Michigan CWD TSE Prion Total Suspect Positive Deer Jumps To 181 to date
Michigan CWD TSE Prion Total Suspect Positive Deer Jumps To 181 with total deer tested 80,131 to date.
Michigan 2019 to December 31, 2019 CWD TSE Prion Total 65 cases positive
https://www.michigan.gov/dnr/0,4570,7-350-79136_79608_90516_90536-501527--,00.html
Michigan Total Captive CWD TSE Prion Positives including trace out and traces in of all captive, breeder, farm, urine mills, antler velvet mills, high or low fence, big or small ranch, THOSE FIGURES ARE STORED UNDERGROUND IN A BUNKER MARKED TOP SECRET, apparently, because MDARD will not release that information to the public apparently...so sad! the public needs to know this, in order to help contain the spread of CWD TSE Prion imo...or stay away from...terry
Sent: Mon, Jan 27, 2020 4:23 pm
Subject: Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?
Michigan Chronic Wasting Disease wild deer only update through January 1, 2020
Subject: CWD TSE Prion better bust a move
i think some hunters that don't read this carefully are going to think this is a cure all for cwd tse contamination. IT'S NOT!
first off, it would take a strong bleach type sodium hypochlorite, that is NOT your moms bleach she uses in her clothes, and store bought stuff.
Concentrated bleach is an 8.25 percent solution of sodium hypochlorite, up from the “regular bleach” concentration of 5.25 percent.Nov 1, 2013 https://waterandhealth.org/disinfect/high-strength-bleach-2/
second off, the study states plainly;
''We found that a five-minute treatment with a 40% dilution of household bleach was effective at inactivating CWD seeding activity from stainless-steel wires and CWD-infected brain homogenates. However, bleach was not able to inactivate CWD seeding activity from solid tissues in our studies.''
''We initially tested brains from two CWD-infected mice and one uninfected mouse using 40% bleach for 5 minutes. The results from these experiments showed almost no elimination of prion seeding activity (Table 4). We then increased the treatment time to 30 minutes and tested 40% and 100% bleach treatments. Again, the results were disappointing and showed less than a 10-fold decrease in CWD-seeding activity (Table 4). Clearly, bleach is not able to inactivate prions effectively from small brain pieces under the conditions tested here.''
''We found that both the concentration of bleach and the time of treatment are critical for inactivation of CWD prions. A 40% bleach treatment for 5 minutes successfully eliminated detectable prion seeding activity from both CWD-positive brain homogenate and stainless-steel wires bound with CWD. However, even small solid pieces of CWD-infected brain were not successfully decontaminated with the use of bleach.''
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659
https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html
i think with all the fear from recent studies, and there are many, of potential, or likelihood of zoonosis, if it has not already happened as scjd, i think this study came out to help out on some of that fear, that maybe something will help, but the study plainly states it's for sure not a cure all for exposure and contamination of the cwd tse prion on surface materials. imo...terry
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
Michigan Total Captive CWD TSE Prion Positives including trace out and traces in of all captive, breeder, farm, urine mills, antler velvet mills, high or low fence, big or small ranch, THOSE FIGURES ARE STORED UNDERGROUND IN A BUNKER MARKED TOP SECRET, apparently, because MDARD will not release that information to the public apparently...so sad! the public needs to know this, in order to help contain the spread of CWD TSE Prion imo...or stay away from...terry
Sent: Mon, Jan 27, 2020 4:23 pm
Subject: Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?
Michigan 2018 CWD TSE Prion Total 62 cases positive
Michigan 2019 to December 31, 2019 CWD TSE Prion Total 65 cases positive
Michigan Total to date CWD TSE Prion 174 cases positive
2019 CWD Testing Goals and Results as of January 24, 2020
Number Positive Total to date 65
PLEASE NOTE, THE ABOVE DOES NOT INCLUDE CAPTIVE FARMED CERVID IN MICHIGAN, AND CWD TSE PRION POSITIVES THERE FROM, TRACE OUT POSITIVES AND SUCH, WHERE THE DEPARTMENT OF AGRICULTURE KEEP THOSE FIGURES CLOSE AT HAND. THESE ARE SEPARATE CWD TSE POSITIVE FIGURES KEPT IN A SECRET BUNKER UNDERGROUND MARKED TOP SECRET, APPARENTLY...TSS
Biol. Rev. (2019), pp. 000–000. 1 doi: 10.1111/brv.12568
The ecology of chronic wasting disease in wildlife
Luis E. Escobar1,∗,† , Sandra Pritzkow2,†, Steven N. Winter1 , Daniel A. Grear3, Megan S. Kirchgessner4, Ernesto Dominguez-Villegas5, Gustavo Machado6 , A. Townsend Peterson7,† and Claudio Soto2,†
snip...
V. ROLE OF THE ENVIRONMENT AND WILDLIFE IN THE SPREAD OF CWD
Experimental studies have shown that infectious prions can enter the environment through saliva, faeces, urine, blood, antler velvet, or placenta tissue from infected animals, and carcasses (Angers et al., 2009; Zabel & Ortega, 2017). Importantly, CWD contamination of the environment via prion shedding in cervid excreta occurs many months before the onset of clinical disease (Mathiason et al., 2009; Plummer et al., 2017). Prions are hardy in the environment, are resistant to most general disinfectants (e.g. heating, most disinfectant chemicals, ultraviolet and ionizing radiation), and can remain infective for years to decades (Georgsson, Sigurdarson & Brown, 2006; Seidel et al., 2007; Smith, Booth & Pedersen, 2011). We recently reported that plants efficiently bind, uptake, retain, and transport infectious prions (Pritzkow et al., 2015). Other natural or man-made components of the environment, such as soil, rocks, wood, metals, and plastic, bind prions and do not diminish infectivity to susceptible species (Pritzkowet al., 2018). While oral ingestion is the most common route of exposure for prion disease, infectious scrapie prions caused 100% mortality via airborne transmission in a laboratory challenge of mice (Haybaeck et al., 2011). One report suggested that prions bound to soil are more infective than free prions, so soil may serve both as an environmental reservoir and a facilitator of CWD prion transmission (Johnson et al., 2007). Soils of different texture, mineralogy, and organic content appear to bind differently to prions and show distinct infectivity rates via oral or aerosolized transmission (Johnson et al., 2007). For example, soils with high organic material content (e.g. high concentration of humic acid) appear to degrade CWD prions faster (Kuznetsova et al., 2018).
Direct exposure of non-cervid animals to CWD-infected cervids could help to spread CWD. For example, hawks, owls, crows, dogs, cats, coyotes, raccoons, skunks, mink, foxes, and opossums that consume deer carcasses could act as spillover hosts and potentially vector spreaders of CWD (Bunk, 2004; Jennelle et al., 2009), although there has been no detection of CWD in any of these species (Fig. 2). Additionally, supplemental wildlife feeding can increase disease transmission by exacerbating deer densities, increasing contact rates, altering normal behaviour, and prolonging exposure to potentially contaminated areas (Thompson, Samuel & Van Deelen, 2008). For example, feeding grounds used to subsidize wild elk during the winter (e.g. in Wyoming) increase the risk of disease transmission (Creech et al., 2012). Similarly, recent detection of CWD PrPSc in ecologically relevant environments, such as natural mineral licks where wildlife obtain minerals from soil and water consumption, suggests a key role of landscape features in CWD transmission risk (Plummer et al., 2018). Thus, identifying where and when CWD occurs in a timely fashion can help inform policies regarding baiting and supplemental feeding of cervids and to consider direct habitat modification with the aim of reducing infectious contact (Sorensen, van Beest & Brook, 2014). Identifying the environmental conditions that facilitate or limit CWD infectivity, as well as the relative importance of CWD transmission from environmental reservoirs versus direct animal–animal transmission, may help to identify potential control methods (Grear et al., 2010).
snip...see;
Michigan Deer
Until further notice, the Michigan Department of Agriculture is allowing cervidae importation on a permit basis ONLY. General information is listed below. Contact Melanie Hart at 517-284-5679 or HartM1@Michigan.gov for information. Completed applications can be submitted to Melanie Hart at HartM1@Michigan.gov.
Dr. Jennifer Sidge Cervids & Small Ruminants sidgej@michigan.gov 517-284-5692
Dr. Nora Wineland State Veterinarian & Division Director winelandn@michigan.gov 517-284-5689
Dr. Nancy Barr Assistant State Veterinarian TB & Ruminant Animals barrn@michigan.gov 517-284-5669
MICHIGAN DEPARTMENT OF AGRICULTURE, CAPTIVE DEER FARMING, AND CHRONIC WASTING DISEASE CWD TSE PRION
Michigan DNR CWD TSE Prion pages, updates, and figures are confusing to me.
Michigan Department of Agriculture Captive Deer Farming and CWD TSE Prion seems more secretive $$$
That's to bad for any fair chase hunters (if any exist anymore) in the state of Michigan, but that's what the USDA et al do, protect the industry at all cost$
I call it state by state, pay to play, trucking cwd tse prion, but that's just my opinion.
SINCE the recent findings of cwd tse prion in captive herds again in Michigan, where 3 positives were found, i have not, and cannot get any information on the depopulation efforts from that herd, CWD IDENTIFIED IN NEWAYGO COUNTY FARMED DEER in 3 white-tailed deer. i had heard nothing about depopulation efforts or update there from, so, i called the number above, was finally connected to a Dr. Sidge, where i was told by Dr. Sidge, that if i was reporting on cwd in captive herds in Michigan, she nor MDARD would give me any figures on the captive positive cwd cases or any more positives if any, or any history there from, depopulation efforts, quarantine efforts, decontamination efforts, NOTHING AT ALL, period. she repeated this, that if i was going to write anything about cwd in captive herds in Michigan, she nor MDARD would not speak to me. that i could look at their website, that's it, where these figures do not exist. i simply wanted to know what the efforts of CWD IDENTIFIED IN NEWAYGO COUNTY FARMED DEER in 3 white-tailed deer were now, had any other positives been found, trace outs etc. had the herd been depopulated and what the test results were? what the total figures on _all_ captive and depopulated positive captive positives there from, to date in Michigan? she told me again, if i was reporting on cwd in captive herds in Michigan, she nor MDARD would give me any figures on the captive positive cwd cases, depopulation efforts, AT ALL, period. i could look at their website, where these figures do not exist. i think i might have repeated myself, but i wanted to make sure you all understand what's going on here.
so, there your are, protect the farmed deer industry at all cost$
TUESDAY, JANUARY 14, 2020
Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm
TUESDAY, JANUARY 07, 2020
Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 174 confirmed to date
CWD IDENTIFIED IN NEWAYGO COUNTY FARMED DEER
For Immediate Release: January 14, 2020
Media Contact: Jessy Sielski, 517-284-5725
LANSING – The Michigan Department of Agriculture and Rural and Development (MDARD) has confirmed chronic wasting disease (CWD) in three white-tailed deer from a Newaygo County deer farm. All three deer were four-and-a-half years old. The samples were submitted for routine testing as part of the state’s CWD surveillance program for farmed deer.
To date, CWD has not been detected in free-ranging deer in Newaygo County. As part of MDARD’s disease response, an investigation will be conducted to rule out exposure of any other farmed deer.
“Chronic wasting disease is a serious disease affecting both farmed and free-ranging deer,” said State Veterinarian Nora Wineland, DVM. “MDARD and the Michigan Department of Natural Resources work together, in partnership with the state’s deer farmers, to ensure the protection of all of Michigan’s deer.”
Since 2008, CWD has been detected in four additional privately-owned cervid facilities from Kent, Mecosta, and Montcalm Counties. The deer farm in Newaygo County is the fifth Michigan farm in which CWD has been detected.
CWD is a fatal neurological disease that affects white-tailed deer, mule deer, elk, and moose. CWD can be transmitted directly from one animal to another, as well as indirectly through the environment. Infected animals may display abnormal behavior, progressive weight loss and physical debilitation. To date, there have been no reported cases of CWD infection in humans. However, as a precaution, the U.S. Centers for Disease Control and the World Health Organization recommend that infected animals not be consumed as food by either humans or domestic animals.
More information about CWD can be found at Michigan.gov/CWD.
''Since 2008, CWD has been detected in four additional privately-owned cervid facilities from Kent, Mecosta, and Montcalm Counties. The deer farm in Newaygo County is the fifth Michigan farm in which CWD has been detected.''
March 30, 2018
Contact: Lt. David Shaw, 616-218-3762
Mecosta County man sentenced following DNR investigation
Game ranch owner falsified information related to chronic wasting disease testing
A Mecosta County game ranch owner has been sentenced on charges resulting from an investigation by the Michigan Department of Natural Resources Law Enforcement Division, in cooperation with the Michigan Department of Agriculture and Rural Development.
Lester Jay Gemmen, 64, of Morley was charged with providing false information regarding the origin of two deer heads that were submitted for disease testing, and for failing to properly maintain fencing at the Super G Ranch. The ranch is a privately owned cervid (POC) facility, a designation that includes game ranches and hunting ranches.
He was sentenced by the 77th District Court to 60 days in jail for each count, ordered to pay $775 in fines and costs and must perform 80 hours of community service.
The investigation began in 2017 after two of the six deer heads submitted by Gemmen tested positive for chronic wasting disease (CWD).
“I commend the detectives from our Special Investigations Unit and our field conservation officers for their thorough, professional approach to this investigation,” said 1st Lt. David Shaw, supervisor of the Special Investigations Unit of the DNR Law Enforcement Division.
The facility’s remaining deer were depopulated and tested, but no further evidence of CWD was found. The facility remains under quarantine, currently preventing ownership of farmed cervids.
The Privately Owned Cervid Program is jointly managed by the DNR and MDARD. There is mandatory CWD testing in all registered herds in Michigan, under the oversight of MDARD. The DNR oversees POC registration and performs inspections of POC facilities. Proper maintenance of POC facilities is critical to protecting Michigan’s free-ranging and privately owned cervid herds.
CWD is a fatal central nervous system disease that affects white-tailed deer, mule deer, elk and moose. It attacks the brain of infected animals, creating small lesions in the brain, which result in death. It is transmitted through direct animal-to-animal contact or by contact with saliva, urine, feces, blood, carcass parts of an infected animal or infected soil. To date, there have been no reported cases of CWD infection in humans. However, as a precaution, the U.S. Centers for Disease Control and Prevention and the World Health Organization recommend that infected animals not be consumed as food by humans or domestic animals.
Since May 2015, CWD-positive deer have been found in Michigan. As of mid-March 2018, 57 free-ranging deer have tested positive for the disease. CWD has not been found in the Upper Peninsula, though it has been discovered in Wisconsin, approximately 40 miles from the western Upper Peninsula border.
The DNR is working with stakeholders to address the status of CWD in Michigan. In the coming weeks, the DNR and the Michigan Natural Resources Commission will host a series of public engagement meetings across the state on CWD. The sessions will provide hunters, business owners and residents with opportunities to share their ideas and observations.
In addition, the DNR, NRC and MDARD are evaluating recommendations from the CWD Working Group, which was created after last year’s CWD Symposium. The symposium brought national and international experts to Michigan to discuss CWD. During the coming months, the DNR, NRC and MDARD will work with stakeholders to develop new CWD regulation recommendations.
FRIDAY, JANUARY 20, 2017
Michigan Chronic wasting disease identified in two Mecosta County farmed deer
FOR IMMEDIATE RELEASE: January 20, 2017
Media contacts: Jessy Sielski (MDARD), 517-284-5725 or Chad Stewart (DNR), 517-282-4810
LANSING – Chronic wasting disease was confirmed this week in two female deer from a Mecosta County deer farm. CWD is a fatal neurological disease that affects white-tailed deer, mule deer, elk and moose. This is the second time the disease has been found in a farmed deer facility in Michigan. In 2008, a white-tailed deer from a Kent County deer farm tested positive.
“Chronic wasting disease is a serious disease affecting both farmed and free-ranging deer,” said MDARD State Veterinarian James Averill, DVM. “We are following the state’s CWD response plan and taking the necessary steps to protect the health and well-being of all of Michigan’s deer populations.” Samples from the two deer were submitted for testing as a part of MDARD’s mandatory CWD surveillance program. All farmed deer facilities licensed with the Michigan Department Natural Resources must participate in this program.
“Any discovery of chronic wasting disease in free-ranging or farmed deer is disappointing,” said Chad Stewart, DNR deer and elk specialist. “It will take significant time and effort – through immediate, targeted surveillance and mandatory checks during the upcoming deer seasons – to understand the current situation. The Michigan DNR remains committed in our efforts to contain this disease and safeguard our valuable wildlife resource.”
MDARD and DNR are implementing the Michigan Surveillance and Response Plan for Chronic Wasting Disease of Free-Ranging and Privately Owned Cervids, and are taking the following steps:
Quarantine the affected farm.
Complete trace investigations to identify the potential sources of infection and possible areas of spread.
Work with the producer to depopulate the facility.
Test all deer from the affected herd for CWD.
Identify all other deer farms in a 15-mile radius, which will undergo a records audit, fence inspection and increased surveillance testing.
Conduct targeted surveillance testing on free-ranging white-tailed deer near the facility.
Have mandatory deer check for hunter-harvested deer in a nine-township area.
An informational meeting for deer farmers is scheduled for:
Wednesday, February 1, 2017, at 7 p.m.Big Rapids Holiday Inn1005 Perry Avenue, Big Rapids, Michigan 49307
In May 2015, CWD was found in a free-ranging deer in Ingham County. Since then, the DNR has tested nearly 12,000 free-ranging deer for CWD; nine deer have tested positive in Ingham and Clinton counties.
CWD is transmitted directly from one animal to another and indirectly through the environment. Infected animals may display abnormal behavior, progressive weight loss and physical debilitation. To date, there is no evidence that CWD presents any risk to humans or other animals outside the deer family, either through contact with an infected deer or from handling venison that came from a CWD-infected deer. However, as a precaution, the U.S. Centers for Disease Control and the World Health Organization recommend that infected animals not be consumed as food by either humans or domestic animals.
More information about CWD – including Michigan’s CWD surveillance and response plan – is available at www.michigan.gov/cwd.
#
January 14, 2018
Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases
WEDNESDAY, DECEMBER 13, 2017
Michigan Chronic Wasting Disease Identified in a Mecosta County Farmed Deer Chronic Wasting Disease Identified in a Mecosta County Farmed Deer
Agency: Agriculture and Rural Development
For immediate release: December 13, 2017 Media contacts: Jessy Sielski (MDARD), 517-284-5725 or Ryan Soulard (DNR), 517-284-6184
LANSING – Chronic wasting disease was confirmed this week in a one-and-a-half-year-old female deer from a Mecosta County deer farm. CWD is a fatal neurological disease that affects white-tailed deer, mule deer, elk and moose. The sample was submitted for testing as a part of the state’s CWD surveillance program.
“The deer farmer who submitted the sample has gone above and beyond any state requirements to protect their deer from disease, and it is unknown at this time how this producer’s herd became infected with CWD,” said Michigan Department of Agriculture and Rural Development State Veterinarian James Averill, DVM. “In partnership with the Department of Natural Resources and the U.S. Department of Agriculture, we are taking the necessary steps to protect the health and well-being of all of Michigan’s deer populations.”
“What we know about CWD is always evolving,” said DNR state wildlife veterinarian, Kelly Straka, DVM. “As new positives are found, we learn more about how it’s transmitted to determine the best way to protect both free-ranging and farmed deer.”
MDARD and DNR are following the Michigan Surveillance and Response Plan for Chronic Wasting Disease of Free-Ranging and Privately Owned Cervids. The positive farm has been quarantined and, based on the plan, DNR and MDARD will take the following steps:
Conduct trace investigations to find possible areas of spread. Identify deer farms within the 15-mile radius and implement individual herd plans that explain the CWD testing requirements and movement restrictions for each herd. These herds will also undergo a records audit and fence inspection. Partner with the USDA on the management of the herd. CWD is transmitted directly from one animal to another and indirectly through the environment. Infected animals may display abnormal behavior, progressive weight loss and physical debilitation. To date, there have been no reported cases of CWD infection in humans. However, as a precaution, the U.S. Centers for Disease Control and the World Health Organization recommend that infected animals not be consumed as food by either humans or domestic animals.
Since May 2015, when the first free-ranging white-tailed CWD positive deer was found in Michigan, the DNR has tested approximately 23,000 deer. Of those tested, as of December 6, 30 cases of CWD have been suspected or confirmed in deer from Clinton, Ingham, Kent and Montcalm counties. This is the first year any free-ranging deer were found CWD positive in Montcalm or Kent counties.
More information about CWD – including Michigan’s CWD surveillance and response plan – is available at http://www.michigan.gov/cwd. ;
###
January 14, 2018
Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases
FRIDAY, MARCH 30, 2018
Michigan Mecosta County man sentenced following DNR investigation Game ranch owner falsified information related to chronic wasting disease testing
MONDAY, AUGUST 25, 2008
CWD FIRST DOCUMENTED IN MICHIGAN
Michigan's First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding Facility Contact: Bridget Patrick (MDA) or Mary Dettloff (DNR) 517-241-2669 or 517-335-3014 Agency: Natural Resources
August 25, 2008 LANSING - The Michigan departments of Agriculture (MDA) and Natural Resources (DNR) today confirmed the state's first case of Chronic Wasting Disease (CWD) in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County.
The state has quarantined all POC facilities, prohibiting the movement of all - dead or alive - privately-owned deer, elk or moose. Officials do not yet know how the deer may have contracted the disease. To date, there is no evidence that CWD presents a risk to humans.
DNR and MDA staff are currently reviewing records from the Kent County facility and five others to trace deer that have been purchased, sold or moved by the owners in the last five years for deer and the last seven years for elk. Any deer that may have come in contact with the CWD-positive herd have been traced to their current location and those facilities have been quarantined.
"Michigan's veterinarians and wildlife experts have been working throughout the weekend to complete their investigation," said Don Koivisto, MDA director. "We take this disease very seriously, and are using every resource available to us to implement response measures and stop the spread of this disease."
CWD is a fatal neurological disease that affects deer, elk and moose. Most cases of the disease have been in western states, but in the past several years, it has spread to some midwestern and eastern states. Infected animals display abnormal behaviors, progressive weight loss and physical debilitation.
Current evidence suggests that the disease is transmitted through infectious, self-multiplying proteins (prions) contained in saliva and other fluids of infected animals. Susceptible animals can acquire CWD by direct exposure to these fluids or also from contaminated environments. Once contaminated, research suggests that soil can remain a source of infection for long periods of time, making CWD a particularly difficult disease to eradicate.
Michigan's First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding Facility: "Currently, one of our top concerns is to confirm that the disease is not in free-ranging deer," said DNR Director Rebecca Humphries. "We are asking hunters this fall to assist us by visiting check stations to allow us to take biological samples from the deer they harvest, so we can perform adequate surveillance of the free-ranging white-tailed deer herd in the area."
Deer hunters this fall who take deer from Tyrone, Soldon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield, and Cannon townships will be required to bring their deer to a DNR check station. Deer taken in these townships are subject to mandatory deer check.
The DNR is also asking hunters who are participating in the private land five-day antlerless hunt in September in other parts of Kent County to visit DNR check stations in Kent County so further biological samples can be taken from free-ranging deer for testing. The DNR is in the process of finding additional locations for check stations in Kent County to make it more convenient for hunters.
The deer that tested positive at the Kent County facility was a doe that had been recently culled by the owner of the facility. Michigan law requires sick deer or culled deer on a POC facility be tested for disease. The samples from the Kent County deer tested "suspect positive" last week at Michigan State University Diagnostic Center for Population and Animal Health, and were sent to the National Veterinary Services Laboratory in Ames, Iowa last Thursday for confirmatory testing. The positive results of those tests were communicated to the state of Michigan today.
Audits of the facility by the DNR in 2004 and 2007 showed no escapes of animals from the Kent County facility were reported by the owner. Also, there were no violations of regulations recorded during the audits.
Since 2002, the DNR has tested 248 wild deer in Kent County for CWD. In summer 2005, a number of those deer had displayed neurological symptoms similar to CWD; however, after testing it was determined the deer had contracted Eastern Equine Encephalitis.
More information on CWD is available on Michigan's Emerging Diseases Web site at www.michigan.gov/chronicwastingdisease.
http://www.michigan.gov/emergingdiseases/0,1607,7-186-25806-198865--,00.html
MICHIGAN SURVEILLANCE AND RESPONSE PLAN FORCHRONIC WASTING DISEASE OF FREE-RANGING ANDPRIVATELY-OWNED/CAPTIVE CERVIDS
TUESDAY, SEPTEMBER 09, 2008
CWD MICHIGAN UPDATE September 5, 2008
CWD Update Chronic Wasting Disease Eradication Program Provided by the Animal Industry Division Michigan Department of Agriculture September 5, 2008
Background: The Michigan departments of Agriculture (MDA) and Natural Resources (DNR) confirmed the state’s first case of Chronic Wasting Disease (CWD) in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County on Monday, August 25, 2008. The state quarantined all POC facilities, prohibiting the movement of all – dead or alive – privately-owned deer, elk, or moose. Officials do not yet know how the deer may have contracted the disease. To date, there is no evidence that CWD presents a risk to humans or to animals other than cervids. MDA Actions: The state-wide quarantine on all privately owned cervid facilities is still in place. Facilities may continue to hold shooting events, but all carcasses* must be held until testing clears the animal/or the quarantine is released. A clarification to the quarantines was published and distributed to law enforcement officials, stakeholders and other interested parties. A questions and answers sheet is available under the livestock link on the www.michigan.gov/chronicwastingdisease website.
The test results from the Kent County cervid breeding facility, where the index case was confirmed, found no additional diseased deer. Epidemiologists are reviewing taxidermy records on a facility related to the index case. Taxidermy operations must be licensed and operators must follow Michigan requirements when conducting business with hunters who have harvested animals from other states. Current Michigan law prohibits the import of free-ranging deer or elk carcasses from states or provinces with CWD. Only de-boned meat, antlers, antlers attached to a scull cap cleaned of all brain and muscle tissue, hides and upper canine teeth may be brought into Michigan. A person that is notified by mail or other means, that a carcass imported into Michigan tested positive for CWD must notify the Michigan DNR.
The first tier of traces from the index facility led to five facilities: three in Kent County, one in Montcalm County, and one in Osceola County. These facilities were quarantined by MDA. Records of sales and purchases have been reviewed and have revealed that two facilities received deer from the index case. Four deer from these two facilities were 2 euthanized, samples were tested at MSU’s DCPAH and were found to be negative on Thursday, September 04, 2008. One of the five facilities in tier one, also a Kent County facility conducts a taxidermy operation on the premises. Taxidermy is of great concern because infectious prions in the bones and spinal tissue of the carcass from CWD positive states can infect deer on the facility. MDA, DNR and USDA staff are investigating the records of the taxidermy operation. The second tier investigation to this point, has quarantined four facilities in Bay, Kent, Mecosta, and Saginaw counties. These facilities only sold to the tier one facilities and did not receive anything. They are quarantined as terminal operations and any deer that die, are culled, or shot for sport must be submitted for CWD testing. POC Facilities Quarantined: All POC facilities, except those that only have reindeer, are under quarantine in Michigan until the disease investigation is complete. Epidemiologists are developing a policy for records review and release of quarantines based on management practices and risk.
Disease Surveillance Table: Index facility Depopulated Tier 1 Tier 2 1 Entire index herd tested negative 5 herds 2 trace outs (four test-negative animals) 3 trace ins 4 none of these 4 facilities trace directly to the index facility DNR Actions: The ban on all baiting and feeding of deer and elk in the Lower Peninsula is in effect. MSU’s Product Center for Agriculture Development is taking calls from bait growers/sellers. The Center is using Michigan Market Maker, an interactive mapping system that connects Agriculture processors and businesses with Michigan growers and marketers. http://mi.marketmaker.uiuc.edu/ Information on the baiting and feeding ban is available on the CWD page of the Emerging Diseases website. A mandatory deer check for hunters who take a deer within the Kent County townships of Tyrone, Solon, Nelson, Sparta, Algoma, Courtland, Alpine, Plainfield, and Cannon, is in effect for the 2008 hunting season. The deer heads will be collected and tested for CWD. All transport of live wild deer, elk, and moose is prohibited statewide, including transport for rehabilitation purposes. Education and Outreach: A town hall meeting is scheduled to take place in Kent County on September 9, 2008 at 6:30 p.m. near Grand Rapids. Representatives from MDA, USDA, DNR and MSU will be there to answer questions about CWD, quarantines and the baiting ban. An update on the disease investigation will be presented to the House of Representatives Committee on Outdoor Recreation and Natural Resources on September 9, 2008 and the Senate Natural Resources, Agriculture, and Hunting and Fishing committees on September 10, 2008. 3 Questions and Answers regarding POC facility quarantines were sent via email to legislative offices, POC facility executive directors, and DNR law enforcement. They are also posted to the MDA, and Emerging Diseases websites. A coordinated communications action plan is in place. MSU Extension, Michigan Deer and Elk Breeders, MUCC, and many other special interest groups have volunteered to assist with information distribution. Information on CWD may be found on the Michigan Emerging Diseases website at www.michigan.gov/emergingdiseases. Corrected on September 8, 2008 – changed from “meat” to “carcasses”.
Summary of Michigan Wildlife Chronic Wasting Disease Surveillance Updated May 1, 2008 by Michigan Department of Natural Resources, Wildlife Disease Laboratory
Consumer Warning September – December 2008
The state's first case of Chronic Wasting Disease (CWD) was confirmed in a three-year old white-tailed deer from a privately owned cervid (POC) facility in Kent County on August 25, 2008. As a result, all POC facilities in Michigan were quarantined. Chronic Wasting Disease (CWD) is a fatal neurological disease that affects deer, elk and moose. Infected animals display abnormal behavior, progressive weight loss and physical debilitation. CWD is believed to be caused by infectious, self-multiplying proteins (prions). Prions are normal cell proteins whose shape has been transformed, causing CWD. To date, CWD is not known to cause or be associated with disease in humans. No increase in human prion disease has been observed in areas of the western United States where CWD has been endemic in cervid populations for decades.
However, because much is still unknown about prion diseases, the Centers for Disease Control and Prevention and the World Health Organization advise that humans do NOT consume animals that have been tested and are known to be infected with CWD. In general, people should not handle or consume wild animals that appear sick or act abnormally, regardless of the cause. CWD prions are primarily found in central nervous system tissues (e.g. brain and spinal cord) and the lymphatic system (e.g. tonsils, lymph nodes and spleen) of infected cervids. Humans should avoid the handling or consumption of these tissues. Hunters should wear disposable gloves while field dressing and de-boning meat from the carcass. Recent research has shown that CWD prions may also be found in the saliva and urine of the infected animal. Experiments conducted suggest that CWD prions can persist in the environment and may indirectly infect other susceptible animals that come into contact with the contaminated environment. The meat product you are receiving has come from a quarantined facility under surveillance for CWD. MDA recommends you take de-boned meat from the carcass, hold the meat product in a freezer and consume it only after the facility of origin receives clarification from MDA that the animal was negative for CWD.
State ponders lifting quarantine of deer breeding farms Posted by Ben Beversluis | Grand Rapids Press September 10, 2008 04:26AM Categories: State News
State officials have found no chronic wasting disease in four deer moved from a Kent County farm where the disease was found for the first time in Michigan.
While that's good news, the investigation now will expand.
But state veterinarian Steve Halstead also said a plan is being developed to start easing the quarantine of some of the state's 559 deer breeding farms. Some, with the cleanest records and no ties to the infected farm, might see their quarantine lifted by the end of the month.
The four tested deer were from farms in Osceola and Montcalm counties. They had been moved from an Algoma Township farm, where in August, a 3-year-old doe was found to be infected.
The tests clear the "first tier" of five deer farms directly connected with the local farm. Now, the investigation will expand to the next tier of farms, numbering in the teens, that supplied or received deer from any of the first-tier farms.
"Now we're looking back upstream, to herds that moved animals into those premises. We're looking where they got their animals from and sent other animals to," Halstead said.
Because of the quality of Michigan's deer stock, the number of deer farms and a ban on importing deer from other states, Michigan farms have extensive movement of deer between farms.
"So the whole state is pretty much touched by movement of deer," Halstead said. The quarantine froze movement to find any links to the infected farm.
"It's big, and we have got to get our arms around this thing."
In fact, the state has begun a five-year surveillance process to track farm-bred deer.
Chronic wasting disease damages deer brains. It first was identified in 1967 in a captive mule deer in Colorado. It was diagnosed in free-ranging elk in 1981, in free-ranging mule deer in 1985, and in white-tailed deer in 1990.
The disease, apparently transmitted through a protein, now is found in several states, including Illinois and Wisconsin.
No diseased wild Michigan deer have been found.
With the quarantine, the state is taking several measures to limit possible spread.
All 51 deer in the Algoma Township herd were destroyed and tested. No others had CWD.
The DNR also is culling deer from a "hot zone" of nine northern Kent County townships. Tests are not yet back on wild deer killed last week.
In all, the state aims to test 300 deer from the area. Any deer killed by hunters in that zone must be brought for testing, and the DNR is strongly encouraging hunters to bring deer killed anywhere in Michigan to check stations. The state also has banned deer baiting anywhere in the Lower Peninsula. Bait piles encourage deer to congregate, which may spread disease.
Meanwhile, Department of Natural Resources, Department of Agriculture and public health officials will host a town hall meeting tonight to discuss what is being done to assess and control the disease, any risks to humans and animals, and what will happen in the future.
MDA-NewsRelease MDA-NewsRelease 9/9/2008 4:09 PM >>> FOR IMMEDIATE RELEASE: September 9, 2008
Chronic Wasting Disease Investigation Results Released State Officials Clarify Deer Facility Quarantines
LANSING - As the Chronic Wasting Disease (CWD) investigation continues, officials with the Michigan departments of Agriculture (MDA) and Natural Resources (DNR) today announced additional negative test results for animals sold from the Kent County CWD-positive privately owned cervid (POC) facility to facilities in Montcalm and Osceola counties. Four animals were removed from Montcalm and Osceola POC facilities, submitted to the Michigan State University (MSU) Diagnostic Center for Population and Animal Health (DCPAH), and all tested negative. The Kent County facility was depopulated on Aug. 26; and the deer were tested and all were negative for CWD. The Montcalm and Osceola county facilities will not have to be depopulated.
We are narrowing the investigation and at the same time clarifying the statewide quarantine requirements for POC facilities. Getting results back in a timely manner assists us eliminating some facilities that received deer from the index herd and additional facilities that sold to the index herd, said MDA State Veterinarian Steven Halstead. Good records are essential in a speedy investigation and the owner kept excellent records. We want to make sure these businesses have complete awareness of what is required of them.
At this time, no live cervid may be transported from a quarantined facility. Whole carcasses must either go to a U.S. Department of Agriculture (USDA) inspected slaughter plant, under official seal, or the meat must be removed from the carcass and no head, spinal tissue, or bones may leave the premises. Violation of quarantine is a felony and may be punishable up to $50,000 in fines and may include prison time.
Shooting ranches are required to provide a consumer warning to clients taking de-boned meat off the premises. A clarification of the statewide quarantine is available on the Michigan Emerging Diseases Web site at www.michigan.gov/chronicwastingdisease.
To control the potential spread of this devastating disease, last week the DNR banned the feeding and baiting of free-ranging deer and elk in the Lower Peninsula; and MDA issued a statewide quarantine banning the movement of deer from all POC facilities.
The DNR will increase testing on animals harvested from the region surrounding the CWD positive Kent County facility this fall, and will greatly expand statewide testing efforts as well.
The Michigan CWD response team is a multi-agency team of experts from the Michigan departments of Agriculture, Community Health, and Natural Resources. Michigan State University and the U.S. Department of Agriculture also participate in the disease investigations.
-##-
-------- Original Message --------
Subject: A Risk-based Audit of the Captive/Privately-owned Cervid Industry in Michigan
Date: Fri, 1 Apr 2005 15:48:08 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000040/!x-usc:mailto:BSE-L@KALIV.UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy #####################
A Risk-based Audit of the Captive/Privatelyowned Cervid Industry in Michigan Michigan Department of Natural Resources Report Series
Issue Report No. 1
March 10, 2005
5.1.2 C/P-OC facility management
5.1.2.1 Fence management
5.1.2.1.1 Status of current regulatory requirements. The OSRPOC (2000) states that all privately owned cervid facilities must have perimeter fencing constructed of continuous woven wire or cyclone fencing for the entire vertical height and be maintained in a condition to prevent the ingress or egress of any cervidae species. A facility owner or representative must inspect the perimeter fencing at least once per month and following any possible physical damage. The facility owner or representative must keep records of fence inspections and submit monthly fence inspection reports by January 15 of each year for the previous year. The fence’s ground edge “shall remain at or below ground level at all times” (OSRPOCF 2000, p. 1), but openings up to 6 inches square can be present to facilitate movement of small mammals and reptiles.
Fence height requirements vary with species. For WTD, sika, fallow, and mule deer, fences must be 10 feet tall. For elk and red deer, fences must be 8 feet tall. Reindeer and caribou require 4.5 foot fences. Regardless of species, fences must “be maintained in a condition to prevent ingress or egress of any cervidae species” (OSRPOCF 2000, p. 1). Facilities that had 8 feet of woven wire with single stranded high-tensile wire as the top 2 feet of fencing, and were licensed for WTD by MDNR prior to April 1, 1998, were considered to be compliant with fence regulations. However, if sections of fence 40 feet and wider were replaced after April 1, 1998, the replacement fence must be 10 feet of woven wire. While the requirements are to prevent “ingress or egress of any cervid”, free-ranging WTD, accomplished jumpers that they are, could nevertheless enter an elk facility with an legal 8 foot fence.
Gates must be constructed of continuous woven wire or cyclone fencing and meet or exceed fence height requirements for species contained in the enclosure. Gates must be adjusted seasonally, or more often if necessary, such that the bottom of the gate extends no higher than 8 inches from the ground along the entire length. 5.1.2.1.2 Inspection. Perimeter fences that house WTD must be 10 feet tall, and those for elk must be 8 feet tall. Yet, examining the minimum fence height reported by inspection teams (Appendix B, Tables 22a,b), nearly half of all facilities inspected were in noncompliance because of low fences; 46.5% of Full Registration, 49.6% of Ranches, 12.5% of Exhibition, and 41.4% of Hobby facilities had fences that were too low for the species housed at 1 or more points along the perimeter fence.
5.1.2.1.3 Materials and construction. Fence regulations state that continuous woven wire must be used for fences, but MDNR and MDA have generally deemed woven wire or materials stronger than woven wire acceptable for purposes of compliance. In general, woven wire is stronger than other fence types, and the regulations were written to prevent weaker type fences from being used to house cervids. Woven wire also allows better ingress and egress of smaller non-cervid species.
WTD are able to jump 8 feet fences with relative ease and are capable of clearing higher fences, if pressed. WTD can and do walk into and out of open gates or even relatively small gaps in fences. Risk of disease transmission from C/P-OC to freeranging cervids or vice versa is increased dramatically when free-ranging deer gain access to enclosures (and subsequently escape from the enclosure) or when C/P-OC
27
escape from enclosures. While audit inspections found many facilities with exemplary fences (e.g., Figure 5.1), many other facilities either used unacceptable or poorly maintained materials (e.g. Figure 5.2) or did not meet minimum height requirements for the species housed (Figure 5.3). Others never repaired storm damage that compromised the integrity of the fence (sometimes completely, e.g. Figure 5.4), had gaps in (Figure 5.5) or under (Figure 5.6) fences which easily allowed deer to pass through in either direction, or had gates which were out of compliance (Figure 5.7). All of these problems increase potential CWD risk to both C/P-OC and free-ranging cervids.
Fence faults did not vary dramatically by class. Facilities averaged approximately 0.5 to 2 faults per facility. A graph of fence faults normalized to faults per mile of fence is presented in Appendix B, Figure 8. Viewed by this measure, the majority of C/P-OC facilities of all classes had no fence faults/mile of fence. However, some facilities, particularly in the Full Registration class, had substantial numbers of fence faults per mile. For example, more than 50 Class IV facilities had up to 5 faults per mile, about 20 had 5 to 10 faults per mile, etc. Inspectors found at least 1 Full Registration facility with more than 100 faults per mile of fence. Defects in fences are often quickly found and exploited, especially by deer, and every fence fault carries a risk of mixing between the C/P-O and free-ranging cervid populations and a risk of disease introduction from one population to the other.
5.1.2.1.4 Maintenance. Current regulations require that fences be inspected monthly for faults. Commendably, nearly all active facilities, 97%, responded that fences were inspected monthly. For active Full Registration and Ranch facilities, 97% were inspected monthly. Fences were reportedly inspected monthly on all Hobby facilities and on 75% of inspected Exhibition facilities. The adequacy of monthly fence inspections depends on the habitat immediately adjacent to the fence. In forested areas, one intense windstorm can cause major fence faults at any time. The OSRPOCF (2000, p. 1) specify that the integrity of fencing needs to be monitored “following any possible physical damage,” which is particularly difficult for large facilities with extensive perimeter fences to maintain. Inspection comments suggest that some facilities inspect fences more than once a month. However, the 3% of facilities that do not inspect fences at least monthly present an increased risk of disease introduction to free-ranging wildlife should they happen to house infected individuals.
5.1.2.1.5 Contact with free-ranging cervids. The majority of C/P-OC in Michigan could make contact with free-ranging cervids at fence lines. Of active Ranch and Full Registration facilities, 94% had potential contact with free-ranging cervids. It has been demonstrated that pens contaminated with feces or carcasses of infected cervids are infective for naïve animals (Miller et al. 2004). It seems likely that saliva is infective as well, given transmission by direct animal to animal contact in experimental studies (Miller and Williams 2003). The possibility exists for CWD exposure through a fence, either from free-ranging deer to C/P-OC or from C/P-OC to free-ranging animals, but the risk is likely lower than that entailed by direct mixing of animals.
28
snip...
Free-ranging cervids were reported to have been found inside enclosures in 3.8% of Full Registration facilities and in 20.0% of Ranch facilities. Only 1 Exhibition facility, reported that free-ranging cervids had been found in the enclosure. If free-ranging cervids can get into the facility, they can likely leave it as well. To the extent that is true, free-ranging animals exposed to C/P-OC can potentially carry infection outside of the facility and infect other wild cervids. Similarly, free-ranging deer can potentially expose C/P-OC to pathogens.
5.1.2.1.6 Escapes and recovery protocol. The OSRPOCF (2000) states that all livestock within the perimeter fence that become located outside the perimeter fence, not under the direct control of the owner for more than 12 hours, will be considered as released. The owner then must report the release within 24 hours of discovery, although outside of normal business hours the owner is allowed to delay the report until the next business day. Consequently, if an escape occurred on Friday evening, over 2 days could elapse before the facility is legally required to report the escape. Animals that are released and then recovered must immediately be placed in an isolation facility that maintains the recovered animals no less than 30 feet from the remainder of the herd. If the animal is not recovered within 48 hours after being discovered as released, MDA will implement a recovery plan. In this plan, MDA is responsible for determining the maximum allowable timeframe for recovery. MDA will also evaluate the cause of the release and may require modifications to fences or facility management practices to prevent further releases. The OSRPOCF specifies that released animals will remain privately owned cervids as long as official identification remains intact and the owner follows MDA procedures for recovery. However, the POCPMA (2000, p. 9) also notes that “an animal that escapes from a facility is considered to be public property if the operator of a cervidae livestock facility does not notify the department (MDA).” Animals that are released and do not bear official identification are not exempted from legal taking under a MDNR permit (e.g., by licensed hunters).
Over the course of audit inspections, C/P-OC representatives reported that during the last 4 years, 464 cervids had escaped from 69 (20%) active Full Registration and 18 (14.4%) Ranch facilities, with 87.9% (408) of those reported escaped animals being from Class IV facilities (Appendix B, Table 9a). However, data obtained from MDA on May 17, 2004 record only 8 reports of released cervids in the last 4 years, less than 2% of all escapes reported by facilities during audit inspections. It is possible that some of these escapes were not reported to MDA because they were recovered before 12 hours elapsed. Other evidence independent of the audit also shows not only that escapes of C/P-OC occur, but that they often go unreported. Each year, escaped C/P-OC turn up among samples of hunter-harvested free-ranging deer submitted for TB and CWD testing (e.g., Figures 5.8, 5.9).
The higher proportion of escapes from Full Registration facilities may in part be due to greater awareness of inventory or may be attributable to more intensive management and better record keeping. While it is possible that escapes actually occurred more often on Class IV facilities, it is also conceivable that Ranch facilities experienced escapes which simply went unnoticed due to larger average facility size. In addition, Ranch facilities are not required to mark all animals on the premises, so it is more difficult to determine if cervids outside the enclosure are free-ranging or escaped captives. Twenty percent of inspected Hobby facilities reported to audit inspectors that escapes had occurred, as did 25% of Exhibition facilities. The most common species to escape (consistent with their predominance among all MI C/P-OC) were WTD and elk, both of which are susceptible to CWD. However, non-native species were also reported escaped. Fence faults and gates left open accounted for many of the escapes (Appendix
36
B, Table 10a). Cervids were reportedly tagged prior to escape on 50% of the Ranches, 81% of Full Registration facilities, 67% of Hobby facilities, and on 50% of Exhibition facilities where cervid escapes were reported. Most facilities used USDA metal eartags or other visible eartags for identification prior to escape. WTD (and elk, in areas of the state where free-ranging elk are present) that bear no identification can quickly blend into the free-ranging population, making recovery and return to captivity much more difficult and transmission of any diseases they may carry much more likely.
Reported recovery rates of escaped C/P-OC were variable among facility classes (Appendix B, Table 9a), but at least 41 escaped animals (8.8%) were never recovered. CWD-infected C/P-OC have been implicated as sources of infection for free-ranging cervids in NE, SD, and SK (Williams et al. 2002), and CWD-infected escaped C/P-O WTD have been documented at large with free-ranging WTD in WI (Joly et al. 2003). Even if subsequently recovered, CWD-infected escaped C/P-OC could potentially act as a source of infection for numerous free-ranging cervids, based on research suggesting that feces from CWD-infected deer are infectious for uninfected deer (Miller et al. 2004). In areas of Michigan where concentrations of C/P-OC facilities as well as relatively high WTD densities (Appendix C, Figure 3) occur, the risks for propagation of CWD among free-ranging deer could be expected to be high once infected.
Three Full Registration facilities and 1 Ranch facility reported intentionally releasing C/P-O WTD into the wild (Appendix B, Tables 11a,b). Intentional release of C/P-OC is a felony in MI (POCPMA 2000, Section 17). The audit data suggest that intentional releases are infrequent, although given the penalties, the numbers noted here, which are based on C/P-OC facility self reports, may be an underestimate.
37
" Captive/Privately Owned Cervid Facility Audit Report
PDF icon An audit of captive/privately owned cervid facilities that house deer, elk and other animals around the state showed that 37 percent of the facilities are not in compliance with current regulations for the industry.
Executive Summary
Synopsis of the report
TSS
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
see also;
Michigan cwd information history of farmed postives
Michigan ANIMAL INDUSTRY DIVISION Annual Report 2018
PROGRAM MANAGER:
ANIMAL INDUSTRY DIVISION
Raising deer and elk in captivity is jointly regulated by the Michigan Departments of Natural Resources (DNR) and Agriculture and Rural Development. The Animal Industry Division (AID) manages the animal health components of farmed deer and elk, including programs for chronic wasting disease (CWD), bovine tuberculosis, and movement.
IMPACT FOR MICHIGAN:
Deer and elk are raised for breeding, meat production, private hunting, animal watching and specialty products. Michigan’s deer farming industry ranks third in the nation in number of farms. Maintaining healthy farmed deer and elk is critical to protecting the health status of the free-ranging population of white-tailed deer and elk in Michigan. Disease surveillance programs provide for early detection of infected individuals and minimizing the spread of disease. Herd certification and accreditation programs minimize the risk of introduction, transmission, and spread of disease in captive cervid populations in the United States.
ACCOMPLISHMENTS:
• Managed the disease investigation and removal of deer from the a CWD positive deer farm identified in December 2017.
• Due to multiple detections of CWD in free-ranging deer, the parameters for being in a designated special surveillance area were modified to include all herds in an affected county. This change created more comprehensive and efficient responses.
• Initiated a comprehensive program review with the DNR to streamline and improve the Farmed Cervid Program.
FARMED CERVID
Cheryl Collins, DVM | 517-284-5686 | CollinsC3@michigan.gov
MEASURING SUCCESS:
MDARD Annual Report | 2018
PROGRAM GOALS:
• Work cooperatively with the Michigan Department of Natural Resources to mitigate impact of Chronic Wasting Disease in both free-ranging and farmed cervids in Michigan.
• Maintain Approved State Status for USDA Chronic Wasting Disease Herd Certification Program.
• Provide excellent customer service in farmed cervid regulatory disease programs by processing CWD Certification and TB Accreditation within 40 days.
• Complete comprehensive program review with Department of Natural Resources to streamline and improve farmed cervid programs.
KEY STAKEHOLDERS
• Michigan deer and elk farmers
• Cervid Advisory Committee
• USDA Animal and Plant Health Inspection Service
• Michigan Department of Natural Resources
• United Deer Farmers of Michigan
LEGAL AUTHORITY:
• Act 466, P.A. 1988, as amended, the Animal Industry Act
• Act 190, P.A. 2000,The Privately Owned Cervidae Producers Marketing Act Memorandum of Understanding with Department of Natural Resources
• 9 Code of Federal Regulations (CFR) Part 55 9 CFR Part 77
• Bovine Tuberculosis Eradication: Uniform Methods and Rules, Effective January 22, 1999
• Chronic Wasting Disease Program Standards, USDA, May 2014 Metric 2017 2018
Percent of herds that the CWD Certification was completed in 40 days 37% 35%
Percent of herds that the TB Accreditation was completed in 40 days 45% 29%
Number of deer and elk imported into Michigan 19 10
Number of herds involved in special surveillance zones around CWD positive free-ranging deer
51 81
Michigan ANIMAL INDUSTRY DIVISION Annual Report 2017
PROGRAM MANAGER:
ANIMAL INDUSTRY DIVISION
The farming of deer and elk (cervid) is jointly regulated by the Animal Industry Division (AID) and the Michigan Department of Natural Resources. AID manages the animal health components of farmed deer and elk, including programs for chronic wasting disease (CWD) and bovine tuberculosis (TB).
IMPACT FOR MICHIGAN:
Raising deer and elk for breeding, meat production, private hunting, animal watching and specialty products helps to ensure a prosperous economy and creates more jobs. Michigan’s deer farming industry ranks third in the nation in number of farms. The deer farming industry continues to grow in Michigan, as 43 percent of farms have been created in the last decade. Additionally, maintaining healthy farmed deer and elk is critical to protecting the health status of the free-ranging population of white-tailed deer and elk in Michigan. Disease surveillance programs can lead to early detection of infected individuals and prevent the spread of disease, while strong herd certification and accreditation programs protect our trade status with other states.
ACCOMPLISHMENTS:
• Successfully managed the depopulation of a farmed deer herd where CWD was detected during routine surveillance.
• Implemented quarantines and herd plans for farmed deer herds in surveillance zones around CWD positive free-ranging animals and CWD positive farmed cervid facility.
• Feedback provided to all farmed deer facilities resulted in increased number of samples submitted for chronic wasting disease testing.
517-284-5686 | collinsc3@michigan.gov
Cheryl Collins, DVM
MEASURING SUCCESS:
MDARD Annual Report | 2016-2017
PROGRAM GOALS:
• Maintain Approved State status in the U.S. Department of Agriculture’s (USDA) CWD Herd Certification Program.
• Efficiently manage the herd inventories and certification processes for the cervid disease surveillance programs.
• Work cooperatively with the Michigan Department of Natural Resources to manage CWD in free-ranging white-tailed deer by having an effective disease control program among farmed deer.
KEY STAKEHOLDERS
• Deer and Elk farmers
• Cervid Advisory Committee
• USDA Animal and Plant Health Inspection Service
• USDA Veterinary Services
• Michigan Department of Natural Resources
• United Deer Farmers of Michigan
LEGAL AUTHORITY:
• Act 466, P.A. 1988, as amended, the Animal Industry Act
• Act 190, P.A. 2000,The Privately Owned Cervidae Producers Marketing Act Memorandum of Understanding with Department of Natural Resources
• 9 Code of Federal Regulations (CFR) Part 55 9 CFR Part 77
• Bovine Tuberculosis Eradication: Uniform Methods and Rules, Effective January 22, 1999
• Chronic Wasting Disease Program Standards, USDA, May 2014 Metric 2016 2017
Average number of days to process CWD Certification 39 55
Average number of days to process TB Accreditation 32 57
Number of deer and elk imported into Michigan 14 19
2015 Michigan annual report not a word on cwd tse prion
Number of Cervids
Tested for CWD 1704 1719 1622 999 665
Number of Cervid Herds in the CWD Certification Program
Not available Not available Not available Not available 96
Michigan CWD response plan outdated
CWD Identified in a Montcalm County Farmed Deer
Agency: Agriculture and Rural Development
For immediate release: March 28, 2019
Media contact: Jessy Sielski (MDARD), 517-284-5725 or Ryan Soulard (DNR), 517-284-6184
LANSING – The Michigan departments of Agriculture and Rural and Development and Natural Resources have confirmed chronic wasting disease in a two-year-old female white-tailed deer from a Montcalm County deer farm. The sample was submitted for routine testing as a part of the state’s CWD surveillance program for farmed deer.
In Montcalm County, 83 CWD-positive free-ranging deer have been identified. This part of the state is an active CWD Management Zone. All deer farms in Michigan are required to submit samples for testing regularly; however, deer farms in a CWD Management Zone are quarantined and must participate in increased surveillance.
As a part of MDARD’s disease response, an investigation will be conducted to rule out exposure of any other farmed deer.
“The test results and age of the deer indicate that this deer was recently infected, emphasizing the importance of early detection through surveillance,” said State Veterinarian Nora Wineland, DVM. “MDARD and DNR work together, in partnership with the state’s deer farmers, to ensure the protection of all of Michigan’s deer.”
“With a disease like CWD, everyone’s actions matter,” said DNR state wildlife veterinarian, Kelly Straka, DVM. “Whether you are a deer producer submitting samples for surveillance or a hunter practicing safe carcass disposal, we all have a role to play in minimizing the risk of disease spread.”
Since May 2015, when the first free-ranging white-tailed CWD-positive deer was found in Michigan, CWD has been confirmed in free-ranging white-tailed deer in the Lower Peninsula from Clinton, Eaton, Gratiot, Ionia, Ingham, Jackson, Kent, and Montcalm counties. Additionally, a CWD-positive deer was found in the Upper Peninsula in Dickinson County in October of last year. Baiting and feeding of deer and elk is not allowed in the Lower Peninsula.
CWD is a fatal neurological disease that affects white-tailed deer, mule deer, elk, and moose. CWD can be transmitted directly from one animal to another, as well as indirectly through the environment. Infected animals may display abnormal behavior, progressive weight loss and physical debilitation. To date, there have been no reported cases of CWD infection in humans. However, as a precaution, the U.S. Centers for Disease Control and the World Health Organization recommend that infected animals not be consumed as food by either humans or domestic animals.
More information about CWD can be found at www.Michigan.gov/CWD.
###
Michigan Farmed CWD
January 20, 2020
Chronic wasting disease identified in Newaygo County farmed deer
March 28, 2019 A farmed deer in Montcalm County has tested positive for deadly chronic wasting disease
Mecosta County man sentenced after Michigan DNR investigates
DAVE MULL|APR 2, 2018
A Mecosta County game ranch owner has been sentenced on charges resulting from a deer CWD-related investigation by the Michigan Department of Natural Resources Law Enforcement Division, in cooperation with the Michigan Department of Agriculture and Rural Development.
Lester Jay Gemmen, 64, of Morley was charged with providing false information regarding the origin of two deer heads that were submitted for disease testing, and for failing to properly maintain fencing at the Super G Ranch. The ranch is a privately owned cervid (POC) facility, a designation that includes game ranches and hunting ranches.
He was sentenced by the 77th District Court to 60 days in jail for each count, ordered to pay $775 in fines and costs and must perform 80 hours of community service.
The investigation began in 2017 after two of the six deer heads submitted by Gemmen tested positive for chronic wasting disease (CWD).
“I commend the detectives from our Special Investigations Unit and our field conservation officers for their thorough, professional approach to this investigation,” said 1st Lt. David Shaw, supervisor of the Special Investigations Unit of the DNR Law Enforcement Division.
Facility ‘depopulated’
The facility’s remaining deer were depopulated and tested, but no further evidence of CWD was found. The facility remains under quarantine, currently preventing ownership of farmed cervids.
The Privately Owned Cervid Program is jointly managed by the DNR and MDARD. There is mandatory CWD testing in all registered herds in Michigan, under the oversight of MDARD. The DNR oversees POC registration and performs inspections of POC facilities. Proper maintenance of POC facilities is critical to protecting Michigan’s free-ranging and privately owned cervid herds.
CWD is a fatal central nervous system disease that affects white-tailed deer, mule deer, elk and moose. It attacks the brain of infected animals, creating small lesions in the brain, which result in death. It is transmitted through direct animal-to-animal contact or by contact with saliva, urine, feces, blood, carcass parts of an infected animal or infected soil. To date, there have been no reported cases of CWD infection in humans. However, as a precaution, the U.S. Centers for Disease Control and Prevention and the World Health Organization recommend that infected animals not be consumed as food by humans or domestic animals.
Since May 2015, the DNR has found CWD-positive deer in Michigan. As of mid-March 2018, 57 free-ranging deer tested positive for the disease. CWD has not been found in the Upper Peninsula, though it has been discovered in Wisconsin, approximately 40 miles from the western Upper Peninsula border.
The DNR is working with stakeholders to address the status of CWD in Michigan. In the coming weeks, the DNR and the Michigan Natural Resources Commission will host a series of public engagement meetings across the state on CWD. The sessions will provide hunters, business owners and residents with opportunities to share their ideas and observations.
In addition, the DNR, NRC and MDARD are evaluating recommendations from the CWD Working Group, which was created after last year’s CWD Symposium. The symposium brought national and international experts to Michigan to discuss CWD. During the coming months, the DNR, NRC and MDARD will work with stakeholders to develop new CWD regulation recommendations.
Visit www.michigan.gov/cwd for more information about the disease, preventive measures and the public meeting schedule.
December 13, 2017 Alice Shea
CWD Confirmed in Deer From Mecosta County Deer Farm
Another Northern Michigan deer has been found with chronic wasting disease, this time in Mecosta County.
The Michigan Department of Agriculture and Rural Development says the disease was confirmed this week in a one-and-a-half-year-old female deer from a Mecosta County deer farm.
News Release: Chronic Wasting Disease Found In Two Mecosta County Deer 26 Jul, 2017
Chronic Wasting Disease Identified on Michigan Deer Farm Details Published: 23 January 2017
br> (Provided by MDNR)
Chronic wasting disease was confirmed this week in two female deer from a Mecosta County deer farm. CWD is a fatal neurological disease that affects white-tailed deer, mule deer, elk and moose. This is the second time the disease has been found in a farmed deer facility in Michigan. In 2008, a white-tailed deer from a Kent County deer farm tested positive.
"Chronic wasting disease is a serious disease affecting both farmed and free-ranging deer," said MDARD State Veterinarian James Averill, DVM. "We are following the state's CWD response plan and taking the necessary steps to protect the health and well-being of all of Michigan's deer populations."
Samples from the two deer were submitted for testing as a part of MDARD's mandatory CWD surveillance program. All farmed deer facilities licensed with the Michigan DNR must participate in this program.
"Any discovery of chronic wasting disease in free-ranging or farmed deer is disappointing," said Chad Stewart, DNR deer and elk specialist. "It will take significant time and effort ñ through immediate, targeted surveillance and mandatory checks during the upcoming deer seasons ñ to understand the current situation. The Michigan DNR remains committed in our efforts to contain this disease and safeguard our valuable wildlife resource."
Chronic wasting disease found in mid-Michigan deer ranch March 16, 2017
Bill Parker Lansing, Mich. — A pair of 3.5-year-old white-tailed does from a high-fence deer hunting ranch in mid-Michigan’s Mecosta County recently tested positive for chronic wasting disease. CWD is an always fatal neurological disease that affects cervids including deer, elk, and moose.
This is the second time the disease has been found in a farmed deer facility in Michigan. In 2008, a 3-year-old doe on a Kent County deer farm also tested positive.
“Chronic wasting disease is a serious disease affecting both farmed and free-ranging deer,” Michigan Department of Agriculture and Rural Development Veterinarian James Averill said in a statement. “We are following the state’s CWD response plan and taking the necessary steps to protect the health and well-being of all of Michigan’s deer populations.”
CWD was found in the two deer through mandatory testing of all deer killed on deer farms and ranches in Michigan.
On May 20, 2015, a six-year-old whitetail doe was confirmed positive for CWD.
After being reported by the landowner, it was found emaciated in Meridian Township, Ingham County. This is the first wild deer found with CWD in Michigan. Prior to this, one captive deer was identified in Kent County in 2008.
Historically, MDNR had tested over 34,000 deer, 1,600 elk, and 70 moose prior to the positive deer, and all were negative for CWD. Genetic tests at MSU suggest the positive wild doe, as well as two additional CWD positive deer, were Michigan deer and are in some manner related. How they became infected is unknown.
Michigan has had a CWD Response Plan in place for over 10 years that was updated in 2012 and it is what both agencies are following at this time. MDNR is following a 10-mile circle concept in which any counties that touch that radius are part of the CWD management unit. Baiting has ceased, surveillance has been increased, within a twomile radius (or nine-township area) they have been harvesting deer with the assistance of USDA Wildlife Services, and controlled movement is placed on all deer harvested in that area this year. In addition, there are less strict movement controls for the remainder of the three-county area involved.
On the MDARD side, a 15-mile circle has been established and three privately-owned cervid (POC) operations exist within that circle. Those operations have 30 cervids, two have only reindeer, a breed never found to have the disease. Although the risk for these POCs to contract the disease is very minimal, the department is monitoring the herd inventories twice a year and surveillance is increased in those facilities.
As of August 20, over 600 deer have been harvested within the two-mile radius since the finds in May and no additional CWD positives have been identified. USDA Wildlife Services will cease their targeted harvesting within the next week or so in preparation for early hunting season. At the end of hunting season, the number of deer harvested, any additional CWD positive finds, and the overall estimated deer population will be analyzed and targeted culls may resume in January if deemed prudent. MDNR will continue to conduct surveillance for a total of three years.
Michigan has had plans in place for HPAI and CWD, has updated those as appropriate, and is prepared. These diseases demonstrate the importance of how we need to be considering the impact of wildlife/domestic animal interactions. The department’s goal is to protect, regulate, and promote animal health and MDARD continues to do its best toward that goal.
In response to question from Commissioner Montri, Dr. Averill advised that MDNR is in the process of re-estimating the deer population in various areas of the state. However, the current area under surveillance for CWD is an area where the deer population is well over 60 deer per square mile.
MONDAY, AUGUST 25, 2008
CWD FIRST DOCUMENTED IN MICHIGAN Michigan's First Case of Chronic Wasting Disease Detected at Kent County Deer Breeding
The test results from the Kent County cervid breeding facility, where the index case was confirmed, found no additional diseased deer. Epidemiologists are reviewing taxidermy records on a facility related to the index case.
2012
News Release: Chronic Wasting Disease Found In Two Mecosta County Deer 26 Jul, 2017•0 Comments January 2017 – Two female deer from a deer farm in Mecosta County have confirmed cases of Chronic Wasting Disease, the Department of Agriculture and Rural development said Friday.
Chronic Wasting Disease is a fatal neurological disease that affects white-tailed deer, mule deer, elk and moose. The Mecosta deer mark the second time the disease has been found in farmed deer, the first being a white-tailed deer on a Kent County farm in 2008.
“Chronic wasting disease is a serious disease affecting both farmed and free-ranging deer,” James Averill, MDARD state veterinarian, said in a statement. “We are following the state’s CWD response plan and taking necessary steps to protect the health and well-being of all of Michigan’s deer populations”.
Samples from the two deer were submitted for testing, as the Department of Natural Resources requires of all licensed deer farms in the state.
“Any discovery of chronic wasting disease in free-ranging or farmed deer is disappointing,” said Chad Stewart, DNR deer and elk specialist. “It will take significant time and effort – through immediate, targeted surveillance and mandatory checks during the upcoming deer seasons – to understand the current situation. The Michigan DNR remains committed in our efforts to contain the disease and safeguard our valuable wildlife resource.”
An informal meeting for deer farmers is scheduled on February 1 at the Big Rapids Holiday Inn at 1005 Perry Avenue.
MDARD and DNR are also implementing surveillance and response plan for the disease and will quarantine the affected farm; complete trace investigations to identify the potential sources of infection and possible areas of spread; test all deer in the herd for the disease; inspect other farms in a 15-mile radius; and have a mandatory deer check for harvested deer in a 9-township area.
Click this link for more information on Chronic Wasting Disease.
Since May 2015 when the first CWD deer was found in Michigan, CWD has been confirmed in free-ranging white-tailed deer in the Lower Peninsula from Clinton, Ionia, Ingham, Jackson, Kent, Gratiot, Eaton, and Montcalm counties. 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.
TUESDAY, NOVEMBER 20, 2018
U.P. CWD Task Force continues work after deer confirmed with disease in Dickinson County
The deer was shot on an agricultural farm about 4 miles from the Michigan-Wisconsin border.
***> In Montcalm County, 83 CWD-positive free-ranging deer have been identified.
***> Since May 2015, when the first free-ranging white-tailed CWD-positive deer was found in Michigan, CWD has been confirmed in free-ranging white-tailed deer in the Lower Peninsula from Clinton, Eaton, Gratiot, Ionia, Ingham, Jackson, Kent, and Montcalm counties. Additionally, a CWD-positive deer was found in the Upper Peninsula in Dickinson County in October of last year. Baiting and feeding of deer and elk is not allowed in the Lower Peninsula.
CWD Identified in a Montcalm County Farmed Deer Agency: Agriculture and Rural Development
For immediate release: March 28, 2019 Media contact: Jessy Sielski (MDARD), 517-284-5725 or Ryan Soulard (DNR), 517-284-6184
LANSING – The Michigan departments of Agriculture and Rural and Development and Natural Resources have confirmed chronic wasting disease in a two-year-old female white-tailed deer from a Montcalm County deer farm. The sample was submitted for routine testing as a part of the state’s CWD surveillance program for farmed deer.
In Montcalm County, 83 CWD-positive free-ranging deer have been identified. This part of the state is an active CWD Management Zone. All deer farms in Michigan are required to submit samples for testing regularly; however, deer farms in a CWD Management Zone are quarantined and must participate in increased surveillance.
As a part of MDARD’s disease response, an investigation will be conducted to rule out exposure of any other farmed deer.
“The test results and age of the deer indicate that this deer was recently infected, emphasizing the importance of early detection through surveillance,” said State Veterinarian Nora Wineland, DVM. “MDARD and DNR work together, in partnership with the state’s deer farmers, to ensure the protection of all of Michigan’s deer.”
“With a disease like CWD, everyone’s actions matter,” said DNR state wildlife veterinarian, Kelly Straka, DVM. “Whether you are a deer producer submitting samples for surveillance or a hunter practicing safe carcass disposal, we all have a role to play in minimizing the risk of disease spread.”
Since May 2015, when the first free-ranging white-tailed CWD-positive deer was found in Michigan, CWD has been confirmed in free-ranging white-tailed deer in the Lower Peninsula from Clinton, Eaton, Gratiot, Ionia, Ingham, Jackson, Kent, and Montcalm counties. Additionally, a CWD-positive deer was found in the Upper Peninsula in Dickinson County in October of last year. Baiting and feeding of deer and elk is not allowed in the Lower Peninsula.
CWD is a fatal neurological disease that affects white-tailed deer, mule deer, elk, and moose. CWD can be transmitted directly from one animal to another, as well as indirectly through the environment. Infected animals may display abnormal behavior, progressive weight loss and physical debilitation. To date, there have been no reported cases of CWD infection in humans. However, as a precaution, the U.S. Centers for Disease Control and the World Health Organization recommend that infected animals not be consumed as food by either humans or domestic animals.
More information about CWD can be found at www.Michigan.gov/CWD.
###
THURSDAY, MARCH 28, 2019
Michigan CWD Identified in a Montcalm County Farmed Deer
TUESDAY, JANUARY 14, 2020
Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm
TUESDAY, DECEMBER 31, 2019
In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
***> 2020 CWD TSE PRION UPDATE GLOBAL MAP 2020
CWD TSE PRION UPDATE GLOBAL MAP 2020
SATURDAY, JANUARY 18, 2020
United States wildlife and wildlife product imports from 2000–2014 and TSE PRION aka Mad Cow Type Disease
***> HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE 1 IN 5,000 NOT ONE IN A MILLION!
***> I urge every Country around the Globe to Declare an Extraordinary Emergency Due To A Foreign Animal Disease Chronic Wasting Disease CWD TSE Prion from the USA, Canada, and Mexico (they have no clue), all of North America should have this Declaration of Emergency against them, just like the one called way back when the shoe was on the other foot with the mad sheep of mad river valley, except this time, it's not a wag the dog false flag, this is for real...terry
SATURDAY, JANUARY 25, 2020
Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date
FRIDAY, JANUARY 24, 2020
Wyoming Game & Fish Discovers CWD-Positive Mule Deer in Pinedale, Discourages Feeding of Wildlife
''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.''
''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''
FRIDAY, JANUARY 24, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020
FRIDAY, JANUARY 17, 2020
North Dakota 11 Positive Chronic Wasting Disease CWD TSE Prion detected since Sept 1, 2019
TUESDAY, JANUARY 07, 2020
Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 174 confirmed to date
TUESDAY, JANUARY 14, 2020
Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm
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
FRIDAY, JANUARY 10, 2020
Minnesota Investigation leads to additional CWD positive deer on Pine County farm
THURSDAY, JANUARY 23, 2020
Wisconsin Confirms CWD Detected In Marquette and Marathon County
WEDNESDAY, JANUARY 08, 2020
Wisconsin Chronic Wasting Disease CWD TSE Prion Positives in Farm-raised Deer in 2019
The majority of the positives have come after 2013 when DATCP began letting some deer farms and hunting ranches continue operating after CWD was detected on their property.
TUESDAY, JANUARY 07, 2020
Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive
THURSDAY, DECEMBER 19, 2019
TEXAS Val Verde County White-tailed Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion State Positive NOW at 147 Confirmed
FRIDAY, DECEMBER 20, 2019
Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission
FRIDAY, DECEMBER 20, 2019
TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY
SUNDAY, JANUARY 05, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion 2019 to 2020 Totals As Of December 3, 2019 399 Confirmed with more pending results
SUNDAY, DECEMBER 22, 2019
Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019
Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...
TUESDAY, DECEMBER 31, 2019 In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus
SUNDAY, AUGUST 02, 2015 TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
TUESDAY, JANUARY 07, 2020
Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 174 confirmed to date
SATURDAY, JANUARY 04, 2020
Mississippi CWD TOTALS JUST ABOUT DOUBLE Since October 1, 2019 To Date Statewide Total is 37 Confirmed
SUNDAY, JANUARY 19, 2020
Missouri CWD TSE Prion 2019-2020 SAMPLING RESULTS TO DATE 25 Positive
THURSDAY, JANUARY 02, 2020
Missouri MDC officially reports more than 20 new cases of Chronic Wasting Disease CWD TSE Prion
FRIDAY, JANUARY 17, 2020
Montana Moose Tests Positive for Chronic Wasting Disease CWD TSE PRION in Libby Area
Montana Fish, Wildlife & Parks 2019 CWD Surveillance Hunter Test Results CWD TSE PRION LOOKS LIKE 136 POSITIVE SO FAR, count them up...
WEDNESDAY, DECEMBER 25, 2019
Montana 16 more deer positive for CWD first time positive hunting district 705 in southeast
SUNDAY, DECEMBER 22, 2019
Illinois CWD TSE Prion 90 CWD-positive deer with 826 confirmed positive Total positives through June 30, 2019
THURSDAY, JANUARY 23, 2020
Canadian Food Inspection Agency (CFIA) has updated the following chapter of the Accredited Veterinarian's Manual: Chapter 13 Chronic Wasting Disease Herd Certification Programs
TUESDAY, JANUARY 21, 2020
2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020
Colorado Chronic Wasting Disease Response Plan December 2018
I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.
snip...
(the map on page 71, cwd marked in red, is shocking...tss)
ORIGIN OF CHRONIC WASTING DISEASE TSE PRION?
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even contemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
”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 it’s 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.
Subject: CWD TSE Prion better bust a move
Folks, the Cervid, and more, are in dire straits if we don’t bust a move now, I’m telling you, it’s going to take all hands on deck, to combat the cwd tse prion, and you will have to hit it from all sides, everything we have, you are either all in, or, you are part of the problem. You let this cwd tse PrP saturate the environment, strains mutate, tse jumps species become zoonotic, if that has not already happened. Some recent video presentations on cwd, and my submission today, to TAHC, for anyone interested, it’s just science 🧬
CWD WEBINAR CWD YESTERDAY! December 11, 2019
Dr. Mckenzie and CIDRAP on CWD TSE Prion
122: Prions and Chronic Wasting Disease with Jason Bartz
Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
''On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. ''
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO
cwd update on Wisconsin from Tammy Ryan...
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?
apparently, no ID though. tell me it ain't so please...
23:00 minute mark
''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
SATURDAY, JANUARY 19, 2019
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission
Greetings TAHC et al,
Thank You Kindly for letting me comment again on cwd tse prion.
My comments 1-8 with updated science in references to back all my concerns up with...
1. ALL CWD TSE PRION RULES MUST BE MADE MANDATORY, voluntary does not work.
2. TAHC MUST BAN THE MOVEMENT OF ALL CERVID BY GAME FARMS, BREEDERS, SPERM MILLS, URINE MILLS, HORN MILLS, VELVET MILLS, HIGH/LOW FENCE, WITH ALL VEHICLES AND FARM EQUIPMENT BEING LIMITED TO ONLY THOSE SITES.
3. ALL CAPTIVE FARMING PUT ON HOLD WITH NO MORE PERMITTED
4. ALL CAPTIVE FARMING CERVID MUST BE TESTED ANNUALLY LIVE AND DEAD AND VERIFIED, THAT OLD BSe of ''just another escapee' does not cut it anymore, see why here;
WEDNESDAY, FEBRUARY 10, 2016
Wisconsin Two deer that escaped farm had chronic wasting disease CWD
436 Deer Have Escaped From Farms to Wild
Tuesday, 18 March 2003 00:00
As the DNR prepared to hand over authority for overseeing game farms to the agriculture department, it sent 209 conservation wardens to 550 farms to collect information, attempt to pinpoint the source of the disease and to learn whether other deer had been exposed to it. The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling. see;
436 Deer Have Escaped From Farms to Wild
Tuesday, 18 March 2003 00:00
TUESDAY, JULY 14, 2015
TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD postive farm Yellow ear tag
5. ALL CAPTIVE FARMING CERVID ON ANY FARM MUST BE KILLED AND INCINERATED, COMPLETE ERADICATION OF ANY CWD POSITIVE HERD
6. 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, QUARANTINE MUST BE FOR AT LEAST 16 YEARS WITH NO MOVEMENT IN OR OUT OF THAT PREMISES
7. TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
***> PLEASE SEE HISTORY OF TEXAS TRUCKING CWD TSE PRION DISEASE AT THE BOTTOM OF MY SUBMISSION, TOO LONG TO POST HERE.
8.CONSIDERING RECENT SCIENCE THAT CWD TSE PRION WILL TRANSMIT ORALLY TO PIGS AND ALSO SCRAPIE TO PIGS BY ORAL ROUTES, CONSIDERING CWD TRANSMIT EASILY TO CERVID BY ORAL ROUTE, CONSIDERING A NEW TSE PRION OUTBREAK IN A NEW LIVESTOCK SPECIES, THE CAMEL, CONSIDERING THE FACT THE USA THAT THE 1997 BSE feed regulation at 589.2000, which remains in effect but which applies only to feed for cattle and other ruminants, and specifically, the new section 589.2001, WAS AND STILL IS A TOTAL AND COLOSSAL FAILURE, AND PROVEN TO BE SO BY RECENT COMMENTS COMING FROM THE FDA, BUT FIRST, COMMENTS FROM DEFRA;
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
***> cattle, pigs, sheep, cwd, tse, prion, oh my!
***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006).
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
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 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" 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.
***> In summary, our results establish aerosols as a surprisingly efficient modality of prion transmission. This novel pathway of prion transmission is not only conceptually relevant for the field of prion research, but also highlights a hitherto unappreciated risk factor for laboratory personnel and personnel of the meat processing industry. In the light of these findings, it may be appropriate to revise current prion-related biosafety guidelines and health standards in diagnostic and scientific laboratories being potentially confronted with prion infected materials. While we did not investigate whether production of prion aerosols in nature suffices to cause horizontal prion transmission, the finding of prions in biological fluids such as saliva, urine and blood suggests that it may be worth testing this possibility in future studies.
Adriano Aguzzi ''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''
WOW!...tss
Rabbits are not resistant to prion infection
Francesca Chianinia,1, Natalia Fernández-Borgesb,c,1, Enric Vidald , Louise Gibbarda , Belén Pintadoe , Jorge de Castroc , Suzette A. Priolaf , Scott Hamiltona , Samantha L. Eatona , Jeanie Finlaysona , Yvonne Panga , Philip Steelea , Hugh W. Reida , Mark P. Dagleisha , and Joaquín Castillab,c,g,2 a
Moredun Research Institute, Penicuik, Near Edinburgh EH26 0PZ, Scotland, United Kingdom; b CIC bioGUNE, Derio 48160, Bizkaia, Spain; g IKERBASQUE, Basque Foundation for Science, Bilbao 48011, Bizkaia, Spain; c Department of Infectology, Scripps Florida, Jupiter, FL 33458; f Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; d Centre de Recerca en Sanitat Animal (CReSA), UAB-IRTA, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain; and e Centro Nacional de Biotecnología (CNB), 28049 Cantoblanco, Madrid, Spain
Edited by Reed B. Wickner, National Institutes of Health, Bethesda, MD, and approved February 16, 2012 (received for review December 6, 2011)
The ability of prions to infect some species and not others is determined by the transmission barrier. This unexplained phenomenon has led to the belief that certain species were not susceptible to transmissible spongiform encephalopathies (TSEs) and therefore represented negligible risk to human health if consumed. Using the protein misfolding cyclic amplification (PMCA) technique, we were able to overcome the species barrier in rabbits, which have been classified as TSE resistant for four decades. Rabbit brain homogenate, either unseeded or seeded in vitro with disease-related prions obtained from different species, was subjected to serial rounds of PMCA. De novo rabbit prions produced in vitro from unseeded material were tested for infectivity in rabbits, with one of three intracerebrally challenged animals succumbing to disease at 766 d and displaying all of the characteristics of a TSE, thereby demonstrating that leporids are not resistant to prion infection. Material from the brain of the clinically affected rabbit containing abnormal prion protein resulted in a 100% attack rate after its inoculation in transgenic mice overexpressing rabbit PrP. Transmissibility to rabbits (>470 d) has been confirmed in 2 of 10 rabbits after intracerebral challenge. Despite rabbits no longer being able to be classified as resistant to TSEs, an outbreak of “mad rabbit disease” is unlikely.
snip...
In summary, after 3 y postchallenge with three different rabbitderived inocula, we have obtained one positive clinical case, one possible preclinical case, two intercurrent deaths, and six animals that have remained healthy. Although the incubation periods do not directly correlate with the degree of susceptibility, these data might indicate that rabbits are poorly susceptible to prion infection. Although the rabbits used in this study were not inbred, they all had identical full-length PrP sequences and, to date, no difference has been detected in the ORF PrP sequence in any other published rabbit PrP sequence placed in GenBank. To further investigate this, two types of second passage experiment were performed; three raPrPTg mice and 10 rabbits were all intracerebrally inoculated using brain homogenate from the clinically affected rabbit. In contrast to 100% of the de novo RaPrPSc-inoculated transgenic mice having succumbed to a standard clinical prion disease and thereby demonstrating a high rate of transmissibility in vivo, two of 10 rabbits developed a TSE (477 and 540 dpi, respectively) to date. A plausible explanation for the evident differences between these two transmission studies would be the high level of rabbit PrPC expression (4- to 6-fold) in the murine model. In addition, it is well known that even if overexpression does not increase susceptibility, it can significantly reduce the incubation time of disease (2). However, the two positive TSE cases in the second rabbit passage, even though 8 rabbits remained clinically normal at 560 dpi, have led us to conclude that rabbits can no longer be considered a prionresistant species. The long incubation times, even after a second passage, might be due to the presence of some unknown, and probably rare, susceptibility factor in rabbits, which may also be present, for example, in equids and canids.
To critically evaluate this risk, several experiments are currently underway to characterize this new prion disease in rabbits and other species to examine its ability to cross the species barrier. In addition, supplementary experiments have been initiated in rabbits and also in transgenic mice that overexpress rabbit PrPC, to evaluate their susceptibilities to other important prion diseases including CWD and BSE. There are several factors that any potential new TSE epidemic would require: (i) the new prion should be efficiently transmitted through the homologous species; (ii) animals should be edible by humans and should be slaughtered at an age at which the disease has developed, thereby increasing the chance that prions have replicated (especially for those prions that require long incubation times); and (iii) the meat and bone meal should be recycled and fed to new members of the same species. In the light of these data and taking into account the previous three factors, it is unlikely there will be an outbreak of “mad rabbit disease,” and consumers of rabbit meat face much less of a risk than consumers of cattle or sheep products.
THURSDAY, AUGUST 08, 2019
Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are;
BSE TESTING (failed terribly and proven to be a sham)
BSE SURVEILLANCE (failed terribly and proven to be a sham)
BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham)
these are facts folks. trump et al just admitted it with the feed ban.
see;
FDA Reports on VFD Compliance
John Maday
August 30, 2019 09:46 AM VFD-Form 007 (640x427)
Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.
SUNDAY, SEPTEMBER 1, 2019
***> FDA Reports on VFD Compliance
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
I STRENUOUSLY URGE TEXAS FDA MODIFY THESE FEED BANS ASAP!
SEE;
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary
View Attachment:View as format pdf
SATURDAY, JANUARY 18, 2020
United States wildlife and wildlife product imports from 2000–2014 and TSE PRION aka Mad Cow Type Disease
***> HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE 1 IN 5,000 NOT ONE IN A MILLION!
***> I urge every Country around the Globe to Declare an Extraordinary Emergency Due To A Foreign Animal Disease Chronic Wasting Disease CWD TSE Prion from the USA, Canada, and Mexico (they have no clue), all of North America should have this Declaration of Emergency against them, just like the one called way back when the shoe was on the other foot with the mad sheep of mad river valley, except this time, it's not a wag the dog false flag, this is for real...terry
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.
snip...see full text submission;
FRIDAY, DECEMBER 20, 2019
Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission
THURSDAY, DECEMBER 19, 2019
TSE surveillance statistics exotic species and domestic cats Update December 2019
THURSDAY, DECEMBER 19, 2019
The emergence of classical BSE from atypical/Nor98 scrapie
FRIDAY, DECEMBER 06, 2019
Estimating relative CWD susceptibility and disease progression in farmed white-tailed deer with rare PRNP alleles
WEDNESDAY, NOVEMBER 20, 2019
Review: Update on Classical and Atypical Scrapie in Sheep and Goats
WEDNESDAY, NOVEMBER 20, 2019
Sheep Are Susceptible to the Bovine Adapted Transmissible Mink Encephalopathy agent by Intracranial Inoculation and Have Evidence of Infectivity in Lymphoid Tissues
***> ''indicating that sheep inoculated with the bovine TME agent harbor infectivity in their lymph nodes despite a lack of detection with conventional immunoassays.''
FRIDAY, NOVEMBER 15, 2019
Southwest Wisconsin CWD, Deer and Predator Study
FRIDAY, NOVEMBER 08, 2019
EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III
WEDNESDAY, OCTOBER 16, 2019
Australia Assessment of bulk wheat from Canada Part B: Animal biosecurity risk advice, CWD TSE Prion concerns are mounting
FRIDAY, MAY 24, 2019
Assessing chronic wasting disease strain differences in free-ranging cervids across the United States
MONDAY, MAY 20, 2019
APHIS, USDA, Announces the Finalized Chronic Wasting Disease Herd Certification Program Standards Singeltary Submissions
CDC
New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES
Mad Camel Disease
Volume 24, Number 6—June 2018 Research
Prion Disease in Dromedary Camels, Algeria Abstract
Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
SNIP...
The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.
Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries. Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).
On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).
Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep. In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.
The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock. https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article ;
***> IMPORTS AND EXPORTS <***
***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***
SUNDAY, JANUARY 12, 2020 2019
USAHA-AAVLD Annual Meeting October 24-30, 2019 Transmissible Spongiform Encephalopathy TSE Prion CWD, Scrapie UPDATE
MONDAY, OCTOBER 07, 2019
Chronic Wasting Disease (CWD) and Government Response Congressional Research Service May 17, 2019
WEDNESDAY, OCTOBER 02, 2019
Chronic Wasting Disease In Cervids: Prevalence, Impact And Management Strategies
WEDNESDAY, JUNE 26, 2019
Subcommittee Hearing: Chronic Wasting Disease: The Threats to Wildlife, Public Lands, Hunting, and Health
video
CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002
CHRONIC WASTING DISEASE
JOINT OVERSIGHT HEARING BEFORE THE SUBCOMMITTEE ON FORESTS AND FOREST HEALTH JOINT WITH THE SUBCOMMITTEE ON FISHERIES CONSERVATION, WILDLIFE AND OCEANS OF THE COMMITTEE ON RESOURCES U.S. HOUSE OF REPRESENTATIVES ONE HUNDRED SEVENTH CONGRESS SECOND SESSION
May 16, 2002
Serial No. 107-117
snip...
Mr. MCINNIS. Today, this joint Subcommittee hearing will explore an issue of immeasurable importance to the growing number of communities in wide-ranging parts of this country, the growing incidence of Chronic Wasting Disease in North America’s wild and captive deer and elk populations. In a matter of just a few months, this once parochial concern has grown into something much larger and much more insidious than anyone could have imagined or predicted.
As each day passes, this problem grows in its size, scope, and consequence. One thing becomes clear. Chronic Wasting Disease is not a Colorado problem. It is a Wisconsin problem or a Nebraska or Wyoming problem. It is a national problem and anything short of a fully integrated, systematic national assault on this simply will not do, which is precisely why we brought our group together here today.
snip...
So this is a disease that is spreading throughout the continent and it is going to require a national response as well as the efforts that are currently taking place in States like Wisconsin, Colorado, Nebraska, Wyoming, the interest they now have down in Texas and some of the neighboring States that have large white-tailed deer population and also elk.
This is a huge issue for us, Mr. Chairman, in the State of Wisconsin. I want to commend Governor McCallum and your staff and the various agencies for the rapid response that you have shown, given the early detection of CWD after the last deer hunting season. The problem that we have, though, is just a lack of information, good science in regards to what is the best response, how dangerous is this disease. We cannot close the door, quite frankly, with the paucity of scientific research that is out there right now in regards to how the disease spreads, the exposure of other livestock herds—given the importance of our dairy industry in the State, that is a big issue—and also the human health effects.
FRIDAY, OCTOBER 04, 2019
Inactivation of chronic wasting disease prions using sodium hypochlorite
i think some hunters that don't read this carefully are going to think this is a cure all for cwd tse contamination. IT'S NOT!
first off, it would take a strong bleach type sodium hypochlorite, that is NOT your moms bleach she uses in her clothes, and store bought stuff.
Concentrated bleach is an 8.25 percent solution of sodium hypochlorite, up from the “regular bleach” concentration of 5.25 percent.Nov 1, 2013 https://waterandhealth.org/disinfect/high-strength-bleach-2/
second off, the study states plainly;
''We found that a five-minute treatment with a 40% dilution of household bleach was effective at inactivating CWD seeding activity from stainless-steel wires and CWD-infected brain homogenates. However, bleach was not able to inactivate CWD seeding activity from solid tissues in our studies.''
''We initially tested brains from two CWD-infected mice and one uninfected mouse using 40% bleach for 5 minutes. The results from these experiments showed almost no elimination of prion seeding activity (Table 4). We then increased the treatment time to 30 minutes and tested 40% and 100% bleach treatments. Again, the results were disappointing and showed less than a 10-fold decrease in CWD-seeding activity (Table 4). Clearly, bleach is not able to inactivate prions effectively from small brain pieces under the conditions tested here.''
''We found that both the concentration of bleach and the time of treatment are critical for inactivation of CWD prions. A 40% bleach treatment for 5 minutes successfully eliminated detectable prion seeding activity from both CWD-positive brain homogenate and stainless-steel wires bound with CWD. However, even small solid pieces of CWD-infected brain were not successfully decontaminated with the use of bleach.''
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659
https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html
i think with all the fear from recent studies, and there are many, of potential, or likelihood of zoonosis, if it has not already happened as scjd, i think this study came out to help out on some of that fear, that maybe something will help, but the study plainly states it's for sure not a cure all for exposure and contamination of the cwd tse prion on surface materials. imo...terry
HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...
* 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]
Wednesday, September 11, 2019
Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion
172. Establishment of PrPCWD extraction and detection methods in the farm soil
Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo Sohn
Foreign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, Korea
ABSTRACT
Introduction: Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2016 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and faeces of TSE-infected animals. Soil can serve as a stable reservoir for infectious prion proteins. We found that PrPCWD can be extracted and detected in CWD contaminated soil which has kept at room temperature until 4 years after 0.001 ~ 1% CWD exposure and natural CWD-affected farm soil through PBS washing and sPMCAb.
Materials and Methods: Procedure of serial PMCAb. CWD contaminated soil which has kept at room temperature (RT) for 1 ~ 4 year after 0.001%~1% CWD brain homogenates exposure for 4 months collected 0.14 g. The soil was collected by the same method once of year until 4 year after stop CWD exposure. We had conducted the two steps. There are two kinds of 10 times washing step and one amplification step. The washing step was detached PrPSc from contaminated soil by strong vortex with maximum rpm. We harvest supernatant every time by 10 times. As the other washing step, the Washed soil was made by washing 10 times soil using slow rotator and then harvest resuspended PBS for removing large impurity material. Last step was prion amplification step for detection of PrPCWD in soil supernatant and the washed soil by sPMCAb. Normal brain homogenate (NBH) was prepared by homogenization of brains with glass dounce in 9 volumes of cold PBS with TritonX-100, 5 mM EDTA, 150 mM NaCl and 0.05% Digitonin (sigma) plus Complete mini protease inhibitors (Roche) to a final concentration of 5%(w/v) NBHs were centrifuged at 2000 g for 1 min, and supernatant removed and frozen at −70 C for use. CWD consisted of brain from natural case in Korea and was prepared as 10%(w/v) homogenate. Positive sample was diluted to a final dilution 1:1000 in NBH, with serial 3:7 dilutions in NBH. Sonication was performed with a Misonix 4000 sonicator with amplitude set to level 70, generating an average output of 160W with two teflon beads during each cycle. One round consisted of 56 cycles of 30 s of sonication followed 9 min 30 s of 37°C incubation. Western Blotting (WB) for PrPSc detection. The samples (20 µL) after each round of amplification were mixed with proteinase K (2 mg/ml) and incubated 37°C for 1 h. Samples were separated by SDS-PAGE and transferred onto PVDF membrane. After blocking, the membrane was incubated for 1 h with 1st antibody S1 anti rabbit serum (APQA, 1:3000) and developed with enhanced chemiluminescence detection system.
Results: We excluded from first to third supernatant in view of sample contamination. It was confirmed abnormal PrP amplification in all soil supernatants from fourth to tenth. From 0.01% to 1% contaminated washed soils were identified as abnormal prions. 0.001% contaminated washed soil did not show PrP specific band (Fig 1). The soil was collected by the same method once of year until 4 year after stop CWD exposure. After sPMCAb, there were no PrPCWD band in from second to fourth year 0.001% washed soil. but It was confirmed that the abnormal prion was amplified in the washing supernatant which was not amplified in the washed soil. we have decided to use soil supernatant for soil testing (Fig. 2). After third rounds of amplification, PrPSc signals observed in three out of four sites from CWD positive farm playground. No signals were observed in all soil samples from four CWD negative farm (Fig. 3).
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.
===
186. Serial detection of hematogenous prions in CWD-infected deer
Amy V. Nalls, Erin E. McNulty, Nathaniel D. Denkers, Edward A. Hoover and Candace K. Mathiason
Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA
CONTACT Amy V. Nalls amy.nalls@colostate.edu
ABSTRACT
Blood contains the infectious agent associated with prion disease affecting several mammalian species, including humans, cervids, sheep, and cattle. It has been confirmed that sufficient prion agent is present in the blood of both symptomatic and asymptomatic carriers to initiate the amyloid templating and accumulation process that results in this fatal neurodegenerative disease. Yet, to date, the ability to detect blood-borne prions by in vitro methods remains difficult.
We have capitalized on blood samples collected from longitudinal chronic wasting disease (CWD) studies in the native white-tailed deer host to examine hematogenous prion load in blood collected minutes, days, weeks and months post exposure. Our work has focused on refinement of the amplification methods RT-QuIC and PMCA. We demonstrate enhanced in vitro detection of amyloid seeding activity (prions) in blood cell fractions harvested from deer orally-exposed to 300 ng CWD positive brain or saliva.
These findings permit assessment of the role hematogenous prions play in the pathogenesis of CWD and provide tools to assess the same for prion diseases of other mammalian species.
Considering the oral secretion of prions, saliva from CWD-infected deer was shown to transmit disease to other susceptible naïve deer when harvested from the animals in both the
and preclinical stages69
of infection, albeit within relatively large volumes of saliva (50 ml). In sheep with preclinical, natural scrapie infections, sPMCA facilitated the detection of PrPSc within buccal swabs throughout most of the incubation period of the disease with an apparent peak in prion secretion around the mid-term of disease progression.70
The amounts of prion present in saliva are likely to be low as indicated by CWD-infected saliva producing prolonged incubation periods and incomplete attack rates within the transgenic mouse bioassay.41
snip...
Indeed, it has also been shown that the scrapie and CWD prions are excreted in urine, feces and saliva and are likely to be excreted from skin. While levels of prion within these excreta/secreta are very low, they are produced throughout long periods of preclinical disease as well as clinical disease. Furthermore, the levels of prion in such materials are likely to be increased by concurrent inflammatory conditions affecting the relevant secretory organ or site. Such dissemination of prion into the environment is very likely to facilitate the repeat exposure of flockmates to low levels of the disease agent, possibly over years.
snip...
Given the results with scrapie-contaminated milk and CWD-contaminated saliva, it seems very likely that these low levels of prion in different secreta/excreta are capable of transmitting disease upon prolonged exposure, either through direct animal-to-animal contact or through environmental reservoirs of infectivity.
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
***>>> 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.
========================
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.
HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...
* 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]
Wednesday, September 11, 2019
Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion
SATURDAY, MARCH 16, 2019
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission
THURSDAY, SEPTEMBER 27, 2018
***> Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model
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]
2018 - 2019
***> This is very likely to have parallels with control efforts for CWD in cervids.
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2
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...
As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.
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.
Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.
Funding This study was funded by DEFRA within project SE1865.
Competing interests None declared.
Saturday, January 5, 2019
Rapid recontamination of a farm building occurs after attempted prion removal
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
***> 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.
***> 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.
Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3
Correspondence
Gudmundur Georgsson ggeorgs@hi.is
1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland
2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland
3 Bethesda, Maryland, USA
Received 7 March 2006 Accepted 6 August 2006
In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. 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. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION
SEE;
Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;
Some unofficial information from a source on the inside looking out -
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
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
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
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.
=========================
***>>> 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.
========================
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.
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
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
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).
Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).
Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.
Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.
Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).
The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.
It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.
Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.
Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.
In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.
In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).
As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).
This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.
This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.
In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.
Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.
The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.
In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).
A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).
This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.
Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
WEDNESDAY, MARCH 13, 2019
CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood
Subject: Prion 2019 Conference
See full Prion 2019 Conference Abstracts
see scientific program and follow the cwd studies here;
Thursday, May 23, 2019
Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts
THURSDAY, DECEMBER 19, 2019
TSE surveillance statistics exotic species and domestic cats Update December 2019
MONDAY, DECEMBER 16, 2019
Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update
***> ''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) <***
What if?
> 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).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
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.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 Conference
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
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
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 detected in spinal cord and brain of some 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 pre-clinical 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.
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..
***> 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. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
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..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
states.
AND ANOTHER STUDY;
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..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip…
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
PRION 2019 ABSTRACTS
1. Interspecies transmission of the chronic wasting disease agent
Justin Greenlee
Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service
ABSTRACT
The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.
53. Evaluation of the inter-species transmission potential of different CWD isolates
Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa
aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile
ABSTRACT
Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.
56. Understanding chronic wasting disease spread potential for at-risk species
Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca
ABSTRACT
Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.
KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates
Thursday, May 23, 2019
Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts
see full Prion 2019 Conference Abstracts
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
snip…full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
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 (216-119-163-189.ipset45.wt.net)
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, just 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 $$$ ***
*** 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).***
FRIDAY, JULY 26, 2019
Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species
TUESDAY, JANUARY 21, 2020
***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020
***> 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) <***
FRIDAY, OCTOBER 25, 2019
Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease
***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
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
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 emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise 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 acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway
***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)
Abstract
Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.
*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
OR
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
OR
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
OR here;
*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.
Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
WEDNESDAY, MAY 29, 2019
Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!
***> 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) <***
THURSDAY, DECEMBER 12, 2019
Heidenhain Variant Creutzfeldt Jakob Disease hvCJD, sporadic spontaneous CJD and the TSE Prion December 14, 2019
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
MONDAY, JANUARY 27, 2020
updated
Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
3:35 PM
0 Comments
