Greetings Welsh Government and Food Standards
Agency Wales,
With great urgency, I would kindly like to
comment on ;
Number: WG18417
Joint
Public Consultation on the Proposed Transmissible Spongiform Encephalopathies
(Wales) Regulations 2013
The European Food Safety Authority (EFSA) and the European Centre for
Disease Prevention and Control jointly advised in 2011 that BSE is the only
animal TSE that has been shown to be a risk to human health and that there is no
epidemiological evidence to suggest that classical scrapie is a risk to human
health.
and
What are the main issues under consideration?
2.1 The main issues under consideration relate to changes in BSE testing
requirements; more proportionate measures for controlling classical scrapie in
sheep flocks and goat herds in which classical scrapie is confirmed; and more
proportionate controls on animal feed. The Welsh Government also wishes to
consult on proposed amendments to the BSE cattle compensation system in light of
identified anomalies in the current system, in addition to a variety of other
proposed technical and procedural amendments to the 2008 Regulations.
2.2 The key specific amendments are summarised and then considered in more
detail below. Other proposed technical amendments, which are considered to have
a negligible impact or have already been implemented administratively, are
listed at Annex A.
What are the main issues under consideration?
2.1
* The main issues under consideration relate to changes in BSE testing
requirements;
* more proportionate measures for controlling classical scrapie in sheep
flocks
* and goat herds in which classical scrapie is confirmed; and
* more proportionate controls on animal feed.
Greetings again Welsh Government and Food
Standards Agency Wales,
with another TSE prion medical blunder
happening just this past week ;
Friday, July 19, 2013
Beaumont Hospital in Dublin
assessing patients for CJD
http://creutzfeldt-jakob-disease.blogspot.com/2013/07/beaumont-hospital-in-dublin-assessing.html
I STRENUOUSLY urge you take my submission with the greatest urgency.
My submission and concerns as follows, and in part mixed in and throughout
the WG18417 Proposed Transmissible Spongiform Encephalopathies
(Wales) Regulations 2013.
First and foremost, I think it is very important for the Welsh Government
and Food Standards Agency Wales, to take a full inventory of your imports from
North America, and other Countries, especially your pet and fish foods, for
reasons and scientific facts I have supplied below.
I think the attempt by Governments around the globe to do away with the
Transmissible Spongiform Encephalopathy TSE prion disease, via weakening of the
BSE TSE prion surveillance, lowering of age limits in testing, weakening the
feed bans, caving in to industry, ignoring all the science of the past 3
decades, ignoring these different atypical TSE prion disease breaking out,
making up new names for these TSE prion disease, and by the way, what ever
happened to the IBNC BSE, and the pathology there, and what about testing there
from?
The USDA, CFIA, with the help of the OIE, have made it there goal to
extinguish all BSE TSE prion trade barriers, before all the science on the TSE
prion disease is in, and are working hard to exempt all TSE prion in all species
from any trade barrier, and the OIE is working right along with them. This
happened December 2003, when the USA lost it’s OIE BSE Gold Card, when BSE was
first documented in the USA, after a long hard fought battle trying to cover mad
cow disease up. This proven time and time again by the OIG and the GAO of the
USA. I will supply url links of submissions I have made to the USDA et al over
the years, since the death of my Mother to the Heidenhain Variant of Creutzfeldt
Jakob Disease i.e. hvCJD ‘confirmed’ 12/14/97. just another happenstance of bad
luck they tell me, that it only happens in the UK, and that it’s a UK disease,
this mad cow disease, that no other animal species TSE prion disease in the
world, at no other location, can transmit a TSE prion disease to a human, and
then basing all trading protocol from country to country, based on this junk
science, destroys the past 3 decades of trying to eradicate the damn disease,
and the OIE, USDA, CFIA, and all the other countries that know better, that just
goes along with this due to trade purposes, just because it’s a long incubating
disease, just because the science is still in it’s infancy, does not mean we
should start ignoring what early science has taught us, and start weakening any
safety protocols there from.
North America has the most documented TSE prion disease in the wild and in
farmed livestock than any other country in the world, excluding the TSE prion
disease documented in zoo animals. Chronic Wasting Disease CWD in cervids is
running rampant, the USA and Canada can’t stop it, while Mexico has not a clue
of any TSE prion disease. The shooting pens, and CWD there from in the USA, is
a real risk factor, one the game farms refuse to admit they are a big problem
with the spreading of the CWD TSE prion disease, fighting tooth and nail
completely ignoring the evolving science on the CWD TSE prion disease, and how
it’s spread, and these antler mills are multiplying from state to state in big
numbers. There is ample evidence of CWD transmission to humans, to warrant a
warning to the world, of the IATROGENIC potential for this TSE prion disease in
cervids, via the multitude of potential routes of infection, via the medical,
dental, surgical, blood, tissue. CWD has now mutated to multiple strains. The
science is there to warrant this very real concern, it’s just the same as with
what happened in the U.K., the industry and USDA inc., are stopping these
concerns to be made public, with the same watered down junk science used in the
beginning of the BSE blunder. you should all be very aware of this, if you come
abroad to North America. DEFRA has put out a warning on CWD TSE prion disease in
the USA and have put out a document I supplied with additional risk factors from
North America, this is supplied below as well.
Another concern is with your assumptions that typical classical scrapie is
not a risk factor for humans, when there _is_ evidence to show otherwise, that
indeed typical scrapie is a risk factor for humans, as with atypical
Scrapie.
The OIE, USDA inc, and the CFIA, have come to the conclusion that neither
typical scrapie nor the atypical Nor-98 scrapie are neither a risk factor for
humans, they have urged the OIE to conclude that atypical Nor-98 to be exempt
from any trading protocols, and indeed have made the Nor-98 atypical scrapie
EXEMPT, and made it legal to trade, and they are also in the works to make
typical scrapie exempt.
typical scrapie consist of many different strains of scrapie, not just one.
and the atypical Nor-98 has very similar features with human
Gerstmann-Sträussler-Scheinker Disease GSS and Variably Protease-Sensitive
Prionopathy VPSPr. I have not seen anywhere in the Bible, or the scrolls of the
Dead Sea, where it was stipulated that indeed typical c-BSE is the only zoonosis
Transmissible Spongiform Encephalopathy TSE prion disease. This is ludicrous in
2013 to still believe this junk science.
With the science to date of the 1st 10 nvCJD victims of Dr. Ironside et al,
and the diagnostic criteria then to diagnose the nvCJD, compared to what Dr.
Gambetti et al diagnosed in their 1st 10, of which young victims are being
diagnosed, but yet changed the name to VPSPr type CJD human TSE, is not
scientific in my opinion. I believe that the UKBSEnvCJD only theory is bogus, it
is not scientific, and should be put to bed once and for all. you cannot have
your cake and eat it too. either Ironside was wrong, or Gambetti is wrong. to
continue this UKBSEnvCJD only myth, will only help continue spread the TSE prion
agent long and far.
typical Scrapie has been studied for decades and decades, and has proven to
be transmitted to non-human primates by their NON-FORCED oral consumption (Gibbs
et al). when you write in absolute terms as this is fact that ‘’BSE is the
only animal TSE that has been shown to be a risk to human health and that there
is no epidemiological evidence to suggest that classical scrapie is a risk to
human health’’ may be true in terms of documentation, but in terms of science to
date, I think you are wishing. I kindly wish to submit the following in good
faith ;
Subject: Food and Rural Affairs on the incidence of transmissible
spongiform encephalopathy in the UK sheep flock has been in each of the last 10
years
CJD: Sheep
Jesse Norman: To ask the Secretary of State for Environment, Food and Rural
Affairs what the incidence of transmissible spongiform encephalopathy in the UK
sheep flock has been in each of the last 10 years for which data is available.
[158834]
Mr Heath [holding answer 12 June 2013]: All cases of transmissible
spongiform encephalopathy (TSE) confirmed in the UK sheep flock between 2003 and
2012 have been either classical or atypical scrapie. Cases by year are given in
the following table:
Classical scrapie Atypical scrapie
Total 2003 444 52 496
2004 337 16 353
2005 229 25 254
2006 157 49 206
2007 37 36 73
2008 9 12 21
2009 9 25 34
2010 1 19 20
2011 49(1) 23 72
2012 2 29 31
(1) 44 classical scrapie cases in 2011 came from a single flock.
THIS atypical Nor-98 scrapie, or BSE in sheep, or IBNC BSE, I don’t know
what they mean here, but seems these happenstance of bad luck twisted up
proteins i.e. atypical, what some claim to be the old timey, old age TSE, the
ones that are _suppose_ to happen spontaneously, if you listen to some
officials, seems strange to have 52 cases in 2003, then only 16 cases in 2004,
and back up to 49 cases in 2006.
or it’s not spontaneous at all.
this is very interesting too ; (1) 44 classical scrapie cases in 2011 came
from a single flock. what ever happened to the IBNC BSE in the UK cattle ?
1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF
CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS
SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN HISTOPATHOLOGY AND
INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS _NOT_ BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT ?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN
ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE,
AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE
AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. ...
Tuesday, November 17, 2009
SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM
THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
"All of the 15 cattle tested showed that the brains had abnormally
accumulated PrP"
2009
''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$
1995
page 9 of 14 ;
30. The Committee noted that the results were unusual. the questioned
whether there could be coincidental BSE infection or contamination with scrapie.
Dr. Tyrell noted that the feeling of the committee was that this did not
represent a new agent but it was important to be prepared to say something
publicly about these findings. A suggested line to take was that these were
scientifically unpublishable results but in line with the policy of openness
they would be made publicly available and further work done to test their
validity. Since the BSE precautions were applied to IBNC cases, human health was
protected. Further investigations should be carried out on isolations from
brains of IBNC cases with removal of the brain and subsequent handling under
strict conditions to avoid the risk of any contamination.
31. Mr. Bradley informed the Committee that the CVO had informed the CMO
about the IBNC results and the transmission from retina and he, like the
Committee was satisfied that the controls already in place or proposed were
adequate. ...
snip... see full text
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA
Final report
IN CONFIDENCE
BSE ATYPICAL LESION DISTRIBUTION
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
Atypical prion protein in sheep brain collected during the British
scrapie-surveillance programme
S. J. Everest1, L. Thorne1, D. A. Barnicle1, J. C. Edwards1, H. Elliott2,
R. Jackman1,† and J. Hope3,†
+ Author Affiliations
1Department of TSE Molecular Biology, Veterinary Laboratories Agency, New
Haw, Addlestone, Surrey KT15 3NB, UK
2Institute for Animal Health, Pirbright Laboratory, Woking, Surrey, UK
3Veterinary Laboratories Agency Lasswade, Pentlands Science Park, Bush
Loan, Penicuik, Midlothian EH26 0PZ, UK
Correspondence J. Hope j.hope@vla.defra.gsi.gov.uk Received 9 March 2005.
Accepted 14 October 2005. Abstract Scrapie of sheep and goats is the most common
prion disease (or transmissible spongiform encephalopathy, TSE) of mammals and
aggregates of abnormal, proteinase-resistant prion protein (PrPSc) are found in
all naturally occurring prion diseases. During active surveillance of British
sheep for TSEs, 29 201 sheep brain stem samples were collected from abattoirs
and analysed for the presence of PrPSc. Of these samples, 54 were found to be
positive by using an ELISA screening test, but 28 of these could not be
confirmed initially by immunohistochemistry. These unconfirmed or atypical cases
were generally found in PrP genotypes normally associated with relative
resistance to clinical scrapie and further biochemical analysis revealed that
they contained forms of PrPSc with a relatively protease-sensitive amyloid core,
some resembling those of Nor98 scrapie. The presence of these atypical forms of
protease-resistant PrP raises concerns that some TSE disorders of PrP metabolism
previously may have escaped identification in the British sheep population.
Previous SectionNext Section ↵†These authors contributed equally to this
work.
Supplementary material is available in JGV Online.
Sunday, August 26, 2012
Susceptibility of young sheep to oral infection with bovine spongiform
encephalopathy decreases significantly after weaning
Wednesday, January 18, 2012
BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE
February 1, 2012
Thursday, April 4, 2013
Variably protease-sensitive prionopathy in the UK: a retrospective review
1991–2008
Brain (2013) 136 (4): 1102-1115. doi: 10.1093/brain/aws366
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until
now. Overall, 5 voles were positive with survival time between 281 and 596
d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like
PrPSc electrophoretic pattern, characterized by low molecular weight PrPres.
These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative
with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus
and the N-terminus. Second passages are in progress from these first successful
transmissions.
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
Monday, January 14, 2013
Gambetti et al USA Prion Unit change another highly suspect USA mad cow
victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes
along with this BSe
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012
Saturday, December 29, 2012
MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
Tuesday, November 6, 2012
Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and
Sporadic CJD, November-December 2012 update
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE
RISE IN NORTH AMERICA
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1
(August 19, 2011) including Texas
Monday, August 9, 2010
Variably protease-sensitive prionopathy: A new sporadic disease of the
prion protein or just more Prionbaloney ?
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $
OR-10 15:25 - 15:40 VARIABLY PROTEASE-SENSITIVE PRIONOPATHY IS
TRANSMISSIBLE IN BANK VOLES Nonno
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009
Sunday, February 10, 2013
Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection
report/CJD
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
see follow-up here about North America BSE Mad Cow TSE prion risk factors,
and the ever emerging strains of Transmissible Spongiform Encephalopathy in many
species here in the USA, including humans ;
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque
"BSE-L in North America may have existed for decades"
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
Sunday, July 21, 2013
Biochemical Characteristics and PrPSc Distribution Pattern in the Brains of
Cattle Experimentally Challenged with H-type and L-type Atypical BSE
Saturday, July 6, 2013
*** Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy
Research Article
Tuesday, July 2, 2013
APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals
Eliminating ALL remaining BSE barriers to export market
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
Terry S.
Singeltary Sr. submission
Thursday, June 13, 2013
Experimental interspecies transmission studies of the transmissible
spongiform encephalopathies to cattle: comparison to bovine spongiform
encephalopathy in cattle
Monday, June 3,
2013
*** Unsuccessful oral transmission of scrapie from British sheep to
cattle
Sunday, July 21, 2013
As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
Thursday,
July 11, 2013
The New Hornographers: The Fight Over the Future of
Texas Deer
interesting article ;
Max Dream, the Madera Bonita Ranch's prized buck, is
a semen-producing cash cow. Mike Wood
Max Dream, the Madera Bonita Ranch's prized buck, is
a semen-producing cash cow.
In magazine advertisements in which Max is backlit in
messianic grandeur, his value can be determined in other ways. Wood sells
half-cubic-centimeter straws of the animal's cryogenically frozen semen (or
about a tenth of a teaspoon) for $5,000 a pop. And breeders will pony up just
for a shot at a fawn boasting the great Max Dream as sire. Bear in mind, a buck
in his prime with an electroejaculator inserted in his rectum can produce 60
straws at a time.
Though Max never leaves the confines of Madera
Bonita, FedEx spreads his cryogenically frozen seed far and wide.
Thursday, July 11, 2013
The New Hornographers: The Fight Over the Future of
Texas Deer
PLEASE SEE FULL TEXT
SUBMISSION ;
Subject: 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
From: "Terry S. Singeltary Sr."
To:
fdadockets@oc.fda.gov
CWD, SCRAPIE, CATTLE, TSE ???
"CWD has been transmitted
to cattle after intracerebral inoculation, although the infection rate was low
(4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD
prions might be transmitted to cattle grazing in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated
animals had lost weight, revealed abnormal clinical signs, and were
euthanatized. Laboratory tests revealed the presence of a unique pattern of the
disease agent in tissues of these animals. These findings demonstrate that when
CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle
develop clinical signs of the disease.
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089
"although the infection rate was low (4 of
13 animals [Hamir et al. 2001])."
shouldn't this be corrected, 86% is
NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr.
P.O. Box 42 Bacliff, Texas USA 77518
UPDATED CORRESPONDENCE FROM AUTHORS
OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY
BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO
CATTLE ;
----- Original Message -----
From:
David Colby
To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday,
March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and
Stanley B. Prusiner1,2 + Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter.
Warm Regards, David Colby
--
David
Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of
Delaware
====================END...TSS==============
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.pdf
breeding cervids, captive shooting pens,
straw bred bucks, antler mills, sperm mills, all these type business are a petri
dish for Chronic Wasting Disease CWD. not that it matters to the TAHC, they been
letting CWD waltz across Texas from the WSMR in NM since around 2002, where I
told them then, it was waltzing across from the TRANS PECOS region. did they
listen? no, and the rest is history. TEXAS is CWD positive now. and YES, CWD
does transmit to other species, and YES, there is a risk factor for humans, and
that risk factor has grown now that there are multiple strains of CWD. these are
the facts as I have come to know them doing daily research of the TSE CWD mad
cow type prion, after loosing my mother to the hvCJD 'confirmed', 15 years ago.
sporadic CJD cases are rising, and the age is getting younger. ...tss
*** 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.
http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf
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.pdf
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.
http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099
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.
http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975
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.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
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 ;
CANADA SEE STEADY INCREASE OF THE SPORADIC
CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss
PLEASE NOTE, type
determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a
steady increase.
please see ;
> 3. Final classification of 50
cases from 2009, 2010, 2011 and 2012 is pending.
CJD Deaths Reported by
CJDSS1, 1994-20122
As of May 31, 2012
Deaths of Definite and
Probable CJD
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
1994 2 0 0 1 0 0 3
1995 3 0 0 0 0 0 3
1996 13 0 0 0 0 0
13
1997 16 0 1 1 0 0 18
1998 22 1 0 1 0 0 24
1999 26 2 2
1 0 0 31
2000 32 0 0 3 0 0 35
2001 27 0 2 1 0 0 30
2002
31 0 2 2 0 1 36
2003 27 1 1 0 0 0 29
2004 42 0 1 0 0 0 43
2005 42 0 0 2 0 0 44
2006 39 0 1 3 1 0 44
2007 35 0 0 4
0 0 39
2008 48 0 1 0 0 0 49
2009 48 0 3 2 0 0 53
2010 34
0 3 0 0 0 37
2011 37 0 2 1 0 1 41
2012 1 0 0 0 0 0 1
Total 525 4 19 22 1 2 573
1. CJDSS began in 1998
2. Data
before 1998 are retrospective and partial, data from 1998 to 2008 are complete,
and data for 2009 - 2012 are provisional
3. Final classification of 50
cases from 2009, 2010, 2011 and 2012 is pending.
CJD Deaths Reported by
CJDSS1, 1994-20122
As of May 31, 2012
USA SEE STEADY INCREASE OF THE SPORADIC
CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss
National Prion Disease Pathology
Surveillance Center
Cases Examined1
(May 18, 2012)
Year
Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996
& earlier 50 32 28 4 0 0
1997 114 68 59 9 0 0
1998 88 52 44
7 1 0
1999 123 74 65 8 1 0
2000 145 103 89 14 0 0
2001
210 120 110 10 0 0
2002 248 149 125 22 2 0
2003 266 168 137 31 0
0
2004 326 187 164 22 0 13
2005 344 194 157 36 1 0
2006
382 196 166 28 0 24
2007 377 213 185 28 0 0
2008 396 232 206 26
0 0
2009 423 256 212 43 1 0
2010 413 257 216 41 0 0
2011
410 257 213 43 0 0
2012 153 82 51 15 0 0
TOTAL 44685 26406 2227
387 6 3
1 Listed based on the year of death or, if not available, on
year of referral;
2 Cases with suspected prion disease for which brain
tissue and/or blood (in familial cases) were submitted;
3 Disease
acquired in the United Kingdom;
4 Disease was acquired in the United
Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 14
cases in which the diagnosis is pending, and 18 inconclusive cases;
6
Includes 17 (16 from 2012) cases with type determination pending in which the
diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of
sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive
Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
Rev 5/18/2012
http://www.cjdsurveillance.com/pdf/case-table.pdf
> 6 Includes
> 17 (16 from 2012) cases with type
determination pending in which the diagnosis of vCJD has been excluded.
> The Sporadic cases include 16 cases of
sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive
Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
*** The discovery of previously
unrecognized prion diseases in both humans and animals (i.e., Nor98 in small
ruminants) demonstrates that the range of prion diseases might be wider than
expected and raises crucial questions about the epidemiology and strain
properties of these new forms. We are investigating this latter issue by
molecular and biological comparison of VPSPr, GSS and Nor98.
*** 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
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html
The TSE prion disease survives ashing to
600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot
cook the TSE prion disease out of meat.
you can take the ash and mix it
with saline and inject that ash into a mouse, and the mouse will go down with
TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after
Biodiesel Production as well.
the TSE prion agent also survives
Simulated Wastewater Treatment Processes.
IN fact, you should also know
that the TSE Prion agent will survive in the environment for years, if not
decades.
you can bury it and it will not go away.
The TSE agent
is capable of infected your water table i.e. Detection of protease-resistant
cervid prion protein in water from a CWD-endemic area.
it’s not your
ordinary pathogen you can just cook it out and be done with. that’s what’s so
worrisome about Iatrogenic mode of transmission, a simple autoclave will not
kill this TSE prion agent.
New studies on the heat resistance of
hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests
an inorganic template of replication
The infectious agents responsible
for transmissible spongiform encephalopathy (TSE) are notoriously resistant to
most physical and chemical methods used for inactivating pathogens, including
heat. It has long been recognized, for example, that boiling is ineffective and
that higher temperatures are most efficient when combined with steam under
pressure (i.e., autoclaving). As a means of decontamination, dry heat is used
only at the extremely high temperatures achieved during incineration, usually in
excess of 600°C. It has been assumed, without proof, that incineration totally
inactivates the agents of TSE, whether of human or animal origin.
http://www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still
Infectious after Biodiesel Production
Histochemical analysis of hamster
brains inoculated with the solid residue showed typical spongiform degeneration
and vacuolation. Re-inoculation of these brains into a new cohort of hamsters
led to onset of clinical scrapie symptoms within 75 days, suggesting that the
specific infectivity of the prion protein was not changed during the biodiesel
process. The biodiesel reaction cannot be considered a viable prion
decontamination method for MBM, although we observed increased survival time of
hamsters and reduced infectivity greater than 6 log orders in the solid MBM
residue. Furthermore, results from our study compare for the first time prion
detection by Western Blot versus an infectivity bioassay for analysis of
biodiesel reaction products. We could show that biochemical analysis alone is
insufficient for detection of prion infectivity after a biodiesel process.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
Detection of protease-resistant cervid
prion protein in water from a CWD-endemic area
The data presented here
demonstrate that sPMCA can detect low levels of PrPCWD in the environment,
corroborate previous biological and experimental data suggesting long term
persistence of prions in the environment2,3 and imply that PrPCWD accumulation
over time may contribute to transmission of CWD in areas where it has been
endemic for decades. This work demonstrates the utility of sPMCA to evaluate
other environmental water sources for PrPCWD, including smaller bodies of water
such as vernal pools and wallows, where large numbers of cervids congregate and
into which prions from infected animals may be shed and concentrated to
infectious levels.
http://www.landesbioscience.com/journals/prion/NicholsPRION3-3.pdf
A Quantitative Assessment of the Amount of
Prion Diverted to Category 1 Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform
encephalopathy;QRA;scrapie;TSE
In this article the development and
parameterization of a quantitative assessment is described that estimates the
amount of TSE infectivity that is present in a whole animal carcass (bovine
spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for
sheep and lambs) and the amounts that subsequently fall to the floor during
processing at facilities that handle specified risk material (SRM). BSE in
cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s
(310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070)
and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical
scrapie, respectively. Lambs contained the least infectivity with a mean of 251
OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical
scrapie. The highest amounts of infectivity falling to the floor and entering
the drains from slaughtering a whole carcass at SRM facilities were found to be
from cattle infected with BSE at rendering and large incineration facilities
with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a
mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14).
The lowest amounts entering drains are from lambs infected with classical and
atypical scrapie at intermediate plants and atypical scrapie at collection
centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The
results of this model provide key inputs for the model in the companion paper
published here.
http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract
SEMEN AND TSE INFECTIVITY
FOR THOSE INTERESTED, PLEASE SEE MORE SCIENCE HERE ON
CWD TSE prion disease ;
Thursday, July 11, 2013
The New Hornographers: The Fight Over the Future of
Texas Deer, Captive shooting pens, and the CWD TSE prion disease
Tuesday, July 02, 2013
National Rifle Association and the Unified Sportsman
of Florida support a Florida ban on the importation of captive deer and cervids
into Florida
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.
Tuesday,
December 18, 2012
A
Growing Threat How deer breeding could put public trust wildlife at risk
Monday,
June 24, 2013
The
Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following
its Discovery
Thursday, June 20, 2013
atypical, BSE, CWD, Scrapie, Captive Farmed shooting pens (livestock),
Wild Cervids, Rectal Mucosa Biopsy 2012 USAHA Proceedings, and CJD TSE prion
Update
Sunday,
June 09, 2013
Missouri
House forms 13-member Interim Committee on the Cause and Spread of Chronic
Wasting Disease CWD
Tuesday,
April 16, 2013
Cervid
Industry Unites To Set Direction for CWD Reform and seem to ignore their
ignorance and denial in their role in spreading Chronic Wasting Disease
Sunday,
January 06, 2013
USDA TO
PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”
Wednesday, January 18, 2012
BSE IN
GOATS CAN BE MISTAKEN FOR SCRAPIE February 1, 2012
Saturday, December 3, 2011
Isolation of Prion with BSE Properties from Farmed Goat Volume 17,
Number
12—December 2011
Sunday,
October 3, 2010
Scrapie,
Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking
?
Tuesday,
February 01, 2011
Sparse
PrP-Sc accumulation in the placentas of goats with naturally acquired
scrapie
Research
article
Thursday, June 2, 2011
USDA
scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND
California
UPDATE
PLEASE NOTE ;
AS of
June 30, 2011,
snip...
INCLUDING 10 POSITIVE GOATS FROM THE SAME HERD (FIGURE 7).
snip...
see
updated APHIS scrapie report ;
Tuesday,
February 01, 2011
Sparse
PrP-Sc accumulation in the placentas of goats with naturally acquired
scrapie
Research
article
snip...
Date:
Tuesday, February 01, 2011 5:03 PM
To: Mr
Terry Singeltary
Subject:
Your comment on BMC Veterinary Research 2011, 7:7
Dear Mr
Singeltary
Thank
you for contributing to the discussion of BMC Veterinary Research 2011, 7:7
.
Your
comment will be posted within 2 working days, as long as it contributes to the
topic under discussion and does not breach patients' confidentiality or libel
anyone. You will receive a further notification by email when the posting
appears on the site or if it is rejected by the moderator.
Your
posting will read:
Mr Terry
Singeltary,
retired
Scrapie
cases Goats from same herd USA Michigan
Comment:
" In spite of the poorly defined effects of PRNP genetics, scrapie strain, dose,
route and source of infection, the caprine placenta may represent a source of
infection to progeny and herd mates as well as a source of persistent
environmental contamination. "
Could
this route of infection be the cause of the many cases of Goat scrapie from the
same herd in Michigan USA ?
Has this
been investigated ?
(Figure
6) including five goat cases in FY 2008 that originated from the same herd in
Michigan. This is highly unusual for goats, and I strenuously urge that there
should be an independent investigation into finding the common denominator for
these 5 goats in the same herd in Michigan with Scrapie. ...
Kind
Regards, Terry
Thursday, January 07, 2010
Scrapie
and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR
2008
In FY
2010, 72 cases of classical Scrapie and 5 cases of Nor-98 like Scrapie were
confirmed...
Scrapie
Nor-98 like case in California FY 2011 AS of December 31, 2010.
Scrapie
cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21
Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases)
Last
herd with infected goats disignated in FY 2008 Michigan 8 cases
Tuesday,
February 01, 2011
Sparse
PrP-Sc accumulation in the placentas of goats with naturally acquired
scrapie
Research
article
"In
spite of the poorly defined effects of PRNP genetics, scrapie strain, dose,
route and source of infection, the caprine placenta may represent a source of
infection to progeny and herd mates as well as a source of persistent
environmental contamination."
Could
this route of infection be the cause of the many cases of Goat scrapie from the
same herd in Michigan USA ?
Has this
been investigated ?
(Figure
6) including five goat cases in FY 2008 that originated from the same herd in
Michigan. This is highly unusual for goats, and I strenuously urge that there
should be an independent investigation into finding the common denominator for
these 5 goats in the same herd in Michigan with Scrapie. ...
Kind
Regards, Terry
SNIP...
Scrapie
Nor-98 like case in California FY 2011 AS of December 31, 2010.
Scrapie
cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21
Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases)
Last
herd with infected goats disignated in FY 2008 Michigan 8 cases
UPDATED
RESPONSE ON MY CONCERNS OF GOAT SCRAPIE IN MICHIGAN ;
-----
Original Message -----
From:
"BioMed Central Comments"
To:
Sent:
Wednesday, February 16, 2011 4:13 AM
Subject:
Your comment on BMC Veterinary Research 2011, 7:7
Your
discussion posting "Scrapie cases Goats from same herd USA Michigan" has been
rejected by the moderator as not being appropriate for inclusion on the
site.
Dear Mr
Singeltary,
Thank
you for submitting your comment on BMC Veterinary Research article (2011, 7:7).
We have read your comment with interest but we feel that only the authors of the
article can answer your question about further investigation of the route of
infection of the five goats in Michigan. We advise that you contact the authors
directly rather than post a comment on the article.
With
best wishes,
Maria
Maria
Kowalczuk, PhD Deputy Biology Editor BMC-series Journals
BioMed
Central 236 Gray's Inn Road London, WC1X 8HB
+44 20
3192 2000 (tel) +44 20 3192 2010 (fax)
W:
www.biomedcentral.com E: Maria.Kowalczuk@biomedcentral.com
Any
queries about this decision should be sent to comments@biomedcentral.com
Regards
BMC
Veterinary Research
SNIP...PLEASE SEE FULL TEXT ;
Tuesday,
February 01, 2011
Sparse
PrP-Sc accumulation in the placentas of goats with naturally acquired
scrapie
Research
article
Scrapie
Nor-98 like case in California FY 2011 AS of December 31, 2010.
Scrapie
cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21
Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases)
Last
herd with infected goats disignated in FY 2008 Michigan 8 cases
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine
spongiform encephalopathy following passage in sheep
Monday,
March 21, 2011
Sheep
and Goat BSE Propagate More Efficiently than Cattle BSE in Human PrP Transgenic
Mice
*** Most
recent positive goat confirmed in April 2013.
Scrapie
Cases in Goats FY 2002 – FY 2013 As of April 30, 2013
***SCRAPIE GOATS CALIFORNIA 13 CASES TO DATE ! ***
(an
unusually high amount of scrapie documented in goats for a happenstance of bad
luck, or spontaneous event, THAT DOES NOT HAPPEN IN OTHER STATES ??? )
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine
spongiform encephalopathy following passage in sheep
Monday,
November 30, 2009
USDA AND
OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
Thursday, December 20, 2012
OIE
GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH
BOVINE MAD COW DISEASE
*** The
discovery of previously unrecognized prion diseases in both humans and animals
(i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases
might be wider than expected and raises crucial questions about the epidemiology
and strain properties of these new forms. We are investigating this latter issue
by molecular and biological comparison of VPSPr, GSS and Nor98.
Tuesday,
April 30, 2013
Transmission of classical scrapie via goat milk
Veterinary Record2013;172:455 doi:10.1136/vr.f2613
ALSO,
SEE CALIFORNIA AND MICHIGAN FOR THE HIGH SCRAPIE RATE IN GOATS ???
THIS
needs to be addressed immediately, as to find the source, route, cause, from
this unusual event...tss
Wednesday, November 28, 2012
Scientific and technical assistance on the provisional results of the
study on genetic resistance to Classical scrapie in goats in Cyprus 1
SCIENTIFIC REPORT OF EFSA
Thursday, March 29, 2012
atypical
Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA
Annual Conference April 11-14, 2011San Antonio, Texas
*** The
discovery of previously unrecognized prion diseases in both humans and animals
(i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases
might be wider than expected and raises crucial questions about the epidemiology
and strain properties of these new forms. We are investigating this latter issue
by molecular and biological comparison of VPSPr, GSS and Nor98.
OR-10:
Variably protease-sensitive prionopathy is transmissible in bank voles
Romolo
Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1
Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi
Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy;
2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy;
3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a
recently described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results.
To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109.
Overall, 3 voles were positive with survival time between 290 and 588 d post
inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the
typical PrP27–30, which was indistinguishable to that previously observed in
BvM109 inoculated with sCJDMM1 cases.
In
BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now.
Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In
contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc
electrophoretic pattern, characterized by low molecular weight PrPres. These
PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with
SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the
N-terminus. Second passages are in progress from these first successful
transmissions.
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The
discovery of previously unrecognized prion diseases in both humans and animals
(i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases
might be wider than expected and raises crucial questions about the epidemiology
and strain properties of these new forms. We are investigating this latter issue
by molecular and biological comparison of VPSPr, GSS and Nor98.
Wednesday, March 28, 2012
VARIABLY
PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up
again $
*** The
discovery of previously unrecognized prion diseases in both humans and animals
(i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases
might be wider than expected and raises crucial questions about the epidemiology
and strain properties of these new forms. We are investigating this latter issue
by molecular and biological comparison of VPSPr, GSS and Nor98.
Increased Atypical Scrapie Detections
Press
reports indicate that increased surveillance is catching what otherwise would
have been unreported findings of atypical scrapie in sheep. In 2009, five new
cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the
exception of Quebec, all cases have been diagnosed as being the atypical form
found in older animals. Canada encourages producers to join its voluntary
surveillance program in order to gain scrapie-free status. The World Animal
Health will not classify Canada as scrapie-free until no new cases are reported
for seven years. The Canadian Sheep Federation is calling on the government to
fund a wider surveillance program in order to establish the level of prevalence
prior to setting an eradication date. Besides long-term testing, industry is
calling for a compensation program for farmers who report unusual deaths in
their flocks.
Thursday, March 29, 2012
atypical
Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA
Annual Conference April 11-14, 2011San Antonio, Texas
Monday,
April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume
17, Number 5-May 2011 However, work with transgenic mice has demonstrated the
potential susceptibility of pigs, with the disturbing finding that the
biochemical properties of the resulting PrPSc have changed on transmission (40).
***The
pathology features of Nor98 in the cerebellum of the affected sheep showed
similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
***
Intriguingly, these conclusions suggest that some pathological features of Nor98
are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
***
These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.
Surprisingly the TSE agent characteristics were dramatically different
v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and
biochemical characteristics similar to those of atypical BSE L in the same mouse
model. Moreover, whereas no other TSE agent than BSE were shown to transmit into
Tg porcine mice, atypical scrapie was able to develop into this model, albeit
with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion
showed similar biological and biochemical characteristics than BSE adapted to
this porcine mouse model. Altogether these data indicate.
(i) the
unsuspected potential abilities of atypical scrapie to cross species
barriers
(ii) the
possible capacity of this agent to acquire new characteristics when crossing
species barrier
These
findings raise some interrogation on the concept of TSE strain and on the origin
of the diversity of the TSE agents and could have consequences on field TSE
control measures.
Friday,
February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
RESEARCH
Emerging
Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Marion
M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh
Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin,
and John Spiropoulos
To
investigate the possibility of oral transmission of atypical scrapie in sheep
and determine the distribution of infectivity in the animals’ peripheral
tissues, we challenged neonatal lambs orally with atypical scrapie; they were
then killed at 12 or 24 months. Screening test results were negative for
disease-specifi c prion protein in all but 2 recipients; they had positive
results for examination of brain, but negative for peripheral tissues.
Infectivity of brain, distal ileum, and spleen from all animals was assessed in
mouse bioassays; positive results were obtained from tissues that had negative
results on screening. These fi ndings demonstrate that atypical scrapie can be
transmitted orally and indicate that it has the potential for natural
transmission and iatrogenic spread through animal feed. Detection of infectivity
in tissues negative by current surveillance methods indicates that diagnostic
sensitivity is suboptimal for atypical scrapie, and potentially infectious
material may be able to pass into the human food chain.
SNIP...
Although
we do not have epidemiologic evidence that supports the effi cient spread of
disease in the fi eld, these data imply that disease is potentially
transmissible under fi eld situations and that spread through animal feed may be
possible if the current feed restrictions were to be relaxed. Additionally,
almost no data are available on the potential for atypical scrapie to transmit
to other food animal species, certainly by the oral route. However, work with
transgenic mice has demonstrated the potential susceptibility of pigs, with the
disturbing fi nding that the biochemical properties of the resulting PrPSc have
changed on transmission (40). The implications of this observation for
subsequent transmission and host target range are currently unknown.
How
reassuring is this absence of detectable PrPSc from a public health perspective?
The bioassays performed in this study are not titrations, so the infectious load
of the positive gut tissues cannot be quantifi ed, although infectivity has been
shown unequivocally. No experimental data are currently available on the
zoonotic potential of atypical scrapie, either through experimental challenge of
humanized mice or any meaningful epidemiologic correlation with human forms of
TSE. However, the detection of infectivity in the distal ileum of animals as
young as 12 months, in which all the tissues tested were negative for PrPSc by
the currently available screening and confi rmatory diagnostic tests, indicates
that the diagnostic sensitivity of current surveillance methods is suboptimal
for detecting atypical scrapie and that potentially infectious material may be
able to pass into the human food chain undetected.
Emerging
Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
why do
we not want to do TSE transmission studies on chimpanzees $
5. A
positive result from a chimpanzee challenged severly would likely create alarm
in some circles even if the result could not be interpreted for man. I have a
view that all these agents could be transmitted provided a large enough dose by
appropriate routes was given and the animals kept long enough. Until the
mechanisms of the species barrier are more clearly understood it might be best
to retain that hypothesis.
snip...
R.
BRADLEY
1: J
Infect Dis 1980 Aug;142(2):205-8
Oral
transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman
primates.
Gibbs CJ
Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and
Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were
transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the
infectious agents only by their nonforced consumption of known infectious
tissues. The asymptomatic incubation period in the one monkey exposed to the
virus of kuru was 36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The
successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by
natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID:
6997404
Recently
the question has again been brought up as to whether scrapie is transmissible to
man. This has followed reports that the disease has been transmitted to
primates. One particularly lurid speculation (Gajdusek 1977) conjectures that
the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible
encephalopathy of mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit scrapie-blood
line and scrapie-exposed sheep and goats to be processed for human or animal
food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by
the finding that some strains of scrapie produce lesions identical to the once
which characterise the human dementias"
Whether
true or not. the hypothesis that these agents might be transmissible to man
raises two considerations. First, the safety of laboratory personnel requires
prompt attention. Second, action such as the "scorched meat" policy of USDA
makes the solution of the acrapie problem urgent if the sheep industry is not to
suffer grievously.
snip...
76/10.12/4.6
Nature.
1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ
Jr, Gajdusek DC.
Nature
236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J.
GIBBS jun. & D. C. GAJDUSEK
National
Institute of Neurological Diseases and Stroke, National Institutes of Health,
Bethesda, Maryland
SCRAPIE
has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca
fascicularis) with an incubation period of more than 5 yr from the time of
intracerebral inoculation of scrapie-infected mouse brain. The animal developed
a chronic central nervous system degeneration, with ataxia, tremor and myoclonus
with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
Suspect
symptoms
What if
you can catch old-fashioned CJD by eating meat from a sheep infected with
scrapie?
28 Mar
01
Like
lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284.
Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his
mother die horribly from a degenerative brain disease. Doctors told him it was
Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent
symptoms, and he demanded an autopsy. It showed she had died of sporadic
Creutzfeldt-Jakob disease.
Most
doctors believe that sCJD is caused by a prion protein deforming by chance into
a killer. But Singeltary thinks otherwise. He is one of a number of campaigners
who say that some sCJD, like the variant CJD related to BSE, is caused by eating
meat from infected animals. Their suspicions have focused on sheep carrying
scrapie, a BSE-like disease that is widespread in flocks across Europe and North
America.
Now
scientists in France have stumbled across new evidence that adds weight to the
campaigners' fears. To their complete surprise, the researchers found that one
strain of scrapie causes the same brain damage in mice as sCJD.
"This
means we cannot rule out that at least some sCJD may be caused by some strains
of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy
Commission's medical research laboratory in Fontenay-aux-Roses, south-west of
Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD
surveillance in Germany, is so concerned by the findings that he now wants to
trawl back through past sCJD cases to see if any might have been caused by
eating infected mutton or lamb.
Scrapie
has been around for centuries and until now there has been no evidence that it
poses a risk to human health. But if the French finding means that scrapie can
cause sCJD in people, countries around the world may have overlooked a CJD
crisis to rival that caused by BSE.
Deslys
and colleagues were originally studying vCJD, not sCJD. They injected the brains
of macaque monkeys with brain from BSE cattle, and from French and British vCJD
patients. The brain damage and clinical symptoms in the monkeys were the same
for all three. Mice injected with the original sets of brain tissue or with
infected monkey brain also developed the same symptoms.
As a
control experiment, the team also injected mice with brain tissue from people
and animals with other prion diseases: a French case of sCJD; a French patient
who caught sCJD from human-derived growth hormone; sheep with a French strain of
scrapie; and mice carrying a prion derived from an American scrapie strain. As
expected, they all affected the brain in a different way from BSE and vCJD. But
while the American strain of scrapie caused different damage from sCJD, the
French strain produced exactly the same pathology.
"The
main evidence that scrapie does not affect humans has been epidemiology," says
Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in
Edinburgh, who was a member of the same team as Deslys. "You see about the same
incidence of the disease everywhere, whether or not there are many sheep, and in
countries such as New Zealand with no scrapie." In the only previous comparisons
of sCJD and scrapie in mice, Bruce found they were dissimilar.
But
there are more than 20 strains of scrapie, and six of sCJD. "You would not
necessarily see a relationship between the two with epidemiology if only some
strains affect only some people," says Deslys. Bruce is cautious about the mouse
results, but agrees they require further investigation. Other trials of scrapie
and sCJD in mice, she says, are in progress.
People
can have three different genetic variations of the human prion protein, and each
type of protein can fold up two different ways. Kretschmar has found that these
six combinations correspond to six clinical types of sCJD: each type of normal
prion produces a particular pathology when it spontaneously deforms to produce
sCJD.
But if
these proteins deform because of infection with a disease-causing prion, the
relationship between pathology and prion type should be different, as it is in
vCJD. "If we look at brain samples from sporadic CJD cases and find some that do
not fit the pattern," says Kretschmar, "that could mean they were caused by
infection."
There
are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere.
Singeltary and other US activists think that some of these people died after
eating contaminated meat or "nutritional" pills containing dried animal brain.
Governments will have a hard time facing activists like Singeltary if it turns
out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's
work on macaques also provides further proof that the human disease vCJD is
caused by BSE. And the experiments showed that vCJD is much more virulent to
primates than BSE, even when injected into the bloodstream rather than the
brain. This, says Deslys, means that there is an even bigger risk than we
thought that vCJD can be passed from one patient to another through contaminated
blood transfusions and surgical instruments.
Monday,
December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob
Disease Are Encoded by Distinct Prion Types
(hmmm,
this is getting interesting now...TSS)
Sporadic
CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular)
deposits,
see also
;
All of
the Heidenhain variants were of the methionine/ methionine type 1 molecular
subtype.
see full
text ;
Monday,
December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob
Disease Are Encoded by Distinct Prion Types
Friday,
March 09, 2012
Experimental H-type and L-type bovine spongiform encephalopathy in
cattle: observation of two clinical syndromes and diagnostic challenges
Research
article
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits
Thursday, February 14, 2013
*** The
Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion
disease
Tuesday,
March 5, 2013
Use of
Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the
Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
FDA
believes current regulation protects the public from BSE but reopens comment
period due to new studies
Tuesday,
March 05, 2013
A closer
look at prion strains Characterization and important implications
Prion
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
Tuesday,
May 28, 2013
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a
methodological outline for evidence-based guidance
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim
McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre,
Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of
Calgary, Canada
Background: Three BSE types (classical and two atypical) have been
identified on the basis of molecular characteristics of the misfolded protein
associated with the disease. To date, each of these three types have been
detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16
Canadian BSE cases based on the biochemical properties of there associated
PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and
relative proteinase K sensitivity of the PrPres from each of the 16 confirmed
Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type
and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and
changes in glycosylation similar to other atypical BSE cases. PK digestion under
mild and stringent conditions revealed a reduced protease resistance of the
atypical cases compared to the C-type cases. N terminal- specific antibodies
bound to PrPres from H type but not from C or L type. The C-terminal-specific
antibodies resulted in a shift in the glycoform profile and detected a fourth
band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries.
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
2012
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE
in these countries.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
The present study demonstrated successful intraspecies transmission of
H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc
in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be
minimally defined by oral transmission of different TSE agents (C-type, L-type,
and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected
cattle have been initiated and are underway to provide information regarding the
extent of similarity in the immunohistochemical and molecular features before
and after transmission.
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
IT is of
my opinion, that the OIE and the USDA et al, are the soul reason, and
responsible parties, for Transmissible Spongiform Encephalopathy TSE prion
diseases, including typical and atypical BSE, typical and atypical Scrapie, and
all strains of CWD, and human TSE there from, spreading around the globe.
I have
lost all confidence of this organization as a regulatory authority on animal
disease, and consider it nothing more than a National Trading Brokerage for all
strains of animal TSE, just to satisfy there commodity. AS i said before, OIE
should hang up there jock strap now, since it appears they will buckle every
time a country makes some political hay about trade protocol, commodities and
futures. IF they are not going to be science based, they should do everyone a
favor and dissolve there organization.
JUST
because of low documented human body count with nvCJD and the long incubation
periods, the lack of sound science being replaced by political and corporate
science in relations with the fact that science has now linked some sporadic CJD
with atypical BSE and atypical scrapie, and the very real threat of CWD being
zoonosis, I believed the O.I.E. has failed terribly and again, I call for this
organization to be dissolved. ...
IN A NUT
SHELL ;
(Adopted
by the International Committee of the OIE on 23 May 2006)
11.
Information published by the OIE is derived from appropriate declarations made
by the official Veterinary Services of Member Countries. The OIE is not
responsible for inaccurate publication of country disease status based on
inaccurate information or changes in epidemiological status or other significant
events that were not promptly reported to the Central Bureau,
Thursday, May 30, 2013
World
Organization for Animal Health (OIE) has upgraded the United States' risk
classification for mad cow disease to "negligible" from "controlled", and risk
further exposing the globe to the TSE prion mad cow type disease
U.S.
gets top mad-cow rating from international group and risk further exposing the
globe to the TSE prion mad cow type disease
Tuesday,
June 11, 2013
Weld
County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant deviations from
requirements in FDA regulations that are intended to reduce the risk of bovine
spongiform encephalopathy (BSE) within the United States
Thursday, June 6, 2013
BSE TSE
PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as
at June 5, 2013
Greetings,
since
our fine federal friends have decided not to give out any more reports on the
USA breaches of the feed ban and surveillance etc. for the BSE TSE prion mad cow
type disease in the USDA livestock, I thought I might attempt it. I swear, I
just don’t understand the logic of the SSS policy, and that includes all of it.
I assure you, it would be much easier, and probably better for the FDA and the
USDA INC., if they would simply put some kind of report out for Pete’s sake,
instead of me doing it after I get mad, because I am going to put it all out
there. the truth.
PLEASE
BE ADVISED, any breach of any of the above classifications OAI, VAI, RTS, CAN
lead to breaches into the feed BSE TSE prion protocols, and CAN lead to the
eventual suspect tainted feed reaching livestock. please, if any USDA official
out there disputes this, please explain then how they could not. paperwork
errors can eventually lead to breaches of the BSE TSE prion mad cow feed ban
reaching livestock, or contamination and exposure there from, as well.
I would
sure like to see the full reports of just these ;
4018
CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR,
OF HP 11/26/2012 OAI Y
9367
3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR
RE, TH HP 2/27/2013 OAI N
9446
DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO
80631-9501 OPR RE, TH HP 10/12/2012 OAI N
9447
DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods 13553 County
Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N
see full
list of the fda mad cow bse feed follies, toward the bottom, after a short brief
update on the mad cow bse follies, and our good friend Lester Crawford that was
at the FDA.
ALSO, I
would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms
Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion
protocols, from the extensive mad cow feed ban warning letters the fda use to
put out for each violations. simply put, this excel format sucks, and the FDA et
al intentionally made it this difficult to follow the usda fda mad cow follies.
this is an intentional format to make it as difficult as possible to follow
these breaches of the mad cow TSE prion safety feed protocols. to have
absolutely no chronological or numerical order, and to format such violations in
a way that they are almost impossible to find, says a lot about just how far the
FDA and our fine federal friends will go through to hide these continued
violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols
there from. once again, the wolf guarding the henhouse $$$
NAI = NO
ACTION INDICATED
OAI =
OFFICIAL ACTION INDICATED
VAI =
VOLUNTARY ACTION INDICATED
RTS =
REFERRED TO STATE
Inspections conducted by State and FDA investigators are classified to
reflect the compliance status at the time of the inspection, based upon whether
objectionable conditions were documented. Based on the conditions found,
inspection results are recorded in one of three classifications:
OAI
(Official Action Indicated) when inspectors find significant objectionable
conditions or practices and believe that regulatory sanctions are warranted to
address the establishment’s lack of compliance with the regulation. An example
of an OAI classification would be findings of manufacturing procedures
insufficient to ensure that ruminant feed is not contaminated with prohibited
material. Inspectors will promptly re-inspect facilities classified OAI after
regulatory sanctions have been applied to determine whether the corrective
actions are adequate to address the objectionable conditions.
VAI
(Voluntary Action Indicated) when inspectors find objectionable conditions or
practices that do not meet the threshold of regulatory significance, but warrant
an advisory to inform the establishment that inspectors found conditions or
practices that should be voluntarily corrected. VAI violations are typically
technical violations of the 1997 BSE Feed Rule. These violations include minor
recordkeeping lapses or conditions involving non-ruminant feeds.
NAI (No
Action Indicated) when inspectors find no objectionable conditions or practices
or, if they find objectionable conditions, those conditions are of a minor
nature and do not justify further actions.
when
sound science was bought off by junk science, in regards to the BSE TSE prion
mad cow type disease, by the USDA, CFIA, WHO, OIE, et al. $$$
when the
infamous, and fraudulently USDA, FSIS, APHIS, FDA, gold card was taken away that
infamous day in December of 2003, all cards were off the table, it was time to
change the science, and change they did. ...tss
snip.
...please see full text ;
Thursday, June 6, 2013
BSE TSE
PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as
at June 5, 2013
Friday,
July 19, 2013
PART 589
-- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED Revised as of April 1,
2013 50# Regular Chicken Feed was found to contain mammalian protein label does
not contain the warning statement
PLEASE REMEMBER ;
The Akron, Ohio-based CJD Foundation said the Center for Disease Control
revised that number in October of 2004 to about one in 9,000 CJD cases per year
in the population group age 55 and older.
HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO
ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???
if not, why not...
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis
full text with source references ;
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease (SEE
VIDEO)
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? (see video at
bottom)
WHO WILL FOLLOW THE CHILDREN FOR CJD SYMPTOMS ???
Saturday, May 2, 2009
U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK
DOWNER COW SCHOOL LUNCH PROGRAM
OUR SCHOOL CHILDREN ALL ACROSS THE USA WERE FED THE MOST HIGH RISK CATTLE
FOR MAD COW DISEASE FOR 4 YEARS I.E. DEAD STOCK DOWNER CATTLE VIA THE USDA AND
THE NSLP.
WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5+ DECADES ???
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH
RISK FOR MAD COW DISEASE ???
you can check and see here ;
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
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...
SNIP...SEE FULL TEXT ;
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
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling
Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is
complete. REASON Possible contamination of dairy animal feeds with ruminant
derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
***
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags,
Recall # V-121-6;
b)
Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall #
V-122-6;
c)
Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d)
Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags,
Recall # V-124-6;
e)
Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f)
Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g)
Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville,
AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall
is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with
ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END
OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
***
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b)
Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c)
Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d)
CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e)
"Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f)
CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag,
Recall # V-105-6;
g)
Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall #
V-106-6;
h)
CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20
Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall #
V-107-6;
i)
CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j)
CO-OP LAYING CRUMBLES, Recall # V-109-6;
k)
CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l)
CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m)
CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur,
AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is
complete.
REASON Animal and fish feeds which were possibly contaminated with
ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END
OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD
COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22
71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a)
PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall #
V-079-6;
b)
ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall
# V-080-6;
c)
PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall
# V-081-6;
d)
Feather Meal, Recall # V-082-6 CODE
a)
Bulk
b)
None
c)
Bulk
d)
Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville,
AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm
initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END
OF ENFORCEMENT REPORT FOR July 12, 2006
###
Friday, October 8, 2010
Scientific reasons for a feed ban of meat-and-bone meal, applicable to
all farmed animals including cattle, pigs, poultry, farmed fish and pet food
Wednesday, July 10, 2013
Prions in the Ocean: A Natural Case of Prion Disease in Dolphins
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in
the EU
Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES
AND FOOD SAFETY a non-profit Swiss Foundation
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject
PRO/AH/EDR>
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim
McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre,
Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of
Calgary, Canada
Background: Three BSE types (classical and two atypical) have been
identified on the basis of molecular characteristics of the misfolded protein
associated with the disease. To date, each of these three types have been
detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16
Canadian BSE cases based on the biochemical properties of there associated
PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and
relative proteinase K sensitivity of the PrPres from each of the 16 confirmed
Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type
and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and
changes in glycosylation similar to other atypical BSE cases. PK digestion under
mild and stringent conditions revealed a reduced protease resistance of the
atypical cases compared to the C-type cases. N terminal- specific antibodies
bound to PrPres from H type but not from C or L type. The C-terminal-specific
antibodies resulted in a shift in the glycoform profile and detected a fourth
band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *It also suggests
a similar cause or source for atypical BSE in these countries.
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
Tuesday, July 2, 2013
APHIS USDA Administrator Message to Stakeholders: Agency Vision and
Goals Eliminating ALL remaining BSE barriers to export market
Welsh Government and Food Standards Agency
Wales Joint Public Consultation on the Proposed Transmissible Spongiform
Encephalopathies (Wales) Regulations 2013
This consultation seeks your views on the 2013
Regulations, which will replace the current Transmissible Spongiform
Encephalopathies (Wales) Regulations 2008 (SI 2008 No. 3154).
Start of
consultation: 08/07/2013
End of
consultation: 02/09/2013
Transmissible spongiform encephalopathies (TSEs) are
fatal brain diseases suffered by a variety of species. The most common
is:
- Bovine Spongiform Encephalopathy (BSE) in
cattle
-
- Scrapie in sheep and goats
-
- Chronic Wasting Disease (CWD) in deer
-
- Feline Spongiform Encephalopathy (FSE) in
cats.
Exposure to BSE through the consumption of infected meat
products is also thought to be the most likely cause of variant
Creutzfeldt-Jakob Disease (vCJD) in humans.
The Regulations provide the necessary powers to
administer and enforce the provisions of Regulation (EC) 999/2001. This concerns
the prevention, control and eradication of BSE and other TSEs relating to
cattle, sheep and goats.
How to respond
Please submit your comments by 02 September
2013, in any of the following ways:
Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
Joint Welsh Government and Food Standards Agency Wales
Consultation Document
Date of issue: 8 July 2013
Action required: Responses by 2 September 2013
Number: WG18417
Overview
Transmissible spongiform encephalopathies (TSEs) are fatal brain diseases,
which include scrapie in sheep and goats and Bovine Spongiform Encephalopathy
(BSE) in cattle.
Regulation (EC) No.999/2001 (‘The EU TSE Regulation’) requires Member
States to implement rules for the prevention, control and eradication of
TSEs.
The purpose of this consultation is to seek views on the proposed
Transmissible Spongiform Encephalopathies (Wales) Regulations 2013, which will
revoke and replace the current TSE (Wales) Regulations 2008, as amended, to
include amendments in response to changes in EU legislation, advice from the
Commission, technical changes and reviews of procedure.
How to respond
Please send hard copy (paper) responses to:
Dave Miles
Welsh Government
Office of the Chief Veterinary Officer
Cathays Park
Cardiff
CF10 3NQ
Tel: 029 20 825461
Further information and related documents
Large print, Braille and alternate language versions of this document are
available on request.
Useful links:
The TSE (Wales) Regulations 2008
The TSE (Wales) (Amendment) (No 2) Regulations 2008
The TSE (Wales) (Amendment) Regulations 2009
The TSE (Wales) (Amendment) Regulations 2010
Contact details
Please contact Dave Miles, as above.
snip...
Part II – Proposed amendments to the 2008 Regulations
What are the main issues under consideration?
2.1 The main issues under consideration relate to changes in BSE testing
requirements; more proportionate measures for controlling classical scrapie in
sheep flocks and goat herds in which classical scrapie is confirmed; and more
proportionate controls on animal feed. The Welsh Government also wishes to
consult on proposed amendments to the BSE cattle compensation system in
2
light of identified anomalies in the current system, in addition to a
variety of other proposed technical and procedural amendments to the 2008
Regulations.
2.2 The key specific amendments are summarised and then considered in more
detail below. Other proposed technical amendments, which are considered to have
a negligible impact or have already been implemented administratively, are
listed at Annex A.
Current position
2.3 The provisions of the EU TSE Regulation are currently administered and
enforced by the TSE (Wales) Regulations 2008, as amended, which came into force
on 31 December 2008.
Evidence for change
2.4 In line with the EU TSE Roadmap, the Welsh Government policy objective
is to have TSE controls in place that maintain consumer and animal health
protection, are based on sound science and best available evidence, are
proportionate to the known risk and are as practical and enforceable as is
reasonable.
2.5 In light of amendments made to the EU TSE Regulation, advice provided
by the Commission and various technical changes and reviews of procedure, the
Welsh Government needs to update and replace the 2008 Regulations accordingly.
This will ensure compliance with EU obligations, bring Welsh legislation into
line with the rest of the UK and support a consistent GB/UK approach.
Summary of key specific changes to be introduced by the proposed TSE
(Wales) Regulations 2013
2.6 The key proposed changes are as follows (NB. all references are to the
2008 Regulations):
• Schedule 2 - Decision 2013/76/EU permitted the UK to stop testing healthy
slaughtered cattle for BSE from 4 February 2013. As a result of this Decision
the Required Method of Operation (RMOP) for the occupier (Food Business Operator
(FBO)) of participating slaughterhouses now exceeds the requirements of the EU
TSE Regulation, leaving many of the requirements redundant. Schedule 2 will be
updated to reflect this Decision (paragraphs 3.1 to 3.4 below refer).
• Schedule 3, paragraph 5 will be amended to clarify the existing
procedures for appealing against the inspector’s decision to kill a BSE cohort
animal; to clarify the option of deferring the killing of a cohort animal; and
to limit appeals against the inspector’s decision to kill a cohort animal to
specific criteria (paragraphs 3.5 and 3.6 below refer).
3
• Schedule 3, paragraph 9 sets out the amount of compensation payable for
BSE, which is set at the average price paid in Great Britain for the age and
category of an animal. The Welsh Government proposes to update the Table of
Categories (paragraphs 3.8 to 3.11 below refer).
• Schedule 4 will be amended to reflect the full range of options now
available under the EU TSE Regulation to control classical scrapie, including
the surveillance (monitoring) option (paragraphs 3.14 to 3.25 below
refer).
• The Welsh Government proposes a new policy to support farmers who are
enrolled within the CSFS Surveillance (monitoring) option, who, on a voluntary
basis, wish to breed scrapie resistance into their flocks (paragraph 3.25 below
refers).
• Schedule 4, paragraphs 6 & 7 will be amended to allow Welsh Ministers
to replace the requirement for killing and complete destruction of animals, as
required in the existing CSFS genotype and cull option, with slaughtering for
human consumption. For animals required to be slaughtered, no compensation will
be payable and farmers will obtain the slaughter price determined by market
forces.
• Schedule 4, Paragraphs 6 and 7 will also be amended to enforce
requirements in the EU TSE Regulation, preventing the feeding of milk and milk
products to ruminants other than on the holding of origin on which classical
scrapie is confirmed or if produced prior to the removal of genetically
susceptible sheep/all goats or where a flock/herd is monitored for further
cases. It will be an offence to use such milk/milk products as feed for
ruminants (except on the holding of origin). If such milk/milk products are used
for feed for non-ruminants it will be an offence:
to export the feed from the UK;
to fail to comply with the documentation and packaging
requirements;
to bring such feed on to a premises with ruminants for storage or use;
and,
to fail to comply with the requirements for transport and cleaning and
disinfection of vehicles.
Part III - Details of Proposed Amendments
Schedule 2 – TSE Monitoring in Bovine Animals
snip...
Food Safety Authority (EFSA) in 2008, the EU adopted Regulation (EC)
No.103/2009 introducing new controls to reduce the risk of spreading BSE or
classical scrapie to ruminant animals in uninfected flocks and herds through
consumption of sheep and goats’ milk and milk products. The new controls also
ensure that sheep and goats’ milk and milk products from flocks and herds in
which TSE is suspected is not placed on the market unless BSE is excluded.
3.13 To administer these controls the following changes are proposed to the
2008 Regulations:
(i) Regulation 15 and Paragraph 4 of Schedule 4 of the 2008 Regulations
would be amended to require an inspector to serve a notice to prohibit the
movement of sheep or goat milk or milk products from a holding on which a TSE is
suspected in sheep or goats.
(ii) A new paragraph will be inserted to enable the enforcement of the EU
TSE Regulation preventing the feeding of milk products to ruminants other than
on the holding of origin.
Classical Scrapie Controls
snip...
Thank
You,
I am
sincerely,
Terry S.
Singeltary Sr.
P.O. Box
42
Bacliff,
Texas USA 77518
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