Friday, January 29, 2010

14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

----- Original Message -----
From: Terry S. Singeltary Sr.
Sent: Friday, January 29, 2010 3:23 PM
Subject: 14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

18.173 page 189

Experimental Challenge of Cattle with H-type and L-type Atypical BSE

A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.

From: xxxx
To: Terry Singeltary
Sent: Saturday, December 05, 2009 9:09 AM
Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'

Your preliminary abstract number: 670

Dear Mr. Singeltary,

On behalf of the Scientific Committee, I am pleased to inform you that your abstract

'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'

WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.

Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.

Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Author: T. Singeltary; Bacliff, TX/US

Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange

This abstract has been ACCEPTED.

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Authors: T. Singeltary; Bacliff, TX/US

Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Body: Background

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.


12 years independent research of available data


I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.

I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion

see page 114 :

Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009


I ask Professor Kong ;

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

Professor Kong reply ;


''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.

Thanks for your interest.''

Best regards,

Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA


I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS


MARCH 26, 2003

Send Post-Publication Peer Review to journal:

Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

Newsdesk 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

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 disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)—the relative of mad cow disease seen among deer and elk in the USA. Although his feverish…

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. FREE FULL TEXT

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.


BY Philip Yam

Yam Philip Yam News Editor Scientific American

Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.


Laying Odds

Are prion diseases more prevalent than we thought?

Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn’t think bovine spongiform encephalopathy was a zoonosis—an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?

Revisiting Sporadic CJD

It’s not hard to get Terry Singeltary going. “I have my conspiracy theories,” admitted the 49-year-old Texan.1 Singeltary is probably the nation’s most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union’s Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.

Singeltary has similar inclinations. ...

DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link auf diesen Artikel im Archiv:

"Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.

Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich verpflichteten sich fünf Unternehmen, darunter Branchenführer wie GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus unverdächtigem Material herzustellen.

"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...

Suspect symptoms

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

28 Mar 01

Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.

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.

Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.

Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.

As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.

"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.

But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.

People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.

But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."

There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.

Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.

Sunday, August 09, 2009

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

Tuesday, August 18, 2009

BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009

Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

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

Greetings List Members,

I was lucky enough to sit in on this BSE conference call today and even managed to ask a question. that is when the trouble started.

I submitted a version of my notes to Sandra Blakeslee of the New York Times, whom seemed very upset, and rightly so.

"They tell me it is a closed meeting and they will release whatever information they deem fit. Rather infuriating."

and i would have been doing just fine, until i asked my question. i was surprised my time to ask a question so quick.

(understand, these are taken from my notes for now. the spelling of names and such could be off.)

[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.

[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]

[host Richard] could you repeat the question?

[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[not sure whom ask this] what group are you with?

[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.

[not sure who is speaking] could you please disconnect Mr. Singeltary

[TSS] you are not going to answer my question?

[not sure whom speaking] NO

from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;

[unknown woman] what group are you with?

[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?

at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.

IF i were another Country, I would take heed to my notes, BUT PLEASE do not depend on them. ask for transcript from;

RBARNS@ORA.FDA.GOV 301-827-6906

he would be glad to give you one ;-)

Rockville Maryland, Richard Barns Host

BSE issues in the U.S., How they were labelling ruminant feed? Revising issues.

The conference opened up with the explaining of the U.K. BSE epidemic winding down with about 30 cases a week.

although new cases in other countries were now appearing.

Look at Germany whom said NO BSE and now have BSE.

BSE increasing across Europe.

Because of Temporary Ban on certain rendered product, heightened interest in U.S.

A recent statement in Washington Post, said the New Administration (old GW) has a list of issues. BSE is one of the issues.

BSE Risk is still low, minimal in U.S. with a greater interest in MBM not to enter U.S.

HOWEVER, if BSE were to enter the U.S. it would be economically disastrous to the render, feed, cattle, industries, and for human health.

(human health-they just threw that in cause i was listening. I will now jot down some figures in which they told you, 'no need to write them down'. just hope i have them correct. hmmm, maybe i hope i don't ???)

80% inspection of rendering

*Problem-Complete coverage of rendering HAS NOT occurred.

sizeable number of 1st time FAILED INITIAL INSPECTION, have not been reinspected (70% to 80%).

Compliance critical, Compliance poor in U.K. and other European Firms.

Gloria Dunason Major Assignment 1998 goal TOTAL compliance. This _did not_ occur. Mixed level of compliance, depending on firm.

Rendering FDA license and NON FDA license

system in place for home rendering & feed 76% in compliance 79% cross contamination 21% DID NOT have system 92% record keeping less than 60% total compliance

279 inspectors 185 handling prohibited materials

Renderer at top of pyramid, significant part of compliance. 84% compliance

failed to have caution statement render 72% compliance & cross contamination caution statement on feed, 'DO NOT FEED TO CATTLE'


1240 FDA license feed mills 846 inspected

"close to 400 feed mills have not been inspected"

80% compliance for feed.

10% don't have system.

NON-FDA licensed mills There is NO inventory on non licensed mills. approximately 6000 to 8000 Firms ??? 4,344 ever inspected. "FDA does not have a lot of experience with"

40% do NOT have caution statement 'DO NOT FEED'.

74% Commingling compliance

"This industry needs a lot of work and only half gotten to"

"700 Firms that were falitive, and need to be re-inspected, in addition to the 8,000 Firms."

Quote to do BSE inspection in 19 states by end of January or 30 days, and other states 60 days. to change feed status??? Contract check and ask questions and pass info.

At this time, we will take questions.

[I was about the third or fourth to ask question. then all B.S.eee broke loose, and i lost my train of thought for a few minutes. picked back up here]

someone asking about nutritional supplements and sourcing, did not get name. something about inspectors not knowing of BSE risk??? the conference person assuring that Steve Follum? and the TSE advisory Committee were handling that.

Some other Dr. Vet, whom were asking questions that did not know what to do???

[Dennis Wilson] California Food Agr. Imports, are they looking at imports?

[Conference person] they are looking at imports, FDA issued imports Bulletin.

[Linda Singeltary ??? this was a another phone in question, not related i don't think] Why do we have non-licensed facilities?

(conference person) other feed mills do not handle as potent drugs???

Dennis Blank, Ken Jackson licensed 400 non FDA 4400 inspected of a total of 6000 to 8000,

(they really don't know how many non licensed Firms in U.S. they guess 6000 to 8000??? TSS)

Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not'

Warren-Maryland Dept. Agr. Prudent to re-inspect after 3 years. concerned of Firms that have changed owners.



############ ############


Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...
Date: Thu, 11 Jan 2001 22:02:47 -0700
From: "Sandy Blakeslee"
To: "Terry S. Singeltary Sr." References: 1

Hi terry -- thanks for all your help. I know it made a difference with the FDA getting out that release.

----- Original Message -----
From: "Terry S. Singeltary Sr."
To: Sent: Thursday, January 11, 2001 2:06 PM
Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...

hi sandy,

From the New York Times, January 11, 2001

Many Makers of Feed Fail to Heed Rules on Mad Cow Disease By SANDRA BLAKESLEE

Large numbers of companies involved in manufacturing animal feed are not complying with regulations meant to prevent the emergence and spread of mad cow disease in the United States, the Food and Drug Administration said yesterday.

The widespread failure of companies to follow the regulations, adopted in August 1997, does not mean that the American food supply is unsafe, Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at the F.D.A., said in an interview.

But much more needs to be done to ensure that mad cow disease does not arise in this country, Dr. Sundlof said.

The regulations state that feed manufacturers and companies that render slaughtered animals into useful products generally may not feed mammals to cud-chewing animals, or ruminants, which can carry mad cow disease.

All products that contain rendered cattle or sheep must have a label that says, "Do not feed to ruminants," Dr. Sundlof said. Manufacturers must also have a system to prevent ruminant products from being commingled with other rendered material like that from chicken, fish or pork. Finally, all companies must keep records of where their products originated and where they were sold.

Under the regulations, F.D.A. district offices and state veterinary offices were required to inspect all rendering plants and feed mills to make sure companies complied. But results issued yesterday demonstrate that more than three years later, different segments of the feed industry show varying levels of compliance.

Among 180 large companies that render cattle and another ruminant, sheep, nearly a quarter were not properly labeling their products and did not have a system to prevent commingling, the F.D.A. said. And among 347 F.D.A.-licensed feed mills that handle ruminant materials - these tend to be large operators that mix drugs into their products - 20 percent were not using labels with the required caution statement, and 25 percent did not have a system to prevent commingling.

Then there are some 6,000 to 8,000 feed mills so small they do not require F.D.A. licenses. They are nonetheless subject to the regulations, and of 1,593 small feed producers that handle ruminant material and have been inspected, 40 percent were not using approved labels and 25 percent had no system in place to prevent commingling.

On the other hand, fewer than 10 percent of companies, big and small, were failing to comply with the record-keeping regulations.

The American Feed Industry Association in Arlington, Va., did not return phone calls seeking comment.

Subject: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Wed, 10 Jan 2001 14:04:21 -0500
From: "Gomez, Thomas M."
Reply-To: Bovine Spongiform Encephalopathy To:

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

USDA/APHIS would like to provide clarification on the following point from Mr. Singeltary's 9 Jan posting regarding the 50 state conference call.

[Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not']

Dr. Detwiler was responding to an announcement made during the call to use the FDA emergency number if anyone wanted to report a cow with signs suspect for BSE. Mr. Singeltary is correct that Dr. Detwiler asked participants to use the FDA emergency number as a last resort to report cattle suspect for BSE. What Mr. Singeltary failed to do was provide the List with Dr. Detwiler's entire statement. Surveillance for BSE in the United States is a cooperative effort between states, producers, private veterinarians, veterinary hospitals and the USDA. The system has been in place for over 10 years. Each state has a system in place wherein cases are reported to either the State Veterinarian, the federal Veterinarian in Charge or through the veterinary diagnostic laboratory system. The states also have provisions with emergency numbers. Dr. Detwiler asked participants to use the systems currently in place to avoid the possibility of a BSE-suspect report falling through the cracks. Use of the FDA emergency number has not been established as a means to report diseased cattle of any nature.

############ ############

Subject: Re: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan.9, 2001
Date: Wed, 10 Jan 2001 13:44:49 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: References: 1

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

Hello Mr. Thomas,

> What Mr. Singeltary failed to do was provide the List with Dr. Detwiler's entire statement.

would you and the USDA/APHIS be so kind as to supply this list with a full text version of the conference call and or post on your web-site? if so when, and thank you. if not, why not?

The system has been in place for over 10 years.

that seems to be a very long time for a system to be in place, and only test 10,700 cattle from some 1.5 BILLION head (including calf crop). Especially since French are testing some 20,000 weekly and the E.U. as a whole, are testing many many more than the U.S., with less cattle, same risk of BSE/TSEs.

Why does the U.S. insist on not doing massive testing with the tests which the E.U. are using? Why is this, please explain?

Please tell me why my question was not answered?

U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

It was a very simple question, a very important question, one that pertained to the topic of BSE/feed, and asked in a very diplomatic way. why was it not answered?

If all these years, we have been hearing that pharmaceutical grade bovines were raised for pharmaceuticals vaccines etc. But yet the USA cannot comply with feed regulations of the ruminant feed ban, PLUS cannot even comply with the proper labelling of the feed, cross contamination etc. Then how in the world can you Guarantee the feed fed to pharmaceutical grade bovine, were actually non ruminant feed?

Before i was ask to be 'disconnected', i did hear someone in the background say 'we can't'-- have him ask the question again.

could you please be so kind, as to answer these questions?

thank you, Terry S. Singeltary Sr. Bacliff, Texas USA

P.S. if you will also notice, i did not post that emergency phone number and do not intend on passing it on to anyone. I was joking when i said i should call and report the whole damn U.S. Herd. So please pass that on to Dr. Detwiler, so she can rest easily.

BUT, they should be reported, some are infected with TSE. The U.S. is just acting as stupid as Germany and other Countries that insist they are free of BSE.


Subject: Report on the assessment of the Georgraphical BSE-risk of the USA July 2000 (not good)
Date: Wed, 17 Jan 2001 21:23:51 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To:

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

Greetings List Members and ALL EU Countries,

Because of this report, and the recent findings of the 50-state BSE Conference call, I respectfully seriously suggest that these Countries and the SSC re-evaluate the U.S.A. G.B.R. to a risk factor of #3.

I attempted to post this to list in full text, but would not accept...

thank you, kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA

Report on the assessment of the Geographical BSE-risk of the USA July 2000



- 29 -

Report on the assessment of the Geographical BSE-risk of the USA July 2000



The current geographical BSE-risk (GBR) level is II, i.e. it is unlikely but cannot be excluded that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.

Stability: Before 1990 the system was extremely unstable because feeding of MBM to cattle happened, rendering was inappropriate with regard to deactivation of the BSE-agent and SRM and fallen stock were rendered for feed. From 1990 to 1997 it improved to very unstable, thanks to efforts undertaken to trace imported animals and exclude them from the feed chain and intensive surveillance. In 1998 the system became neutrally stable after the RMBM-ban of 1997.

External challenges: A moderate external challenge occurred in the period before 1990 because of importation of live animals from BSE-affected countries, in particular from the UK and Ireland. It cannot be excluded that some BSE-infected animals have been imported by this route and did enter the US rendering and feed production system. The efforts undertaken since 1990 to trace back UK-imported cattle and to exclude them from the feed chain reduced the impact of the external challenge significantly.

Interaction of external challenges and stability: While extremely unstable, the US system was exposed to a moderate external challenge, mainly resulting from cattle imports from the UK. It can not be excluded that BSE-infectivity entered the country by this route and has been recycled to domestic cattle. The resulting domestic cases would have been processed while the system was still very unstable or unstable and would hence have initiated a number of second or third generation cases. However, the level of the possible domestic prevalence must be below the low detection level of the surveillance in place.

As long as there are no changes in stability or challenge the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent will remain at the current level.



The available information was suitable to carry out the GBR risk assessment.

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Report on the assessment of the Geographical BSE-risk of the USA July 2000


2.1 Overall appreciation of the ability to identify BSE-cases and to eliminate animals at risk of being infected before they are processed

· Before 1989, the ability of the system to identify (and eliminate) BSE cases was limited. · Since 1990 this ability is significantly improved, thanks to a good BSE-surveillance and culling system (contingency plan). · Today the surveillance should be able to detect clinical BSE-cases within the limits set by an essential passive surveillance system, i.e. some cases might remain undetected.

2.2 Overall appreciation of the ability to avoid recycling BSE-infectivity, should it enter processing

· Before 1997 the US rendering and feed producing system would not have been able to avoid recycling of the BSE agent to any measurable extent. If the BSE-agent was introduced the feed chain, it could probably have reached cattle. · After the introduction of the RMBM-to-ruminants-ban in August 1997 the ability of the system to avoid recycling of BSE-infectivity was somewhat increased. It is still rather low due to the rendering system of ruminant material (including SRM and fallen stock) and the persisting potential for cross-contamination of cattle feed with other feeds and hence RMBM.

2.3 Overall assessment of the Stability

· Until 1990 the US BSE/cattle system was extremely unstable as RMBM was commonly fed to cattle, the rendering system was not able to reduce BSE-infectivity and SRM were rendered. This means that incoming BSE infectivity would have been most probably recycled to cattle and amplified and the disease propagated. · Between 1990 and 1995 improvements in the BSE surveillance and the efforts to trace back and remove imported cattle gradually improved the stability but the system remained very unstable. In 1998 the system became unstable because of an RMBM-ban introduced in 1997. After 1998 the ban was fully implemented and the system is regarded to be neutrally stable since 1998. The US system is therefore seen to neither be able to amplify nor to reduce circulating or incoming BSE-infectivity.


A moderate external challenge occurred in the period 1980-1989 because of importation of live animals from the UK. imports from other countries are regarded to have been negligible challenges. · As a consequence of this external challenge, infectivity could have entered the feed cycle and domestic animals could have been exposed to the agent. These domestic BSE-incubating animals might have again entered processing, leading to an internal challenge since 1991. · This internal challenge could have produced domestic cases of BSE, yet prevalence levels could have been below the detection limits of the surveillance system until now. (According to US calculations, the current surveillance

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Report on the assessment of the Geographical BSE-risk of the USA July 2000

system could detect clinical incidence of 1-3 cases per year per million adult cattle, i.e. in absolute numbers 43-129 cases per year). Between 1990 und 1995, with the exclusion of the imported animals from Europe from the feed chain, the effect of the external challenges decreased.


4.1 Interaction of stability and challenqe

· In the late 80s, early 90s a moderate external challenges met an extremely unstable system. This would have amplified the incoming BSE-infectivity and propagated the disease. · With the exclusion of the imported animals from Europe from the feed chain between 1990 and 1995 the effect of the external challenge decreased. · Before 1998 an internal challenge, if it developed, would have met a still unstable system (inappropriate rendering, no SRM ban, RMBM ban only after 1997) and the BSE-infectivity could have been recycled and amplified. · After 1998 the neutrally stable system could still recycle the BSE-agent but due to the RMBM-ban of 1997 the BSE-infectivity circulating in the system would probably not be amplified.

4.2 Risk that BSE-infectivity enters processing

· A very low processing risk developed in the late 80s when the UK-imports were slaughtered or died. It increased until 1990 because of the higher risk to be infected with BSE of cattle imported from the UK in 1988/89, as these animals could have been processed prior to the back-tracing of the UK-imports in 1990. · From 1990 to 1995 a combination of surviving non-traced UK imports and some domestic (pre-)clinical cases could have arrived at processing resulting in an assumed constant low but non-negligible processing risk. · After 1995 any processing risk relates to assumed domestic cases arriving at processing. · The fact that no domestic cases have been shown-up in the BSE-surveillance is reassuring - it indicates that BSE is in fact not present in the country at levels above the detection limits of the country's surveillance system. This detection level has been calculated according to US-experts to be between 1 & 3 clinical cases per million adult cattle per year.

Note: The high turnover in parts of the dairy cattle population with a young age at slaughter makes it unlikely that fully developed clinical cases would occur (and could be detected) or enter processing. However, the theoretical infective load of the pre-clinical BSE-cases that under this scenario could be processed, can be assumed to remain relatively low.

4.3 Risk that BSE-infectivity is recycled and propagated

· During the period covered by this assessment (1980-1999) the US-system was not able to prevent propagation of BSE should it have entered, even if this ability was significantly improved with the MBM-ban of 1997. · However, since the likelihood that BSE-infectivity entered the system is regarded to be small but non-negligible, the risk that propagation of the disease took place is also small but not negligible.

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Report on the assessment of the Geographical BSE-risk of the USA July 2000


5.1 The current GBR

The current geographical BSE-risk (GBR) level is II, i.e. it is unlikely but cannot be excluded that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.

5.2 The expected development of the GBR

As long as there are no changes in stability or challenge the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent remains at the current level.

5.3 Recommendations for influencin.q the future GBR

· As long as the stability of the US system is not significantly enbanced above neutral levels it remains critically important to avoid any new external challenges. · All measures that would improve the stability of the system, in particular with regard to its ability to avoid recycling of the BSE-agent should it be present in the cattle population, would reduce, over time, the probability that cattle could be infected with the BSE-agent. Possible actions include: removal of SRMs and/or fallen stock from rendering, better rendering processes, improved compliance with the MBM-ban including control and reduction of cross-contamination. · Results from an improved intensive surveillance programme, targeting at risk sub-populations such as adult cattle in fallen stock or in emergency slaughter, could verify the current assessment.


The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.


Tuesday, January 26, 2010

Establishing a Fully Integrated National Food Safety System with Strengthened Inspection, Laboratory and Response Capacity Draft 09/24/09

2009-2010 ***

Monday, December 14, 2009 R.I.P. MOM DOD

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

> 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.

Thursday, January 07, 2010

Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008

Monday, September 1, 2008


Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009


Monday, November 23, 2009


Tuesday, August 11, 2009

Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants

Brian S. Appleby, MD; Kristin K. Appleby, MD; Barbara J. Crain, MD, PhD; Chiadi U. Onyike, MD, MHS; Mitchell T. Wallin, MD, MPH; Peter V. Rabins, MD, MPH

Sunday, May 10, 2009

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission) TO :

May 8, 2009

Greetings again Dr. Freas, TSEAC et al,



Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [] Monday, January 08,200l 3:03 PM freas ...

Thursday, January 28, 2010

Multiorgan Detection and Characterization of Protease-Resistant Prion Protein in a Case of Variant CJD Examined in the United States

Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009


5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

my comments to PLosone here ;

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

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Friday, January 15, 2010

New York Firm Recalls Beef Carcass That Contains Prohibited Materials (BSE)

New York Firm Recalls Beef Carcass That Contains Prohibited Materials


Congressional and Public Affairs (202) 720-9113 Atiya Khan

WASHINGTON, January 15, 2010 - Jerry Hayes Meats Inc., a Newark Valley, N.Y., establishment is recalling approximately 490 pounds of a beef carcass that may not have had the spinal column removed, which is not compliant with regulations that require the removal of spinal cord and vertebral column from cattle over 30 months of age, the U.S. Department of Agriculture's Food Safety and Inspection Service (FSIS) announced today.

Spinal cord and vertebral column are considered a specified risk material (SRM) and must be removed from cattle over 30 months of age in accordance with FSIS regulations. SRMs are tissues that are known to contain the infective agent in cattle infected with Bovine Spongiform Encephalopathy (BSE), as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.

The products subject to recall include: 1- "BEEF CARCASS," which bears the establishment number "EST. 04488 M" inside the USDA mark of inspection.

The product was packed on January 7, 2010, and sold to a single customer in New York.

The problem was discovered through routine FSIS inspection activities. FSIS has received no reports of illnesses associated with consumption of this product.

FSIS routinely conducts recall effectiveness checks to verify recalling firms notify their customers (including restaurants) of the recall and that steps are taken to make certain that the product is no longer available to consumers.

Media and consumers with questions about the recall should contact the company's owner, Jerry Hayes at (607) 642-9598.

The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.

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 $$$

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

my comments to PLosone here ;

Thursday, January 14, 2010


> FSIS has received no reports of illnesses associated with consumption of this product.

Here we go again. This to me is very misleading, why don't they post the rest of the science on TSE and incubation periods ? The FSIS et al know damn good and well that your not going to eat this product and fall over dead immediately or in the next few days, weeks, months from a mad cow type disease i.e. Transmissible Spongiform Encephalopathy. It takes years, decade, and or decades for a TSE to become clinical and kill. Once the TSE is clinical, you better have your things in order, your going to die. ...

Science 23 November 2001: Vol. 294. no. 5547, pp. 1726 - 1728 DOI: 10.1126/science.1066838


Estimation of Epidemic Size and Incubation Time Based on Age Characteristics of vCJD in the United Kingdom Alain-Jacques Valleron,1 Pierre-Yves Boelle,1 Robert Will,2 Jean-Yves Cesbron3

1 Epidemiology and Information Sciences, INSERM U444, CHU Saint-Antoine, Université Pierre et Marie Curie et Assistance Publique-Hôpitaux de Paris, 27 rue Chaligny, 75012 Paris, France. 2 National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Edinburgh EH4 2XU, UK. 3 Immunité Anti-Infectieuse JE 2236, UFR de Médecine de Grenoble, Université Joseph Fourier, Domaine de la Merci, 38706 La Tronche, France.


The distribution of the vCJD incubation period that best fits the data within the framework of our model has a mean of 16.7 years, with a standard deviation of 2.6 years. The 95% upper percentile of this distribution is 21.4 years. The 95% confidence interval (CI) of the estimates of the mean and standard deviation is relatively narrow: The 95% CI for the estimate of the mean incubation period is 12.4 to 23.2 years, and the 95% CI of the standard deviation is 0.9 to 8 years (10). The decrease in susceptibility to infection in exposed subjects older than 15 years, as estimated from the parameter , was found to be very sharp: 16% per year of age (CI: 12 to 23%). This means that, under the best fitting hypothesis, an individual aged 20 years in 1981 had 55% less risk of becoming infected than a child aged 15 years (99.9% for an individual aged 70).

Interpretation Incubation periods of infection with human prions can exceed 50 years. In human infection with BSE prions, species-barrier effects, which are characteristic of cross-species transmission, would be expected to further increase the mean and range of incubation periods, compared with recycling of prions within species. These data should inform attempts to model variant CJD epidemiology.


a. MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College London, London WC1N 3BG, UK b. Papua New Guinea Institute of Medical Research, Goroka, EHP, Papua New Guinea c. Centre for International Health, Curtin University, Perth, Australia

Correspondence to: Prof John Collinge

WHAT about iatrogenic CJD there from these animal and human typical and atypical TSE's in the USA i.e. Friendly Fire and or 'The Pass It Forward' mode of transmission, and incubation periods there of ??? did not tell the public about that either ?


Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth hormone

E A Croes, G Roks, G H Jansen, P C G Nijssen, C M van Duijn ...............................................................

J Neurol Neurosurg Psychiatry 2002;72:792-793

A 47 year old man is described who developed pathology proven Creutzfeldt-Jakob disease (CJD) 38 years after receiving a low dose of human derived growth hormone (hGH) as part of a diagnostic procedure. The patient presented with a cerebellar syndrome, which is compatible with iatrogenic CJD. This is the longest incubation period described so far for iatrogenic CJD. Furthermore, this is the first report of CJD after diagnostic use of hGH. Since the patient was one of the first in the world to receive hGH, other cases of iatrogenic CJD can be expected in the coming years.

Prion diseases are potentially transmissible. Human to human transmission was first reported in 1974, when a 55 year old woman was described who developed symptoms of Creutzfeldt-Jakob disease (CJD) 18 months after a corneal transplant.1 Since then, transmission has been reported after stereotactic electroencephalographic (EEG) depth recording, human growth hormone (hGH) and gonadotrophin treatment, and dura mater transplantation.2-5 More than 267 patients with iatrogenic CJD are known today and their number is growing.6 The most important iatrogenic cause of CJD is still contaminated cadaveric hGH. Exposure to contaminated hGH occurred before 1985, when recombinant growth hormone became available. In a recent study, incubation periods in 139 patients with hGH associated CJD were found to range from 5-30 years, with a median of 12 years.6 One of the factors influencing incubation time is genotype on polymorphic codon 129 of the prion protein gene.7 The incubation time is significantly shorter in people who are homozygous for either methionine or valine on this polymorphism.7

We describe the second patient with hGH related CJD in the Netherlands. The patient developed the disease 38 years after hGH injections. To our knowledge, this is the longest incubation period described for any form of iatrogenic CJD. Further-more, our patient was not treated with hGH but only received a low dose as part of a diagnostic procedure.


This patient presented at the age of 47 years with paraesthesia in both arms for six months, difficulty with walking for four weeks, and involuntary movements of mainly the upper extremities of two weeks' duration. He did not notice any change in cognitive function, although his twin sister had noticed minor memory disturbances. There was no family history of neurological disease. During childhood the patient had experienced a growth delay compared with his twin sister and with the average in the Netherlands. When he was 9 years old, a nitrogen retention test with 6 IU hGH over five days was performed to exclude growth hormone deficiency. Since the result was not decisive, a quantitative amino acid test was performed, which measures 30 amino acids during fasting and one, two, and three hours after growth hormone injection. No abnormal amino acid concentrations were found making the diagnosis of primordial dwarfism most likely. Therefore, no treatment with hGH was given.

On neurological examination we found a slight dysarthria without aphasia. Cranial nerve function was normal. Walking was unstable and wide based. During movements of the upper extremities myoclonic jerks were present. Sensation, muscle tone, and strength were normal. Co-ordination was impaired in all four limbs with a disturbed balance. Tendon reflexes were brisk at the arms and increased at the legs with a clonus in the ankle reflex. Plantar responses were both normal. On the mini mental state examination, the patient scored 30/30. Routine laboratory investigation, thyroid function, vitamin concentrations (B-1, B-6, B-12, and E), and copper metabolism were normal. Admission EEG examination showed generalised arrhythmic slow activity with diffuse spikes and spike waves. EEG examination two months later showed a further slowing of the rhythm with bilateral diphasic sharp waves but was not typical for CJD. Cerebral magnetic resonance imaging was normal. Cerebrospinal fluid examination showed 1 cell/3 µl, normal glucose and protein concentrations, and a strongly positive 14-3-3 protein test. The patient was homozygous for methionine on the PRNP codon 129 polymorphism. On clinical grounds, CJD was diagnosed. Within one month the patient's condition deteriorated rapidly and because of severe disturbances in coordination and progressive myoclonus he became bedridden. An eye movement disorder developed with slow saccadic and dysmetric eye movements. Temperature became unstable with peaks of 39°C without an infectious focus, for which a disorder of autoregulation was presumed. Until a very advanced stage, cognitive function was intact. The patient died five months after admission. The diagnosis of CJD was confirmed at necropsy. The brain weighed 990 g and showed clear cortical and cerebellar atrophy. Spongiosis, neuronal loss, and gliosis were found predominantly in the putamen, caudate nucleus, and basotemporal and cerebellar cortex; the cerebellum was the most severely affected of these. Vacuoles ranged from 2-12 µm. No amyloid or Kuru plaques were found. Immunohistochemical staining (3F4 antibody 1:1000, Senetek, USA) was clearly positive for prion protein accumulation in a "synaptic" distribution. Most deposition was found in the stratum moleculare of the cerebellum.


We describe a 47 year old patient who developed pathology proven CJD 38 years after hGH injections. The patient was never treated with hGH but received a small dose as part of a diagnostic procedure. The onset of CJD was signalled by prodromal symptoms of paraesthesia followed by a rapidly progressive ataxia. The disease presentation and course with predominantly cerebellar and eye movement disorders are compatible with iatrogenic CJD caused by hGH treatment.6 8

Growth hormone treatment was first described in 1958 but hGH was not produced on a larger scale from human pituitary glands until the beginning of the 1960s. In the Netherlands growth hormone extraction started in 1963 and was soon centrally coordinated. Until 1979 growth hormone was extracted non-commercially from pituitaries by a pharmaceutical company. In 1971 commercial products also became available. Our patient was one of the first to receive hGH in the Netherlands but the origin of this product was not recorded. A causal relation can therefore not be established with full certainty, but coincidentally receiving growth hormone and developing this very rare disease is unlikely. Since the clinical course in this relatively young patient is in accordance with an iatrogenic cause, we think the probability is high that the hGH injections explain the development of CJD in this patient.

The first Dutch patient with hGH related CJD died in 1990. 9 During several periods from 1963 to 1969 she received intramuscular injections of hGH. During an unknown period the hGH was derived from South America. At age 39, 27 years after starting the treatment, she developed an ataxic gait, slurred speech, sensory disorders, and myoclonus, but her cognitive function remained normal. Postmortem examination of the brain confirmed the diagnosis of CJD.9 Following the identification of this patient, a retrospective study was started to trace all 564 registered hGH recipients who were treated before May 1985. Until January 1995, none of these was suspected of having CJD.10 Since 1993 prospective surveillance for all forms of human prion disease has been carried out in the Netherlands and, apart from the patient described above, a further two patients with iatrogenic CJD have been identified, who developed the disease after dura mater transplantation.11

An incubation period as long as 38 years had never been reported for iatrogenic CJD. Huillard d'Aignaux et al7 studied the incubation period in 55 patients with hGH related CJD in a cohort of 1361 French hGH recipients. The median incubation period was between 9 and 10 years. Under the most pessimistic model, the upper limit of the 95% confidence interval varied between 17 and 20 years. Although the infecting dose cannot be quantified, it can be speculated that the long incubation period in our patient is partly explained by the administration of a limited amount of hGH. This hypothesis is supported by experimental models, in which higher infecting doses usually produce shorter incubation periods.6 Since our patient was one of the first in the world to receive hGH, this case indicates that still more patients with iatrogenic CJD can be expected in the coming years. Another implication of our study is that CJD can develop even after a low dose of hGH. This case once more testifies that worldwide close monitoring of any form of iatrogenic CJD is mandatory.


We are grateful to M Jansen PhD MD for his search for the origin of the growth hormone and P P Taminiau MD. CJD surveillance in the Netherlands is carried out as part of the EU Concerted Action on the Epidemiology of CJD and the the EU Concerted Action on Neuropathology of CJD, both funded through the BIOMED II programme, and is supported by the Dutch Ministry of Health. This surveillance would not have been possible without the cooperation of all Dutch neurologists and geriatricians. ........................................

Authors' affiliations

E A Croes, G Roks*, C M van Duijn, Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands

P C G Nijssen, Department of Neurology, St Elisabeth Hospital, PO Box 90151, 5000 LC Tilburg, Netherlands

G H Jansen, Department of Pathology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands

*Also the Department of Neurology, St Elisabeth Hospital

Correspondence to: Professor C M van Duijn, Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands;

Received 27 December 2001 In revised form 1 March 2002 Accepted 12 March 2002

Competing interests: none declared


1 Duffy P, Wolf J, Collins G, et al. Possible person-to-person transmission of Creutzfeldt-Jakob disease. N Engl J Med 1974;290:692-3.

2 Bernoulli C, Siegfried J, Baumgartner G, et al. Danger of accidental person-to-person transmission of Creutzfeldt-Jakob disease by surgery. Lancet 1977;i:478-9.

3 Koch TK, Berg BO, De Armond SJ, et al. Creutzfeldt-Jakob disease in a young adult with idiopathic hypopituitarism: possible relation to the administration of cadaveric human growth hormone. N Engl J Med 1985;313:731-3.

4 Cochius JI, Burns RJ, Blumbergs PC, et al. Creutzfeldt-Jakob disease in a recipient of human pituitary-derived gonadotrophin. Aust NZ J Med 1990;20:592-3.

5 Thadani V, Penar PL, Partington J, et al. Creutzfeldt-Jakob disease probably acquired from a cadaveric dura mater graft: case report. J Neurosurg 1988;69:766-9.

6 Brown P, Preece M, Brandel JP, et al. Iatrogenic Creutzfeldt-Jakob disease at the millennium. Neurology 2000;55:1075-81.

7 Huillard d'Aignaux J, Costagliola D, Maccario J, et al. Incubation period of Creutzfeldt-Jakob disease in human growth hormone recipients in France. Neurology 1999;53:1197-201.

8 Billette de Villemeur T, Deslys JP, Pradel A, et al. Creutzfeldt-Jakob disease from contaminated growth hormone extracts in France. Neurology 1996;47:690-5.

9 Roos RA, Wintzen AR, Will RG, et al. Een patiënt met de ziekte van Creutzfeldt-Jakob na behandeling met humaan groeihormoon. Ned Tijdschr Geneeskd 1996;140:1190-3.

10 Wientjens DP, Rikken B, Wit JM, et al. A nationwide cohort study on Creutzfeldt-Jakob disease among human growth hormone recipients. Neuroepidemiology 2000;19:201-5.

11 Croes EA, Jansen GH, Lemstra AF, et al. The first two patients with dura mater associated Creutzfeldt-Jakob disease in the Netherlands. J Neurol 2001;248:877-81.

J Neurol Neurosurg Psychiatry 1994;57:757-758 doi:10.1136/jnnp.57.6.757
Research Article
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
C J Gibbs, Jr,
D M Asher,
A Kobrine,
H L Amyx,
M P Sulima,
D C Gajdusek
+ Author Affiliations

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.

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

my comments to PLosone here ;

Saturday, January 16, 2010

Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al


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Thursday, January 14, 2010




05-10 1/12/10




I. PURPOSE This notice provides the Food Safety and Inspection Service (FSIS) inspection program personnel with instructions regarding the collection of brain samples for the Animal and Plant Health Inspection Service’s (APHIS) Bovine Spongiform Encephalopathy (BSE) ongoing surveillance plan.


A. Approved Alternative Off-Site Sample Collection

1. APHIS will provide for the collection of brain (obex) samples from an allocated number of cattle 30 months and older condemned for any reason on ante-mortem inspection, and from cattle of any age displaying Central Nervous System (CNS) symptoms, at federally-inspected slaughter establishments that have agreements with APHIS under the approved alternative off-site sample collection program.

2. At such establishments, FSIS inspection program personnel will not collect brain samples. They will provide the following to plant management:

a. condemn tag (Z-tag) numbers (not the Z-tag itself); and

b. disposition information (i.e., the reason for condemnation under 9 CFR Part 309).

B. Brain Sample Collection of Cattle Displaying CNS Symptoms

1. At Federally-inspected establishments not under the approved alternative off-site sample collection program, FSIS Public Health Veterinarians (PHVs):


a. will collect appropriate BSE samples from cattle of all ages that display CNS symptoms, or

b. will not collect the samples for BSE testing if the slaughter establishment has made or plans to make arrangements with APHIS, whereby the samples from cattle condemned for CNS symptoms will be collected at a location other than on the official plant premises.

2. Certain Alternative Off-Site Agreements that were in place during Enhanced Surveillance may no longer be in effect and establishments will need to initiate new agreements with APHIS and potential collectors.


A. Upon receipt of this notice, the FSIS PHV is to hold an awareness meeting with the establishment. At this meeting, the FSIS PHV should ask the management whether:

1. it is under APHIS’ approved alternative off-site sample collection program for collecting allocated samples (paragraph II. A.); and

2. if not, whether:

a. FSIS is to collect brain samples from cattle displaying CNS symptoms (paragraph II. B. 1.a.); or

b. the establishment needs time to engage in making arrangements with APHIS for the off-site brain sample collection of such cattle (paragraph II. B. 1. b.).

B. If during the awareness meeting establishment management states that it plans to work with APHIS to begin off-site sampling, until APHIS approves that arrangement, or until FSIS is advised that an off-site agreement will not be forthcoming, FSIS PHVs are to:

1. identify all CNS animals condemned on ante-mortem with a "U. S. Condemned” tag;

2. contact the APHIS Area Veterinarian-In-Charge (AVIC) so the AVIC can collect the brain sample;

3. ensure that the animals are humanely euthanized, unless APHIS requests otherwise; and

4. not allow them to move off the premise of the establishment, unless APHIS requests otherwise.

C. In a memorandum of interview (MOI), the FSIS PHV is to document who was present at the awareness meeting, the date and time of the meeting, how the


establishment plans to proceed based on the choices set out in A. above, and any documents shared with management.

D. If the establishment plans to work with APHIS to begin off-site sampling, the FSIS PHV is to update the MOI as to whether an agreement was reached and in general, what the agreement was.

E. The FSIS PHV is to maintain a copy of the memorandum of interview in the official government file, provide a copy to the plant management, and electronically mail a copy to the APHIS AVIC as changes occur.


A. The FSIS PHV is to complete the condemnation form, FSIS Form 6000-13 (Certification of Ante-mortem or Post-mortem Disposition of Tagged Animals) and FSIS Form 6150-1 (Identification Tag – Ante-mortem). The FSIS PHV should pay special attention when providing a full description of the reason for the condemnation on FSIS Form 6000-13 and fill out fully FSIS Form 6150-1.

B. Incoming animal identification, except the Z-tag, should be left on these animals since it will be needed at the approved alternative off-site collection location to fill out collection forms. Z-tags will be removed prior to any carcasses leaving the official establishment.

NOTE: Information supplied to plant management to take to the approved alternative off-site collection sites needs to be complete and accurate. FSIS PHVs need to provide a full description of the reason for the condemnation on FSIS Form 6000-13, APHIS will use this information to triage which condemned animals are sampled.


A. If the establishment does not have an agreement with APHIS for off-site sampling of cattle with CNS symptoms, the FSIS PHV will collect the brain samples from cattle showing signs of CNS symptoms. The FSIS PHV is to make all final disposition decisions regarding whether to condemn cattle in accordance with 9 CFR part 309.

NOTE: FSIS PHVs can also find information regarding BSE sampling (e.g., forms, sampling supply information) at:

//Outlook Public Folders/All PublicFolders/ OPPD/PDD/BSE_Training_Info/

B. The FSIS PHV, or the establishment under the supervision of the FSIS PHV, should promptly remove the head in order to collect the brain sample. If the establishment does not arrange to remove the head, the FSIS PHV may need to collect the brain sample as a priority over other ante-mortem or post-mortem procedures.

C. The FSIS PHV should collect the brain sample either in the inedible area of the establishment or in another area set aside for such collection to prevent the creation of


an insanitary condition. Establishment personnel and FSIS inspection program personnel are to take proper sanitary measures before returning to edible areas of the establishment after brain sample collection, in accordance with 9 CFR 416.5.

D. In situations where the FSIS PHV has missed the last FedEx pick-up for the day, or the FSIS PHV collected the sample on a day when FedEx does not pick up, the PHV is to refrigerate the samples until the next available FedEx pick-up day. Remember, the sample is not to pass through or to be stored in areas of the establishment where the establishment produces edible product. The FSIS PHV is to maintain the sample’s chain-of-custody.

E. The FSIS PHV is to verify the collection, documentation, and control of all animal identification associated with cattle condemned during ante-mortem inspection that are to be sampled by FSIS. The FSIS PHV is to attach the “U. S. Condemned” tag to cattle condemned during ante-mortem inspection in accordance with 9 CFR 309.13. This documentation will facilitate traceback in the event that the sample result is positive for BSE. The documentation should include records in accordance with 9 CFR 320.1.

F. The FSIS PHV is to verify that the presence of condemned cattle or parts does not create insanitary conditions (9 CFR part 416). The establishment is responsible for the disposal of the condemned cattle in accordance with 9 CFR part 314. The FSIS PHV also is to verify that the establishment maintains records regarding the disposal of the condemned cattle in accordance with 9 CFR 320.1.

G. Inspection program personnel may inform the establishment that it may choose to hold the carcass and parts until testing results are available. If the establishment chooses to dispose of any carcass or parts before it receives test results, inspection program personnel are to advise the establishment that it must dispose of the carcass in one of the following ways:

1. render it at a facility for non-animal feed use (e.g., biofuel or cement);

2. alkaline digestion;

3. incineration; or

4. lined land fills.

H. Documentation for Cattle Showing Signs of CNS Symptoms

1. For locations without high-speed internet connections, the FSIS PHV is to forward the completed BSE Surveillance Information System (BSE-SIS) sample collection sheets to the APHIS,VS office by FAX or by e-mail. The follow site lists the VS office FAX numbers and e-mail where available:

2. The APHIS AVIC in each area office may assist with sample delivery verification and troubleshooting. The FSIS PHV can get copies of BSE-SIS forms by contacting the local APHIS office.


3. The FSIS PHV is to enter the relevant information into the BSE-SIS at locations with high-speed connections and proceed as instructed in the training materials. FSIS PHVs may get the training from AgLearn or may contact the District Office if they need a copy of the BSE Surveillance Information System (BSE-SIS) training CD and for assistance in getting permission to have access to BSE-SIS.


A. The FSIS PHV will receive, by e-mail, a report from the AVIC on the BSE test results. The AVIC will also send copies of the results to the District Office.

B. If the test is negative (reported as “not detected”), any carcasses and parts the establishment has held may be released for rendering or other disposal in accordance with 9 CFR 314.

C. If the test is inconclusive, the FSIS PHV will receive supervisory instruction on further actions.

D. For any sample confirmed positive for BSE, the FSIS PHV is to verify that the establishment disposes of the carcasses and parts in the proper manner as set out in paragraph V. G.


A. After sampling cattle showing signs of CNS symptoms, the FSIS PHV (or designee) is to enter the relevant information for each sample into eADRS.

B. The FSIS PHV (or designee) is to enter each ante-mortem condemned animal in eADRS under the applicable pathological condition

C. For each relevant disease condition, in the “Add Daily Totals” window, the FSIS PHV is to select the “Update BSE Details” button if FSIS sampled one or more of the condemned animals for BSE. Selecting this button opens the “Update BSE Details” screen.

D. On the “Update BSE Details” screen, the FSIS PHV is to enter the number of animals sampled and the applicable “U.S. Condemned” Z-tag number for each sampled animal.

E. After entering the relevant information, the FSIS PHV is to click the “Save” button and proceed to the next disease condition.

F. For additional information on entering BSE sample information, refer to Section 7 of the eADRS User Guide.


A. In a rare situation, such as when an animal is condemned by the FSIS PHV on ante-mortem for rabies, the FSIS PHV should contact their District Office, who will advise APHIS. In these cases, APHIS will see that the animal is tested for rabies. APHIS will work with the laboratory to get appropriate samples forwarded for BSE surveillance from rabies negative animals.

B. Rabies booster vaccination for PHVs collecting BSE samples is still highly recommended. PHVs can be reimbursed for rabies vaccinations or boosters. Rabies vaccinations are volunatry. Only PHVs who are actually involved with BSE sample collection will be eligible for reimbursement on the vaccination series. PHVs should make arrangements for the vaccinations with their private physician. PHVs should contact their Front-line supervisor for approval on reimbursement prior to beginning the three shot vaccination series.

Refer questions regarding this notice to the Policy Development Division through askFSIS at or by telephone at 1-800-233-3935.

Assistant Administrator Office of Policy and Program Development



04-10 1/12/10





This notice reminds inspection program personnel (IPP) that the tonsils from cattle of all ages are among the materials identified as specified risk materials (SRMs) under 9 CFR 310.22(a). Lingual and palatine tonsils must be removed from finished product per FSIS Directive 6100.4. See attachment 1 for related questions and answers.

IPP may review pictures and guidance materials on removal of lingual and palatine tonsils from tongues and beef market heads at the following link:

IPP are to continue to verify that establishments are properly addressing removal of SRMs, including lingual and palatine tonsils, as set out in FSIS Directive 6100.4, Verification Instructions Related to Specified Risk Materials. See attachment 2 of this notice or the above link to access a helpful tool for use when verifying the requirements of 9 CFR 310.22. To verify that the establishment has in place adequate head dressing procedures to remove the designated lingual and palatine tonsils from beef tongues and beef market heads, off-line IPP are to include direct observation of the plant’s tonsil removal procedures and finished product (processed beef tongues and market heads prior to packaging) on a regular and recurring basis whenever HACCP 01 and 02 procedures are scheduled. Off-line inspectors are to effect a regulatory control action in accordance with 9 CFR 500.2 if the establishment is observed not properly removing tonsils. The regulatory control action is to remain in place until the establishment has implemented effective corrective actions.

Refer questions regarding this notice to the Policy Development Division through askFSIS at or by telephone at 1-800-233-3935.

Assistant Administrator Office of Policy and Program Development


Audit Report

Animal and Plant Health Inspection Service

Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II


Food Safety and Inspection Service

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III

Report No. 50601-10-KC January 2006

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain

Our prior report identified a number of inherent problems in identifying and testing high-risk cattle. We reported that the challenges in identifying the universe of high-risk cattle, as well as the need to design procedures to obtain an appropriate representation of samples, was critical to the success of the BSE surveillance program. The surveillance program was designed to target nonambulatory cattle, cattle showing signs of CNS disease (including cattle testing negative for rabies), cattle showing signs not inconsistent with BSE, and dead cattle. Although APHIS designed procedures to ensure FSIS condemned cattle were sampled and made a concerted effort for outreach to obtain targeted samples, industry practices not considered in the design of the surveillance program reduced assurance that targeted animals were tested for BSE.

In our prior report, we recommended that APHIS work with public health and State diagnostic laboratories to develop and test rabies-negative samples for BSE. This target group is important for determining the prevalence of BSE in the United States because rabies cases exhibit clinical signs not inconsistent with BSE; a negative rabies test means the cause of the clinical signs has not been diagnosed.

APHIS agreed with our recommendation and initiated an outreach program with the American Association of Veterinary Laboratory Diagnosticians, as well as State laboratories. APHIS also agreed to do ongoing monitoring to ensure samples were obtained from this target population.

Although APHIS increased the samples tested from this target group as compared to prior years, we found that conflicting APHIS instructions on the ages of cattle to test resulted in inconsistencies in what samples were submitted for BSE testing. Therefore, some laboratories did not refer their rabies negative samples to APHIS in order to maximize the number tested for this critical target population. In addition, APHIS did not monitor the number of submissions of rabies negative samples for BSE testing from specific laboratories.


An NVSL official stated that APHIS is not concerned with rabies negatives samples from cattle less than 30 months of age. This position, however, is contrary to APHIS’ published target population.

Our prior audit recognized the significant challenge for APHIS to obtain samples from some high-risk populations because of the inherent problems with obtaining voluntary compliance and transporting the carcasses for testing. USDA issued rules to prohibit nonambulatory animals (downers) from entering the food supply at inspected slaughterhouses. OIG recommended, and the International Review Subcommittee33 emphasized, that USDA should take additional steps to assure that facilitated pathways exist for dead and nonambulatory cattle to allow for the collection of samples and proper disposal of carcasses. Between June 1, 2004, and May 31, 2005, the APHIS database documents 27,617 samples were collected showing a reason for submission of nonambulatory and 325,225 samples were collected with reason of submission showing "dead."

APHIS made extensive outreach efforts to notify producers and private veterinarians of the need to submit and have tested animals from these target groups. They also entered into financial arrangements with 123 renderers and other collection sites to reimburse them for costs associated with storing, transporting, and collecting samples. However, as shown in exhibit F, APHIS was not always successful in establishing agreements with non-slaughter collection sites in some States. APHIS stated that agreements do not necessarily reflect the entire universe of collection sites and that the presentation in exhibit F was incomplete because there were many collection sites without a payment involved or without a formal agreement. We note that over 90 percent of the samples collected were obtained from the 123 collection sites with agreements and; therefore, we believe agreements offer the best source to increase targeted samples in underrepresented areas.

We found that APHIS did not consider industry practices in the design of its surveillance effort to provide reasonable assurance that cattle exhibiting possible clinical signs consistent with BSE were tested. Slaughter facilities do not always accept all cattle arriving for slaughter because of their business requirements. We found that, in one State visited, slaughter facilities pre-screened and rejected cattle (sick/down/dead/others not meeting business

Downers and Cattle that Died on the Farm standards) before presentation for slaughter in areas immediately adjacent or contiguous to the official slaughter establishment. These animals were not inspected and/or observed by either FSIS or APHIS officials located at the slaughter facilities.

FSIS procedures state that they have no authority to inspect cattle not presented for slaughter. Further, APHIS officials stated they did not believe that they had the authority to go into these sorting and/or screening areas and require that the rejected animals be provided to APHIS for BSE sampling. Neither APHIS nor FSIS had any process to assure that animals left on transport vehicles and/or rejected for slaughter arrived at a collection site for BSE testing. FSIS allows slaughter facilities to designate the area of their establishment where federal inspection is performed; this is designated as the official slaughter establishment.34

We observed animals that were down or dead in pens outside the official premises that were to be picked up by renderers. Animals that were rejected by plant personnel were transported off the premises on the same vehicles that brought them to the plant.35

A policy statement36 regarding BSE sampling of condemned cattle at slaughter plants provided that effective June 1, 2004, FSIS would collect BSE samples for testing: 1) from all cattle regardless of age condemned by FSIS upon ante mortem inspection for CNS impairment, and 2) from all cattle, with the exception of veal calves, condemned by FSIS upon ante mortem inspection for any other reason.

FSIS Notice 28-04, dated May 20, 2004, informed FSIS personnel that, "FSIS will be collecting brain samples from cattle at federally-inspected establishments for the purpose of BSE testing." The notice further states that, "Cattle off-loaded from the transport vehicle onto the premises of the federally-inspected establishment (emphasis added), whether dead or alive, will be sampled by the FSIS Public Health Veterinarian (PHV) for BSE after the cattle have been condemned during ante mortem inspection. In addition, cattle passing ante mortem inspection but later found dead prior to slaughter will be condemned and be sampled by the FSIS PHV."

APHIS has the responsibility for sampling dead cattle off-loaded onto plant-owned property that is adjoining to, but not considered part of, the "official premises.37 FSIS procedures38 provide that "Dead cattle that are off-loaded to facilitate the off-loading of live animals, but that will be re-loaded onto the transport vehicle, are not subject to sampling by FSIS.

While performing our review in one State, we reviewed the circumstances at two slaughter facilities in the State that inspected and rejected unsuitable cattle before the animals entered the official receiving areas of the plants. This pre-screening activity was conducted in areas not designated by the facility as official premises of the establishment and not under the review or supervision of FSIS inspectors. The plant rejected all nonambulatory and dead/dying/sick animals delivered to the establishment. Plant personnel refused to offload any dead or downer animals to facilitate the offloading of ambulatory animals. Plant personnel said that the driver was responsible for ensuring nonambulatory animals were humanely euthanized and disposing of the carcasses of the dead animals. Plant personnel informed us that they did not want to jeopardize contracts with business partners by allowing unsuitable animals on their slaughter premises.

In the second case, one family member owned a slaughter facility while another operated a livestock sale barn adjacent to the slaughter facility. The slaughter facility was under FSIS’ supervision while the sale barn was not. Cattle sometimes arrived at the sale barn that were sick/down/dead or would die or go down while at the sale barn. According to personnel at the sale barn, these animals were left for the renderer to collect. The healthy ambulatory animals that remained were marketed to many buyers including the adjacent slaughter facility. When the slaughter facility was ready to accept the ambulatory animals for processing, the cattle would be moved from the sale barn to the slaughter facility where they were subject to FSIS’ inspection.

We requested the slaughter facilities to estimate the number of cattle rejected on a daily basis (there were no records to confirm the estimates). We visited a renderer in the area and found that the renderer had a contract with APHIS to collect samples for BSE testing. In this case, although we could not obtain assurance that all rejected cattle were sampled, the renderer processed a significant number of animals, as compared to the slaughter plants’ estimates of those rejected. Due to the close proximity (less than 5 miles) of the renderer to the slaughter facilities, and the premium it paid for dead cattle that were in good condition, there was a financial incentive for transport drivers to dispose of their dead animals at this renderer.

USDA/OIG-A/50601-10-KC Page 25

In our discussions with APHIS officials in Wisconsin and Iowa, they confirmed that there were plants in their States that also used pre-screening practices. On May 27, 2005, we requested APHIS and FSIS to provide a list of all slaughter facilities that pre-screened cattle for slaughter in locations away from the area designated as the official slaughter facility. Along with this request, we asked for information to demonstrate that either APHIS or FSIS confirmed there was a high likelihood that high-risk animals were sampled at other collection sites.

In response to our request, the APHIS BSE Program Manager stated that APHIS did not have information on slaughter plants that pre-screen or screen their animals for slaughter suitability off their official plant premises. To their knowledge, every company or producer that submits animals for slaughter pre-sorts or screens them for suitability at various locations away from the slaughter facility. For this reason, USDA focused its BSE sample collection efforts at other types of facilities such as renderers, pet food companies, landfills, and dead stock haulers. Further, in a letter to OIG on June 14, 2005, the administrators of APHIS and FSIS noted the following:

"…we believe that no specific actions are necessary or appropriate to obtain reasonable assurance that animals not presented for slaughter are being tested for BSE. There are several reasons for our position. First, we do not believe that the practice is in fact causing us to not test a significant enough number of animals in our enhanced surveillance program to invalidate the overall results. Second, OIG has concluded that because of the geographical proximity and business relationships of the various entities involved in the case investigated, there is reasonable assurance that a majority of the rejected cattle had been sampled. Third, it is also important to remember that the goal of the enhanced surveillance program is to test a sufficient number of animals to allow us to draw conclusions about the level of BSE (if any) in the American herd…We believe that the number we may be not testing because of the "pre-sorting" practice does not rise to a significant level. The number of animals tested to date has far exceeded expectations, so it is reasonable to infer that there are few of the animals in question, or that we are testing them at some other point in the process…APHIS estimated…there were approximately 446,000 high risk cattle…[and APHIS has]…tested over 375,000 animals in less than 1 year. This indicated that we are missing few animals in the high-risk population, including those that might be pre-sorted before entering a slaughter facility’s property."


APHIS notes that for the current surveillance program, it had established regional goals and APHIS was not trying to meet particular sampling levels in particular States. However, we believe that it would be advantageous for APHIS to monitor collection data and increase outreach when large geographical areas such as the above States do not provide samples in proportion to the numbers and types of cattle in the population.

We also disagree with APHIS/FSIS’ contention that because they have tested over 375,000 of their 446,000 estimate of high risk cattle, few in the high-risk population are being missed, including those that might be pre-screened before entering a slaughter facility’s property. In our prior audit, we reported that APHIS underestimated the high-risk population; we found that this estimate should have been closer to 1 million animals (see Finding 1). We recognize that BSE samples are provided on a voluntary basis; however, APHIS should consider industry practice in any further maintenance surveillance effort. Animals unsuitable for slaughter exhibiting symptoms not inconsistent with BSE should be sampled and their clinical signs recorded. However, this cited industry practice results in rejected animals not being made available to either APHIS or FSIS veterinarians for their observation and identification of clinical signs exhibited ante mortem. Although these animals may be sampled later at other collection sites, the animals are provided post mortem without information as to relevant clinical signs exhibited ante mortem. For these reasons, we believe APHIS needs to

USDA/OIG-A/50601-10-KC Page 27

observe these animals ante mortem when possible to assure the animals from the target population are ultimately sampled and the clinical signs evaluated.



Date: June 21, 2007 at 2:49 pm PST

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduledfor May 2007.


Topics that will be covered in ongoing or planned reviews under Goal 1 include:

soundness of BSE maintenance sampling (APHIS), implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),


The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.


Office of the United States Attorney District of Arizona

FOR IMMEDIATE RELEASE For Information Contact Public Affairs

February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625Cell: (602) 525-2681



Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, FarmFresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.

Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin.


Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department ofAgriculture, Office of Inspector General. The prosecutionis being handled by Robert Long, Assistant U.S. Attorney, District ofArizona, Phoenix.CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee)# # #

Thursday, June 26, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

Saturday, April 5, 2008


Tuesday, July 1, 2008

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

Friday, August 8, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed

Thursday, October 15, 2009

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009

Sunday, October 18, 2009

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009

Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009


----- Original Message ----- From: "Terry S. Singeltary Sr." To: Sent: Thursday, November 05, 2009 9:25 PM Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009

Thursday, November 12, 2009

BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009

Thursday, March 19, 2009


Sunday, September 6, 2009




Monday, July 27, 2009



''nobody has ever ask''

''they dont want our comment''

''they don't want to know, the don't care''

''i have tried repeatedly''

''level of absolute ignorance''

''Entire policy was driven...heard from mr. laycraft, so now, after time has passed, it's ok for Canada, cattle under 30 month, to the USA, THAT'S ALL THAT MATTERED!


''yes, i think prions are bad to eat, and you can die from them''


Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009

Monday, November 23, 2009



the myth that cattle under 30 months of age are free from BSE/TSE is just that, a myth, and it's a false myth !

Information released on 2 February 2005 Summary of information requested What statistics are available on cattle less than 30 months of age found to have BSE? Information released VLA has recorded approximately 100 cases of BSE in cattle of 30 months of age or under during the entire period of the BSE epidemic (1986 - 2005). The figure is approximate as for 51 of these the age is only estimated. This is because farmers did not have accurate documentation to confirm birth date. This was not a requirement at the time. We can confirm that of the 100 cases, 49 were under 30 months of age, of these the youngest case was 20 months old.

Youngest confirmed case 20 Months, Oldest confirmed case 22 Years, Data valid to 01 April 2008

BSE Youngest and oldest cases by year of onset - GB 20 months, 21 months, (8) 24 months, see complete list of younger than 30 month ;

BSE Youngest Japan 21 months, 23 months

The implications of the Swiss result for Britain, which has had the most BSE, are complex. Only cattle aged 30 months or younger are eaten in Britain, on the assumption, based on feeding trials, that cattle of that age, even if they were infected as calves, have not yet accumulated enough prions to be infectious. But the youngest cow to develop BSE on record in Britain was 20 months old, showing some are fast incubators. Models predict that 200-300 cattle under 30 months per year are infected with BSE and enter the food chain currently in Britain. Of these 3-5 could be fast incubators and carrying detectable quantities of prion.


PLoS ONE. 2008; 3(8): e2969. Published online 2008 August 13. doi: 10.1371/journal.pone.0002969. PMCID: PMC2493038

Copyright This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production


Monday, November 16, 2009

CANADA, USA, specified risk materials (SRMs), Environment, Fertilizer, AND Politics, just more BSe

The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.

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 $$$

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

my comments to PLosone here ;


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