TEXAS One sorghum DDGS sample out of 168 DG samples was contaminated with
bovine spongiform encephalopathy, but the transmission route of the bovine
spongiform encephalopathy agent could not be clearly defined.
***UDATED CORRECTION BY AUTHOR...SEE AFTER THE ORIGINAL ARTICLE...TSS
***UDATED CORRECTION BY AUTHOR...SEE AFTER THE ORIGINAL ARTICLE...TSS
UPDATED CORRECTION BY AUTHOR AND EMAIL SENT TO ME ;
From: Kyung-Min Lee
Sent: Thursday, October 01, 2015 1:39 PM
Cc: CJD-L@LISTS.AEGEE.ORG ;
cjdvoice@yahoogroups.com ; bloodcjd@yahoogroups.com ; jcattanach@foodprotection.org ;
cnc3@psu.edu ; dloynachan@foodprotection.org ;
lhovey@foodprotection.org ; Timothy J. Herrman
Subject: RE: TEXAS CONFIRMATION OF BOVINE SPONGIFORM
ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG
SAMPLES
Dear
Terry S. Singeltary Sr.
Thank
for your interest and concern about our published article entitled “Evaluation
of Selected Nutrients and Contaminants in Distillers Grains from Ethanol
Production in Texas”. I should apologize you and others that there were some
errors and misleading statements in this article due to inappropriate
terminology. The statement you were concerned about was corrected to "One
sorghum DDGS out of 168 DG samples was contaminated with animal protein
prohibited for use in ruminant feed and was channeled to poultry feed." We
requested the journal editor to correct some errors and the relevant statements,
or to withdraw the article from the journal.
Again
I sincerely apologize for any confusion and inconvenience this may cause.
Thanks.
best
wishes,
Kyung-Min
Kyung-Min Lee, Ph. D.
Research Scientist
Office of the Texas State Chemist
Research Scientist
Office of the Texas State Chemist
Texas A&M AgriLife Research
P.O. Box 3160, College Station, TX 77841-3160
Phone: 979-845-4113 (ext 132)
Email:kml@otsc.tamu.edu
Fax: 979-845-1389
P.O. Box 3160, College Station, TX 77841-3160
Phone: 979-845-4113 (ext 132)
Email:kml@otsc.tamu.edu
Fax: 979-845-1389
snip...end...tss
corrected...
Sunday, September 27, 2015
TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE
SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
kind regards, terry
1st mad cow that got away $$$
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.
ONE HUNDRED EIGHTH CONGRESS
COMMITTEE ON GOVERNMENT REFORM
May 13,2004
The Honorable Ann M. Veneman Secretary of Agriculture Department of
Agriculture1400 Independence Avenue, SW Washington, DC 20250
Dear Madam Secretary:
I am writing to express concern that the recent failure of the U.S.
Department of Agriculture (USDA) to test a Texas cow with neurological syrnptoms
for bovine spongifonnencephalopathy (BSE) may reflect wider problems in the
surveillance program. USDA apparently does not keep track of how many cows
condemned for central nervous system symptoms are tested for BSE nor does it
require that suspect carcasses be held pending testing...
FULL TEXT ;
The 2nd mad cow that almost got away, brain samples laid up somewhere for 7
months, so the BSE MRR risk policy, so the BSE MRR risk policy, the legal
trading of all strains of TSE prions was ratified. after an act of Congress and
scientist from around the world complaining about it to the OIG, the sample was
finally sent to Weybridge and CONFIRMED. ...
Release No. 0336.05 Contact: USDA Jim Rogers 202-690-4755 FDA Rae Jones
301-827- 6242
Printable version Email this page
U.S. Department of Agriculture (USDA) Food and Drug Administration
(FDA)
Investigation Results of Texas Cow That Tested Positive for Bovine
Spongiform Encephalopathy (BSE) Aug. 30, 2005
The U.S. Department of Agriculture's Animal and Plant Health Inspection
Service (APHIS) and the U.S. Department of Health and Human Services' Food and
Drug Administration (FDA) have completed their investigations regarding a cow
that tested positive for bovine spongiform encephalopathy (BSE) in June 2005.
The agencies conducted these investigations in collaboration with the Texas
Animal Health Commission and the Texas Feed and Fertilizer Control
Service.
Our results indicate that the positive animal, called the index animal, was
born and raised on a ranch (termed the "index farm") in Texas. It was a cream
colored Brahma cross approximately 12 years old at the time of its death. It was
born prior to the implementation of the 1997 feed ban instituted by FDA to help
minimize the risk that a cow might consume feed contaminated with the agent
thought to cause BSE. The animal was sold through a livestock sale in November
of 2004 and transported to a packing plant. The animal was dead upon arrival at
the packing plant and was then shipped to a pet food plant where it was sampled
for BSE. The plant did not use the animal in its product, and the carcass was
destroyed in November 2004.
APHIS attempted to trace all adult animals that left the index farm after
1990, as well as all progeny born within 2 years of the index animal's death.
Together, these animals are called animals of interest.
During the course of the investigation, USDA removed and tested a total of
67 animals of interest from the farm where the index animal's herd originated.
All of these animals tested negative for BSE. 200 adult animals of interest were
determined to have left the index farm. Of these 200, APHIS officials determined
that 143 had gone to slaughter, two were found alive (one was determined not to
be of interest because of its age and the other tested negative), 34 are
presumed dead, one is known dead and 20 have been classified as untraceable. In
addition to the adult animals, APHIS was looking for two calves born to the
index animal. Due to record keeping and identification issues, APHIS had to
trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter
channels, four are presumed to have entered feeding and slaughter channels and
one calf was untraceable.
To determine whether contaminated feed could have played a role in the
index animal's infection, FDA and the Texas Feed and Fertilizer Control Service
conducted a feed investigation with two main objectives: 1) to identify all
protein sources in the animal=s feed history that could potentially have been
the source of the BSE agent, and 2) to verify that cattle leaving the herd after
1997 were identified by USDA as animals of interest and were rendered in
compliance with the 1997 BSE/ruminant feed rule.
The feed history investigation identified 21 feeds or feed supplements that
were used on the farm since 1990. These feed ingredients were purchased from
three retail feed stores and were manufactured at nine feed mills. This
investigation found that no feed or feed supplements used on the farm since 1997
were formulated to contain prohibited mammalian protein. Due to this finding,
FDA has concluded that the animal was most likely infected prior to the 1997
BSE/ruminant feed rule.
The investigation into the disposition of herd mates from this farm
involved visits to nine slaughter plants and eight rendering plants. The
investigation found that all of the rendering plants were operating in
compliance with the BSE/ruminant feed rule. A review of the inspection history
of each of these rendering firms found no violations of the FDA feed ban
rule.
APHIS and FDA are very pleased with the results of their investigations,
which show the animals of interest did not present a threat to livestock and
that the ruminant feed rule is being followed. The U.S. maintains an
interlocking system of safeguards designed to prevent BSE from entering the
human and animal food chain. USDA also remains vigilant in its attempt to find
BSE in the United States. To date, there have been more than 450,000 animals
tested in the last 14 months and only two BSE positive animals found in this
country.
For more information on USDA's epidemiological investigation and a copy of
the report, please visit the APHIS website at http://www.aphis.usda.gov/lpa/issues/bse/bse.html
or
For more information on FDA's feed investigation, please visit the FDA's
website at
Last Modified: 08/31/2005
Aug 30, 2005 USDA Texas BSE Investigation—Final Epidemiology Report
TSS REPORT ON 2ND TEJAS MAD COW Mon, 22 Nov 2004 17:12:15 -0600 (the one
that did NOT get away, thanks to the Honorable Phyllis Fong)
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr." To: Carla Everett References: <[log in
to unmask]> <[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food
chain?
and i see the TEXAS department of animal health is ramping up forsomething,
but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you
confirm???terry
==============================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 –0600
From: Carla Everett To: "Terry S. Singeltary Sr." References: <[log in
to unmask]>
The USDA has made a statement, and we are referring all callers to the USDA
web site. We have no information about the animal being in Texas. Carla
At 09:44 AM 11/19/2004, you wrote:
>Greetings Carla,
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow
is from
>TEXAS. can you comment on this either way please?
>>thank you,
>Terry S. Singeltary Sr.
>>
===================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
<[log in to unmask] us> <[log in to unmask]> <[log in to unmask]
us> <[log in to unmask]>
our computer department was working on a place holder we could postUSDA's
announcement of any results. There are no results to be announced tonightby
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something.
At 06:05 PM 11/22/2004, you wrote:>why was the announcement on your TAHC
site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of animal.
>>>>>>
==========================
THEN, 7+ MONTHS OF COVER-UP BY JOHANN ET AL! no doubt about it now
$$$
NO, it's not pretty, hell, im not pretty, but these are the facts, take em
or leave em, however, you cannot change them.
with kindest regards,
I am still sincerely disgusted and tired in sunny Bacliff, Texas USA
77518
Terry S. Singeltary Sr.
FULL 130 LASHINGS TO USDA BY OIG again
News Release Texas Animal Health Commission Box l2966 * Austin, Texas 78711
* (800) 550-8242 * FAX (512) 719-0719 Bob Hillman, DVM * Executive Director For
info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710,
or ceverett@tahc.state.tx.us
For immediate release---
State-Federal Team Responds to Texas BSE Case
The US Department of Agriculture announced June 29 that genetic testing has
verified that an aged cow that tested positive for Bovine Spongiform
Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for
laboratory testing were initially collected from the animal in November 2004,
and the carcass was incinerated and did not enter the human food, animal feed or
fertilizer supply system. While tests in November indicated the animal did not
have BSE, retesting in England in June confirmed the animal had the disease. The
Texas Animal Health Commission (TAHC), the state’s livestock and poultry health
regulatory agency, and USDA have jointly assigned a state-federal team to
conduct the epidemiological investigation and response.
“The TAHC and US Department of Agriculture’s Veterinary Services are
working with a complement of experts from federal and state animal health, food
safety, public health and feed regulatory agencies to ensure the continued
safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state
veterinarian and executive director of the TAHC, the state’s livestock and
poultry health regulatory agency. “Epidemiological investigations are thorough
and focus on verifying the herd of origin, and when, where and how the animal
and potentially, any herd mates, were exposed to the abnormal prion, or disease
agent, that causes BSE. Additionally, epidemiology investigations trace the
infected animal’s movement and herd mates. Animals potentially exposed to the
disease will be depopulated, with proper disposal. The animals will not be
introduced into the human or animal food chain.”
The USDA’s BSE testing protocol requires testing of emaciated or injured
cattle, cattle that exhibit central nervous system disorder, cattle unable to
rise or to walk normally, and cattle that die of unknown causes. Since June 1,
2004, brain tissue samples from more than 394,000 cattle have been tested in the
U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr.
Hillman noted. BSE surveillance has been conducted in the U.S. since l990.
The U.S. has taken preventive measures against the introduction of BSE
since l989, when prohibitions were placed on cattle and other ruminants from
BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was
extended to all of Europe.
Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned
the use of ruminant-derived protein (from animals such as cattle and sheep) in
feed for cattle and other ruminants. There is no evidence that BSE spreads from
live animal to animal in the herd, but cattle can be exposed by eating feed that
contains rendered protein from infected animals. “These measures taken by the
USDA and the FDA are safeguards that work to protect livestock, and ultimately,
our meat supply,” he said.
--30--
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
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
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
LET's go back to the infamous TOKEN, charade, that happened on January 30,
2001, at the Texas Purina feed lot around Gonzales. NOW remember, this thing was
set up from the word go, as to some big showing that the FDA was DOING SOMETHING
BIG. let's look at exactly what was said then, and then i will run some figures
by you, of what banned mad cow feed has gone into commerce, of which most was
fed out. but, as wrong as the comments made were about what amount of infectious
material will kill a cow in this statement, even if you were to go by those
wrong figures of about .......... oh what was it ???
''FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of prohibited
material. These animals weigh approximately 600 pounds.''
you can take that with how ever many grains of salt you wish, but i read
that as saying, it was only 5 1/2 grams, and the old cow ways 600 pounds, so
know way that even if the feed was tainted, there was not enough to cause
disease. the fda, usda et al, knew at that exact moment when they wrote that
statement, they knew then that the 5 1/2 grams was enough to kill a small herd
of cows. it was old science. but again, they chose to deceive. THIS WAS 2001,
and it's now 2009, and they still are choosing to deceive, and the new
administration appears willing to continue the USA mad cow charade. NOW, since
the charade at the purina mill in 2001, i am going to list a few figures of
suspect, banned mad cow feed that went out into commerce, even in 2008, 2007,
2006, back a few years, and you can compare, what enormous amounts of banned
suspect mad cow feed and other products continue to go out. when you consider,
and they knew all along, that .005 grams is lethal, my God, how much of this
poison was consumed? WASHINGTON, June 26, 2008 - Beltex Corporation, doing
business as Frontier Meats, a Fort Worth, Texas, establishment, is recalling
approximately 2,850 pounds of fresh cattle heads which may contain specified
risk materials (SRMs), the U.S. Department of Agriculture's Food Safety and
Inspection Service announced today.
Data reported as of: 05/10/2008
Search by: State = TX, and FDA District = DAL-DO, and Firm Type = FR,HF,NL,
and Last BSE Insp Date From 01/01/2007 To 05/31/2008 and BSE Program Risk =
DP,HP,NP, and Last BSE District Decision = OAI, and Handles Feed for Rum.
Animals = Y,N,R Sort by: Last BSE District Decision FDA District DAL-DO Firm Id
(FEI) 3006607060 Firm Name Texas Legend Ranch Street Address 2803 Highway 473
City Kendalia State TX Zip Code 78027-2016 Opr. Status OPR Firm Type(s) FR, OF
Prgm Risk NP Last BSE Insp Date 03/25/2008 Last BSE Dist. Dcsn'' OAI Handles
Feed for Rum. Animals? Y
snip...end
An OAI inspection classification occurs when significant objectionable
conditions or practices were found and regulatory sanctions are warranted in
order to address the establishment's lack of compliance with the regulation. An
example of an OAI inspection classification would be findings of manufacturing
procedures insufficient to ensure that ruminant feed is not contaminated with
prohibited material. Inspections classified with OAI violations will be promptly
re-inspected following the regulatory sanctions to determine whether adequate
corrective actions have been implemented.
CORRECTIONS: VETERINARY MEDS -- CLASS II PRODUCT: Buckeye 26% Hi Fat Swine
Mix, Sandy Lake 40% Hog Supplement, 100 lb. containers, flexible plastic burlap
bags. Recall #V-026-1.
CODE: None are used.
MANUFACTURER: Sandy Lake Mills, Sandy Lake, PA. RECALLED BY: Manufacturer,
by telephone and visit. Firm initiated recall complete.
DISTRIBUTION: Pennsylvania.
QUANTITY: Seven containers, each weighing 100 pounds.
REASON: The product contains prohibited material (ruminant animal proteins)
used as an ingredient in the finished product swine feed. The product is not
labeled with the required caution statement "Do Not Feed to Cattle or Other
Ruminants."
________
PRODUCT: Custom Vaquero Supplement for Cattle identified by Purina Mills.
Recall #V-027- 1. CODE: 7V87. MANUFACTURER: Purina Mills, Inc., Gonzalez, Texas.
RECALLED BY: Manufacturer, contacted the one consignee on January 17, 2001.
DISTRIBUTION: Texas.
QUANTITY: 44,355 pounds.
REASON: The ruminant feed product contains meat and bone meal (MBM) of
bovine origin.
look at the table and you'll see that as little as 1 mg (or 0.001 gm)
caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in
primates Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian
Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to non-human
primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months
after exposure, whereas the other remained free of disease at 76 months. On the
basis of these findings and data from other studies, we made a preliminary
estimate of the food exposure risk for man, which provides additional assurance
that existing public health measures can prevent transmission of BSE to
man.
snip...
BSE bovine brain inoculum 100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01
mg Primate (oral route)* 1/2 (50%) Cattle (oral route)* 10/10 (100%) 7/9 (78%)
7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%) RIII mice (ic ip route)* 17/18 (94%)
15/17 (88%) 1/14 (7%) PrPres biochemical detection The comparison is made on the
basis of calibration of the bovine inoculum used in our study with primates
against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of
animals surviving at the time of clinical onset of disease in the first positive
animal (%). The accuracy of bioassays is generally judged to be about plus or
minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula
Published online January 27, 2005
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral
Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6;
Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique,
France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious
Disease control, Sweden; 5Georg August University, Germany; 6German Primate
Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to
contract BSE through contaminated food. For this purpose, BSE brain was titrated
in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this, to
assess the risk for humans. Secondly, we aimed at examining the course of the
disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE
brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals
were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the onset of
the clinical phase. However, there are differences in the clinical course
between orally and intracerebrally infected animals that may influence the
detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years).
However, there are rapid progressors among orally dosed monkeys that develop
simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study "BSE
in primates" supported by the EU (QLK1-2002-01096).
Calves were challenged by mouth with homogenised brain from confirmed cases
of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were
then left to develop BSE, but were not subjected to the normal stresses that
they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in some
of the groups, but it appears as if those in the 1 and 10g challenge groups most
closely fit the picture of incubation periods seen in the epidemic. Experiments
in progress indicate that oral infection can occur in some animals with doses as
low as 0.01g and 0.001g. .........
It is clear that the designing scientists must also have shared Mr
Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100 grams) was probably given with the benefit of hindsight;
particularly if one considers that later in the same answer Mr Bradley expresses
his surprise that it could take as little of 1 gram of brain to cause BSE by the
oral route within the same species. This information did not become available
until the "attack rate" experiment had been completed in 1995/96. This was a
titration experiment designed to ascertain the infective dose. A range of
dosages was used to ensure that the actual result was within both a lower and an
upper limit within the study and the designing scientists would not have
expected all the dose levels to trigger infection. The dose ranges chosen by the
most informed scientists at that time ranged from 1 gram to three times one
hundred grams. It is clear that the designing scientists must have also shared
Mr Bradley's surprise at the results because all the dose levels right down to 1
gram triggered infection.
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken
on feed used at a Texas feedlot that was suspected of containing meat and bone
meal from other domestic cattle -- a violation of FDA's 1997 prohibition on
using ruminant material in feed for other ruminants. Results indicate that a
very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in
total, five-and-one-half grams - approximately a quarter ounce -- of prohibited
material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin
(therefore not likely to contain infected material because there is no evidence
of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy
Commissioner, "The challenge to regulators and industry is to keep this disease
out of the United States. One important defense is to prohibit the use of any
ruminant animal materials in feed for other ruminant animals. Combined with
other steps, like U.S. Department of Agriculture's (USDA) ban on the importation
of live ruminant animals from affected countries, these steps represent a series
of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing
that it is voluntarily purchasing all 1,222 of the animals held in Texas and
mistakenly fed the animal feed containing the prohibited material. Therefore,
meat from those animals will not enter the human food supply. FDA believes any
cattle that did not consume feed containing the prohibited material are
unaffected by this incident, and should be handled in the beef supply clearance
process as usual. ...
snip...
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in
TEXAS was enough to kill 100 cows.
PRODUCT: Custom Vaquero Supplement for Cattle identified by Purina Mills.
Recall #V-027- 1. CODE: 7V87. MANUFACTURER: Purina Mills, Inc., Gonzalez, Texas.
RECALLED BY: Manufacturer, contacted the one consignee on January 17, 2001.
DISTRIBUTION: Texas. QUANTITY: 44,355 pounds. REASON: The ruminant feed product
contains meat and bone meal (MBM) of bovine origin.
PRODUCT: a) Manna Pro Floating Fish Food for Catfish . Recall #V-028-1; b)
Manna Pro Floating Fish Food - 26% For All Freshwater Fish. Recall #V-029-1.
Both are packaged in 50 pound, plastic-lined, paper sacks. CODE: a) 10160164,
12090164, 01050264, 03020264, and 03140264; b) 09110164, 09190164, 09230164,
10090164, 10160164, 11170164, 12090164 and 3200264. MANUFACTURER: Doane Pet
Care, Brentwood, Tennessee. RECALLED BY: Manufacturer, by telephone on March 26,
2001. Firm-initiated recall complete. DISTRIBUTION: California, Pennsylvania,
Ohio, Kansas, Colorado, Georgia, and Florida. QUANTITY: 27,300 pounds of Catfish
Food and 86,100 pounds of Freshwater Fish. REASON: The products, which contain
meat by-products, were shipped without the required BSE warning label.
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
Australia
COMMONWEALTH OF AUSTRALIA Official Committee Hansard SENATE RURAL AND
REGIONAL AFFAIRS AND TRANSPORT REFERENCES COMMITTEE Reference: Import
restrictions on beef FRIDAY, 5 FEBRUARY 2010 CANBERRA BY AUTHORITY OF THE
SENATE
RRA&T 2 Senate Friday, 5 February 2010 RURAL AND REGIONAL AFFAIRS AND
TRANSPORT
[9.03 am]
BELLINGER, Mr Brad, Chairman, Australian Beef Association
CARTER, Mr John Edward, Director, Australian Beef Association
CHAIR—Welcome. Would you like to make an opening statement?
Mr Bellinger—Thank you. The ABA stands by its submission, which we made on
14
December last year, that the decision made by the government to allow the
importation of beef from BSE affected countries is politically based, not
science based. During this hearing we will bring forward compelling new evidence
to back up this statement. When I returned to my property after the December
hearing I received a note from an American citizen. I will read a small excerpt
from the mail he sent me in order to reinforce the dangers of allowing the
importation of beef from BSE affected countries. I have done a number of press
releases on this topic, and this fellow has obviously picked my details up from
the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He
states, and rightfully so:
snip...end
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
We have shown that cattle-adapted TME is the third cattle prion strain
(joining classical and L-type BSE) to be transmissible both to non-human
primates and transgenic mice overexpressing human PrP. However, the successful
transmission of raccoon TME to primate, inducing a disease with similar features
as cattle TME, extends this notion to TME-related strains independent of host
origin. Pathological, biochemical and bioassay investigations converged to
demonstrate the similarity between cattle-adapted TME and L-BSE.
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, Val erie 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...TSS
===============
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
*** Moreover, transmission experiments to non-human primates suggest that
some TSE agents in addition to Classical BSE prions in cattle (namely L-type
Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME)
and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
*** These atypical BSE cases constitute an unforeseen first threat that
could sharply modify the European approach to prion diseases.
Second threat
snip...
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a
Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have
attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you
will find in the paper, we have managed to associate the alternate phenotype to
type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim
any further sub-classification in respect of Heidenhain variant CJD or Vicky
Rimmer's version. It will take further studies, which are on-going, to establish
if there are sub-types to our initial finding which we are now reporting. The
main point of the paper is that, as well as leading to the expected new variant
CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an
alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can
be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
<>
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial
College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44
(0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until
9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
================
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
===============
***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
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
PRION CONFERENCE 2014 HELD IN ITALY RECENTLY CWD BSE TSE UPDATE
> First transmission of CWD to transgenic mice over-expressing bovine
prion protein gene (TgSB3985)
PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping
up the future of prion research
Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First
transmission of CWD to transgenic mice over-expressing bovine prion protein gene
(TgSB3985)
Friday, August 14, 2015
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation
P.150: Zoonotic potential of L-type BSE prions: A new prion disease in
humans?
Emilie Jaumain,1 Stéphane Haïk,2 Isabelle Quadrio,3 Laetitia Herzog,1
Fabienne Reine,1 Armand Perret-Liaudet,3 Human Rezaei,1 Hubert Laude,1 Jean-Luc
Vilotte,4 and Vincent Béringue1 1INR A (Institut National de la Recherche
Agronomique); UR892; Virologie Immunologie Moléculaires; Jouy-en-Josas, France;
2IN SERM; Equipe maladie d’Alzheimer et maladies à Prions; CRicm; UMRS 1127; CNR
S; UPMC. R.; ICM, Hôpital de la Salpêtrière; Paris, France; 3Neurobiologie, CMRR
, Gériatrie, Hospices Civils de Lyon, Université Lyon 1-CNR S UMR5292-IN SERM
U1028; Lyon, France; 3INR A; UMR1313; Génétique Animale et Biologie Intégrative;
Jouy-en-Josas, France
Two novel prion strains, referred to as BSE-L and BSE-H, have been
recognized in bovines through active prion surveillance programs, both being
distinct from the epizootic, ‘classical’, BSE strain (C-BSE). Both H and L-types
have been detected worldwide as rare cases occurring in aged animals. Like C-BSE
prions, H- and L-types prions can propagate with relative ease in foreign
species or in transgenic mouse lines expressing heterologous PrP sequences. A
prion exhibiting biological properties similar to C-BSE agent sometimes emerged
from these cross-species transmissions. Previously, L-type prions were shown to
transmit to transgenic mice expressing human PrP with methionine at codon 129
with higher efficacy than C-BSE prions. Here, we examined whether L-type prions
propagate without any apparent transmission barrier in these mice and whether
such ‘humanised’ L-type prions share biological properties with CJD prions.
L-type prions and a panel of human CJD cases with various genotypes at codon 129
and electrophoretic PrPres signatures were serially transmitted by intracerebral
route to human PrP mice. The biological phenotypes induced by these agents were
compared by all the standard methods currently used to distinguish between prion
strains. At each passage, L-type prions were also transmitted back to bovine PrP
mice to assess whether the agent has evolved upon passaging on the human PrP
sequence. L-type prions transmitted to human PrP mice at 100% attack rate,
without notable alteration in the mean incubation times over 5 passages. At each
passage, ‘humanized’ L-type prions were able to transmit back to bovine PrP
transgenic mice without apparent transmission barrier, as based on the survival
time and the restoration of a L-type BSE phenotype. Comparison of mean
incubation times on primary and subsequent passages in human PrP mice showed no
overlap between L-type and sporadic CJD agents. While the electrophoretic
signature and regional distribution of PrPres in L-type diseased mouse brains
resembled that seen after transmission of MM2 CJD strain type, both agents
exhibited distinct resistance of the associated PrPres molecules to protease
denaturation.
In summary, L-type prions can be passaged on the human PrP sequence without
any obvious transmission barrier. The phenotype obtained differs from the
classical CJD prion types known so far. Careful extrapolation would suggest that
the zoonotic transmission of this agent could establish a new prion disease type
in humans.
========Prion2013==========
2012 ATYPICAL L-TYPE BASE BSE TSE PRION CALIFORNIA ‘confirmed’ Saturday,
August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
Saturday, September 12, 2015
The Canadian Management of Bovine Spongiform Encephalopathy in Historical
and Scientific Perspective, 1990-2014
>>>We propose that Canadian policies largely ignored the implicit
medical nature of BSE, treating it as a purely agricultural and veterinary
issue. In this way, policies to protect Canadians were often delayed and
incomplete, in a manner disturbingly reminiscent of Britain’s failed management
of BSE. Despite assurances to the contrary, it is premature to conclude that BSE
(and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of
Canada’s past: BSE remains very much an issue in Canada’s present.
<<<
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. ...
Wednesday, September 23, 2015
NIH Availability for Licensing AGENCY: [FR Doc. 2015–24117 Filed 9–22–15;
8:45 am] Detection and Discrimination of Classical and Atypical L-Type BSE
Strains by RT-QuIC
Tuesday, September 22, 2015
Host Determinants of Prion Strain Diversity Independent of Prion Protein
Genotype
*** 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.
Thursday, September 24, 2015
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE
Prion Testing
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
*** see past warnings about cwd from Shannon Tompkins of the Houston
Chronicle
*** see video and latest transmission studies and warnings below.
Thursday, September 10, 2015
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory
Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
FDA TSE PRION MAD COW CIRCUS AND TRAVELING ROAD SHOW (their words)
Saturday, September 19, 2015
*** An interview with Professor John Collinge: VIDEO Director of the MRC
Prion Unit Part of the Hayward Gallery's History Is Now ***
Saturday, March 21, 2015
*** Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence
Rates Increasing
*** HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL
CDC ***
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European ***
the patient had resided in Kuwait, Russia and Lebanon. The completed
investigation did not support the patient's having had extended travel to
European countries, including the United Kingdom, or travel to Saudi Arabia. The
specific overseas country where this patient’s infection occurred is less clear
largely because the investigation did not definitely link him to a country where
other known vCJD cases likely had been infected.
Sunday, December 14, 2014
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report ***
Thursday, July 30, 2015
Professor Lacey believes sporadic CJD itself originates from a cattle
infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is
much too high to be mere chance
Terry S. Singeltary Sr.
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