Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TESTING
Important Chronic Wasting Disease (CWD) Program News
The USDA has recently adopted new federal regulations and standards for the
National CWD Program. The TAHC is currently working with interested parties to
modify current TAHC regulations to be consistent with the new federal
regulations and standards.
One major change that was adopted as a result of the new federal
regulations is the sample collection for diagnostic testing of CWD.
Under the old regulations, owners were only required to collect and submit
a sample of the obex (brainstem) to the laboratory for testing. The new federal
changes require owners to collect and submit a sample of both the obex and
retropharyngeal lymph nodes for a more complete diagnostic testing.
The TAHC has discussed these changes with the Texas A&M Veterinary
Medical Diagnostic Laboratory (TVMDL.) Currently the TVMDL has been testing
samples of the obex for a lab charge of $40. TVMDL has modified their testing
protocol to now test both the obex and retropharyngeal lymph nodes for an
additional fee of only $5 for a total lab fee of $45. The request to test both
samples must be documented on the form upfront.
If you use another laboratory for your testing it is recommended that you
contact the lab to discuss specifics about the testing of both samples and lab
charges.
If you have any questions regarding the CWD program please feel free to
contact your Regional TAHC office.
Stay tuned for more information and details on changes.
Texas Animal Health Commission www.tahc.texas.gov 800-550-8242
Greetings,
Texas and other states are well known for the infamous OBEX ONLY TSE PRION
TESTING, and how useless it really has been, but certified to MISS cases, of
which is why it has been used for so long. USDA officials have known this for a
decade or more.
now, we will stray from CWD here at first and look at past history of
testing the obex only TSE prion mad cow type disease, then back to CWD, but
first, just out ;
Dissociation between Transmissible Spongiform Encephalopathy (TSE)
Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a
Murine Transgenic Model of TSE Disease
Karen Dobie and
Rona Barron
+ Author Affiliations
Neurobiology Division, The Roslin Institute & R(D)SVS, Easter Bush,
Midlothian, United Kingdom
ABSTRACT
Most current diagnostic tests for transmissible spongiform encephalopathies
(TSE) rely on the presence of proteinase K (PK)-resistant PrPSc (PrP-res) in
postmortem tissues as an indication of TSE disease. However, a number of studies
have highlighted a discrepancy between TSE infectivity and PrP-res levels in
both natural and experimental cases of TSE disease. Previously, we have shown
high TSE infectivity levels in the brain tissue of mice that have a clinical TSE
disease with associated vacuolar pathology but little or no detectable PrP-res.
Here, the levels of TSE infectivity and PrP-res within a peripheral tissue of
this mouse model were investigated. Biochemical analysis showed that low levels
of PrP-res were present in the spleen tissue in comparison to the levels
observed in the spleen of mice infected with ME7 or 79A. However, upon
subpassage of brain and spleen tissue from clinically ill mice with little or no
PrP-res detectable, similar short incubation periods to disease were observed,
indicating that infectivity levels were similarly high in both tissues. Thus,
the discrepancy between PrP-res and TSE infectivity was also present in the
peripheral tissues of this disease model. This result indicates that peripheral
tissues can contain higher levels of infectivity given the correct combination
of host species, PrP genotype, and TSE agent. Therefore, the assumption that the
levels of peripheral infectivity are lower than those in the central nervous
system is not always correct, and this could have implications for current food
safety regulations.
FOOTNOTES
Received 19 December 2012.
Accepted 7 March 2013.
Address correspondence to Rona Barron, rona.barron@roslin.ed.ac.uk.
Published ahead of print 13 March 2013
Copyright © 2013, American Society for Microbiology. All Rights Reserved.
Wednesday, April 24, 2013
Dissociation between Transmissible Spongiform Encephalopathy (TSE)
Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a
Murine Transgenic Model of TSE Disease
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
Greetings BSE-L members et al,
THIS seems to be another lesson on 'how not to find BSE' via the 'statutory
(obex only) diagnostic criteria'. However, this was some 10 years before Dr.
Detwiler was warning of this very practice, and how they would be 'MISSING'
cases of BSE if USED, which the USDA et al seemed to use as the 'GOLD STANDARD'.
NOW we see the UK used it. This seems to put a different light on the true
numbers of BSE mad cow cases that were documented, or, better yet, how many were
NOT documented $$$ IN THE USA AND ABROAD ???
============
ATYPICAL LESION DISTRIBUTION (RBSE 92/21367)
A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in
Aberdeenshirer submitted as a suspect BSE case in the negative study (SE0203),
has been diagnosed as BSE negative on standard, statutory (obex only),
diagnostic criteria at CVL.
Further examination by Dr Jeffrey at Lasswade, as required by the project
design, has revealed vacuolar change in the septal nucleus and putamen which
co-localised with PrP immunoreactivity. No significant lesions were found in any
other part of the brain, neither was PrP found in the medulla.
It is important to note that examination of four brain blocks used earlier
in the epidemic would not have detected the lesion but a 16 block study (as used
in the very days of BSE) would.
FURTHER INFORMATION
The herd of origin has had 15, HB, suspect cases of BSE since July 1989 and
a further case is still alive.
2. Of the 15, eight have been confirmed by standard histopathology and
seven diagnosed negative (including the above case).
3. Fixed brain tissue from the negative cases exists at Lasswade (because
they always collect whole brain in Scotland) but has not so far been examined
further. No frozen tissue was collected so neither SAF nor PrP detection (by
immunoblotting) has been attempted.
4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.
FURTHER ACTION IN PROGRESS
1. The brain tissue from the negative cases will be examined in detail by
conventional histopathology and ICC.
2. Kevin Taylor and his veterinary colleagues have been alerted to the
situation.
OTHER RECOMMENDED ACTIONS
1. TRANSMISSION Attempt transmission from the 'case' to standard mice
strains. (Note: In regard to strain typing, formalin may have modified strain
phenotype - we need to discuss with NPU). Further transmission studies (eg in
cattle) might be suggested if primary transmission in mice fails. These
proposals have funding implications.
CODE 18-77
93/2.17/1.1
2. PrP GENOTYPING - Although only fixed brain tissue is available we are
considering genotyping from parents/offspring/fixed brain. As a first step we
are attempting to extract DNA from the fixed brain and to amplify the PrP gene
by PCR.
3. John Wilesmith has interrogated the data base for the herd history.
Other than the high proportion of negative cases nothing significant is
apparent.
4. Familial relationships between suspect (including positive and negative)
cases in this herd could be examined and tracings of breeding animals
initiated.
5. Consideration might be given to collecting frozen spinal cord from new
cases in this herd or in dispersals from it for (SAF/PrP examination).
CONCLUSIONS
1. At present it is unclear whether or not this is a singleton incident or
whether the other negative cases in this herd show a similar lesion.
2. The discovery might indicate the existence of a different strain of BSE
from that present in the general epidemic or an unusual response by an
individual host.
3. If further atypical lesion distribution cases are revealed in this herd
then implications of misdiagnosis of 'negative' cases in other herds may not be
insignificant.
4. If this is a new strain all the implications need to be considered
including whether or not to proceed with the further investigation of future
cases negative for BSE on obex examination alone and from which whole brains are
available (as in Scotland) or collected in the future. Also perhaps
investigation of the tissue distribution of infectivity in these animals might
be considered.
5. Animal and public health controls in place should be sufficient since
all tissues (other than brain for diagnosis) are incinerated.
We observe that Dr Tyrrell would wish to be informed of this at an early
opportunity and that the SEAC would wish to discuss it at their meeting in
April.
R BRADLEY
M DAWSON
17 February 1993
CVO - for information and comment on further action please
cc Mr K C Taylor
Dr B J Shreeve
93/2.17/1.2
This minute is re-issued with a wider distribution.
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
Mr Scudamore
Mr R C Lowson
Dr D Matthews
Mr I Robertson
Dr K MacOwan
Mr C Randall
Mr J W Wilesmith
Mr G A H Wells
Dr M Jeffrey
Dr M Simmons
93/2.17/1.3
IN CONFIDENCE
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)
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
========
NOW, what about the 'obex only' mode of testing used by the USDA et al for
TSE, prions $$$ works for them too, a sure fire way NOT TO FIND MAD COW DISEASE
$$$
NOW, read the following please, and then ask yourself, WHY the USDA et al
were ONLY TESTING THE OBEX PART OF THE BRAIN in USA cattle for BSE $$$
BECAUSE they knew that would be the least likely way to find BSE/TSE in USA
cattle $$$...TSS
=========
Discussion
In the five cats in this study with a spongiform encephalopathy, fibrils
were observed by electron microscopy and their major protein, Prpsc, was
identified by SDS-PAGE and Western blot. The fibrils were similar to those
described in sheep with scrapie (Rubenstein and others 1987, Gibson and others
1987, Scott and others 1987, Dawson and others 1987), cattle with bovine
spongiform encephalopathy (Wells and others 1987, Hope and others 1988, Scott
and others 1990) and humans with Creutzfeldt-Jakob disease (Merz and others
1984).
In sheep with scrapie, fibrils can be readily detected in several areas of
the brain, including cerebral cortex (Stack and others 1991).
By contrast, the frequency with which fibrils were detected in cattle with
BSE, DEPENDED ON THE REGION OF THE BRAIN SAMPLED; THE HIGHEST YIELD BEING
OBTAINED FROM MEDULLA, MIDBRAIN, THALAMUS AND BASAL NUCLEI WHERE VACUOLA CHANGES
ARE PRESENT (Scott and others 1990). This correlation between PrPsc accumulation
and vacuolar pathology is also well established in laboratory animal models of
scrapie (Bruce and others 1989). Because of the widespread distribution of
changes in FSE (Whatt and others 1991) and the requirement, in the present
study, not to compromise the histopathological examination of the brain, the
frontal region of the cerebrum was therefore selected for fibril and PrPsc
examinations. However, studies of the sensitivity of fibril detection in
different parts of the brain in cats with FSE are required to determine whether
detection can be made as readliy in other regions as in the frontal cerebral
cortex.
IT IS OF INTEREST, that fibrils were detected in the brains of 3 cats
(cases 9, 13, & 18) WITHOUT histopathological evidence of spongiform
encephalopathy, and that in only one of them, (case 9), a Western blot for
modified PrP was positive. There are precedents for the occurrence of abnormal
PrP in the organs of animals incubation scrapie prior to clinical signs and/or
spongiform encephalopathy...
snip...
(please see full text (and one might start downloading these documents for
future use, as some disappear never to re-appear, as in some of the FDA's.
...TSS)
PLEASE NOTE *
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...
AND THE USDA ET AL KNEW IT TOO ;
"These 9,200 cases were different because brain tissue samples were
preserved with formalin, which makes them suitable for only one type of
test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in
the bovine, and these were probably from the most high risk cattle pool, the
ones the USDA et al, SHOULD have been testing. ...TSS
USDA 2003
We have to be careful that we don't get so set in the way we do things that
we forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain stem
and we're looking in only one area. In Norway, they were doing a project and
looking at cases of Scrapie, and they found this where they did not find lesions
or PRP in the area of the obex. They found it in the cerebellum and the
cerebrum. It's a good lesson for us. Ames had to go back and change the
procedure for looking at Scrapie samples. In the USDA, we had routinely looked
at all the sections of the brain, and then we got away from it. They've recently
gone back. Dr. Keller: Tissues are routinely tested, based on which tissue
provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another
important thing to get across to the public is that the negatives do not
guarantee absence of infectivity. The animal could be early in the disease and
the incubation period. Even sample collection is so important. If you're not
collecting the right area of the brain in sheep, or if collecting
lymphoreticular tissue, and you don't get a good biopsy, you could miss the area
with the PRP in it and come up with a negative test. There's a new, unusual form
of Scrapie that's been detected in Norway. We have to be careful that we don't
get so set in the way we do things that we forget to look for different emerging
variations of disease. We've gotten away from collecting the whole brain in our
systems. We're using the brain stem and we're looking in only one area. In
Norway, they were doing a project and looking at cases of Scrapie, and they
found this where they did not find lesions or PRP in the area of the obex. They
found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had
to go back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got away
from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides
an 'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
END...TSS
==========
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE
sampling FROM HEALTHY USDA CATTLE)
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services. In addition to the targeted sample population (those
cattle that were more than 30 months old or had other risk factors for BSE), the
owner submitted to USDA, or caused to be submitted, BSE obex (brain stem)
samples from healthy USDA-inspected cattle. As a result, the owner fraudulently
received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1
include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for
specified risk material (SRM) violations and improved inspection controls over
SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in
future semiannual reports as the relevant audits and investigations are
completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to a
processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began
an investigation. On Friday and throughout the weekend, FDA investigators
inspected the slaughterhouse, the rendering facility, the farm where the animal
came from, and the processor that initially received the cow from the
slaughterhouse.
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That material is
being held by the firm, which is cooperating fully with FDA.
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve
Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick
to assure the public earlier this week that the third case of mad cow disease
did not pose a risk to them, but what federal officials have not acknowledged is
that this latest case indicates the deadly disease has been circulating in U.S.
herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is thought
that cows usually contract the disease from contaminated feed they consume as
calves. The concern is that humans can contract a fatal, incurable,
brain-wasting illness from consuming beef products contaminated with the mad cow
pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before one
year ago" because of the agency's reluctance to retest the Texas cow that
initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector
general.
"Everything they did on the Texas cow makes everything they did before 2005
suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as
bovine spongiform encephalopathy, or BSE, did not significantly threaten human
or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk
either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers
should be troubled by the USDA's secrecy and its apparent plan to dramatically
cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the
USDA's surveillance program and the failure of the USDA to reveal really
important details," Halloran told UPI. "Consumers have to be really concerned if
they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it
has proposed, even in light of a third case, scaling back the program to 40,000
tests annually.
"They seem to be, in terms of actions and policies, taking a lot more
seriously the concerns of the cattle industry than the concerns of consumers,"
Halloran said. "It's really hard to know what it takes to get this
administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow
tissue into cattle feed (which is thought to spread the disease) and removal of
the most infectious parts of cows, such as the brain and spinal cord, protect
consumers. But the agency glosses over the fact that both of these systems have
been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has
been criticized by the Government Accountability Office in two reports, the most
recent coming just last year. The GAO said the FDA's enforcement of the ban
continues to have weaknesses that "undermine the nation's firewall against
BSE."
USDA documents released last year showed more than 1,000 violations of the
regulations requiring the removal of brains and spinal cords in at least 35
states, Puerto Rico and the Virgin Islands, with some plants being cited
repeatedly for infractions. In addition, a violation of similar regulations that
apply to beef exported to Japan is the reason why Japan closed its borders to
U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system.
The USDA insists the prevalence of mad cow disease is low, but the agency has
provided few details of its surveillance program, making it difficult for
outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without
having a breakdown of the tested population by age and risk status," Elizabeth
Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern,
Switzerland, a company that provides advice on reducing mad cow risk to industry
and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be
able to go away a little bit for (the USDA) if they would just publish a
breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's
surveillance plan via the Freedom of Information Act in May 2004 but nearly two
years later has not received any corresponding documents from the agency,
despite a federal law requiring agencies to comply within 30 days. This leaves
open the question of whether the USDA is withholding the information, does not
have the information or is so haphazardly organized that it cannot locate
it.
Mumford said the prevalence of the disease in U.S. herds is probably quite
low, but there have probably been other cases that have so far gone undetected.
"They're only finding a very small fraction of that low prevalence," she
said.
Mumford expressed surprise at the lack of concern about the deadly disease
from American consumers. "I would expect the U.S. public to be more concerned,"
she said.
Markus Moser, a molecular biologist and chief executive officer of
Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is
that if people are infected, the mad cow pathogen could become "humanized" or
more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical
procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul
Brown is Senior Research Scientist in the Laboratory of Central Nervous System
... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."
........TSS
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform
Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and
Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat
Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
THIS is just ONE month report, of TWO recalls of prohibited banned MBM,
which is illegal, mixed with 85% blood meal, which is still legal, but yet we
know the TSE/BSE agent will transmit blood. we have this l-BSE in North America
that is much more virulent and there is much concern with blood issue and l-BSE
as there is with nvCJD in humans. some are even starting to be concerned with
sporadic CJD and blood, and there are studies showing transmission there as
well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD
COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that
reaches commerce is ever returned via recall, very, very little. this was 2007,
TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN
THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow
feed that was in ALABAMA in one of the links too, this is where the infamous
g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the
USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
snip...see full text ;
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
Friday, April 19, 2013
APHIS 2013 Stakeholder Meeting (March 2013) BSE TSE PRION
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Friday, April 19, 2013
FDA BSE TSE PRION NEWS FEED AND ANNUAL INSPECTION OF FEED MILLS REPORTS HAS
CEASED TO EXIST
Monday, March 25, 2013
Minnesota Firm Recalls Bone-In Ribeye That May Contain Specified Risk
Materials Recall Release CLASS II RECALL FSIS-RC-024-2013
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
Wednesday, March 20, 2013
GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to
Expand Its Use of Reported Health Problems to Oversee Product
From: Terry S. Singeltary Sr.
Sent: Tuesday, March 19, 2013 2:46 PM
To: gomezj@gao.gov
Cc: siggerudk@gao.gov ; youngc1@gao.gov ; oighotline@gao.gov
Wednesday, February 20, 2013
World Organization for Animal Health Recommends United States' BSE Risk
Status Be Upgraded
Statement from Agriculture Secretary Tom Vilsack:
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and
TSE prion disease
Friday, April 19, 2013
Bovine Spongiform Encephalopathy (BSE) Feed Safety Support Program Grants
Fiscal Year 2011: October 1, 2010 - September 30, 2011 FDA
USDA-APHIS-VS Chronic Wasting Disease National Program
Patrice N. Klein of USDA APHIS VS – National Center for Animal Health
Programs provided an update on the agency’s CWD–related activities:
CWD Rule Update: The amended final rule on chronic wasting disease (CWD) is
currently in departmental clearance. The rule will set minimum standards for
interstate movement and establish the national voluntary Herd Certification
Program (HCP). Farmed/captive cervid surveillance testing: Through FY2010, VS
conducted surveillance testing on approximately 20,000 farmed /captive cervids
by the immunohistochemistry (IHC) standard protocol. As of September 15, 2011,
approximately 19,000 farmed /captive cervids were tested by IHC for CWD with
funding to cover lab costs provided through NVSL.
Farmed/captive cervid CWD status: The CWD positive captive white-tailed
deer (WTD) herd reported in Missouri (February 2010) was indemnified and
depopulation activities were completed in June 2011. All depopulated animals
were tested for CWD and no additional CWD positive animals were found.
In FY 2011, CWD was reported in two captive elk herds in Nebraska
(December, 2010 and April 2011, respectively).
To date, 52 farmed/captive cervid herds have been identified in 11 states:
CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI.
Thirty-nine were elk herds and 13 were WTD herds. At this time, eight CWD
positive herds remain – six elk herds in Colorado and the two elk herds in
Nebraska.
Wild Cervid surveillance: In FY 2009 funding supported surveillance in
approximately 74,330 wild cervids in 47 cooperating States. Wild cervid CWD
surveillance totals are pending for fiscal year 2010 (2010 – 2011 calendar year)
due to seasonal surveillance activities and completion of final cooperative
agreement reporting to APHIS.
In fiscal year 2011, there are 15 ‘tier 1’ States, 20 ‘tier 2’ States, and
15 ‘tier 3’ States. Two new ‘tier 1’ States, Minnesota and Maryland, were added
in fiscal year 2011 based on the new CWD detections in a free-ranging
white-tailed deer in southeastern Minnesota and in western Maryland.
Consequently, Delaware was upgraded to ‘tier 2’ status as an adjacent State to
Maryland. For FY 2011, 45 States and 32 Tribes will receive cooperative
agreement funds to complete wild cervid surveillance and other approved work
plan activities. Based on FY 2012 projected budget reductions, future
cooperative agreement funds will be eliminated.
APHIS CWD Funding: In FY2011, APHIS received approximately $15.8 million in
appropriated funding for the CWD Program. The President’s FY 2012 budget
proposes to reduce program funding for CWD by $13.9 million, leaving the program
with a request of $1.925 million to provide some level of Federal coordination
for the national herd certification program (HCP).
Consequently, APHIS is planning to amend its role in the program to one of
Federal coordination. Based on the projected FY 2012 budget, funding for CWD
cooperative agreements and indemnity funding for States and Tribes will be
eliminated. Under this scenario, the States or cervid industry producers will
likely be responsible for the costs of surveillance testing and indemnity for
appraisal, depopulation, and disposal of CWD-positive animals.
Commodity Health Line Structure: In the FY 2012 budget, livestock
commodities regulated by USDA have been organized into ‘Commodity Health Line’
structures or groupings. APHIS’ Equine, Cervid and Small Ruminant (ECSR) Health
line supports efforts to protect the health and thereby improve the quality and
productivity of the equine, cervid and small ruminant industries. Activities
supported by the ECSR Health line range from monitoring and surveillance to
investigation and response actions undertaken when health issues relevant to the
industry are identified. APHIS also maintains regulations and program standards
which guide ECSR activities at both the Federal and State/Tribal level.
The ECSR Health line funds essential activities necessary to maintain
current ECSR surveillance and program operations while providing the flexibility
to respond to new and emerging industry-specific health concerns. APHIS’ current
activities include Scrapie, Chronic Wasting Disease (CWD), Slaughter Horse
Transport, and Brucellosis/Tuberculosis in cervids. Overall, APHIS will use
funding from the ECSR Health Line Item to support Agency efforts in the
following mission areas: prevention, preparedness and communication; monitoring,
surveillance and detection; response and containment; and continuity of
business, mitigation and recovery
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie
and CWD in inoculated deer. Interspecies transmission studies afford the
opportunity to better understand the potential host range and origins of prion
diseases. We inoculated white-tailed deer intracranially (IC) and by a natural
route of exposure (concurrent oral and intranasal inoculation) with a US scrapie
isolate. All deer inoculated by the intracranial route had evidence of PrPSc
accumulation and those necropsied after 20 months post-inoculation (PI) (3/5)
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6
months PI did not have clinical signs, but had widespread distribution of PrPSc.
This highlights the facts that 1) prior to the onset of clinical signs PrPSc is
widely distributed in the CNS and lymphoid tissues and 2) currently used
diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical
signs. The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile consistent with CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 months PI. Tissues from these deer were positive for scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
Committee Business:
The Committee discussed and approved three resolutions regarding CWD. They
can be found in the report of the Reswolutions Committee. Essentially the
resolutions urged USDA-APHIS-VS to:
Continue to provide funding for CWD testing of captive cervids
Finalize and publish the national CWD rule for Herd Certification and
Interstate Movement
Evaluate live animal test, including rectal mucosal biopsy, for CWD in
cervids
how many states have $465,000., and can quarantine and purchase there from,
each cwd said infected farm, but how many states can afford this for all the cwd
infected cervid game ranch type farms ???
? game farms in a state X $465,000., do all these game farms have insurance
to pay for this risk of infected the wild cervid herds, in each state ???
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
Form 1100-001
(R 2/11)
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Information Item: Almond Deer Farm Update
FOR: DECEMBER 2011 BOARD MEETING
TUESDAY
TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief
SUMMARY:
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
Generation of a new form of human PrPSc in vitro by inter-species
transmission from cervids prions
Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, 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 77030, 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. Running Title: Conversion of human PrPC by cervid PrPSc
Keywords: Prion / transmissible spongiform encephalopathy / infectivity /
misfolded prion protein / prion strains * To whom correspondence should be
addressed. University of Texas Houston Medical School, 6431 Fannin St, Houston,
TX 77030. Tel 713-5007086; Fax 713-5000667; E-mail Claudio.Soto@uth.tmc.edu The
latest version is at http://www.jbc.org/cgi/doi/10.1074/jbc.M110.198465
JBC Papers in Press.
Published on January 4, 2011 as Manuscript M110.198465 Copyright 2011 by
The American Society for Biochemistry and Molecular Biology, Inc. 5, Downloaded
from www.jbc.org by guest, on November 11, 2012 2
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion
disorder of increasing prevalence within the United States that affects a large
population of wild and captive deer and elk. Determining the risk of
transmission of CWD to humans is of utmost importance, considering that people
can be infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the misfolded 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 conversion of human PrPC, but only
after the CWD prion strain has been stabilized by successive passages in vitro
or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct
biochemical pattern that differs from any of the currently known forms of human
PrPSc. Our results also have profound implications for understanding the
mechanisms of prion species barrier and indicate that the transmission barrier
is a dynamic process that depend on the strain and moreover the degree of
adaptation of the strain. If our findings are corroborated by infectivity
assays, they will imply that CWD prions have the potential to infect humans, and
that this ability depends on CWD strain adaptation.
Various studies aimed to analyze the transmission of CWD to transgenic mice
expressing human PrP have consistently given negative results (9-11), indicating
a strong species barrier. This conclusion is consistent with our many failed
experiments to attempt converting human PrPC with natural CWD, even after
pushing the PMCA conditions (see figure 1). We found successful conversion only
after adaptation of the CWD prion strain by successive passages in vitro or in
cervid transgenic mice. We are not aware that in any of the transgenic mice
studies the inoculum used was a previously stabilized CWD strain. Although, it
has been shown that strain stabilization in vitro by PMCA (17;26) and in vivo
using experimental rodents (36) has similarities with the strain adaptation
process occurring in natural hosts, we cannot rule out that the type of CWD
strain adaptation that is required to produce strains transmissible to humans
may take much longer time in cervids or not occur at all. An important
experiment will be to study transmissibility to humanized transgenic mice of CWD
passed experimentally in deer several times. Besides the importance of our
results for public health in relation to the putative transmissibility of CWD to
humans, our data also illustrate a very important and novel scientific concept
related to the mechanism of prion transmission across species barriers. Today
the view is that species barrier is mostly controlled by the degree of
similarity on the sequence of the prion protein between the host and the
infectious material (4). In our study we show that the strain and moreover the
stabilization of the strain plays a major role in the inter-species
transmission. In our system there is no change on the protein sequence, but yet
strain adaptation results in a complete change on prion transmissibility with
potentially dramatic consequences. Therefore, our findings lead to a new view of
the species barrier that should not be seen as a static process, but rather a
dynamic biological phenomenon that can change over time when prion strains
mature and evolve. It remains to be investigated if other species barriers also
change upon progressive strain adaptation of other prion forms (e.g. the
sheep/human barrier).
Our results have far-reaching implications for human health, since they
indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc,
suggesting that CWD might be infectious to humans. Interestingly our findings
suggest that unstable strains from CWD affected animals might not be a problem
for humans, but upon strain stabilization by successive passages in the wild,
this disease might become progressively more transmissible to man.
Generation of a New Form of Human PrPScin Vitro by Interspecies
Transmission from Cervid Prions*
Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A.
Mastrianni‖ and Claudio Soto‡,1 + Author Affiliations
From the ‡Mitchell Center for Alzheimer's Disease and Related Brain
Disorders, Department of Neurology, University of Texas Medical School at
Houston, Houston, Texas 77030, the §Departments of Microbiology, Immunology, and
Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of
Kentucky Medical Center, Lexington, Kentucky 40506, the ¶Institute of Pathology,
Case Western Reserve University, Cleveland, Ohio 44106, and the ‖Department of
Neurology, The University of Chicago, Chicago, Illinois 60637 1 To whom
correspondence should be addressed: University of Texas Medical School at
Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax:
713-500-0667; E-mail: claudio.soto@uth.tmc.edu.
Abstract
Prion diseases are infectious neurodegenerative disorders that affect
humans and animals and that result from the conversion of normal prion protein
(PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD)
is a prion disorder of increasing prevalence within the United States that
affects a large population of wild and captive deer and elk. Determining the
risk of transmission of CWD to humans is of utmost importance, considering that
people can be infected by animal prions, resulting in new fatal diseases. To
study the possibility that human PrPC can be converted into the misfolded form
by CWD PrPSc, we performed experiments using the protein misfolding cyclic
amplification technique, which mimics in vitro the process of prion replication.
Our results show that cervid PrPSc can induce the conversion of human PrPC but
only after the CWD prion strain has been stabilized by successive passages in
vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a
distinct biochemical pattern that differs from that of any of the currently
known forms of human PrPSc. Our results also have profound implications for
understanding the mechanisms of the prion species barrier and indicate that the
transmission barrier is a dynamic process that depends on the strain and
moreover the degree of adaptation of the strain. If our findings are
corroborated by infectivity assays, they will imply that CWD prions have the
potential to infect humans and that this ability progressively increases with
CWD spreading.
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
The overall diagnostic specificity was 99.8%. Selective use of antemortem
rectal biopsy sample testing would provide valuable information during disease
investigations of CWD-suspect deer herds.
Tuesday, April 09, 2013
EFFICACY OF ANTEMORTEM RECTAL BIOPSIES TO DIAGNOSE AND ESTIMATE PREVALENCE
OF CHRONIC WASTING DISEASE IN FREE-RANGING COW ELK (CERVUS ELAPHUS NELSONI)
Monday, March 18, 2013
PROCEEDINGS ONE HUNDRED AND FIFTEENTH ANNUAL MEETING of the UNITED STATES
ANIMAL HEALTH ASSOCIATION September 29 – October 5, 2011
see updated 2012 RESOLUTIONS
Monday, April 01, 2013
Dr. Deer/Dough from Texas on Wisconsin’s CWD implementation survey, is now
available
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, April 02, 2013
IMPORTANT: Cervid Industry and State Veterinarians on Rewriting Chronic
Wasting Disease Rule
Friday, April 12, 2013
Federal Protocol on Chronic Wasting Disease (CWD) - Darrel Rowledge,
Alliance for Public Wildlife
Saturday, April 13, 2013
Tennessee Launches CWD Herd Certification Program in the wake of
legislation for game farms
Thursday, March 29, 2012
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT
CALLING KETTLE BLACK
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, December 18, 2012
A Growing Threat How deer breeding could put public trust wildlife at risk
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
SNIP...SEE ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
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
*** 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.
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Wednesday, April 24, 2013
Dissociation between Transmissible Spongiform Encephalopathy (TSE)
Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a
Murine Transgenic Model of TSE Disease
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
Thursday, May 02, 2013
Pennsylvania Game Commission has established the state’s second Disease
Management Area in parts of four counties in response to three hunter-killed
deer that tested positive for CWD
FOR IMMEDIATE RELEASE: May 01, 2013
TSS
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