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From: TSS ()
Subject: Re: NIH says it will preserve CJD brains
Date: June 1, 2005 at 11:11 am PST

In Reply to: NIH says it will preserve CJD brains posted by TSS on May 31, 2005 at 3:09 pm:

June 1, 2005

Dear Honorable Senator John Cornyn,

I would like to take this time to thank you for your efforts in our quest to find the truth about our
loved ones death to this hideous disease and your efforts to help us preserve our loved ones brain
and tissue samples that was difficult to donate (for the sake of science in finding answers about TSE).
I sent out many letters for help to many TEXAS GOVERNMENT OFFICIALS asking for help
about this, you were the only one that took action. THANK YOU! I believe it was your intervention
in my request to NIH that helped get this in writing, that NIH will NOT destroy those samples. IT was
a ludicrous thought from the beginning, but politics as usual. I wish I could sit down with you and show
you what your fellow Gov. Scientists are NOT telling you about new studies coming out about human
and animal TSEs aka mad cow disease around the globe, and what they have NOT been doing for the
last 25 to 30 years. I also hope that you stand up and slam down President Bush's BSE MRR policy.
THIS policy will do nothing more than make legal the trading of all strains of TSE, thus, 25 to 20 years
of trying to eradicate this deadly disease will go down the drain. WE must adhere to the BSE GBR risk
assessments and make them even stronger to include all strains of TSE.

IN closing, I must say that while very happy that NIH will NOT destroy those tissue samples, I was very
disturbed about Dr. Story C. Landis comments that ;

"The tissues that are discarded are those that have either decayed to an extent that renders them no longer appropriate for research or those for which we do not have sufficient identification," Landis wrote.

"Which ones" are being destroyed? asked Terry Singeltary, who is involved with several CJD patient groups.

"With a system like this, they could destroy whatever and whenever they wanted, for whatever reason they wanted," Singeltary, whose mother died of CJD in 1997, told UPI.

"It's a perfect excuse to discard some suspicious tissue resembling vCJD or some atypical TSE related to animal TSEs in the USA," he added.


Sir, if the USDA et al are capable of rendering a stumbling and staggering suspect BSE mad cow in TEXAS,
then have it ordered destroyed, rendered, all tissues, brain, spinal cord and all destroyed so all evidence of any
TSE is gone, without any TSE testing what so ever. IF the USDA et al are capable of NOW refusing to use
the proper and most sensitive BSE/TSE testing technique to find BSE/TSE cases in the USA cattle i.e. WESTERN
BLOT (they used this to confirm the first mad cow in the USA, but since then have refused to use to confirm the
positive, positive, inconclusives because the WB worked so good the first time). All one has to do is look at the some
of the cases in Japan and you will see why the USDA et al decided not to use WB any more;

IF one looks at Japan BSE # 8 and # 9 BSE case ;

8. 6/10/2003 Holstein Steer 13/1/2001 23 mths

9. 4/11/1003 Holstein Steer 13/1/2002 21 mths

IF USDA et al are capable of covering up BSE TSE in the USA bovine, then what are we to think of what
NIH was trying to do with our loved ones CJD brain and tissue samples? WE have many TSEs in many
species in the USA. WE have had for decades. WE still know very very little about them, but the thought
of destroying those tissues were preposterous and very suspicious. THE TSE agent has been in the USA
bovine herd for decades, just not documented. IT has been proven there are more strains of TSE in the
BOVINE than one, it was even shown that USA sheep scrapie transmitted to USA bovine will NOT look
like UK BSE. Now we have a new strain of TSE in cattle that does NOT look like nvCJD in humans,
but very very similar to the sporadic CJD. WITH all this Sir, it is paramount that all human and animal TSE
are reportable in every state, and most importantly of ALL age groups. THIS is not the case now. only about
32 states have CJD reportable, and some of those have age limits on them. THIS is not acceptable. ALL animal for
human and animal consumption must be tested for TSE. Scrapie of sheep and goat is rampant in the USA,
we know nothing of those atypical Vermont sheep yet, due to the blatant irresponsibility of the USDA et al
for putting off those mouse bio assays for over 2 years. who knows about the BSE in sheep and goats that have
been imported here over the decades. CWD in deer and elk spreading faster than a wild fire. TME in mink.
Undocumented TSE in bovines in USA, all this rendered and fed back to animals for human animal consumption.
SOMEONE must step up to the plate and make them accountable. YOU have made a start. THANK YOU!


AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure 3). There were 11 new infected and source flocks reported in March (Figure 4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 39 (Figure 6), with 1 flock released in March. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN addition, as of March 31, 2005, 225 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat cases was reported in January 2005. New infected flocks, source flocks, and flocks released or put on clean-up plans for FY 2005 are depicted in Figure 10. ...


-------- Original Message --------
Subject: Re: hello Dr. Sutton...question please...scrapie...TSS
Date: Thu, 20 May 2004 14:36:09 -0400

Dear Mr. Singeltary,

The Western blot tests on these animals were completed in April of this
year. That means that we can begin the mouse inoculations. To get the
results of the Western blot tests, you will need to submit a Freedom of
Information Act request through our FOIA office. The FAX number there is

Have a nice day,

Jim Rogers

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

Subject: Sheep
Date: Sat, 12 Jun 2004 14:26:04 EDT

Mr. Singeltary.

I hope this finds you well. As you are aware I left the USDA last year. I can only update you on the sheep before that time. Contact was established with the UK on doing the bioassay studies. They agreed. However, we were prioritized after their own needs, hence the delay. I am aware that there are now additional labs in Europe running the mouse bioassay strain typing. You will have to contact USDA for further word.

Linda Detwiler


-------- Original Message -------- Subject: re-85th Meeting of SEAC - 30.11.04
Date: Tue, 21 Dec 2004 16:56:55 -0000
From: "Barlow, Tom (SEAC)"
To: "''"

Dear Mr Singeltary Thank you for you enquiry to the SEAC secretariat about mouse bioassays commissioned by the USDA to investigate TSE cases in imported sheep. After making a number of enquiries, it appears that Defra were not involved with this work. However, it is possible that a UK research laboratory wascontacted by the USDA about such tests but I have been unable to find outany further information. You may wish to make further enquiries with theUSDA.Yours sincerely Tom Barlow Dr Tom Barlow Spongiform Encephalopathy Advisory Committee (SEAC) SecretariatArea 108, 1A Page Street, London SW1P 4PQTel: 0207 904 6267


Published online before print February 17, 2004, 10.1073/pnas.0305777101

Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease

Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli *
*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.


C.C. and G.Z. contributed equally to this work.

||To whom correspondence should be addressed.

E-mail: .

-------- Original Message --------
Subject: Re: Research Project: Study of Atypical Bse Project Number: 3625-32000-073-07
Date: Sun, 2 Jan 2005 11:21:30 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
References: <>

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

Greetings list members,

I was going over the data from the 1st documented BSE/TSE cow
in the USA and find it disturbing they thought it important enough
to use WB to verify there immunohistochemistry test then. HOWEVER,
on the 3, 4, and 5 mad cow in the USA, they refused to use WB
to confirm this. I guess it worked so well the first time they could not
afford to use it again. (please note the 2nd USA mad cow was the
one in TEXAS they cover-up after witnessing the stumbling and staggering
cow and then refusing to BSE/TSE test it, just decided to send to
the render to get rid of all evidence. SO, if you count that Texas cow,
there would have most likely have been 5 confirmed cases of BSE/TSE in
the USA, if they would have used the WB like they did on the first cow)...

TSEs Touch Off
ARS Research

A year ago this month, a group of ARS
scientists and technicians gave up their Christmas time off and even
delayed family vacations to provide characterization of the first case
of bovine spongiform encephalopathy (BSE)—commonly called mad cow
disease—to be found in the United States.

On December 23, 2003, a Canadian cow shipped to slaughter from a farm in
Mabton, Washington, had come up presumptively positive for BSE in
testing by USDA's Animal and Plant Health Inspection Service (APHIS),
which has diagnostic responsibility and regulatory oversight for BSE
issues. APHIS had already used the "gold standard" diagnostic
immunohistochemistry test, which was originally developed by ARS. But
for the first U.S. case of BSE, APHIS wanted additional scientific
information that could be provided by the Western blot test.

So APHIS put in a high-priority call to veterinary medical officer
Juergen Richt and his colleagues at the Virus and Prion Diseases of
Livestock Laboratory, which is part of ARS's National Animal Disease
Center (NADC) in Ames, Iowa.

"We had experience with the Western blot test and we had all the
reagents on hand," explains Richt. "So we put our holiday plans on hold
and got everything ready so that APHIS would have verification of the
results from the immunohistochemistry test." ........... snip

full text;


Terry S. Singeltary Sr. wrote:

> ##################### Bovine Spongiform Encephalopathy
> #####################
> Research Project: Study of Atypical Bse
> Location:
> Virus and Prion Diseases of Livestock
> Project Number: 3625-32000-073-07
> Project Type: Specific C/A
> Start Date: Sep 15, 2004
> End Date: Sep 14, 2007
> Objective:
> The objective of this cooperative research project with Dr. Maria
> Caramelli from the Italian BSE Reference Laboratory in Turin, Italy,
> is to conduct comparative studies with the U.S. bovine spongiform
> encephalopathy (BSE) isolate and the atypical BSE isolates identified
> in Italy. The studies will cover the following areas: 1. Evaluation of
> present diagnostics tools used in the U.S. for the detection of
> atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate
> and other typical BSE isolates with atypical BSE cases. 3. Studies on
> transmissibility and tissue distribution of atypical BSE isolates in
> cattle and other species.
> Approach:
> This project will be done as a Specific Cooperative Agreement with the
> Italian BSE Reference Laboratory, Istituto Zooprofilattico
> Sperimentale del Piemonte, in Turin, Italy. It is essential for the
> U.S. BSE surveillance program to analyze the effectiveness of the U.S
> diagnostic tools for detection of atypical cases of BSE. Molecular
> comparisons of the U.S. BSE isolate with atypical BSE isolates will
> provide further characterization of the U.S. BSE isolate. Transmission
> studies are already underway using brain homogenates from atypical BSE
> cases into mice, cattle and sheep. It will be critical to see whether
> the atypical BSE isolates behave similarly to typical BSE isolates in
> terms of transmissibility and disease pathogenesis. If transmission
> occurs, tissue distribution comparisons will be made between cattle
> infected with the atypical BSE isolate and the U.S. BSE isolate.
> Differences in tissue distribution could require new regulations
> regarding specific risk material (SRM) removal.
>> Differences in tissue distribution could require new regulations
>> regarding specific risk material (SRM) removal.


full text ;

It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32

The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33

The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34

The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.

Visit to USA ... info on BSE and Scrapie

WHY is USA insisting _now_ not to use WB, when on the 1st _confirmed_ case Dec. 23, 2003
USA mad cow, WB was used ???

maybe this is the reason ;

JAPAN BSE # 8 & 9 cow

8. 6/10/2003 Holstein Steer 13/10/2001 23 mths
No clinical signs WB+, IHC-, HP-

9. 4/11/2003 Holstein Steer 13/1/2002
21 mths No clinical signs WB+, IHC-, HP-


More information on the first 11 Japanese BSE-cases can be found on the website of the Japanese Embassy in the US:

it's gonna be a long year........


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

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

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

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

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

PMID: 6997404

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)


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 increases.



Canada and the United States have been raised to level III (presence of BSE likely but not confirmed, or confirmed at a lower level) following a new assessment taking into account the most recent evidence. EFSAs Scientific Expert Working Group on geographic BSE risk assessment also evaluated the status of Mexico and South Africa which were classified as level III.

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 decisions
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

With kindest Regards,
I am sincerely,

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


WASHINGTON, DC 20510-4305
April 26,2005
Mr. Terry SingeltaryP.O. Box 42Bacliff, Texas 77518
Dear Mr. Singeltary:
In response to your recent request for my assistance, I have contacted the National Institutes ofHealth.
I will write you again as soon as I receive a reply.
I appreciate having the opportunity to represent you in the United States Senate and to be ofservice in this matter.


United States Senator


WASHINGTON, DC 20510-4305

May 18,2005

Mr. Terry Singeltary
P.O. Box 42Bacliff,
Texas 77518

Dear Mr. Singeltary:

Enclosed is the reply I received from the Department of Health and Human Services in
response to my earlier inquiry on your behalf. I hope this will be useful to you.
I appreciate having the opportunity to represent you in the United States Senate.
Thank you for taking time to contact me.

United States Senate

National Institutes of HealthNational Institute of NeurologicalDisorders and Stroke
Building 31, Room 8A52
31 Center Dr., MSC 2540
Bethesda, Maryland 20892-2540
Phone: 301-496-9746
Fax: 301-496-0296

May 10, 2005

The Honorable John CornynUnited States SenatorOccidental Tower5005 LBJ Freeway, Suite 1150Dallas, Texas 75244-6199

Dear Senator Cornyn:

Your letter to the National Institutes of Health (NIH) forwarding correspondence from Mr. Terry
S. Singeltary, Sr., has been forwarded to me for reply. Mr. Singeltary is concerned about thepreservation of Creutzfeldt-Jakob disease (CJD) brain samples that have been maintained by theNational Institute of Neurological Disorders and Stroke (NINDS) Intramural Research programfor many years.
I am sorry to learn that Mr. Singeltary's mother died of CJD and can certainly understand hisdesire that any tissues that could help investigators unravel the puzzle of this deadly disease arepreserved. I hope he will be pleased to learn that all the brains and other tissues with potential tohelp scientists learn about CJD are, and will continue to be, conserved. (The tissues that arediscarded are those that have either decayed to an extent that renders them no longer appropriatefor research or those for which we do not have sufficient identification.)
The purpose of gathering these brains and tissues is to help scientists learn about CJD. To that
end, some of the NINDS-held samples are distributed to investigators who can demonstrate thatthey have a compelling research or public health need for such materials. For example, sampleshave been transferred to NIH grantee Dr. Pierluigi Gambetti, who heads the National PrionDiseases Pathology Surveillance Center at Case Western Reserve University in Ohio and workswith the Centers for Disease Control and Prevention to monitor all cases of CJD in the UnitedStates. Dr. Gambetti studies the tissues to learn about the formation, physical and chemicalproperties, and pathogenic mechanisms of prion proteins, which are believed to be involved inthe cause of CJD. Samples have also been transferred to Dr. David Asher, at the U.S. Food andDrug Administration, for use in assessing a potential diagnostic test for CJD.

Page 2 - The Honorable John Cornyn

in closing, we know that donating organs and tissue from loved ones is a very difficult andpersonal choice that must often be made at the most stressful of times. We at the NINDS aregrateful to those stalwart family members who make this choice in the selfless hope that it willhelp others afflicted with CJD. We also know the invaluable contribution such donations maketo the advancement of medical science, and we are dedicated to the preservation of all of thetissue samples that can help in our efforts to overcome CJD.

I hope this information is helpful to you in responding to Mr. Singeltary.

Story C. Landis, Ph.D.
Director, National Institute ofNeurological Disorders and Stroke

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