ACA Council Convenes to Assess Federal CWD Reform
Possibilities
November 18, 2013
Claims
USAHA Trip a Success; Looks for Options to Assist States with Border
Issues
AYR, NE-
The American Cervid Alliance Leadership Council convened Monday, November 18,
2013, to review the USAHA conference and discuss options in regard to Federal
CWD policy and state border closings.
The council examined possible
scenarios that could exist in regard to the CWD Program Standards. In San Diego
at the USAHA conference, Dr. John Clifford said the final version of standards,
known as Version 23, was ready for public comment. After several concerns from
industry leaders, Dr. Clifford offered to hold the advancement of the standards
and offered to give a personal review and compare to Version 18. Version 18 was
the version crafted by cervid industry representatives and state veterinarians
last April. ACA council members speculated there could only be a few possible
outcomes: Dr Clifford could send Version 23 forward to public comment, create a
blend of Version 23 and Version 18 and then move forward, or ask for a new
document to be re-drafted. Council leaders discussed the pros and cons of each
scenario.
Clint Patty and Kevin Fowler of the ACA’s law firm on
retainer were on the call to answer questions from council members regarding
various scenarios that could potentially occur. Travis Lowe, who takes notes
and minutes of the council meetings, is distributing a complete list of the
scenarios for the members to share with their home association boards of
directors. Moderator Eric Mohlman advised the council members to start
discussion with their home boards to know how they feel about each scenario.
The ACA recapped the recent border shutdown to CWD-susceptible cervid
species in New York and discussion centered around whether shutting down
interstate commerce was legal. The council also received updates on the pending
wild elk relocation project from Kentucky to Wisconsin. Cervid leaders feel
Wisconsin’s importation of wild elk should be held to the same importation
requirements as farmed cervids. Rhonda Brakke gave an update that the second
Iowa legal case with the Iowa Department of Natural Resources is currently
underway.
Discussion was held on the ongoing assault of inaccurate
negative press in Missouri by conservation groups seeking to shut down boarders
to cervid movement into that state. Travis Lowe stated at the cervid
leaders/USDA meeting in September in Washington DC, that USDA/APHIS was asked to
help with messaging to the state agriculture and conservation agencies. Lowe,
representing the Kansas Cervid Breeders Association, stated the KCBA is
preparing to send a letter to Dr TJ Myers of USDA/APHIS requesting the USDA to
help reinforce that there is no science to prove that CWD has had any
significant impact on wild deer populations. A motion was made by Charly Seale,
representing the Exotic Wildlife Association, for the ACA to draft a letter to
be sent to Dr. TJ Myers requesting USDA/APHIS to assist by offering a positive
statement to the Missouri agencies, and encourage ACA member associations to do
the same. Donald Hill, councilman for the Missouri Whitetail Deer & Hunting
Ranch Association, seconded of the motion and stated his association would
greatly welcome the help. The Seale motion was unanimously adopted.
ACA leaders extolled the recent trip to San Diego for the United States
Animal Health Association conference as a huge success. Almost all of the
proposed objectives previously approved by the council had been accomplished.
ACA Leaders stressed the importance of USAHA and urged state associations to
budget for a representative next year. Charly Seale told the council, “As an
industry we would not have the opportunities we had this year if our industry
did not have several representatives attend the conference. We need more faces
under their own state association flag to press our issues with key decision
makers.” Next year’s USHA conference is in Kansas City, Missouri.
Saturday, October 19, 2013
ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE
PRION DISEASE)
Eric Mohlman advised the Alliance that he has had several
discussions with key USAHA leaders about the possibly of approving the ACA as an
allied organization and board member of USAHA. Currently, three of the national
cervid associations, which include the North American Elk Breeders Association,
North American Deer Farmers Association, and Exotic Wildlife Association, serve
on the board of directors. The possibility of the ACA having its own seat, as
an allied organization representing thirty cervid associations, would increase
the presence of the industry voice on the national level. A motion was made by
Kim Kafka of the North American Elk Breeders Association, seconded by Brian
Wagner of the Minnesota Elk Breeders Association, to approve the ACA moving
forward to seek the USAHA Board seat. The motion was adopted unanimously,
22-0. The Alliance nominated two council members to serve as the interim
representative for the ACA, if approved. The nominees were Eric Mohlman and
Laurie Seale. After the roll call vote, Laurie Seale was approved by a vote of
13-7. Next year the ACA will conduct a nominating vetting process for the 2014
USAHA Conference representative.
Wednesday, September 04, 2013
***cwd - cervid captive livestock
escapes, loose and on the run in the wild ***
Thursday, August 08, 2013
***
Characterization of the first case of naturally occurring chronic wasting
disease in a captive red deer (Cervus elaphus) in North America ***
Monday, June 24, 2013
*** The
Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following
its Discovery ***
Tuesday, June 11, 2013
***
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in
Pennsylvania ***
***
USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.” ***
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd
Pennsylvania Update May 28, 2013
6
doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine
began on October 18, 2012, still ongoing, Lake Charles premises.
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Sunday, January 27, 2013
Indiana 6 deer missing from farm pose health risk to state herds INDIANA
Wisconsin : 436 Deer Have Escaped From Farms to Wild
Date: March 18, 2003 Source: Milwaukee Journal Sentinel
Contacts: LEE BERGQUIST lbergquist@journalsentinel.com
State finds violations, lax record keeping at many sites, report
says
A
state inspection of private deer farms, prompted by the discovery of chronic
wasting disease, found that 436 white-tailed deer escaped into the wild,
officials said Tuesday
The
Department of Natural Resources found that captive deer have escaped from
one-third of the state's 550 deer farms over the lifetime of the operations. The
agency also uncovered hundreds of violations and has sought a total of 60
citations or charges against deer farm operators.
These and other findings come as state officials say they are still no
closer to understanding how the fatal deer disease got to Wisconsin.
Since the discovery a little more than a year ago, chronic wasting
disease has thrown both deer hunting and management of Wisconsin's 1.4 million
deer herd into tumult. Fewer hunters went into the woods last year, and a
booming deer population has the DNR worried that the number of whitetails could
grow out of control.
Tuesday's findings were presented to the state Department of
Agriculture, Trade and Consumer Protection. The DNR had regulated deer farms,
but the authority was transferred to the Agriculture Department on Jan. 1. Now
agriculture regulators oversee elk, deer and other captive cervids.
Solving the problem
Stricter regulations - and closer attention to the operations of game
farms - should cut down on future violations, officials from the two agencies
said. Tougher reporting requirements also will help authorities keep better
track of the movement of animals, they said.
Permanent rules take effect in June, and include tighter controls on
moving animals and requiring the reporting of escaped animals within 48 hours.
There will be mandatory testing of every deer age 16 months or older that
dies.
Almost from the start of the state's battle against chronic wasting
disease, game farm operators came under scrutiny because their business involves
the buying and selling of captive deer and elk across state lines. When the
disease was first discovered here Feb. 28, 2002, Wisconsin became the first
state to have the disease east of the Mississippi River.
A
representative of the deer industry said Tuesday that the DNR is trying to shift
blame for chronic wasting disease to his industry.
"The state of Wisconsin has spent a year chasing chronic wasting
disease, and they have made zero progress," said Gary Nelson, president of
Whitetails of Wisconsin. "In the past, they have essentially collected our fees
and ignored us. Now that they have discovered CWD, they are looking for someone
to blame."
A
DNR representative agreed that the agency could have done a better job keeping
tabs on deer farms.
"We're not pointing fingers," said Karl Brooks, a conservation warden
with the DNR. "But two things that we know for sure is that there is CWD in the
wild deer population, and we have found CWD on game farms."
CWD
found on 2 farms
Seven deer have tested positive for the disease on game farms - one on a
Portage County farm and six on a Walworth County farm - since the disease was
discovered in three wild deer killed near Mount Horeb in western Dane County.
One deer that tested positive on the Walworth County farm escaped and roamed
free for six months.
Regulations have only begun to catch up to the captive deer industry,
and "unfortunately, it took CWD to get us there," said agriculture secretary Rod
Nilsestuen at a news briefing in Madison.
As
the DNR prepared to hand over authority for overseeing game farms to the
agriculture department, it sent 209 conservation wardens to 550 farms to collect
information, attempt to pinpoint the source of the disease and to learn whether
other deer had been exposed to it.
The
audit found that most farms were in compliance, but the DNR found many
violations and instances of poor record keeping. Also in numerous instances,
fences did not stop wild and captive deer from intermingling.
At
least 227 farms conducted part of their business on a cash basis, making it hard
to track animal movement with financial records.
For
example, both the Internal Revenue Service and the state Department of Revenue
have been contacted about a deer farm near Wild Rose in Waushara County that is
suspected of selling six large bucks for $45,000 in cash and not using live deer
shipping tags as required.
The
DNR found that game farm operators have more deer in captivity than their
records show, which is "due in part because the owners of a number of large deer
farm operations were unable to accurately count the number of deer within their
fences," the audit found.
Hundreds of deer escape
The
DNR found a total of 671 deer that escaped farms - 436 of which were never found
- because of storm-damaged fences, gates being left open or the animals jumping
over or through fences.
In
one example in Kewaunee County, a deer farmer's fence was knocked down in a
summer storm. Ten deer escaped, and the farmer told the DNR he had no intention
of trying to reclaim them. The DNR found five of the deer, killed them and cited
the farmer for violation of a regulation related to fencing.
Another deer farmer near Mishicot, in Manitowoc County, released all
nine of his whitetails last summer after he believed the discovery of chronic
wasting disease was going to drive down the market for captive deer.
The
DNR found 24 instances of unlicensed deer farms and issued 19 citations.
Journal Sentinel correspondent Kevin Murphy contributed to this
report.
Game Farms Inspected
A
summary of the findings of the Department of Natural Resources' inspection of
550 private white-tailed deer farms in the state: The deer farms contained at
least 16,070 deer, but the DNR believes there are more deer in captivity than
that because large deer farms are unable to accurately count their deer. 671
deer had escaped from game farms, including 436 that were never found.
24
farmers were unlicensed. One had been operating illegally since 1999 after he
was denied a license because his deer fence did not meet minimum
specifications.
Records maintained by operators ranged from "meticulous documentation to
relying on memory." At least 227 farms conducted various portions of their deer
farm business with cash. Over the last three years, 1,222 deer died on farms for
various reasons. Disease testing was not performed nor required on the majority
of deer. Farmers reported doing business with people in 22 other states and one
Canadian province.
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Sunday, November 03, 2013
Wisconsin Second CWD deer found in Portage County
how many states have $465,000., and can quarantine and purchase there from,
each cwd said infected farm, but how many states can afford this for all the cwd
infected cervid game ranch type farms ???
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of
land for $465,000 for the Statewide Wildlife Habitat Program in Portage County
and approve the restrictions on public use of the site.
SUMMARY:
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Thursday, February 09, 2012
Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Monday, February 13, 2012
Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild
Deer Herd oppose HB3164
Tuesday, February 14, 2012
Oppose Indiana House Bill 1265 game farming cervids
Wednesday,
February 15, 2012
West
Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED
CWD
2013
State Agriculture Commissioner Walt Helmick speaks Wednesday to the West
Virginia Food Policy Council at Tamarack on ways to grow the state’s
agricultural economy. One item he proposed is for the state to expand its deer
farming industry, but explained the Legislature would need to move control of
the state’s deer farming program from the Division of Natural Resources to his
department. Brandi Underwood
Thursday, November 14, 2013
West Virginia Ag Commissioner Pushing for Control of Deer Farming risks
spreading CWD
Wednesday, August 21, 2013
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE
D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
snip...
5. On July 16, 2012, DNR received a notice from the Texas Veterinary
Medical Diagnostic Lab ("Texas Vet Lab”) that a sample from an adult male deer
killed at Pine Ridge tested presumptively positive for CWD. (DNR has an
agreement with the Texas Vet Lab to run these preliminary tests.) Because the
Texas Vet Lab found this presumptive positive result, protocols required the
sample to be sent to the National Veterinary Services Laboratory ("National
Lab”) in Ames, Iowa for final confirmation. On July 18, 2012, the National Lab
confirmed the positive CWD result in the deer.
6. On
July 19, 2012, DNR notified the Brakkes of the positive test by phone. Mr.
Brakke was out of state.
7. On
July 23, 2012, DNR met with the Brakkes to initiate an epidemiological
investigation. This investigation would help determine where the infected deer
came from and make preliminary assessments about the extent of the exposure. The
Brakkes provided information including their herd inventory and photographic
evidence of the animals killed on the date the infected deer was killed. Also
present at this meeting were representatives from the Iowa Department of
Agriculture and Land Stewardship ("IDALS"), the United States Department of
Agriculture ("USDA") and the Iowa Whitetail Deer Association, an Iowa non-profit
organization. IDALS regulates breeding programs that sometimes populate hunting
preserves. USDA regulates interstate transport of captive deer; its veterinarian
designated as the Area Veterinarian in Charge would have been involved to
determine if the diseased captive deer are or may have been moved through
interstate commerce and/or transport.
8.
Based on information provided by the Brakkes, DNR concluded that captive deer
killed on the Hunting Preserve on the same day as the infected deer were located
in Florida, New Hampshire, Tennessee and Iowa. Between July 27, 2012 and August
6, 2012, DNR worked with law enforcement officials from those other states to
collect samples from the antlers of those deer for DNA testing. These tests
would help to identify the origin of the infected deer and verify Brakke's prior
documents that the infected deer came from the breeding facility run by the Tom
and Rhonda Brakke in Cerro Gordo County, Iowa ("Brakke’s Breeding Facility").
These samples were obtained in a manner to preserve the chain of custody.
9. On
August 10, 2012, the Wyoming Game and Fish Wildlife Forensic and Fish Health
Laboratory ("Wyoming Lab") provided DNR results for the seven specimens provided
to it. (DNR has an agreement with the Wyoming Lab to conduct DNA testing.) The
results confirmed that the infected deer originated from the Brakke's Breeding
Facility.
10. On
August 13, 2012, DNR notified the Brakkes of the DNA results by telephone. DNR
advised the Brakkes that they would need to meet with DNR to develop a plan to
address the CWD infection at the Hunting Preserve. DNR would have also been
communicating with IDALS consistent with the Plan.
11. On
September 7, 2012, DNR and the Brakkes executed an agreement ("Agreement") to
depopulate the Hunting Preserve by January 31, 2013, and to clean and disinfect
the Hunting Preserve. It also contained a general Compliance with Laws
provision, which required the Brakkes to comply with all applicable federal,
state and local laws and regulations, including without limitation the rules
described in 571 Iowa Administrative Code section 115.10 related to the
maintenance of a
--------------------------------------------------------------------------------
Page 4
IOWA
DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE
D/B/A PINE RIDGE HUNTING PRESERVE
quarantine
on the Quarantined Premises and the prohibition of deer movement in or out of
the Quarantined Premises.
12.
The Brakkes depopulated the Hunting Preserve, as specified in the Agreement,
from September 10, 2012 to January 31, 2013. As part of this effort, the
Brakkes, the staff and their customers killed 199 captive deer and nine captive
elk. The DNR obtained 170 CWD samples. (Samples were not taken from fawns and
one adult female who was killed in a manner that made sampling impossible.) Of
these 199 deer, two additional adult male deer tested positive for CWD.
Information provided by the Brakkes confirmed that these two additional deer
originated from the Brakke Breeding Facility.
13.
DNR installed, with the Brakke's permission, an interior electric fence on
October 1 and 2, 2012.
14.
The Brakkes cleaned and disinfected, under DNR supervision, the feeders and
ground surrounding the feeders on April 5, 2013.
15. On
April 26, 2013, the Brakkes hand-delivered a notice to the DNR’s Chief of Law
Enforcement Bureau, notifying the DNR that they would no longer operate a
hunting preserve on the Quarantined Premises. The Brakkes did not reveal any
plans to remove the fence around the Quarantined Premises or to remove the gates
to and from the Quarantined Premises in this April 26, 2013 letter.
16. On
June 3, 2013, DNR became aware that sections of the exterior fence surrounding
the Quarantined Premises had been removed and that some, if not all, of the
exterior gates to and from the Quarantined Premises were open.
17. On
June 4, 2013, DNR received reports from the public in the area that four wild
deer were observed inside the Quarantined Premises.
18. On
June 5, 2013, DNR conducted a fence inspection, after gaining approval from
surrounding landowners, and confirmed that the fenced had been cut or removed in
at least four separate locations; that the fence had degraded and was failing to
maintain the enclosure around the Quarantined Premises in at least one area;
that at least three gates had been opened; and that deer tracks were visible in
and around one of the open areas in the sand on both sides of the fence,
evidencing movement of deer into the Quarantined Premises.
IV.
CONCLUSIONS OF LAW
snip...
Wednesday,
August 21, 2013
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE
D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
PLEASE STUDY THIS MAP !
SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION
RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
SNIP...
CWD Zoonotic Potential, Species Barriers, and Strains
Current Understanding of the CWD Species Barrier
Strong evidence of zoonotic transmission of BSE to humans has led to
concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions
are present nearly ubiquitously throughout diseased hosts, including in muscle,
fat, various glands and organs, antler velvet, and peripheral and CNS tissue
(2,14,15). Thus, the potential for human exposure to CWD by handling and
consumption of infectious cervid material is substantial and increases with
increased disease prevalence.
Interspecies transmission of prion diseases often yields a species-barrier
effect, in which transmission is less efficient compared with intraspecies
transmission, as shown by lower attack rates and extended incubation periods
(3,28). The species barrier effect is associated with minor differences in PrPc
sequence and structure between the host and target species (3). Prion strain
(discussed below) and route of inoculation also affect the species barrier
(3,28). For instance, interspecies transmission by intracerebral inoculation is
often possible but oral challenge is completely ineffective (29).
Most epidemiologic studies and experimental work have suggested that the
potential for CWD transmission to humans is low, and such transmission has not
been documented through ongoing surveillance (2,3). In vitro prion replication
assays report a relatively low efficiency of CWD PrPSc-directed conversion of
human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are
resistant to CWD infection (31); these findings indicate low zoonotic potential.
However, squirrel monkeys are susceptible to CWD by intracerebral and oral
inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans
than squirrel monkeys, are resistant to CWD infection (32). Regardless, the
finding that a primate is orally susceptible to CWD is of concern.
Interspecies transmission of CWD to noncervids has not been observed under
natural conditions. CWD infection of carcass scavengers such as raccoons,
opossums, and coyotes was not observed in a recent study in Wisconsin (22). In
addition, natural transmission of CWD to cattle has not been observed in
experimentally controlled natural exposure studies or targeted surveillance (2).
However, CWD has been experimentally transmitted to cattle, sheep, goats, mink,
ferrets, voles, and mice by intracerebral inoculation (2,29,33).
CWD is likely transmitted among mule, white-tailed deer, and elk without a
major species barrier (1), and other members of the cervid family, including
reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD
infection. Black-tailed deer (a subspecies of mule deer) and European red deer
(Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34).
Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation
(35). Continued study of CWD susceptibility in other cervids is of considerable
interest.
Reasons for Caution
There are several reasons for caution with respect to zoonotic and
interspecies CWD transmission. First, there is strong evidence that distinct CWD
strains exist (36). Prion strains are distinguished by varied incubation
periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions
(3,32). Strains have been identified in other natural prion diseases, including
scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions
from CWD-positive deer and elk isolates resulted in identification of >2
strains of CWD in rodent models (36), indicating that CWD strains likely exist
in cervids. However, nothing is currently known about natural distribution and
prevalence of CWD strains. Currently, host range and pathogenicity vary with
prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with
CWD strain. In addition, diversity in host (cervid) and target (e.g., human)
genotypes further complicates definitive findings of zoonotic and interspecies
transmission potentials of CWD.
Intraspecies and interspecies passage of the CWD agent may also increase
the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial
passage naturally as the disease continues to emerge. In vitro and in vivo
intraspecies transmission of the CWD agent yields PrPSc with an increased
capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission
can alter CWD host range (38) and yield multiple novel prion strains (3,28). The
potential for interspecies CWD transmission (by cohabitating mammals) will only
increase as the disease spreads and CWD prions continue to be shed into the
environment. This environmental passage itself may alter CWD prions or exert
selective pressures on CWD strain mixtures by interactions with soil, which are
known to vary with prion strain (25), or exposure to environmental or gut
degradation.
Given that prion disease in humans can be difficult to diagnose and the
asymptomatic incubation period can last decades, continued research,
epidemiologic surveillance, and caution in handling risky material remain
prudent as CWD continues to spread and the opportunity for interspecies
transmission increases. Otherwise, similar to what occurred in the United
Kingdom after detection of variant CJD and its subsequent link to BSE, years of
prevention could be lost if zoonotic transmission of CWD is subsequently
identified,
SNIP...
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
see much more here ;
recently, a report came out in the U.K., about risk factors from entry of
CWD from the USA.
I think you might find interest there ;
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...
SNIP...SEE ;
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
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population (Chronic Wasting
Disease CWD TSE prion aka mad deer disease)
Wednesday, September 25, 2013
Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE
PRION 2013
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
EMC 1 Terry S. Singeltary Sr. Vol #: 1
PLEASE SEE FULL TEXT SUBMISSION ;
Thursday, October 03, 2013
TAHC ADOPTS CWD RULE THAT the amendments *remove* the requirement for a
specific fence height for captives
Texas Animal Health Commission (TAHC)
ANNOUNCEMENT
October 3, 2013
Sunday, September 01, 2013
***
hunting over gut piles and CWD TSE prion disease
Monday, October 07, 2013
The importance of localized culling
in stabilizing chronic wasting disease prevalence in white-tailed deer
populations
Wednesday, September 25, 2013
USDA Officials: CWD Standards Going to Public Comment Soon
Sunday, November 3, 2013
***
Environmental Impact Statements; Availability, etc.: Animal Carcass Management
[Docket No. APHIS-2013-0044]
OLD
HISTORY ON CWD AND GAME FARMS IN USA
Chronic Wasting Disease TSE prion aka mad deer to Humans ?
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
The chances of a person
or domestic animal contracting CWD are “extremely remote,” Richards said. The
possibility can’t be ruled out, however. “One could look at it like a game of
chance,” he explained. “The odds (of infection) increase over time because of
repeated exposure. That’s one of the downsides of having CWD in free-ranging
herds: We’ve got this infectious agent out there that we can never say never to
in terms of (infecting) people and domestic livestock.”
https://www.avma.org/News/JAVMANews/Pages/121201a.aspx
P35
ADAPTATION
OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN
OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department
of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is
increasingly important for the diagnosis and biological definition of these
infectious pathogens. Although well-established in scrapie and, more recently,
in BSE, comparatively little is known about the possibility of prion strains in
chronic wasting disease (CWD), a disease affecting free ranging and captive
cervids, primarily in North America. We have identified prion protein variants
in the white-tailed deer population and demonstrated that Prnp genotype affects
the susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic
region.
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdfPRION2013
CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats,
blood, and mother to offspring transmission
Sunday, July 21, 2013
***
As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in
free-ranging and captive cervid species in North America, and there is evidence
suggesting the existence of multiple CWD strains. The susceptibility of human
CNS and peripheral organs to the various CWD prion strains remains largely
unclear. Current literature suggests that the classical CWD strain is unlikely
to infect human brain, but the potential for peripheral infection by CWD in
humans is unknown. We detected protease-resistant PrpSc in the spleens of a few
humanized transgenic mice that were intracerebrally inoculated with natural CWD
isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated
mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral
challenge with such PrpSc-positive humanized mouse spleen already led to prion
disease in most animals.
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison
of the ability of sheep, cattle and deer prion disease isolates to convert
normal human prion protein to its pathological isoform in a cell-free system
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki
Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and
Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain
Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh,
UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food
Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious
Pathogen Research Section; Central Research Laboratory; Japan Blood Products
Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku
University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division;
The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush;
Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic
prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans.
In contrast, classical scrapie in sheep is thought to offer little or no danger
to human health. However, a widening range of prion diseases have been
recognized in cattle, sheep and deer. The risks posed by individual animal prion
diseases to human health cannot be determined a priori and are difficult to
assess empirically. The fundamemal event in prion disease pathogenesis is
thought to be the seeded conversion of normal prion protein (PrPC) to its
pathological isoform (PrPSc). Here we report the use of a rapid molecular
conversion assay to test whether brain specimens from different animal prion
diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type
BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain
homogenates were tested for their ability to seed conversion of human PrPC to
PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed
human PrPSc was detected by protease digestion and western blotting using the
antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to
PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion
diseases tested only chronic wasting disease appeared to have the capability ro
convert human PrPC to PrPSc. The results were consistent whether the human PrPC
came from human brain, humanised transgenic mouse brain or from cultured human
cells and the effect was more pronounced for PrPC with methionine at codon 129
compared with that with valine.
Conclusion. Our results show that none of the tested animal prion
disease isolates are as efficient as C-type BSE and vCJD in converting human
prion protein in this in vitro assay.
***However, they also show that there is no absolute barrier ro
conversion of human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats,
blood, and mother to offspring transmission
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and
Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal
muscle from CWD-infected cervids suggests prevention of such tissue in the human
diet as a precautionary measure for food safety, pending on further
clarification of whether CWD may be transmissible to humans.
PPo3-7:
Prion Transmission from Cervids to Humans is Strain-dependent
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi
Gambetti and Liuting Qing Department of Pathology; Case western Reserve
University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial
Sloan-Kettering Cancer Center; New York, NY USA
Key words: CWD, strain, human transmission
Chronic wasting disease (CWD) is a widespread prion disease in cervids
(deer and elk) in North America where significant human exposure to CWD is
likely and zoonotic transmission of CWD is a concern. Current evidence indicates
a strong barrier for transmission of the classical CWD strain to humans with the
PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD
strains. What remain unknown is whether individuals with the PrP-129VV/MV
genotypes are also resistant to the classical CWD strain and whether humans are
resistant to all natural or adapted cervid prion strains. Here we report that a
human prion strain that had adopted the cervid prion protein (PrP) sequence
through passage in cervidized transgenic mice efficiently infected transgenic
mice expressing human PrP, indicating that the species barrier from cervid to
humans is prion strain-dependent and humans can be vulnerable to novel cervid
prion strains. Preliminary results on CWD transmission in transgenic mice
expressing human PrP-129V will also be discussed.
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A.
Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and
related Brain disorders; Dept of Neurology; University of Texas Houston Medical
School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular
Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky
Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve
University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago;
Chicago, IL USA
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of
cervids is a prion disorder of increasing prevalence within the United States
that affects a large population of wild and captive deer and elk. CWD is highly
contagious and its origin, mechanism of transmission and exact prevalence are
currently unclear. The risk of transmission of CWD to humans is unknown.
Defining that risk is of utmost importance, considering that people have been
infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the infectious form by CWD
PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification
(PMCA) technique, which mimic in vitro the process of prion replication. Our
results show that cervid PrPSc can induce the pathological conversion of human
PrPC, but only after the CWD prion strain has been stabilized by successive
passages in vitro or in vivo. Interestingly, this newly generated human PrPSc
exhibits a distinct biochemical pattern that differs from any of the currently
known forms of human PrPSc, indicating that it corresponds to a novel human
prion strain. Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD
Isolates
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin,
Germany
Key words: CWD, strains, FT-IR, AFM
Chronic wasting disease (CWD) is one of three naturally occurring forms of
prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie
in sheep. CWD is contagious and affects captive as well as free ranging cervids.
As long as there is no definite answer of whether CWD can breach the species
barrier to humans precautionary measures especially for the protection of
consumers need to be considered. In principle, different strains of CWD may be
associated with different risks of transmission to humans. Sophisticated strain
differentiation as accomplished for other prion diseases has not yet been
established for CWD. However, several different findings indicate that there
exists more than one strain of CWD agent in cervids. We have analysed a set of
CWD isolates from white-tailed deer and could detect at least two biochemically
different forms of disease-associated prion protein PrPTSE. Limited proteolysis
with different concentrations of proteinase K and/or after exposure of PrPTSE to
different pH-values or concentrations of Guanidinium hydrochloride resulted in
distinct isolate-specific digestion patterns. Our CWD isolates were also
examined in protein misfolding cyclic amplification studies. This showed
different conversion activities for those isolates that had displayed
significantly different sensitivities to limited proteolysis by PK in the
biochemical experiments described above. We further applied Fourier transform
infrared spectroscopy in combination with atomic force microscopy. This
confirmed structural differences in the PrPTSE of at least two disinct CWD
isolates. The data presented here substantiate and expand previous reports on
the existence of different CWD strains.
2012
Envt.06:
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2
Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6
and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food
Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS
USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa,
ON Canada
†Presenting author; Email: emmanuel.comoy@cea.fr
The constant increase of chronic wasting disease (CWD) incidence in North
America raises a question about their zoonotic potential. A recent publication
showed their transmissibility to new-world monkeys, but no transmission to
old-world monkeys, which are phylogenetically closer to humans, has so far been
reported. Moreover, several studies have failed to transmit CWD to transgenic
mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the
only animal prion disease for which a zoonotic potential has been proven. We
described the transmission of the atypical BSE-L strain of BSE to cynomolgus
monkeys, suggesting a weak cattle-to-primate species barrier. We observed the
same phenomenon with a cattleadapted strain of TME (Transmissible Mink
Encephalopathy). Since cattle experimentally exposed to CWD strains have also
developed spongiform encephalopathies, we inoculated brain tissue from
CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice
overexpressing bovine or human PrP. Since CWD prion strains are highly
lymphotropic, suggesting an adaptation of these agents after peripheral
exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid
brains using the oral route. Nearly four years post-exposure, monkeys exposed to
CWD-related prion strains remain asymptomatic. In contrast, bovinized and
humanized transgenic mice showed signs of infection, suggesting that CWD-related
prion strains may be capable of crossing the cattle-to-primate species barrier.
Comparisons with transmission results and incubation periods obtained after
exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted
TME) will also be presented, in order to evaluate the respective risks of each
strain.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal
muscle from CWD-infected cervids suggests prevention of such tissue in the human
diet as a precautionary measure for food safety, pending on further
clarification of whether CWD may be transmissible to humans.
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
now, let’s see what the authors said about this casual link, personal
communications years ago. 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
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
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 ;
Saturday, October 6, 2012
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES 2011 Annual Report
Thursday, November 21, 2013
***Assessing the susceptibility of transgenic mice over-expressing deer
prion protein to bovine spongiform encephalopathy***
WHAT about the sporadic CJD TSE proteins
?
WE now know that some cases of sporadic CJD are linked to atypical BSE
and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and
all it’s sub-types $$$
Sunday, August 11, 2013
Creutzfeldt-Jakob
Disease CJD cases rising North America updated report August 2013
Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010
http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html
> In 12 of 15 hospitals with
neurosurgical incidents, a decision was made to notify patients of their
potential exposure.
TSS
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