Sunday, September 27, 2015

TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES

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

 
J Food Prot. 2015 Oct;78(10):1861-9. doi: 10.4315/0362-028X.JFP-15-157.

 
Evaluation of Selected Nutrients and Contaminants in Distillers Grains from Ethanol Production in Texas.

 
Lee KM1, Herrman TJ2. Author information 1Office of the Texas State Chemist, Texas A&M AgriLife Research, Texas A&M University System, College Station, Texas 77841, USA. kml@otsc.tamu.edu. 2Office of the Texas State Chemist, Texas A&M AgriLife Research, Texas A&M University System, College Station, Texas 77841, USA.

 
Abstract

 
This study evaluated distillers grain (DG) by-products produced in different ethanol plants and supplemented in animal diets in Texas, based on samples analyzed from 2008 to 2014. The samples were assessed for concentration, occurrence, and prevalence of selected nutrients and contaminants. Protein and sulfur contents of DG were largely different between corn and sorghum by-products as well as wet distillers grain with solubles and dry distillers grain with solubles (DDGS), indicating a significant effect of grain feedstock and dry-grind process stream on DG composition and quality. Salmonella was isolated in 4 DDGS samples out of a total of 157 DG samples, a percentage (2.5%) that is much lower than the percentage of Salmonella-positive samples found in other feed samples analyzed during the same period. A small amount of virginiamycin residue was found in 24 corn DDGS, 1 corn wet distillers grain with solubles, and 2 sorghum DDGS samples out of 242 samples in total. 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. The concentrations of aflatoxin and fumonisin DG by-products averaged 3.4 μg/kg and 0.7 mg/kg, respectively. Among contaminated corn DG samples, five DDGS samples for aflatoxin contained a higher concentration than the U.S. Food and Drug Administration action level for use in animal feed, whereas no sample for fumonisin was found above the action level. The study results raised some important issues associated with the quality and use of DG by-products, suggesting several approaches and strategies for their effective and safe use as a feed ingredient to promote animal and human health and welfare.

 
PMID: 26408135 [PubMed - in process]

 
http://www.foodprotection.org/publications/journal-of-food-protection/

 
I don’t guess I am smart enough to have access to this journal, but found this abstract, and found this study of Selected Nutrients and Contaminants in Distillers Grains from Ethanol Production in Texas, and the fact they found BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES in 2015, I find this disturbing, but does not surprise me. ($$$) ...terry


UPDATED CORRECTION BY AUTHOR AND EMAIL SENT TO ME ;


From: Kyung-Min Lee
Sent: Thursday, October 01, 2015 1:39 PM
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
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
 
 
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

 
a review of the TSE prion aka mad cow type disease in Texas, what I call the Texas mad cow two step, or the mad cow TSE Prion follies of the TAHC $$$

 

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.