BSE may have caused second strain of CJD

November 28, 2002 The Guardian (London) by James Meikle

Measures to protect the public from BSE-like diseases were called into serious question last night as researchers suggested that the BSE epidemic in cattle might have caused two separate fatal brain conditions, not one as thought.

Their stunning conclusion, that eating cheap cow meat might be responsible for some cases of sporadic CJD, as well as variant CJD 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, 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 this is not related to what you read in the newspapers, 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 fitted with 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 three strains 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.

Haemophiliac 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 haemophiliacs 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."

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