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Judge DreadJudge Dread Member Posts: 2,372 ✭✭✭✭✭
edited November 2002 in General Discussion
DUUUUHHHH! AWWWWW!!!!! now they find what I have being posting for 4 years is true.....(I know were it comes from also)....this thing can be the end of the world as we know it......
Live and let die ???


BSE Now Thought To Cause
From Dr. Patricia Doyle, PhD

Hello Jeff - This is very important information. It means that the cause of SOME cases of 'traditional' or 'normal' CJD may be a direct result of eating BSE-infected meat. Until now, medical science has insisted that 'traditional' CJD has been around for a number of years and was NOT caused by Mad Cow/BSE meat...which is the KNOWN cause of what is called vCJD (variant) in humans.

If we take this one LOGICAL step further, we might be inclined to theorize that some cases of CJD and sporadic CJD might have been the direct result of eating Chronic Wasting Disease infected deer, elk and moose.

The cases of CJD and sCJD resulting from CWD would be cases in the US. The CDC and other authoritarian organizations which claim the US does not have any BSE "mad cow" disease in its beef or dairy industry are NOT correct if one considers the above hypothesis as it pertains to Chronic Wasting Disease and sCJD and CJD resulting from eating the CWD-infected meat.

Patricia Doyle

BSE May Have Caused Some Cases Of CJD As Well As vCJD

By James Meikle
The Guardian - UK

Measures to protect the public from bovine spongiform encephalopathy (BSE)-like diseases were called into serious question last night as researchers suggested that the BSE epidemic in cattle might have caused 2 separate fatal brain conditions, not one as thought. Their stunning conclusion, that eating cheap cow meat might be responsible for some cases of sporadic Creutzfeldt-Jakob disease (CJD), as well as variant CJD [abbreviated as vCJD or CJD (new var.) in ProMED-mail] or human BSE, will cause further reassessment of risks still posed by food and by infection through cross-contamination of surgical instruments and blood.

Experiments with mice by John Collinge and colleagues at University College London appear to strengthen the possibility that more animals, and by extension humans, can act as infective carriers of the killer diseases well before full-blown symptoms occur. They cast another shadow over the safety of sheep, reinforcing concerns that they were infected with BSE as well as scrapie, a disease not known to be harmful to humans, and that one disease had "masked" the other.

The Department of Health will have to reconsider the operation and size of its compensation scheme for families that have a human BSE sufferer. The money is not available for sporadic CJD victims or relatives, and there is no way yet that scientists can distinguish between cases that arose from spontaneous changing in the form of the prion protein linked to both diseases, and those that might be diet-related. The research, outlined in the journal of the European Molecular Biology Organisation (EMBO) [see comment below], could mean huge changes in the counselling of sporadic CJD patients and their families. Professor Collinge said last night: "When you counsel those who have the classical sporadic disease, you tell them that it arises spontaneously out of the blue. I guess we can no longer say that."

The results come from a continuing long term study of laboratory mice [engineered to express] the human prion protein, then injected in the brain with BSE-infected material. Some showed a molecular signature indistinguishable from human BSE; others a signature the same as that left by one of 3 forms of sporadic CJD.

Deaths from sporadic CJD reported in Britain in the 1990s peaked at around 60 a year between 1997 and 1999, far more than the 28 variant CJD cases in 2000, the worst year so far for variant CJD. Urgent reviews will be made as to whether some sporadic cases might be BSE-related, although hard evidence would be extremely difficult to find. The pattern of infectivity through the body is markedly different between sporadic CJD and variant CJD, meaning surveillance might now become more complicated.

There are no blood tests yet available. Hemophiliac patients who were treated with blood clotting factors by the Scottish blood transfusion service between 1987 and 1989 are being informed that one donor of blood for the concentrates had later contracted variant CJD. All hemophiliacs in Scotland are now treated with genetically engineered substitutes, but these are not universally available in England, where warnings of possible contamination have been issued several times. The Haemophilia Society last night said it would increase pressure on the Department of Health to ensure that alternatives were available to patients in England.

Gillian Turner, of the CJD Support Network, said: "This research will be welcomed by many families who have been affected by sporadic CJD. They have been concerned for a long time that it was diet-related." Lester Firkins, of the Human BSE Foundation, said: "This could throw all the work that people have been doing on modelling [the possible spread of diseases] up in the air again. You might see clustering of cases if you have more numbers."

Sporadic CJD was identified in 1920s. The disease affects mainly the middle-aged and elderly. The incidence is roughly one in a million, between 29 and 63 a year since 1990. The disease is found worldwide. Time between obvious symptoms and death is typically a few months. Until now it has been assumed that a normal prion protein in the brain spontaneously changed into abnormal dangerous form. BSE or similar diseases could now be factor

vCJD was identified in 1996, with the average age of onset in the late 20s. Found mainly in Britain: 129 cases with 117 deaths so far, plus 6 in France, 1 each in Italy, Ireland, Canada & the USA. Largely blamed on consumption of cheap cattle meat and offal during 1980s. Tough food controls were meant to have significantly reduced risk. Concern remains over whether sheep might also have become infected with BSE and entered the food chain. First symptoms often [imitate] psychological problems. Duration is often well over a year. Several physical symptoms are similar to sporadic CJD.,2763,849293,00.html



The scientific paper upon which this report is based is published in the current issue of the EMBO Joural, Vol. 21, No. 23, 6358-6368, 2002.

Title: BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein.

Authors: Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth and John Collinge. MRC Prion Unit and Department of Neuro-degenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK.

Abstract: Variant Creutzfeldt-Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrP\Sc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.

In an interview with the London Times Health Editor, Professor Collinge stated that the number of cases of sporadic CJD cases had been increasing at about the same rate as the vCJD figures, and that the Swiss had reported recently a 2 to 3 fold increase in sporadic CJD. He also expressed concern that the transgenic mouse experiments had revealed instances of subclinical infection; although appearing normal in life, these mice when examined post-mortem exhibited extensive brain lesions. Subtle changes in mice are hard to detect, but changes might be more obvious in humans in terms of psychiatric symptoms. A subclinical form of CJD in humans would increase the hazard of transmission of disease via surgical instruments.

Professor Collinge stated that it was now a matter of urgency to conduct a large scale study of tonsil tissue in order to establish how widespread CJD infection is. He said that he remained concerned about the ultimate size of the CJD epidemic. The tonsil study that has been carried out so far employed a relatively crude test. He stated that new cases of kuru, the neurological disease caused by cannibalism some 50 years ago are still coming to light. Consequently these are very early days for a human prion epidemic, which could have a 30 year incubation period. - Mod.CP]

[see also: CJD, increased incidence - Switzerland 20020714.4756 CJD, long incubation period 20020612.4478 CJD, surgical instrument re-use - UK 20021030.5671 CJD, suspected cluster - USA (Wisconsin) 20020721.4827 CJD (new var.) - UK: 10th Annual Report 20020711.4727 CJD (new var.) - UK: update Sep 2002 20020908.5258 2001 ---- CJD, death rate increase - Switzerland 20011225.3110 CJD, surgical transmission? - Canada (Ontario) 20010512.09 2000 ---- CJD, possible surgical transmission - USA (Louisiana) 20001027.1872] ..................cp/jw

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