Maryland DNR reported that 53 WTD sampled within Allegany and Washington counties in 2021 tested positive for chronic wasting disease CWD
Maryland DNR reported that 53 WTD sampled within Allegany and Washington counties in 2021 tested positive for chronic wasting disease CWD
Chronic Wasting Disease Detected in 53 Deer in Western Maryland
May 18, 2022
Positive Samples Were Entirely Within Existing Management Area
Map of chronic wasting disease management area in Allegany and Washington counties
The Maryland Department of Natural Resources reported that 53 white-tailed deer sampled within Allegany and Washington counties in 2021 tested positive for chronic wasting disease, a neurodegenerative disease found in deer and elk. All of Maryland’s positive samples were found within the existing Chronic Wasting Disease Management Area.
“Chronic wasting disease continues to spread both regionally and nationally, and we continue to monitor this disease using the best science available to minimize the impact on our deer population and this valuable resource,” Wildlife and Heritage Service Director Paul Peditto said.
Since 1999, the department has tested more than 11,500 deer for chronic wasting disease. A total of 710 samples were collected in 2021 from Allegany, Frederick, Garrett, Montgomery, and Washington counties. Despite the increasing occurrence of positive cases within Allegany and Washington counties, to date, chronic wasting disease has not been detected outside of the existing Chronic Wasting Disease Management Area.
Chronic wasting disease was first confirmed in Maryland in February 2011. Since then, Maryland, Pennsylvania, Virginia, and West Virginia have all documented chronic wasting disease in the region. The latest findings bring the number of positive cases in Maryland to 133. The 2021 sampling marks an increase in cases, but Maryland’s positive sampling remains lower compared to other states in the region.
Concerns about chronic wasting disease should not stop anyone from hunting deer or enjoying venison. Research suggests the disease cannot be naturally transmitted to humans. However, as a general safety precaution, it is recommended that hunters avoid consuming the meat of sick animals, as well as the brain, lymph nodes, or spinal column of any deer — all of which are normally removed during the butchering process.
More information on chronic wasting disease in Maryland is available on the DNR website. Anyone with questions may contact the department at 410-260-8540.
https://news.maryland.gov/dnr/2022/05/18/chronic-wasting-disease-detected-in-53-deer-in-western-maryland/
see Maryland CWD;
https://dnr.maryland.gov/wildlife/Pages/hunt_trap/CWD_in_Maryland.aspx
Chronic Wasting Disease (CWD) In Maryland Maryland Deer Hunters' Attitudes Toward Chronic Wasting Disease
Maryland’s Chronic Wasting Disease Response Plan
What is CWD?
Chronic Wasting Disease (CWD) is a fatal neurological disease of deer, moose and elk, including white-tailed deer and mule deer. The disease causes degeneration of the brain and eventual death. In the early stages of the disease, an infected animal may not show any signs that it is sick. As the disease progresses, animals will show signs of weight loss, generally accompanied by behavioral changes. In later stages, affected animals may show emaciation, excessive drooling, increased drinking and urination, listlessness, stumbling, trembling, loss of fear of humans and nervousness.
CWD is not caused by a bacteria or virus. It is classified as a prion disease. A prion is an altered protein that causes other normal proteins to change and cause sponge-like holes in the brain. CWD is related to, but different from, scrapie in sheep, Bovine Spongiform Encephalopathy (BSE or mad cow disease) in cattle and Creutzfelt-Jacob Disease (CJD) in humans. These diseases also attack the brain and cause deterioration and eventual death. CWD was first identified in the 1960s in a Colorado research facility and since that time has been found in multiple states and Canadian provinces. It is unknown whether sika deer are susceptible to CWD.
CWD appears to be passed between animals via saliva and possibly feces and urine. Animals can also become infected through direct contact with an environment (i.e., soils) that is contaminated with the prions. At this time it is unclear whether transmission between females and their fetuses (maternal transmission) can occur. CWD may be transmitted more readily within overpopulated herds and at feeding stations where direct physical contact among individuals is more likely. There is currently no evidence that CWD is transmissible to humans. Public health officials recommend that human exposure to CWD be avoided and recommend not consuming venison from infected deer. There are basic precautions, outlined below, that hunters should take to minimize any risk associated with CWD.
Status of CWD in Maryland
The Department of Natural Resources has tested 11,592 deer for CWD since 1999. The disease was detected for the first time in Maryland from a deer taken by a hunter in November 2010. To date, 133 infected deer have been documented in the state.
In Allegany County, sixty-six of the deer originated in Harvest Management Unit 233, including three on Billmeyer Wildlife Management Area, twenty-two on Green Ridge State Forest, and one on Sideling Hill Wildlife Management Area. Twenty-two positive deer have been detected in Allegany County Harvest Management Unit 231 near Cumberland, and eight have been detected in Harvest Management Unit 232, including one on Warrior Mountain Wildlife Management Area.
In Washington County, twenty-two positive deer have been detected in Harvest Management Unit 250, including three on Woodmont Natural Resources Management Area and one on Sideling Hill Wildlife Management Area. Ten positive deer have been found in Washington County Harvest Management Unit 251, including one on Indian Springs Wildlife Management Area. Five have been found in Harvest Management Unit 252.
Number of White-tailed Deer that have Tested Positive for Chronic Wasting Disease by Harvest Management Unit (HMU) in Maryland, 2010 – 2021.
County HMU Number Positive
Allegany 230 0
231 22
232 8
233 66
234 0
Washington 250 22
251 10
252 5
Total 133
* White-tailed deer harvested on public lands are included in the appropriate private land HMU code.
The department has been testing deer for CWD with increasing intensity since 1999. Initially, only deer that appeared to have classic CWD symptoms were tested. Beginning in 2002, the department began more intensive sampling and collected samples from deer in all counties of the state. In 2010, sampling efforts were focused on Allegany and western Washington counties due to the presence of positive cases in nearby West Virginia and Virginia. West Virginia first detected CWD in Hampshire County in 2005 and it was found in Frederick County, Virginia in early 2010. Pennsylvania documented a deer positive for CWD in 2012.
Sampling is conducted on road-kills and deer brought by hunters to cooperating deer processors. Staff remove the brain stem and certain lymph nodes and those tissues are sent to a laboratory for testing. Any samples that test positive by the first lab are then sent to the USDA National Veterinary Services Laboratories for confirmation. This testing takes several months to complete. Positive samples are traced back to the hunter that harvested the deer.
The Maryland Department of Agriculture, Maryland Department of Health & Mental Hygiene, the Southeastern Cooperative Wildlife Disease Study, and the United States Department of Agriculture are integral partners in all CWD surveillance plans to assist in monitoring wild deer populations, protect domestic animals and preserve human health.
Deer Hunters and CWD
Concerns over CWD should not stop hunters from enjoying the hunting season or any venison they may acquire. CWD has not been shown to be transmissible to humans. However, it is recommended that hunters field-dressing or butchering deer should take the same precautions as they would to protect against other pathogens or diseases. It is also recommended to not consume venison from infected deer.
The following common-sense precautionary measures are recommended for the safe handling, field-dressing and home processing of venison:
Avoid shooting or handling a deer that appears sick.
Wear latex or rubber gloves when field-dressing or butchering deer.
Remove all internal organs.
Remove the meat from the bones and spinal column if home processing a deer
Do not use household knives or utensils when field-dressing or home processing a deer.
Avoid cutting through bones or the spinal column (backbone).
If you saw off antlers or through a bone, or if you sever the spinal column with a knife, be sure to disinfect these tools prior to using them for the butchering or removal of meat.
Always wash hands and instruments thoroughly after dressing and processing game meat.
Use a 50/50 solution of household chlorine bleach and water to disinfect tools and work surfaces. Wipe down counters and let them dry; soak knives for one hour.
Deer Urine Lures and CWD
Recent research has shown that deer urine can contain infected prions. Until more is known about whether commercial deer lures pose a realistic risk of spreading CWD, we recommend that hunters use caution when placing natural urine-based lures in the environment and suggest the following:
Whenever possible, avoid using natural urine lures and instead use synthetic lures. Research has shown synthetic lures to be as effective as natural lures. Hunters should avoid placing deer lures on the ground or on vegetation where deer can come into contact with them. Deer lures can be safely placed above deer height, yet still allow air currents to disperse the scent and attract deer.
Hunters should not place urine-based lures on their skin or clothing.
CWD Management
Due to the detection of CWD in Allegany and Washington counties, the department has created a Chronic Wasting Disease Management Area (CWDMA) to help slow the spread of the disease. The current CWDMA (see map below) consists of all public and private lands in Allegany and Washington counties. Currently, whole deer carcasses cannot be transported out of the CWDMA unless they are transported to an approved processor or taxidermist (see below).
Whole deer carcasses or deer parts cannot be transported out of the CWDMA, except for:
Meat with no part of the spinal column, backbone, or head attached,
Hind quarters and front shoulders with no spinal column or backbone attached, (hunters MUST have checked in their deer and obtained a confirmation number in order to transport a quartered deer)
Cleaned hide with no head attached,
Skull plate cleaned of all meat and brain tissue,
Antlers with no meat or soft tissue attached,
Finished taxidermy mounts or tanned hides,
Whole deer carcasses or parts being transported directly to the meat processors or taxidermists listed below, or to the landfill located within Allegany or Washington County.
Currently, the following taxidermists and meat processors are approved to prepare or process deer carcasses or deer parts taken from within Maryland’s CWDMA. This provision provides an opportunity for hunters harvesting deer within Maryland’s CWDMA to transport carcasses or other deer parts directly to one of these approved businesses for meat processing, taxidermy services or for preparation for transport to another taxidermist.
If you choose to quarter your deer in the field, it is permissible to leave the carcass remains at the kill site when hunting on Department of Natural Resources public lands. Hunters should obtain permission when hunting on private lands. Whenever possible, the department encourages hunters to bag the remains and dispose of them in a landfill. It is not permissible to leave or dispose of carcass remains in public parking areas, along roadways or near other public use areas.
Meat Processors
Allegany County
- B&B Country Meats, Frostburg, MD, 301-689-6225
- B&B Butchering, Orleans, MD, 301-478-2558
Washington County
- Banzhoff’s Custom Butchering, Williamsport, 301-223-9326
- Ernst Market, Clear Spring, MD, 301-842-2292
- Holsinger's Meats and Deli, Maugansville, MD, 301-733-9263
- Leitersburg Butcher Shop, Hagerstown, MD, 301-491-9911
- Mountain Trail Butchers, Clear Spring, 301-842-1407
- Sunnyland/Ray Burger's Meats, Williamsport, MD, 301-223-9637
- Wolford’s Meat Shop, Big Pool, 301-842-3156
Frederick County
- Clint’s Cuts, Mt. Airy, 301-865-5120
- KD Deer Processing, Frederick, 240-285-6143
- Pry's Deer Processing, Knoxville, 301-834-8752
- Rob’s Deer Shop, Rocky Ridge, 301-271-7780
- Wolfe's Deer Shop, Thurmont, MD, 240-549-2613
Taxidermists
Allegany County
- Brian McKinley, Cumberland, 240-580-4148
- Donnie Burley, Cumberland, 301-707-6272
- Richard Kroll, Barton, 301-359-5010
- Robert Friend, Westernport, 301-359-9784
- Steven Fairgrieve, Barton, 301-707-9261
Washington County
- Draper's Taxidermy, Fairplay, 301-582-3173
- Fairview Wildlife Studio, Hagerstown, 301-791-1568
- Kaetzel's Taxidermy, Smithsburg, 301-667-2495
- Kline’s Taxidermy, Smithsburg, 301-416-0201
- Martin's Taxidermy Studio, Boonsboro, 301-432-5909
- Millstone Taxidermy, Hancock, 240-520-7226
- Mountin' Man Taxidermy, Knoxville, MD, 301-834-5197
- Quirauk Mountain Skull Works, Cascade, 301-331-6916
- South Mountain Taxidermy, Boonsboro, 301-432-6006
Frederick County
- Baker Taxidermy, Frederick, 240-674-2752
- Brian Keane Taxidermy, Frederick, 301-682-9210
- Carder's Taxidermy, Ijamsville, 240-674-9146
- Geisinger Taxidermy, Thurmont, 301-271-0501
- Natalie's Taxidermy, Myersville, 240-315-3471
- Roger's Taxidermy, Thurmont, 301-606-7015
- Young's Wildlife, Frederick, 301-788-3860
Please note: Due to the significant enlargement of the CWDMA, dumpsters will no longer be furnished for carcass disposal. Carcasses can either be quartered in the field, taken to an approved processor or taxidermist listed above, or disposed of at the Allegany or Washington County landfill for a fee. Whole carcasses are still permitted to be transported freely about within the CWDMA to private residences, hunting camps, etc.
Please also check the department website for updates on CWD surveillance and management in Maryland. Hunter assistance and cooperation is essential to the department’s efforts to monitor and manage CWD in Maryland. 2022 Chronic Wasting Disease Management Area Map
2020 Chronic Wasting Disease Map for Maryland
Carcass Importation Ban
The primary objective in the management of CWD is to prevent or slow its spread into new areas. One possible mode of disease transmission is by the movement and disposal of infected carcasses. In an effort to minimize the risk for disease spread, Maryland, along with many other states, has adopted regulations that prohibit the importation of whole carcasses and certain carcass parts of deer, moose and elk harvested from states that have CWD.
A person may bring only the following parts of a dead deer, elk, or moose into Maryland from another state or province’s designated CWD containment, surveillance, or management area: (1) meat with no part of the spinal column or head attached; (2) hind quarters and front shoulders with no spinal column or backbone attached; (3) meat without backbone; (4) cleaned hide with no head attached; (5) skull plate cleaned of all meat and brain tissue; (6) antlers with no meat or soft tissue attached; (7) upper canine teeth, also known as buglers, whistlers, or ivories; and (8) finished taxidermy mounts or tanned hides.
Importation of whole deer, elk, moose or other cervid carcasses is prohibited from CWD positive areas identified within the states and provinces listed in the link below. To get the latest information on CWD positive areas in any of these states or provinces call the number listed or go to www.cwd-info.org
Any person who imports or possesses a cervid carcass or part of a cervid that was tested for chronic wasting disease in another state or province and is notified that the cervid tested positive, must report the test results to the Maryland Department of Natural Resources within 24 hours of receiving such notification- by telephone at 301-334-4255 or by email to jonathank.trudeau@maryland.gov.
Travelers may pass through Maryland with cervid carcasses, provided that no parts are disposed of or remain in the state.
If you hunt deer, elk, moose or other cervids in other states and/or provinces, particularly those in which CWD has been detected, check with the respective fish and wildlife agencies regarding special regulations or specific advice for hunters. Also check with your home state fish and wildlife agency to ensure that animals lawfully killed elsewhere may be imported and possessed in your state. Additional information can be found at the CWD Alliance website www.cwd-info.org
Taking Deer Carcasses out of Maryland
Because Maryland is considered a CWD positive state, deer hunters must follow carcass importation regulations in other states when they transport a deer carcass out of Maryland (see www.cwd-info.org).
The surrounding states of Delaware, Pennsylvania, Virginia, and West Virginia each have specific regulations as to whether they will allow whole deer carcasses or only parts of carcasses to enter from Maryland. Likewise, the regulations for each of these states vary as to whether they apply to deer from anywhere in Maryland, or just to deer taken within the CWDMA. Hunters are strongly encouraged to check state regulations before transporting deer carcasses.
Travelers may pass through Maryland with cervid carcasses, provided that no parts are disposed of or remain in the state.
How You Can Help
You can help by reporting any deer that are emaciated, unhealthy or acting abnormally to the by calling 410-260-8540. You can also help by cooperating if department staff ask permission to collect brain tissue samples from deer you harvested.
https://dnr.maryland.gov/wildlife/Pages/hunt_trap/CWD_in_Maryland.aspx
Maryland Passes On CWD Testing During The 2020-2021 Hunting Seasons, Chooses To Play Prion Poker Instead
Maryland Passes On CWD TSE Prion Testing During The 2020-2021 Hunting Seasons
Maryland passes on CWD testing
Jan 27, 2021
Citing COVID-19 protocols, the Maryland Wildlife and Heritage Service, an arm of the Department of Natural Resources, chose to forego sampling of hunter-harvested deer for chronic wasting disease during the 2020-2021 hunting seasons.
“Due to safety protocols designed to prevent spread of COVID-19, and protect our staff and the public, DNR was unable during 2020-21 to collect the random, hunter-harvest chronic wasting disease samples that are part of the normal disease monitoring protocol,” an agency spokesman said in an email. “We do however continue to take samples from any sick deer that are reported to us by the public, when it is safe to do so. We will resume normal sample collection in the fall deer season provided it is safe to do so.”
This decision leaves the agency with a gap in sampling data and marks the first year such testing has not taken place since the presence of the fatal disease was discovered in 2010. The first West Virginia case was known in 2005 and came from Hampshire County.
All told, about 10,000 Maryland deer have been sampled during that time frame with 80 turning up positive for CWD. During the 2019-2020 seasons, 706 deer were sampled and 28 were positive.
CWD presence is concentrated in the eastern portion of Allegany County and the western portion of Washington County. It has not been confirmed west of Cumberland or east of Washington County.
As part of deer management, WHS divides private lands in the state into Hunting Management Units. The numbers assigned to those units can be seen in the illustration accompanying this column. Public hunting lands, such as state forests and wildlife management areas, are given separate numbers, even though they lie within a unit encompassing private land.
For example, the Billmeyer Wildlife Management Area is HMU 243, but exists within the borders of HMU 233.
Considering that, here are where the 80 deer with CWD have turned up: HMU 231 – 12 deer; HMU 232 – 3; HMU 233 – 27; HMU 242 (Green Ridge State Forest) – 15; HMU 243 (Billmeyer Wildlife Management Area) – 3; HMU 246 (Sideling Hill Wildlife Management Area) – 1; HMU 250 – 13; HMU 251 – 4; HMU 252 – 1; HMU 267 (Woodmont Natural Resources Management Area) – 1.
snip...see full text;
''the Maryland Wildlife and Heritage Service, an arm of the Department of Natural Resources, chose to forego sampling of hunter-harvested deer for chronic wasting disease during the 2020-2021 hunting seasons.''
this is terrible news, cwd tse prion will not go anywhere while Maryland flounders, CWD will just continue to amplify and multiply, and it will be there in full force when Maryland finally gets back to testing for cwd. seems to be just another game of CWD Prion Poker, and when you play Prion Poker, you lose. ...terry
FRIDAY, OCTOBER 09, 2020
Maryland detects additional 28 positives from last year's CWD TSE Prion sampling, total stands at 80 confirmed cases to date
TUESDAY, MAY 28, 2019
Maryland Chronic Wasting Disease Detected in 25 Deer
WEDNESDAY, FEBRUARY 21, 2018
Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties
SATURDAY, MARCH 04, 2017
Maryland DNR Six Deer Test Positive for Chronic Wasting Disease
TUESDAY, MARCH 29, 2016
Maryland Department of Natural Resources Five Deer Test Positive for Chronic Wasting Disease ONE OUTSIDE CWD MANAGEMENT ZONE
SUNDAY, NOVEMBER 27, 2011
Chronic Wasting Disease Found In A White-Tailed Deer In Maryland
Thursday, February 10, 2011
Chronic Wasting Disease Found In A White-Tailed Deer In Maryland
Chronic Wasting Disease CWD TSE Prion of Cervid
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION MAD COW TYPE DISEASE
THE tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
MONDAY, APRIL 19, 2021
Evaluation of the application for new alternative biodiesel production process for rendered fat including Category 1 animal by-products (BDI-RepCat® process, AT) ???
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!
QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !
FRIDAY, APRIL 30, 2021
Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems...
Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years
Published: May 9, 2007
snip...
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
snip...
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
***> 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.
KOREA CWD UPDATE 2022
FRIDAY, MARCH 18, 2022
Korea Chronic Wasting Disease CWD TSE PrP Update Increase of Positive Cases and Polymorphisms of the prion-related protein gene
IN 235 elks, 22 elks (9.4%) were infected with CWD.
IN 257 red deer, 78 red deer (30.4%) were infected with CWD.
IN 150 sika deer, 16 sika deer (10.7%) were infected with CWD.
***> 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.
Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).
Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document
Pathogens. 2020 Apr; 9(4): 311.
Published online 2020 Apr 23. doi: 10.3390/pathogens9040311
PMCID: PMC7238116
PMID: 32340296
Long-Term Incubation PrPCWD with Soils Affects Prion Recovery but Not Infectivity
Alsu Kuznetsova,1 Debbie McKenzie,2 Catherine Cullingham,3 and Judd M. Aiken1,*
Abstract
Chronic wasting disease (CWD) is a contagious prion disease of cervids. The infectious agent is shed from animals at the preclinical and clinical stages of disease where it persists in the environment as a reservoir of CWD infectivity. In this study, we demonstrate that long-term incubation of CWD prions (generated from tg-mice infected with deer or elk prions) with illite, montmorillonite (Mte) and whole soils results in decreased recovery of PrPCWD, suggesting that binding becomes more avid and irreversible with time. This continual decline of immunoblot PrPCWD detection did not correlate with prion infectivity levels. Bioassay showed no significant differences in incubation periods between mice inoculated with 1% CWD brain homogenate (BH) and with the CWD-BH pre-incubated with quartz or Luvisolic Ae horizon for 1 or 30 weeks. After 55 weeks incubation with Chernozem and Luvisol, bound PrPCWD was not detectable by immunoblotting but remained infectious. This study shows that although recovery of PrPCWD bound to soil minerals and whole soils with time become more difficult, prion infectivity is not significantly altered. Detection of prions in soil is, therefore, not only affected by soil type but also by length of time of the prion–soil interaction.
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4. Conclusions
The binding of prions to soil minerals and other soil constituents impacts PrPCWD recovery. During extended incubation with soils, PrP signal on immunoblots continuously declined until it was no longer detectable after 25 weeks in soils with loamy-clay texture and Mte minerology. PrPCWD infectivity did not, however, decrease after 30 weeks incubation with quartz and the Luvisolic Ae soil horizon. At 55 weeks incubation in Chernozem and Luvisol, CWD-BH remained infectious. We studied a wide variety of soil types (from prairie, mountain and boreal regions) and showed decreased PrPCWD signal recovery (as measured by immunoblotting) with retention of infectivity. The decrease in PrPCWD recovery was particularly dramatic in soils from the prairie region. Regardless of soil minerology, texture and humus content, detection of PrPCWD in environmental soil samples is a challenge after long-term incubation. These findings provide important information on the behavior of prions in natural environments, but complicate analysis of environmental samples.
Keywords: prion protein, soil, CWD, prolonged incubation, CWD infectivity, prion detection
Prion. 2012 Jul 1; 6(3): 302–308. doi: 10.4161/pri.20025 PMCID: PMC3399538 PMID: 22561162
Temperature influences the interaction of ruminant PrPTSE with soil
Ben C. Maddison, 1 Jonathan P. Owen, 1 Maged A. Taema, 2 George Shaw, 3 and Kevin C. Gough 2 , *
Abstract
Ovine scrapie and cervid chronic wasting disease can be transmitted in the absence of animal-to-animal contact, and environmental reservoirs of infectivity have been implicated in their spread and persistence. Investigating environmental factors that influence the interaction of disease-associated PrP with soils is imperative to understanding what is likely to be the complex role of soil in disease transmission. Here, we describe the effects of soil temperature on the binding/desorption and persistence of both ovine scrapie- and bovine BSE-PrPTSE. Binding of PrPTSE to a sandy loam soil at temperatures of 4°C, 8–12°C and 25–30°C demonstrated that an increase in temperature resulted in (1) a decrease in the amount of PrPTSE recovered after 24 h of interaction with soil, (2) an increase in the amount of N-terminal cleavage of the prion protein over 11 d and (3) a decrease in the persistence of PrPTSE on soil over an 18 mo period.
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In the present study we investigated the effects of soil temperature in the range 4°C to 30°C on the interaction of BSE- and scrapie-PrPTSE with a complex soil matrix. Lower soil temperatures resulted in increased levels of PrPTSE recovery and persistence over an 18-mo incubation period. A low soil temperature also resulted in less cleavage of the N-terminal domain of PrPTSE after an 11-d interaction. These effects of temperature on PrPTSE-soil interaction were likely to be exerted through both microbial activity and abiotic cleavage mechanisms. Together, the data indicate that for the recoverable fraction of PrPTSE, soils at lower temperature may release increased levels of PrPTSE.
A recent study using transmissible mink encephalopathy reported a correlation between the level of desorption of PrPTSE from soil and the infectivity titer of the sample.25 If such a correlation is also true for ovine scrapie and bovine BSE, the data presented here indicate that the bioavailability of prions in soil for the environmental transmission of scrapie or BSE may be influenced by the temperature of the soil. However, it remains to be seen whether the reported influence of temperature on prion interaction with a sandy-loam soil is consistent with other soil types. Of course, it should also be considered that temperature would be just one of a range of factors influencing the bioavailability of prions from soil; other factors would likely include soil type, prion strain and the biological matrix of the prion source. Scrapie and CWD are known to be spread by environmental routes and therefore understanding the range of factors that influence the persistence of environmental prions is vital in developing eradication programmes.
Keywords: BSE, environment, prion, scrapie, soil, transmission
Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
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***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
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Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
source reference Prion Conference 2015 abstract book
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
Sandra Pritzkow,1 Rodrigo Morales,1 Fabio Moda,1,3 Uffaf Khan,1 Glenn C. Telling,2 Edward Hoover,2 and Claudio Soto1, * 1Mitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, 6431 Fannin Street, Houston, TX 77030, USA
2Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA
3Present address: IRCCS Foundation Carlo Besta Neurological Institute, 20133 Milan, Italy *Correspondence: claudio.soto@uth.tmc.edu http://dx.doi.org/10.1016/j.celrep.2015.04.036
SUMMARY
Prions are the protein-based infectious agents responsible for prion diseases. Environmental prion contamination has been implicated in disease transmission. Here, we analyzed the binding and retention of infectious prion protein (PrPSc) to plants. Small quantities of PrPSc contained in diluted brain homogenate or in excretory materials (urine and feces) can bind to wheat grass roots and leaves. Wild-type hamsters were efficiently infected by ingestion of prion-contaminated plants. The prion-plant interaction occurs with prions from diverse origins, including chronic wasting disease. Furthermore, leaves contaminated by spraying with a prion-containing preparation retained PrPSc for several weeks in the living plant. Finally, plants can uptake prions from contaminated soil and transport them to aerial parts of the plant (stem and leaves). These findings demonstrate that plants can efficiently bind infectious prions and act as carriers of infectivity, suggesting a possible role of environmental prion contamination in the horizontal transmission of the disease.
INTRODUCTION
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DISCUSSION
This study shows that plants can efficiently bind prions contained in brain extracts from diverse prion infected animals, including CWD-affected cervids. PrPSc attached to leaves and roots from wheat grass plants remains capable of seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc naturally excreted in urine and feces from sick hamster or cervids was enough to efficiently contaminate plant tissue. Indeed, our results suggest that the majority of excreted PrPSc is efficiently captured by plants’ leaves and roots. Moreover, leaves can be contaminated by spraying them with a prion-containing extract, and PrPSc remains detectable in living plants for as long as the study was performed (several weeks). Remarkably, prion contaminated plants transmit prion disease to animals upon ingestion, producing a 100% attack rate and incubation periods not substantially longer than direct oral administration of sick brain homogenates.
Finally, an unexpected but exciting result was that plants were able to uptake prions from contaminated soil and transport them to aerial parts of the plant tissue. Although it may seem farfetched that plants can uptake proteins from the soil and transport it to the parts above the ground, there are already published reports of this phenomenon (McLaren et al., 1960; Jensen and McLaren, 1960;Paungfoo-Lonhienne et al., 2008). The high resistance of prions to degradation and their ability to efficiently cross biological barriers may play a role in this process. The mechanism by which plants bind, retain, uptake, and transport prions is unknown. We are currently studying the way in which prions interact with plants using purified, radioactively labeled PrPSc to determine specificity of the interaction, association constant, reversibility, saturation, movement, etc.
Epidemiological studies have shown numerous instances of scrapie or CWD recurrence upon reintroduction of animals on pastures previously exposed to prion-infected animals. Indeed, reappearance of scrapie has been documented following fallow periods of up to 16 years (Georgsson et al., 2006), and pastures were shown to retain infectious CWD prions for at least 2 years after exposure (Miller et al., 2004). It is likely that the environmentally mediated transmission of prion diseases depends upon the interaction of prions with diverse elements, including soil, water, environmental surfaces, various invertebrate animals, and plants.
However, since plants are such an important component of the environment and also a major source of food for many animal species, including humans, our results may have far-reaching implications for animal and human health. Currently, the perception of the riskfor animal-to-human prion transmission has beenmostly limited to consumption or exposure to contaminated meat; our results indicate that plants might also be an important vector of transmission that needs to be considered in risk assessment.
ACCEPTED MANUSCRIPT
Genotype by Environment Interactions for Chronic Wasting Disease in Farmed U.S. White-tailed Deer
Christopher M Seabury, Mitchell A Lockwood, Tracy A Nichols G3 Genes|Genomes|Genetics, jkac109,
Published: 10 May 2022
Abstract
Despite implementation of enhanced management practices, chronic wasting disease (CWD) in U.S. white-tailed deer (Odocoileus virginianus; hereafter WTD) continues to expand geographically. Herein, we perform the largest genome-wide association analysis (GWAA) to date for CWD (n = 412 CWD-positive; n = 758 CWD-non-detect) using a custom Affymetrix Axiom® single nucleotide polymorphism (SNP) array (n = 121,010 SNPs), and confirm that differential susceptibility to CWD is a highly heritable (h2 = 0.611 ± 0.056) polygenic trait in farmed U.S. WTD, but with greater trait complexity than previously appreciated. We also confirm PRNP codon 96 (G96S) as having the largest-effects on risk (P ≤ 3.19E-08; Phenotypic Variance Explained ≥ 0.025) across three U.S. regions (Northeast, Midwest, South). However, 20 CWD-positive WTD possessing codon 96SS genotypes were also observed, including one that was lymph node and obex positive. Beyond PRNP, we also detected 23 significant SNPs (P-value ≤ 5E-05) implicating ≥ 24 positional candidate genes; many of which have been directly implicated in Parkinson’s, Alzheimer’s and prion diseases. Genotype-by-environment (GxE) interaction GWAA revealed a SNP in the lysosomal enzyme gene ARSB as having the most significant regional heterogeneity of effects on CWD (P ≤ 3.20E-06); with increasing copy number of the minor allele increasing susceptibility to CWD in the Northeast and Midwest; but with opposite effects in the South. In addition to ARSB, 38 significant GxE SNPs (P-value ≤ 5E-05) were also detected, thereby implicating ≥ 36 positional candidate genes; the majority of which have also been associated with aspects of Parkinson’s, Alzheimer’s and prion diseases.
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Conclusions
Herein, we perform the largest GWAA to date for CWD in WTD, thereby further confirming that differential susceptibility to CWD is a highly heritable, polygenic trait in farmed U.S. WTD, but with greater overall complexity than previously postulated or reported; as evidenced by significant GxE interactions, the general paucity of moderate or large-effect SNPs, and conversely, the large number of SNPs displaying small effects on risk.
We also confirm PRNP codon 96 as the largest-effect region of the WTD genome across three U.S. regions (Northeast, Midwest, South).
However, the proportion of phenotypic variance explained (PVE) by PRNP SNPs alone cannot be expected to facilitate a successful CWD eradication program, as further evidenced by 20 CWD positive WTD possessing the codon 96SS genotype enrolled in the present study; including one that was both lymph node and obex positive.
Finally, we provide the first evidence linking naturally occurring genetic variation in a lysosomal GAG catabolism gene (ARSB) to differences in CWD susceptibility in farmed U.S. WTD, but also further confirm the involvement of genes underlying other neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and various prion diseases of mammals, including scrapie and sporadic CJD.
Data availability Accession codes are as follows: Data (DRYAD: https://doi.org/10.5061/dryad.wh70rxwnt). ;
White-tailed Deer, Chronic Wasting Disease, GxE Interaction, GWAA, PRNP Issue Section: Investigation
Published: 07 October 2021
Review on PRNP genetics and susceptibility to chronic wasting disease of Cervidae
Katayoun Moazami-Goudarzi, Olivier Andréoletti, Jean-Luc Vilotte & Vincent Béringue
Veterinary Research volume 52, Article number: 128 (2021) Cite this article
Abstract
To date, chronic wasting disease (CWD) is the most infectious form of prion disease affecting several captive, free ranging and wild cervid species. Responsible for marked population declines in North America, its geographical spread is now becoming a major concern in Europe. Polymorphisms in the prion protein gene (PRNP) are an important factor influencing the susceptibility to prions and their rate of propagation. All reported cervid PRNP genotypes are affected by CWD. However, in each species, some polymorphisms are associated with lower attack rates and slower progression of the disease. This has potential consequences in terms of genetic selection, CWD diffusion and strain evolution. CWD also presents a zoonotic risk due to prions capacity to cross species barriers. This review summarizes our current understanding of CWD control, focusing on PRNP genetic, strain diversity and capacity to infect other animal species, including humans.
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CWD positive animals with extended time before they succumb to disease likely represent a source of chronic prion shedding within populations and may contribute to environmental contamination.
***> CWD positive animals with extended time before they succumb to disease likely represent a source of chronic prion shedding within populations and may contribute to environmental contamination. <***
Genes (Basel) . 2021 Sep 10;12(9):1396. doi: 10.3390/genes12091396.
Selective Breeding for Disease-Resistant PRNP Variants to Manage Chronic Wasting Disease in Farmed Whitetail Deer
Nicholas Haley 1, Rozalyn Donner 1, Kahla Merrett 1, Matthew Miller 1, Kristen Senior 1
Affiliations expand
PMID: 34573378 DOI: 10.3390/genes12091396
Abstract
Chronic wasting disease (CWD) is a fatal transmissible spongiform encephalopathy (TSE) of cervids caused by a misfolded variant of the normal cellular prion protein, and it is closely related to sheep scrapie. Variations in a host's prion gene, PRNP, and its primary protein structure dramatically affect susceptibility to specific prion disorders, and breeding for PRNP variants that prevent scrapie infection has led to steep declines in the disease in North American and European sheep. While resistant alleles have been identified in cervids, a PRNP variant that completely prevents CWD has not yet been identified. Thus, control of the disease in farmed herds traditionally relies on quarantine and depopulation. In CWD-endemic areas, depopulation of private herds becomes challenging to justify, leading to opportunities to manage the disease in situ. We developed a selective breeding program for farmed white-tailed deer in a high-prevalence CWD-endemic area which focused on reducing frequencies of highly susceptible PRNP variants and introducing animals with less susceptible variants. With the use of newly developed primers, we found that breeding followed predictable Mendelian inheritance, and early data support our project's utility in reducing CWD prevalence. This project represents a novel approach to CWD management, with future efforts building on these findings.
Keywords: CWD; PRNP; deer; prion; resistance; selective breeding; susceptibility.
***> While resistant alleles have been identified in cervids, a PRNP variant that completely prevents CWD has not yet been identified.
In Moore et al., reindeer carrying allele E had longer survival-times following intracranial exposure [24]. In the same experiment, a reindeer with a genotype carrier of E, found dead without showing clinical signs ~13 months post-intracranial inoculation, had no histopathological lesions or PrPSc deposition at post-mortem examination.
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Our data support the notion that PRNP genetic variation modulates CWD susceptibility rather than conferring complete resistance. This is in agreement with experimental observations of reindeer-developing CWD after intracranial inoculation regardless of PRNP genotype [24].
***> Our data support the notion that PRNP genetic variation modulates CWD susceptibility rather than conferring complete resistance.
Published: 27 May 2021
White-tailed deer S96 prion protein does not support stable in vitro propagation of most common CWD strains
Alicia Otero, Camilo Duque Velásquez, Judd Aiken & Debbie McKenzie
Scientific Reports volume 11, Article number: 11193 (2021) Cite this article
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Abstract
PrPC variation at residue 96 (G/S) plays an important role in the epidemiology of chronic wasting disease (CWD) in exposed white-tailed deer populations. In vivo studies have demonstrated the protective effect of serine at codon 96, which hinders the propagation of common CWD strains when expressed in homozygosis and increases the survival period of S96/wt heterozygous deer after challenge with CWD. Previous in vitro studies of the transmission barrier suggested that following a single amplification step, wt and S96 PrPC were equally susceptible to misfolding when seeded with various CWD prions. When we performed serial prion amplification in vitro using S96-PrPC, we observed a reduction in the efficiency of propagation with the Wisc-1 or CWD2 strains, suggesting these strains cannot stably template their conformations on this PrPC once the primary sequence has changed after the first round of replication. Our data shows the S96-PrPC polymorphism is detrimental to prion conversion of some CWD strains. These data suggests that deer homozygous for S96-PrPC may not sustain prion transmission as compared to a deer expressing G96-PrPC.
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The protective effect of S96 and H95 alleles was further demonstrated by experimental oral infection in white-tailed deer expressing these amino acid substitutions19. Among the alleles of the PRNP gene associated with a lower CWD incidence and extended preclinical phase, S96 has the highest allelic frequency (~ 25%) after the wt allele in several white-tailed deer populations from the United States and Canada26,27,31. Subsequent independent transmission and epidemiological studies have demonstrated that deer homozygous and heterozygous for S96-PrPC are, compared to wt/wt deer, less susceptible to CWD infection, present prolonged survival times, show delayed prion accumulation and are generally at a significantly earlier stage of disease when deer herds are depopulated23,31,32,33.
***> Subsequent independent transmission and epidemiological studies have demonstrated that deer homozygous and heterozygous for S96-PrPC are, compared to wt/wt deer, less susceptible to CWD infection, present prolonged survival times,
Prion protein polymorphisms associated with reduced CWD susceptibility limit peripheral PrPCWD deposition in orally infected white-tailed deer
Alicia Otero1 , Camilo Duque Velásquez4,5, Chad Johnson3 , Allen Herbst2,5, Rosa Bolea1 , Juan José Badiola1 , Judd Aiken2,5 and Debbie McKenzie4,5*
Abstract
Background: Chronic wasting disease (CWD) is a prion disease affecting members of the Cervidae family. PrPC primary structures play a key role in CWD susceptibility resulting in extended incubation periods and regulating the propagation of CWD strains. We analyzed the distribution of abnormal prion protein (PrPCWD) aggregates in brain and peripheral organs from orally inoculated white-tailed deer expressing four different PRNP genotypes: Q95G96/ Q95G96 (wt/wt), S96/wt, H95/wt and H95/S96 to determine if there are substantial differences in the deposition pattern of PrPCWD between different PRNP genotypes.
Results: Although we detected differences in certain brain areas, globally, the different genotypes showed similar PrPCWD deposition patterns in the brain. However, we found that clinically affected deer expressing H95 PrPC , despite having the longest survival periods, presented less PrPCWD immunoreactivity in particular peripheral organs. In addition, no PrPCWD was detected in skeletal muscle of any of the deer.
Conclusions: Our data suggest that expression of H95-PrPC limits peripheral accumulation of PrPCWD as detected by immunohistochemistry. Conversely, infected S96/wt and wt/wt deer presented with similar PrPCWD peripheral distribution at terminal stage of disease, suggesting that the S96-PrPC allele, although delaying CWD progression, does not completely limit the peripheral accumulation of the infectious agent.
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The significantly longer incubation periods observed in deer with H95-PRNP alleles may not impact secretion of CWD (i.e., less CWD secreted over longer time periods). The emergence of new CWD strains could implicate a zoonotic potential [20].
Keywords: Prions, Prion diseases, Chronic wasting disease, CWD, PrPCWD, Peripheral tissues, Polymorphisms, Deer
***> Selective Breeding
***> less susceptible to CWD infection, present prolonged survival times...
this is very disturbing. with all the hype about selective breeding with different alleles, and presenting longer survival times with cwd, this would only allow the spreading of the cwd tse prion to last longer in the given environment imo., and as such has been stated in scientific literature...terry
With cervids, however, resistance based on the PRNP allele alone is not absolute, and is better characterized as a delayed progression [18,25]
Volume 23, Number 9—September 2017 Research Letter
Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
Allen Herbst1, Camilo Duque Velásquez1, Elizabeth Triscott, Judd M. Aiken, and Debbie McKenzieComments to Author Author affiliations: University of Alberta, Edmonton, Alberta, Canada
Abstract
Human and mouse prion proteins share a structural motif that regulates resistance to common chronic wasting disease (CWD) prion strains. Successful transmission of an emergent strain of CWD prion, H95+, into mice resulted in infection. Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD
In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.'' c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§
Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g
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Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.
THURSDAY, DECEMBER 16, 2021
Detection of CWD prions in naturally infected white‑tailed deer fetuses and gestational tissues by PMCA
THURSDAY, DECEMBER 16, 2021
RT‑QuIC detection of CWD prion seeding activity in white‑tailed deer muscle tissues
***> Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaoui, Irina Zemlyankina, Sheng Chun Chang, Maria Immaculata Arifin, Vincent Beringue, Debbie McKEnzie, Hermann M Schatzl, Sabine Gilch
Affiliations:
1 Department of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine; Hotchkiss Brain Institute; University of Calgary, Calgary, Canada
2 Université Paris-Saclay, INRAE, UVSQ, VIM, 78 350 Jouy-en-Josas, France
3 Department of Biological Sciences, Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada
*Corresponding author. Email: sgilch@ucalgary.ca
This article is a preprint and has not been certified by peer review [what does this mean?].
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide the strongest evidence to date supporting the zoonotic potential of CWD prions, and their probable materialization in humans using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestations, with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results are the first evidence that CWD can infect humans with a distinctive clinical presentation, signature, and tropism, and might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD management.
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Discussion Our findings strongly suggest that CWD is an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
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Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C and N termini, with a molecular weight between 6 and 8 kDa 48-51. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7 – 8 kDa fragment (Figure 2 and 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
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CWD in humans might remain subclinical but with PrPSc deposits in the brain (e.g., mouse #328; Figure 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
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Taking this into consideration, our study is the strongest proof-of-principal that CWD is transmissible to humans. Using humanized mice, we demonstrated the zoonotic potential of CWD. Furthermore, our findings provide striking insights into how CWD might manifest in humans and the impact it may have on human health. We have used Wisc-1/CWD1, one of the most common CWD strains, notably WTD prions, which have been shown to be more prone to generate human prions in vitro 43. This implies a high risk of exposure to this strain, e.g., through consumption or handling of infected carcasses, in contrast to rarer CWD strains, and therefore, an actual risk for human health. In addition, CWD surveillance in humans should encompass a wider spectrum of tissues/organs tested and include new criteria in the diagnosis of potential patients.
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132
also, see;
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.
snip...
The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
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.
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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 ;
==================
https://www.nature.com/articles/srep11573
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
''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
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Professor Kongs reply to me just this month about above grant study that has NOT been published in peer reveiw yet...
=================================
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:
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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:
Dear Terry,
An excellent piece of review as this literature is desperately 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
***> ''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) <***
***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...
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
*** 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.
***> 1st and foremost your biggest problem is 'VOLUNTARY'! AS with the BSE 589.2001 FEED REGULATIONS, especially since it is still voluntary with cervid, knowing full well that cwd and scrapie will transmit to pigs by oral route. VOLUNTARY DOES NOT WORK! all animal products should be banned and be made mandatory, and the herd certification program should be mandatory, or you don't move cervid. IF THE CWD HERD CERTIFICATION IS NOT MANDATORY, it will be another colossal tse prion failure from the start.
***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.
***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently.
***> 4th Captive Farmed Cervid, 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?
***> 5th QUARANTINE OF ALL FARMED CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY, AND THEIR PRODUCTS, that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT near long enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 to 21 years.
***> 6th America BSE 589.2001 FEED REGULATIONS CWD TSE Prion
***> 7TH TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
***> 8TH ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK.
***> 9TH ANY STATE WITH DOCUMENTED CWD, INTERSTATE, NATIONAL, AND INTERNATIONAL MOVEMENT OF ALL CERVID, AND ALL CERVID PRODUCTS MUST BE HALTED!
***> 10TH BAN THE SALE OF STRAW BRED BUCKS AND ALL CERVID SEMEN AND URINE PRODUCTS
***> 11th ALL CAPTIVE FARMED CERVID AND THEIR PRODUCTS MUST BE CWD TSE PRION TESTED ANNUALLY AND BEFORE SALE FOR CWD TSE PRION
SEE FULL SCIENCE REFERENCES AND REASONINGS ;
***> 2nd USA should declare a Declaration of Extraordinary Emergency due to CWD, and all exports of cervid and cervid products must be stopped internationally, and there should be a ban of interstate movement of cervid, until a live cwd test is available.
***> 3rd Captive Farmed cervid ESCAPEES should be made mandatory to report immediately, and strict regulations for those suspect cwd deer that just happen to disappear. IF a cervid escapes and is not found, that farm should be indefinitely shut down, all movement, until aid MIA cervid is found, and if not ever found, that farm shut down permanently.
***> 4th Captive Farmed Cervid, 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?
***> 5th QUARANTINE OF ALL FARMED CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY, AND THEIR PRODUCTS, that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT near long enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 to 21 years.
***> 6th America BSE 589.2001 FEED REGULATIONS CWD TSE Prion
***> 7TH TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
***> 8TH ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK.
***> 9TH ANY STATE WITH DOCUMENTED CWD, INTERSTATE, NATIONAL, AND INTERNATIONAL MOVEMENT OF ALL CERVID, AND ALL CERVID PRODUCTS MUST BE HALTED!
***> 10TH BAN THE SALE OF STRAW BRED BUCKS AND ALL CERVID SEMEN AND URINE PRODUCTS
***> 11th ALL CAPTIVE FARMED CERVID AND THEIR PRODUCTS MUST BE CWD TSE PRION TESTED ANNUALLY AND BEFORE SALE FOR CWD TSE PRION
SEE FULL SCIENCE REFERENCES AND REASONINGS ;
Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
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)
CWD AND SCRAPIE TRANSMIT TO PIGS BY ORAL ROUTES
2021 Transmissible Spongiform Encephalopathy TSE Prion End of Year Report 2020
CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020
zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum
4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein.
***> PIGS, WILD BOAR, CWD <***
***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE
HYPOTHOSIS AND SPECIFIC AIMS
HYPOTHOSIS
BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS
Final Report – CJD Foundation Grant Program A.
Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.
Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018
Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.
Interpretive Summary:
The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
LINE TO TAKE
3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:-
"There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.
DO Hagger RM 1533 MT Ext 3201
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
cattle are highly susceptible to white-tailed deer CWD and mule deer CWD
***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, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
SNIP...
price of prion poker goes up for cwd to cattle;
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
AUG. 11, 2017
RE: Inactivation of porcine endogenous retrovirus in pigs using CRISPR-Cas9
seems that the USA feed ban for ruminant protein is still a serious problem, so there seems to still be a risk factor for pigs and Transmissible Spongiform Encephalopathy TSE prion disease. now with the updated science showing that pigs are susceptible to the Chronic Wasting Disease TSE Prion ORALLY, and cwd running rampant in the USA, any use of porcine organs should be tested for the CWD TSE Prion...
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
SUNDAY, AUGUST 06, 2017
USA Chronic Wasting Disease CWD TSE Prion Emergency Response Plan Singeltary et al
TUESDAY, AUGUST 8, 2017
Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2016-0092]
Terry S. Singeltary Sr.
FRIDAY, FEBRUARY 11, 2022
Passage of the CWD agent through meadow voles results in increased attack rates and decreased incubation periods in raccoons
TUESDAY, APRIL 26, 2022
Susceptibility of Beavers to Chronic Wasting Disease
Saturday, April 9, 2022
***> EFSA EU Request for a scientific opinion on the monitoring of Chronic Wasting Disease (CWD) EFSA-Q-2022-00114 M-2022-00040 Singeltary Submission
TUESDAY, MARCH 29, 2022
OIE Agent causing chronic wasting disease (CWD) TSE Prion of Cervid
WEDNESDAY, APRIL 13, 2022
UT Health Soto receives $13 million NIH grant to further research on chronic wasting disease
Michigan’s 2021 deer seasons included targeted CWD surveillance, 25 positive deer
April 14, 2022
Hunters encouraged to share harvest results via online survey
Buck walking through lush green forest
Though Michigan’s 2021 deer hunting seasons ended in late January 2022, the Michigan Department of Natural Resources is continuing to accept feedback from hunters about their experiences. Hunter harvest surveys have been sent to a random sample of the state’s deer hunters. In addition, hunters can take a brief online survey. Final harvest survey results will be presented later this summer.
Initial data from Michigan’s 2021 deer hunting seasons – including chronic wasting disease testing results and deer license sales information – was presented at Thursday’s meeting of the Michigan Natural Resources Commission in Lansing, with highlights shared below.
A shift in CWD testing
The DNR has finalized its 2021 surveillance efforts for chronic wasting disease, ultimately testing just over 7,200 deer. The more targeted testing goals are part of the department’s new region-by-region strategy aimed at detecting new outbreaks rather than revisiting known ones.
“We want to thank hunters for their cooperation in helping us meet our CWD surveillance goals,” said DNR Director Dan Eichinger. “Strategic testing for chronic wasting disease is of primary importance for the department, and we couldn’t meet these goals without the committed assistance of deer hunters.”
Eichinger also praised the work of deer processors, taxidermists and local businesses that help collect samples for testing, and other key partners who provide necessary assistance to the department.
In all, 25 CWD-positive deer were confirmed in 2021. Three cases of CWD were detected in Isabella County, which represents a new county where the disease has been found. (Since Michigan’s first confirmation of a CWD-positive wild deer in 2015, CWD has been detected in white-tailed deer in Clinton, Dickinson, Eaton, Gratiot, Ingham, Ionia, Jackson, Kent and Montcalm counties.)
Doe walking through late summer forest “It was not unexpected to find positive cases in Isabella County, as these detections were fairly close to where we’ve identified cases in Montcalm and northern Gratiot County,” said DNR deer and elk specialist Chad Stewart. “Our main areas of infection remain in parts of Montcalm and northeast Kent counties, as well as southern Jackson County, where we knew CWD existed going into the 2021 hunting season.”
Despite the department’s finding of 25 positive animals last year, Stewart cautioned against comparing the low number of positives with the high number of deer tested and concluding there is not a problem.
“The distribution of our samples greatly affects the number of positives we expect to find. Intensive collection of samples in known CWD locations like Montcalm and Kent counties would certainly lead to a high number of positives being detected,” he said. “Our goal this year was to begin to understand what CWD looks like in areas that are historically under-sampled, and we made a lot of strides on that front.”
Stewart said that chronic wasting disease is going to be a problem for parts of Michigan’s deer herd in the future: “Once it becomes established, it is unlikely that we can reverse course on the disease. Prevention and early detection remain our best options for CWD management.”
Hunter walking across plain while sun shines brightly CWD surveillance moving forward
For Michigan’s 2021 deer seasons, the DNR started a multiyear process of strategic, focused CWD surveillance in regions around the state. Last year’s surveillance occurred mainly in the three tiers of counties near the Ohio border. Over the next few years, the remainder of the state will be systematically sampled to determine if CWD is present in other areas where it hasn’t yet been identified.
Hunter numbers
While there was a temporary rise in hunter numbers during the COVID-19 pandemic, participation is declining in Michigan. The trend is not new, nor is it only being observed here. States across the country are feeling the financial pressure of reduced hunter numbers, because sales of hunting licenses comprise a large portion of the funding for critical conservation work.
“Nationwide, hunting has seen a gradual decline over the last several decades,” said Eichinger. “The trend is likely due to a combination of factors including generations of hunters who are aging out of the sport, and younger generations that are less likely to participate in hunting due to societal changes and more competition for their attention.”
Deer hunter numbers in 2021 were down nearly 4% over the previous year with close to 600,000 hunters purchasing a deer license. Hunter number declines are in line with past years going back to peak participation in the mid 90’s.
“While the trend in hunter participation is discouraging, we know that hunting remains an important part of Michigan’s outdoor heritage,” Eichinger said. “That’s why we encourage experienced hunters to introduce the sport to new hunters wherever they can. Spending time with veteran hunters can reduce the learning curve, increase safety and instill a sense of excitement and appreciation for our state’s natural resources.”
To learn more about deer management, CWD and deer hunting in Michigan, and to access the 2021 deer harvest survey, visitMichigan.gov/Deer.
Michigan Chronic Wasting Disease CWD TSE Prion Update
CWD in Michigan
Since May 2015 when the first CWD deer was found in Michigan, CWD has been confirmed in a number of townships in the Lower Peninsula. As of October 2018, a CWD positive deer was found in the Upper Peninsula in Dickinson County. CWD was also found in August 2008 at a Kent County deer farm facility and in January 2017 in two captive deer that were from a deer farm facility in Mecosta County.
CWD TESTING RESULTS
MICHIGAN CWD CAPTIVE
11/4/2021 2, 3 Y Male MI Kent Elk Breeder Yes Yes 0 Depopulated
7/15/2021 4 Y Female MI Montcalm WTD Breeder No No 109 Quarantine
4/18/2021 2.5 Y Male MI WTD Shooter No No ukn Quarantine
3/3/2021 4 Y Male MI Montcalm WTD Shooter No NA 14 Quarantine
12/2019 3, 4.5 Y Males MI Newaygo WTD Shooter No No >600 Quarantine
4/2019 2.5 Y Female MI Montcalm WTD Breeder No NA 113 Depopulated
12/2017 1.5 Y Female MI Mecosta WTD Breeder Yes Yes 525 Quarantined
1/2017 2Y Female MI Mecosta WTD & Sika deer Shooter No NA 71 Depopulated
Michigan:
September, 2019: NVSL confirmed CWD in a two year old female white-tailed deer in Montcalm County. The doe was a natural addition to the breeding herd which consists of 50 white-tailed deer. This herd is not enrolled in the Federal HCP, is within a CWDendemic area, and is under quarantine.
Michigan: One new CWD positive herd
Hunt preserve of >600 WTD, not in HCP, populated and under quarantine
Farmed Cervid Chronic Wasting Disease Management and Response Activities 2021 Cooperative Agreements
snip...see full text;
MONDAY, MAY 09, 2022
Michigan MDARD: Chronic Wasting Disease Confirmed in a Farmed White-Tailed Deer from Mecosta County
FRIDAY, FEBRUARY 18, 2022
Michigan Chronic Wasting Disease CWD TSE Prion Update February 2022
WEDNESDAY, MAY 18, 2022
Wisconsin Walworth County Deer Farm Tests Positive for CWD
Wisconsin two white-tailed deer at a Waukesha County farm have tested positive for chronic wasting disease (CWD)
Waukesha County Deer Farm Tests Positive for CWD
FOR IMMEDIATE RELEASE: February 10, 2022
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) has confirmed that two white-tailed deer at a Waukesha County farm have tested positive for chronic wasting disease (CWD). The samples were confirmed by the National Veterinary Services Laboratories in Ames, Iowa.
Both affected animals were 3-year-old bucks. The 9-acre farm had been under quarantine since November 2021 after white-tailed deer moved from its herd tested positive at an Eau Claire County ranch. It will remain under quarantine while DATCP and the U.S. Department of Agriculture (USDA) veterinarians and staff conduct the epidemiological investigation.
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 http://farm-raised deer program: https://datcp.wi.gov/Pages/Programs_Services/FarmRaisedDeer.aspx
###
Wisconsin Lawmakers should end their frolic with ‘Hunter Nation’
Kevin Wilson
CWD hunters
It’s time for Wisconsin lawmakers to work with hunters, anglers and trappers to address chronic wasting disease and other challenges to the state’s natural resources.
Patrick Durkin
Wisconsin this month fortified its standing as the capital of the world for chronic wasting disease by verifying the plague in wild deer in 38 of the state’s 72 counties.
Yep, Wisconsin now has more counties with CWD in free-ranging deer than it does counties without. We passed the halfway mark Jan. 11 when the Department of Natural Resources reported two adult bucks in Monroe County and one deer in Oconto County tested positive for the always-fatal disease.
We started the 2021 hunting seasons with CWD in 34 counties but made it 35 when the DNR confirmed a sick adult doe Oct. 29 in Fond du Lac County. We then reached the halfway point Dec. 12 when the DNR confirmed a sick yearling (18 months old) buck in Vilas County.
And just think what we’d find if we searched aggressively for CWD. All four newly christened CWD counties found their first cases despite modest sampling efforts. Hunters in Monroe County have provided a respectable 373 samples during the current testing year, but hunters in Oconto provided only 162; Vilas, 161; and Fond du Lac, 105.
The 2021 sampling year ends March 31, but it’s safe to report that 25 Wisconsin counties will end the year with less than 100 samples tested, given the hunt is largely over.
As of Jan.15, Wisconsin has confirmed 9,450 CWD cases since discovering the disease in three deer shot west of Madison in November 2001. The DNR has documented 1,283 cases statewide so far this year after testing 16,165 samples. That’s 8% of all tests, which is similar to 2020’s rate.
CWD sampling declined this past fall, with 2,749 fewer samples (-14.5%) statewide than in 2020 (18,914). Most samples come from the DNR’s southern farmland zone, where sampling fell 22% from 9,3892 a year ago to 7,277.
Despite the decline, 1,234 deer (17%) have tested positive so far in that zone, which is 4 percentage points lower than the 2020 total. For perspective, when the DNR tested similar numbers (7,097 deer) in the Southern farmlands in 2010, it found 219 (3%) CWD cases, or 5.6 times fewer doomed deer.
Elsewhere, CWD cases more than doubled from 19 to 39 in central Wisconsin’s farmlands this year, accounting for 40% of the zone’s historical total of 98 cases. In addition, deer baiting is now banned in 58 Wisconsin counties. The 14 counties where the controversial practice remains are Douglas, Bayfield, Ashland, Iron, Sawyer, Rusk, Price, St. Croix, Pierce, Lincoln, Brown, Manitowoc, Kewaunee and Door.
Iowa County again leads the state with 315 cases this year, or 31% of the 1,026 samples provided. Next was Richland, 270 cases (21% positive); Sauk, 222 (25%); Dane, 151 (17%); Grant, 80 (14%); and Columbia, 72 (15%).
Cooperation from hunters remains poor as indifference reigns. In Sauk County, hunters tested only 15% of the 6,002 deer they registered during the 2021 gun, crossbow and archery seasons. Further, Dane County hunters tested 23.5% of 3,833 registered deer; Richland County, 24% of 5,228; Iowa County, 28% of 3,607; Grant County, 0.09% of 6,176; and Columbia County, 0.08% of 6,007.
A soon-to-be released DNR survey from 2019 also found that 70% of Wisconsin hunters have never submitted a deer for CWD testing. The survey also found that 33% of hunters who get their deer tested don’t wait for results before eating it.
Despite such dismal numbers, GOP lawmakers are ignoring the mess by distracting everyone with the Wisconsin Sporting Freedom Act. This bag of stale air from the Kansas-based group Hunter Nation doesn’t even mention CWD.
We pause here to ask, “Sporting Freedom Act”? What is that? Do politicians think they can just insert “freedom” in a bill’s title, and we’ll snap to attention and salute? As silly as “freedom fries” sounded in February 2003, at least the word choice made sense. You’ll recall folks were mad at France for not supporting the war in Iraq, and urged restaurants to purge “French” from their menus.
Again I ask: Sporting Freedom Act? Freedom from what? Science? Biology? A future for deer hunting in Wisconsin?
If you think that’s harsh, explain how mandating the annual raising and releasing of 200,000 pheasants and 100,000 brook trout is relevant to liberty and freedom, or wise fish and wildlife management?
And how about the act’s “turkey hunting simplification” bill? Luke Hilgemann, CEO/president of Hunter Nation, recently wrote that our current spring turkey season confuses Wisconsin hunters. Really? Name someone who’s puzzled. True, our current season of six weeklong hunting periods might baffle your average lobbyist, state senator, assembly-creature, and Gov. Scott Walker’s four appointees to the Natural Resources Board. But Wisconsin’s spring season wins praise from 70% to 80% of turkey hunters surveyed annually.
Another bill in the “Freedom Act” infuriates many retired conservation wardens and the Wisconsin Hunter Education Instructor Association. The Mentored Hunt Bill (SB-611 and AB-670) would allow beginning hunters to earn their hunter-education certificate by simply taking an online course and then going afield with a licensed adult hunter, not a certified instructor.
Yes, that shortcut was allowed the past year because of COVID-19, and it sounded OK the first time I read it, but I was wrong. It doesn’t deserve our Legislature’s permanent blessing.
Hilgemann also recently wrote: “Hunting … in Wisconsin is a sacred tradition (and the Freedom Act sends) a strong message about our heritage and way of life. Not only does the Wisconsin Sporting Freedom Act reform rules for hunters and anglers, it helps ensure that future generations still have access to the resources that help these sacred traditions thrive through proactive resource management.”
Huh? You’ll find more substance in a bag of cheetos. Hunter Nation and its GOP backers insult Wisconsin’s hunting heritage by ignoring all the work of recent decades that made hunting so safe.
The WHEIA notes that conservation wardens annually investigated 174 hunting accidents, including 17 deaths, from 1956 to 1966 in Wisconsin. The state’s hunter education program began in 1967. Since then, over 17,000 volunteer instructors helped reduce those numbers to an annual average of 21 accidents and 1.8 deaths.
Y’know, we don’t need Hunter Nation messing with our programs. It’s time GOP lawmakers stop frolicking with these amateurs and get serious about addressing CWD and other obvious challenges to our natural resources.
That won’t happen, however, if hunters, anglers and trappers don’t hold lawmakers accountable with emails, letters, phone calls and votes.
Hunter Nation exposed this Legislature’s scarcity of thinkers and leaders. They must be told what to do.
— Patrick Durkin is a free-lance writer who covers outdoors recreation in Wisconsin. Contact him at patrickdurkin56@gmail.com, or at @patrickdurkinoutdoors.com on Facebook and Instagram.
Kevin Wilson
very sad, indeed very sad...
Wisconsin CWD TSE Prion Spreads To More Wild Deer In New Counties of Monroe and Oconto
FOR IMMEDIATE RELEASE: 2022-01-11
Contact: Scott Roepke, DNR Area Wildlife Supervisor
Scott.Roepke@wisconsin.gov or 715-284-1403
DNR CONFIRMS CWD IN WILD DEER HARVESTED IN MONROE COUNTY
BAITING AND FEEDING BANS RENEWED FOR MONROE COUNTY
MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) confirms two wild deer tested positive for chronic wasting disease (CWD) in Monroe County during the fall 2021 hunting season. The two deer were adult bucks harvested in the towns of Ridgeville and Glendale. These are the first confirmed wild positive cases of CWD in Monroe 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 Monroe County.
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 Monroe county 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.
Information on how to have deer tested during the 2021-2022 hunting seasons is available here.
The DNR will hold a virtual informational meeting on Thursday, Feb. 3 from 6-8 p.m. to discuss CWD in Monroe County. Members of the public are 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.
MEETING DETAILS
WHAT: CWD In Monroe County
WHEN: 6-8 p.m. Feb. 3, 2022
WHERE: Join by Zoom here.
Join by phone: 833-548-0282, Meeting ID: 818 9196 0967
FOR IMMEDIATE RELEASE: 2022-01-11
Contact: Janet Brehm, Peshtigo Area Wildlife Supervisor
Janet.Brehm@wisconsin.gov or 715-409-3277
DNR CONFIRMS CWD IN WILD DEER HARVESTED IN OCONTO COUNTY
BAITING AND FEEDING BANS RENEWED FOR OCONTO AND MENOMINEE COUNTIES, ONGOING FOR SHAWANO COUNTY
Wisconsin DNR news release
The Wisconsin DNR confirms CWD in a wild deer harvested in Oconto County. Baiting and feeding bans are renewed for Oconto and Menominee Counties and remain in effect for Shawano County.
Photo credit: Wisconsin DNR
MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) confirms a wild deer tested positive for chronic wasting disease (CWD) in the Town of Underhill in Oconto County. The deer was a one-year-old hunter-harvested buck taken during the 2021 gun deer season. This is the first confirmed wild positive case of CWD in Oconto County.
Following state law, the DNR will renew a three-year baiting and feeding ban in Oconto County as well as a two-year ban in Menominee County, as the deer was harvested within 10 miles of the county line. Shawano County is also within 10 miles of the Oconto positive’s harvest location, but is already under a longer three-year baiting and feeding ban due to a positive CWD detection at a captive deer 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.
Those harvesting deer within 10 miles of the newly detected positive case are especially encouraged to have their harvested adult deer tested for CWD. The Farmland Zone of Oconto County has an either-sex extended archery and crossbow deer hunt through Jan. 31, 2022; harvest authorizations are still available for purchase with your license. Collecting CWD samples is essential for assessing where and to what extent CWD occurs in deer across the state.
Information on how to have deer tested during the 2021-22 hunting seasons is available here.
Successful CWD management depends in part on citizen involvement in the decision-making process through local County Deer Advisory Councils (CDAC). The DNR and the Oconto and Shawano CDACs will hold a public meeting on the status of CWD and a response plan for sampling wild deer in Oconto and Shawano County. The virtual meeting is open to all members of the public and will take place on Tuesday, Feb. 1 from 6-8 p.m. via Zoom. The public may also call in to the meeting by dialing 888-475-4499, meeting ID 871 6740 0821.
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.
MEETING DETAILS:
WHAT: CWD In Oconto County
WHEN: 6-8 p.m. Feb. 1, 2022
WHERE: Join by Zoom here.
Join by phone: 888-475-4499, Meeting ID: 871 6740 0821
FOR IMMEDIATE RELEASE: 2022-01-07
Contact: DNR Office of Communications
VIRTUAL CWD RESPONSE PLAN REVIEW COMMITTEE MEETING JAN. 12
MADISON, Wis. – The Wisconsin Department of Natural Resources (DNR) today announced it will host the Chronic Wasting Disease Response Plan Review Committee meeting on Wednesday, Jan. 12 from 9 a.m. to 1:30 p.m.
The DNR’s 15-year CWD Response Plan, in effect through 2025, helps guide the department’s approach to addressing CWD in Wisconsin. The plan was developed to fulfill its public trust responsibility to manage wildlife and ensure the health of Wisconsin’s wildlife populations. As part of the plan’s implementation, the department will review progress toward meeting its goals and objectives every five years.
The committee is comprised of a group of stakeholders representing conservation, business and hunting organizations and tribal governments. During its meetings, the committee will develop input on the plan’s implementation and actions to consider as it completes this second five-year review.
Chronic wasting disease is a fatal, infectious nervous system disease of deer, moose, elk and reindeer/caribou. The Wisconsin DNR began monitoring the state's wild white-tailed deer population for CWD in 1999. The first positives were found in 2002.
More information on CWD is available on the DNR's CWD webpage.
Additional information on the DNR’s CWD Response Plan is available on the DNR’s website.
WHAT: CWD Response Plan Review Committee Meeting
WHEN: 9 a.m. – 1:30 p.m. Jan. 12, 2022
WHERE: The public is invited to watch live on the DNR’s YouTube channel here.
There is no registration required to attend, and a recording of the meeting will be posted to the DNR website.
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:
###
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:
###
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
###
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
Chronic wasting disease in a Wisconsin white-tailed deer farm
WEDNESDAY, JANUARY 12, 2022
Wisconsin CWD TSE Prion Spreads To More Wild Deer In New Counties of Monroe and Oconto
WEDNESDAY, JANUARY 12, 2022
Wisconsin CWD TSE Prion Spreads To More Wild Deer In New Counties of Monroe and Oconto
SUNDAY, AUGUST 15, 2021
Wisconsin CWD TSE Prion 2021 Update Wild Cervid 8,174 Positive To Date
THURSDAY, AUGUST 12, 2021
Wisconsin Deer Farms in Sauk, Taylor Counties Test Positive for CWD TSE Prion
FRIDAY, JANUARY 22, 2021
Wisconsin DNR CONFIRMS CWD IN WOOD COUNTY WILD DEER; RENEWS BAITING AND FEEDING BANS
TUESDAY, JANUARY 12, 2021
Wisconsin CWD TSE Prion 8,101 Positive With Wild Deer Testing Positive for CWD in Germania in Southwestern Shawano County
snip...see full text;
THURSDAY, FEBRUARY 10, 2022
Wisconsin two white-tailed deer at a Waukesha County farm have tested positive for chronic wasting disease (CWD)
Minnesota CWD detected in a wild deer in Grand Rapids prompts DNR to update disease response plan
CWD detected in a wild deer in Grand Rapids prompts DNR to update disease response plan
March 22, 2022
The Minnesota Department of Natural Resources (DNR) is updating its chronic wasting disease response plan after the discovery of a wild white-tailed deer infected with CWD within the city of Grand Rapids. The response plan update will better reflect a statewide approach to disease surveillance, management, control and education.
This is the first time CWD has been detected in wild deer in this deer permit area, so the DNR is also taking immediate steps to understand the prevalence of the disease in wild deer in the Grand Rapids area. The agency will work with local road authorities to collect samples from road-killed deer and is exploring opportunities for targeted culling where it can be performed safely.
“We’ve always looked at CWD as a disease that could impact the entire state, yet implemented disease management actions as needed in each area where CWD was found,” said Kelly Straka, the DNR’s wildlife section manager. “This new discovery doesn’t make CWD a statewide problem, but it does mean we need to take more of a statewide approach.”
While the surveillance outlined in the DNR’s current response plan made this detection possible, the finding of CWD in Grand Rapids highlights the need for an enhanced statewide sampling approach.
The enhanced statewide surveillance will include:
Updating the DNR’s CWD response plan this spring
Investigating options for hunters to use a self-mailing kit for free testing statewide
Expanding the taxidermist network (Partner Sampling Program) statewide
Upgrading and improving current design for self-service stations
The DNR will seek public input as it explores and implements the ideas above and other options for enhanced statewide surveillance.
“The DNR has taken an aggressive approach to managing CWD in Minnesota,” said DNR Commissioner Sarah Strommen. “We will continue this strong approach as we address this latest finding and as we update our statewide CWD response plan. The health of Minnesota’s wild deer herd remains a top priority for the DNR.”
There now are eight areas spread across Minnesota, from north to south, where CWD has been found in wild or farmed deer. Despite these detections, the disease remains rare in Minnesota. Fewer than 1% of deer have tested positive for CWD in areas where the disease has consistently been detected during the past five years.
Since 2002, DNR has tested 106,000 deer statewide and 153 have tested positive. Most of those cases occurred in southeastern Minnesota.
The DNR received confirmation of the Grand Rapids CWD infection on March 15. A Grand Rapids resident reported to the DNR in mid-February that an adult doe had died in his backyard. DNR staff collected the carcass and submitted a lymph node sample for CWD testing.
Results of a full necropsy showed the deer died from a collision with a vehicle, not CWD. The deer showed no clinical signs of the disease but final test results confirmed the infection.
Active surveillance for CWD has not occurred in the location where the infected deer was found (deer permit area 179) since 2004. The DNR conducted CWD surveillance to the west and north of Grand Rapids in fall 2021 in DPAs 197, 169, 184 and 110 in response to captive deer infected with CWD on a Beltrami County farm. More than 1,800 samples were tested and CWD was not detected. To the west and south of Grand Rapids, a CWD management zone exists in DPA 604. Surveillance has been ongoing in this area since 2017. Two wild deer detections have been found in the 6,300 deer tested since surveillance began.
More information about CWD and what the DNR is doing to limit disease spread and protect the health of Minnesota’s white-tailed deer is available on the DNR website.
***> Minnesota Board of Animal Health Report Concurrent Authority Regulating Farmed White-tailed Deer and CWD TSE Prion
Minnesota Board of Animal Health
Report: Concurrent Authority Regulating Farmed
White-tailed Deer
As required by Minnesota Session Law 2021, 1st Special Session, Chapter 6 02/01/2001
Report to the Minnesota Legislature Minnesota Department of Natural Resources
500 Lafayette Road Saint Paul, MN 55155 (Phone) 651-296-6157 info.dnr@state.mn.us dnr.state.mn.us
As requested by Minnesota Statute 3.197: This report cost approximately $37,368 to prepare, including staff time and contracting expenses.
Upon request, this material will be made available in an alternative format such as large print, Braille or audio recording. Printed on recycled paper.
Contents
Background 1
Work Accomplished to Date 2
Inspections of Farmed White-tailed Deer Facilities 2
Data Sharing and Analysis - Animal Health Information System 3
Internal Communications 3 Concurrent Authority Implementation Challenges 3
Ongoing Challenges to Managing CWD 5
Compliance Inspections and Enforcement 5
Movement 6
Costs of CWD Surveillance in Wild and Farmed White-tailed Deer 6
Recommendations 7
Roles and Responsibilities 7
Communication 7
Recommendations for Rule and Statute Changes to Address CWD Challenges 7
Appendix A: DNR Project Plan-Captive Cervid Facilities Co-Management 9
Background
The 2021 Minnesota State Legislature, in a special session ending in July 2021, issued direction to the Minnesota Department of Natural Resources (DNR) and the Board of Animal Health (BAH) by amending Chapter 35.155 as follows:
2021 Minn. Laws 1st Sp. Sess. Chap. 6 Art. 2 Sec. 17
Subd. 14. Concurrent authority; regulating farmed white-tailed deer.
(a) The commissioner of natural resources and the Board of Animal Health possess concurrent authority to regulate farmed white-tailed deer under this section, sections 35.92 to 35.96, and any administrative rules adopted pursuant to this section or sections 35.92 to 35.96. This does not confer to the commissioner any additional authorities under chapter 35, other than those set forth in sections 35.155 and 35.92 to 35.96, and any administrative rules adopted thereto.
(b) By February 1, 2022, the commissioner of natural resources, in conjunction with the Board of Animal Health, must submit a report to the chairs and ranking minority members of the legislative committees and divisions with jurisdiction over the environment and natural resources and agriculture on the implementation of the concurrent authority under this section. The report must include:
(1) a summary of how the agencies worked together under this section, including identification of any challenges;
(2) an assessment of ongoing challenges to managing chronic wasting disease in this state; and
(3) recommendations for statutory and programmatic changes to help the state better manage the disease.
In the 2005 legislative special session, the Legislature amended the farmed cervid program statutes to give authority over farmed cervids to the BAH; prior to this change, the DNR had managed the state’s farmed cervid program. The DNR continues to manage regulation of other similar commercial activities, including taxidermies, commercial minnow/fish harvest, logging, and commercial decorative forest products.
This report fulfills the requirements to report to the Legislature by February 1, 2022, summarizing how the agencies worked together under concurrent authority, describing ongoing challenges to managing chronic wasting disease (CWD) and providing recommendations for moving forward.
Work Accomplished to Date
Upon enactment of 2021 Min. Laws 1st Sp. Session, Chapter 6 Art. 2 Sec. 17, the DNR created a farmed cervid project plan entitled Captive Cervid Facilities Co-Management Project Plan (see Appendix A) and assembled a project team. The project team’s plan contains deliverables including completion of an early set of at least 40 inspections of white-tailed deer facilities with BAH staff, development and implementation of data management and protocols, and engagement with the BAH on recommendations for policy and programmatic changes to reduce the spread of CWD. In October 2021, the BAH’s internal cervid program staff organized a similar farmed cervid project team and established a weekly interagency meeting with the DNR project team to discuss the activities taking place under concurrent authority.
Inspections of Farmed White-tailed Deer Facilities
Immediately upon passage of concurrent authority legislation, the BAH engaged with the DNR to provide structured training on program management, conducting epidemiological investigations, and monitoring whitetailed deer movement. This education progressed into real-time field training during joint BAH and DNR farm inspections. Additionally, BAH staff provided guidance and instruction to the DNR in email communications, reference documents and written processes. This training was initially provided to support BAH inspectors during field activities, with an eventual goal of DNR staff conducting inspections independently in the future.
DNR and BAH staff conducted joint inspections of white-tailed deer farms. Initially, BAH served as the lead inspector while the DNR took an active learning role. As inspections progressed into the late fall and early winter, the DNR took a more active role, offering suggestions to mitigate interaction between farmed and wild white-tailed deer and helping BAH inspectors determine compliance. From the end of August to December 2021, DNR and BAH inspectors jointly inspected 50 registered Cervidae farms and identified 17 compliance infractions:
• 10 farms with inadequate fencing;
• 2 farms with inadequate redundant gating;
• 2 herd owners’ failure to submit death reports within the required timeline;
• 1 herd owner’s failure to submit samples for CWD testing;
• 1 farm where inspectors could not visualize official ID, and
• 1 farm with official identification missing.
During the inspections, DNR staff closely evaluated the potential for farmed and wild deer to interact near fence lines, since this is a potential risk for the spread of CWD. DNR found:
• Good deer cover or habitat at the fence line on 35 farms.
• Close or direct contact potential between farmed and wild deer on 22 farms. Evidence included feces, rubs/scrapes, tracks, and wild deer sightings in the vicinity of the fence.
• At least one water, feed, or mineral station within 10 feet of the perimeter fence on 23 farms; 17 farms had at least one feeder within 10 feet of the fence.
This new information shows that wild and farmed deer have the potential to interact at fence lines; given that, it reinforces the need for strong fencing requirements and compliance. Further, it highlights the potential for exclusionary fencing to offer additional safeguards for separation of wild and farmed deer.
Data Sharing and Analysis - Animal Health Information System
The BAH uses CoreOne by Trace First as its animal health information system. This system contains data for animals regulated by the BAH, including farmed white-tailed deer herds and mixed-species herds. The DNR and BAH considered multiple options to determine how the DNR could access needed data from the BAH database. The most important factors were data privacy and cost. Minnesota Government Data Practices statutes regulate access to data the BAH maintains. Ultimately, to provide DNR staff with only the data necessary for concurrent management, the BAH, DNR and Minnesota IT Services (MNIT) staff worked with CoreOne by Trace First to create a second, separate database that contained only data related to farmed white-tailed deer herds. The vendor copied farms with mixed-species herds data, and permanently moved data related to farms with only white-tailed deer herds, from the BAH system into the DNR database.
The DNR just recently obtained access to view data in this separate system. However, access is limited to a readonly testing phase through the end of January 2022. Because of this limitation, and the desire to limit duplicate data entry, the DNR has been unable to enter data into the new database. Given this, the DNR has not yet assigned dedicated staff to enter or manage this system. There will be a final migration of white-tailed deer farm data into the new DNR database on Feb. 1, 2022. This process will solidify the new DNR CoreOne database as the system of record for farmed white-tailed deer moving forward; however, both agencies will maintain access to this database.
Internal Communications
Both agencies have internal teams working on the white-tailed deer program. The DNR project team meets weekly with a standing agenda to discuss topics surrounding farmed white-tailed deer and concurrent authority. The agenda covers farm inspections, data management, communications, and emergent issues such as escapes, movement bans and compliance issues. The BAH also holds an internal weekly meeting and supplies meeting notes to the DNR.
In addition, the DNR and BAH staff hold weekly joint meetings that include similar agendas as the internal meetings but also cover interagency communication topics, training and education, and stakeholder communications. These meetings keep the agencies informed on current activities under the concurrent authority.
Concurrent Authority Implementation Challenges
One significant challenge has been establishing a mutual understanding of what concurrent authority looks like operationally. Although BAH and DNR have different skills and mandates, both agencies agree CWD is a common threat for farmed and wild white-tailed deer and other cervids, and that joint management offers strategic benefits. The agencies are engaging in discussions on how to optimize concurrent authority to contain and manage CWD.
The challenges related to farm inspections, data documentation, and communications identified thus far are:
• Farm inspections: Up to three DNR and BAH staff members have participated in each of the 50 inspections conducted since concurrent authority was enacted. Training and educating DNR staff is necessary during this transition period. To date, DNR staff have not taken the lead in any part of the inspection process. There is a need to clarify roles and scope for BAH and DNR inspectors in the farminspection process. Additionally, concurrent authority in general, and DNR staff presence on farms in particular, has caused concern among some herd owners. There have been at least two incidents of strong resistance to these changes by herd owners. BAH anticipated this response and developed a policy that it would not conduct an inspection unless a producer allowed DNR staff on premises.
• Data sharing and analysis. In addition to continued training for DNR staff on the CoreOne system, and the potential hiring of additional data entry staff, maintaining two systems for mixed species farms will be an ongoing challenge. Since the BAH currently maintains the exclusive regulation and data ownership of farmed non-white-tailed deer species, including those in mixed species herds, there will be a continued need for BAH staff to manage data in both systems. Some duplication of data will be required in certain cases: for example, maintaining a current list of certified CWD sample collectors. Due to the complex nature of certain program data, such as inventories, a go-live date of Feb. 1, 2022 means some 2021 data will still need to be entered. As a result, BAH staff will have to duplicate that remaining data in both systems. Reporting activities will be more complicated now that data are split between two databases. Not only will new platforms with reporting criteria need to be developed and connected to the DNR system, there also will be a significant amount of data-combining needed for reports involving multiple species of farmed cervids. Additional protocols will need to be determined in the future as the new system moves into a live phase.
• Internal communication. Significant progress has been made to improve communication between agencies since concurrent authority was granted. Prior to October 2021, each agency worked fairly independently to develop plans. Since then, the DNR and BAH have been addressing the challenges of consistent flow and clarity between the two agencies and developing a mutually agreed-upon vision for concurrent authority and its implementation.
• Public communication. Coordination between the DNR and BAH surrounding public communication is a work in progress. In January 2019 (prior to concurrent authority), a Memorandum of Understanding (MOU) was finalized between the DNR and BAH that contained protocols for sharing information between agencies and communicating with the public. These protocols must be reviewed to make this agreement operational under concurrent authority.
Ongoing Challenges to Managing CWD
CWD is a fatal, neurologic disease that affects cervids including white-tailed deer, mule deer, elk, moose, reindeer, and others. Minnesota is home to approximately 1 million free-ranging white-tailed deer, about 3,000 moose, and several hundred free-ranging elk. The discovery of CWD in Minnesota in either free-ranging or farmed cervid populations represents a risk to all susceptible species.
The primary risk factors facilitating the introduction of CWD into Minnesota—or its spread within the state—are the movement of live cervids and high-risk carcass parts (e.g., brain, spinal column). In wild populations, live cervid movements are typically limited to their distinct home ranges and migratory patterns attributed to each species. In the farmed cervid industry, movement of live cervids through sales and exchanges can cover hundreds of miles. Cervid carcasses can also move long distances, from harvest locations to homes, taxidermists or meat processors. Both types of movements can contribute to CWD spread through direct contact or environmental contamination.
Minnesota has addressed the risk of hunter-mediated interstate carcass movements with a blanket ban that restricts the import of any whole cervid carcass from anywhere outside of Minnesota, including Canada, regardless of chronic wasting disease status. Successful out-of-state hunters may only bring back quarters, deboned meat, cleaned skull plates, and finished taxidermy mounts. Similarly, Minnesota imposes intrastate carcass movements of cervids harvested within CWD management zones until CWD test results are received, with the exception of quarters or deboned meat, and provides dumpsters to reduce the instances of carcasses left on the landscape in high-risk areas. For farmed cervid carcasses, Minnesota does not allow cervid carcass movement from a CWD endemic area, except for cut and wrapped meat, quarters or other portions of meat with no part of the spinal column or head attached. Carcasses may not be imported into Minnesota from a herd infected with or exposed to CWD.
It is understood that the concurrent authority granted and referred to in this report is limited to white-tailed deer. Because chronic wasting disease affects additional cervid species, the following sections refer to the ongoing challenges in managing CWD risk to all susceptible animals in the state.
Compliance Inspections and Enforcement
An important component of managing CWD is the regulation of cervid farms. There have been inconsistencies noted in compliance inspections and enforcement activities. Communication with herd owners regarding regulations and other contributing factors to disease spread between wild and farmed herds, such as methods to evaluate the potential for wild and farmed deer interactions near the fence, will aid in managing overall risk. Consistent and firm enforcement of statutes and rules must take place, regardless of which agency has the authority.
Movement
Interstate Movement
Current Minnesota Rules prohibit the import of live cervids from herds infected or exposed to CWD, as well as herds existing in counties where CWD has been detected in free-ranging cervid populations. Interstate movement of live cervids is permitted if the originating herd participates in a federal CWD certification program; however, most of the herds discovered to have CWD in the United States in the past 5 years have been Level 6 (highest level of certification) at the time of disease discovery. This suggests the certification program does not adequately address disease risk. The lack of a validated ante-mortem test for CWD, which would indicate illness or infection sustained before death, allows movement of infected live cervids early in the incubation period of the disease, often months or years before the disease is identified on the source premises. This built-in delay in disease discovery exposes other cervid herds receiving these infected animals, as well as the free-ranging cervid populations that exist in the surrounding area, to increased risk of CWD.
Intrastate Movement
Movement within states (intrastate) holds similar CWD risks as movement between states (interstate). CWD certification status has not proven to be an accurate indicator of a facility’s disease status. Of the 12 farmed cervid herds confirmed with CWD in Minnesota, all but one were at a Level 6 certification status at the time of disease discovery. Further, spread of CWD among farmed herds through intrastate movements has spread the disease hundreds of miles across Minnesota, increasing risk to wild populations through fence-line contact and mechanical movement of prions.
Currently, the BAH defines “CWD Endemic Areas” as 15-mile radius circles around wild CWD-positive deer, and farmed herds within these areas have movement restrictions. However, any movement of deer from CWD endemic areas increases the risk of disease spread.
Costs of CWD Surveillance in Wild and Farmed White-tailed Deer
The State of Minnesota covers the cost of CWD testing of all farmed Cervidae over 12 months of age that die or are killed. In addition, testing is required of newborns over six months of age that die or are killed in herds that are quarantined with CWD-exposed animals in the herd. In 2021, Minnesota spent $55,176 on CWD testing of farmed cervids.
Additionally, Minnesota spent approximately $2.9M in fiscal year 2021 on additional CWD-related activities such as sampling and testing hunter-harvested deer, conducting targeted culling, CWD surveillance planning and deer movement studies.
Each new CWD-positive farmed herd results in a minimum of 3 years of wild deer surveillance at a cost to Minnesota of $300,000 to $500,000. The cost increases if the disease has migrated into the wild population and mitigation and management efforts must continue.
Recommendations
As concurrent authority for farmed white-tailed deer continues, the DNR and BAH recommend the responsibilities that fall under Minnesota statutes 35.155, 35.92 to 35.96, and any administrative rules adopted, be assigned to agencies and acted on in a predictable, coordinated way. DNR and BAH will develop a new interagency MOU to create a shared vision, address all responsibilities, and create a transition plan to implement agreed upon actions and roles. The agencies will continue planning to assess the benefit of revising statutes and rules related to the division of responsibilities between themselves.
Roles and Responsibilities
The DNR and BAH have defined a list of activities involved in the regulation of farmed white-tailed deer and further clarified which activities best fit the skills and mandates of each agency. Examples of activities include inspections and follow up, tracking white-tailed deer movement, data entry and management, and rule development. The agencies will continue to refine roles and responsibilities and will formalize this in an interagency MOU.
Communication
Coordinated communication with Minnesotans and specific stakeholder groups, such as deer farmers and deer hunters, is critically important.
While the 2019 MOU between the DNR and BAH related to roles and responsibilities around cervid management provides a strong foundation, the agencies agree that a coordinated effort must continue to address this important priority.
Recommendations for Rule and Statute Changes to Address CWD Challenges
The BAH has been pursuing changes to Minnesota Rules Chapter 1721 for cervid program rules modifications for approximately two years. The agency has enlisted the assistance of a rules advisory team, held numerous virtual listening sessions for many diverse groups and communicated publicly during the process. The change to concurrent authority occurred during this rules process. The BAH paused its rules process after the legislative change, intending to pick up the important and imperative work with DNR rule writing staff for the white-tailed deer portion of the rules. The BAH recommends the DNR provide designated staff to continue this work in cooperation with the BAH.
The DNR has identified areas of CWD transmission risk it believes can be mitigated through changes to rule and statute. These changes have the potential to benefit both wild cervids and the farmed cervid industry. • Fence deficiencies: Perimeter fences are the last line of defense in keeping farmed deer secure inside the enclosure and keeping wild deer out. Fences must meet specifications and be free of defects to promote animal containment and reduce escapes.
o DNR recommends reducing the time allowed for repair of fence deficiencies from 45 days to 14 days (Statute 35.155, Subd. 4). This change would be further supported in Rule 1721.0380 General Requirements: Subp. 3. Inspections B with a reduction in time allowed for repair from 45 to 14 days. Further, a change to Inspections A to reduce the window for reinspection from 3 months to 30 days will help ensure fence deficiencies are corrected in a timely manner.
• Spread of CWD through interstate and intrastate movement: We must minimize the risk of deer moving between herds spreading disease. To accomplish this, we must be able to account for all animals in a herd, ensure they are properly identified, and inventories are accurate.
o DNR recommends statutory and rule changes that require all white-tailed deer fawns be tagged within 14 days of birth, physical inventories occur on 2-year intervals to verify ID of all animals in the herd, and record keeping that includes age, sex, species, date of birth/acquisition, and parentage (Statute 35.155 Farmed Cervidae, Subd 6, 7; Rules 1721.0390 Animal Identification, 1721.0380, Subp. 10. Record Keeping, 1721.0380 General Requirements).
o DNR recommends prohibiting import of cervids from any herd originating from a state or province where CWD has been detected in either farmed or wild deer. This would also prohibit all movement of live cervids that originate from a herd within a CWD Management Zone, except direct to slaughter (Statute 35.155 Farmed Cervidae, Subd 12; Rules 1721.0400 Importation of Farmed Cervidae, 1721.0410. Intrastate Movement of Farmed Cervidae).
• Rapid detection of CWD within a herd, timely depopulations, and containment of prions in the environment: To increase the opportunity to detect CWD early within a herd, it’s important to test all animals upon death.
o DNR recommends requiring CWD testing upon death for all deer ≥6 months, reporting the death within 7 days, and submitting all collected tissue samples within 7 days to an appropriate laboratory (Statute 35.155 Farmed Cervidae, Subd 11, Rules 1721.0420 CWD).
o DNR recommends that herd owners who fail to test all dead deer for CWD have movement restrictions on their herd.
o DNR recommends that herds confirmed with CWD be required to be depopulated within 30 days by the owner if an indemnification application is not submitted (Rule 1721.0420 CWD). Also, all herd depopulation plans will be required to include perimeter fencing requirements maintained for 20 years to reduce risk of spread to wild cervids (Statute 35.155 Farmed Cervidae, Subd 11, Rules 1721.0420 Subp. 2, CWD).
Appendix A: DNR Project Plan-Captive Cervid Facilities Co-Management
Project Plan
Captive Cervid Facilities Co-Management
DRAFT as of July 22, 2021
Background (Why We’re Doing This)
During the 2021 special legislative session, the state legislature passed a law directing the MN Department of Natural Resources (DNR) and the Board of Animal Health (BAH) to concurrently manage farmed cervid facilities containing whitetailed deer. Part of this concurrent authority provision requires a report to the legislature by February 1, 2022, detailing how the agencies have worked together, an assessment of ongoing challenges to managing Chronic Wasting Disease (CWD) in the state, and recommendations for further statutory and programmatic changes to address the disease. The report and associated activities require focused effort by both agencies to ensure appropriate response. The Commissioner’s Office has established this high-priority project within the DNR’s Enforcement (ENF) and Fish and Wildlife (FAW) divisions to ensure our own agency’s capabilities to work as an effective partner toward that end, and to do our part alongside BAH to make tangible progress.
The current political and operating environment both pose numerous risks, given the high profile of CWD within the state, concerns about the disease’s spread, and the inherent challenges of two state agencies with overlapping but different missions working together quickly and effectively. Nevertheless, the Commissioner’s Office and project team are confident that our work can reflect the best values of the agency and state work: science-driven and fact-based decision-making; accountability to taxpayers and legislature for activities undertaken; and strong partnership with and respect for BAH, captive cervid facility owners, and other stakeholders.
Goals and Deliverables (What We’ll Do Together)
We want to achieve the following broad goals as a project team and agency:
• Prevent the spread of CWD in both farmed and wild cervid populations;
• Ensure compliance of all farmed cervid facilities with relevant state laws and rules;
• Fulfill the legislative requirements for farmed cervid facilities containing white-tailed deer;
• Identify deficiencies of existing laws and rules, provide recommendations in the February report, and keep working beyond that report to make thoughtful changes to those laws and rules; and
• Demonstrate a strong, effective relationship between DNR and BAH.
• Biosecurity Compliance – biosecurity rules must be adhered to by field staff or others going on farmed cervid premises for inspections, enforcement, or other types of site visits to prevent the spread and introduction of disease to and from the premises.
To make progress toward these goals, we will focus on the following specific deliverables during the timeline of this project:
• Immediate rules progress. Engage the current rules package under consideration by the BAH and seek tangible, positive changes regarding farmed cervid facility management that will demonstrate early engagement with the state legislature’s directives.
• Staff capacity. Hire, designate, develop, and/or train staff within the FAW and ENF divisions to establish long-term capacity for inspections, compliance assurance, and related ongoing statutory obligations.
• Data capacity. Engage BAH and Minnesota IT Services (MNIT) to develop and implement the data governance, management, and equitable sharing processes required for effective concurrent authority over farmed cervid facilities containing white-tailed deer.
• Early set of inspections. 40 white-tailed deer facilities would be inspected prior to the legislative report. Facilities inspections would be targeted to get an equitable cross section of facilities of all types and sizes across the state. This would represent a clear, tangible mark of progress that, like the data capacity and immediate rules progress, would improve the quality of the mandated report. At least one representative from FAW and ENF Divisions will be on every inspection. BAH and DNR would be completing inspections together to ensure the inspection process is done in a consistent manner. However, FAW and ENF Divisions would complete inspections without BAH if they are otherwise unable to complete inspections as needed or in the timeline provided within the project plan.
• Communications plan. As we release the report to the legislature, the project will have a communications plan ready to ensure legislators, conservation organizations, the media and public are aware of the work and understand its context and importance. Part of the message should also indicate what next steps may happen, and how to engage future process. The DNR will solicit comments from BAH on the communications.
• Mandated report. Submit a report by February 1, 2022, to the appropriate legislative authority on the implementation of the concurrent authority, as required by the recent law. This report will detail how the agencies have worked together, an assessment of ongoing challenges to managing Chronic Wasting Disease (CWD) in the state, and recommendations for further statutory and programmatic changes to address the disease.
In Scope (What We’ll Do and Discuss to Get the Deliverables)
Analysis of existing policies and rules, and proposals for changes. The fundamental driver of this project is the state legislature’s desire to see things change, to improve outcomes on CWD disease spread. All relevant policies, procedures, and rules are on the table. A science-driven, fact-based approach to policy analysis is essential.
Partnership with the BAH and MNIT. While this project contains deliverables and activities that DNR has some control over, we cannot succeed without our colleagues in BAH and MNIT. This project’s initial focus is on the internal activities we need to conduct immediately, to ensure success. The team’s priority will be to transition to the concurrent inspection, enforcement, and investigation authority implementation in collaboration with the BAH. After completion of the report and draft rules, the project’s leadership will shift the focus toward the more collaborative and longer-term activities required for ultimate success. The activities related to data are particularly complex and will require close partnership, early on.
Engagement with farmed cervid facilities’ owners and other key stakeholders. Effective and thoughtful communication and outreach strategies will be crucial to early and long-term success. The best compliance outcomes are from parties who are informed, engaged, and educated on the regulations’ purpose. We can and should seek their input at appropriate points in the rulemaking and policy analysis process, during and after this project. An initial list of such stakeholders is below.
Out of Scope (What We’ll Set Aside So We Can Focus on the Deliverables)
Wild and farmed cervid species beyond white-tailed deer. While the report and policy components of this project may point out known/discovered interactions between farmed white-tailed deer and other cervid species, the primary focus should be on farmed white-tailed deer. In addition, any enforcement or compliance activities will focus only on what the legislation directs.
Activities beyond winter 2022. For the sake of project focus, this outline is only for those activities that will lead up to the generation, submission, and presentation of a successful legislative report. Certainly, those activities (e.g., hiring staff) will set us up for long term success. New deliverables we design, for which we cannot complete a tangible milestone by February 2022, whether on our own as an agency or in partnership with BAH, will have their own project definition developed and dedicated resources to work on.
Roles and Responsibilities (Who Will Do What)
Most of the project’s roles and responsibilities fall to staff within the ENF and FAW divisions; there are also resources assigned from Operations Services Division (OSD) and MNIT at DNR. As noted above, as the project progresses, project leadership may either adjust this work or generate a new project that would express partnership roles for BAH staff, with their consent and full participation.
snip...
Again, there will be multiple activities that can and must continue beyond the scope of this project. Executive and managing sponsors should consider developing a longer-term planning framework that tracks additional necessary work, such as the development of an advisory group, additional staffing needs, ongoing policy-making processes, long-run enforcement and compliance activities, and how the agency will pursue the recommendations generated by the report. Logistics (Where and How We’ll Do All of This)
Given the multiple deliverables that are part of this project, there will be multiple “sub-teams”:
• Immediate rules changes. Led by Michelle Carstensen.
• Report generation. Led by the project managers.
• Policy analysis (including the interagency consulting team). Led by [TBD].
• First set of early inspections. FAW and ENF will conduct facility inspections. Led by project managers or TBD designees.
• Data protocols. Led by Bruce Anderson.
• Others as needed
The logistics for each team will be a bit different, given the wide differences in timeline and product. Common risks for each sub-team to consider while progressing: Coordination with BAH. Interagency collaboration can be challenging even under the best of circumstances. Here, the time pressures, staffing pressures, and political visibility of the issue all contribute to very high risk of process failure.
In particular, a team from BAH consisting of Linda Glaser, Annie Balghiti and Courtney Wheeler and DNR staff consisting of Michelle Carstensen, Robert Gorecki and Chris Balzer immediately will be assigned to the project. Project managers and managing sponsors should consider how to coordinate these contacts. Closer collaboration on this project, and inclusion of key BAH personnel on the full project team, should be an early consideration. This will help efficiency with communication and logistics for all moving parts.
• Issue complexity. CWD spread is well-recognized as a complex public policy issue involving multiple state and federal agencies; a wide range of stakeholder groups with strongly differing opinions; and natural limits to what testing and observation can tell us in a timely manner.
• COVID-19 protocols. While some staff may be returning from telework (or never did), a large portion of relevant staff should still be presumed teleworking for at least some of the time, early in the project timeline. Sub-teams should carefully consider the safety of all colleagues and partners when scheduling meetings, inspections, and other project activities.
• Public perception and political pressure. The entire project faces the well-known risk of misperceptions or mischaracterization by some members of the public as to what the DNR (or any state agency) can reasonably accomplish, as well as what enforcement activities may be reasonable. Project team members can minimize these risks and their impact by committing to themselves and each other an approach of mutual respect toward differing
perspectives, and a collaborative approach to colleagues who may disagree. Whatever the final product, all project team members must stand behind it.
• Data Collection and Dissemination Protocols. All staff must adhere to data practices regulations under MN Statute: 13.643 Subd. 6. Animal premises data: There are implications for the public (or not public) status of certain data that will require training and careful practice. Close coordination with both agencies’ Data Practices Compliance Officials will be a key strategy in minimizing the risk of inappropriate data use. Data collection will benefit from a data management plan.
The full project team should check in at least monthly. Sub-teams should check in at least weekly. Project managers should consult with managing sponsors (and if desired, the project facilitator) at their discretion, but no less frequently than biweekly.
March 7, 2022 4:39 PM
Proposed moratorium on new deer farms moves on to environment committee
By Rob Hubbard
How widespread are chronic wasting disease and COVID-19 in deer that live on Minnesota farms?
We don’t really know.
A comprehensive study hasn’t been undertaken on the farmed deer of Minnesota, but an Iowa study completed in 2021 found 80% of the sampled deer on farms there tested positive for COVID-19, according to Kevin Dupuis, chairman of the Fond du Lac Band of Lake Superior Chippewa.
That’s one reason Rep. Rick Hansen (DFL-South St. Paul) is sponsoring HF3273, a bill that would prohibit the Board of Animal Health from approving new registrations for the possession of farmed white-tailed deer.
On Monday, the House Agriculture Finance and Policy Committee voted 8-4 along party lines to refer the bill to the House Environment and Natural Resources Finance and Policy Committee.
The bill’s companion, SF3169, sponsored by Sen. John Marty (DFL-Roseville), awaits action by the Senate Agriculture and Rural Development Finance and Policy Committee.
“The first step is to stop the bleeding, and that is to issue no new registrations,” Hansen said. “There is precedence for this, about 20 years ago, with registrations for commercial turtle harvesting. … Last fall, we had testimony that there had been six to 10 new registrations per year.”
Craig Engwall, executive director of the Minnesota Deer Hunters Association, said his approximately 20,000-member organization supported the bill’s proposed moratorium at its recent annual meeting.
“Chronic wasting disease is a strong focus [for the organization], and we virtually unanimously supported a moratorium on new registrations as a means of protecting the wild deer herd,” he said. “On Feb. 1, the DNR and the Board of Animal Health issued their joint report finding that there was about a 34% infraction rate on their inspected farms. These included inadequate fencing, inadequate gates, refusing inspection. We believe we’ve reached the point where the wild deer herd is under significant threat.”
Representing the Minnesota Deer Farmers Association, Tim Spreck said the bill would do “irreparable damage” to the deer-farming industry. “We’re trying to drive the deer-farming industry into oblivion, one cut at a time. We don’t want to be bought out. We don’t want to go away.”
Rep. Rob Ecklund (DFL-International Falls) noted it was the first time he’d heard committee discussion of the state “buying out” the deer farming industry.
“Let’s clean up this industry,” Ecklund said. “I’ve never said let’s eliminate it. I think it has value. I’ve just been trying to protect the wild deer herd.”
When Rep. Paul Anderson (R-Starbuck) asked Hansen if he would support a buyout, Hansen replied, “No, because it would just turn into a publicly funded auction.”
“I think the mistakes have been delicate ones,” Anderson said. “And I think this takes a sledgehammer to things. I think this is too severe and strict on the deer farmers.”
Feb 14 2022 4:05PM
Deer farmers could face more requirements to safeguard against chronic wasting disease
By Brian Hall
In a continuing effort to eradicate and control the spread of chronic wasting disease, Minnesota deer farmers could be forced to test their entire herd.
Sponsored by Rep. Rob Ecklund (DFL-International Falls), HF2814 would require owners of farmed white-tailed deer to test their animals for the disease by October. Additional testing would be required for animals who test positive for chronic wasting disease.
The bill includes a $250,000 appropriation to the Board of Animal Health for the testing and would establish a requirement for a soil test before sale or transfer of land where the disease was detected while farming cervids, including deer, moose and elk.
Following a 9-3 vote by the House Agriculture Finance and Policy Committee Monday, the bill was sent to the House Environment and Natural Resources Finance and Policy Committee without recommendation, in part, due to questions surrounding the testing used for the deer and soil.
The real-time quaking-induced conversion test has not been approved by the U.S. Department of Agriculture.
Rep. Rob Ecklund
“Approval is expected in the near future,” Ecklund said. “We go to great lengths and take all precautions in protecting our meat and food supply. The RTQuIC test is one more tool that we have available to protect the industry.”
Several Republicans felt the bill was being considered too early given the test hasn’t been approved by the USDA.
Rep. Paul Anderson (R-Starbuck) said that the bill was originally going to be laid over before a late addition recommended it be moved on. Because of the time, Anderson said members didn’t feel an urgency in putting amendments forward.
“Given what we’ve heard today, we do need to slow down,” said Rep. John Burkel (R-Badger).
Ecklund said there’s approximately 3,500 captive white-tailed deer in the state.
“If we do find any problems through the use of this technology, then we would know the areas in the state that need the most attention,” he said.
The companion, SF3037, is sponsored by Sen. John Marty (DFL-Roseville) and awaiting action by the Senate Agriculture and Rural Development Finance and Policy Committee.
“We’ve been fighting CWD for five years,” Ecklund said. “I’d like to get to the bottom of what’s going on here.”
He later added: “If we had something in our swine population, if we had something in our turkey population, if we had something in our cattle population, it would be all hands on deck to make sure that we were addressing this.”
''Several Republicans felt the bill was being considered too early given the test hasn’t been approved by the USDA.''
''Rep. Paul Anderson (R-Starbuck) said that the bill was originally going to be laid over before a late addition recommended it be moved on. Because of the time, Anderson said members didn’t feel an urgency in putting amendments forward.''
“Given what we’ve heard today, we do need to slow down,” said Rep. John Burkel (R-Badger).''
''Ecklund said there’s approximately 3,500 captive white-tailed deer in the state.''
“We’ve been fighting CWD for five years, ” Ecklund said. “I’d like to get to the bottom of what’s going on here.”
END
***> WHILE republicans and captive lobbyist continue to flounder, CWD continues to spread, it's the name of the game...terry
SATURDAY, JANUARY 29, 2022
Minnesota Chronic Wasting Disease CWD PrP 146 WILD Positive To Date
Minnesota captive cwd to date???
TUESDAY, MARCH 08, 2022
Minnesota Board of Animal Health Report Concurrent Authority Regulating Farmed White-tailed Deer and CWD TSE Prion
FRIDAY, JANUARY 28, 2022
Chronic Wasting Disease Transmission Risk Assessment for Farmed Cervids in Minnesota and Wisconsin
MONDAY, OCTOBER 11, 2021
Minnesota DNR temporarily bans farmed deer movement into and within state to protect state’s wild white-tailed deer
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
North Dakota Game and Fish Department reports 26 deer tested positive during the 2021 hunting season
CWD Test Results
Wed, 02/23/2022
With most chronic wasting disease testing completed, the North Dakota Game and Fish Department reports 26 deer tested positive during the 2021 hunting season.
Fourteen were from hunting unit 3F2, eight from unit 3A1, and one was found in unit 3B1. Single positive deer were also found in three units (3C, 3D1 and 3E2) where the disease had not been previously detected.
CWD is a fatal disease of deer, moose and elk that can cause long-term population declines as infection rates climb.
The estimated infection rates in unit 3F2 were 4.9% in mule deer and 3% in whitetail deer. In unit 3A1, the estimated infection rate in mule deer was 6.9%. Approximately 4.9% of hunters turned in heads for testing in units where the Department was focusing surveillance efforts.
Game and Fish will use its 2021 surveillance data to guide its CWD management strategy moving forward. More information about CWD can be found at gf.nd.gov/cwd.
North Dakota NDGF Deer in Minnesota Suspected of CWD, Surveillance Expands to Unit 2B
Deer in Minnesota Suspected of CWD, Surveillance Expands to Unit 2B
Thu, 11/04/2021
Following Wednesday’s announcement from the Minnesota Department of Natural Resources of a suspected case of chronic wasting disease in a wild deer southwest of Climax, Minn., the state Game and Fish Department is increasing its Hunter-Harvested Surveillance efforts to include Unit 2B in eastern North Dakota.
Hunters in deer gun Unit 2B are encouraged to submit the head of their harvested animal for testing in Fargo, Grand Forks or Hillsboro. Game and Fish Department staff will also be stationed at the Hillsboro location on Saturdays and Sundays from 10 a.m. – 6 p.m. through the deer gun season to sample deer heads hunters wish to keep.
Game and Fish wildlife veterinarian Dr. Charlie Bahnson said CWD is a fatal brain disease of deer that can cause long-term population effects as infection rates climb.
“It is a different disease than epizootic hemorrhagic disease that was detected in many parts of the state this fall,” Bahnson added. “Hunter-Harvest Surveillance provides information that is critical to track and manage CWD.”
Heads of adult or yearling deer can be dropped off at these collection sites:
Fargo – NDSU Veterinary Diagnostic Lab, 4035 19th Ave. N. Grand Forks – Tractor Supply Co., 4460 32nd Ave. S. Hillsboro – Cenex, 105 Sixth St. SW
More information on CWD, including collection locations, is available on the Game and Fish website, gf.nd.gov.
CWD Test Results Tue, 01/19/2021
With most chronic wasting disease testing completed, the North Dakota Game and Fish Department reports 18 deer tested positive during the 2020 hunting season.
Fourteen were from hunting unit 3F2, two were from unit 3A1 and one was from unit 4B. A white-tailed deer harvested in unit 3A2 also tested positive and was the first detection in the unit.
CWD is a fatal disease of deer, moose and elk that can cause long-term population declines as infection rates climb.
The estimated infection rates in unit 3F2 were 5.1% in mule deer and 2.2% in whitetail deer. It was less than 2% in other positive units. Approximately 7% of hunters turned in heads for testing in units where the Department was focusing surveillance efforts.
Game and Fish will use its 2020 surveillance data to guide its CWD management strategy moving forward. More information about CWD can be found at gf.nd.gov/cwd.
Minnesota CWD suspected in a wild deer harvested along northwestern Minnesota’s border
DNR News Release
For Immediate Release:
Nov. 3, 2021
For more information: Contact DNR Information Center by email or call 888-646-6367.
CWD suspected in a wild deer harvested along northwestern Minnesota’s border
Area deer hunters asked to submit samples for testing at stations in Climax, Neilsville The first suspected case of chronic wasting disease in a wild deer along Minnesota’s border with North Dakota has prompted the Minnesota Department of Natural Resources to implement voluntary CWD sampling for all deer harvested in this area during the 2021 firearms season.
Hunters who harvest deer in permit areas 261 and 262, which are located between Moorhead on the south and Oslo on the north, are strongly encouraged to leave samples at self-service stations in Neilsville and Climax. Once exact locations are established for these two stations, details and instructions will be available on the DNR website, alongside information about sampling stations in CWD surveillance, management and control zones.
Preliminary test results from a deer harvested southwest of Climax strongly indicate a CWD infection. Confirmation of the initial result is expected next week.
No cases of CWD had been reported in wild or captive deer in nearby areas, and no CWD sampling requirements were in place. The hunter voluntarily collected the sample and paid for a private test. When preliminary results came back positive, the hunter contacted the DNR.
“Thanks to this hunter’s early discovery, we have the chance to act quickly and be proactive,” said Seth Goreham, acting wildlife research manager for the DNR. “We’re asking hunters to submit samples so we can determine the extent of CWD in the area and take steps to help control the spread.”
Testing is free for deer harvested in permit areas 261 and 262 as well as any other deer permit area designated a CWD surveillance, management or control zone. Hunters outside a CWD zone can collect lymph node samples and pay a small fee for a CWD test. Complete video instructions on how to properly collect a lymph node sample and laboratory information is available on the DNR website.
CWD is a fatal neurological disease that affects cervids, including white-tailed deer. It is found globally and in about half of the states in the U.S. CWD remains relatively rare in Minnesota, but is a concern as there is no known cure.
The DNR continues to take aggressive steps to combat CWD and its spread. So far 118 cases of CWD have been documented in Minnesota’s wild deer herd, most of them in the southeastern part of the state. The disease is also being actively and aggressively managed near Bemidji, the Brainerd Lakes area and in the south metropolitan area.
Complete information about CWD is available on the DNR website at mndnr.gov/cwd.
###
A CWD-positive white-tailed deer buck harvested in hunting unit 3A2 in 2020 altered deer management strategies in that and surrounding units. The goal is to minimize the CWD prevalence rate and reduce spread of the disease outside infected units; therefore, a more aggressive harvest strategy remains in the northwestern part of the state. From the 2020 surveillance, CWD-positive deer were detected in 3A1 (two mule deer), 3A2 (one white-tailed deer), 3F2 (nine mule deer and five white-tailed deer) and 4B (one mule deer). Increased surveillance will continue in these units to better understand CWD prevalence.
MONDAY, JANUARY 11, 2021
North Dakota 18 deer tested positive for CWD during the 2020 hunting season, with most testing completed
Oct. 25, 2021
Hunters Encouraged to Have Deer Tested for CWD
The North Dakota Game and Fish Department will continue its Hunter-Harvested Surveillance program during the 2021 hunting season by sampling deer for chronic wasting disease from select units in the central and western portion of the state.
Samples will be tested from deer taken from units 2H, 2I, 2J1, 2J2, 2K1, 2K2, 3A1, 3A2, 3A3, 3A4, 3B1, 3B3, 3C, 3E1, 3E2, 3F1, 3F2, 4A, 4B and 4C.
CWD is a slow-moving brain disease of deer, moose and elk that can cause population-level impacts under high infection rates.
“Many folks are aware of the fairly bad epizootic hemorrhagic disease year we’ve had,” said Game and Fish veterinarian Dr. Charlie Bahnson. “While EHD is a different disease from CWD, it illustrates the impact diseases can have on our wildlife populations. And unlike EHD, which is cyclical, CWD can become an increasing, annual pressure on our herd.”
Knowing where CWD is in the state and how many deer are infected is critical for managing the disease.
“One major goal is to confidently determine what areas do not have CWD,” Bahnson said. “We need to test a lot of deer to make that assessment, which is why hunters’ willingness to help is so important.”
Hunters are encouraged to drop off heads of adult or yearling deer at collection locations. Fawns and head-shot deer cannot be tested. Hunters wishing to keep the heads can bring them to a Game and Fish district office during business hours to have them sampled.
Results will be provided within four weeks, barring delays, by visiting My Account on the department’s website, gf.nd.gov, where you can also add or update contact information. Click Additional Info for CWD results for lottery licenses or Inbox for results for first-come, first-served licenses.
Hunters should note whole carcasses or heads of deer taken from units 3A1, 3A2, 3B1, 3F2, 4B and 4C may not be transported outside of the unit. Exception: hunters can transport whole deer carcasses between adjoining CWD carcass restricted units.
More information on CWD, including transportation restrictions, is available at the Game and Fish website.
North Dakota Outdoors
AUGUST-SEPTEMBER 2021 • NUMBER 2 • VOLUME LXXXIV
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A CWD-positive white-tailed deer buck harvested in hunting unit 3A2 in 2020 altered deer management strategies in that and surrounding units. The goal is to minimize the CWD prevalence rate and reduce spread of the disease outside infected units; therefore, a more aggressive harvest strategy remains in the northwestern part of the state. From the 2020 surveillance, CWD-positive deer were detected in 3A1 (two mule deer), 3A2 (one white-tailed deer), 3F2 (nine mule deer and five white-tailed deer) and 4B (one mule deer). Increased surveillance will continue in these units to better understand CWD prevalence.
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Baiting Restrictions in North Dakota Hunters are reminded it is unlawful to hunt big game over bait, or place bait to attract big game for the purpose of hunting, in deer units 3A1, 3A2, 3A3, 3A4, 3B1, 3C west of the Missouri River, 3E1, 3E2, 3F1, 3F2, 4A, 4B and 4C. The restriction is in place to help slow the spread of chronic wasting disease, a fatal disease of deer, moose and elk that can cause long-term population declines if left unchecked. In addition, baiting for any purpose is prohibited on all North Dakota Game and Fish Department wildlife management areas. Hunting big game over bait is also prohibited on all U.S. Fish and Wildlife Service national wildlife refuges and waterfowl production areas, U.S. Forest Service national grasslands, U.S. Army Corps of Engineers managed lands, and all North Dakota state trust, state park and state forest service lands. More information on CWD can be found at the Game and Fish website, gf.nd.gov
North Dakota CWD Big Game Transport Rules, Hunting Big Game Over Bait, 26 deer have tested positive to date Big Game Transport Rules
Hunting Big Game Over Bait
Tue, 01/19/2021
With most chronic wasting disease testing completed, the North Dakota Game and Fish Department reports 18 deer tested positive during the 2020 hunting season.
Fourteen were from hunting unit 3F2, two were from unit 3A1 and one was from unit 4B. A white-tailed deer harvested in unit 3A2 also tested positive and was the first detection in the unit.
CWD is a fatal disease of deer, moose and elk that can cause long-term population declines as infection rates climb.
The estimated infection rates in unit 3F2 were 5.1% in mule deer and 2.2% in whitetail deer. It was less than 2% in other positive units. Approximately 7% of hunters turned in heads for testing in units where the Department was focusing surveillance efforts.
Game and Fish will use its 2020 surveillance data to guide its CWD management strategy moving forward. More information about CWD can be found at gf.nd.gov/cwd.
CWD Surveillance Continued
Since 2009, 26 deer have tested positive for chronic wasting disease in the state. Those animals that tested positive were from hunting units in parts of southwestern and northwestern North Dakota
Testing in North Dakota for the invariably fatal disease began in 1998 with roadkilled, sick and suspect animals. In the early 2000s, Game and Fish increased CWD surveillance efforts by annually collecting samples from hunter-harvested deer, elk and moose Typically, surveillance efforts from hunter-harvested deer focuses on a third of the state on a rotating basis, and those areas where wildlife managers are trying to manage for CWD. In 2020, given the COVID situation, Department wildlife managers prioritized efforts and focused resources and personnel in the southwestern and northwestern parts of the state where the disease continued to be of greater concern CWD test results for the 2020 deer gun season weren’t available at the time of publication.
***North Dakota CWD TSE Prion
North Dakota, to date, CWD has been detected in 26 cervid (personal communication Dr. Charlie Bahnson, wildlife veterinarian for the North Dakota Game and Fish Department...November 23, 2020).
FEBRUARY 2020 • NUMBER 7 • VOLUME LXXXII
Eight deer taken during the 2019 North Dakota deer gun season tested positive for chronic wasting disease, according to Dr. Charlie Bahnson, wildlife veterinarian for the North Dakota Game and Fish Department.
All were antlered deer taken from areas previously known to have CWD – six from unit 3F2 and two from 3A1. Bahnson said six of the eight were mule deer, with two whitetails from unit 3F2. CWD was not detected in any deer harvested in the eastern portion of the state where hunterharvested surveillance was conducted last fall. In addition, no elk or moose tested positive.
“Only about 15% of hunters submit heads for testing in units where CWD has been found, so the infection rate is more meaningful than the raw number of positive animals found,” Bahnson said. “Approximately 3% of harvested mule deer were infected with CWD in unit 3F2, and roughly 2% in unit 3A1. Our infection rate in whitetails in 3F2 was about 1%.
“Overall,” he continued, “we could probably live with these current infection rates long-term, but they suggest an upward trend and we’ve certainly seen an expansion in the known distribution of the disease. We need to continue to try to limit the spread within our herds as best as we can.”
CWD is a fatal disease of deer, moose and elk that can cause long-term population declines if left unchecked.
Bahnson said the eight positive deer put the total at 11 detected since September 1. As previously reported, two mule deer taken in September tested positive for CWD – one was harvested during the archery season from deer gun unit 4B, and one during the youth season in unit 3A1. CWD was also detected in a whitetailed deer from unit 3F2 that was euthanized in December following a report from the public that it appeared sick and was displaying erratic behavior.
Game and Fish will use its 2019 surveillance data to guide its CWD management strategy moving forward. More information about CWD is available on the Game and Fish Department’s website, gf.nd.gov/cwd.
Taking aim at chronic wasting disease: Fatal deer disease a focus as rifle hunting season approaches
Written By: Brad Dokken | Nov 4th 2019 - 8am.
To date, 17 deer – all wild – have tested positive for CWD in North Dakota, Bahnson said. First detected in 2009 in south-central North Dakota, CWD in the past year has been found in northwest North Dakota and, most recently, McKenzie County in the North Dakota Badlands, where a mule deer buck shot with a bow in September in hunting Unit 4B tested positive.
The deer in 4B was tested as part of a routine sampling effort. A second mule deer buck taken during the September youth season in Unit 3A1 in Divide County also tested positive.
Both deer appeared perfectly healthy, Bahnson said. That’s been the case with most of the nearly 30,000 deer Game and Fish has tested since it began sampling for the disease in 2002, he said.
Deer found near Williston tests positive for CWD
Written By: Forum staff reports | Mar 19th 2019 - 2pm.
BISMARCK — A white-tailed deer found dead just south of Williston in late February has been confirmed positive for chronic wasting disease (CWD), according to Dr. Charlie Bahnson, wildlife veterinarian for the North Dakota Game and Fish Department.
The find means CWD is much farther south than previously thought, officials said.
CWD is a fatal disease of deer, moose and elk that can cause long-term population declines if left unchecked. Since 2009, 14 other deer have tested positive for CWD in North Dakota; 13 from Grant and Sioux counties in hunting unit 3F2 in the southwest, and the other taken last fall from the northwest in Divide County.
The deer found near Williston is the first documented case of a mortality due to CWD in North Dakota. Previous deer found with CWD were hunter harvested before they became sick. This latest deer was severely emaciated and had an empty digestive tract, officials said.
The Game and Fish Department will collect additional samples for testing through targeted removal over the next week or so. In addition to the targeted removal and testing, Game and Fish will review the need to amend the current CWD proclamation to reflect the new CWD positive.
Chronic Wasting Disease Detected in McKenzie County
Two mule deer taken in September tested positive for chronic wasting disease, including one during the archery season from deer gun unit 4B in McKenzie County, where CWD had not previously been found. The other deer was harvested during the youth season in unit 3A1 in Divide County where CWD was first detected last fall.
North Dakota Game and Fish Department wildlife veterinarian Dr. Charlie Bahnson said the finding in 4B marks the first detection of CWD in the badlands.
“This is an iconic place to hunt big game where people travel to from across the state,” Bahnson said. “By no means does this first detection spell doom for hunting in this area, as long as we are proactive in trying to keep infection rates from climbing. We also need to reduce the chance of CWD spreading to new areas.”
Game and Fish will review its CWD management strategy after the deer rifle season and will consider making revisions for next season. While unit 4B does not have carcass transportation restrictions in place for 2019, Bahnson does recommend that hunters in 4B submit their deer for testing, and avoid transporting high-risk carcass parts, such as the brain and spinal column, outside of the hunting unit.
North Dakota CWD 2020
NORTH DAKOTA CAPTIVE CERVID FARMING
THURSDAY, NOVEMBER 04, 2021
North Dakota NDGF Deer in Minnesota Suspected of CWD, Surveillance Expands to Unit 2B
TUESDAY, MARCH 03, 2020
North Dakota Eight deer taken during the 2019 deer gun season tested positive for chronic wasting disease CWD TSE Prion
FRIDAY, JANUARY 17, 2020
North Dakota 11 Positive Chronic Wasting Disease CWD TSE Prion detected since Sept 1, 2019
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WEDNESDAY, FEBRUARY 23, 2022
North Dakota Game and Fish Department reports 26 deer tested positive during the 2021 hunting season
Texas Chronic Wasting Disease CWD TSE Prion Confirmed Positive Jumps By 91 Total To Date 361 Cases
TEXAS CWD TRACKING
CWD Positive
Confirmation Date Free Range/Captive County Source Species Sex Age
Pending Breeder Deer Kimble Facility #6 White-tailed Deer Unknown 3.5
Pending Breeder Deer Hunt Facility #9 White-tailed Deer M 1.9
N/A Free Range Hartley N/A Mule Deer M 5.5
2022-01-25 Free Range Medina N/A White-tailed Deer F 5.5
2022-01-12 Breeder Deer Hunt Facility #9 White-tailed Deer M 1.5
2022-01-12 Breeder Deer Hunt Facility #9 White-tailed Deer F 3.5
2022-01-12 Breeder Release Site Medina Facility #3 Red Deer F 4.5
2022-01-12 Free Range Hartley N/A White-tailed Deer M 3.5
2022-01-12 Free Range Hartley N/A Mule Deer M 5.5
2022-01-12 Free Range Hartley N/A Mule Deer M 4.5
2022-01-12 Free Range Hartley N/A Mule Deer M 5.5
2022-01-12 Free Range Hartley N/A Mule Deer F 3.5
2022-01-12 Breeder Deer Kimble Facility #6 White-tailed Deer Unknown 5.5
2022-01-12 Free Range Hartley N/A Mule Deer M 3.5
2022-01-12 Free Range Hartley N/A Mule Deer M 7.5
2022-01-10 Free Range Medina N/A White-tailed Deer M 4.5
2022-01-10 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.3
2022-01-10 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 5.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 5.4
2022-01-06 Free Range Medina N/A White-tailed Deer M 2.5
2021-12-28 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2021-12-28 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2021-12-13 Free Range Medina N/A White-tailed Deer M 3.5
2021-12-13 Breeder Deer Duval Facility #13 White-tailed Deer F 4.4
2021-12-13 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 8.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.1
Showing 1 to 100 of 361 entries Previous Next
National CWD Tracking Map
“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).
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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
TEXAS CWD TSE PRP
SATURDAY, FEBRUARY 26, 2022
Texas Chronic Wasting Disease CWD TSE Prion Confirmed Positive Jumps By 91 Total To Date 361 Cases
FRIDAY, APRIL 30, 2021
Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
WEDNESDAY, DECEMBER 04, 2013
Chronic Wasting Disease CWD and Land Value concerns?
TUESDAY, APRIL 13, 2021
Implications of farmed-cervid movements on the transmission of chronic wasting disease
TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
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
THURSDAY, AUGUST 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD
THURSDAY, FEBRUARY 17, 2022
Captive Cervids and their Contribution to CWD
MONDAY, MAY 02, 2022
Arkansas has detected 1,324 case of CWD TSE Prion in Cervid AS OF 31 MAR 2022
MONDAY, MAY 09, 2022
Ohio 9 ADDITIONAL CWD-POSITIVE DEER CONFIRMED IN WYANDOT, MARION COUNTIES
MONDAY, APRIL 11, 2022
Pennsylvania new DMA 7 created when CWD recently was detected at a captive facility in Lycoming County
MONDAY, MAY 09, 2022
Colorado CWD TSE Prion Detected in 40 of 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds
THURSDAY, MARCH 31, 2022
North Carolina Wildlife Commission Announces First Chronic Wasting Disease CWD-Positive TSE PrP Deer
TUESDAY, MARCH 08, 2022
Alabama Second Case of CWD Confirmed in Northwest
WEDNESDAY, MAY 18, 2022
Upper Midwest tribal natural resource managers' perspectives on chronic wasting disease outreach, surveillance, and management
SUNDAY, MAY 08, 2022
USA National Prion Disease Pathology Surveillance Center Surveillance Update April 11th, 2022
Terry S. Singeltary Sr., Bacliff, Texas USA 77518, flounder9@verizon.net Galveston Bay, on the bottom...
posted by Terry S. Singeltary Sr. at
11:16 AM
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