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Officials await tests on man for human Mad Cow Disease Texas

flounder

Well-known member
sadly, this is not about terry, it's about science, most folks (not all) on this board seem to have forgotten about sound science.

there is much more to this than the hamburger eating adolescents only theory, there's much more to the mad cow story than this.

I respectfully and strenuously urge you all watch and listen to these two testimonies.

bash me, disrespect me and the dead, cuss me, do what you want, but take the time to listen to this. if you don't have realplayer, download it. it takes about two minutes here ;

http://www.real.com/


then instead of listening to some money crubbing industry ladden government paid scientist, listen to some real science for a change.

Stanley Prusiner, Nobel Peace Prize winner on the PRION

http://maddeer.org/video/embedded/prusiner.html

Steven DeArmond, Professor of Neuropathology

http://maddeer.org/video/embedded/dearmond.html

DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN

''they don't wanna know, the dont' care''

http://maddeer.org/video/embedded/prusinerclip.html


24 Jul 00 Trade Statistics: UK to US Compiled by Terry S.Singeltary Sr of Bacliff, Texas

[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these? Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.

Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]

10 January 1990 COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION

COMMITTEE ON SAFETY OF MEDICINES WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY

SURGICAL CATGUT SUTURES 2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to Licence Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licenced catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K. IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;

3006.10.0000: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE MATERIALS AND STERILETISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE; AND SIMILAR STERILE MATERIAL U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD ---> Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 10,801 3,116 143,058 40,068

Belgium . . . . . . . . . --- --- 107 14 France . . . . . . . . . 81 49 2,727 1,132 Switzerland . . . . . . . --- --- 1,357 1,693 United Kingdom . . . . . 1,188 242 35,001 5,564

U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date Subheading 300210: ANTISERA AND OTHER BLOOD FRACTIONS, AND MODIFIED IMMUNOLOGICAL PRODUCTS

3002.10.0010: HUMAN BLOOD PLASMA U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 25,740 1,827 270,357 20,476 Belgium . . . . . . . . . 14 8 145 60 France . . . . . . . . . --- --- 134 60 Netherlands . . . . . . . --- --- 11 5 Switzerland . . . . . . . 10,462 597 86,101 5,894 United Kingdom . . . . . --- --- 335 62

3002.10.0020: NORMAL HUMAN BLOOD SERA, WHETHER OR NOT FREEZE-DRIED U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 1,039 817 19,056 22,678 Austria . . . . . . . . . --- --- 9,194 18,707 Belgium . . . . . . . . . --- --- 22 15 Netherlands . . . . . . . 353 2 6,733 41 Switzerland . . . . . . . 374 218 1,084 440 United Kingdom . . . . . --- --- 1 4

3002.10.0030: HUMAN IMMUNE BLOOD SERA U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 1,926 461 14,484 3,563 ... United Kingdom . . . . . 2 8 464 192

3002.10.0040: FETAL BOVINE SERUM (FBS) U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 2,727 233 131,486 8,502 ... Belgium . . . . . . . . . --- --- 17 32 United Kingdom . . . . . 329 82 743 756

3002.10.0090: OTHER BLOOD FRACTIONS NOT ELSEWHERE SPECIFIED OR INCLUDED U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 88,467 27,343 944,412 309,947 ... United Kingdom . . . . . 1,887 2,300 26,823 23,585

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

http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/Imports/30/300290.html

U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300290: HUMAN BLOOD; ANIMAL BLOOD PREPARED FOR THERAPEUTIC, ETC. USES; TOXINS, CULTURES OF MICRO-ORGANISMS (EXCLUDING YEASTS) AND SIMILAR PRODUCTS NESOI

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 36,178 643 250,982 11,604 ... United Kingdom . . . . . 584 39 11,292 588

http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-Month/Imports/05/051199.html


U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date

Subheading 051199: ANIMAL PRODUCTS, NESOI; DEAD HORSES AND OTHER EQUINE ANIMALS, BOVINE ANIMALS, SHEEP, GOATS AND POULTRY, UNFIT FOR HUMAN CONSUMPTION, NESOI

0511.99.2000: PARINGS AND SIMILAR WASTE OF RAW HIDES OR SKINS; GLUE STOCK, NOT ELSEWHERE SPECIFIED OR INCLUDED U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

0511.99.4024: DAIRY CATTLE EMBRYOS U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Number)

<--- Mar 1999 --- <--- 1999 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . --- --- 53 16 Canada . . . . . . . . . --- --- 9 3 France . . . . . . . . . --- --- 44 13

0511.99.4050: ANIMAL PRODUCTS NOT ELSEWHERE SPECIFIED OR INCLUDED; DEAD ANIMALS OF CHAPTER 1, UNFIT FOR HUMAN CONSUMPTION U.S. Imports for Consumption: March 1999 and 1999 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Mar 1999 --- <--- 1999 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 718,476 2,313 2,206,867 4,739 Belgium . . . . . . . . . --- --- 13 18 France . . . . . . . . . 1,088 14 1,489 20 United Kingdom . . . . . 11 3 38 9

http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/Imports/30/300220.html


U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300220: VACCINES FOR HUMAN MEDICINE

3002.20.0000: VACCINES FOR HUMAN MEDICINE U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 25,702 26,150 550,258 378,735 Belgium . . . . . . . . . 14,311 12,029 248,041 199,036 France . . . . . . . . . 3,902 4,859 87,879 92,845 Switzerland . . . . . . . 716 353 9,303 4,271 United Kingdom . . . . . 4,075 1,172 162,960 47,148

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

http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/Imports/30/300230.html


U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300230: VACCINES FOR VETRINARY MEDICINE

List of (6-digit) Subheadings in this (2-digit) Chapter Next (6-Digit) Subheading ... Descending ... Ascending

Latest Monthly Data

Switch from U.S. Imports to U.S. Exports

About These Trade Data Tables

3002.30.0000: VACCINES FOR VETRINARY MEDICINE U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 --- <--- 1998 YTD --- Country Quantity Value Quantity Value

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

WORLD TOTAL . . . . . . . 6,528 237 87,149 2,715 Canada . . . . . . . . . --- --- 2,637 305 Federal Rep. of Germany --- --- 104 5 Netherlands . . . . . . . 138 64 472 192 New Zealand . . . . . . . 6,390 173 83,882 1,895 United Kingdom . . . . . --- --- 54 318

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

http://www.ita.doc.gov/industry/otea/Trade-Detail/Latest-December/Imports/30/300610.html

U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date

Subheading 300610: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE MATERIALS AND STERILE TISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE; STERILE HAEMOSTATICS, ETC.

3006.10.0000: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE MATERIALS AND STERILETISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE; AND SIMILAR STERILE MATERIAL U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

Belgium . . . . . . . . . --- --- 107 14 Federal Rep. of Germany 1,795 356 16,878 3,741 France . . . . . . . . . 81 49 2,727 1,132

Subject: Re: exports from the U.K. of it's MBM to U.S.??? Date: Tue, 8 Feb 2000 14:03:16 +0000 From: [email protected] To: [email protected] (Receipt Notification Requested) (Non Receipt Notification Requested)

Terry meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as "flours and meals of meat or offals (including tankage), unfit for human consumption; greaves". UK exports of this to the US are listed below:

Country Tonnes

1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990

Subject: Re: Imports of MBM or Ruminants to the U.S. from foreign Countries with the potential risk of BSE... Date: Tue, 28 Dec 1999 17:19:15 -0500 From: Linda Detwiler To: [email protected] (Receipt Notification Requested)

I have attached the file ibov96.txt containing all of the bovine imports for 1996.

Subject: [Fwd: IMPORTED UK AND NETHERLANDS BEEF?] -Reply Date: Thu, 3 Sep 1998 6:54:00 -0400 From: Linda Detwiler To: [email protected] (Receipt Notification Requested)

I will check on this as I had not heard about the UK. The Netherlands would not have suprised me as they did not have a case until March 1997. ... now my question would be, how many of these animals that fed on MBM's from these countries, were imported to the United States, via 3rd country routes??? i will give you that answer below...TSS

Marva Thompson Foreign Trade Reference Room 202/482-2185

"The U.S. is apparently still importing beef, pork, sheep, and lamb from countries in which BSE is found [this is probably completely legal under regulations applicable at time of import-- webmaster]:

Bovine anmls bnlss ex prcssd frozen/U.S. Imports for Consumption 1997 year to date (custom value, in thousands of dollars) (units of quantity: kilograms)

United Kingdom 37,122 kilograms, 43 thousand dollars Netherlands 56,260 kilograms, 413 thousand dollars Canada 18,141,481 kilograms, 23,914 million dollars

Livers of bovine animals, edible, frozen. U.S. Imports for consumption

Netherlands 19,230 kilograms, 25 thousand dollars Canada 160,632 kilograms, 147 thousand dollars

Tongues of bovine animals, edible, frozen U.S. Imports for consumption

Netherlands 1,047 kilograms, 4 thousand dollars Canada 767,859 kilograms, 2,028 million

Hi-qulty beef cuts w/bone in prcssd f/c u.S. Imports for consumption

Canada 25,332 kilograms, 37 thousand dollars

Beef cuts w/bone in excpt prcdssd fr/ch u.S. Imports for consumption

Netherlands 5,276 kilograms, 30 thousand dollars Canada 117,142 kilograms, 353 thousand dollars

Meat bovine anmls cuts w/bone ex prrocssd fr us imports for consumption

Netherlands 51,836 kilograms, 444 thousand dollars Canada 120,955,010 kilograms, 253,199 million

Cattle hides, whole, fresh or wet-salt u.S. Imports for consumption

Belgium 1,270 pieces, 112 thousand dollars United kingdom 36 pieces, 3 thousand dollars Ireland 12,797 pieces, 839 thousand dollars Italy 50 pieces, 10 thousand dollars Fr germany 2,500 pieces, 36 thousand dollars Canada 1,405,430 pieces, 67,320 million dollars

Hides/skins bovine anmls nesoi whole frh/wet-saltd u.S. Imports for consumption

United kingdom 13 pieces, 1 thousand dollars Italy 4 pieces, 4 thousand dollars Germany 9,455 pieces, 139 thousand dollars Canada 567,816 pieces, 17,196 million dollars

Cattle hides, whole, fresh or wet-salted u.S. Imports for consumption

1998 year to date Italy 7 pieces, 2 thousand dollars Ireland 1,408 pieces, 85 thousand dollars France 25 pieces 2 thousand dollars Canada 965,355 pieces, 37,244 million dollars

Hides and skins of bovine animals, whole, nesoi, fresh or wet-salted U.S. Imports for consumption

United kingdom 18 pieces, 3 thousand dollars Sweden 1 pieces, 1 thousand dollars Italy 2 pieces, 2 thousand dollars Germany 5,565 pieces, 72 thousand dollars Canada 84,327 pieces, 2,257 million dollars

Sheep, lamb skins, no wool, nesoi, pickled not split, u.S. Imports for Consumption

United kingdom 9,504 pieces, 88 thousand dollars Sheep, lamb skins, no wool, nesoi, pickled, split u.S. Imports for Consumption

United Kingdom 149,580 pieces, 1,212 million dollars Netherlands 50,400 pieces, 267 thousand dollars Italy 4,175 pieces, 64 thousand dollars France 13,644 pieces, 57 thousand dollars Canada 131,642 pieces, 241 thousand dollars

Flawed inspection of food is a danger, senate panel told 9-11-98 Knight Rider Tribune News

The government's current system to check food imports for possible health dangers is dangerously flawed, experts in the food business told a Senate subcommittee Thursday. U.S. inspectors check only 2 percent of all foreign shipments and consistently issue low penalties to importers who break the rules, experts said. Unscrupulous importers typically import large amounts of products that will not pass (Food and Drug Administration) inspection, said a former West Coast customs broker.

He said importers easily bypass inspections by docking at high-volume ports, such as Los Angeles-Long Beach and New York, where the inspection force is stretched thin. Inspections are so low there they virtually pass right through.

Subject: MBM/U.K. imports of MBM to the U.S./BSE Inquiry http://www.bse.org.uk/dfa/dfa25.htm Date:Mon, 10 Apr 2000 15:14:21 -0700 From: "Terry S. Singeltary Sr." To: [email protected]

69. On 14 February 1990, Mr Meldrum wrote a letter to the Chief Veterinary Officers of a number of countries. [76] On 15 February 1990, Mrs Attridge and other officials were sent a copy of the letter of 14 February 1990 and a list of the countries to which it had been sent. They were stated to be the countries which had imported ruminant based meat and bone meal from the United Kingdom. The countries listed were Norway; Sweden, Switzerland, Czechoslovakia, Hungary, Nigeria, Thailand, South Africa, Malaysia, Taiwan, Hong Kong, South Korea, Japan, Canada, USA, Turkey, Kenya, Malta, Libera, Lebanon, Saudi Arabia, Sri Lanka, Puerto Rico, Curacao, Finland.[77] The letter from Mr Meldrum included the following: Although we have kept the Office Internationale des Epizooties (OIE) fully informed about this new disease, and they will shortly be disseminating information and recommendations to member countries, I am writing to you on a personal basis to ensure that you are aware of all the developments in relation to BSE, including its likely cause. The majority of our findings have now been published in the Veterinary Record.?[78]

70. On 20 February 1990, Dr Pickles wrote to Ms Verity (APS/CMO). Dr Pickles? minute included the following: 1. Mr Meldrum is arguing that MAFF have already taken all the necessary and responsible steps to warn importing countries of the BSE dangers in UK meat and bone meal. Yet the action taken so far overseas suggest the message has not got through, or where it has this has been late. The first nation that woke up to the danger did so a year after our own feed ban. It seems even now several EC countries neither ban our imports or the general feeding of ruminant protein. It also seems the OIE and CVO have yet to inform the rest of the world. 2. I do not see how this can be claimed to be responsible?. We do not need an expert group of the Scientific Veterinary Committee to tell us British meat and bone meal is unsafe for ruminants. I fail to understand why this cannot be tackled from the British end which seems to be the only sure way of doing it, preferably by banning exports. As CMO says in his letter of 3 January surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries.??[79]

http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh

Thursday, July 24, 2008
Prion diseases are efficiently transmitted by blood transfusion in sheep
Submitted April 18, 2008 Accepted June 28, 2008

http://vcjdblood.blogspot.com/2008/07/prion-diseases-are-efficiently.html

10 people killed by new CJD-like disease

Public release date: 9-Jul-2008

Since Gambetti's team wrote a paper describing an initial 11 cases referred to his centre between 2002 and 2006 (Annals of Neurology, vol 63, p 697), another five have come to light. "So it is possible that it could be just the tip of the iceberg," Gambetti says.

snip...end

http://www.eurekalert.org/pub_releases/2008-07/ns-tpk070908.php

sporadic CJD, the big lie

Thursday, July 10, 2008 A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008

http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html

Thursday, July 10, 2008 A New Prionopathy update July 10, 2008

http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html

Saturday, June 21, 2008 HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008

http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html


Docket No. 2005N-0373 RIN number 0910-AF54 Use of Materials Derived From Cattle in Medical Products REOPENING COMMENT PERIOD Date: March 30, 2007 at 11:37 am PST

http://madcowfeed.blogspot.com/2008/07/docket-no-2005n-0373-and-rin-number.html


Sunday, July 20, 2008
Red Cross told to fix blood collection or face charges 15 years after warnings issued, few changes made to ensure safety

http://vcjdblood.blogspot.com/2008/07/red-cross-told-to-fix-blood-collection.html


Greetings again Dr. Freas et al at FDA,

THIS was like closing the barn door after the mad cows got loose. not only the red cross, but the FDA has failed the public in protecting them from the TSE aka mad cow agent. TSE agent i.e. bse, base, cwd, scrapie, tme, and any sub strains thereof. we do not know if these strains will or have transmitted to humans as subclinical TSE or clinical disease, and we do not know if they have or will transmit second, third, forth passage via friendly fire i.e. multiple potential routes via medical, surgical, pharmaceutical etc.

Saturday, December 08, 2007 Transfusion Transmission of Human Prion Diseases http://vcjdblood.blogspot.com/2006/12/vcjd-case-study-highlights-blood.html

Tuesday, October 09, 2007 nvCJD TSE BLOOD UPDATE

http://vcjdblood.blogspot.com/2007/10/nvcjd-tse-blood-update.html

Saturday, December 08, 2007 Transfusion Transmission of Human Prion Diseases

http://vcjdblood.blogspot.com/2007/12/transfusion-transmission-of-human-prion.html

Saturday, January 20, 2007 Fourth case of transfusion-associated vCJD infection in the United Kingdom

http://vcjdtransfusion.blogspot.com/2007/01/fourth-case-of-transfusion-associated.html

http://vcjdblood.blogspot.com/


vCJD case study highlights blood transfusion risk 9 Dec 2006 by Terry S. Singeltary Sr. THIS was like closing the barn door after the mad cows got loose. not only the red cross, but the FDA has failed the public in protecting them from the TSE aka mad cow agent. TSE agent ie bse, base, cwd, scrapie, tme, ... vCJD case study highlights blood transfusion risk - http://vcjdblood.blogspot.com/


Saturday, July 26, 2008
Creutzfeldt-Jakob Disease in Recipients of Corneal Transplants

http://creutzfeldt-jakob-disease.blogspot.com/2008/07/creutzfeldt-jakob-disease-in-recipients.html



FDA FAILED US

http://fdafailedus.blogspot.com/


SCIENCE BUSHWHACKED

http://sciencebushwhacked.blogspot.com/



kind regards,
terry
 

flounder

Well-known member
Mrs.Greg said:
:shock: Whoa.....all along I've believed Terrys mom died from vCJD,now I find out it was sporadic :evil: Guess I mostly ignored his posts. I'm not one for saying get rid of anyone either but I'm thinking now why are we allowing someone with a bogus cause come on here and spew hatred for the cattle industry. :???:


sadly Mrs., Greg, you have taken the low road. I am sorry to see this, and sorry to disappoint you, but my cause is not bogus, and I never once said my mother died from nothing but hvCJD, whatever the source and route is thereof. hvCJD is but one of many phenotypes of the infamous sporadic CJDs documented at 6 different phenotypes, (with NOW, new atypical unknown phenotypes to add to those 6). you and your followers on this board may not want to know the route and source of sporadic CJDs, but there are many others that do. sadly, people are dying from human TSE, and it is very apparent nobody on this board wants to know the route and source.


Mrs. Greg, my stance has never been but as follows ;


hvCJD has been around a long time, so have different strains of TSE, cwd, scrapie, and some strain of TSE in cattle here in the USA, if you go by sound science that was ignored ;

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 feeding 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.

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf


sporadic CJD is not a single strain, but multiple strains of human TSE i.e. sporadic CJD, that to date, the route and source has not been confirmed.


and for you Mrs, Greg, let me make this perfectly clear of what my mother died from ;


Subject: Creutzfeldt-Jakob Disease Presenting with Confusion and Visual Disturbance and hvCJD i.e. Heidenhain Variant CJD case report Date: July 18, 2007 at 12:31 pm PST

TO The Editor-in-Chief,

Archives of Iranian Medicine, Editorial Office,

Academy of Medical Sciences of I.R.Iran,

P.O. Box: 19395-4655, Tehran, Iran.

TSS submission to the following study, comments and submission to follow ;

Arch Iranian Med 2007; 10 (3): 397 – 400 Archives of Iranian Medicine, Volume 10, Number 3, July 2007 397

Creutzfeldt-Jakob Disease Presenting with Confusion and Visual Disturbance

Masoud Nikanfar MD*, Mehdi Farhoudi MD•**, Monireh Halimi MD***, Fereidoon Ashrafian-Bonab MD***, Kaveh Mehrvar MD†

Creutzfeldt-Jakob disease is increasingly being reported in the last three decades as a result of increased awareness for the disease. Various studies have reported an annual incidence of 0.5 – 1.5 cases of Creutzfeldt-Jakob disease per million of general population. However, in our country, like other developing countries, the disease is still under-reported. Herewith, we described our clinical experience with an autopsy-proven case of Creutzfeldt-Jakob disease.

Archives of Iranian Medicine, Volume 10, Number 3, 2007: 397 – 400.

Introduction

Prions can cause neurodegenerative diseases that have long incubation periods and progress inexorably once the clinical symptoms appear. So far, five human prion diseases have been recognized including Kuru, Creutzfeldt-Jakob disease (CJD), variant Creutzfeldt-Jakob disease (vCJD also known as new variant CJD), Gerstmann-Straussler-Scheinker (GSS) syndrome, and fatal familial insomnia (FFI).1, 2 Bovine spongiform encephalopathy (BSE), one of prion infections affecting animals, was responsible for a more widespread public attention with its possible link to vCJD.3, 4 These human prion diseases share certain common neuropathologic features including neuronal loss, proliferation of glial cells, absence of an inflammatory response, and the presence of small vacuoles within the neutrophils, which produces a spongiform appearance. The current theory is that prion diseases are associated with the accumulation of an abnormal form of a host cell protein, the so-called “prion protein” (PrP).5 This paper describes the clinical experience with an autopsy-proven case of CJD managed at the Department of Neurology of Razi Hospital, Tabriz, North-West of Iran.

Case Report

A 71-year-old woman referred to our hospital on May 3, 2004 with a one and a half-month history of visual symptoms accompanied by transient confusion and disorientation and dystonic posture in her right arm. Her family members reported that she had transient attacks of agitation, hallucinations, and confusional state with a duration of about 15 minutes. After each attack, she became normal without any memories of attacks. Gradually, the frequency of these attacks increased. Meanwhile, she complained of transient visual problems such as macropsy, micropsy, blurred vision, and color vision disturbance. She had also transient dystonic posture in her right arm. Before admission, she also developed a mild left-sided hemiparesis. She was visited by a psychiatrist who prescribed haloperidol and clonazepam with no beneficial effect; her condition became worse progressively. On admission, she had mild confusion, and headache, and vertigo. General examination was normal. In neurologic examination, she had a left hemiparesis, left central hemifacial weakness, no in her right arm. All biochemical laboratory tests of plasma and urine were normal. Cerebrospinal fluid analysis was normal. In brain computed tomography (CT) and magnetic resonance imaging (MRI), multiple lacunar infarctions and senile atrophy were reported. In her first electroencephalogram (EEG), generalized slow sharp waves appeared in all montages (Figure 1A). The patient’s general condition and level of consciousness progressively deteriorated during hospitalization. After 15 days, she developed myoclonie seizures — first in her right arm and then generalized. In the next EEG, there was progressive slowness and periodic sharp waves. In her last EEG, slow and disorganized background activity that was interrupted by repetitive discharges of large sharp waves in all montages — about one cycle per second — were recorded (Figure 1B, C). She was intubated and finally on June 9, 2004, she died of sepsis. In pathologic study performed two days after death, the spongiform encephalopathy was documented. Histopathologic examination revealed no Kuru plaque in Congo red and PAS staining. No inflammatory infiltration was present (Figure 2). Discussion

snip...full text ;

http://www.ams.ac.ir/AIM/07103/0023.pdf

Greetings Editor-in-Chief et al Archives of Iranian Medicine, Editorial Office,

I kindly wish to submit the following to the Authors of the above study, and to the Archives of Iranian Medicine, Editorial Office, Academy of Medical Sciences of I.R.Iran.

THESE symptoms are very similar of which my mother had i.e. Heidenhain Variant Creutzfeldt Jakob Disease. I can remember her and her right arm, and she would stretch her arm against the wall, ...... strange reading this. also, clinical onset of disease to death similar, approx. 12+ weeks, and of course my mother went blind at onset, again, with similar symptoms. ODD, they don't even mention the Heidenhain Variant of CJD, one of six documented phenotypes of the sporadic CJDs to date, with 'unknown' phenotype of Sporadic CJD growing in USA (14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins). ...TSS

The Heidenhain Variant of Creutzfeldt-Jakob Disease

Stefan Kropp, MD; Walter J. Schulz-Schaeffer, MD; Michael Finkenstaedt, MD; Christian Riedemann, MD; Otto Windl, PhD; Bernhard J. Steinhoff, MD; Inga Zerr, MD; Hans A. Kretzschmar, MD; Sigrid Poser, MD

Arch Neurol. 1999;56:55-61.

Objective To investigate whether typical neuropathological and radiological findings can be identified in patients with the clinical diagnosis of the Heidenhain variant of Creutzfeldt-Jakob disease (CJD).

Design Case study. The clinical symptoms, neuropathological findings, electroencephalograms, magnetic resonance images, and cerebrospinal fluid samples of 14 Heidenhain cases were evaluated. Neuropathological changes were compared with those in a group of 14 patients with ataxia as the leading clinical sign.

Setting A university hospital, base of the German National Creutzfeldt-Jakob Disease Surveillance Study.

Patients Medical records of 169 neurologically examined patients with prospectively classified and neuropathologically confirmed CJD were analyzed.

Main Outcome Measure Difference in neuropathological and radiological findings between patients with the Heidenhain variant and other patients with CJD.

Results Of 169 patients with confirmed CJD, 20% showed characteristic clinical findings such as blurred vision, visual field restriction, metamorphopsia, or cortical blindness. Disease course of the Heidenhain group, as compared with the group of all patients with definite CJD, was significantly shorter (5.7 months vs 7.5 months; P=.02, t test). Neuropathological examination of patients with the Heidenhain variant showed most pronounced changes in the occipital lobe but less damage in the cingulate gyrus and basal ganglia compared with 14 patients with CJD who had ataxia as the leading clinical sign. Eleven (92%) of 12 genetically analyzed Heidenhain cases were homozygous for methionine at codon 129 of the prion protein gene (PRNP). In 9 of 9 cases, the 14-3-3 protein was present. In 7 (78%) of 9 cases, the level of neuron-specific enolase was elevated, with a concentration above 35 ng/mL. Periodic sharp-wave complexes were observed in 11 (78%) of the 14 cases. In 7 (63%) of 11 patients, magnetic resonance images showed symmetric hyperintensities in the basal ganglia in the T2- and proton-weighted sequence. In 4 of 11 cases the T2- and proton density–weighted images showed a pronounced signal increase confined to the gray matter of the occipital and visual cortex. Isolated atrophy of the visual cortex was noticeable in 2 of 11 cases.

Conclusions The clinical presentation of the Heidenhain variant of CJD was shown to correlate with the neuropathological findings of gliosis and nerve cell loss. In patients with visual disorders of unclear origin and signs of dementia, the differential diagnosis of a Heidenhain variant of CJD must be taken into consideration.

From the Departments of Neurology (Drs Kropp, Riedemann, Zerr, and Poser), Neuropathology (Drs Schulz-Schaeffer, Windl, and Kretzschmar), Neuroradiology (Dr Finkenstaedt), and Clinical Neurophysiology (Dr Steinhoff), Georg-August-University Göttingen, Göttingen, and the MR/CT Institute Hamburg, Hamburg (Dr Finkenstaedt), Germany.

http://archneur.ama-assn.org/cgi/content/abstract/56/1/55

full text pdf ;

http://archneur.ama-assn.org/cgi/reprint/56/1/55.pdf

Of Illusions, Hallucinations and Creutzfeldt-Jakob Disease (Heidenhain’s Variant)

http://neuro.psychiatryonline.org/cgi/reprint/17/1/124.pdf

Creutzfeldt-Jakob Disease Presenting with Visual Blurring, Diplopia and Visual Loss: Heidenhain’s Variant

K E Lee,*MBBS, MRCP (UK), N K Loh,**MBBS, MRCP (UK), M Med (Int Med), A K Y Tan,***FAMS, MBBS, MRCP (UK), W L Lee,† MBBS (Hons), MRCP (UK), M Med (Paed), H T L Tjia,‡ FAMS, MBBS, M Med (Int Med)

http://www.annals.edu.sg/pdf_nov98/leeke.pdf


Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'

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

FAX COVER SHEET

DATE: 4-23-98

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

FROM: Gerald Campbell

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

Number of Pages (including cover sheet):

Message:

*CONFIDENTIALITY NOTICE*

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

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

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

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

Autopsy NO.: AU-97-00435

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

FINAL AUTOPSY DIAGNOSIS

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

***TYPE: Anatomic(A) or Clinical(C) Diagnosis. IMPORTANCE: 1-immediate cause of death (COD); 2.ureterlying COD; 3-contributory COD: 4.concomitant, significant; 5-incidental ***

Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date; Time: 01/30/98 - 0832

Page: 1 Continued .... --------------

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

Pathology Report

Autopsy NO,: AU-97-00435

MICROSCOPIC DESCRIPTION: The spongiform change is evident in all areas of neocortex, varying from mild to moderate in severity with only very mild neuronal loss and gliosis. In the bilateral occipital lobes, there is severe loss cortical neurons and gliosis, with a corresponding pallor of the underlying white matter. There is only minimal, focal spongiform change in corpus striatum, lentiform nuclei, thalamus, hippocampus, brainstem and cerebellum. There is no significant loss of neurons from the lateral geniculate nucleus, and the optic chiasm and tracts are well-myelinated.

SECTIONS TAKEN: N-l) Pituitary, N-2) Right frontal, N-3) Right inferior frontal, N-4) Right caudate putamen. N-5) Right lentiform nuclei, N-6) Right hippocampus, N-7) optic chiasm. N-8) Left inferior temporal lobe, N-9) Right inferior occipital, N-10} Cerabellum. N-l1) Midbrain, N-12) Pons, N-13) Medulla.

FINAL DIAGNOSES: BRAIN: 1. Clinical history of rapidly progressive dementia, clinically consistent with Creutzfeldt-Jakob Disease.

a. spongiform encephalopathy, most Severe in occipital lobes, consistent with Heidenhain variant of Creutzfeldt-Jakob disease.

b. Ventriculer enlargement, moderate, consistent with atrophy. 1. Communicating spherical enlargement of occipital horn of left lateral ventricle (possible incidental congenital anomaly).

DURA; Left subdural hemorrhage, recent, minimal.

PITUITARY: Severe capillary congestion.

COMMENTS; See also western blot report from Dr. Gambetti's lab Amyloid stains are not completed for this case as of this date. The results, which are not essential for the diagnosis, will be reported separately in an addendum.

(this was hand written notes) no amyloid evident in the special stains. no evidence of plaques.GAE

Gerald A. Campbell, M.D., Pathologist Division of Neuropathology

(Electronic Signature}. (Gross: 01/16/98 Final: 02/08/98

Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date: Time: 02/09/98 - 1120

Page 2 END OF REPORT -------

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

Date/Time of Death: 12/14/97 Autopsy No.: AU-97-00435

NEUROPATHOLOGY CONSULTATION

CLINICAL HISTORY This patient was a 63-year-old white female with recent onset of progressive dementia. She was well until September of this year, when she noted a decrease in her visual activity and was found to have visual field defects as well. MRI revealed no lesions in the orbits or optic pathways. She was admitted to the hospital with the working diagnosis of bilateral optic neuropathy for a course of intravenous methylprednisolone, but her vision continued to deteriorate. She developed increasing memory and speech impairment, weakness and myoclonus. She died on 12/14/97, approximately three and one-half months after her symptoms started.

Date/Time of Death: 12/14/97 13:30 Date/Time Autopsy: 12/15/97 15:00 Pathologist Resident: PENCIL/FERNANDEZ

GROSS DESCRIPTION: Submitted are the brain, convexity dura and pituitary gland.

The pituitary gland is very dark and almost hemorrhagic in appearance, but has no obvious hematoma. It is submitted totally for histology.

The right convexity dura has diffuse but minimal subdura hemorrhage, and the dura is otherwise unremarkable.

The brain is normally developed with normal size for an adult and is symmetric externally. It does not have apparent sulcal widening. There is mild congestion of the leptomeninges, which are transparent. There is no evidence of inflammatory exudete. There is no evidence of internal softenings or other lesions externally. The cerebral arteries have focal atherosclerosis, but are without significant compromise of the vessels lumens. There is no evidence of aneurysms or malformations.

The hemispheres are sliced coronally revealing, a ventricular system which is mildly enlarged. The cortical ribbon is normal in thickness throughout most of the brain, except for the inferior and medial occipital lobes bilaterally, where the cortex is firm, thin and has a brownish discoloration, more severely so on the left than the right. In addition there is a spherical enlargement of the left occipital horn of the lateral ventricle which communicates with the remainder of the lateral ventricle. The tissue of the white matter around this enlargement is somewhat softer then in other areas. Other areas of the brain are grossly unremarkable. The brainstem and cerebellum are sliced transversely, revealing normal development and no evidence of gross changes or lesions.

DICTATED BY: GERALD A. CAMPBELL, M.D., PATHOLOGIST 01/16/98

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Patient Account: 90000014-518 Med. Rec. No,: (0160)118511Q

Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex:F Race:C Admitting Dr.: Attending Dr: Date/Time Admitted: 12/14/97 1228

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

FINAL AUTOPSY REPORT Autopsy Office (409)772-2858 Autopsy No.: AU-97-00435

CLINICAL SUMMARY:

This is a 63-year-old white female with a recent onset of progressive dementia. Her past medical history is significant for hypothyroidism. She was well until September of this year, when she noted visual difficulty. By mid-October, she could not read the newspaper. She was found to have a decrease in visual acuity and visual field defects. One week after her initial evaluation, a panel of blood tests showed no significant abnormalities and a MRI revealed some periventricular white matter "plaque-like" areas but no lesions in the orbits or optic pathways.

The patient had continued deterioration and distortion of her vision. The visual field defects increased, and she was found to have paracentral scotomas which were thought to be consistent with bilateral optic neuropathy. Early in November, she was admitted to the hospital for a course of intravenous methyl prednisolone.

During her hospital stay, she was noted to have short term memory and speech impairment; her vision did not improve. She was discharged with the diagnosis of Creutzfeldt-Jakob disease.

Later, the patient developed progressive dementia with marked impairment of speech and memory. She had complete visual loss, increased weakness and myoclonus. She died on December 14, 1997.

MF /AV 12/16/97

Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01//30/98 - 0832 Page: 2 Continued .... --------------

Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr.: Date / Time Admitted : 12/14/97 1228

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

AU-97-00435

GROSS DESCRIPTION:

EXTERNAL EXAMINATION: The body is that of a 63-year-old well-nourished, well-developed white female. There is no rigor mortis present, and there is unfixed dependent lividity on the posterior surface. The head is normocephalic with a moderate amount of gray, medium length scalp hair. The irides are blue with equal pupils measuring 0.4 mm in diameter. The nares are patent with no exudate. Dentition is fair. Buccal membranes are normal. There is normal female hair distribution. The chest does not have increased anterior-posterior diameter. The abdomen is slightly protuberant. Lymph node enlargement is not present. The extremities are unremarkable. The genitalia are those of a normal female. Two well-healed remote scars are identified in the abdomen: one in the right upper quadrant and another in the superpubic area.

BRAIN: The brain weighs 1450 gm. The gyri and sulci display a normal pattern without edema or atrophy. The meninges show no abnormalities. The circle of Willis, basilar and vertebral arteries show no significant atherosclerosis. The brain is fixed in formalin for later examination by a neuropathologist (see neuropathology report). No indentation of the cingulate gyri, unci or molding of the cerebellar tonsils are noted.

SPINAL CORD: The spinal cord is not removed.

PITUITARY GLAND: The pituitary gland is removed and is fixed in formalin for subsequent examination by a neuropathologist.

MF /AV 12/16/97

Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 - 0832

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Patient Account : 90000014-518 Med. Rec. No.: (0160)118511Q patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr,: Date/Time Admitted: 12/14/97 1228

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

Pathology Report AU-97-00435

MICROSCOPIC DESCRIPTION:

BRAIN: Histologic examination of multiple sampled areas of the brain showed the characteristic features of Creutzfetdt-Jakob disease. These were present in most sections, but were particularly prominent in the occipital cortex. The spongiform degeneration was seen in the neuropil of the gray matter as multiple vacuoles amoung numerous reactive astrocytes and occasional neuronal cell bodies. These changes were most notable in the basal layer of the cortex. PAS and amyloid stains will be performed on selected sections to asses the presence of plaques.

MF /MF 01/28/98

Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 - 0832

Page: 4 Continued .... --------------

Patient Account: 90000014-518 Med. Rec. No.: (0160}118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr.: Date / Time Admitted : 12/14/97 1228

UTMB University of Texas Medical Branch Galveston, Texas 775550-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report

Autopsy office (409)772-2858 Autopsy No.: AU-97-00435

FINAL AUTOPSY REPORT

CLINICOPATHOLOGIC CORRELATION:

The clinical findings in this case strongly suggest the diagnosis of Creutzfeldt-Jakob disease: progressive dementia, typical EEG changes, visual disturbances and myoclonus. These characteristics indicate this is a "probable case of CJD", according the criteria set by the EC Surveillance Group of Creutzfeldt-Jakob Disease in Europe (1).

The definitive diagnosis of Creutzfeldt-Jakob disease, however, is established by neuropathologic findings. There are three changes that are classically described and considered diagnostic: spongiform change, neuronal loss and astrocytic gliosis. The presence of these can vary significantly in proportion and distribution and often correlate with clinical symptoms. This permits classification of the disease into several variants.

Three variants of Creutzfeldt-Jakob disease have been proposed by Roos and Gajdusek (2): frontopyramidal, with pyramidal or lower motor neuron involvement; occipitoparietal {Heidenhain), characterized by disorders in higher cortical function and vision; and diffuse, with cerebral, cortical, basal ganglia, thalamic, cerebellar, midbrain and spinal cord involvement.

Histological examination from multiple samples of the brain in this case revealed astrocytic gliosis, spongiform degeneration and neuronal loss. Although these changes were seen in most sections, they were most prominent in the occipital cortex. This correlates very well with the clinical history of visual disturbances. Based on this finding, the present case corresponds to the Heidenhain variant. It is not uncommon for Creutzfeldt-Jakob disease to present with visual symptoms as the initial manifestation of the disease. Vargas et al (3) has reported three cases with these characteristics.

There have been numerous and significant advances in our understanding of Creutzfeldt-Jakob disease and prion diseases in general. These have been reviewed in several papers written recently, including one by Horowich and Weissman (4).

In summary, this 63 year old female with a history of visual disturbances and dementia of rapid progression was found to have the neuropathologic changes characteristic of Creutzfeldt-Jakob disease, predominantly in the occipital cortex. The occipital tropism and consequent visual symptoms indicate this case corresponds to the Heidenhain variant.

REFERENCES:

Patient Name: POULTER, BARBARA Patient location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 * 0832

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Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr.: Date / Time Admitted : 12/14/97 1228

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

Autopsy No.: AU-97-00435

FINAL AUTOPSY REPORT

CLINICOPATHOLOGIC CORRELATION:

1. Budka H, et al: Tissue handling in suspected Creutzfeldt-Jakob disease (CJD) and other human spongiform encephalopathies (prion diseases), Brain Pathology. 5:319-322,1995.

2. Roos R, Gajdusek DC, Gibbs CJ Jr: The clinical characteristics of transmissible Creutzfeldt-Jakob disease. Brain 96: 1-20, 1973.

3. Vargas ME, et al: Homonymous field defect as the first Manifestation of Creutzfeldt-Jakob disease. American Journal of Ophthalmology. 119:497-504, 1995.

4. Horowich AL, Weissman JS: Deadly conformations - protein misfolding in prion disease. Cell Vol.89, 499-510, 1997.

MF /MF 01/28/98

SCOT D. PENCIL, M.D., PATHOLOGIST MARTIN FERNANDEZ, M.D. 01/29/98 (Electronic Signature)

Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 - 0832

Page: 6 END OF REPORT --------------

The University of Texas Medical Branch at Galveston

Gerald A, Campbell, Ph.D., M.D, Associate Professor and Director Division of Neuropathology Department of Pathology

February 26, 1998

Pierluigi Gambetti, M.D. Professor Institute of Pathology Case Western Reserve University 2085 Adelbert Road Cleveland Ohio 44106

Dear Dr, Gambetti:

Enclosed please find the microscopic slides and autopsy report from our patient, Barbara Poulter (Hosp.# 11851lQ, Autopsy # AU97-435). These slides are being sent for consultation at the request of Mr. Singletary, Ms. Poulter's son and next of kin. We will also send frozen tissue from the brain on dry ice next week, and someone will call you on the day the tissue is shipped. Please return the slides when you have finished with your examination. If you need any further information, please do not hesitate to call me. Thanks for your assistance with this case.

Sincerely, Gerald A. Campbell ------------------ CASE WESTERN RESERVE UNIVERSITY

February 26, 1988

Gerald Campbell, M.D,, PhD. Division of Neuropathology, G85 University TX Medical Branch Galveston, TX 77555-0785

Dear Dr. Campbell,

As per our telephone conversation concerning a recent case of CJD, I Will be willing to examine slides and the frozen tissue on western blotting, I will issue a report to you about our conclusions. Below is my address, Our Fed Ex number is XXXXXXXXXXXXXXX.

Thank your for your assistance in this matter,

Best personal regards,

Pierluigi Gambetti, M.D.

PG:In

Division of Neuropathology Pierluigi Gambetti, M.D. Director Institute Of Neuropathology 2085 Adelbert Road Cleveland, Ohio 44106

Phone 216-368-0587 Fax 216-368-2546 ------------------ CASE WESTERN RESERVE UNIVERSITY

February 27, 1998

Dr. Gerald A. Campbell The University of Texas Medical Branch at Galveston Division of Neuropathology, G85 Galveston. TX 77555-0785

Dear Dr. Campbell,

We are in receipt of the slides you sent on Mrs. Barbara Poulter (your #: AU97-435;our#098-28).

Best personal regards, Pierluigi Gambetti, M.D.

PG:sb

Division of Neuropathology Pierluigi Gambetti, M.D., Director ----------------------------------- CASE WESTERN RESERVE UNIVERSITY

March 30, 1998

Dr. Gerald A, Campbell The University of Texas Medical Branch at Galveston Division of Neuropathology Department of Pathology Galveston, Texas

Dear Dr Campbell,

We performed Western immunoblot analysis on the frozen tissue from your case #AU97-435 (our #098-28). The Immunoblot reveals the presence of protease-resistant prion protein (PrPres) confirming the diagnosis of prion disease. The immunoblot pattern of PrPres is consistent with the diagnosis of Creutzfeldt-Jakob disease.

Thank you for referring to us this interesting case.

Sincerely,

Piero Parchi, M.D.

Pierluigi Gambetti, M.D.

PP:sb

Division of Neuropathology Pierluigi Gambetti, M.D., Director Case Western Reserve University

This Autopsy report is for the use of anyone, who is trying to understand this hideous disease CJD. I hope it can be beneficial for some in researching human TSE. Please remember, this was my Mom, and to use this with great respect.

thank you, kind regards,

Terry S. Singeltary Sr., Bacliff, Texas USA

-------------------------------

BARBARA FREDERICK POULTER

DIED 12-14-97

If I had one last thing I could tell you, it would be, I love you. I'm sorry for the stupid argument we had the last few months, BEFORE this hideous disease ROARED through your body. BUT, I PROMISE MOM, YOUR DEATH WILL NOT GO UNANSWERED!

HEIDENHAN VARIANT CREUTZFELDT JAKOB DISEASE

We got a call from my Mother around the end of Oct. saying "the damn'est thing has happened, I can't see, and if I'm talking to you and I don't make sense, bare with me, I'll come back". It was a shock to all of us. It seems that a few days before, she was crossing the ferry and became frightened because she was having problems seeing. She explained it as looking down a tunnel or not being able to see from the sides, and seeing brown spots.

We had NOT been talking, over something, we had NO control of, for a few months. So I did not know she had been having these visual problems, until she was blind. These were her first symptoms. From that point on, I was with her most everyday. I had to cross the Galveston/Bolivar ferry, and its about 30 minutes each way, so as the disease progressed, it gave me a great deal of time to think. When the visual problems started, it was about 2 weeks later, and she was blind. That led to coordination, and balance problems starting. But as this hideous disease progresses, it just GOES. You don't seem to catch up with it. It was like a fire in a hurricane. We would go out and get her things she needed one day, and the next day it would be obsolete, because the disease had gone to another stage. So you started over. Her coordination and balancing led to being in a wheel-chair. She was starting to get these trembles. I also noticed how her hands and feet started to go inward. Her speech was nothing more than jerble at this time, and this was probably about the 6th week, (at this point we had to tie her to the wheel chair, to keep her from falling out). The trembles had turned into SEVERE JERKS, that at times would take 3 of us to hold her down. I will never forget that....About her 8th week she became comatose....She died around the 10th week. I had spent the night, she had problems through the night, so the nurse came. She checked her out and comforted us, (HOSPICE IS A WONDERFUL ORGANIZATION). The nurse said she seemed to be alright and that it would probably be alright to go home for a few hours. I was on the Ferry, going back to Galveston, when I got the call, she was gone. What can you do, Mom was gone, and I was stuck on the Damn Ferry, going the wrong direction.

She knew what she had. I remember, before she had lost her speech completely. After a doctors conference, and CJD had come up. She heard us say CJD, and she screamed, SHE knew! At that point, I didn't know what was, much less, CREUTZFELDT JAKOB DISEASE.....I have learned a lot since. I have learned I truly miss my Mom and I am MAD as hell that she is gone!

Terry/MADSON!!!

SYMPTOMS:

VISION - BLIND IN ABOUT 10 TO 14 DAYS

COORDINATION AND MUSCLE CONTROL SWALLOWING DIFFICULTY CONFUSION AND DEMENTIA SPEECH PROBLEMS HALLUCINATIONS TREMBLES TOO SEVERE JERKING LOSS OF WEIGHT HANDS AND FEET GREW INWARD UPPER TRUNK STIFFNESS, SHOULDER, UPPER ARM

http://www.fortunecity.com/healthclub/cpr/798/terry.htm

Back to MANY FACES OF CJD

http://www.fortunecity.com/healthclub/cpr/798/cjd.htm

From: Jeff (webwizard.vegsource.org) Subject: Very interesting letter from son of CJD victim -- and alleged connection to cows

Date: April 22, 1998 at 19:53:42 EST

This was sent to Oprah Winfrey, reprinted here by permission:

I am the madson of a deadmom who died of madcow.(heidenhain variant creutzfeldt-jacob disease.) I sat with her for 10 weeks and watched as this hideous disease ate her brain up. She wrote in her journal that she started to see brown spots on sept. 27, 1997. These were her first symptoms -- apprx.10 days later she was blind, about 2 weeks later she had lost control of her coordination, walking, and speech.

She would get these uncontrollable jerks that at times would take 3 of us to hold her down. Around the 8th week she was totally bedridden. She died in the 10th week on 12-14-97. THANK GOD!

If you ever see this disease, as I did with my mom, you will truly believe that madcow is here. I truly believe that is what my mom died of. They can call it what ever they want to.

Now, I will take this a step further. My neighbor's mother also died of c.j.d. She died on 12-14-96, they had diagnosed it as Alzheimers, until the autopsy he demanded ruled out alzheimers and ruled in c.j.d.

About a month ago my neighbor called me over, he had been going through some old boxes of his mom's and came across some pills he thought I should see. When I read the ingredients I just about sh*t!

INGREDIENTS: vacuum dried bovine brain, bone meal, bovine eye, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. It was a cow in a pill! This woman taking these pills died of c.j.d. Could it be madcow in a pill?

I called the texas dept. of health (T.D.H.) the next day, and the following day they were out here and got the pills. I had located the manufacture and called with a bogus story and a list of doctors that would prescribe them in houston. The T.D.H. called a few days later, asking for the list of doctors, their phone numbers, and told me they would take it from there. I need not pursue it any further!

Not to long ago, 4 or 5 weeks, a girl showed up at my door. She had called crying a week earlier and could not talk. She had seen a story on T.V. about my mother. Anyway, when I first saw her I knew she had seen it too (madcow). Her mother had died of c.j.d. on 2-14-97.

This disease is here and you can call it what ever you want, c.j.d., n.v.c.j.d., hvCJD, b.s.e. or madcow, for what it is. But, that young man who died of n.v.c.j.d. in England, Steve Churchhill, had the exact same symptoms as my mother. There is also a girl in Ft. Worth Texas who called me. She had seen an article about my mom in the dallas morning news. Her dad had died of c.j.d. so far we have come up with about 18 people who has died of c.j.d. in texas, 15 confirmed. I have heard from other people its up to 32.

I am tired of hearing this crap about nv-cjd being in just young people. That same old line about how nv-cjd victims are much younger and their clinical course from first sign of symptoms to death is much longer. Any diseases clinical course is going to be longer in younger people, because their body and organs are much younger and healthier. But, in the end, their brains are full of spongiform holes, just like the older folks. Just because the plaques are more extreme, does not mean its a different disease. Could it not be just a more extreme case of typical c.j.d.????

Greed is what it is all about. They banned feeding cattle to cattle. But, are still allowed to feed those downer cows to pork and poultry. Then they are still allowed to feed the pork and poultry byproducts back to the cows. Now Dr. Gibbs writes that the prion-protien can survive the digestinal track and composting process. So the prion-protein goes right back to the cow. We must ban feeding all animals to animals. Its just an endless cycle of greed thats killing people.

I have requested that further test be done on my moms brain.(frozen tissue, paraffeine sections and serum) be sent to case western reserve university in Cleveland, Ohio. Dr. Pierre Lugi Gambetti.

I hope you find some interest in this. I just don't believe we are being told everything. The gov. lied about asbestos for 75 years.

P.S.-- the results from Case Western Reserve University, on my Mothers Brain, came back positive for the prion protein PrPres, confirming the prion disease.........

kind regards,

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

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

-------- 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" <[email protected]> To: "'[email protected]'"

<[email protected]>



Dear Terry,



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

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

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

you for your interest in the paper.



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

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

phenotype to type 2 PrPSc, the commonest sporadic CJD.

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

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

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

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

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

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

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.



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

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



Emmanuel Asante

<<Asante et al 2002.pdf>> ____________________________________

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:

[email protected]k. (until 9/12/02)

New e-mail: [email protected] (active from now)

____________________________________



2008

10 people killed by new CJD-like disease

Public release date: 9-Jul-2008

Since Gambetti's team wrote a paper describing an initial 11 cases referred to his centre between 2002 and 2006 (Annals of Neurology, vol 63, p 697), another five have come to light. "So it is possible that it could be just the tip of the iceberg," Gambetti says.

snip...end

http://www.eurekalert.org/pub_releases/2008-07/ns-tpk070908.php


sporadic CJD, the big lie

Thursday, July 10, 2008 A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008

http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html


Thursday, July 10, 2008 A New Prionopathy update July 10, 2008

http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html


MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html


Saturday, June 21, 2008 HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008

http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html



http://www.usda.gov/oig/webdocs/50601-10-KC.pdf

Communicated by: Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]

http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html

http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963

There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf

JOURNAL OF NEUROLOGY

MARCH 26, 2003

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

disease in the United States

Email Terry S. Singeltary:

[email protected]

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?

http://www.neurology.org/cgi/eletters/60/2/176#535

THE PATHOLOGICAL PROTEIN

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

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.

http://www.thepathologicalprotein.com/

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

http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

2 January 2000 British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117

15 November 1999 British Medical Journal vCJD in the USA * BSE in U.S.

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406



see full text ;


Tuesday, July 29, 2008
Heidenhain Variant Creutzfeldt Jakob Disease Case Report


snip...


WHY were they planning to destroy all CJD tissue samples donated ???

Washington Times - Washington,DC,USA NIH may destroy human brain collection

By Steve Mitchell Medical Correspondent

Washington, DC, Mar. 24 (UPI) -- The National Institutes of Health may discard part or all of a rare collection that includes hundreds of human brain samples from patients that suffered from a disorder similar to mad cow disease -- unless another researcher or institution takes them on, United Press International has learned.


snip...


http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html



kind regards,
terry
 

Kato

Well-known member
You say your cause is not bogus. Please enlighten us as to exactly what your cause is. I think we've all figured it out, but it would be nice to hear it from you anyway.

Is the purpose of the incessant posts to cause all of us to quit raising cattle? It's not going to happen.

Is it to stop people from eating beef? I don't think you'll find an audience here.

Exactly what is it? Maybe if you admit to your true agenda, we can have a dialogue that means something, because all the long drawn out postings aren't being read anyway.

Unless you are willing to engage in a real conversation, I would think you are pretty much wasting your and our time here. :!:
 

Mrs.Greg

Well-known member
Terry,I'm not saying I don't sympathize with you on the loss of your mom,I do very much,I lost my mom when I was 16 my dad when I was 32. I understand the hurt. I also have watched a person die fron CJD,my 4 wonderful nephews gramma died in pretty well the same manner your mom did,its horrifying to say the least.BUT its has been looked into VERY well here in Canada and in NO WAY has it been linked to beef at all. It was sporadic.My brother-in law and his family also miss thier mom but have not become inbittered and vengeful,they don't put blame on ranchers or the beef industry,heck they still buy beef from us. I'm sure your mom would be sad to know you've takin her cause so far that you feel hurting an industry and a large group of really good people working thier butts off to put the best and safest product out to the buying public.
 

flounder

Well-known member
Kato said:
You say your cause is not bogus. Please enlighten us as to exactly what your cause is. I think we've all figured it out, but it would be nice to hear it from you anyway.

Is the purpose of the incessant posts to cause all of us to quit raising cattle? It's not going to happen.

Is it to stop people from eating beef? I don't think you'll find an audience here.

Exactly what is it? Maybe if you admit to your true agenda, we can have a dialogue that means something, because all the long drawn out postings aren't being read anyway.

Unless you are willing to engage in a real conversation, I would think you are pretty much wasting your and our time here. :!:



i agree, i am wasting my time here. ...thanks, terry
 

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