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Blood transfusions have been identified as a potential route of infection for variant Creutzfeldt-Jakob disease (vCJD), for which there is no treatment or cure.
At least 15 people known to have had blood transfusions from donors who subsequently developed vCJD are to be warned that they could be at risk. There are potentially thousands more treated with blood plasma products who could face a much smaller risk.
John Reid, the Health Secretary, told the House of Commons yesterday that the evidence was not conclusive. It involves a patient unidentified, at the request of the family, by sex, age or place of residence, who died of vCJD this autumn. The patient had had a blood transfusion in 1996, using blood from a donor who was at the time apparently healthy. The donor developed the symptoms of vCJD three years later and died.
The possibility exists that the donor’s blood was contaminated with the agent responsible for vCJD long before symptoms of the disease appeared, and that this was passed on to the recipient. The incubation period between the transfusion and the appearance of disease in the recipient, six and a half years, is consistent with this scenario.
It is still possible, Mr Reid said, that both donor and recipient had caught the disease independently, by eating contaminated beef. “It is impossible to be sure which was the route of infection,” he said. “However, the possibility of this being transfusion-related cannot be discounted.”
As a result, all those known to have had blood from donors who subsequently developed vCJD are to be contacted by the Health Protection Agency, with the assistance of the National Blood Service. “All will be told about the circumstances of their case and have the opportunity to discuss the risks with an expert counsellor,” Mr Reid said.
Sir Liam Donaldson, the Chief Medical Officer, said that deciding to contact these individuals, when there is no way of testing them for vCJD or of treating them if they develop it, had been “very, very difficult”. The CJD incidents panel had discussed it at length, he said, before deciding that contacting them was the right thing to do.
A further and potentially much larger group of patients is also likely to be contacted. These are people who were treated with blood plasma products before the end of 1999, when supplies of these products were switched to US sources. These people, including haemophiliacs, used products prepared from pooled plasma coming from thousands of donors. That means that a single contaminated donation could have affected the entire pool, and many recipients.
Offset against that, however, the infectious agent would be very much diluted. “The CJD incidents panel considers the risk for this group to be even lower than for those who received whole blood,” Mr Reid said.
The emergence of a possible link between blood and vCJD is not entirely unexpected. Animal experiments have shown that such a link is possible, and a series of precautionary measures have already been taken.
The news will be potentially disastrous, however, for the National Blood Service. One possibility now to be reconsidered is to exclude from the blood donor register any would-be donor who had received a previous blood transfusion. In the worst case, this could exclude 15 per cent of donors, Angela Robinson, medical director of the service, said. This could leave Britain with a blood shortage and medical experts would have to balance risks. Excluding donors on the basis of an unproven risk could expose patients and victims of accidents to a real risk, Dr Robinson said.
In October the expert committee on the microbiological safety of blood and tissues for transplantation advised that excluding blood recipients from giving blood was not necessary. Now it has been asked to look at it again.
Frances Hall, secretary of the Human BSE Foundation, whose son Peter died from vCJD in 1996, said the news came as a complete shock. “The information from this death seems to make it more likely that blood can carry the disease,” she said. “It is going to be very frightening for people who have received blood transfusions from victims.”
Threat from rogue proteins
Variant CJD is caused by a protein in the brain folding itself into the wrong shape and changing its behaviour. It can be transmitted by the consumption of beef contaminated with the rogue proteins, which also cause BSE (“mad cow” disease).
When vCJD emerged in 1996, nobody had any idea how many cases would occur. There were then no tests to identify it in meat, and there are still none to identify it in blood. Some experts suggested that hundreds of thousands of people might be infected.
In fact, there have been just 143 cases up to the beginning of this month. The number of new cases has been falling over the past three years, but the outbreak is not over. So far, all victims have had the same genetic make-up, shared by about 40 per cent of the population. The other 60 per cent may also still be vulnerable.
If blood is an alternative source of infection, that could also increase the numbers. The incubation period for such cases is likely to be shorter than in food-borne infection, because it would be human-to-human transmission with no “species barrier” to overcome.
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