Wednesday, February 12, 2014
News Release
For Immediate Release 2/7/2014 Contact Megan Kirchgessner, Wildlife
Veterinarian, 804-837-5666 Nelson Lafon, Deer Project Coordinator, (540)
569-0023
VDGIF Recognizes Assistance of Hunters, Reports Two New CWD Positives in
Frederick County
RICHMOND, VA - Two new cases of chronic wasting disease (CWD) were detected
in Frederick County during the 2013 hunting season. One deer, a 2.5 year old
doe, was killed on November 30, 2013, in close proximity to the cluster of five
CWD-positive deer harvested in Virginia since 2009. Additionally, a 1.5 year old
buck was killed on November 23, 2013, approximately 10 miles southeast of the
previously reported cluster. The location of this positive is not surprising,
given that many male white-tailed deer disperse miles from their place of birth
during their second year. Due to the proximity of this new positive to the
eastern border of the current Containment Area (CA), changes to the CA
boundaries are expected for the 2014 hunting season.
The Virginia Department of Game and Inland Fisheries (VDGIF) would like to
thank all of the hunters in Frederick and Shenandoah counties for their
excellent cooperation during CWD sample collection this past fall. VDGIF plans
to continue collecting CWD samples on the first three Saturdays of regular
firearms season during future hunting seasons, along with other management
options implemented after the initial detection of CWD in 2009. These management
actions include: prohibiting the feeding of deer year-round both in and near the
CA, prohibiting the movement of deer carcasses and parts out of the CA (with
exceptions), restricting the disposal of deer wastes from the CA, prohibiting
the rehabilitation of deer in the CA, and maintaining liberal seasons and bag
limits on private lands in an attempt to reduce the deer population. The CA is
currently localized to western Frederick and Shenandoah counties, but will
likely be expanded for the 2014 hunting season.
As of February, 2014, CWD has been detected in 23 states and two Canadian
provinces. The disease is a slow, progressive neurological (brain and nervous
system) disease found in deer, elk, and moose in North America. The disease
ultimately results in death of the animal. Symptoms exhibited by CWD-infected
deer include staggering, abnormal posture, lowered head, drooling, confusion,
and marked weight loss. There is no evidence that CWD can be naturally
transmitted to humans, livestock, or pets. More information on CWD can be found
on the VDGIF website at: www.dgif.virginia.gov/wildlife/diseases/cwd/.
> There is no evidence that CWD can be naturally transmitted to humans,
livestock, or pets. More information on CWD can be found on the VDGIF website
at: www.dgif.virginia.gov/wildlife/diseases/cwd/.
now, decades later ;
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA
snip...
This highlights the facts that
1) prior to the onset of clinical signs PrPSc is widely distributed in the
CNS and lymphoid tissues and
2) currently used diagnostic methods are sufficient to detect PrPSc prior
to the onset of clinical signs.
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile consistent with CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 months PI. Tissues from these deer were positive for scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
2011 Annual Report
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
2011 Annual Report
In Objective 1, Assess cross-species transmissibility of transmissible
spongiform encephalopathies (TSEs) in livestock and wildlife, numerous
experiments assessing the susceptibility of various TSEs in different host
species were conducted. Most notable is deer inoculated with scrapie, which
exhibits similarities to chronic wasting disease (CWD) in deer suggestive of
sheep scrapie as an origin of CWD.
snip...
4. Accomplishments
1. Deer inoculated with domestic isolates of sheep scrapie.
Scrapie-affected deer exhibit 2 different patterns of disease associated prion
protein. In some regions of the brain the pattern is much like that observed for
scrapie, while in others it is more like chronic wasting disease (CWD), the
transmissible spongiform encephalopathy typically associated with deer.
his work conducted by ARS scientists at the National Animal Disease Center,
Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may
have been the origin of CWD. This is important for husbandry practices with both
captive deer, elk and sheep for farmers and ranchers attempting to keep their
herds and flocks free of CWD and scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
snip...
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by potential natural routes of inoculation.
In-depth analysis of tissues will be done to determine similarities between
scrapie in deer after intracranial and oral/intranasal inoculation and chronic
wasting disease resulting from similar routes of inoculation.
see full text ;
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** 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.”
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.
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.
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html
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 ;
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Saturday, March 09, 2013
*** Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest
Incubation Time Model for Prion Diseases
*** NOR IS THE FDA recalling this CWD positive elk meat for the well being
of the dead elk ;
Wednesday, March 18, 2009 Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk
products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO,
NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
___________________________________
PRODUCT
a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each
package is approximately 2 lbs., and each case is approximately 16 lbs.; Item
number 755125, Recall # F-129-9;
b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;
c) Elk Meat, French Rack, Chilled. Item number 755132, Recall #
F-131-9;
d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;
e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall #
F-133-9;
f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall #
F-134-9;
CODE
Elk Meats with production dates of December 29, 30, and 31
RECALLING FIRM/MANUFACTURER
Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009
and press release on February 9, 2009.
Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is
ongoing.
REASON
Elk products contain meat derived from an elk confirmed to have Chronic
Wasting Disease (CWD).
VOLUME OF PRODUCT IN COMMERCE
Unknown
DISTRIBUTION
NV, CA, TX, CO, NY, UT, FL, OK
___________________________________
Monday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
snip...
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a
new prion strain
Date: August 25, 2007 at 12:42 pm PST
our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions.
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
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
pens, pens, PENS ???
*** 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. ...
also, see where even decades back, the USDA had the same thought as they do
today with CWD, not their problem...see page 27 below as well, where USDA stated
back then, the same thing they stated in the state of Pennsylvania, not their
damn business, once they escape, and they said the same thing about CWD in
general back then ;
”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 veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
”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 veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
sound familiar $$$
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
Monday, October 08, 2012
VDGIF has discovered four positive cases of CWD in Virginia Updated
9/24/2012
Thursday, March 15, 2012
CWD VIRGINIA TWO NEW CASES
Wednesday, February 15, 2012
West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE
WARNED CWD
Monday, January 17, 2011
Ten Additional Deer Test Positive for Chronic Wasting Disease in West
Virginia
Friday, December 17, 2010
CWD positive in western Frederick County VA VDGIF December 16, 2010
W.Va. DNR Reports Results from Spring 2010
CWD Surveillance Efforts In Hampshire County; CWD Containment Area Expanded
Joe Manchin III, Governor Frank Jezioro, Director
News Release: June 28, 2010
Thursday, January 21, 2010
Chronic Wasting Disease Found in White-tailed Deer in Virginia
Friday, January 15, 2010
Sixteen Additional Deer Test Positive for Chronic Wasting Disease In
Hampshire County, West Virginia
West Virginia Division of Natural Resources
www.wvdnr.gov
Friday, May 29, 2009
Seven Deer Test Positive for Chronic Wasting Disease During 2009 Spring
Collections in Hampshire County, West Virginia
Thursday, May 08, 2008
Eleven Deer Test Positive for Chronic Wasting Disease During Spring
Collections in Hampshire County, West Virginia West Virginia Division of Natural
Resources
www.wvdnr.gov
Monday, December 17, 2007
Five Additional Deer Test Positive for Chronic Wasting Disease In Hampshire
County, West Virginia
Monday, December 17, 2007
Five Additional Deer Test Positive for Chronic Wasting Disease In Hampshire
County, West Virginia
West Virginia Division of Natural Resources
www.wvdnr.gov
West Virginia:
The following press release (shortened for inclusion on this update) was
issued by the West Virginia Department of Natural Resources on December 17,
2007: Five Additional Deer Test Positive for Chronic Wasting Disease in
Hampshire County, West Virginia. Preliminary test results have detected the
Chronic Wasting Disease (CWD) agent in five hunter-harvested deer collected in
Hampshire County during the 2007 deer firearms hunting season. “As part of our
agency’s ongoing and intensive CWD surveillance effort, samples were collected
from 1,285 hunter-harvested deer brought to game checking stations in Hampshire
County,” noted Frank Jezioro, Director for the West Virginia Division of Natural
Resources (DNR). The five CWD positive deer included one 2.5 year-old doe, two
2.5 year-old bucks, one 3.5 year-old buck, and one 4.5 year-old buck. Four of
the five deer were harvested within the Hampshire County CWD Containment Area
(i.e., that portion of Hampshire County located North of U.S. Route 50). The
fifth deer was also harvested in Hampshire County, but it was killed outside the
CWD Containment Area near Yellow Springs, West Virginia. CWD has now been
detected in a total of 19 deer in Hampshire County (i.e., one road-killed deer
confirmed in 2005, four deer collected by the DNR in 2005, five deer collected
by the DNR in 2006, one hunter-harvest deer taken during the 2006 deer season,
three deer collected by the DNR in 2007 and five hunter-harvested deer taken
during the 2007 deer season). Operating within guidelines established by its CWD
– Incident Response Plan, the DNR has taken the steps necessary to implement
appropriate management actions designed to control the spread of this disease,
prevent further introduction of the disease, and possibly eliminate the disease
from the state. Full text of the press release is at:
West Virginia DNR CWD information is available at:
Wednesday, February 15, 2012
West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE
WARNED CWD OPPOSE Senate Bill 421 and this move to DE-REGULATE deer farms.
Friday, February 17, 2012
Deer Farming Bill Hits a Snag in West Virginia 02/17/2012
Wednesday, September 04, 2013
***cwd - cervid captive livestock escapes, loose and on the run in the
wild...
Wednesday, January 01, 2014
APHIS-2006-0118-0100 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE Prion
disease Singeltary submission to Scottish Parliament
Thursday, October 10, 2013
*** CJD REPORT 1994 increased risk for consumption of veal and venison and
lamb
Thursday, November 21, 2013
Assessing the susceptibility of transgenic mice over-expressing deer prion
protein to bovine spongiform encephalopathy
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Monday, February 3, 2014
Evaluation of the zoonotic potential of transmissible mink encephalopathy
TSE Prion disease
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ???
Friday, January 10, 2014
*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ???
Monday, January 13, 2014
*** Prions in Variably Protease-Sensitive Prionopathy: An Update Pathogens
2013
Pathogens 2013, 2, 457-471; doi:10.3390/pathogens2030457
Wednesday, January 15, 2014
*** INFECTION PREVENTION AND CONTROL OF CJD, VCJD AND OTHER HUMAN PRION
DISEASES IN HEALTHCARE AND COMMUNITY SETTINGS Variably Protease-Sensitive
Prionopathy (VPSPr) January 15, 2014
Sunday, January 19, 2014
*** National Prion Disease Pathology Surveillance Center Cases Examined1 as
of January 8, 2014 ***
Thursday, January 23, 2014
Medical Devices Containing Materials Derived from Animal Sources (Except
for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]
Tuesday, February 11, 2014
Novant Health Forsyth Medical Center Information on potential CJD exposure
TSS
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