Statement
Release No. 0345.15 Contact: USDA Office of Communications
202-720-4623
Statement from Agriculture Secretary Tom Vilsack on the Country of Origin
Labeling Requirements for Beef and Pork
WASHINGTON, Dec. 18, 2015 – Agriculture Secretary Tom Vilsack today
released the following statement regarding the language in the omnibus bill
repealing the country of origin labeling requirements for beef and pork
products.
"The omnibus bill repealed the country of origin labeling (COOL)
requirements for muscle cuts of beef and pork, and ground beef and pork.
Effective immediately, USDA is not enforcing the COOL requirements for muscle
cut and ground beef and pork outlined in the January 2009 and May 2013 final
rules."
USDA will be amending the COOL regulations as expeditiously as possible to
reflect the repeal of the beef and pork provisions. In addition, all imported
and domestic meat will continue to be subject to rigorous inspections by USDA to
ensure food safety.
#
USDA is an equal opportunity provider and employer. To file a complaint of
discrimination, write: USDA, Office of the Assistant Secretary for Civil Rights,
Office of Adjudication, 1400 Independence Ave., SW, Washington, DC 20250-9410 or
call (866) 632-9992 (Toll-free Customer Service), (800) 877-8339 (Local or
Federal relay), (866) 377-8642 (Relay voice users).
USDA Looking at Voluntary COOL Program
Yesterday at 10:12 AM in Agriculture
- See more at: http://wnax.com/news/180081-usda-looking-at-voluntary-cool-program/#sthash.XHiqeF6q.dpuf
LMAO !!!
yep, that voluntary mad cow feed ban worked so well, (NOT), we are now
suppose to believe voluntary cool will work?
any voluntary move on COOL and that would/will be a joke.
USDA, OIE et al are already the laughing stock of the globe in animal
disease, when it comes to the TSE prion disease aka mad cow type disease.
Veterinary Record 2015;177:381 doi:10.1136/vr.h5454 News and Reports One
health THE World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
THE World Organisation for Animal Health (OIE) and the Institut Pasteur
have agreed to strengthen their cooperation in the fields of animal disease and
zoonosis research, education, surveillance and control, in line with the One
Health concept, through a new collaborative agreement.
The Institut Pasteur is
Veterinary Record 2015;177:379 doi:10.1136/vr.h5446
News and Reports
Defra seeks a dialogue on animal import controls Defra is seeking ‘ideas
and discussion’ as part of a review in England of the Trade in Animals and
Related Products Regulations 2011. The Regulations govern veterinary border
controls for live animals and products of animal origin.
>THE World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research<
please forgive me if I don’t believe you $$$
I remember...
>>>PARIS -- The World Organization for Animal Health said on
Wednesday it had lowered to the safest level the official risk of six countries
for mad cow disease, a move expected to open international market access for
their beef exports. These countries are France, Ireland, Switzerland, the Czech
Republic, Cyprus and the Lichtenstein.<<<
THIS move is _not_ based on science, but on corporate profits and big ag.
to say now that France is a "negligible risk", would be like saying North
America is a "negligible risk", which is preposterous. not based on sound
science, but on greed and special interest. the only _move_ this ‘’BSE mad cow
negligible risk’’ assessment makes, is a move to increase global Transmissible
Spongiform Encephalopathy prion mad cow type disease, via the legal trading of
the TSE prion aka mad cow type disease via the BSE MRR i.e. Minimal Risk Region
policy, a policy set up to fail from the start. please, for whatever God you
pray to sake, please be warned.
‘’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.’’
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,
Tuesday, May 19, 2015
COUNTRY OF ORIGIN LABELING COOL H.R. 2393 Agriculture Chairman K. Michael
Conaway (R-TX) Fears of US imports infected with mad cow disease is emerging as
an issue in trans-Pacific trade talks
Wednesday, March 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
Friday, April 4, 2014
China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa
and Saudi Arabia still retain BSE-related closures
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
The OIE is nothing more than a trading brokerage for the Transmissible
Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is
still in the midst of a mad cow disease outbreak with atypical BSE cases still
growing. mad cow disease is so bad in France, as with the USA, they stopped
testing for mad cow disease (France altogether and the USA to figures so low,
you would only detect a case of mad cow disease, only by chance).
from the inside looking out ;
Quote: Maybe familirise yourself with the OIE. The primary concern is
animal health of the world they are the animal version of the WHO. It is a long
way down from that ivory tower but here we go, until pressured by the USA
representatives a country could not export animals for 6 years after finding a
BSE/BASE positive animal so under the old rules the US would not be able to
export anywhere in the world for another 4 1/2 years. Who got the risk levels
system put in to allow some trade - your US representatives. You guys want to
change rules - OK , but you do not get special rules that only apply to the US.
As i have told you before Sand h I market all my own slaughter animals and you
know that, so don't do the whole holier than thow act.
With all due respect, it is obvious that you know little about the OIE and
how it actually works. Having been to their offices in Paris and talked
personally with the Head of the Animal Test Section, you would choke if you knew
how many lobby groups attend that office daily. There is a steady stream of paid
lobby groups that have one goal in life and that is to sway the Section Heads of
each department within the OIE to suit the needs of different jurisdictions
around the world, which curiously enough, also includes the USA and Canada.
Anyone can go there and chat with them - providing they can provide valid cause
to be let in. To say that the only goal of the OIE is animal health is actually
only part of their function. They are more than that and my discussions with Dr.
Diaz there has showed me that. But to blindly make a statement regarding what
they do when you have no idea what they actually do is like eating the skin of
the orange and not knowing what is actually under.
Interestingly you state that the US Government applied pressure (to the
OIE) I assume and that is a great example of the lobby groups doing their job.
So, at the end of the day, one can safely assume that it is the pressure applied
by certain influential lobby groups that will determine a likely outcome to an
apparent OIE directive. Man alive, isn't it great to live in a democracy wherein
the people get to make the choices and not just some "other" interested party or
group - say like........Cargill or Tyson for example?
So, one last question, question?
Who wags the tail of that dog?? And for what reason other than one that is
purely associated with trade and international agreements and greed?
And you think it is so simply explainable.
end...tss
Subject: UPDATED WHO Guidelines include tissues from Cervidae affected with
Chronic Wasting Disease (CWD)
Distribution of infectivity in animal tissue and body fluids
Introduction
A.2.1 The following table (Table A2) presents a guide to the possible
presence of TSE infectivity in various tissues and body fluids of cattle
(exposed naturally or experimentally and orally to first passage BSE agent),
sheep and goats (exposed naturally to scrapie agents and potentially to the BSE
agent) irrespective of the stage of incubation. Table A2 has been updated in
June 2010 taking account of the updated WHO Guidelines published in 2010 (WHO,
2010).
*** A.2.2 This is the first time that the WHO Guidelines include tissues
from Cervidae affected with Chronic Wasting Disease (CWD). CWD has not been
reported in Europe despite some surveillance for it and there are no specific
regulations in force. Should information on TSE infectivity in CWD be required,
for example in regard to Cervidae in zoos or in animals in transit through our
ports,*** please see updated 2010 WHO Guidelines.
The inclusion of infectivity data in CWD in these Tables was considered
important for three reasons: 1) CWD is continuing its spread to new regions of
North America, 2) infectivity has been convincingly demonstrated in several
bodily secretions and excretions of infected deer and 3) CWD is the only form of
animal Transmissible Spongiform Encephalopathies (TSE) that exists in the wild
and, although not presently considered to be an important concern for human,
could pose serious problems of control in the future, especially as a potential
source of infection in other animal species.
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing
***
Wednesday, March 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
Friday, April 4, 2014
China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa
and Saudi Arabia still retain BSE-related closures
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
It is clear that the designing scientists must also have shared Mr
Bradleys surprise at the results because all the dose levels right down to 1
gram triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
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...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
*** Monday, October 26, 2015 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations 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.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Monday, October 26, 2015
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical
BSE investigations
Saturday, December 12, 2015
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
December 28, 2015 at 2:21am
*** Australian government assessing risk of importing beef from US, Japan
and the Netherlands
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67
PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in
unusual brain location and PrPsc detection by PMCA only.
***IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
Sunday, October 25, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.
DATES: The comment period for the proposed rule published on September 10,
2015 (80 FR 54660-54692) is reopened. We will consider all comments that we
receive on or before December 9, 2015. ...
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I
kindly submit the following ;
>>>The last major revision of the scrapie regulations occurred on
August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket
No. 97-093-5) a final rule amending part 79 by imposing additional restrictions
on the interstate movement of sheep and goats.<<<
Indeed, much science has changed about the Scrapie TSE prion, including
more science linking Scrapie to humans. sadly, politics, industry, and trade,
have not changed, and those usually trump sound science, as is the case with all
Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing
animals and the OIE. we can look no further at the legal trading of the Scrapie
TSE prion both typical and atypical of all strains, and CWD all stains. With as
much science of old, and now more new science to back this up, Scrapie of all
types i.e. atypical and typical, BSE all strains, and CWD all strains, should be
regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE,
and all trading partners to take heed to the latest science on the TSE prion
disease, all of them, and seriously reconsider the blatant disregards for human
and animal health, all in the name of trade, with the continued relaxing of TSE
Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set
up to fail in the first place. If the world does not go back to the ‘BSE RISK
ASSESSMENTS’, enhance, and or change that assessment process to include all TSE
prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we
continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’
PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they
will continue to mutate and spread among species of human and animal origin, and
they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Evaluation of the zoonotic potential of transmissible mink
encephalopathy
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Ruchoux,
Marie-Madeleine - item Durand, Valerie - item Luccantoni-Freire, Sophie - item
Dehen, Capucine - item Correia, Evelyne - item Casalone, Cristina - item Richt,
Juergen item Greenlee, Justin item Torres, Juan Maria - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Pathogens Publication Type: Peer Reviewed Journal Publication
Acceptance Date: July 30, 2013 Publication Date: July 30, 2013 Citation: Comoy,
E.E., Mikol, J., Ruchoux, M., Durand, V., Luccantoni-Freire, S., Dehen, C.,
Correia, E., Casalone, C., Richt, J.A., Greenlee, J.J., Torres, J.M., Brown, P.,
Deslys, J. 2013. Evaluation of the zoonotic potential of transmissible mink
encephalopathy. Pathogens. 2:(3)520-532.
Interpretive Summary: Cases of bovine spongiform encephalopathy (BSE) or
mad cow disease can be subclassified into at least 3 distinct disease forms with
the predominate form known as classical BSE and the others collectively referred
to as atypical BSE. Atypical BSE can be further subdivided into H-type and
L-type cases that are distinct from classical BSE and from each other. Both of
the atypical BSE subtypes are believed to occur spontaneously, whereas classical
BSE is spread through feeding contaminated meat and bone meal to cattle.
Transmissible mink encephalopathy (TME) is another prion disease that transmits
to cattle and show similarities to L-type BSE when subjected to laboratory
testing. The purpose of this study was to use non-human primates (cynomologous
macaque) and transgenic mice expressing the human prion protein to determine if
TME could represent a potential risk to human health. TME from two sources
(cattle and raccoons) was able to infect non-human primates and transgenic mice
after exposure by the intracranial route. This result suggest that humans may be
able to replicate TME prions after an exposure that allows infectious material
access to brain tissue. At this time, it is unknown whether non-human primates
or transgenic mice would be susceptible to TME prions after oral exposure. The
results obtained in these animal models were similar to those obtained for
L-type BSE. Although rare, the existence of TME and that it transmits to cattle,
non-human primates, and transgenic mice suggest that feed bans preventing the
feeding of mammalian tissues to cattle should stay in place and that regular
prion surveillance during the slaughter should remain in place. Parties with
interest in the cattle and beef industries and regulatory officials responsible
for safe feeding practices of cattle will be interested in this work. Technical
Abstract: Successful transmission of Transmissible Mink Encephalopathy (TME) to
cattle supports the bovine hypothesis to the still controversial origin of TME
outbreaks. Human and primate susceptibility to classical Bovine Spongiform
Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques assume
a low cattle-to-primate species barrier: we therefore evaluated the zoonotic
potential of cattle-adapted TME. In less than two years, this strain induced in
cynomolgus macaques a neurological disease similar to L-BSE and distinct from
c-BSE. TME derived from another donor species (raccoon) induced a similar
disease with shorter incubation periods.
*** L-BSE and cattle-adapted TME were also transmissible to transgenic mice
expressing human PrP. Interestingly, secondary transmissions to transgenic mice
expressing bovine PrP showed the maintenance of prion strain features for the
three tested bovine prion strains (cattle TME, c-BSE and L-BSE) regardless of
intermediate host.
*** Thus, TME is the third animal prion strain transmissible to both
macaques and humanized transgenic mice, suggesting zoonotic potentials that
should be considered in the risk analysis of animal prion diseases for human
health.
*** Moreover, the similarities between TME and L-BSE are highly suggestive
of a link between those strains, and of the presence of L-BSE decades prior to
its identification in USA and Europe.
Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies 2014 Annual Report
1a.Objectives (from AD-416): 1. Investigate the pathobiology of atypical
transmissible spongiform encephalopathies (TSEs) in natural hosts. A.
Investigate the pathobiology of atypical scrapie. B. Investigate the
pathobiology of atypical bovine spongiform encephalopathy (BSE). 2. Investigate
the horizontal transmission of TSEs. A. Assess the horizontal transmission of
sheep scrapie in the absence of lambing. B. Determine routes of transmission in
chronic wasting disease (CWD) infected premises. C. Assess oral transmission of
CWD in reindeer. 3. Investigate determinants of CWD persistence. A. Determine
CWD host range using natural routes of transmission. B. Investigate the
pathobiology of CWD.
1b.Approach (from AD-416): The studies will focus on three animal
transmissible spongiform encephalopathy (TSE) agents found in the United States:
bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic
wasting disease (CWD) of deer, elk, and moose. The research will address sites
of accumulation, routes of infection, environmental persistence, and ante mortem
diagnostics with an emphasis on controlled conditions and natural routes of
infection. Techniques used will include clinical exams, histopathology,
immunohistochemistry and biochemical analysis of proteins. The enhanced
knowledge gained from this work will help mitigate the potential for
unrecognized epidemic expansions of these diseases in populations of animals
that could either directly or indirectly affect food animals.
3.Progress Report: Research efforts directed toward meeting objective 1 of
our project plan, Investigate the pathobiology of atypical transmissible
spongiform encephalopathies (TSEs) in natural hosts, include work in previous
years starting with the inoculation of animals for studies designed to address
the pathobiology of atypical scrapie, atypical bovine spongiform encephalopathy
(BSE), as well as a genetic version of BSE. Animals inoculated with atypical
scrapie have not yet developed disease. Atypical BSE animals have developed
disease and evaluation of the samples is currently underway. Animals inoculated
with a genetic version of BSE have developed disease and the manuscript has been
published (2012). In addition, we have investigated the possibility that
atypical scrapie was present earlier than previously detected in the national
flock by analyzing archived field isolates using methods that were unavailable
at the time of original diagnosis. Sample quality was sufficiently degraded that
modern methods were not suitable for evaluation. In research pertaining to
objective 2, Investigate the horizontal transmission of TSEs, we have initiated
a study to determine if cohousing non-lambing scrapie inoculated sheep is
sufficient to transmit scrapie to neonatal lambs. At this time, scrapie free
ewes have lambed in the presence of scrapie inoculated animals and the lambs are
cohoused with these inoculated animals.
4.Accomplishments 1. Evaluated enzyme immunoassay for rapid identification
of prion disease in livestock. Scrapie of sheep and bovine spongiform
encephalopathy of cattle are diseases that cause damage to the central nervous
system including the retina in the eye. The infectious agent is an abnormal
protein called a prion that has misfolded from its normal state and is resistant
to breakdown by the host cells. Current diagnostic methods require the testing
of brain material, which can be difficult to collect and may lead to
contamination of the environment and exposure of personnel to the infectious
agent. Eyes can be readily collected without opening the skull. ARS researchers
at Ames, Iowa demonstrated that the enzyme immunoassay results using eyes of
negative controls or samples collected from sheep or cattle with clinical signs
were in agreement with approved confirmatory assays (western blot or
immunohistochemistry). These results indicate the retina is a useful tissue for
rapid diagnosis of prion disease in clinically ill sheep and cattle and could be
considered to greatly increase the number of samples submitted for prion disease
diagnosis with a minimal investment of time and limited exposure of personnel to
prion agents.
2. Evaluated E211K cattle as a model for inherited human prion disease.
Prion diseases cause damage to the central nervous system of animals and humans.
The infectious agent is an abnormal protein called a prion that has misfolded
from its normal state and is resistant to breakdown by the host cells and thus
accumulates and damages those cells. Some forms of prion disease are genetic and
can be inherited. Current models of genetic prion disease in humans rely on
mouse models expressing either the human prion protein (E200K) or a combination
of both mouse and human sequences. In addition to being an entirely artificial
system these mouse models have a short lifespan making them a less than ideal
system to study a naturally occurring genetic disorder with a long incubation
time and late onset of disease. Cattle, however, exhibit a number of
similarities to humans with regard to prion disease and perhaps most notable is
the late onset of genetic prion disease. ARS researchers at Ames, Iowa have
produced cattle containing both 1 and 2 chromosome copies of the cattle prion
gene (E211K) and evaluated many aspects of this prion protein from cattle
including protein stability, protein expression levels and ratios, as well as
evidence of oxidative stress. Taken together, these results highlight the
differences between mouse models of genetic prion disease and a naturally
occurring prion disease system in cattle and suggest that cattle will provide a
more relevant understanding of genetic prion disease in humans than do current
rodent models.
Review Publications Smith, J.D., Greenlee, J.J. 2014. Detection of
misfolded prion protein in retina samples of sheep and cattle by use of a
commercially available enzyme immunoassay. American Journal of Veterinary
Research. 75(3):268-272. Haldar, S., Beveridge, A.J., Wong, J., Singh, A.J.,
Galimberti, D., Borroni, D., Zhu, X., Blevins, J., Greenlee, J., Perry, G.,
Mukhopadhyay, C.K., Schmotzer, C., Singh, N. 2014. A low-molecular-weight
ferroxidase is increased in the CSF of sCJD Cases: CSF ferroxidase and
transferrin as diagnostic biomarkers for sCJD. Antioxidants & Redox
Signaling. 19(14):1662-1675.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=421870&fy=2014
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=421870
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
*** Evidence for zoonotic potential of ovine scrapie prions
HervƩ Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, FrƩdƩric Lantier,4, SƩverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier AndrƩoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
***The serial transmission of different scrapie isolates in these mice led
to the propagation of prions that are phenotypically identical to those causing
sporadic CJD (sCJD) in humans.***
***These results demonstrate that scrapie prions have a zoonotic potential
and raise new questions about the possible link between animal and human
prions.***
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
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Tuesday, December 15, 2015
*** Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts
Study: Chronic Wasting Disease kills 19% of deer herd annually
North America CWD TSE Prion Out of Control
Saturday, December 12, 2015
*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
***
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat. you can take the ash and
mix it with saline and inject that ash into a mouse, and the mouse will go down
with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?
to the breeders and industry that care more about their bottom dollar,
ignore science, and the ones crying about their poor deer being
slaughtered...crying me a river$$$
CENSORED, RAW, AND UNCUT...
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
from the other side of the fence... today’s Singeltary Sunday School class
‘thinking outside of the box, God’s Wrath’ at the bottom. ...tss
Wednesday, March 18, 2015
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
(8 cases CWD in wild to date Texas)
Wednesday, March 25, 2015
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, December 24, 2015
*** Infectious disease spread is fueled by international trade ***
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Thursday, December 24, 2015
Revisiting the Heidenhain Variant of Creutzfeldt-Jakob Disease: Evidence
for Prion Type Variability Influencing Clinical Course and Laboratory Findings
Article type: Research Article
Congress is all set to give NIH it's largest increase in 12 years.
Included in the bill: $350 million increase for Alzheimer’s research and an
$85 million increase for the BRAIN Initiative, the project to map the human
brain.
Full story at: http://ow.ly/VYKBv
great news, with not a minute to spare...
Evidence for human transmission of amyloid-Ī² pathology and cerebral amyloid
angiopathy
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-? pathology and cerebral
amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
snip...see full text ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Wednesday, September 2, 2015
Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses
in an Alzheimer’s Disease Database
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
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 Gƶttingen, 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...
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
The Pathological Protein:
Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases
Philip Yam
''Answering critics like Terry Singeltary, who feels that the US
undercounts CJD, Schonberger _conceded_ that the current surveillance system has
errors but stated that most of the errors will be confined to the older
population''....end
RIP MOM DOD December 14, 1997 confirmed Heidenhain Variant of Creutzfeldt
Jakob Disease hvCJD...
these blogs are for educational use. I do not advertise or make money from
them.
MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget,
and never let them forget...
kindest regards, terry
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
