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From: TSS (
Subject: Re: Emory University Hospital in Atlanta LIES TO PUBLIC IN MAD COW MEDIA BLITZ TO CALM NERVES
Date: October 11, 2004 at 10:19 am PST

In Reply to: Emory University Hospital in Atlanta LIES TO PUBLIC IN MAD COW MEDIA BLITZ TO CALM NERVES posted by TSS on October 11, 2004 at 9:29 am:

-------- Original Message --------
Subject: Emory University Hospital in Atlanta LIES TO PUBLIC IN MAD COW MEDIA BLITZ TO CALM NERVES
Date: Mon, 11 Oct 2004 12:24:22 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy

Contact Information:
Cindy Sanders 404-686-8538; 404-686-5500, ID # 12831 (pager)
Kathi Baker 404-791-3437; 404-686-5500, ID # 14455 (pager)
Janet Christenbury 404-226-2945, 404-686-5500, ID # 14596 (pager)

Emory Hospital Suspects case of Rare CJD: Notifying Surgical Patients

October 01, 2004

ATLANTA - Emory officials believe Creutzfeldt-Jakob disease (CJD), an
extremely rare degenerative disease, is the probable diagnosis of an
Emory University Hospital patient following a brain biopsy, and are
taking steps on the basis of that assumption. Given the rarity of this
disease, the definitive test is done by a national laboratory in
Cleveland, Ohio. Due to time requirements and the complexity of
analysis, the results are not expected for several weeks.

Nevertheless, the Hospital is in the process of notifying 98 brain and
spine surgery patients of the remote possibility they may have been
exposed to the protein that causes CJD, a very rare disease that occurs
at the rate of only one person per million per year worldwide.

Emory physicians said potential exposures might have occurred following
the September 10 brain biopsy of a patient who later received a
preliminary diagnosis of CJD.

After the biopsy, the surgical equipment used was sterilized according to
the Hospital's normal procedures, which call for instruments to be
cleaned in a solution and heated to 270 degrees Fahrenheit for four
minutes in a prevacuum surgical autoclave.

There have been no known cases of CJD transmitted by surgical
instruments in the past 28 years since the routine use of these
sterilization techniques. However, certain enhanced sterilization
measures are recommended specifically for instruments used in cases of
CJD by bodies such as the World Health Organization (WHO).

As a first precaution, on September 15, following receipt of preliminary
biopsy results, all neurosurgical equipment was re-sterilized according
to WHO guidelines for CJD. On Monday, September 27, all hospital
surgical equipment was re-sterilized according to the same enhanced
guidelines as a further precaution.

"Although we believe the chances of an exposure are extremely small, we
cannot guarantee they are zero. That is why Emory is taking every
possible step to deal with this matter," said Allan Levey, MD, PhD,
Chair of Neurology, Emory School of Medicine.

William Bornstein, MD, PhD, Chief Quality Officer, Emory Healthcare
said,"All sterilized surgical equipment in the hospital has been
resterilized using the enhanced procedures recommended for this rare
disease. We have also instituted a new policy that exceeds hospital
norms and calls for
treating every brain biopsy as a potential case of CJD and sterilizing
the instruments using the enhanced process, no matter how unlikely CJD
may appear at the time."

Hospital officials have also written to 418 non-neurosurgical patients
who were operated on in the hospital between September 10-27, describing
the events to them and explaining that any risks to non-neurosurgical
patients are even lower, if any. There are only six known cases of CJD
transmitted by surgical equipment, and all six of these patients had
brain procedures.All of those cases occurred in the 1970s before current
standards of sterilization, such as those used by Emory Hospital, were

CJD is an unusually rare, progressive degenerative disease of the brain
usually presenting as premature dementia and gradual loss of muscular
coordination. It is believed to be caused by the accumulation of an
abnormal protein, called a prion, found in nerve cells. Sporadic CJD,
which has no identified underlying cause, occurs at a rate of one case
per million people per year worldwide. It is not the disease known
popularly as "mad cow disease."

"It is Emory's policy to notify patients when we become aware of these
types of issues. It is also true, unfortunately, that there is no
diagnostic test to determine whether they have been exposed, nor are
there any known means of prevention or treatment," says Dr. Bornstein.
"We believe the risk is extremely low, but we also believe we have an
obligation to share our initial findings with our patients."

"The well-being of our patients is always our first concern," said John
Fox,President and Chief Executive Officer of Emory Healthcare. "We want to
assure our patients that we are taking every step possible to ensure
quality patient care."

The Emory Health Connection, a call center staffed by registered nurses,
is available to speak with patients who would like more information.
Emory is also making physicians available to patients and their families.

About Emory Hospitals
Emory Hospitals include Emory University Hospital, a 579-bed hospital
located on the Emory University campus in northeast Atlanta, Emory
Crawford Long Hospital, a 511-bed, community-based hospital in midtown
and Wesley Woods Hospital, a 100-bed geriatric hospital located on the
Emory campus.Emory Hospitals are components of Emory Healthcare, the
largest and most comprehensive health care system in Georgia. Other
components of Emory Healthcare are: The Emory Clinic, the Emory
Children's Center, the jointly owned Emory-Adventist Hospital, and EHCA,
LLC, a limited liability company created in collaboration with HCA


Creutzfeldt-Jakob Disease Information
(Information from National Institute of Neurological Disorders and
Stroke, National Institutes of Health)

What is Creutzfeldt-Jakob Disease?
Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, invariably
fatal brain disorder. Typically, onset of symptoms occurs at about age
60. There are three major categories of CJD: sporadic CJD, hereditary
CJD, and acquired CJD. There is currently no single diagnostic test for
CJD. The first concern is to rule out treatable forms of dementia such
as encephalitis or chronic meningitis. The only way to confirm a
diagnosis of CJD is by brain biopsy or autopsy. In a brain biopsy, a
neurosurgeon removes a small piece of tissue from the patient's brain so
that is can be examined by a neurologist. Because a correct diagnosis of
CJD does not help the patient, a brain biopsy is discouraged unless it
is need to rule out a treatable disorder. While CJD can be transmitted
to other people, the risk of this happening is extremely small.

Is there any treatment?
There is no treatment that can cure or control CJD. Current treatment is
aimed at alleviating symptoms and making the patient as comfortable as
possible. Opiate drugs can help relieve pain, and the drugs clonazepam
and sodium valproate may help relieve involuntary muscle jerks.

What is the prognosis?
About 90 percent of patients die within 1 year. In the early stages of
disease, patients may have failing memory, behavioral changes, lack of
coordination and visual disturbances. As the illness progresses, mental
deterioration becomes pronounced and involuntary movements, blindness,
weakness of extremities, and coma may occur.

What research is being done?
The leading scientific theory at this time maintains that CJD is caused
by a type of protein called a prion. The harmless and the infectious
forms of the prion protein are nearly identical, but the infectious form
takes a different folded shape than the normal protein. Researchers are
examining whether the transmissible agent is, in fact, a prion and
trying to discover factors that influence prion infectivity and how the
disorder damages the brain. Using rodent models of the disease and brain
tissue from autopsies, they are also trying to identify factors that
influence the susceptibility to the disease and that govern when in life
the disease appears.


Alzheimer's Association
225 North Michigan Avenue
17th Floor
Chicago, IL 60601-7633
Tel: 312-335-8700 800-272-3900
Fax: 312-335-1110

Centers for Disease Control and Prevention (CDCP)
U.S. Department of Health and Human Services
1600 Clifton Road, N.E.
Atlanta, GA 30333
Tel: 800-311-3435 404-639-3311/404-639-3543

Creutzfeldt-Jakob (CJD) Foundation Inc.
P.O. Box 5312
Akron, OH 44334
Tel: 800-659-1991
Fax: 330-668-2474 305-893-9050

Atlanta Hospital Cancels 'Mad Cow' Alert, FL - 56 minutes ago
... were sighs of relief from patients at Emory University Hospital in
Atlanta who have learned
they weren't exposed to the human version of mad cow disease, after ...
Emory University Hospital in Atlanta LIES TO PUBLIC IN MAD COW MEDIA
10/11/04 (0)



> There have been no known cases of CJD transmitted by surgical
> instruments in the past

> 28 years since the routine use of these sterilization techniques.

YEP, but this does not mean that it is not happening. THIS is like
saying that there is _no known_ BSE/TSE
in the USA cattle, but we all know this is not so. WE all know TSE have
been in the USA cattle for decades,
we have simply been lied to about that as well...

Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared
practices, we obtained a careful history of feed ingredients used over
the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer
or dead dairy
cattle and a few horses. Sheep had never been fed....


full text;

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough


July 13, 2004

IG Audit Finds Multiple Flaws in Mad Cow Surveillance Plan
Rep. Waxman raises questions about the effectiveness and credibility of
USDA's response to mad cow disease, citing an audit by the USDA
Inspector General that finds systemic deficiencies in the Department's
surveillance plan and new evidence that USDA misled the public in the
wake of the detection of an infected cow in Washington State.

- Letter to USDA

IG Draft Audit

May 13, 2004

Failure To Test Staggering Cow May Reflect Wider Problems
Rep. Waxman raises concerns that the recent failure of USDA to test an
impaired cow for BSE may not be an isolated incident, citing the failure
of USDA to monitor whether cows condemned for central nervous system
symptoms are actually tested for mad cow disease.

- Letter to USDA



No mad cow results for nearly 500 cows

By Steve Mitchell
United Press International
Published 8/11/2004 11:23 AM

WASHINGTON, Aug. 11 (UPI) -- The U.S. Department of Agriculture failed
to test for mad cow disease or collect the correct portion of the brain
on nearly 500 suspect cows over the past two years -- including some in
categories considered most likely to be infected -- according to agency
records obtained by United Press International.

The testing problems mean it may never be known with certainty whether
these animals were infected with the deadly disease. Department
officials said these animals were not included in the agency's final
tally of mad cow tests, but the records, obtained by UPI under the
Freedom of Information Act, indicate at least some of them were counted...



Steve Mitchell is UPI's Medical Correspondent. E-mail
Copyright © 2001-2004 United Press International

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8

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

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.

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

PMID: 8006664 [PubMed - indexed for MEDLINE]

IMPORTS FROM CANADA [takes a few minutes to load]

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2



File Format: PDF/Adobe Acrobat -

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

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

Asante/Collinge et al, that BSE transmission to the 129-methionine

genotype can lead to an alternate phenotype that is indistinguishable

from type 2 PrPSc, the commonest _sporadic_ CJD;

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML
Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of
those who provided comments in response to Docket No. ...
Meager 8/18/01 Terry S. Singeltary Sr ...

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food
Facilities, Section 305
Comment Number: EC-254 [TSS SUBMISSION]

Dockets Entered On October 2, 2003 Table of Contents, Docket #,
Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr.
Vol #: 1, ...

Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2.
... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...

Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1

Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... - 05-20-2003
- Cached

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

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:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


Volume 3, Number 8 01 August 2003


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 search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.

Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.

Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.

Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunterstwo of whom were friendswho died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very


he complained in a letter to the Journal of the American Medical

Association (JAMA 2003; 285: 733). I hope that the CDC does not

continue to expect us to still believe that the 85% plus of all CJD

cases which are sporadic are all spontaneous, without route or source.<<<

actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...

Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.






BY Philip Yam

Yam Philip Yam News Editor Scientific American

IN light of Asante/Collinge et al findings that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: (until 9/12/02)

New e-mail: (active from now)



full text ;

AND the new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic

Creutzfeldt-Jakob disease

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk
(GBR) of the United States of America (USA)
Publication date: 20 August 2004

Adopted July 2004 (Question N° EFSA-Q-2003-083)

* 167 kB Report

* 105 kB Summary

Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working
Group on the Assessment of the Geographical Bovine Spongiform
Encephalopathy (BSE) Risk (GBR) were asked by the European Commission
(EC) to provide an up-to-date scientific report on the GBR in the United
States of America, i.e. the likelihood of the presence of one or more
cattle being infected with BSE, pre-clinically as well as clinically, in
USA. This scientific report addresses the GBR of USA as assessed in 2004
based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached
domestic cattle in the middle of the eighties. These cattle imported in
the mid eighties could have been rendered in the late eighties and
therefore led to an internal challenge in the early nineties. It is
possible that imported meat and bone meal (MBM) into the USA reached
domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle
imports from BSE risk countries were slaughtered or died and were
processed (partly) into feed, together with some imports of MBM. This
risk continued to exist, and grew significantly in the mid 90’s when
domestic cattle, infected by imported MBM, reached processing. Given the
low stability of the system, the risk increased over the years with
continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is
likely but not confirmed that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. As long as there are no
significant changes in rendering or feeding, the stability remains
extremely/very unstable. Thus, the probability of cattle to be
(pre-clinically or clinically) infected with the BSE-agent persistently

From: Terry S. Singeltary Sr. []
Sent: Tuesday, July 29, 2003 1:03 PM
Cc:;; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

Greetings FDA,


PLUS, if the USA continues to flagrantly ignore the _documented_ science
to date about the known TSEs in the USA (let alone the undocumented TSEs
in cattle), it is my opinion, every other Country that is dealing with
BSE/TSE should boycott the USA and demand that the SSC reclassify the
USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the
SSC to _flounder_ any longer on this issue, should also be regarded with
great suspicion as well. NOT to leave out the OIE and it's terribly
flawed system of disease surveillance. the OIE should make a move on CWD
in the USA, and make a risk assessment on this as a threat to human
health. the OIE should also change the mathematical formula for testing
of disease. this (in my opinion and others) is terribly flawed as well.
to think that a sample survey of 400 or so cattle in a population of 100
million, to think this will find anything, especially after seeing how
many TSE tests it took Italy and other Countries to find 1 case of BSE
(1 million rapid TSE test in less than 2 years, to find 102 BSE cases),
should be proof enough to make drastic changes of this system. the OIE
criteria for BSE Country classification and it's interpretation is very
problematic. a text that is suppose to give guidelines, but is not
understandable, cannot be considered satisfactory. the OIE told me 2
years ago that they were concerned with CWD, but said any changes might
take years. well, two years have come and gone, and no change in
relations with CWD as a human health risk. if we wait for politics and
science to finally make this connection, we very well may die before any
or changes are made. this is not acceptable. we must take the politics
and the industry out of any final decisions of the Scientific community.
this has been the problem from day one with this environmental man made
death sentence. some of you may think i am exaggerating, but you only
have to see it once, you only have to watch a loved one die from this
one time, and you will never forget, OR forgive...yes, i am still very
angry... but the transmission studies DO NOT lie, only the politicians
and the industry do... and they are still lying to this day...TSS

4 University studies showing that from 3 to 33 % of victims diagnosed
with Alzheimer's,
after autopsy, actually had CJD.

NO CJD surveillance to speak of in USA, kinda like BSE/TSE surveillance
of............ 'don't look, don't find' and or 'shoot, shovel, and shut
the hell up'.

4.5 million _diagnosed_ with Alzheimer's? some 19 million by 2050?

HOW much is actually a human TSE?

ALL animals for human/animal consumption must be tested for TSE.

ALL human TSEs must be made reportable Nationally and Internationally...
nothing less///

Terry S. Singeltary Sr. P.O. BOX 42 Bacliff, TEXAS USA

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