deer F 2.260273973
2021-09-14 Breeder Deer Medina Facility #4 White-tailed Deer F 6.205479452
2021-07-07 Free Range El Paso N/A Mule Deer F 6.5
2021-06-30 Breeder Deer Hunt Facility #9 White-tailed Deer F 3
2021-06-30 Breeder Deer Hunt Facility #9 White-tailed Deer F 3
2021-06-30 Breeder Deer Hunt Facility #9 White-tailed Deer F 3
2021-06-30 Breeder Deer Hunt Facility #9 White-tailed Deer F 3
2021-06-28 Breeder Deer Uvalde Facility #8 White-tailed Deer F 5
2021-06-28 Breeder Deer Uvalde Facility #8 White-tailed Deer F 2
2021-06-28 Breeder Deer Uvalde Facility #8 White-tailed Deer F 5
2021-06-28 Breeder Deer Uvalde Facility #8 White-tailed Deer F 11.01369863
2021-06-28 Breeder Deer Uvalde Facility #8 White-tailed Deer F 7
2021-06-28 Breeder Deer Uvalde Facility #8 White-tailed Deer F 4
2021-06-28 Breeder Deer Uvalde Facility #8 White-tailed Deer F 4
Showing 1 to 24 of 270 entries Previous Next
SNIP...SEE ALL;
Oh, Deer, CWD, Heading Off a Wildlife Epidemic Texas Real Estate Research Center TAMU
Texas A & M University
Texas Real Estate Research Center
Oh, Deer
Heading Off a Wildlife Epidemic
Charles E. Gilliland (Aug 18, 2021)
The Takeaway
Landowners in certain parts of the state need to be aware of chronic wasting disease, which can greatly reduce the number of deer. While there are no known cures or ways to eradicate the disease, the Texas Parks and Wildlife Department is taking measures to reduce its spread.
snip...
Because the spread of CWD is evolving, regulations can change quickly. Therefore, anyone involved in hunting activity should consult the most recent Outdoor Annual for the latest regulations. To reduce the chances of spreading the disease, TPWD regulations also restrict the movement of live deer from CWD zones.
Impact on Rural Landowners CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections.
As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
____________________
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
SATURDAY, DECEMBER 04, 2021
TPWD CWD TSE PRION TRACKER UPDATE TEXAS 270 CONFIRMED TO DATE POSTIVE CAPTIVE AND WILD
TERRIBLE NEWS for Texas for sure, and the good Doctor brings much needed attention to a topic no one wants to talk about, and i have been trying to bring awareness to this very topic for decades, 5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!
QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !
3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?
Trucking CWD TSE Prion
MONDAY, MARCH 05, 2018
TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES
SATURDAY, JULY 09, 2016
Texas Intrastate – within state movement of all Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium
PENNSYLVANIA CWD TSE PRION CAPTIVE CERVID INDUSTRY
SUNDAY, JANUARY 23, 2022
Pennsylvania Chronic Wasting Disease CWD TSE PrP Surveillance 2021 2022 Update
CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION
***> cattle, pigs, sheep, cwd, tse, prion, oh my!
***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006).
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
Published: 06 September 2021
Chronic wasting disease: a cervid prion infection looming to spillover
Alicia Otero, Camilo Duque Velásquez, Judd Aiken & Debbie McKenzie
Veterinary Research volume 52, Article number: 115 (2021)
Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years
Published: May 9, 2007
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Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.
snip...
***> This is very likely to have parallels with control efforts for CWD in cervids. <***
Paper
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough BSc (Hons), PhD Claire Alison Baker BSc (Hons) Steve Hawkins MIBiol Hugh Simmons BVSc, MRCVS, MBA, MA Timm Konold DrMedVet, PhD, MRCVS … See all authors
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
Abstract
The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. Post‐decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. Twenty‐four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie‐positive during the bioassay, samples of dust collected within the barn were positive by month 3. The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
***>This is very likely to have parallels with control efforts for CWD in cervids.
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
Gudmundur Georgsson1, Sigurdur Sigurdarson2, Paul Brown3
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
imageTimm Konold1*, imageStephen A. C. Hawkins2, imageLisa C. Thurston3, imageBen C. Maddison4, imageKevin C. Gough5, imageAnthony Duarte1 and imageHugh A. Simmons1
1Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK
2Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK
3Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK
4ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
5School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie-affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).
Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).
Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.
Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.
Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).
The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.
It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.
Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.
Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.
In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.
In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).
As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).
This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.
This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.
In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.
Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.
The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.
In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).
A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).
This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.
Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018
P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer
Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1)
(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada.
Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer.
Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection.
Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD.
SOURCE REFERENCE 2018 PRION CONFERENCE ABSTRACT
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Horizontal transmission of chronic wasting disease in reindeer
Author
item MOORE, SARAH - ORISE FELLOW item KUNKLE, ROBERT item WEST GREENLEE, MARY - IOWA STATE UNIVERSITY item Nicholson, Eric item RICHT, JUERGEN item HAMIR, AMIRALI item WATERS, WADE item Greenlee, Justin
Submitted to: Emerging Infectious Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/29/2016
Publication Date: 12/1/2016
Citation: Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.
Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.
***> Scrapie vs Chronic Wasting Disease CWD TSE Prion ???
172. Establishment of PrPCWD extraction and detection methods in the farm soil
Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo Sohn
Foreign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, Korea
Conclusions: Our studies showed that PrPCWD persist in 0.001% CWD contaminated soil for at least 4 year and natural CWD-affected farm soil. When cervid reintroduced into CWD outbreak farm, the strict decontamination procedures of the infectious agent should be performed in the environment of CWD-affected cervid habitat.
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. ***These circumstances represent a potential threat to blood, blood products, and plasma supplies.
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
3.2.1.2 Non‐cervid domestic species
The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.
For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).
In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).
A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
Nathaniel D. Denkers ,Clare E. Hoover ,Kristen A. Davenport,Davin M. Henderson,Erin E. McNulty,Amy V. Nalls,Candace K. Mathiason,Edward A. Hoover
Published: August 20, 2020
We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
ARS RESEARCH Generation of human chronic wasting disease in transgenic mice
Publication Acceptance Date: 9/8/2021
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Generation of human chronic wasting disease in transgenic mice
Author item WANG, ZERUI - Case Western Reserve University (CWRU) item QIN, KEFENG - University Of Chicago item CAMACHO, MANUEL - Case Western Reserve University (CWRU) item SHEN, PINGPING - Case Western Reserve University (CWRU) item YUAN, JUE - Case Western Reserve University (CWRU) item Greenlee, Justin item CUI, LI - Jilin University item KONG, QINGZHONG - Case Western Reserve University (CWRU) item MASTRIANNI, JAMES - University Of Chicago item ZOU, WEN-QUAN - Case Western Reserve University (CWRU)
Submitted to: Acta Neuropathologica Publication Type: Peer Reviewed Journal Publication Acceptance Date: 9/8/2021 Publication Date: N/A Citation: N/A
Interpretive Summary: Prion diseases are invariably fatal neurologic diseases for which there is no known prevention or cure. Chronic wasting disease (CWD) is the prion disease of deer and elk and is present in farmed and free ranging herds throughout North America. To date there is no clear evidence that the CWD agent could be transmitted to humans. This manuscript describes the use of an in vitro technique, cell-free serial protein misfolding cyclic amplification (sPMCA), to generate a CWD prion that is infectious to transgenic mice expressing the human prion protein. This study provides the first evidence that CWD prions may be able to cause misfolding in the human prion protein. This information will impact medical experts and those involved in making policy for farmed cervids and wildlife.
Technical Abstract: Chronic wasting disease (CWD) is a cervid spongiform encephalopathy or prion disease caused by the infectious prion or PrPSc, a misfolded conformer of cellular prion protein (PrPC). It has rapidly spread in North America and also has been found in Asia and Europe. In contrast to the zoonotic mad cow disease that is the first animal prion disease found transmissible to humans, the transmissibility of CWD to humans remains uncertain although most previous studies have suggested that humans may not be susceptible to CWD. Here we report the generation of an infectious human PrPSc by seeding CWD PrPSc in normal human brain PrPC through the in vitro cell-free serial protein misfolding cyclic amplification (sPMCA). Western blotting confirms that the sPMCA-induced proteinase K-resistant PrPSc is a human form, evidenced by a PrP-specific antibody that recognizes human but not cervid PrP. Remarkably, two lines of humanized transgenic (Tg) mice expressing human PrP-129Val/Val (VV) or -129Met/Met (MM) polymorphism develop prion disease at 233 ± 6 (mean ± SE) days post-inoculation (dpi) and 552 ± 27 dpi, respectively, upon intracerebral inoculation with the sPMCA-generated PrPSc. The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns. We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.
''The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns.''
''We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.''
Published: 26 September 2021
Generation of human chronic wasting disease in transgenic mice
Zerui Wang, Kefeng Qin, Manuel V. Camacho, Ignazio Cali, Jue Yuan, Pingping Shen, Justin Greenlee, Qingzhong Kong, James A. Mastrianni & Wen-Quan Zou
Acta Neuropathologica Communications volume 9, Article number: 158 (2021)
Abstract
Chronic wasting disease (CWD) is a cervid prion disease caused by the accumulation of an infectious misfolded conformer (PrPSc) of cellular prion protein (PrPC). It has been spreading rapidly in North America and also found in Asia and Europe. Although bovine spongiform encephalopathy (i.e. mad cow disease) is the only animal prion disease known to be zoonotic, the transmissibility of CWD to humans remains uncertain. Here we report the generation of the first CWD-derived infectious human PrPSc by elk CWD PrPSc-seeded conversion of PrPC in normal human brain homogenates using in vitro protein misfolding cyclic amplification (PMCA). Western blotting with human PrP selective antibody confirmed that the PMCA-generated protease-resistant PrPSc was derived from the human PrPC substrate. Two lines of humanized transgenic mice expressing human PrP with either Val or Met at the polymorphic codon 129 developed clinical prion disease following intracerebral inoculation with the PMCA-generated CWD-derived human PrPSc. Diseased mice exhibited distinct PrPSc patterns and neuropathological changes in the brain. Our study, using PMCA and animal bioassays, provides the first evidence that CWD PrPSc can cross the species barrier to convert human PrPC into infectious PrPSc that can produce bona fide prion disease when inoculated into humanized transgenic mice.
Snip...
It is worth noting that the annual number of sporadic CJD (sCJD) cases in the USA has increased, with the total number of suspected and confirmed sCJD cases rising from 284 in 2003 to 511 in 2017 (https://www.cdc.gov/prions/cjd/occurrence-transmission.html). The greatly enhanced CJD surveillance and an aging population in the USA certainly contributed to the observed increase in annual sCJD case numbers in recent years, but the possibility cannot be excluded that some of the increased sCJD prevalence is linked to CWD exposure.
In the present study, using serial protein misfolding cyclic amplification (sPMCA) assay we generate PrPSc by seeding CWD prions in normal human brain homogenates. Importantly, we reveal that two lines of humanized Tg mice expressing human PrP-129VV and 129MM develop prion diseases upon intracerebral inoculation of the abnormal PrP generated by sPMCA. We believe that our study provides the first opportunity to dissect the clinical, pathological and biochemical features of the CWD-derived human prion disease in two lines of humanized Tg mice expressing two major human PrP genotypes, respectively.
***> ''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***
***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<***
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<***
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***
''The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns.''
''We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.''
Published: 26 September 2021
Generation of human chronic wasting disease in transgenic mice
Zerui Wang, Kefeng Qin, Manuel V. Camacho, Ignazio Cali, Jue Yuan, Pingping Shen, Justin Greenlee, Qingzhong Kong, James A. Mastrianni & Wen-Quan Zou
Acta Neuropathologica Communications volume 9, Article number: 158 (2021)
Abstract
Chronic wasting disease (CWD) is a cervid prion disease caused by the accumulation of an infectious misfolded conformer (PrPSc) of cellular prion protein (PrPC). It has been spreading rapidly in North America and also found in Asia and Europe. Although bovine spongiform encephalopathy (i.e. mad cow disease) is the only animal prion disease known to be zoonotic, the transmissibility of CWD to humans remains uncertain. Here we report the generation of the first CWD-derived infectious human PrPSc by elk CWD PrPSc-seeded conversion of PrPC in normal human brain homogenates using in vitro protein misfolding cyclic amplification (PMCA). Western blotting with human PrP selective antibody confirmed that the PMCA-generated protease-resistant PrPSc was derived from the human PrPC substrate. Two lines of humanized transgenic mice expressing human PrP with either Val or Met at the polymorphic codon 129 developed clinical prion disease following intracerebral inoculation with the PMCA-generated CWD-derived human PrPSc. Diseased mice exhibited distinct PrPSc patterns and neuropathological changes in the brain. Our study, using PMCA and animal bioassays, provides the first evidence that CWD PrPSc can cross the species barrier to convert human PrPC into infectious PrPSc that can produce bona fide prion disease when inoculated into humanized transgenic mice.
Snip...
It is worth noting that the annual number of sporadic CJD (sCJD) cases in the USA has increased, with the total number of suspected and confirmed sCJD cases rising from 284 in 2003 to 511 in 2017 (https://www.cdc.gov/prions/cjd/occurrence-transmission.html). The greatly enhanced CJD surveillance and an aging population in the USA certainly contributed to the observed increase in annual sCJD case numbers in recent years, but the possibility cannot be excluded that some of the increased sCJD prevalence is linked to CWD exposure.
In the present study, using serial protein misfolding cyclic amplification (sPMCA) assay we generate PrPSc by seeding CWD prions in normal human brain homogenates. Importantly, we reveal that two lines of humanized Tg mice expressing human PrP-129VV and 129MM develop prion diseases upon intracerebral inoculation of the abnormal PrP generated by sPMCA. We believe that our study provides the first opportunity to dissect the clinical, pathological and biochemical features of the CWD-derived human prion disease in two lines of humanized Tg mice expressing two major human PrP genotypes, respectively.
i thought i might share some news about cwd zoonosis that i got, that i cannot share or post to the public yet, i promised for various reasons, one that it will cause a shit storm for sure, but it was something i really already knew from previous studies, but, i was told that ;
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''As you can imagine, 2 and 5 (especially 5) may raise alarms. The evidence we have for 4 are not as strong or tight as I would like to have. At this point, please do not post any of the points publicly yet, but you can refer to points 1-3 in private discussions and all 5 points when discussing with relevant public officials to highlight the long-term risks of CWD zoonosis.''
====================
so, i figure your as about as official as it gets, and i think this science is extremely important for you to know and to converse about with your officials. it's about to burn a whole in my pocket. this is about as close as it will ever get for cwd zoonosis to be proven in my time, this and what Canada Czub et al found with the Macaques, plus an old study from cjd surveillance unit back that showed cjd and a 9% increase in risk from folks that eat venison, i will post all this below for your files Sir. i remember back in the BSE nvCJD days, from when the first BSE case in bovine was confirmed around 1984 maybe 83, i forget the good vets named that screwed it up first, Carol something, but from 83ish to 95 96 when nvCJD was linked to humans from BSE in cattle, so that took 10 to 15 years. hell, at that rate, especially with Texas and cwd zoonsis, hell, i'll be dead before it's official, if ever, so here ya go Sir. there was a grant study on cwd zoonosis that had been going on for some time, i followed it over the years, then the grant date for said study had expired, so, i thought i would write the good Professor about said study i.e. Professor Kong, CWRU et al. i will post the grant study abstract first, and then after that, what reply i got back, about said study that i was told not to post/publish...
CWD ZOONOSIS GRANT FIRST;
===============
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; (3) Reliable essays can be established to detect CWD infection in humans; and (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency Agency National Institute of Health (NIH) Institute National Institute of Neurological Disorders and Stroke (NINDS) Type Research Project (R01) Project # 1R01NS088604-01A1 Application # 9037884 Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND) Program Officer Wong, May Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2015-09-30 Budget End 2016-07-31 Support Year 1 Fiscal Year 2015 Total Cost $337,507 Indirect Cost $118,756
snip...
Professor Kongs reply to me just this month about above grant study that has NOT been published in peer reveiw yet...
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Here is a brief summary of our findings:
snip...can't post, made a promise...tss
On Sat, Apr 3, 2021 at 12:19 PM Terry Singeltary <flounder9@verizon.net> wrote:
snip...
end...tss
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CWD ZOONOSIS THE FULL MONTY TO DATE
International Conference on Emerging Diseases, Outbreaks & Case Studies & 16th Annual Meeting on Influenza March 28-29, 2018 | Orlando, USA
Qingzhong Kong
Case Western Reserve University School of Medicine, USA
Zoonotic potential of chronic wasting disease prions from cervids
Chronic wasting disease (CWD) is the prion disease in cervids (mule deer, white-tailed deer, American elk, moose, and reindeer). It has become an epidemic in North America, and it has been detected in the Europe (Norway) since 2016. The widespread CWD and popular hunting and consumption of cervid meat and other products raise serious public health concerns, but questions remain on human susceptibility to CWD prions, especially on the potential difference in zoonotic potential among the various CWD prion strains. We have been working to address this critical question for well over a decade. We used CWD samples from various cervid species to inoculate transgenic mice expressing human or elk prion protein (PrP). We found infectious prions in the spleen or brain in a small fraction of CWD-inoculated transgenic mice expressing human PrP, indicating that humans are not completely resistant to CWD prions; this finding has significant ramifications on the public health impact of CWD prions. The influence of cervid PrP polymorphisms, the prion strain dependence of CWD-to-human transmission barrier, and the characterization of experimental human CWD prions will be discussed.
Speaker Biography Qingzhong Kong has completed his PhD from the University of Massachusetts at Amherst and Post-doctoral studies at Yale University. He is currently an Associate Professor of Pathology, Neurology and Regenerative Medicine. He has published over 50 original research papers in reputable journals (including Science Translational Medicine, JCI, PNAS and Cell Reports) and has been serving as an Editorial Board Member on seven scientific journals. He has multiple research interests, including public health risks of animal prions (CWD of cervids and atypical BSE of cattle), animal modeling of human prion diseases, mechanisms of prion replication and pathogenesis, etiology of sporadic Creutzfeldt-Jacob disease (CJD) in humans, normal cellular PrP in the biology and pathology of multiple brain and peripheral diseases, proteins responsible for the α-cleavage of cellular PrP, as well as gene therapy and DNA vaccination.
SUNDAY, JULY 25, 2021
North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk
''Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro.''
MONDAY, JULY 19, 2021
***> U Calgary researchers at work on a vaccine against a fatal infectious disease affecting deer and potentially people
Prion Conference 2018 Abstracts
BSE aka MAD COW DISEASE, was first discovered in 1984, and it took until 1995 to finally admit that BSE was causing nvCJD, the rest there is history, but that science is still evolving i.e. science now shows that indeed atypical L-type BSE, atypical Nor-98 Scrapie, and typical Scrapie are all zoonosis, zoonotic for humans, there from.
HOW long are we going to wait for Chronic Wasting Disease, CWD TSE Prion of Cervid, and zoonosis, zoonotic tranmission to humans there from?
Studies have shown since 1994 that humans are susceptible to CWD TSE Prion, so, what's the hold up with making CWD a zoonotic zoonosis disease, the iatrogenic transmissions there from is not waiting for someone to make a decision.
Prion Conference 2018 Abstracts
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1)
(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.
Background
Chronic wasting disease (CWD) is a prion disease of deer and elk that has been identified in freeranging cervids in 23 US states. While there is currently no epidemiological evidence for zoonotic transmission through the consumption of contaminated venison, studies suggest the CWD agent can cross the species barrier in experimental models designed to closely mimic humans. We compared rates of human prion disease in states with and without CWD to examine the possibility of undetermined zoonotic transmission.
Methods
Death records from the National Center for Health Statistics, case records from the National Prion Disease Pathology Surveillance Center, and additional state case reports were combined to create a database of human prion disease cases from 2003-2015. Identification of CWD in each state was determined through reports of positive CWD tests by state wildlife agencies. Age- and race-adjusted mortality rates for human prion disease, excluding cases with known etiology, were determined for four categories of states based on CWD occurrence: highly endemic (>16 counties with CWD identified in free-ranging cervids); moderately endemic (3-10 counties with CWD); low endemic (1-2 counties with CWD); and no CWD states. States were counted as having no CWD until the year CWD was first identified. Analyses stratified by age, sex, and time period were also conducted to focus on subgroups for which zoonotic transmission would be more likely to be detected: cases <55 years old, male sex, and the latter half of the study (2010-2015).
Results
Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states (rate ratio [RR]: 1.12, 95% confidence interval [CI] = 1.01 - 1.23), as did low endemic states (RR: 1.15, 95% CI = 1.04 - 1.27). Moderately endemic states did not have an elevated mortality rate (RR: 1.05, 95% CI = 0.93 - 1.17). In age-stratified analyses, prion disease mortality rates among the <55 year old population were elevated for moderately endemic states (RR: 1.57, 95% CI = 1.10 – 2.24) while mortality rates were elevated among those ≥55 for highly endemic states (RR: 1.13, 95% CI = 1.02 - 1.26) and low endemic states (RR: 1.16, 95% CI = 1.04 - 1.29). In other stratified analyses, prion disease mortality rates for males were only elevated for low endemic states (RR: 1.27, 95% CI = 1.10 - 1.48), and none of the categories of CWD-endemic states had elevated mortality rates for the latter time period (2010-2015).
Conclusions
While higher prion disease mortality rates in certain categories of states with CWD in free-ranging cervids were noted, additional stratified analyses did not reveal markedly elevated rates for potentially sensitive subgroups that would be suggestive of zoonotic transmission. Unknown confounding factors or other biases may explain state-by-state differences in prion disease mortality.
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P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2)
(1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.
Prion disease is a fatal progressive neurodegenerative disease due to deposition of an abnormal protease-resistant isoform of prion protein. Typical symptoms include rapidly progressive dementia, myoclonus, visual disturbance and hallucinations. Interestingly, in patients with prion disease, the abnormal protein canould also be found in the peripheral nervous system. Case reports of prion deposition in peripheral nerves have been reported. Peripheral nerve involvement is thought to be uncommon; however, little is known about the exact prevalence and features of peripheral neuropathy in patients with prion disease.
We reviewed autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017. We collected information regarding prion protein diagnosis, demographics, comorbidities, clinical symptoms, physical exam, neuropathology, molecular subtype, genetics lab, brain MRI, image and EMG reports. Our study included 104 patients. Thirteen (12.5%) patients had either subjective symptoms or objective signs of peripheral neuropathy. Among these 13 patients, 3 had other known potential etiologies of peripheral neuropathy such as vitamin B12 deficiency or prior chemotherapy. Among 10 patients that had no other clear etiology, 3 (30%) had familial CJD. The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%). The Majority of cases wasere male (60%). Half of them had exposure to wild game. The most common subjective symptoms were tingling and/or numbness of distal extremities. The most common objective finding was diminished vibratory sensation in the feet. Half of them had an EMG with the findings ranging from fasciculations to axonal polyneuropathy or demyelinating polyneuropathy.
Our study provides an overview of the pattern of peripheral neuropathy in patients with prion disease. Among patients with peripheral neuropathy symptoms or signs, majority has polyneuropathy. It is important to document the baseline frequency of peripheral neuropathy in prion diseases as these symptoms may become important when conducting surveillance for potential novel zoonotic prion diseases.
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P177 PrP plaques in methionine homozygous Creutzfeldt-Jakob disease patients as a potential marker of iatrogenic transmission
Abrams JY (1), Schonberger LB (1), Cali I (2), Cohen Y (2), Blevins JE (2), Maddox RA (1), Belay ED (1), Appleby BS (2), Cohen ML (2)
(1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.
Background
Sporadic Creutzfeldt-Jakob disease (CJD) is widely believed to originate from de novo spontaneous conversion of normal prion protein (PrP) to its pathogenic form, but concern remains that some reported sporadic CJD cases may actually be caused by disease transmission via iatrogenic processes. For cases with methionine homozygosity (CJD-MM) at codon 129 of the PRNP gene, recent research has pointed to plaque-like PrP deposition as a potential marker of iatrogenic transmission for a subset of cases. This phenotype is theorized to originate from specific iatrogenic source CJD types that comprise roughly a quarter of known CJD cases.
Methods
We reviewed scientific literature for studies which described PrP plaques among CJD patients with known epidemiological links to iatrogenic transmission (receipt of cadaveric human grown hormone or dura mater), as well as in cases of reported sporadic CJD. The presence and description of plaques, along with CJD classification type and other contextual factors, were used to summarize the current evidence regarding plaques as a potential marker of iatrogenic transmission. In addition, 523 cases of reported sporadic CJD cases in the US from January 2013 through September 2017 were assessed for presence of PrP plaques.
Results
We identified four studies describing 52 total cases of CJD-MM among either dura mater recipients or growth hormone recipients, of which 30 were identified as having PrP plaques. While sporadic cases were not generally described as having plaques, we did identify case reports which described plaques among sporadic MM2 cases as well as case reports of plaques exclusively in white matter among sporadic MM1 cases. Among the 523 reported sporadic CJD cases, 0 of 366 MM1 cases had plaques, 2 of 48 MM2 cases had kuru plaques, and 4 of 109 MM1+2 cases had either kuru plaques or both kuru and florid plaques. Medical chart review of the six reported sporadic CJD cases with plaques did not reveal clinical histories suggestive of potential iatrogenic transmission.
Conclusions
PrP plaques occur much more frequently for iatrogenic CJD-MM cases compared to sporadic CJDMM cases. Plaques may indicate iatrogenic transmission for CJD-MM cases without a type 2 Western blot fragment. The study results suggest the absence of significant misclassifications of iatrogenic CJD as sporadic. To our knowledge, this study is the first to describe grey matter kuru plaques in apparently sporadic CJD-MM patients with a type 2 Western blot fragment.
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P180 Clinico-pathological analysis of human prion diseases in a brain bank series
Ximelis T (1), Aldecoa I (1,2), Molina-Porcel L (1,3), Grau-Rivera O (4), Ferrer I (5), Nos C (6), Gelpi E (1,7), Sánchez-Valle R (1,4)
(1) Neurological Tissue Bank of the Biobanc-Hospital ClÃnic-IDIBAPS, Barcelona, Spain (2) Pathological Service of Hospital ClÃnic de Barcelona, Barcelona, Spain (3) EAIA Trastorns Cognitius, Centre Emili Mira, Parc de Salut Mar, Barcelona, Spain (4) Department of Neurology of Hospital ClÃnic de Barcelona, Barcelona, Spain (5) Institute of Neuropathology, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona (6) General subdirectorate of Surveillance and Response to Emergencies in Public Health, Department of Public Health in Catalonia, Barcelona, Spain (7) Institute of Neurology, Medical University of Vienna, Vienna, Austria.
Background and objective:
The Neurological Tissue Bank (NTB) of the Hospital Clínic-Institut d‘Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain is the reference center in Catalonia for the neuropathological study of prion diseases in the region since 2001. The aim of this study is to analyse the characteristics of the confirmed prion diseases registered at the NTB during the last 15 years.
Methods:
We reviewed retrospectively all neuropathologically confirmed cases registered during the period January 2001 to December 2016.
Results:
176 cases (54,3% female, mean age: 67,5 years and age range: 25-86 years) of neuropathological confirmed prion diseases have been studied at the NTB. 152 cases corresponded to sporadic Creutzfeldt-Jakob disease (sCJD), 10 to genetic CJD, 10 to Fatal Familial Insomnia, 2 to GerstmannSträussler-Scheinker disease, and 2 cases to variably protease-sensitive prionopathy (VPSPr). Within sCJD subtypes the MM1 subtype was the most frequent, followed by the VV2 histotype.
Clinical and neuropathological diagnoses agreed in 166 cases (94%). The clinical diagnosis was not accurate in 10 patients with definite prion disease: 1 had a clinical diagnosis of Fronto-temporal dementia (FTD), 1 Niemann-Pick‘s disease, 1 Lewy Body‘s Disease, 2 Alzheimer‘s disease, 1 Cortico-basal syndrome and 2 undetermined dementia. Among patients with VPSPr, 1 had a clinical diagnosis of Amyotrophic lateral sclerosis (ALS) and the other one with FTD.
Concomitant pathologies are frequent in older age groups, mainly AD neuropathological changes were observed in these subjects.
Discussion:
A wide spectrum of human prion diseases have been identified in the NTB being the relative frequencies and main characteristics like other published series. There is a high rate of agreement between clinical and neuropathological diagnoses with prion diseases. These findings show the importance that public health has given to prion diseases during the past 15 years. Continuous surveillance of human prion disease allows identification of new emerging phenotypes. Brain tissue samples from these donors are available to the scientific community. For more information please visit:
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P192 Prion amplification techniques for the rapid evaluation of surface decontamination procedures
Bruyere-Ostells L (1), Mayran C (1), Belondrade M (1), Boublik Y (2), Haïk S (3), Fournier-Wirth C (1), Nicot S (1), Bougard D (1)
(1) Pathogenesis and control of chronic infections, Etablissement Français du Sang, Inserm, Université de Montpellier, Montpellier, France. (2) Centre de Recherche en Biologie cellulaire de Montpellier, CNRS, Université de Montpellier, Montpellier, France. (3) Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Université Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.
Aims:
Transmissible Spongiform Encephalopathies (TSE) or prion diseases are a group of incurable and always fatal neurodegenerative disorders including Creutzfeldt-Jakob diseases (CJD) in humans. These pathologies include sporadic (sCJD), genetic and acquired (variant CJD) forms. By the past, sCJD and vCJD were transmitted by different prion contaminated biological materials to patients resulting in more than 400 iatrogenic cases (iCJD). The atypical nature and the biochemical properties of the infectious agent, formed by abnormal prion protein or PrPTSE, make it particularly resistant to conventional decontamination procedures. In addition, PrPTSE is widely distributed throughout the organism before clinical onset in vCJD and can also be detected in some peripheral tissues in sporadic CJD. Risk of iatrogenic transmission of CJD by contaminated medical device remains thus a concern for healthcare facilities. Bioassay is the gold standard method to evaluate the efficacy of prion decontamination procedures but is time-consuming and expensive. Here, we propose to compare in vitro prion amplification techniques: Protein Misfolding Cyclic Amplification (PMCA) and Real-Time Quaking Induced Conversion (RT-QuIC) for the detection of residual prions on surface after decontamination.
Methods:
Stainless steel wires, by mimicking the surface of surgical instruments, were proposed as a carrier model of prions for inactivation studies. To determine the sensitivity of the two amplification techniques on wires (Surf-PMCA and Surf-QuIC), steel wires were therefore contaminated with serial dilutions of brain homogenates (BH) from a 263k infected hamster and from a patient with sCJD (MM1 subtype). We then compared the different standard decontamination procedures including partially and fully efficient treatments by detecting the residual seeding activity on 263K and sCJD contaminated wires. We completed our study by the evaluation of marketed reagents endorsed for prion decontamination.
Results:
The two amplification techniques can detect minute quantities of PrPTSE adsorbed onto a single wire. 8/8 wires contaminated with a 10-6 dilution of 263k BH and 1/6 with the 10-8 dilution are positive with Surf-PMCA. Similar performances were obtained with Surf-QuIC on 263K: 10/16 wires contaminated with 10-6 dilution and 1/8 wires contaminated with 10-8 dilution are positive. Regarding the human sCJD-MM1 prion, Surf-QuIC allows us to detect 16/16 wires contaminated with 10-6 dilutions and 14/16 with 10-7 . Results obtained after decontamination treatments are very similar between 263K and sCJD prions. Efficiency of marketed treatments to remove prions is lower than expected.
Conclusions:
Surf-PMCA and Surf-QuIC are very sensitive methods for the detection of prions on wires and could be applied to prion decontamination studies for rapid evaluation of new treatments. Sodium hypochlorite is the only product to efficiently remove seeding activity of both 263K and sCJD prions.
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WA2 Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Schatzl HM (1, 2), Hannaoui S (1, 2), Cheng Y-C (1, 2), Gilch S (1, 2), Beekes M (3), SchulzSchaeffer W (4), Stahl-Hennig C (5) and Czub S (2, 6)
(1) University of Calgary, Calgary Prion Research Unit, Calgary, Canada (2) University of Calgary, Faculty of Veterinary Medicine, Calgary, Canada, (3) Robert Koch Institute, Berlin, Germany, (4) University of Homburg/Saar, Homburg, Germany, (5) German Primate Center, Goettingen, Germany, (6) Canadian Food Inspection Agency (CFIA), Lethbridge, Canada.
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were found in spinal cord and brain of euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and preclinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
See also poster P103
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
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WA16 Monitoring Potential CWD Transmission to Humans
Belay ED
Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA.
The spread of chronic wasting disease (CWD) in animals has raised concerns about increasing human exposure to the CWD agent via hunting and venison consumption, potentially facilitating CWD transmission to humans. Several studies have explored this possibility, including limited epidemiologic studies, in vitro experiments, and laboratory studies using various types of animal models. Most human exposures to the CWD agent in the United States would be expected to occur in association with deer and elk hunting in CWD-endemic areas. The Centers for Disease Control and Prevention (CDC) collaborated with state health departments in Colorado, Wisconsin, and Wyoming to identify persons at risk of CWD exposure and to monitor their vital status over time. Databases were established of persons who hunted in Colorado and Wyoming and those who reported consumption of venison from deer that later tested positive in Wisconsin. Information from the databases is periodically cross-checked with mortality data to determine the vital status and causes of death for deceased persons. Long-term follow-up of these hunters is needed to assess their risk of development of a prion disease linked to CWD exposure.
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P166 Characterization of CJD strain profiles in venison consumers and non-consumers from Alberta and Saskatchewan
Stephanie Booth (1,2), Lise Lamoureux (1), Debra Sorensen (1), Jennifer L. Myskiw (1,2), Megan Klassen (1,2), Michael Coulthart (3), Valerie Sim (4)
(1) Zoonotic Diseases and Special Pathogens, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg (2) Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg (3) Canadian CJD Surveillance System, Public Health Agency of Canada, Ottawa (4) Division of Neurology, Department of Medicine Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton.
Chronic wasting disease (CWD) is spreading rapidly through wild cervid populations in the Canadian provinces of Alberta and Saskatchewan. While this has implications for tourism and hunting, there is also concern over possible zoonotic transmission to humans who eat venison from infected deer. Whilst there is no evidence of any human cases of CWD to date, the Canadian CJD Surveillance System (CJDSS) in Canada is staying vigilant. When variant CJD occurred following exposure to BSE, the unique biochemical fingerprint of the pathologic PrP enabled a causal link to be confirmed. However, we cannot be sure what phenotype human CWD prions would present with, or indeed, whether this would be distinct from that see in sporadic CJD. Therefore we are undertaking a systematic analysis of the molecular diversity of CJD cases of individuals who resided in Alberta and Saskatchewan at their time of death comparing venison consumers and non-consumers, using a variety of clinical, imaging, pathological and biochemical markers. Our initial objective is to develop novel biochemical methodologies that will extend the baseline glycoform and genetic polymorphism typing that is already completed by the CJDSS. Firstly, we are reviewing MRI, EEG and pathology information from over 40 cases of CJD to select clinically affected areas for further investigation. Biochemical analysis will include assessment of the levels of protease sensitive and resistant prion protein, glycoform typing using 2D gel electrophoresis, testing seeding capabilities and kinetics of aggregation by quaking-induced conversion, and determining prion oligomer size distributions with asymmetric flow field fractionation with in-line light scattering. Progress and preliminary data will be presented. Ultimately, we intend to further define the relationship between PrP structure and disease phenotype and establish a baseline for the identification of future atypical CJD cases that may arise as a result of exposure to CWD.
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Source Prion Conference 2018 Abstracts
Volume 24, Number 8—August 2018 Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)
Abstract Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.
snip...
Discussion Characterization of the transmission properties of CWD and evaluation of their zoonotic potential are important for public health purposes. Given that CWD affects several members of the family Cervidae, it seems reasonable to consider whether the zoonotic potential of CWD prions could be affected by factors such as CWD strain, cervid species, geographic location, and Prnp–PRNP polymorphic variation. We have previously used an in vitro conversion assay (PMCA) to investigate the susceptibility of the human PrP to conversion to its disease-associated form by several animal prion diseases, including CWD (15,16,22). The sensitivity of our molecular model for the detection of zoonotic conversion depends on the combination of 1) the action of proteinase K to degrade the abundant human PrPC that constitutes the substrate while only N terminally truncating any human PrPres produced and 2) the presence of the 3F4 epitope on human but not cervid PrP. In effect, this degree of sensitivity means that any human PrPres formed during the PMCA reaction can be detected down to the limit of Western blot sensitivity. In contrast, if other antibodies that detect both cervid and human PrP are used, such as 6H4, then newly formed human PrPres must be detected as a measurable increase in PrPres over the amount remaining in the reaction product from the cervid seed. Although best known for the efficient amplification of prions in research and diagnostic contexts, the variation of the PMCA method employed in our study is optimized for the definitive detection of zoonotic reaction products of inherently inefficient conversion reactions conducted across species barriers. By using this system, we previously made and reported the novel observation that elk CWD prions could convert human PrPC from human brain and could also convert recombinant human PrPC expressed in transgenic mice and eukaryotic cell cultures (15).
A previous publication suggested that mule deer PrPSc was unable to convert humanized transgenic substrate in PMCA assays (23) and required a further step of in vitro conditioning in deer substrate PMCA before it was able to cross the deer–human molecular barrier (24). However, prions from other species, such as elk (15) and reindeer affected by CWD, appear to be compatible with the human protein in a single round of amplification (as shown in our study). These observations suggest that different deer species affected by CWD could present differing degrees of the olecular compatibility with the normal form of human PrP.
The contribution of the polymorphism at codon 129 of the human PrP gene has been extensively studied and is recognized as a risk factor for Creutzfeldt-Jakob disease (4). In cervids, the equivalent codon corresponds to the position 132 encoding methionine or leucine. This polymorphism in the elk gene has been shown to play an important role in CWD susceptibility (25,26). We have investigated the effect of this cervid Prnp polymorphism on the conversion of the humanized transgenic substrate according to the variation in the equivalent PRNP codon 129 polymorphism. Interestingly, only the homologs methionine homozygous seed–substrate reactions could readily convert the human PrP, whereas the heterozygous elk PrPSc was unable to do so, even though comparable amounts of PrPres were used to seed the reaction. In addition, we observed only low levels of human PrPres formation in the reactions seeded with the homozygous methionine (132 MM) and the heterozygous (132 ML) seeds incubated with the other 2 human polymorphic substrates (129 MV and 129 VV). The presence of the amino acid leucine at position 132 of the elk Prnp gene has been attributed to a lower degree of prion conversion compared with methionine on the basis of experiments in mice made transgenic for these polymorphic variants (26). Considering the differences observed for the amplification of the homozygous human methionine substrate by the 2 polymorphic elk seeds (MM and ML), reappraisal of the susceptibility of human PrPC by the full range of cervid polymorphic variants affected by CWD would be warranted.
In light of the recent identification of the first cases of CWD in Europe in a free-ranging reindeer (R. tarandus) in Norway (2), we also decided to evaluate the in vitro conversion potential of CWD in 2 experimentally infected reindeer (18). Formation of human PrPres was readily detectable after a single round of PMCA, and in all 3 humanized polymorphic substrates (MM, MV, and VV). This finding suggests that CWD prions from reindeer could be more compatible with human PrPC generally and might therefore present a greater risk for zoonosis than, for example, CWD prions from white-tailed deer. A more comprehensive comparison of CWD in the affected species, coupled with the polymorphic variations in the human and deer PRNP–Prnp genes, in vivo and in vitro, will be required before firm conclusions can be drawn. Analysis of the Prnp sequence of the CWD reindeer in Norway was reported to be identical to the specimens used in our study (2). This finding raises the possibility of a direct comparison of zoonotic potential between CWD acquired in the wild and that produced in a controlled laboratory setting. (Table).
The prion hypothesis proposes that direct molecular interaction between PrPSc and PrPC is necessary for conversion and prion replication. Accordingly, polymorphic variants of the PrP of host and agent might play a role in determining compatibility and potential zoonotic risk. In this study, we have examined the capacity of the human PrPC to support in vitro conversion by elk, white-tailed deer, and reindeer CWD PrPSc. Our data confirm that elk CWD prions can convert the human PrPC, at least in vitro, and show that the homologous PRNP polymorphisms at codon 129 and 132 in humans and cervids affect conversion efficiency. Other species affected by CWD, particularly caribou or reindeer, also seem able to convert the human PrP. It will be important to determine whether other polymorphic variants found in other CWD-affected Cervidae or perhaps other factors (17) exert similar effects on the ability to convert human PrP and thus affect their zoonotic potential.
Dr. Barria is a research scientist working at the National CJD Research and Surveillance Unit, University of Edinburgh. His research has focused on understanding the molecular basis of a group of fatal neurologic disorders called prion diseases.
Acknowledgments We thank Aru Balachandran for originally providing cervid brain tissues, Abigail Diack and Jean Manson for providing mouse brain tissue, and James Ironside for his critical reading of the manuscript at an early stage.
This report is independent research commissioned and funded by the United Kingdom’s Department of Health Policy Research Programme and the Government of Scotland. The views expressed in this publication are those of the authors and not necessarily those of the Department of Health or the Government of Scotland.
Author contributions: The study was conceived and designed by M.A.B. and M.W.H. The experiments were conducted by M.A.B. and A.L. Chronic wasting disease brain specimens were provided by G.M. The manuscript was written by M.A.B. and M.W.H. All authors contributed to the editing and revision of the manuscript.
Prion 2017 Conference Abstracts
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009.
21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS ABSTRACTS REFERENCE
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
SATURDAY, FEBRUARY 23, 2019
Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019
TUESDAY, NOVEMBER 04, 2014
Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011
Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
> However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven.
if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler ===============
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
snip...see full text;
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results regarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasized by the finding that some strains of scrapie produce lesions identical to the once which characterize the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the scrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
reference...
RB3.20
TRANSMISSION TO CHIMPANZEES
1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :
3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.
R. Bradley
23 September 1990
CVO (+Mr Wells' comments)
Dr T W A Little
Dr B J Shreeve
90/9.23/1.1.
http://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
IN CONFIDENCE CHIMPANZEES
CODE 18-77 Reference RB3.46
Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.
She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.
Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.
We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists or media. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.
The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.
I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.
Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.
CVO cc Dr T Dr B W A Little Dr B J Shreeve
R Bradley
26 September 1990
90/9.26/3.2
http://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf
this is tse prion political theater here, i.e. what i call TSE PRION POKER...tss
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.
snip...
PAGE 26
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province! ...page 26.
snip...see;
IN CONFIDENCE
PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASE OF ANIMALS IN THE USA
GAH WELLS
REPORT OF A VISIT TO THE USA
APRIL-MAY 1989
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man.
***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough.
***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
1985
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
THURSDAY, JANUARY 20, 2022
Wisconsin this month fortified its standing as the capital of the world for Chronic Wasting Disease CWD TSE PrP
WEDNESDAY, JANUARY 12, 2022
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA, what if?
MONDAY, DECEMBER 27, 2021
RT-QuIC detection of pathological prion protein in subclinical goats following experimental oral transmission of L-type BSE
MONDAY, JANUARY 17, 2022
Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie
WEDNESDAY, DECEMBER 8, 2021
Importation of Sheep, Goats, and Certain Other Ruminants AGENCY: Animal APHIA, USDA, FINAL RULE [Docket No. APHIS–2009–0095] RIN 0579–AD10
wtf are they thinking, $$$, that's all they are thinking...terry
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
12:42 PM
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