Friday, September 3, 2010

Dutch report positive test for mad cow disease

Subject: Dutch report positive test for mad cow disease

Dutch report positive test for mad cow disease

AMSTERDAM, Sept 3 Fri Sep 3, 2010 7:00am EDT

AMSTERDAM, Sept 3 (Reuters) - A 10-year-old cow in the Netherlands has tested positive for BSE, more commonly known as "mad cow" disease, the first such result in more than two years, the Dutch government said on Friday.

The government ministry responsible for food quality said the animal tested positive for the brain-wasting disease bovine spongiform encephalopathy at a slaughterhouse.

It was the first positive test for BSE in the country since May 2008, the ministry said in a statement.

A spokesman for the ministry told Reuters the cow's meat was withdrawn from the food chain after a first positive test, while a second test confirmed the result.

All cows sent to slaughter in the country are tested and held aside for the results before their meat enters the system.

Mad cow disease is of particular concern because it has been known to cause a related brain-wasting disease in humans who have eaten contaminated meat.

Three people have died in the Netherlands from Creutzfeldt-Jakob disease after eating meat from a BSE positive cow. The last reported death was in January 2009. (Reporting by Ben Berkowitz; editing by James Jukwey)

Na twee jaar weer BSE-koe aangetroffen Persbericht 03-09-2010

Er is een geval van BSE vastgesteld. Het gaat om een ruim tien jaar oude koe die op het slachthuis is getest. Dit past in de verwachting van het Centraal Veterinair Instituut in Lelystad dat Nederland in de komende jaren af en toe een besmette koe zal tegenkomen.

Het ministerie van LNV is blij dat Nederland ondanks een zeer intensief testprogramma gedurende een periode van ruim twee jaar geen enkel geval van BSE aantrof. Het laatste geval was in mei 2008. In 2009 testte Nederland 405.000 runderen op BSE.,1640333&_dad=portal&_schema=PORTAL&p_news_item_id=2007820

BSE For some years now the Netherlands has been taking measures to prevent BSE (Bovine Spongiforme Encephalopathy) in its cattle herd. All EU measures were implemented, though the Netherlands has also anticipated European regulation and introduced additional measures of its own.

In spite of all these efforts the Netherlands has not been free of BSE. It was first diagnosed in the Netherlands in 1997.

Measures taken by the Dutch Government Over the years a broad package of measures has been built up to combat BSE. This is partly aimed at food safety, partly at the eradication of BSE. These measures follow the recommendations of the Office International des Epizoties (OIE), and Decisions of the EU.

The measures involve:

Tracking down diseased or suspect cattle. Since 1989 it is been compulsory for owners and veterinarians to report any cattle that show symptoms of BSE to the authorities. Evaluation of the animal's health at the slaughterhouse, prior to slaughter. Compulsory removal of risk material on slaughter; This measure was introduced in the Netherlands in 1997. It has applied to all European Member States since 1 October 2000. Treatment of animal by-products used in animal feed at 133°C and 3 bar during 20 min. since the seventies. A ban on the use of animal protein in animal feed for domestic farm animals (such as cattle). Testing for BSE on all slaughtered cattle older than 30 months. Further information on the most important measures is given below.

Removal of risk material The most important measure taken to protect the consumer against BSE is the decision that so-called risk material must be removed in the slaughterhouse. The disease-causing prions do not occur in the whole animal. They are concentrated in the brains, spinal cord and some other risk material. This material is removed on slaughter and incinerated, and so eliminated from the food chain. Disease-causing organisms have never been found in meat taken from cattle muscle (steak, etc.). The removal of risk material has been compulsory since 1997.

Ban on animal protein The aim is to eliminate BSEby removing the most important source of infection (infected animal protein).

Since 1989 there has been a ban in the Netherlands on the use of remains of ruminants in ruminant feed (cattle, sheep and goats). This ban has been tightened on a number of occasions. Since 1994 no animal protein originating from mammals (previously ruminants) may be used in ruminant feed. Since 1999 the production of feed for ruminants and feed for non-ruminants containing animal protein is totally separated. This measures prevents any contamination of feed for ruminants with animal protein. Since 1 January 2001 feed containing animal protein from mammals is not only banned for ruminants, but also for all domestic farm animals, such as pigs and chickens. Compulsory BSE test From 1 January 2001 all cattle older than 30 months presented for slaughter are subjected to a rapid BSE test, approved by the European Commission. In order to carry out these tests a piece of brain tissue is removed from the cattle. If the result is positive the final diagnosis is made by traditional microscopic study of brain tissue, according to OIE.

In addition to the testing of cattle older than 30 months, risk material is removed from slaughtered cattle intended for human consumption.,1640387&_dad=portal&_schema=PORTAL&p_document_id=111059&p_node_id=5550285&p_mode=,1640440&_dad=portal&_schema=PORTAL&p_node_id=8887325

J Neurol. 2007 July; 254(7): 958–960. Published online 2007 April 21. doi: 10.1007/s00415-006-0360-3. PMCID: PMC2779429

Copyright © Steinkopff-Verlag 2007

The first case of variant Creutzfeldt-Jakob disease in the Netherlands

Eurosurveillance, Volume 11, Issue 26, 29 June 2006 Articles C van Duijn1, H Ruijs2, A Timen2


Citation style for this article: van Duijn C, Ruijs H, Timen A.

Second probable case of vCJD in the Netherlands.

Euro Surveill. 2006;11(26):pii=2991.

Available online:

Date of submission:

Second probable case of vCJD in the Netherlands

TO DATE, 3 CASES OF nvCJD have been documented in the Netherlands ;

vCJD cases Worldwide (Netherlands = 3 cases nvCJD documented to date August 2010)

Country 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 Alive Total

Netherlands 1 1 1 3

Total Cases of Sporadic CJD (Deaths)

Sporadic CJD: Definite and probable cases

Country 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 Total

Netherlands 12 18 8 14 18 17 19 10 14 18 12 20 20 22 15 16 11 264


let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.

This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$


In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.

Saturday, August 14, 2010

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

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

Wednesday, July 28, 2010

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

Tuesday, August 03, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein

Monday, August 9, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?

Sunday, August 29, 2010

Prion Disease Round Table Conducted Wednesday December 11, 2003 at Denver, Colorado R-CALF-USA Sponsored (REVISITED AUGUST 2010)

Friday, August 27, 2010


Thursday, August 19, 2010


Thursday, August 19, 2010

SCRAPIE CANADA UPDATE Current as of 2010-07-31 The following table lists sheep flocks and/or goat herds confirmed to be infected with scrapie in Canada in 2010.

Current as of: 2010-07-31

14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America

update October 2009

T. Singeltary

Bacliff, TX, USA


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


12 years independent research of available data


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


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

Wednesday, March 31, 2010

Atypical BSE in Cattle

Friday, May 14, 2010

Prion Strain Mutation Determined by Prion Protein Conformational Compatibility and Primary Structure

Published Online May 13, 2010 Science DOI: 10.1126/science.1187107 Science Express Index

Thursday, June 03, 2010

Prion Strain Mutation and Selection John Collinge MEDICINE

Wednesday, August 18, 2010

Incidence of CJD Deaths Reported by CJD-SS in Canada as of July 31, 2010

Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)


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

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

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.-

Physician Discharge Summary, Parkland Hospital, Dallas Texas

Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team

Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence.She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers.

The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.

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

Monday, March 29, 2010

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


Thursday, August 12, 2010

USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010

Thursday, August 12, 2010

Seven main threats for the future linked to prions


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