Thursday, October 22, 2015

Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened

Former Ag Secretary talks women in agriculture

 

By Jane Fyksen

 

As part of the U.S. Department of Agriculture’s recent women-in-agriculture focus, Ann Veneman shared her perspective as the first-and-only woman who has held the title of U.S. Secretary of Agriculture.

 

snip...

 

What has been your most memorable experience, either as Secretary of Agriculture or in any other official role?

 

snip...

 

Throughout the government, we had to reassess programs and processes to consider potential risks and vulnerabilities to help ensure the protection of our food supply. We had several other challenging crises during my tenure as Secretary of Agriculture, including the discovery of the first case of Mad Cow Disease or Bovine Spongiform Encephalopathy in 2003. I was honored to work beside so many dedicated, career USDA staff, who helped lead our agency successfully through the many policy initiatives we spearheaded.

 


 

a review of the mad cow debacle by USDA et al under Agriculture Secretary Ann Veneman ;

 

US SENATOR AND STAN THE MAN SLAM USDA ''DAMNING TESTIMONY''

 

Senator Michael Machado from California

 

''USDA does not know what's going on''.

 

''USDA is protecting the industry''.

 

''SHOULD the state of California step in''

 

Stanley Prusiner

 

''nobody has ever ask us to comment''

 

''they don't want us to comment''

 

''they never ask''

 

i tried to see Venemon, after Candian cow was discovered with BSE. went to see lyle. after talking with him... absolute ignorance... then thought I should see Venemon... it was clear his entire policy was to get cattle bonless beef prods across the border... nothing else mattered...

 

his aids confirmed this... 5 times i tried to see Venemon, never worked... eventually met with carl rove the political... he is the one that arranged meeting with Venemon... just trying to give you a sense of the distance... healh public safety...

 

was never contacted...

 

yes i believe that prions are bad to eat and you can die from them... END

 

Dr. Stan bashing Ann Veneman - 3 minutes

 


 

 Recall Authority and Mad Cow Disease: Is the Current System Good for Californians?

 

Tuesday, February 24, 2004

 

JOINT HEARING

 

AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND SELECT COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER, Chairs

 

ALL VIDEOS OF THIS HEARING HAVE BEEN REMOVED FROM THE WWW, LIKE IT NEVER HAPPENED...but we know different...TSS

 

-------- Original Message -------- Subject: Re: Congressman Henry Waxmans's Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW Date: Wed, 9 Jun 2004 16:48:31 -0500 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de References: 40A8CD52.1070308@wt.net

 

######## Bovine Spongiform Encephalopathy #########

 

USA BSE RED BOOK

 

October 1998

 

BSE Red Book 2.1-36

 

7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer will advise the READE(3 Director concerning laboratory capabilities and appropriate laboratory examinations to be conducted to provide needed results as rapidly as possible. This individual will assist with interpretation of results.

 

seems that if the 'enhanced BSE/TSE testing program' is to test some 400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.

 

BSE Red Book 2.1-39

 

7.6 Depopulation Procedures

 

Under no circumstances may BSE suspects be sent fo slaughhter or rendering.

 

snip...

 

BSE Red Book 2.1-40

 

7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed animal has moved to rendering or animal feed manufacturing. Field personel should arrange for the carcass to be transported to and examined by a qualified veterinary pathologist or field veterinary medical officer. After the pathologic examination has been completed and the necessary diagnostic specimens have been obtained, field personnel should arrange for disposal of the carcass. Before a method of disposal is selected, there are many factors that must be considered, and often other State and Federal agencies must be consulted. The environmental and legal impacts of the operation must be considered. Upon recommendation of the State or Federal agencies, VS may consider other disposal methods.

 

snip...

 

7.7.3 Rendering Because BSE is spread by rendered animal protein, BSE-suspect and confirmed carcasses must not be rendered, unless the rendered material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or carcasses have moved to rendering or animal feed manufacturing.

 

snip...

 

7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be rendered. Producers, feed mills, and rendering establishments should adhere to U.S. State and local rendering policies and FDA regulations concerning the feeding of rendered animal protein to ruminants.

 

TSS

 

Terry S. Singeltary Sr. wrote:

 

 ######## Bovine Spongiform Encephalopathy #########

 

ONE HUNDRED EIGHTH CONGRESS CONGRESS OF THE UNITED STATES HOUSE OF REPRESENTATIVES COMMITTEE ON GOVERNMENT REFORM 2157 RAYBURN HOUSE OFFICE BUILDING WASHINGTON, DC 20515-6143

 

> www.house.gov/reform > > May 13, 2004 > > The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400 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 symptoms for bovine spongiform encephalopathy (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. Effective surveillance and control of BSE in the United States require a reliable system for ensuring that potentially infected cows are tested and that no infected materials enter the animal or human food supply.

 

Under USDA regulations, any cow that exhibits signs of central nervous system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS) personnel at the plant.1 According to a 1997 Animal and Plant Health Inspection Service (APHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "[i]t is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."3

 

The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

1 9 CFR 309.4.

 

2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or Investigation of Adult Cattle With Clinical Signs of Central Nervous System (CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine Spongiform Encephalopathy (BSE) (June 11,1997). 3 Id.

 

4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4, 2004).

 

The Honorable Ann M. Veneman May 13,2004 Page 2

 

This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:

 

Based on information provided by the Food Safety and Inspection Service (FSIS), the number of adult cattle (2 years of age or greater) condemned at slaughter due to CNS signs is much greater than the number whose brains have been collected for testing.6

 

Despite recognizing the problem more than six years ago, however, USDA apparently did not adopt procedures to ensure that these samples would be collected. In March 2004, the Government Reform Committee asked USDA to provide, for each of the last five years, the number of BSE tests performed on cattle condemned by FSIS inspectors on the basis of CNS symptoms.7 In response, USDA provided information on the numbers of cattle condemned for CNS symptoms by FSIS, but replied that "[i]t is not possible to determine, from the data we currently collect, how many of these cattle were tested by APHIS for BSE."8 It thus appears that not only does USDA not routinely track the gap between the number of condemned and tested cattle, but that USDA could not even calculate this gap when requested to do so by Congress.

 

There also appears to be a lack of clarity regarding the disposition of cattle with CNS symptoms while BSE tests are pending. In the past, companies could send cattle awaiting BSE testing results for rendering, which would allow their remains to be used in feed for animals other than ruminants, such as pigs and chickens. After this incident, both FDA and USDA policy appear to have changed — in different ways.

 

USDA policy has apparently shifted to requesting that companies not send cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS states, "it is requested — though not required — that [the cattle] not go to inedible rendering until the sample comes

 

USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating Place (May 5, 2004).

 

6 USDA APHIS, supra note 2.

 

7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of Agriculture Ann M. Veneman (Mar. 8, 2004).

 

8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1 (Mar. 22- 2004).

 

The Honorable Ann M. Veneman May 13,2004 Page 3

 

back negative."9 There is no explanation of why this course of action is requested, but not required.

 

FDA policy also appears to have shifted towards prohibiting the use of carcasses of cattle with CNS symptoms and indeterminate BSE status in certain types of animal feed. On April 30, FDA requested that the rendering company holding the remains of the Texas cow either destroy them or use them exclusively in swine feed. m the case that the remains are included in swine feed, FDA "will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs."10

 

Any confusion over what to do with cattle condemned for CNS symptoms awaiting testing for BSE seems unnecessary. The obvious approach is to require companies either to destroy the carcasses or hold them until test results become available. Such a policy would avoid any need for complicated traceback procedures after the discovery of a positive result. According to the information provided to the Committee by USDA, the FSIS has condemned only 200 to 250 cows per year because of signs of central nervous system damage." Mandating the destruction or holding of their carcasses would have minimal economic impact.

 

The experience with the BSE-infected cow in Washington State illustrates the prudence of waiting for the results of BSE tests. Prior to December 2003, USDA permitted cattle that were sampled as part of the BSE surveillance program to enter commerce even while BSE tests were pending. As a result, when the BSE-infected cow was discovered, it had already entered the food supply. This led to a complicated and partially successful traceback procedure in which hundreds of thousands of pounds of beef had to be destroyed. Because of this debacle, USDA quickly developed a new policy to require holding all carcasses from the human food chain during BSE testing.

 

I appreciate that you have taken steps to enhance the safety of the U.S. food supply since the discovery of BSE in the United States. I urge you to consider the lessons of this latest

 

9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary Services, and William Smith, Assistant Administrator, Office of Field Operations, Food Safety and Inspection Service, to VSMT, Regional Directors, Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).

 

10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20, 2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).

 

11 The yearly totals of FSIS antemortem CNS condemnation for all adult cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The database for 2003 had not yet closed.

 

The Honorable Ann M. Veneman May 13,2004 Page 4

 

incident. USDA should develop a process that ensures the tracking of cattle condemned for CNS signs and should institute a policy requiring all carcasses with pending BSE tests to be destroyed or held. If there are any statutory barriers to these steps, please do not hesitate to let me know.

 

Sincerely,

 

XXXXX X. XXXXXX

 

Henry A. Waxman

 

Ranking Minority Member

 

Congressman Henry Waxmans's Letter to the Honorable Ann Veneman

 


 

TSS

 


 

*** Qualitative Analysis of BSE Risk Factors in the United States

 

February 13, 2000 at 3:37 pm PST (BSE red book)

 


 

Tuesday, July 14, 2009 U.S.

 

*** Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book

 

Date: February 14, 2000 at 8:56 am PST

 

WHERE did we go wrong $$$

 


 

*********-------- Original Message --------**********

 

Subject: re-USDA's surveillance plan for BSE aka mad cow disease

 

Date: Mon, 02 May 2005 16:59:07 -0500

 

From: "Terry S. Singeltary Sr."

 

To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us

 

Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............

 

snip...

 

There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...

 

Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx

 

Date: June 14, 2005 at 1:46 pm PST In

 

Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:

 

Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS

 

MAD COW IN TEXAS NOVEMBER 2004. ...TSS

 

-------- Original Message --------

 

Director, Public Information Carla Everett ceverett@tahc.state.tx.us

 

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 for something, 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: ...sniptss

 

our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by 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.>>>>>>

 

==========================

 

-------- Original Message --------

 

Director, Public Information Carla Everett ceverett@tahc.state.tx.us

 

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

 

==============================

 


 


 

2004, highly suspect stumbling and staggering mad cow reported, however, NO TESTING DONE, ON ORDERS FROM AUSTIN $

 

May 4, 2004

 

Statement on Texas Cow With Central Nervous System Symptoms

 

On Friday, April 30th, 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.

 

Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison)...

 


 

USDA regulations, any cow that exhibits signs of central nervous system (CNS)

 

According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."

 

The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

May 13,2004

 

Page 2

 

snip...

 

The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:

 


 

USDA did not test possible mad cows

 

By Steve Mitchell

 

United Press International

 

Published 6/8/2004 9:30 PM

 

WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims ittested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.

 


 


 

""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

 

THIS WAS DONE FOR A REASON!

 

THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

 

TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS CONFIRMED

 

THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP

 

JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED

 

OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7 MONTHS LATER

 

TEXAS MAD COW

 

THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i confirmed this case 7 months earlier to the TAHC, and then, only after i contacted the Honorable Phyllis Fong and after an act of Congress, this animal was finally confirmed ;

 

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.

 


 

Executive Summary In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.

 

snip...

 

Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having received an animal of interest. The herd was placed under hold order on 7/27/05. The herd inventory was conducted on 7/28/05. The animal of interest was not present within the herd, and the hold order was released on 7/28/05. The person who thought he sold the animal to the owner of Trace Herd 3 had no records and could not remember who else he might have sold the cow to. Additionally, a search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.

 

Trace Herd 4 The owner of Trace Herd 4 was identified as having received one of the COI through an order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were examined individually by both State and Federal personnel for all man-made identification and brands. The animal of interest was not present within the herd. Several animals were reported to have died in the herd sometime after they arrived on the premises in April 2005. A final search of GDB records yielded no further results on the eartag of interest at either subsequent market sale or slaughter. With all leads having been exhausted, this animal of interest has been classified as untraceable. The hold order on Trace Herd 4 was released on 8/23/05.

 

Trace Herd 5 The owner of Trace Herd 5 was identified as having received two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple pastures. During the course of the herd inventory, the owner located records that indicated that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was subsequently found alive. Upon completion of the herd inventory, the other animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.

 

Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having received an animal of interest and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on two pastures. A herd inventory was conducted and the animal of interest was not present within the herd. The owner of Trace Herd 6 had very limited records and was unable to provide further information on where the cow might have gone after he purchased her from the livestock market. A search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. Additionally, many of the animals presented for sale by the owner of the herd had been re-tagged at the market effectually losing the traceability of the history of that animal prior to re-tagging. The animal of interest traced to this herd was classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.

 

Trace Herd 7 The owner of Trace Herd 7 was identified as having received an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple pastures in multiple parts of the State, including a unit kept on an island. The island location is a particularly rough place to keep cattle and the owner claimed to have lost 22 head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the animal of interest was not found present within Trace Herd 7. A GDB search of all recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to locate the identification tag of the animal of interest. The cow was subsequently classified as untraceable. It is quite possible though that she may have died within the herd, especially if she belonged to the island unit. The hold order on Trace Herd 7 was released on 8/8/05.

 


 

*** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***

 


 

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. ...

 


 

Tuesday, November 02, 2010

 

*** BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

 


 

THE SECRET MAD COW POSITIVE TEST, THAT WAS COVERED UP

 

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...

 

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

 


 

***********2015*********

 

spontaneous atypical BSE ???

 

don’t let anyone fool you. spontaneous TSE prion disease is a hoax in natural cases, never proven.

 

all one has to do is look at France. France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow disease in numbers they could find any with, after those atypical BSE cases started showing up. shut down the testing to numbers set up by OIE that are so low, you could only by accident find a case of BSE aka mad cow disease. and this brilliant idea by the WHO et al, to change the name of mad cow disease, thinking that might change things is preposterous. it’s all about money now folks, when the OIE, USDA and everyone else went along and made the TSE prion disease aka mad cow type disease a legal trading commodity by the BSE MRR policy, I would say everyone bit off more then they can chew, and they will just have to digest those TSE Prions coming from North America, and like it, and just prey you don’t get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE prion disease in the decades to come, and or pass it to some other poor soul via the iatrogenic medical surgical tissue friendly fire mode of transmission i.e. second hand transmission. it’s real folks, just not documented much, due to lack of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is tracked down and documented, and put into the academic and public domain, which very seldom happens. ...

 

As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.

 


 

FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$

 

so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

19 May 2010 at 21:21 GMT

 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

snip...see link ;

 

Saturday, May 09, 2015

 

Expression of genes involved in the T cell signalling pathway in circulating immune cells of cattle 24 months following oral challenge with Bovine Amyloidotic Spongiform Encephalopathy (BASE)

 


 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 


 

*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***

 

THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.

 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. ***We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. ***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

===============

 

***thus questioning the origin of human sporadic cases...

 

===============

 


 

***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 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.

 

==========================================

 

P.108: Successful oral challenge of adult cattle with classical BSE

 

Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada

 

Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, 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. Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.

 


 

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

 


 

Thursday, July 24, 2014

 

*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations

 


 

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

 


 

IBNC Tauopathy or TSE Prion disease, it appears, no one is sure

 

Singeltary et al

 

03 Jul 2015 at 16:53 GMT

 


 

Wednesday, July 15, 2015 *** Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?

 


 

THE last documented mad cow in the USA was in California, was an Atypical BSE BASE TSE prion aka mad cow type disease, the most lethal strain documented to date, and of which has now been linked to sporadic CJD. we have not heard much about BSE aka mad cow disease, due to the Governments covering up mad cow disease. all one as to do is look at the BSE MRR, which is a doctrine for the legal trading of the Transmissible Spongiform Encephalopathy TSE prion disease around the globe. you can thank the OIE, USDA, WTO, just to name a few off the top of my head. it's all about trade folks, nothing else matters, when it comes to the TSE prion disease, due to the long incubation period, and no trace back efforts, even though that once clinical, all of the tse prion disease are fatal. then the federal governments continue to ignore more updated and ongoing sound science, peer review science, that indeed sporadic cjd is linked to not only atypical BSE mad cow disease, but also to atypical scrapie i.e the Nor-98 and typical scrapie as well. or the fact that the 1997 ruminant feed ban aka mad cow feed ban was and still is a terrible failure. but they don’t print that. ...just saying. now, you think I am crazy for saying this....now think back to asbestos and tobacco, and how those two man made killers were covered up for 100 years as cancer causing and killers, by our fine federal friends. for your fileS, use as you wish, but it’s the truth as I have come to know it from daily research of all said science, since my mothers demise to the heidenhain variant of creutzfeldt jakob disease i.e. hvcjd. ...just made a promise to mom, never forget, and never let them forget. ...kind regards, terry

 

Sunday, October 18, 2015

 

World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research

 


 

Thursday, May 28, 2015

 

OIE cuts six European countries' mad cow risk level, while increasing risk factors for humans to the BSE TSE PRION DISEASE around the globe

 


 

Wednesday, May 27, 2015

 

BSE Case Associated with Prion Protein Gene Mutation

 


 

Wednesday, July 15, 2015

 

Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?

 


 

Thursday, October 1, 2015

 

H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation

 

Master Obi-Wan Kenobi, Kemosabe...THIS IS NOT GOOD GOOSE!...grasshopper...tonto...tss

 


 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.

 

*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

see page 176 of 201 pages...tss

 


 

Thursday, July 24, 2014

 

*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations

 


 

Saturday, 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 ***

 


 

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

 


 

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. <<<

 


 

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

 


 

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, October 3, 2015

 

Wales Welsh Government Written Statement - Isolated case of Classical Bovine spongiform encephalopathy detected in deceased bovine

 


 

Wednesday, October 21, 2015

 

*** TAHC CHRONIC WASTING DISEASE CWD TSE PRION REPORT OCTOBER 2015 ***

 


 

cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?

 

Sunday, August 23, 2015

 

TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas

 

from the other side of the fence... today’s Singeltary Sunday School class ‘thinking outside of the box, God’s Wrath’ at the bottom. ...tss

 


 

TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS) BURNS

 

Tuesday, August 11, 2015

 

Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker

 


 

Wednesday, March 18, 2015

 

*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

 


 

Wednesday, March 25, 2015

 

*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015

 


 

Wednesday, July 01, 2015

 

*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer

 


 

Tuesday, July 21, 2015

 

*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***

 


 

Thursday, August 06, 2015

 

*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY

 


 

Friday, August 07, 2015

 

*** Texas CWD Captive, and then there were 4 ?

 


 

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. ...terry

 


 

Saturday, October 03, 2015

 

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

 


 

Friday, October 09, 2015

 

Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015

 


 

Monday, August 24, 2015

 

Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD

 


 

Sunday, October 18, 2015

 

*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015

 


 

Monday, August 31, 2015

 

Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date

 


 

Saturday, September 05, 2015

 

Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for Money, while mad deer and elk disease silently spreads

 


 

Friday, August 14, 2015

 

*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation

 


 

Friday, August 14, 2015

 

Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015

 


 

Tuesday, September 22, 2015

 

*** Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype

 


 

Friday, August 28, 2015

 

Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection

 


 


 

 Thursday, March 29, 2012

 

*** atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 

P03.141

 

Aspects of the Cerebellar Neuropathology in Nor98

 

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

 

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 


 

PR-26

 

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS

 

R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway

 

Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.

 

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.

 

119

 


 

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

 

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations

 

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

 

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

 

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 

Authors

 

Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.

 

Content

 

Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

 

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

 

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

 

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

 

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

 

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

 

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

 


 

Friday, February 11, 2011

 

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

 


 

Monday, December 14, 2009

 

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types

 

(hmmm, this is getting interesting now...TSS)

 

Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,

 

see also ;

 

All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

 


 

Saturday, July 6, 2013

 

Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy

 

Research Article

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 

Authors

 

Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.

 

Content

 

Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

 

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

 

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

 

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

 

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

 

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

 

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

 


 

Friday, February 11, 2011

 

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

 


 

Saturday, August 14, 2010

 

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

 

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

 


 

***The successful oral transmission of C.J.D. and scrapie to primates (Gibbs et al., 1980) and the close resemblance between the properties of the transmissible agent in the two conditions (Gibbs and Gajdusek, 1976) has raised the possibility that the human disease is contracted from sheep. No direct evidence is available and the concept is based on inference and interesting but unconvincing anecdotes

 

(Alter et al., 1971; Lo Russo et al., 1980; Kamin and Patten, 1984). The patient discovered in this study who had never been known to eat meat suggests that eating scrapie infected meat cannot be the only source of C.J.D. in man. C.J.D. occurs in countries in which natural scrapie has not been observed (Galvez et al., 1980; Kondo and Kuroiwa, 1982) and no relationship was discovered in France (Chatelain et al., 1981) between the geographic distribution of scrapie and the incidence of C.J.D. A similar investigation could not be carried out in England and Wales as notification of scrapie to the Ministry of Agriculture is inconsistent and sheep farmers often destroy affected animals without seeking veterinary advice for fear of financial loss.

 

A detailed residential history was obtained in cases and controls. Although over-representation of cases was discovered in certain areas, similar but distinct areas of previous residence common to an apparent excess of controls was discovered. If C.J.D. does have a prolonged incubation period extending to decades the detailed study of residential history may, however, establish potential contact between individual cases which would be otherwise undetectable. The detailed study of individual cases in the prospective study has revealed the possibility of tenuous but extraordinarily coincidental contact between patients.

 

This may only be a reflection of intensive investigation, but if C.J.D. is transmitted by relatively minor surgical or dental procedures many years prior to death it is only by the systematic study of individual cases that potential cross-contamination may be discovered.

 

***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent.

 

snip...see full text here;

 


 

why do we not want to do TSE transmission studies on chimpanzees $

 

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

snip...

 

R. BRADLEY

 


 

1: J Infect Dis 1980 Aug;142(2):205-8

 

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

 

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

 

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

 

snip...

 

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

 

PMID: 6997404

 


 

Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

 

Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

 

snip...

 

76/10.12/4.6

 


 

Nature. 1972 Mar 10;236(5341):73-4.

 

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

 

Gibbs CJ Jr, Gajdusek DC.

 

Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

 

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

 

C. J. GIBBS jun. & D. C. GAJDUSEK

 

National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

 

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

 


 


 


 

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, November 23, 2014

 

*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European ***

 


 

*** ANOTHER UPDATE FOR THE HISTORY OF CJD IN TEXAS, THE CJD CLUSTER BACK IN 1997, AND THE 38 YEAR OLD WOMEN WHOM HAD WORKED FOR TYSON, SLAUGHTERING CATTLE, THAT DIED WITH CJD...TSS ***

 

CJD NE TEXAS CLUSTER

 

Creutzfeldt-Jakob Disease in Northeast Texas

 

J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated. http://www.jifsan.umd.edu/tse/Rawlings.htm

 

Monday, March 29, 2010

 

CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER

 

URGENT, PLEASE NOTE ;

 

>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<

 

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.

 

She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.- Physician Discharge Summary, Parkland Hospital, Dallas Texas Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence. She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers. The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.

 


 

Monday, March 29, 2010

 

CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER

 

URGENT, PLEASE NOTE ;

 

>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<

 

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.

 


 

Singeltary family experience with CJD Listserve 22 May 98

 

Hello, my name is Terry S. Singeltary Sr. and on 12-14-97 my mother died of heidenhan variant CJD, she died a very hidious death. Next, on 12-14-96 exactly one year earlier,my neighbors' mother died from C.J.D. Ii have autopsies to confirm both cases.not to long after my mother had passed away,my neighbor called me and said that I needed to see something. He had been going through a box that he had come across of his mothers. Inside was a bottle of nutritional supplements called IPLEX; INGREDIANTS;VACUUM DRIED BOVINE BRAIN,BONE MEAL,BOVINE EYE,VEAL BONE,BOVINE LIVER POWDER,BOVINE ADRENAL,VACUUM DRIED BOVINE KIDNEY,AND VACUUM DRIED PORCINE STOMACH, it's a cow in a pill. Now this woman taking these pills,died of C.J.D.there was a big article in the Galveston Daily News about all of this. I called the Texas Dept. Of Health and they came and got the pills the next day. Julie Rawlings at the texas dept. of health told me last week that the manufacturer has clammed up on them and will not cooperate anymore. They are referring all matters to their lawyers now.how can this be? Why doesn't the federal government intervEne?

 

Since the story came out in the galv. news on april 27,1998.a girl called me and told me of her father dying in late 94 or early 95 of C.J.D. in galveston. She told me that my mothers doctor was also her fathers doctor.now my mothers doctor would always mention the OTHER CASE but that's as far as it went.NOW i know why,her father was a BUTCHER AT A MEAT MARKET IN GALVESTON UNTIL HE RETIRED.

 

Makes me wonder? Did mom ever eat any beef that had come from that meat market in the last 30 or 40 years? MADCOW is here and you can call it whatever you want to. I saw it, my mother died from it. At times she would jerk so bad it would take 3 of us to hold her down.10 weeks start to finish,and she was gone.this disease that they claim is a different disease in younger folks (nvcjd) is the same damn thing. Just because it last longer and the plaques are a little more extreme,could it not be just a more extreme case of C.J.D. any young person with any disease will last longer than a older person with the same disease, because their body and organs are much younger and healthier.

 

The manufacturer of IPLEX is Standard Process Inc., Palmyra, Wisconsin.1-800-558-8740. I hope you find some interest in this.if you need more details,please don't hesitate to contact me."

 

With thanks,

 

Terry S. Singeltary

 

Texas cluster web site 21 May 98 Mark V. Gregg 512-458-7677 fax 512-458-7616 Director, Public Health Professional Education Texas Department of Health 1100 West 49th Street T-803 Austin, Texas 78756

 

"We've developed a CJD Web page here at the Texas Department of Health. In addition to some general information, the page links to the CDC's CJD page as well as a 1996 issue of our biweekly morbidity and mortality newsletter, the Disease Prevention News, which is also available on the Web. Our Infectious Disease Epidemiology and Surveillance (IDEAS) Division is currently investigating what we believe to be a cluster of CJD in a small area in East Texas. The Division's number is on the Web page if you wanted to follow up with specifics."

 


 


 

North American Equity Research

 

New York

 

13 January 2004

 

BSE (Mad Cow) Update:

 

Do Reports of sCJD Clusters Matter?

 

SNIP...SEE FULL TEXT ;

 


 

GLOBAL CLUSTERS OF CJD

 


 

Tuesday, July 29, 2008

 

Heidenhain Variant Creutzfeldt Jakob Disease Case Report

 

snip...

 

Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'

 

DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785

 

FAX COVER SHEET

 

DATE: 4-23-98

 

TO: Mr. Terry Singeltary @ -------

 

FROM: Gerald Campbell

 

FAX: (409) 772-5315 PHONE: (409) 772-2881

 

Number of Pages (including cover sheet):

 

Message:

 

*CONFIDENTIALITY NOTICE*

 

This document accompanying this transmission contains confidential information belonging to the sender that is legally privileged. This information is intended only for the use of the individual or entry names above. If you are not the intended recipient, you are hereby notified that any disclosure, copying distribution, or the taking of any action in reliances on the contents of this telefaxed information is strictly prohibited. If you received this telefax in error, please notify us by telephone immediately to arrange for return of the original documents. -------------------------- Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Admitting Race: C

 

Attending Dr.: Date / Time Admitted : 12/14/97 1228 Copies to:

 

UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report

 

FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858

 

Autopsy NO.: AU-97-00435

 

AUTOPSY INFORMATION: Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00 Pathologist/Resident: Pencil/Fernandez Service: Private Restriction: Brain only

 

FINAL AUTOPSY DIAGNOSIS

 

I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

 

snip...see full text ;

 


 

Mad cow disease: Could it be here?

 

Man's stubborn crusade attracts experts' notice By Carol Christian | August 5, 2001

 


 

TSS

 

From: Terry S. Singeltary Sr. Sent: Monday, June 02, 2014 9:09 PM To: BSE-L@LISTS.AEGEE.ORG Cc: CJD-L ; CJDVOICE CJDVOICE ; bloodcjd bloodcjd Subject: Re: [BSE-L] Texas: Variant Creutzfeldt-Jakob Disease CONFIRMED death aka mad cow disease confirmed, infection likely occurred overseas

 

remember what deep throat told me long ago ;

 

DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)

 

The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why????than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....

 

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!

 

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...

 

Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"

 

again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

 

You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)

 

END...TSS

 

Date: Tue, 9 Jan 2001 16:49:00 -0800

 

From: "Terry S. Singeltary Sr."

 

Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de

 

######### Bovine Spongiform Encephalopathy #########

 


 

we get them young cases of tse prion disease in Texas, that is not related to anything $$$ money and politics will buy anything, especially junk science... sporadic ffi and sporadic gss ;

 

NOT THIS CASE !!! but another one a while back in Texas...see ;

 

We report a case of a 33-year-old female who died of a prion disease for whom the diagnosis of sFI or FFI was not considered clinically. Following death of this patient, an interview with a close family member indicated the patient's illness included a major change in her sleep pattern, corroborating the reported autopsy diagnosis of sFI.

 


 

sporadic FFI or nvCJD Texas style ???

 


 

Creutzfeldt-Jakob Disease Surveillance in Texas

 


 

Sunday, July 11, 2010

 

CJD or prion disease 2 CASES McLennan County Texas population 230,213 both cases in their 40s

 


 


 

*** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***

 


 

Monday, November 3, 2014

 

USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014

 

National Prion Disease Pathology Surveillance Center Cases Examined1 (October 7, 2014)

 

***6 Includes 11 cases in which the diagnosis is pending, and 19 inconclusive cases;

 

***7 Includes 12 (11 from 2014) cases with type determination pending in which the diagnosis of vCJD has been excluded.

 

***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob disease (sCJD),

 

***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)

 

***and 21 cases of sporadic Fatal Insomnia (sFI).

 


 

Thursday, January 15, 2015

 

*** 41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report

 


 

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type disease

 

what is CJD ? just ask USDA inc., and the OIE, they are still feeding the public and the media industry fed junk science that is 30 years old.

 

why doesn’t some of you try reading the facts, instead of rubber stamping everything the USDA inc says.

 

sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and there is much concern now for CWD and risk factor for humans.

 

My sincere condolences to the family and friends of the House Speaker Becky Lockhart. I am deeply saddened hear this.

 

with that said, with great respect, I must ask each and every one of you Politicians that are so deeply saddened to hear of this needless death of the Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am seriously going to ask you all this...I have been diplomatic for about 17 years and it has got no where. people are still dying. so, are you all stupid or what??? how many more need to die ??? how much is global trade of beef and other meat products that are not tested for the TSE prion disease, how much and how many bodies is this market worth?

 

Saturday, January 17, 2015

 

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease

 


 

*** 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 ***

 


 

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 ***

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

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)

 


 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

 


 

Friday, October 09, 2015

 

An alarming presentation level II trauma center of Creutzfeldt-Jakob disease following a self-inflicted gunshot wound to the head

 


 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

 

Terry S. Singeltary, Sr Bacliff, Tex

 

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.

 


 

26 March 2003

 

Terry S. Singeltary, retired (medically) CJD WATCH

 

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

 


 

2 January 2000

 

British Medical Journal

 

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

 


 

15 November 1999

 

British Medical Journal

 

vCJD in the USA * BSE in U.S.

 


 

The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI

 

Tracking spongiform encephalopathies in North America

 

Original

 

Xavier Bosch

 

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...

 


 

Suspect symptoms

 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01

 

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...

 


 

just made a promise to mom DOD 12/14/97 confirmed hvCJD. never forget, and never let them forget. ...

 

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net

 

Galveston Bay, on the bottom...

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