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BSE Timeline

Mike

Well-known member
INDEPTH: MAD COW
Timeline of BSE in Canada and the U.S.

CBC News Online | Oct. 23, 2006

Canadian Slant......My Words :lol:

Oct. 23, 2006:
The U.S. Department of Agriculture is scheduled to respond to R-CALF's appeal of its decision to allow Canadian cattle and beef products into the U.S.

August 23, 2006
The Canadian Food Inspection Agency (CFIA) confirmed a BSE case in an old Alberta cow. No part of the animal entered the food chain, and because it was eight to 10 years old, the animal may have contracted the disease before Canada banned the use of cattle parts in cattle feed, the agency said. It's the fifth case in 2006.

July 10, 2006:
The Canadian Food Inspection Agency (CFIA) reports a potential case of BSE in an Alberta dairy cow. The four-year-old cow did not enter the human or animal food system, the agency says.

July 4, 2006:
The CFIA confirms a diagnosis of BSE in a 15-year-old beef cow from Manitoba. Officials say the animal did not enter the food system and there is almost no chance the cow could have passed the disease to its offspring.

June 26, 2006:
The CFIA announces new rules that would ban cattle tissues that could transmit BSE from pet foods, livestock feed and fertilizer. The new rules widen the ban, which previously applied only to cattle and ruminant feed.

April 16, 2006:
The CFIA confirms the presence of mad cow disease in a cow at a farm in the Fraser Valley in British Columbia. Officials say no part of the dairy cow entered the human or animal food systems, and there's no risk of the disease spreading from the dead cow.

March 13, 2006:
The U.S Department of Agriculture confirms that a cow in Alabama has tested positive for mad cow disease. The department's chief veterinarian, John Clifford, says the cow spent its last year on a farm in Alabama, but officials are still trying to determine where the cow was born and raised.

Jan. 23, 2006:
The Canadian Food Inspection Agency confirms Canada's fourth case of BSE since the first one was recorded in May 2003. The animal was discovered on the Alberta farm where it was born - and no part of it entered the food chain, the agency said.

Jan. 22, 2006:
Preliminary tests on a dead cow in Alberta suggest the animal might have had bovine spongiform encephalopathy (BSE), according to officials with the Canadian Food Inspection Agency.

Dec. 12, 2005:
Japan eases the ban it imposed on Canadian and American beef two years earlier. Cattle younger than 21 months would be allowed into the country as long as high-risk materials such as the spinal cords and heads have been removed. By the end of the month, Canadian beef would once again be in Japanese supermarkets.

Oct. 14, 2005:
A United States court denies an appeal from R-CALF, a Montana-based lobby group, to extend the Canadian beef ban. The Canadian Cattlemen's Association has a final legal obstacle in Montana, where a lower court judge may rehear the case and reinstate the border ban.

July 18, 2005:
A truck carrying live Canadian cattle from Elmwood, Ont., crosses the border at Lewiston, N.Y., the first to do so after a 26-month ban on cattle imports was lifted.

July 14, 2005:
A three-judge panel of the U.S. Ninth Circuit Court of Appeals overturns a temporary injunction that banned importation of Canadian cattle. U.S. Agriculture Secretary Mike Johanns later announces that the U.S. border is "immediately" open to live Canadian cattle.

June 24, 2005:
The U.S. Department of Agriculture announces that tests have confirmed the second case of mad cow disease in the United States.

June 10, 2005:
The U.S. Department of Agriculture announces that it is investigating another possible case of BSE, but that the animal did not enter the human food or feed chain. It says the test will take several weeks.

June 6, 2005:
Japan confirms its 20th case of mad cow disease.

April 14, 2005:
The U.S. Department of Agriculture admits there were problems with the samples taken from the two cows in 1997, but insists the two cows did not have BSE.

April 12, 2005:
A CBC News investigation raises questions about two suspected cases of mad cow disease in the U.S. in 1997. The investigation found that brain parts necessary for a proper diagnosis went missing.
» More on the investigation

March 29, 2005:
The federal government will give farmers $1 billion to help them through hard times brought on by a high Canadian dollar, low prices, drought and the closed border with the U.S. Payments will begin next month and the sum will be split between grain and oilseed producers, and cattle farmers. Farmers have received about $2 billion in mad cow relief since last March, but the industry is expected to be in the red again for what will be the third year in a row.

March 2, 2005:
U.S. District Judge Richard Cebull grants a temporary injunction to stop Washington from reopening the border to Canadian cattle, scheduled for March 7. The Ranchers-Cattlemen Action Legal Fund, United Stockgrowers of America (R-CALF USA), filed a lawsuit claiming that reopening the border would cause immediate and irreparable damage.

Feb. 9, 2005:
The United States is set to reopen its border to Canadian cattle on March 7. Agriculture Minister Andy Mitchell and a group of government officials had been lobbying for several days in Washington for the reopening. But trade regulations have been tightened, and fewer cattle are expected to cross the border than before it was closed.

Jan. 13, 2005:
The Canadian Cattlemen's Association announces that it's discussing the possible cull or slaughter of the 1.76 million cattle born before 1997 to help restore faith in Canada's beef industry.

Jan. 12, 2005:
U.S. Agriculture Secretary Ann Veneman announces that the border will reopen March 7 as planned, but she's monitoring the latest BSE investigation very closely and has sent an American team to join the probe.

Jan. 11, 2005 – Fourth case in N.A.:
The CFIA announces that a third case of mad cow disease has been found in Alberta. Agency staff say the animal was born after the 1997 ban on feeding cattle remains to cattle, but became infected by eating leftover feed produced before the ban came into effect.

Jan 3. 2005:
Officials confirm that a second case of BSE has been found in Alberta.

Jan. 7, 2005:
CFIA officials tracking 141 cattle from the same farm that raised Canada's second confirmed case of BSE say cattle infected with the disease may have been eaten by people. The agency says the risk that cattle carried the infection into the human food chain is "very low."

Dec. 30, 2004:
The CFIA says initial tests may have turned up another case of BSE - in a 10 year old dairy cow. The federal agency offers few other details, saying complete test results would be available within a few days.

Dec. 29, 2004:
The U.S. Department of Agriculture announces that young live cattle from Canada will be allowed across the border into the United States beginning March 7, 2005.

Dec. 1, 2004:
U.S. President George W. Bush makes his first official visit to Canada and says the process that will open the American border to Canadian beef will take a few months. That night, he dines on Alberta beef at an official dinner.

Sept. 10, 2004:
Federal Agriculture Minister Andy Mitchell announces another $488 million in aid to the Canadian cattle industry. Ottawa's plans include increasing slaughterhouse capacity, expanding foreign markets for Canadian beef and direct aid to farmers.

Aug. 12, 2004:
A group of cattle producers called Canadian Cattlemen for Fair Trade files a lawsuit against the U.S. government seeking $150 million under a provision of NAFTA. The group says its members have suffered because of the U.S. decision to close the border to Canadian beef in May 2003.

Aug. 3, 2004:
Alberta's auditor general reports that the province's meat packers nearly tripled their profits because of mad cow disease. Cattle prices dropped, but consumer demand remained high, so packers didn't change their prices. But the packers did not receive money from a provincial program designed to help cattle producers, the auditor says.

June 15, 2004:
The Alberta government reports that more than 10 per cent of the province's $400 million in mad cow aid went to two meat-packing companies: Lakeside Farm Industries and Cargill Foods. The province's agriculture minister says they got the biggest cheques because they have the most invested in the industry.

May 13, 2004:
MPs from the Conservative party and Bloc Québécois block a House of Commons motion to impose fines on meat packers Lakeside and Cargill for refusing to release financial information. The all-party agriculture committee asked for fines of $250,000 until the companies open their books to federal auditors.

May 6, 2004:
The House of Commons finds Lakeside and Cargill in contempt of Parliament for refusing to give financial statements to the federal agriculture committee.

July 9, 2004:
Ottawa announces it will bring in new regulations to prevent animal parts linked to BSE from being fed to pets and to livestock such as chicken and pigs. The new rules would complement existing rules against using animal parts in feed for ruminants, such as cows and sheep.

April 18, 2004:
The U.S. lifts import restrictions on ground beef, bone-in cuts of beef and offal from animals younger than 30 months. The import of live cows and meat from older animals from Canada is still banned.

March 30, 2004:
The financial records of five of Canada's largest meat packers are subpoenaed to determine whether the companies profited unfairly from the mad cow crisis. The investigation is instigated by complaints that farmers have been getting low prices since BSE was found, but consumers are not paying less for their beef in stores.

Jan. 6, 2004:
Officials from the U.S. and Canada announce that DNA tests confirm a cow that tested positive for mad cow disease in Washington state was born in Alberta. The cow's DNA matched samples from the bull that sired her and from a calf she gave birth to while in Canada.

Dec. 27, 2003:
American officials announce that an ear tag on an American cow diagnosed with BSE suggests that it was imported from Canada as part of a herd of 74 dairy cows from Alberta. Officials with the CFIA say DNA tests will confirm whether the cow did indeed come from Canada.

Dec. 25, 2003:
Scientists in the U.K. confirm on Christmas Day that a cow in Washington state did have mad cow disease. Canada decides not to expand its U.S. beef import restrictions.

Dec. 24, 2003:
Mexico, Russia, Brazil, South Africa, Hong Kong, Japan, Singapore, Taiwan, Malaysia and South Korea are among the countries to ban the import of American beef. (The European Union already bans U.S. beef because of concerns about the use of growth hormones.) Canada restricts imports of cattle-related products from the U.S. to dairy products, cattle destined for immediate slaughter and boneless beef cuts from cattle under 30 months of age.


Dec. 23, 2003:
The U.S. announces its first apparent case of bovine spongiform encephalopathy (BSE), in a Holstein cow in Washington state. U.S. Secretary of Agriculture Ann Veneman confirmed the discovery, saying the animal was a "downer," one that is too sick to walk. Veneman said the USDA is taking "all appropriate actions" to deal with the situation, but told a hastily called news conference that "the risk to human health from BSE is extremely low."


TEXT: U.S. Secretary of Agriculture's announcement



Nov. 4, 2003:
Japan confirms that a bull it killed in October had mad cow disease. The 21-month-old Holstein tested positive on Oct. 29. The bull had been housed in a slaughterhouse in Hiroshima state in western Japan. It's the ninth mad cow case for Japan since the illness was discovered in the country in 2001 and its second in less than a month. Japan banned Canadian beef earlier in 2003 after a single case of mad cow disease was discovered in Alberta.



Nov. 4, 2003:
B.C. Agriculture Minister John van Dongen announces as much as $7.3 million in assistance for ranchers still suffering from the mad cow crisis. Ranchers are suffering from low prices for their cattle and a shortage of feed brought on by the summer drought, according to van Dongen.



Oct. 20, 2003:
CBC News reports that Canadian cattle could be moving across the border into the United States by early December. The U.S. Office of Management and Budget, which manages White House regulatory policies, is expected to end the ban on imports of live Canadian cattle under 30 months old. The ruling would apply to cattle from all regions across Canada.



Sept. 11, 2003:
Almost four months after a single case of BSE was found in Alberta, beef shipments from that province begin crossing into the United States. So far though, shipments of live cattle are still not allowed – only selected cuts from cattle under 30 months old.



Sept. 4, 2003:
Canadian beef producers ask the federal agriculture minister to approve a mass slaughter of 620,000 cattle. Terry Hildebrandt, the president of the Agricultural Producers Association of Saskatchewan, says the size of the Canadian herd needs to be reduced by 12 per cent immediately to prevent further damage to the sagging beef industry.



Sept. 1, 2003:
More than 450,000 kilograms of beef are served for free at hundreds of barbecues across Canada in an effort to pull the country's beef industry out of a slump caused by a single case of BSE.



Aug. 28, 2003:
The Alberta government announces that Canadian beef could be moving across the U.S. border within days. Terry Willock of Alberta Agriculture said officials have been told the United States began to issue import permits. Those permits will allow the first shipments of Canadian beef into the United States since a single case of mad cow disease slammed the border shut three months earlier.



Aug. 11, 2003:
Mexico announces it partially lifted its ban on Canadian beef imports. The move comes just three days after the U.S. made a similar decision. Like the U.S., Mexico will still ban the importation of live Canadian cattle, but the ban will be lifted for boneless meat cuts from cattle under 30 months of age, as well as lambs and goats under 12 months of age.



Aug. 9, 2003:
The U.S. Department of Agriculture announces it is easing its total ban on Canadian beef, which was imposed May 20. The announcement was a shot in the arm for Canada's beef industry. The beef trade between Canada and the United States was almost $2 billion in 2002. That market was completely lost since the border closed in May. The cost has been estimated at $11 million per day, and 5,000 jobs in Canada.



Aug. 8, 2003:
Tory Leader Peter MacKay announces that former prime minister Brian Mulroney is willing to lead a delegation to Washington to convince the Americans to re–open the border to Canadian beef. The Conservative plan is sent in a letter to Prime Minister Jean Chrétien.



July 30, 2003:
In a meeting with Canadian Agriculture Minister Lyle Vanclief, Japan's agriculture minister, Yoshiyuki Kamei, says he won't budge on his country's ban of Canadian beef. Vanclief said he tried to convince Kamei that science was on Canada's side. Vanclief outlined all the steps Canada has taken to ensure the safety of Canadian beef. "In just about every case we've been ahead of what's been happening and what has happened in the last few years in Japan."



July 26, 2003:
2,000 ranchers gather near a border crossing between Alberta and Montana to eat free hamburgers and discuss how to lift a ban on Canadian beef exports. The producers from both countries held a barbecue and urged politicians to remove the trade restriction imposed after a single case of mad cow disease was reported in Canada in May 2003.



July 25, 2003:
The government of Alberta announces it will put another $79 million into programs to help farmers hard hit by the mad cow crisis. Provincial Agriculture Minister Shirley McClellan says the money will be used to pay producers who keep cattle from slaughter, in the hope that will boost prices. The Stranded Beef program pays for the storage of Canadian beef that is sitting in bonded warehouses in foreign markets, held up by the ban.



July 19, 2003:
Ottawa announces that, to reduce the risk of mad cow disease, Canada's beef industry must remove certain parts of cattle carcasses. Beginning July 24, slaughterhouses must get rid of "specified risk materials" (SRMs), such as brains and spinal cords, from the bodies of cattle older than 30 months. The new safeguards were outlined by federal Agriculture Minister Lyle Vanclief and federal Health Minister Minister Anne McLellan.



July 15, 2003:
Alberta Premier Ralph Klein says Canada may have to consider trade sanctions against Japan and the United States unless they allow imports of Canadian beef. Klein said the bans, originally imposed because one Alberta cow was found to have mad cow disease (bovine spongiform encephalopathy) on May 20, have no scientific basis and are more about politics than food safety. Klein wasn't calling for immediate action, but he suggested sanctions may be the only way to end the dispute. "Something is going to have to be done."



July 14, 2003:
A Canadian beef industry official expresses sympathy Monday for Japanese officials who refuse to let Canadian beef into their country. Japan went through its own mad cow crisis two years ago, Ted Haney, president of the Canadian Beef Export Association, told CBC Newsworld. "The minister of agriculture lost his job. The entire government was called into question," he said. "That crisis still haunts many regulators in Japan." As a result, they need their comfort zone raised, Haney said.



July 12, 2003:
Federal Agriculture Minister Lyle Vanclief fails to persuade Japan to start importing Canadian beef again even though officials insist the animals are free of mad cow disease. "I'm frustrated that scientific data isn't getting through to the world," Vanclief told reporters after an 80-minute meeting with his Japanese counterpart, Yoshiyuki Kamei, in Ottawa. Japan is not prepared to lift its ban on Canadian beef, although Vanclief said he's not sure why.



July 10, 2003:
Federal and provincial agriculture ministers wraps up a two-day meeting promising to work harder on convincing the world that Canadian beef is safe from mad cow disease. They agree to move quickly on recent recommendations about the way animals are slaughtered. Parts of cows that might be infected with BSE, such as brains and spinal cords, will be removed from all carcasses that are being processed into human or animal feed. Details are not released on the exact new rules or a timetable for implementing them.



July 9, 2003:
Mexico's ambassador to Canada says his country may soon reopen its borders to Canadian beef. Maria Teresa Garcia de Madero doesn't give a firm date, but says her country would be the first to once again import Canadian beef. Mexico is Canada's second-largest beef market, buying $197 million in beef last year. Almost 99 per cent of the beef was from Alberta. The border has been closed since May when Canadian officials announced a single cow in Alberta had been diagnosed with bovine spongiform encephalopathy (BSE).



July 8, 2003:
Provincial and territorial governments announce they are considering limits on American beef if the U.S. doesn't reopen its border to the Canadian product. The U.S. banned Canadian beef after a single case of mad cow disease was reported in Alberta in May. Since then, Canada's 90,000-plus beef producers have lost an estimated $11 million per day.



June 26, 2003:
Health Minister Anne McLellan and Agriculture Minister Lyle Vanclief promise a quick response to recommendations from an international team of experts looking into Canada's handling of a mad cow case. The four-person investigative team examined how the CFIA handled the case of the cow from Alberta that was diagnosed with BSE.

The team's recommendations included:



Removing certain animal tissues from products destined for human consumption,
Reviewing animal feed restrictions,
Strengthening tracking and tracing systems,
Improving disease testing and surveillance,
Improving disease awareness among producers, veterinarians and the public.
June 9, 2003:
Western premiers say Ottawa should provide $360 million in compensation to help the cattle industry recover from lost revenue from the mad cow scare. The proposed Canada Temporary Slaughter Cattle Disaster Assistance program would run until Aug. 31 or until the U.S. opens the border to Canadian cattle exports.

June 8, 2003:
Alberta Premier Ralph Klein accuses the federal government of a double standard because Ottawa relaxed employment insurance rules for workers affected by SARS in Ontario but not for Western beef industry workers. "We think the federal government should treat B.C., Alberta, Saskatchewan and wherever beef is produced the same as Ontario," he said.

June 7, 2003:
A team of international scientists arrives in Regina to examine Canada's response to the mad cow outbreak. The scientists - from Europe, New Zealand and the United States - were invited by Canadian officials, who hope the international review, plus negative tests on 1,400 cattle, should help make the case that Canadian beef is safe. No second case of BSE has turned up yet.

May 30, 2003:
Tests on three more cattle herds linked to Canada's only case of mad cow disease show all of the animals were free of the disease. Three hundred and seventy animals, including the infected cow's last herd, have been slaughtered and tested. All of the tests have come back negative.

May 29, 2003:
Federal Agriculture Minister Lyle Vanclief says it's unhelpful for any province to talk about banning Alberta cattle because of fears about mad cow disease. He made the comment in response to reports that Ontario Agriculture Minister Helen Johns is looking at ways the province could prevent Prairie cattle from entering her province. Meanwhile, cattle farmers are struggling to find ways of disposing of dead cattle that normally would end up in rendering plants in Canada and the United States. Since the incidence of mad cow disease, demand for the cattle has dropped 50 per cent.

May 28, 2003:
Agriculture officials announce they plan to kill up to 700 more cattle as they try to determine how a single Alberta cow wound up with mad cow disease, and whether more cattle are infected. More than 1,000 animals will have been slaughtered in the wake of the mad cow infection discovered earlier in May in a cow that was sent to slaughter in January.

May 27, 2003:
Manitoba conservation officials say they are deciding how to dispose of hundreds of tonnes of cattle parts. This comes two days after the province's largest rendering plant, Rothsay, announced it would no longer process the parts because it can't sell them south of the border. The United States stopped importing beef from Canada because of the mad cow disease scare.

May 26, 2003:
Abattoirs have so far slaughtered nearly 400 cows during the investigation of a single case of mad cow disease in Alberta, according to federal officials. Two entire herds - including the 192-head northern Alberta herd where the infected cow last lived, and another in Saskatchewan where it might have stayed for up to four years - have been killed and the animals' brains tested for bovine spongiform encephalopathy.

May 25, 2003:
Officials say there's no evidence that more than one animal on a ranch in Alberta had mad cow disease. Preliminary tests on the herd of 150 cattle come back negative for bovine spongiform encephalopathy.

May 24, 2003:
Investigators from the CFIA add three British Columbia farms to the quarantine list, but stress that so far there's only one known case of the disease. Sixteen farms are now under quarantine including 11 in Alberta, two in Saskatchewan and three in B.C.

May 23, 2003:
At least seven ranches in Alberta and two ranches in Saskatchewan are quarantined because of concerns over mad cow disease. Food inspectors say the quarantines are merely a precaution and that there is no evidence that more than one cow in Canada has been diagnosed with bovine spongiform encephalopathy.

May 20, 2003:
The World Reference Laboratory confirms the cow had BSE. Within hours, the US announces a ban on all imports of Canadian beef. In Canada, federal and provincial agriculture ministers take to the airwaves to reassure the public that the diseased cow didn't go into the food system and that the animal's home ranch is quarantined.

May 17-19, 2003:
A federal lab tests the cow on May 17 and 18. As with previous findings, this test does not rule out BSE. Specimens are sent to the World Reference Laboratory in Britain on May 19.

May 16, 2003:
The cow killed in Alberta in January is tested for pneumonia and BSE, even though it didn't show symptoms of BSE. The provincial lab notified the CFIA later that day.

Jan. 31, 2003:
A cow was killed in northern Alberta. It was deemed unfit for consumption because it was underweight and suspected of having pneumonia. The head was kept for testing.

Aug. 23, 2002:
Marwyn Peaster, who farms near Wanham, Alta., buys the cow along with others at a cattle auction.

Summer or Fall 1998:
Cow sold to Saskatchewan farm, where it lives for four years and gives birth to four calves.

1997:
The CFIA bans the use of brains, spinal cords and other parts, known as specified risk material, or SRM, in cattle feed. The policy also applies to the remains of animals such as sheep, goats, bison, elk and deer. However, cattle can still be fed the remains of chickens, hogs and other animals, and cow blood is still used in cattle feed.

Spring 1997:
A female Black Angus cow is born and later sold to an Alberta farmer.

1993:
A single cow in Red Deer, Alta., is found with BSE. The cow had been imported from Britain in 1987. The herd of origin is destroyed along with other cattle determined to be at risk.

1992:
The CFIA implements a national BSE surveillance program. All animals with clinical signs of the disease are tested, as are some animals with no clinical signs. In May 2003, federal Agriculture Minister Lyle Vanclief said the number of samples tested in Canada was double the international standard set by the OIE, the international organization that collects and analyses information on animal disease control.
 

flounder

Well-known member
FOR IMMEDIATE RELEASE
Statement
May 4, 2004
Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA



Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.

Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.

####





http://www.fda.gov/bbs/topics/news/2004/NEW01061.html




about that other mad cow they did document in TEXAS, the atypical one ;



http://bse-atypical.blogspot.com/



http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html



4th CASE VCJD VIA BLOOD TRANSFUSION, BSE, BASE, AND SPORADIC CJD

Bacliff, Texas USA Jan 24, 07


By Terry S Singeltary



http://bloodindex.org/news_zone.php



4th CASE VCJD VIA BLOOD TRANSFUSION, BSE, BASE, AND SPORADIC CJD

Bacliff, Texas USA Jan 24, 07


By Terry S Singeltary PART I



http://bloodindex.org/view_news_zone.php?id=206



4th CASE VCJD VIA BLOOD TRANSFUSION, BSE, BASE, AND SPORADIC CJD

Bacliff, Texas USA Jan 24, 07


By Terry S Singeltary PART II


http://bloodindex.org/view_news_zone.php?id=207



truth and JUSTICE !!!



18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...

4. Members had received information about the notification by the Health
Protection Agency (HPA) of recipients of four batches of plasma products
that had been produced from blood donated by individuals that had later
developed variant Creutzfeldt Jakob Disease (vCJD). THESE batches HAD NOT
been included in a similar notification exercise in 2004, as the fate of
these products COULD NOT BE TRACED at that time. The fourteenth annual
report of the National CJD Surveillance Unit had been published. The
European Food Safety Authority (EFSA) had issued a consultation on a revised
methodology for geographical bovine spongiform encephalopathy (BSE) risk
assessment. Members could submit individual responses. Submission of a SEAC
response was under consideration.

snip...

ITEM 9 - ANY OTHER BUSINESS

snip...

***$$$***

64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.
Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a
mouse model it was possible to alleviate the pathological changes of prion
disease by suppressing expression of the prion protein gene after infection.


http://www.seac.gov.uk/minutes/95.pdf


TSS



----- Original Message -----
From: "Terry S. Singeltary Sr." <[email protected]>
To: "Bovine Spongiform Encephalopathy" <[email protected]>
Cc: <[email protected]>; <[email protected]>;
<[email protected]>; "Sustainable Agriculture Network Discussion Group"
<[email protected]>
Sent: Thursday, January 18, 2007 10:47 AM
Subject: [BLOODCJD] Fourth case of transfusion-associated vCJD infection in
the United Kingdom



Subject: Fourth case of transfusion-associated vCJD infection in the United
Kingdom
Date: January 18, 2007 at 8:32 am PST


Fourth case of transfusion-associated vCJD infection in the United Kingdom

Editorial team ([email protected]), Eurosurveillance
editorial office

A suspected case of variant Creutzfeldt-Jakob disease (vCJD) has recently
been diagnosed in a patient in the United Kingdom (UK), who received a blood
transfusion from a donor who later developed vCJD [1]. This is the fourth
case of probable transfusion transmission of vCJD infection in the UK. Three
of the four recipients developed symptoms of vCJD.
The first symptomatic case of vCJD associated with blood transfusion was
identified in December 2003. This individual developed vCJD six and a half
years after transfusion of red cells donated by an individual who developed
symptoms of vCJD three and a half years after donation.

A second case of vCJD 'infection' was identified a few months later in a
person who had received red cells from a donor who developed symptoms of
vCJD 18 months after donation. This patient (the second case) died from
causes unrelated to vCJD five years after transfusion. Post-mortem
investigations found abnormal prion protein in the spleen and a cervical
lymph node., However, prion protein was not found in the brain, and no
pathological features of vCJD were found.

A third case developed symptoms of vCJD six years after receiving a
transfusion of red blood cells, and died two years and eight months later.
The donor of the blood involved developed vCJD about 20 months after
donating it.

These three cases have been published as case reports and in the findings of
the ongoing collaborative study between the National Blood Services, the
National CJD Surveillance Unit, and the Office for National Statistics. This
study aims to collect evidence about transmission of CJD or vCJD via the
blood supply [2,3,4,5].

The new, fourth case is in a patient who developed symptoms of vCJD eight
and a half years after receiving a transfusion of red blood cells from a
donor who developed vCJD about 17 months after this blood was donated [1].
The donor to this case also donated the vCJD-implicated blood transfused to
the third case. As for all other reported clinical vCJD cases that have been
tested for genotype, this patient is a methionine homozygote at codon 129 of
the prion protein gene. The patient is currently alive.

All four cases had received transfusions of non-leucodepleted red blood
cells between 1996 and 1999. Since October 1999, leucocytes have been
removed from all blood used for transfusion in the UK. The effect of
leucodepletion on the reduction of the risk of transmission of vCJD from an
infective donation is uncertain.

This fourth case of vCJD infection associated with blood transfusion further
increases the level of concern about the risk of vCJD transmission between
humans by blood transfusion, although much remains unknown. This reinforces
the importance of the existing precautions that have been introduced to
reduce the risk of transmission of vCJD infection by blood and blood
products [6]. No cases of vCJD have been associated with fractionated plasma
products. The small group of living recipients of vCJD-implicated blood
transfusion in the UK have been informed of their potential exposure to vCJD
by blood transfusion, asked to take certain precautions to reduce the risk
of onward person-to-person transmission of vCJD during health care, and
offered specialist neurological evaluation and advice.

This article has been adapted from reference 1


References:
Health Protection Agency. Fourth case of variant CJD associated with blood
transfusion (press release). Press release, 18 January 2007.
(http://www.hpa.org.uk/hpa/news/articles/press_releases/2007/070118_vCJD.htm
)
Llewelyn CA, Hewitt PE, Knight RSG, Amar K, Cousens S, Mackenzie J, et al.
Possible transmission of variant CJD disease by blood transfusion. Lancet
2004; 363:417-21.
Peden AH, Head MW, Ritchie DL, Bell JE, Ironside JW. Preclinical vCJD after
blood transfusion in a PRNP codon 129 heterozygous patient. Lancet 2004 ;
364: 527-9.
Wroe SJ, Pal S, Siddique D, Hyare H, Macfarlane R, et al Clinical
presentation and pre-mortem diagnosis of blood transfusion-associated
variant CJD. Lancet 2006;368:2061-67.
Hewitt PE, Llewelyn CA, Mackenzie J, Will RG. Creutzfeldt-Jakob disease and
blood transfusion: results of the UK Transfusion Medicine Epidemiology
review study. Vox Sang. 2006;91(3):221-230.
Department of Health [London]. Further precautions to protect blood supply.
Press release 2004/0104, 16 March 2004.
(http://www.dh.gov.uk/PublicationsAndStatistics/PressReleases/PressReleasesN
otices/fs/en?CONTENT_ID=4076608&chk=MTwE%2Bl)

http://www.eurosurveillance.org/ew/2007/070118.asp#4


FDA NVCJD BLOOD LATEST RECALLS

PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-0576-7;
b) Red Blood Cells, Recall # B-0577-7;
c) Fresh Frozen Plasma, Recall # B-0578-7;
d) Recovered Plasma, Recall # B-0579-7
CODE
a) Units: 4588939, 4685381,4800041, 4892978, 4882799,
4883439, 4956157;
b) Unit: 4662465;
c) Units: 4800041, 4883439;
d) Units: 4588939, 4662465, 4685381, 4800041, 4892978,
4882799, 4956157
RECALLING FIRM/MANUFACTURER
Recalling Firm: Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma
City, OK, by fax on March 11, 2005. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk
for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
17 units
DISTRIBUTION
OK, MS, MI, CA, and Switzerland
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-0580-7;
b) Recovered Plasma, Recall # B-0581-7
CODE
a) and b) Unit: 5346932
RECALLING FIRM/MANUFACTURER
Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by
fax on October 27, 2005. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk
for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
OK and Switzerland

______________________________
PRODUCT
a) Red Blood Cells Leukocytes, Recall # B-0582-7;
b) Recovered Plasma, Recall # B-0583-7
CODE
a) and b) Unit: 5208304
RECALLING FIRM/MANUFACTURER
Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by
fax on April 20, 2006. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased riskfor
variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
OK and Switzerland

______________________________
PRODUCT
Source Plasma, Recall # B-0585-7
CODE
Units: 02JWIB9722, 02JWIC0263, 02JWIC0607, 02JWIC4253, 02JWIC4904,
02JWIC5216, 02JWID2018, 02JWID2958, 02JWID3310, 02JWID8505, 02JWID8842,
02JWID9390, 02JWID9844, 02JWIE0468, 02JWIE0836, 02JWIE1435, 02JWIE1812,
02JWIE2609, 02JWIE3289, 02JWIE3887, 02JWIE4309, 02JWIE4818, 02JWIE5277,
02JWIE5825, 03JWIA0857, 03JWIA1249, 03JWIA1850, 03JWIA2192, 03JWIA2825,
03JWIA3180, 03JWIA3724, 03JWIA4092, 03JWIA4691, 03JWIA5042, 03JWIA5586,
02JWIC1157, 02JWIC1458, 02JWIC2095, 02JWIC2551, 02JWIC3031, 02JWIC3491,
02JWIC3975, 02JWIC6689, 02JWIC7051, 02JWIC7609, 02JWIC7898, 02JWIC8547,
02JWIC8906, 02JWIC9494, 02JWIC9793, 02JWID0630, 02JWID1144, 02JWID1592,
02JWID3884, 02JWID4247, 02JWID4827, 02JWID5189, 02JWID5713, 02JWID6578,
02JWID6926, 02JWID7624, 02JWID7970
RECALLING FIRM/MANUFACTURER
BioLife Plasma Services L.P., Janesville, WI, by fax on April 7, 2003. Firm
initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk
for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
62 units
DISTRIBUTION
MI and Austria

______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-0586-7;
b) Recovered Plasma, Recall # B-0587-7
CODE
a) and b) Unit: 4499508
RECALLING FIRM/MANUFACTURER
Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by
fax on February 27, 2006. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk
for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
OK and Switzerland

______________________________


PRODUCT
a) Red Blood Cells, Leukocytes Reduced, Recall # B-0644-7;
b) Recovered Plasma, Recall # B-0645-7
CODE
a) and b) Units: 5219381, 4759725
RECALLING FIRM/MANUFACTURER
Oklahoma Blood Institute, Sylvan N. Goldman Center, Oklahoma City, OK, by
facsimile on December 3, 2005 or by electronic notification on December 4,
2005. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at increased risk for new
variant Creutzfeldt-Jakob Disease (nvCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
4 units
DISTRIBUTION
OK, VA, and Switzerland

______________________________


END OF ENFORCEMENT REPORT FOR JANUARY 17, 2007

###


http://www.fda.gov/bbs/topics/enforce/2007/ENF00987.html


----- Original Message -----
From: Terry S. Singeltary Sr.
To: [email protected]
Cc: [email protected] ; [email protected]
Sent: Wednesday, November 29, 2006 1:24 PM
Subject: TSE advisory committee for the meeting December 15, 2006 [TSS
SUBMISSION]


November 29, 2006


Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,


a kind and warm Holiday Greetings to you all.


i kindly wish to submit the following to the TSE advisory committee for the
meeting December 15, 2006,
about the assessment for potential exposure to vCJD in human plasma-derived
antihemophilic factor (FVIII) products
manufactured from U.S. plasma donors and related communication material ;


http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm


i see the media picked up on this as a 'low risk', from what the gov. agency
perceived to be to them;


http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines


however, i seem to disagree. from my primitive ciphering, i see it another
way. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2%
which is 1 in 50 or twenty per thousand or 20,000 per million. also, what
about the mixed genotypes/mixed susceptibility? what about the silent
carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN
strain or phenotype? this risk assessment is just more BSe to me. just
another in a long line of industry fed crap. i pray that my assessment is
the one that is wrong. but it is THEY who roll the dice with your life. it
is THEY who refuse to regulate an industry that has run amok. just from a
recall aspect of potentially tainted blood, and these are just recent
recalls ;


PRODUCT
Source Plasma, Recall # B-0054-7
CODE
Units: 03MMNC5465, 03MMNC6361, 03MMNC6801, 03MMNC7510, 03MMNC7891,
03MMNC8252, 03MMNC8801, 03MMNC9144, 03MMND1122, 03MMND1478, 03MMND1969,
03MMND2350, 03MMND2825, 03MMND3211, 03MMND3708, 03MMND4072, 03MMND4588,
03MMND4831, 03MMND5320, 03MMND5719, 03MMND6268, 03MMND6683, 03MMND7228,
03MMND7656, 03MMND8211, 03MMND8652, 03MMND9195, 03MMND9618, 03MMNE0628,
03MMNE0884, 03MMNE1597, 03MMNE1979, 03MMNE2644, 03MMNE3064, 03MMNE3707,
03MMNE4122, 03MMNE4750, 03MMNE5080, 03MMNE5876.......SNIP




full text ;


http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf


Greetings again Dr. Freas et al at FDA,


NOW, here we are in 2006, worried and still fumbling around with what should
have been
done long, long ago ;


Subject: 91ST MEETING OF THE SEAC MEETING LONDON 24TH FEB 2006
Date: March 10, 2006 at 7:36 am PST
1

© SEAC 2006

NINETY FIRST MEETING OF THE SPONGIFORM

ENCEPHALOPATHY ADVISORY COMMITTEE

The Spongiform Encephalopathy Advisory Committee held its 91st

meeting in London on 24th February 2006.


snip...


MEDICAL IMPLANTS CONTAINING BOVINE MATERIAL

SEAC considered the risk to human health from medical implants

that include bovine material sourced from the USA. This material

was used for a wide range of medical devices, some of which are

life saving and for which there are no alternative products.

SEAC considered that the source of the animal was crucial to

manage the risk. The committee suggested that other

precautionary steps be taken where practicable, such as using

material from young animals, sourcing material from countries with

good surveillance procedures and a low prevalence of disease. ......


snip...


http://www.seac.gov.uk/minutes/final90.pdf


A BIT OF HISTORY ON THIS TOPIC


TWA LITTLE minute


http://www.bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf


COMMERCIAL IN CONFIDENCE


http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf


NOT FOR PUBLICATION


http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf


http://www.bseinquiry.gov.uk/yb/1988/11/04003001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf


NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE


snip...

I was quite prepared to believe in unofficial pituitary hormones, also in
the 1970's, whether as described by Dr. Little, or in other circumstances,
for animal use.

snip...

The fact that there were jars of pituitaries (or extract) around on shelves
is attested by the still potent 1943 pituitaries, described in Stockell
Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill.
Having taken the trouble to collect them, they were not lightly thrown
out...


http://www.bseinquiry.gov.uk/files/ws/s467bx.pdf


more on the 1968 medicine act, they forgot to follow


http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf


8. The Secretary of State has a number of licences. We understand that
the inactivated polio vaccine is no longer being used. There is a stock
of smallpox vaccine. We have not been able to determine the source
material. (Made in sheep very unlikely to contain bovine ingredients).

http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf


although 176 products do _not_ conform to the CSM/VPC
guidelines.


http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf


Draft cover letter to product licence holders (considered by Human and Vet
Medicines including deer)


http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/02/22011001.pdf


(It was noted with concern that hormone extracts could be manufactured by a
veterinary surgeon for administration to animals under his care without any
Medicines Act Control.)


http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/07010001.pdf


TWA LITTLE STATEMENT 331


http://www.bseinquiry.gov.uk/files/ws/s331.pdf




SNIP...



ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bare
with me)

THE USA is in a most unique situation, one of unknown circumstances with
human and animal TSE.
THE USA has the most documented TSE in different species to date, with
substrains growing in those
species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here
with different strains),
and we know that sheep scrapie has over 20 strains of the typical scrapie
with atypical scrapie documented
and also BSE is very likely to have passed to sheep. all of which have been
rendered and fed back to animals
for human and animal consumption, a frightening scenario. WE do not know the
outcome, and to play with human
life around the globe with the very likely TSE tainted blood from the USA,
in my opinion is like playing Russian roulette,
of long duration, with potential long and enduring consequences, of which
once done, cannot be undone.
These are the facts as i have come to know through daily and extensive
research of TSE over 9 years, since 12/14/97.
I do not pretend to have all the answers, but i do know to continue to
believe in the ukbsenvcjd only theory of transmission
to humans of only this one strain from only this one TSE from only this one
part of the globe, will only lead to further failures,
and needless exposure to humans from all strains of TSE, and possibly many
more needless deaths from TSE via a multitude of
proven routes and sources via many studies with primates and rodents and
other species. ...

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

********************************************************
 

Kathy

Well-known member
Neurotoxicology. 2006 May;27(3):437-44. Epub 2006 Feb 14.

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.
Universite Francois Rabelais de Tours, Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, 31 Avenue Monge, 37200 Tours, France. [email protected]

The exchange between copper and seven transition metals is studied in a bovine brain obex homogenate according to the redox status of the medium. In reductive conditions, almost all the studied metals can substitute for copper when it is in the reduced form Cu+. This substitution is reversible, since copper uptake as Cu++ is restored in an oxidizing medium but only Co++, Ni++ and Mn++, in this decreasing order, can substitute perfectly for copper in bovine brain homogenate. To study free radical effects on bovine brain proteins, at first a copper substitution was processed in order to inhibit superoxide dismutase-like protective properties against free radicals in copper metalloproteins. Manganese was selected since a brain copper decrease correlated with a manganese increase is well-known in transmissible spongiform encephalopathies. Results for bovine brain homogenate, initially negative in the Western blot Prionics test, indicate that the substitution of manganese for copper in a reducing medium and exposure to UVA-induced free radicals produce proteinase K resistant prion. These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities may be involved in transmissible spongiform encephalopathies.

PMID: 16481041

The replacement of copper by other metals, like manganese, is not enough to cause a positive on the Western blot Prionics test. However, once these manganese loaded prions were exposed to UVA-induced free radicals the Prionics test was positive.

Biochem Biophys Res Commun. 2007 Jan 26;352(4):884-8. Epub 2006 Dec 1.

Decreased brain copper due to copper deficiency has no effect on bovine prion proteins.

Legleiter LR, Ahola JK, Engle TE, Spears JW.
Department of Animal Science and Interdepartmental Nutrition Program, North Carolina State University, Raleigh, NC, USA.

Copper (Cu) is believed to be integral in prion biology and the lack of Cu or replacement by other metal ions on prions may be involved in prion diseases. This theory has not been evaluated in the bovine. Thus, mature cows were used to determine the effects of Cu deficiency on brain Cu concentrations and prion functional characteristics. Two Cu states were induced, Cu-adequate (n=4) and Cu-deficient (n=4). Copper deficiency resulted in decreased (44%) brain Cu concentrations but had no effect on prion concentrations. Based on Western blot analysis, the molecular weights, glycoform distributions, and elution profiles of brain prions were not affected by Cu status. Importantly, Cu status did not affect prion proteinase degradability as all prions were completely degraded by proteinase K. In conclusion, Cu status affected bovine brain Cu concentrations but had no detectable effects on brain prion protein characteristics.

PMID: 17157816

This work by North Carolina researchers, while on the correct track, is misleading because the research is INCOMPLETE.

It was interesting to note than when they put 8 mature angus cows into this program, all animals were initially copper deficient.

What they are missing here is oxidative stress in the brain. A 1 year study of mature cattle purposefully fails to expose the problems which will occur in animals born to copper deficient mothers, and living many years with the copper deficiency.

Then what environment these animals are exposed to will certainly affect the levels of oxidative stress they must deal with (in their brains, and other tissues). Inhalation of radionuclides, or metals like mercury (which forms a gaseous toxin at room temperature, ie: Hg vapourizes at room temperature) will induce massive amounts of oxidative stress if these particles are inhaled, absorbed or consumed (137Cs, 90Sr, 210Pb, 210Bi, 238U, 131I, 54Mn, 40K, 60Co, mercury).

Other sources of UVA like energy, are sound. Although it is very common for many of the CJD hotspots to exist in people who live, or work, at high altitudes, there are other ways of causing oxidative stress.

Int J Radiat Biol. 2005 Apr;81(4):299-307.

Exposure to chronic noise and fractionated X-ray radiation elicits biochemical changes and disrupts body weight gain in rat.

Michaud D, Miller S, Ferrarotto C, Keith S, Bowers W, Kumarathsan P, Marro L, Trivedi A.
Consumer and Clinical Radiation Protection Bureau, Health Canada, Ottawa, Canada. [email protected]

The aim was to assess the developmental and biochemical effects resulting from separate and combined exposures to radiation and noise in adult male Sprague-Dawley rats. For 21 days, animals were exposed daily (1) to whole-body 121 kVp X-ray exposure (cumulative dose=5 Gy), (2) to random intermittent noise band-limited between 0.4 and 20 kHz; 2 h day(-1) 86 decibels (dB) and (3) to combined exposures. Control animals were housed under ambient noise conditions 55 dB A-weighted (dBA) and sham-exposed to X-rays. Body weight gain was significantly reduced in animals exposed to either X-rays or noise, and the loss was more pronounced in animals exposed to both conditions. Neither plasma adrenocorticotropic hormone (ACTH) nor corticosterone was altered by the treatment conditions. This study corroborated previous reports that ionizing radiation exposure increased plasma levels of 8-hydroxy-2'-deoxyguanosine (8-OHDG), but no effect was observed in animals co-exposed to chronic noise. Plasma big-endothelin-1 (Big ET-1) was significantly reduced in animals exposed to a combination of noise and X-rays. The results indicated that (1) adaptation to chronic noise appeared to occur at the level of the hypothalamic pituitary adrenal (HPA) response, in spite of a compromise in overall body weight gain; and (2) ionizing radiation exposure might alter systems activated by stressor exposure and/or act independently to influence health outcomes.

PMID: 16019939

This last Canadian study clearly shows there is a detrimental effect from to "body weight gain" in rats exposed to sound and ionizing radiation, with the loses in weight being most significant when exposed to both simultaneously.

What actual situations is this study trying to simulate? Battlefield exposure to DU while shooting DU rounds from a missle launcher, perhaps. Or, exposure of humans and animals to ionizing radiation (high background levels of radionuclides from DU, nuclear power stations etc) while having repeated exposure to "sonic booms" from military jet planes or the Concorde?

Mark Purdey high-lighted this epidemiological significance at all TSE hotspots. Britain used to subjected to multiple, daily fly-overs by the supersonic military jets at very low altitudes, and the Concorde flight paths. Interestingly, a CJD connection is associated with the Concorde take-off local in New York, etc.

Since TSEs are not as simple as copper being replaced by another metal, I would certainly hope that Spears, Legleiter, etc. would not stop their research at this point. Examining the offspring of these copper - /manganese+ cattle after a few years/months with continued copper deficient diet and mangese overburden, coupled with an environment which would induce long-term oxidative stressors in the brain (like UVA from various sources, sound disturbances (86dBA and up), might actually lead to "cause(s)".

A positive Prionics test after treating the copper depleted and manganese rich prion proteins with UVA - is nothing to sneeze at. Sit up and pay attention!!
 

flounder

Well-known member
Kathy said:
Neurotoxicology. 2006 May;27(3):437-44. Epub 2006 Feb 14.

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

snip...


What actual situations is this study trying to simulate? Battlefield exposure to DU while shooting DU rounds from a missle launcher, perhaps. Or, exposure of humans and animals to ionizing radiation (high background levels of radionuclides from DU, nuclear power stations etc) while having repeated exposure to "sonic booms" from military jet planes or the Concorde?

Mark Purdey high-lighted this epidemiological significance at all TSE hotspots. Britain used to subjected to multiple, daily fly-overs by the supersonic military jets at very low altitudes, and the Concorde flight paths. Interestingly, a CJD connection is associated with the Concorde take-off local in New York, etc.

Since TSEs are not as simple as copper being replaced by another metal, I would certainly hope that Spears, Legleiter, etc. would not stop their research at this point. Examining the offspring of these copper - /manganese+ cattle after a few years/months with continued copper deficient diet and mangese overburden, coupled with an environment which would induce long-term oxidative stressors in the brain (like UVA from various sources, sound disturbances (86dBA and up), might actually lead to "cause(s)".

A positive Prionics test after treating the copper depleted and manganese rich prion proteins with UVA - is nothing to sneeze at. Sit up and pay attention!!




so kathy, you now claim that cjd is caused by not only nuclear radiation, but now the CJD in New York is caused by Concord jet takeoffs. jimminey cricket, you never fail to crack me up girlfriend :shock: :lol: :lol2: :help:
 

rkaiser

Well-known member
Cracked up all right Terry. You are so focused that you can not see the picture that Kathy and the late Mark Purdey are, and were trying to paint.
Have another snort of that crack Terry and get back to reading the one and only thing that you believe, and skim ove the rest while you are on a downer.

You are as simple as Oldtimer when it comes to this stuff are'nt you?
 

Kathy

Well-known member
The common thread is that multiple factors are capable of creating the protease resistant prion.

UVA is ultraviolet radiation from 320 to 400 nm, invisible rays of energy.

Definition of Ionizing Radiation.
Ionization vs. Excitation: Excitation transfers enough energy to an orbital electron to displace it further away from the nucleus.

In ionization the electron is removed, resulting in an ion pair (the newly freed electron(-) and the rest of the atom(+))

Ionizing Radiation: Any electromagnetic or particulate radiation capable of producing ion pairs by interaction with matter. Scope limited to X and gamma rays, alpha particles, beta particles (electrons), neutrons, and charged nuclei.

Particularly important biologically since media can be altered (e.g., ionized atom in DNA molecule may be altered, thereby causing cell death, or a change in cell reproduction, division, or mutation).

Health Effects:
Generalizations: Biological effects are due to the ionization process that destroys the capacity for cell reproduction or division or causes cell mutation. The effects of one type of radiation can be reproduced by any other type.

Therefore, it is important to note this last sentence: "The effects of one type of radiation can be reproduced by any other type."

Ultrasound is acoustic (sound) energy in the form of waves having a frequency above the human hearing range.

The electromagnetic radiation spectrum is the complete range of the wavelengths of electromagnetic radiation, beginning with the longest radio waves (including those in the audio range) and extending through visible light (a very small part of the spectrum) all the way to the extremely short gamma rays that are a product of radioactive atoms.

"The effects of one type of radiation can be reproduced by any other type."

A surge suppressor (sometimes optimistically called a "surge protector") is a device inserted in the alternating current (AC) utility line and/or telephone line to prevent damage to electronic equipment from voltage "spikes" called transients. A more accurate term for this type of device is "transient suppressor."

Free Radic Biol Med. 2007 Jan 1;42(1):79-89. Epub 2006 Sep 27.

Prion protein does not redox-silence Cu(2+), but is a sacrificial quencher of hydroxyl radicals.

Nadal RC, Abdelraheim SR, Brazier MW, Rigby SE, Brown DR, Viles JH.
School of Biological and Chemical Sciences, Queen Mary, University of London, Mile End Road, London E1 4NS, UK.

Oxidative stress is believed to play a central role in the pathogenesis of prion diseases, a group of fatal neurodegenerative disorders associated with a conformational change in the prion protein (PrP(C)). The precise physiological function of PrP(C) remains uncertain; however, Cu(2+) binds to PrP(C) in vivo, suggesting a role for PrP(C) in copper homeostasis. Here we examine the oxidative processes associated with PrP(C) and Cu(2+). (1)H NMR was used to monitor chemical modifications of PrP fragments. Incubation of PrP fragments with ascorbate and CuCl(2) showed specific metal-catalyzed oxidation of histidine residues, His(96/111), and the methionine residues, Met(109/112). The octarepeat region protects His(96/111) and Met(109/112) from oxidation, suggesting that PrP(90-231) might be more prone to chemical modification. We show that Cu(2+/+) redox cycling is not 'silenced' by Cu(2+) binding to PrP, as indicated by H(2)O(2) production for full-length PrP. Surprisingly, although detection of Cu(+) indicates that the octarepeat region of PrP is capable of reducing Cu(2+) even in the absence of ascorbate, H(2)O(2) is not generated unless ascorbate is present. Full-length PrP and fragments cause a dramatic reduction in detectable hydroxyl radicals in an ascorbate/Cu(2+)/O(2) system; however, levels of H(2)O(2) production are unaffected. This suggests that PrP does not affect levels of hydroxyl radical production via Fentons cycling, but the radicals cause highly localized chemical modification of PrP(C).

PMID: 17157195

PrPC is acting like a surge suppressor in the synaptic zone; preventing cellular damage by hydroxyl radicals, when copper is bound to it. When manganese binds to PrPC and it is exposed to "electromagnetic energy spectrum" (in the study above UVA) the protein becomes protease resistant and tests positive with the Prionics Western Blot test kit.

The manganese contaminated prion protein, once it becomes protease resistant, would shut down the cellular protection systems against oxidative stress, and would initiate automatic cell death (aptosis).

Mn + PrPC + UVA (or other sources of the electromagnetic spectrum) equals a POSITIVE Prionics Western Blot test!
 

Kathy

Well-known member
Med Hypotheses. 2003 Jun;60(6):797-820.

Does an infrasonic acoustic shock wave resonance of the manganese 3+ loaded/copper depleted prion protein initiate the pathogenesis of TSE?

Purdey M.
Elworthy, Taunton, Somerset, UK. [email protected]

Intensive exposures to natural and artificial sources of infrasonic acoustic shock (tectonic disturbances, supersonic aeroplanes, etc.) have been observed in ecosystems supporting mammalian populations that are blighted by clusters of traditional and new variant strains of transmissible spongiform encephalopathy (TSE). But TSEs will only emerge in those 'infrasound-rich' environments which are simultaneously influenced by eco-factors that induce a high manganese (Mn)/low copper (Cu)-zinc (Zn) ratio in brains of local mammalian populations. Since cellular prion protein (PrPc) is a cupro-protein expressed throughout the circadian mediated pathways of the body, it is proposed that PrP's Cu component performs a role in the conduction and distribution of endogenous electromagnetic energy; energy that has been transduced from incoming ultraviolet, acoustic, geomagnetic radiations. TSE pathogenesis is initiated once Mn substitutes at the vacant Cu domain on PrPc and forms a nonpathogenic, protease resistant, 'sleeping' prion. A second stage of pathogenesis comes into play once a low frequency wave of infrasonic shock metamorphoses the piezoelectric atomic structure of the Mn 3+ component of the prion, thereby 'priming' the sleeping prion into its fully fledged, pathogenic TSE isoform - where the paramagnetic status of the Mn 3+ atom is transformed into a stable ferrimagnetic lattice work, due to the strong electron-phonon coupling resulting from the dynamic 'Jahn-Teller' type distortions of the oxygen octahedra specific to the trivalent Mn species. The so called 'infectivity' of the prion is a misnomer and should be correctly defined as the contagious field inducing capacity of the ferrimagnetic Mn 3+ component of the prion; which remains pathogenic at all temperatures below the 'curie point'. A progressive domino-like 'metal to ligand to metal' ferrimagnetic corruption of the conduits of electromagnetic superexchange is initiated. The TSE diseased brain can be likened to a solar charged battery on continuous charge; where the Mn contaminated/Cu depleted circadian-auditory pathways absorb and pile up, rather than conduct the vital life force energies of incoming ultra violet, acoustic and geomagnetic radiation. Instead of harnessing these energies for the body's own bio-rhythmic requirements, an infrasonic shock induced metamorphosis of the Mn atom intervenes; initiating an explosive pathogenesis that perverts the healthy pathways of darkness and light; Cu prions are replaced by hyperpolarized Mn 3+ prions that seed self perpetuating 'cluster bombs' of free radical mediated neurodegeneration. TSE ensues.

PMID: 12699706
 

flounder

Well-known member
rkaiser said:
Cracked up all right Terry. You are so focused that you can not see the picture that Kathy and the late Mark Purdey are, and were trying to paint.
Have another snort of that crack Terry and get back to reading the one and only thing that you believe, and skim ove the rest while you are on a downer.

You are as simple as Oldtimer when it comes to this stuff are'nt you?


dang rkeiser, you need to lay off that old crow, stop smoking whatever kathy has been smoking, and read the facts. the concord jet or nuclear radiation does not cause cjd or mad cow disease. ......



Greetings Ranchers and board members,


Kathy wrote in another thread, but yet never documented;

> didn't say that OPs caused prion disease, but that they contributed greatly
> to the UK experience,

and again, could your please reference this materials with scientific data, instead
of hearsay please ???


you can argue the origin of TSE until all the mad cows on earth come home to roost.


i.e. ;


Phosmet induces up-regulation of surface levels of the cellular prion protein.
Neuroreport. 9(7):1391-1395, May 11, 1998.
Gordon, Irit 1; Abdulla, Elizabeth M. 1; Campbell, Iain C. 1; Whatley, Stephen A. 1,2
Abstract:
CHRONIC (2 day) exposure of human neuroblastoma cells to the organophosphate pesticide phosmet induced a marked concentration-dependent increase in the levels of PrP present on the cell surface as assessed by biotin labelling and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable and non-releasable forms of PrP were increased on the plasma membrane. These increases appear to be due to post-transcriptional mechanisms, since PrP mRNA levels as assessed by Northern blotting were unaffected by phosmet treatment. These data raise the possibility that phosmet exposure could increase the susceptibility to the prion agent by altering the levels of accessible PrP.

(C) Lippincott-Raven Publishers.



http://www.neuroreport.com/pt/re/neuroreport/abstract.00001756-199805110-00026.htm;jsessionid=DOEcw0d3vPau1LEbPM42DrGrWVZnF06cF115hTGLe07ro2BZx8d3!586698740!-949856144!9001!-1





BUT, amplification and transmission is the most important factor in stopping the

spread of the TSE agent. WE have known for decades what factors involve the amplification

and transmission, yet the industries involved CHOSE to ignore this science until the incubation

period in humans and animals started to catch up with society.



would it not have been more easy and very much less expensive for MAFF/USDA et al to jump on the OP
bandwagon and save the industry, if OP theory had any credence to it at all? and why did they not?


transmission studies DO NOT LIE !

show me the data that ops are in all the primate/mouse transmission studies?


EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Scientific Steering Committee
OPINION ON
ORGANOPHOSPHATE (OP) POISONING AND
HYPOTHETICAL INVOLVEMENT IN THE ORIGIN OF BSE
Background
In its opinion on possible links between BSE and Organophosphates adopted on 25-26 June
1998 and in its opinion on Hypotheses on the origin and transmission of BSE adopted on 29-
30 November 2001 the SSC concluded that there is no scientific evidence in support of the
hypothesis of an OP origin of BSE.
The issue of organophosphate poisoning has not been dealt with by the SSC so far. The
concerns expressed in the enquiries cover mainly intoxication by occupational exposure of
shepherds and farmers to OPs upon use against ecto-parasites, especially in sheep dipping and
treatment of cattle against Warble Fly infestation. Risks from residues are addressed to a
lesser extend.
In early 2003, a large number of additional enquiries on the issue have been addressed to
European Commission’s Health and Consumer Directorate General. Four of these with
substantial enclosures were by one person. Most of them are addressing both issues: chronic
organophosphate (OP) poisoning and the origin of BSE.
Information provided with the enquiries
In addition to numerous newspaper and magazine articles the enclosures to the enquiries
provide the Material Safety Data Sheet on diazinon, the OHSA Occupational Safety and
Health Guideline for Tetraethylpyrophosphate (TEPP), an US agency Hazardous Substances
Fact Sheet on crufomate, company safety information sheets, some correspondence with UK
authorities including their activities to improve safe use of these chemicals. The information
regarding claimed OP chronic poisoning of cases presented does not provide evidence, neither
for OPs being the cause for diseases nor for their exclusion (i.e., “very low” bloodcholinesterase
levels, provided without data or comparison with the normal distribution of
values; successful treatment of a patient for OP clearance without giving any OP data). It
C:\WINNT\Temporary Internet Files\SSC_Last_OP_Final.doc 2
seems however, that due to insufficient, non-prudent use of the safety requirements undue
exposures of shepherds and farmers have occurred.
There is no additional information on the claimed involvement of OPs in the origin of BSE.
This applies for both, the hypotheses on the direct effect of OPs as well as on their
hypothetical role for Cu-deficiency to be involved in the origin of BSE (Cu binding of prion
protein is known). New publications are mentioned in one enquiry but they have not yet been
provided. In an Internet search no recent scientifically valid publications were traceable. The
SSC had been informed that research would be launched on this hypothesis, but no
information has been provided so far on its status or on results.
Conclusions
a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines – addressed in the enquiries – provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf



Studies on the Putative Interactions between the Organophosphorus Insecticide Phosmet and Recombinant Mouse PrP and its Implication in the BSE Epidemic
I. Shaw1, C. Berry2, E. Lane1, P. Fitzmaurice1, D. Clarke3 and A. Holden1

(1) Centre for Toxicology, University of Central Lancashire, Preston, UK
(2) Department of Morbid Anatomy, The Royal London Hospital, London, UK
(3) CLRC Daresbury Laboratory, Warrington, UK


Abstract It has been suggested that exposure of cattle to the ectoparasiticide Phosmet in the 1980s caused a conformational change in the cellular prion protein (PrPC) to form the BSE prion (PrPSC), which initiated the epidemic of bovine spongiform encephalopathy (BSE).
Recombinant mouse cellular prion (r[mouse]PrPC) was exposed to the organophosphorus pesticide Phosmet in vitro and the conformation of the prion before and after exposure was monitored using circular dichroism (CD) spectroscopy, utilizing synchrotron radiation at the Council for the Central Laboratory of the Research Councils (CLRC) facilities at Daresbury, UK. Metabolites of Phosmet, generated in situ by rat microsomes, were investigated in the same way, to determine whether they might initiate the conformational change due to their high chemical reactivity.
Our studies showed that exposure of r[mouse]PrPC to Phosmet or microsomes-generated metabolites of Phosmet did not result in the conformational change in the protein from -helix to -pleated sheet that is characteristic of the PrPC to PrPSC conversion and, therefore, Phosmet is very unlikely to have initiated the BSE epidemic by a simple direct mechanism of conformational change in the prion protein.
bovine spongiform encephalopathy - circular dichroism spectroscopy - insecticide - organophosphate - Phosmet - prion - protein conformation



http://www.springerlink.com/(bmbpjj55ksv02p2wiismj555)/app/home/contribution.asp?referrer=parent&backto=issue,3,9;journal,31,74;linkingpublicationresults,1:103009,1



transmission studies do not lie, amplification and transmission!


i see NO properties of high levels of Manganese in the diet, combined with low levels of copper, in any of these primate
transmission studies.

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

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


Oral Transmission And Early Lymphoid Tropism Of Chronic Wasting Disease
Prpres In Mule Deer Fawns

Publication: Journal Of General Virology
Publication Request Approval Date: June 25, 1999

Interpretive Summary: Chronic wasting disease is a transmissible
spongiform encephalopathy or prion disease of deer and elk. CWD is a
member of the family of diseases that includes sheep scrapie and bovine
spongiform encephalopathy (BSE). The natural route of transmission of
these diseases in ruminant animals is unknown but oral exposure to
contaminated feeds, bedding, or tissues is presumed to be a major source
of infection. In this study, mule deer fawns were orally fed an
infectious homogenate and sacrificed at intervals to examine the
lymphoid tissue of the alimentary tract for signs of infection. Prion
protein was detected as early as 42 days and was evident in all fawns
after 53 days. This paper provides an improved procedure for detecting
prions in early infection, establishes a protocol for accelerated study
of transmission routes, and supports the hypothesis that oral exposure
may reflect the initial pathway of CWD infection in deer.

Technical Abstract: Mule deer fawns were inoculated orally with a brain
homogenate prepared from mule deer with naturally occurring chronic
wasting disease (CWD), a prion induced transmissible spongiform
encephalopathy. Fawns were necropsies and examined for PrP-res, a
protein marker for infection, at 10, 42, 53, 77, 78 and 80 days post
inoculation using an immunohistochemistry assay modified to enhance
sensitivity. PrP-res was detected in alimentary-tract- associated
lymphoid tissues as early as 42 days post inoculation and in all fawns
after 53 days. These results indicated that CWD PrP-res can be detected
at least 16 months before clinical signs would be expected to appear and
may reflect the initial pathway of CWD infection in deer.

http://nps.ars.usda.gov/publication...gnum=0000103091

Establishing the transmission of BSE to mink

44. Transmissible mink encephalopathy ("TME") is a rare disease of ranch
reared mink, first recognised in the USA. It had been assumed to be
scrapie in mink and, like BSE, outbreaks have epidemiological
features consistent with a foodborne infection, but it has never been
possible to demonstrate that scrapie infected sheep brain tissue is
pathogenic to mink by oral exposure. In an incident of TME in
Stetsonville, Wisconsin, USA in 1985 Dr Richard Marsh observed that
although the rancher fed 'dead stock', mainly in the form of cattle
carcasses, sheep tissues had never been fed. Studies in the USA of
this incident showed not only that cattle inoculated intracerebrally
with the mink brain developed a fatal spongiform encephalopathy, but
also that the cattle passaged agent remained pathogenic for
mink by either intracerebral inoculation or feeding. In the absence of
reports of a clinical disease homologous to BSE in domestic cattle,
these findings prompted the suggestion that a rare or occult
form of such a disease might exist in the USA. Comparison of the
biological properties of the BSE
12
pathogen with those of the Stetsonville isolate was therefore of
considerable interest in relation to hypotheses concerning possible
origins of BSE and potential for subclinical infection in cattle.
45. Proposals to carry out studies with mink in the USA were developed
in collaboration with, the United States Department of Agriculture
("USDA") Agricultural Research Service ("ARS") and the
Department of Veterinary Science, University of Wisconsin, Madison,
Wisconsin, USA. On 30th October, 1990 I attended a CVL/NPU BSE R&D
meeting at the NPU in Edinburgh (YB90/10.30/1.1). I reported that brain
material from BSE affected cows and a control cow (not fed meat and
bonemeal) had been sent coded to Mr Mark Robinson (USDA) for
transmission studies in mink. The studies were conducted from February
1991 under the control and principal funding of USDA-ARS. The results,
discussed at the tenth CVL/NPU BSE R&D meeting on 27th April, 1993
(YB93/4.27/1.1) indicated that mink were indeed susceptible to BSE and,
in contrast to previous attempts to transmit scrapie to the species,
were susceptible by the oral route of inoculation. The collaboration
resulted in the publication of a paper: Robinson, M.M. et al (1994)
Experimental infection of mink with bovine spongiform encephalopathy.
Journal of General Virology 75, 2151-2155 (J/JVIR /75/2151).

snip...


http://www.bseinquiry.gov.uk/files/ws/s065a.pdf

BSE TO MINK CONFIRMED

http://www.bseinquiry.gov.uk/files/yb/1993/04/27001001.pdf


1: Proc Natl Acad Sci U S A 2001 Mar 27;98(7):4142-7

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

Lasmezas CI, Fournier JG, Nouvel V, Boe H, Marce D, Lamoury F, Kopp N,
Hauw JJ, Ironside J, Bruce M, Dormont D, Deslys JP.

Commissariat a l'Energie Atomique, Service de Neurovirologie, Direction
des Sciences du Vivant/Departement de Recherche Medicale, Centre de
Recherches du Service de Sante des Armees 60-68, Fontenay-aux-Roses,
France. [email protected]

There is substantial scientific evidence to support the notion that
bovine spongiform encephalopathy (BSE) has contaminated human beings,
causing variant Creutzfeldt-Jakob disease (vCJD). This disease has
raised concerns about the possibility of an iatrogenic secondary
transmission to humans, because the biological properties of the
primate-adapted BSE agent are unknown. We show that (i) BSE can be
transmitted from primate to primate by intravenous route in 25 months,
and (ii) an iatrogenic transmission of vCJD to humans could be readily
recognized pathologically, whether it occurs by the central or
peripheral route. Strain typing in mice demonstrates that the BSE agent
adapts to macaques in the same way as it does to humans and confirms
that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. The agent responsible for French iatrogenic
growth hormone-linked CJD taken as a control is very different from vCJD
but is similar to that found in one case of sporadic CJD and one sheep
scrapie isolate. These data will be key in identifying the origin of
human cases of prion disease, including accidental vCJD transmission,
and could provide bases for vCJD risk assessment.


http://www.ncbi.nlm.nih.gov/entrez/...1&dopt=Abstract

this next one frightens me the most, you might want to read
it twice, and really think about it...TSS

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

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

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

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

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

http://www.ncbi.nlm.nih.gov/entrez/...4&dopt=Abstract

Proc Natl Acad Sci U S A 1999 Mar 30;96(7):4046-51

Natural and experimental oral infection of nonhuman primates by bovine
spongiform encephalopathy agents.

Bons N, Mestre-Frances N, Belli P, Cathala F, Gajdusek DC, Brown P.

Ecole Pratique des Hautes Etudes, Laboratoire de Neuromorphologie
Fonctionnelle, Universite Montpellier II, 34095-Montpellier cedex 5, France.

Experimental lemurs either were infected orally with the agent of bovine
spongiform encephalopathy (BSE) or were maintained as uninfected control
animals. Immunohistochemical examination for proteinase-resistant
protein (prion protein or PrP) was performed on tissues from two
infected but still asymptomatic lemurs, killed 5 months after infection,
and from three uninfected control lemurs. Control tissues showed no
staining, whereas PrP was detected in the infected animals in tonsil,
gastrointestinal tract and associated lymphatic tissues, and spleen. In
addition, PrP was detected in ventral and dorsal roots of the cervical
spinal cord, and within the spinal cord PrP could be traced in nerve
tracts as far as the cerebral cortex. Similar patterns of PrP
immunoreactivity were seen in two symptomatic and 18 apparently healthy
lemurs in three different French primate centers, all of which had been
fed diets supplemented with a beef protein product manufactured by a
British company that has since ceased to include beef in its veterinary
nutritional products. This study of BSE-infected lemurs early in their
incubation period extends previous pathogenesis studies of the
distribution of infectivity and PrP in natural and experimental scrapie.
The similarity of neuropathology and PrP immunostaining patterns in
experimentally infected animals to those observed in both symptomatic
and asymptomatic animals in primate centers suggests that BSE
contamination of zoo animals may have been more widespread than is
generally appreciated.

http://www.ncbi.nlm.nih.gov/entrez/...0&dopt=Abstract

1: Vet Rec 1993 Apr 17;132(16):403-6

Experimental transmission of BSE and scrapie to the common marmoset.

Baker HF, Ridley RM, Wells GA.

Division of Psychiatry, Clinical Research Centre, Harrow, Middlesex.

Two young male common marmosets (Callithrix jacchus) were injected
intracerebrally and intraperitoneally with a crude brain homogenate
prepared from a cow with bovine spongiform encephalopathy (BSE). Two
other marmosets were similarly injected with brain homogenate from a
sheep with natural scrapie. The two animals injected with scrapie
material developed neurological signs 38 and 42 months after injection
and the two animals injected with BSE material developed neurological
signs after 46 and 47 months. Post mortem examination of the brains
revealed spongiform encephalopathy especially in the basal nuclei and
diencephalon of all the animals and, in addition, involvement of the
cerebral cortex of the marmosets injected with scrapie material. The
experiment extends the host range of experimental BSE to include a
primate species.

http://www.ncbi.nlm.nih.gov/entrez/...8&dopt=Abstract


1: J Gen Virol 1991 Mar;72 ( Pt 3):589-94

Epidemiological and experimental studies on a new incident of
transmissible mink encephalopathy.

Marsh RF, Bessen RA, Lehmann S, Hartsough GR.

Department of Veterinary Science, University of Wisconsin-Madison 53706.

Epidemiological investigation of a new incident of transmissible mink
encephalopathy (TME) in Stetsonville, Wisconsin, U.S.A. in 1985 revealed
that the mink rancher had never fed sheep products to his mink but did
feed them large amounts of products from fallen or sick dairy cattle. To
investigate the possibility that this occurrence of TME may have
resulted from exposure to infected cattle, two Holstein bull calves were
injected intracerebrally with mink brain from the Stetsonville ranch.
Each bull developed a fatal spongiform encephalopathy 18 and 19 months
after inoculation, respectively, and both bovine brains passaged back
into mink were highly pathogenic by either intracerebral or oral
inoculation. These results suggest the presence of a previously
unrecognized scrapie-like infection in cattle in the United States.

http://www.ncbi.nlm.nih.gov/entrez/...3&dopt=Abstract

1: Ital J Neurol Sci 1983 Apr;4(1):61-4

Creutzfeld-Jakob disease in the province of Siena: two cases transmitted
to monkeys.

Fieschi C, Orzi F, Pocchiari M, Nardini M, Rocchi F, Asher D, Gibbs C,
Gajdusek D.

Two cases of histopathologically documented Creutzfeldt-Jakob disease
were observed in the same area of the province of Siena in 1974-1975.
The transmission of the disease was obtained through brain homogenates
and lymphnodes in one of the two cases. This confirms that the agent is
present in other tissues besides the brain and underlines further the
analogies between Creutzfeld-Jakob disease and scrapie.

http://www.ncbi.nlm.nih.gov/entrez/...0&dopt=Abstract


1: Dev Biol Stand 1993;80:9-13

Transmission of human spongiform encephalopathies to experimental
animals: comparison of the chimpanzee and squirrel monkey.

Asher DM, Gibbs CJ Jr, Sulima MP, Bacote A, Amyx H, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, NIH, Bethesda, MD 20992.

The agents of kuru and Creutzfeldt-Jakob disease have been consistently
transmitted from patients with those diseases to chimpanzees and
squirrel monkeys, as well as to other new-world primates, with average
incubation periods of two or three years. No other animals have been
found so consistently susceptible to the agents in human tissues. More
rapid and convenient assays for the infectious agents would greatly
facilitate research on the spongiform encephalopathies of humans.

http://www.ncbi.nlm.nih.gov/entrez/...9&dopt=Abstract


1: J Vet Diagn Invest 2001 Jan;13(1):91-6

Preliminary findings on the experimental transmission of chronic wasting
disease agent of mule deer to cattle.

Hamir AN, Cutlip RC, Miller JM, Williams ES, Stack MJ, Miller MW,
O'Rourke KI, Chaplin MJ.

National Animal Disease Center, ARS, USDA, Ames, IA 50010, USA.

To determine the transmissibility of chronic wasting disease (CWD) to
cattle and to provide information about clinical course, lesions, and
suitability of currently used diagnostic procedures for detection of CWD
in cattle, 13 calves were inoculated intracerebrally with brain
suspension from mule deer naturally affected with CWD. Between 24 and 27
months postinoculation, 3 animals became recumbent and were euthanized.
Gross necropsies revealed emaciation in 2 animals and a large pulmonary
abscess in the third. Brains were examined for protease-resistant prion
protein (PrP(res)) by immunohistochemistry and Western blotting and for
scrapie-associated fibrils (SAFs) by negative-stain electron microscopy.
Microscopic lesions in the brain were subtle in 2 animals and absent in
the third case. However, all 3 animals were positive for PrP(res) by
immunohistochemistry and Western blot, and SAFs were detected in 2 of
the animals. An uninoculated control animal euthanized during the same
period did not have PrP(res) in its brain. These are preliminary
observations from a currently in-progress experiment. Three years after
the CWD challenge, the 10 remaining inoculated cattle are alive and
apparently healthy. These preliminary findings demonstrate that
diagnostic techniques currently used for bovine spongiform
encephalopathy (BSE) surveillance would also detect CWD in cattle should
it occur naturally.

http://www.ncbi.nlm.nih.gov/entrez/...4&dopt=Abstract

P.S. the study above confirmed 5 cows and 1 goat transmission of CWD to cattle,
of the final stages of the study. ...tss

Published online before print March 20, 2001, 10.1073/pnas.041490898
Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,dagger, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas KoppDagger , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce||, Dominique Dormont*, and Jean-Philippe Deslys*

snip...


Discussion

One aim of this study was to determine the risk of secondary transmission to humans of vCJD, which is caused not by a primarily human strain of TSE agent but by the BSE strain having passed the species barrier to humans. This risk is tightly linked to the capacity of the BSE agent to adapt to primates and harbor enhanced virulence (i.e., induce disease after a short incubation period and provoke disease even if highly diluted) and to its pathogenicity after inoculation by the peripheral route. With respect to the latter, there are huge variations between different TSE agent strains and hosts. For example, the BSE agent is pathogenic to pigs after i.c. inoculation but not after oral administration (23). Thus, we wanted to know to what extent the BSE/vCJD agent is pathogenic to humans by the i.c. and i.v. routes. To achieve this, we used the macaque model. To monitor the evolution of the BSE agent in primates, but also to verify the identity of French vCJD, we conducted parallel transmission to C57BL/6 mice, allowing strain-typing. The experimental scheme is depicted in Fig. 1.

Characterization of the BSE Agent in Primates. The identity of the lesion profiles obtained from the brains of the French patient with vCJD, two British patients with vCJD, and nonhuman primates infected with BSE provides experimental demonstration of the fact that the BSE agent strain has been transmitted to humans both in the U.K. and in France. Further, it lends support to the validity of the macaque model as a powerful tool for the study of vCJD. As far as the evolution of the BSE agent in primates is concerned, we observed an interesting phenomenon: at first passage of BSE in macaques and with vCJD, there was a polymorphism of the lesion profile in mice in the hippocampal region, with about half of them harboring much more severe vacuolation than the mice inoculated with cattle BSE. At second passage, the polymorphism tended to disappear, with all mice showing higher vacuolation scores in the hippocampus than cattle BSE mice. This observation suggests the appearance of a variant of the BSE agent at first passage in primates and its clonal selection during second passage in primates. The lesion profiles showed that it was still the BSE agent, but the progressive appearance of a "hippocampal signature" hallmarked the evolution toward a variant by essence more virulent to primates.

Characterization of the CJD and Scrapie Strains. Controls were set up by transmitting one French and one U.S. scrapie isolate from ruminants as well as French sCJD and iCJD cases from humans. None of these revealed a lesion profile or transmission characteristics similar or close to those of BSE or vCJD, respectively, thus extending to the present French scrapie isolate the previous observation that the BSE agent was different from all known natural scrapie strains (4, 24).
The lesion profiles of sCJD and iCJD differed only slightly in severity of the lesions, but not in shape of the profile, revealing the identity of the causative agents. One of us reported the absence of similarity between sCJD (six cases) and U.K. scrapie (eight cases) in transmission characteristics in mice (4). Herein, we made the striking observation that the French natural scrapie strain (but not the U.S. scrapie strain) has the same lesion profile and transmission times in C57BL/6 mice as do the two human TSE strains studied. This strain "affiliation" was confirmed biochemically. There is no epidemiological evidence for a link between sheep scrapie and the occurrence of CJD in humans (25). However, such a link, if it is not a general rule, would be extremely difficult to establish because of the very low incidence of CJD as well as the existence of different isolates in humans and multiple strains in scrapie. Moreover, scrapie is transmissible to nonhuman primates (26). Thus, there is still a possibility that in some instances TSE strains infecting humans do share a common origin with scrapie, as pointed out by our findings.

Transmission of vCJD and BSE to Nonhuman Primates. vCJD transmitted readily to the cynomolgus macaque after 2 years of incubation, which was comparable to the transmission obtained from first-passaged macaque BSE and much shorter than the interspecies transmission of BSE. Starting with 100 mg of BSE-macaque brain material, dilutions up to 4 µg still provoked disease. These data suggest that the BSE agent rapidly adapts to primates accompanied by enhanced virulence.
Examination of macaque brain inoculated with vCJD revealed a similar pathology to that with second-passage BSE. The distribution of vacuolation and gliosis, as well as the pattern of PrP deposition, including the dense, sometimes florid plaques, were similar to the human vCJD and the BSE hallmarks of the first passage (1, 2). These data show that the phenotype of BSE in primates is conserved over two passages. Moreover, they confirm that the BSE agent behaves similarly in humans and macaques, a precious finding that will prove useful in the near future for the design of pathogenesis or therapeutic studies. Because of the number of macaques examined in this study, we can now reliably state that the pathology, in particular the PrP deposition pattern provoked by BSE, is similar in older and very young animals. However, plaque deposition is greater, and mature florid plaques were more numerous, in the young, which may be correlated with a longer duration of the clinical phase observed in this animal (2). This is important with regard to the fact that vCJD has been diagnosed mainly in teenagers and young adults, which raises the concern that older patients may have been misdiagnosed because of an alternative phenotype of the disease. One should bear in mind, however, that cynomolgus macaques are all homozygotes for methionine at codon 129 of the PrP gene. Thus, our observations may not be relevant to humans carrying one or both valine alleles; however, all patients with vCJD reported to date have been M/M at this position (27).

Intravenous Transmissions to Nonhuman Primates. Brain pathology was identical in macaques inoculated i.c. and i.v. The i.v. route proved to be very efficient for the transmission of BSE, as shown by the 2-year survival of the animals, which is only 5 months longer than that obtained after inoculating the same amount of agent i.c. As the i.v. injection of the infectious agent implies per se a delayed neuroinvasion compared with a direct inoculation in the brain, this slight lengthening of the incubation period cannot, at this stage, be interpreted as a lower efficiency of infection as regards the i.c. route.
These data should be taken into account in the risk assessment of iatrogenic vCJD transmission by i.v. administration of biological products of human origin. They also constitute an incentive for a complete i.v. titration.
Conclusions

From BSE and vCJD transmissions in nonhuman primates, a number of conclusions can be drawn that are of major importance for human health: (i) human-adapted BSE appears to be a variant of the BSE agent that is more virulent for humans than cattle BSE and is efficiently transmitted by the peripheral route; (ii) the detection of vCJD in unusually young patients is probably not because of a lack of diagnosis of cases in older patients, thus raising the question of the source of human contamination with BSE early in life; and (iii) iatrogenic transmissions from patients with vCJD would be readily recognized by using the same diagnostic criteria as those applied to vCJD [clinical and pathological criteria (27) comprising neuronal loss and gliosis in the thalamus correlated with high MRI signal (28, 29)], whether such contaminations had occurred by the central or i.v. route. Primary and iatrogenic cases of vCJD could be distinguished on the basis of the patient's clinical history.

The risk assessment of biological products of human origin, notably those derived from blood, has been deeply modified by the appearance of vCJD. We confirm that the BSE agent has contaminated humans not only in the U.K. and the Republic of Ireland but also in France, and we show that its pathogenic properties for primates are being enhanced by a primary passage in humans. Considering the flow of potentially contaminated bovine-derived products between 1980 and 1996, it is obvious that further vCJD cases may occur outside the U.K. Thus, and in the light of the present study, it is necessary to sustain worldwide CJD surveillance regardless of national BSE incidence and to take all precautionary measures to avoid iatrogenic transmissions from vCJD.

snip...

http://www.pnas.org/cgi/content/full/041490898v1



MRC-43-00 [ ] [Text only version of this site] [Print this page]
Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a ?sub-clinical? form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the ?species barrier? - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a ?sub-clinical? form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust.

Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011 (OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly formed MRC Prion Unit based at The Imperial College School of Medicine at St Mary?s Hospital. He is also a member of the UK Government?s Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in 1999, and its work includes molecular genetic studies of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease) in animals. In some circumstances prions from one species of animals can infect another and it is clear that BSE has done this to cause the disease variant CJD in the UK and France. It remains unclear how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain (also known as 263K) which infects hamsters, and until now was assumed not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRC?s expenditure of £345 million is invested in over 50 of its Institutes and Units, where it employs its own research staff. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with a spend of some £600 million in the current financial year 1999/2000. The Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42 different countries to promote and foster research with the aim of improving human and animal health. As well as funding major initiatives in the public understanding of science, the Wellcome Trust is the country's leading supporter of research into the history of medicine.

©2002 Medical Research Council

http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm


and for Gods sake, if someone is smearing this [email protected] all over there kids
heads for lice and did not come up with a TSE, i would say this is good case study;


1) None of our animals that contracted BSE were treated with OP's, even
in utero.
2) My kids were treated with OP's as infants to control head lice. This
seems to be endemic as infection waves in UK primary schools (and
possibly elsewhere).
3) One might argue if the continued use of british beef in the UK was
ethical, none the less it happened. We have a duty to learn from it, not
least a duty to learn on behalf of those people who died so horribly....


NOPE, greed and money is the name of the game, they have known for decades;


STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

To minimise the risk of farmers' claims for compensation from feed
compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by
maintaining the availability of meat and bone meal as a raw
material in animal feeds, and ensuring time is available to make any
changes which may be required.

snip...

THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at
handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which
contain illegal traces of ruminant protein. More likely, a few positive
test results will turn up but proof that a particular feed mill knowingly
supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct
linkage between feed milling _practices_ and actual BSE cases,
the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf



BUT, i applaud ranchers that understand the TSE science and not the hype that surrounds it such as 'reader the second' ;


>>>Look, Mark Purdey, I applaud you for your perserverance, your bravery in taking on the establishment, and your creativity. It may well be that you were instrumental in bringing the familial and other genetic clusters in Slovenia to the attention of science.

I acknowledge that you suffered but your suffering sir is NOTHING compared to the suffering of the families afflicted with CJD and variant CJD and to the extent that your writings are used to ignore public health threats and to avoid taking public health measures that may well protect humans from CJD, then your writings are being ill used. You should acknowledge that and if you do not, I will pay no further attention to you.

Your supporters use your writings to (1) deny that CJD is transmissable from person to person, e.g., via contaminated surgical instruments or tissue or blood donations; (2) reject totally the strong hypothesis that variant CJD is due to the BSE epidemic in the UK being "pushed" over the species barrier. They claim that all cases of human CJD are due to metal contamination. It is they who are perverting your theories and therefore subjecting you to ridicule. Unless you deny these things as well and in which case, you should be ignored since in the case of (1) you deny fact and in the case of (2) you reject a hypothesis that must be accepted for the time being and must lead our public health measures given its strength.

NO ONE has denied that the ultimate cause of TSEs is unknown. However TSEs ARE transmissable between species, albeit not easily, and they are certainly transmissable among the same species. The suffering of the individual and his/her family who contracts CJD or variant CJD is hideous beyond description. If TSEs are your life work, you had better be taking that into consideration.<<<


>>>This is a danger to ranchers and to all humans<<<


INDEED there is;


CJD FARMERS WIFE 1989

http://www.bseinquiry.gov.uk/files/yb/1989/10/13007001.pdf

http://www.bseinquiry.gov.uk/files/yb/1989/10/13003001.pdf


20 year old died from sCJD in USA in 1980 and a 16 year
old in 1981. A 19 year old died from sCJD in
France in 1985. There is no evidence of an iatrogenic
cause for those cases....

http://www.bseinquiry.gov.uk/files/yb/1995/10/04004001.pdf

cover-up of 4th farm worker ???

http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf

http://www.bseinquiry.gov.uk/files/yb/1995/10/20006001.pdf

CONFIRMATION OF CJD IN FOURTH FARMER

http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.pdf

now story changes from;

SEAC concluded that, if the fourth case were confirmed, it would be
worrying, especially as all four farmers with CJD would have had BSE
cases on their farms.

to;

This is not unexpected...

was another farmer expected?

http://www.bseinquiry.gov.uk/files/yb/1995/11/13010001.pdf

4th farmer, and 1st teenager

http://www.bseinquiry.gov.uk/files/yb/1996/02/27003001.pdf

2. snip...
Over a 5 year period, which is the time period on which the advice
from Professor Smith and Dr. Gore was based, and assuming a
population of 120,000 dairy farm workers, and an annual incidence
of 1 per million cases of CJD in the general population, a
DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN
an individual in the general population to develop CJD. Using the
actual current annual incidence of CJD in the UK of 0.7 per
million, this figure becomes 7.5 TIMES.

3. You will recall that the advice provided by Professor Smith in
1993 and by Dr. Gore this month used the sub-population of dairy
farm workers who had had a case of BSE on their farms -
63,000, which is approximately half the number of dairy farm
workers - as a denominator. If the above sums are repeated using
this denominator population, taking an annual incidence in the general
population of 1 per million the observed rate in this sub-population
is 10 TIMES, and taking an annual incidence of 0.7 per million,
IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than
that in the general population...

http://www.bseinquiry.gov.uk/files/yb/1995/01/31004001.pdf



and for those that believe this was a spontaneous event or a happen-stance of bad luck from a spontatneous misfolding PrP, well, dream on. ...TSS



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

Creutzfeldt-Jakob disease


http://www.pnas.org/cgi/content/abstract/0305777101v1


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

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

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

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

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

http://www.pnas.org/cgi/content/full/041490898v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


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

ALL human TSEs must be made reportable Nationally and Internationally, OF ALL AGES...



P.S. MORE ON KATHY'S AND RKEISER'S LOW FLYING CONCORDS ;



18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...


64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.
Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a
mouse model it was possible to alleviate the pathological changes of prion
disease by suppressing expression of the prion protein gene after infection.


http://www.seac.gov.uk/minutes/95.pdf



3:00 Afternoon Refreshment Break, Poster and Exhibit Viewing in the Exhibit
Hall


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse


Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years. ***These results indicate that BASE is
transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.

6:30 Close of Day One


http://www.healthtech.com/2007/tse/day1.asp





AND WHY WOULD TSE IN THE USA BOVINE LOOK LIKE UK BSE ???

WHEN TRANSMISSION STUDIES WERE DONE ON USA SCRAPIE TO USA BOVINE, IT LOOKED NOTHING LIKE UK BSE. USDA et al have known this for eons..............tss



Page 14 of 17

Wilbur Clarke (reference the Mission, Texas scrapie transmission transmission to cattle study) is now the State Veterinarian for Montana based at Helena.

I was given confidential access to sections from the Clarke scrapie-cattle transmission experiment. Details of the experimental design were as supplied previously by Dr. Wrathall (copy of relevant information appended). Only 3 animals (2 inoculated with 2nd pass Suffolk scrapie and 1 inoculated with Angora goat passaged scrapie) showed clinical signs. Clinical signs were characterised by weakness, ''a stilted hindlimb gait'', disorientation, ataxia and, terminally, lateral recumbency. The two cattle from which I examined material were inocluated at 8 months of age and developed signs 36 months pi (goat scrapie inoculum) and 49 months pi (one of the Suffolk scrapie inoculated) respectively. This latter animal was killed at 58 months of age and so the clinical duration was only 1 month. The neuropathology was somewhat different from BSE or the Stetsonville TME in cattle. Vacuolar changes were minimal, to the extent that detection REQUIRED CAREFUL SEARCHING. Conversely astrocyte hypertrophy was a widespread and prominent feature. The material requires DETAILED NEUROPATHOLOGICAL ASSESSMENT BUT WHETHER OR NOT THIS WILL BE DONE REMAINS A QUESTION.

Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases

{the following was written but with a single line marked through it ''first passage (by this route)}...TSS

resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.

snip...

Appendix 3

VISIT TO USA - DR A E WRATHALL - INFO OH BSE AND SCRAPIE

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has successfully transmitted ovine and caprine scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is:-

Expt A6 Her x Jer calves born in 1978 were inoculated as follows with a 2nd Suffolk scrapie passage:-

i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml. 1/6 went down after 48 months with a scrapie/BSE-like disease.

Expt B6 Her or Jer or HxJ calves were inoculated with angora Goat virus 2/6 went down similarly after 36 months.

Expt CMice inoculated from brains of calves/cattle in expts A • B were resistant, only 1/20 going down with scrapie and this was thereason given for not publishing.

Diagnosis in A, B, C was by histopath. No reports on SAT were given.

2. Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally- (and naturally) infected sheep by ET. He had found difficulty in obtaining embryos from naturally infected sheep (cf SPA).
3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control Scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary fetus.
6. A western blotting diagnostic technique (? on PrP) shows some promise.
7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated
17/33 wished to drop it

6/33 wished to develop it

9/13/2005

33

Page 15 of 17

8/33 had few sheep and were neutral

Information obtained from Dr Wrathall's notes of a meeting of the U.S. Animal Health Association at Little Rock, Arkansas Nov. 1988.

end...TSS

>> Differences in tissue distribution could require new regulations >> regarding specific risk material (SRM) removal.

snip...end

full text 33 PAGES ;

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf

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.

http://www.bseinquiry.gov.uk/

1: J Infect Dis. 1994 Apr;169(4):814-20.

Intracerebral transmission of scrapie to cattle.

Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl HD, DeBey BM, Robinson MM.

USDA, Agriculture Research Service, National Animal Disease Center, Ames, IA 50010.

To determine if sheep scrapie agent(s) in the United States would induce a disease in cattle resembling bovine spongiform encephalopathy, 18 newborn calves were inoculated intracerebrally with a pooled suspension of brain from 9 sheep with scrapie. Half of the calves were euthanatized 1 year after inoculation. All calves kept longer than 1 year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis, general weakness, and permanent recumbency. The incubation period was 14-18 months, and the clinical course was 1-5 months. The brain from each calf was examined for lesions and for protease-resistant prion protein. Lesions were subtle, but a disease-specific isoform of the prion protein was present in the brain of all calves. Neither signs nor lesions were characteristic of those for bovine spongiform encephalopathy.

MeSH Terms: Animals Brain/microbiology* Brain/pathology Cattle Cattle Diseases/etiology* Cattle Diseases/pathology Encephalopathy, Bovine Spongiform/etiology* Encephalopathy, Bovine Spongiform/pathology Immunoblotting/veterinary Immunohistochemistry Male Motor Neurons/physiology Prions/analysis Scrapie/pathology Scrapie/transmission* Sheep Sleep Stages Time Factors

Substances: Prions

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8133096&dopt=Citation

9/13/2005



Page 16 of 17

Intracerebral transmission of scrapie to cattle FULL TEXT PDF;

SNIP...

Discussion

WE conclude that American sources of sheep scrapie are transmissible to cattle by direct intracerebral inoculation but the disease induced is NOT identical to BSE as seen in the United Kingdom. While there were similarities in clinical signs between this experimental disease and BSE, there was no evidence of aggressiveness, hyperexcitability, hyperesthesia (tactile or auditory), or hyperemetria of limbs as has been reported for BSE (9). Neither were there extensive neurologic lesions, which are primary for BSE, such as severe vacuolation of neurons and neuropil or neuronal necrosis and gliosis. Although some vacuolation of neuropil, chromotolysis in neurons, and gliosis were seen in the brains of some affected calves, these were industinguishable from those of controls. Vacuolated neurons in the red nucleus of both challenged and normal calves were considered normal for the bovines as previously described (50).

PrP-res was found in ALL CHALLENGED CALVES REGARDLESS OF CLINCIAL SIGNS, and the amount of PrP-res positively related to the length of the incubation. ...

snip...

WE also conclude from these studies that scrapie in cattle MIGHT NOT BE RECOGNIZED BY ROUTINE HISTOPATHOLOGICAL EXAMINATION OF THE BRAIN AND SUGGEST THAT DETECTION OF PrP-res by immunohistochemistry or immunoblotting is necessary to make a definitive diagnosis. THUS, undiagnosed scrapie infection could contribute to the ''DOWNER-COW'' syndrome and could be responsible for some outbreaks of transmissible mink encephalopathy proposed by Burger and Hartsough

(8) and Marsh and harsough (52). ...

snip...

Multiple sources of sheep affected with scrapie and two breeds of cattle from several sources were used inthe current study in an effort to avoid a single strain of either agent or host. Preliminary results from mouse inoculations indicate multiple strains of the agent were present in the pooled inoculum (unpublished data). ...

Transmission of the sheep scrapie to cattle was attempted in 1979 by using intracerebral, intramuscular, subcutaneous, and oral routes of inoculation of 5, 8- to 11-month old cattlw with a homologous mixture of brain from 1 affected sheep (61, 62). ONE of the 5 cattle develped neurologic signs 48 months after inoculation. Signs were disorientation, incoordination, a stiff-legged stilted gait, progressive difficulty in rising, and finally in terminal recumbency. The clinical course was 2.5 months. TWO of the 5 cattle similarly inoculated with brain tissue from a goat with scrapie exhibited similar signs 27 and 36 months after incoluation. Clinical courses were 43 an 44 days. Brain lesions of mild gliosis and vacuolation and mouse inoculation data were insufficient to confirm a diagnosis of scrapie. This work remained controversial until recent examination of the brains detected PrP-res in all 3 cattle with neurologic disease but in none of the unaffected cattle (62). Results of these studies are similar to ours and underscore the necessity of methods other than histopathology to diagnose scrapie infection in cattle. We believe that immunologic techniques for detecting PrP-res currently provide the most sensitive and reliable way to make a definitive diagnosis...

http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf

Visit to USA ... info on BSE and Scrapie

http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf





FULL TEXT 98 PAGES ;



http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf



i reacon kathy's and rkeiser's concord jets been flying too low over mission texas too :lol2: :lol2: :lol: :roll:



SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html




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



THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006


The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he ha
 

flounder

Well-known member
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006


The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before
one year ago" because of the agency's reluctance to retest the Texas cow
that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end


http://www.upi.com/





CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ...
Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central
Nervous System ... Address for correspondence: Paul Brown, Building 36, Room
4A-05, ...


http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm


TSS
 

flounder

Well-known member
Clinical, neuropathological and immunohistochemical features of sporadic and variant forms of Creutzfeldt–Jakob disease in the squirrel monkey (Saimiri sciureus)

Lawrence Williams1, Paul Brown2, James Ironside3, Susan Gibson4, Robert Will3, Diane Ritchie3, Thomas R. Kreil5 and Christian Abee1

1 Department of Veterinary Sciences, Michale E. Keeling Center for Comparative Medicine and Research, University of Texas MD Anderson Cancer Center, Bastrop, TX, USA
2 Bethesda, MD, USA
3 National CJD Surveillance Unit, Western General Hospital, Edinburgh, UK
4 Department of Comparative Medicine, College of Medicine, University of South Alabama, Mobile, AL, USA
5 Global Pathogen Safety, Baxter Bioscience, Vienna, Austria


Correspondence
Lawrence Williams
[email protected]

The squirrel monkey (Saimiri sciureus) has been shown to be nearly as susceptible as the chimpanzee to experimentally induced Creutzfeldt–Jakob disease (CJD), and has been used extensively in diagnostic and pathogenetic studies. However, no information is available concerning the clinicopathological characteristics of different strains of human transmissible spongiform encephalopathy (TSE) in this species, in particular, strains of sporadic and variant CJD (sCJD and vCJD, respectively). Brain homogenates from patients with sCJD or vCJD were inoculated intracerebrally at dilutions of 10–1 or 10–3 into the left frontal cortex of squirrel monkeys. Animals were kept under continuous clinical surveillance during the preclinical and clinical phases of disease, and regularly underwent standardized behavioural testing. Brains from three animals in the sCJD and vCJD groups were examined histopathologically and immunohistochemically for the presence of pathognomonic misfolded protein (PrPTSE). Overall, incubation periods and durations of illness were slightly shorter in monkeys infected with sCJD than in those infected with vCJD, but the earliest signs of illness (ataxia and tremors) were the same in both groups. Clinical disease in the sCJD monkeys was somewhat more severe and of shorter duration. Post-mortem examinations revealed distinctive patterns of spongiform change and PrPTSE distribution in the brains of sCJD and vCJD animals, similar to those seen in humans except that amyloid plaques were not present. PrPTSE was uniformly absent from peripheral lymphoid tissues in both groups of animals. Human strains of sCJD and vCJD cause distinguishable clinicopathological features in the squirrel monkey that can provide a baseline for the evaluation of future therapeutic studies.





http://vir.sgmjournals.org/cgi/content/abstract/88/2/688



TSS
 

Kathy

Well-known member
When manganese binds to PrPC and it is exposed to "electromagnetic energy spectrum" (in the study above UVA) the protein becomes protease resistant and tests positive with the Prionics Western Blot test kit.

The manganese contaminated prion protein, once it becomes protease resistant, would shut down the cellular protection systems against oxidative stress, and would initiate automatic cell death (aptosis).

Mn + PrPC + UVA (or other sources of the electromagnetic spectrum) equals a POSITIVE Prionics Western Blot test!

Neurotoxicology. 2006 May;27(3):437-44. Epub 2006 Feb 14.

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.
Universite Francois Rabelais de Tours, Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, 31 Avenue Monge, 37200 Tours, France. [email protected]

The exchange between copper and seven transition metals is studied in a bovine brain obex homogenate according to the redox status of the medium. In reductive conditions, almost all the studied metals can substitute for copper when it is in the reduced form Cu+. This substitution is reversible, since copper uptake as Cu++ is restored in an oxidizing medium but only Co++, Ni++ and Mn++, in this decreasing order, can substitute perfectly for copper in bovine brain homogenate. To study free radical effects on bovine brain proteins, at first a copper substitution was processed in order to inhibit superoxide dismutase-like protective properties against free radicals in copper metalloproteins. Manganese was selected since a brain copper decrease correlated with a manganese increase is well-known in transmissible spongiform encephalopathies. Results for bovine brain homogenate, initially negative in the Western blot Prionics test, indicate that the substitution of manganese for copper in a reducing medium and exposure to UVA-induced free radicals produce proteinase K resistant prion. These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities may be involved in transmissible spongiform encephalopathies.
PMID: 16481041

initially negative results, tested Positive after the Manganese contaminated prion proteins were subjected to UVA.

Health Effects:
Generalizations: Biological effects are due to the ionization process that destroys the capacity for cell reproduction or division or causes cell mutation. The effects of one type of radiation can be reproduced by any other type.

Therefore, it is important to note this last sentence: "The effects of one type of radiation can be reproduced by any other type."

The electromagnetic radiation spectrum is the complete range of the wavelengths of electromagnetic radiation, beginning with the longest radio waves (including those in the audio range) and extending through visible light (a very small part of the spectrum) all the way to the extremely short gamma rays that are a product of radioactive atoms.


Do not dismiss the FACT that in the Deloncle study above:

Mn + PrPC(deficient in copper) + UVA(electromagnetic energy) = POSITIVE Western Blot Prionics test.
 
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