LONDON -- Two and a half years after the "mad-cow disease" scare hit the United Kingdom, British beef is back. Domestic consumption has rebounded, and the European Union this week voted to lift its ban on exports.
Scientists generally believe that, following the slaughter of 2.5 million cattle and other precautions, people now can eat British beef without fear of the brain disease that killed tens of thousands of British cattle and, many scientists believe, was passed to 31 people as well. "It is now just a matter of time before top-quality British beef is enjoyed across the world once again," says Ben Gill, head of the U.K.'s National Farmers Union.
But that doesn't mean the scare is over. It has taken a new turn. The latest concern isn't about British beef, but British blood. Some scientists now fear that the disease could be passed through transfusions of blood from people who once ate infected beef, and as a result harbor the infectious agent.
The risk remains hypothetical. Scientists aren't sure whether the disease can be spread through blood at all. But new research suggests it is possible, and there is no laboratory test to screen the blood.
Destroying Plasma
So the British government, under criticism for having reacted too slowly to the mad-cow problem in the past, is taking no chances this time. In an unprecedented and controversial decision to reduce the risk of infection, it has begun destroying nearly all the plasma -- the liquid part of blood that is used to make products for hemophiliacs, burn victims and others -- from all blood donations in Britain. It is replacing the plasma with supplies from the U.S., where there have been no reported cases of the disease.
In addition, the government has begun removing and destroying the white blood cells. These are part of the immune system, and they are suspected of playing a role in the disease's progress. By next year, both actions should be fully in place.
"We're erring on the side of caution," says Sue Cunningham, a spokeswoman for Britain's National Blood Service.
Is It Necessary?
In the U.S., some suggest the British are overreacting, especially in their decision to destroy plasma. "This response is based on a theoretical risk only, and therefore I feel it is a bit extreme," says Richard Davey, chief medical officer of the American Red Cross. Paul Brown, a senior research scientist at the National Institutes of Health, calls the policy "an archconservative position" that represents "ultimate caution," although he says he can't argue with it. "If you can afford to do it, that's fine," he says. "It costs a fortune."
Indeed, the British actions are expected to cost $165 million a year -- half of the National Blood Service's budget -- and increase the cost of blood products. But Michael Rawlins, who heads the government advisory board on medicine safety that recommended destroying plasma, says the decision was unanimous. "We fervently hope it's a waste of money," he says. "Because if it isn't, we're in real trouble."
Much remains a mystery about "mad-cow" disease, which is formally called bovine spongiform encephalopathy, or BSE. The fatal illness suffered by the 31 victims has been labeled "new-variant Creutzfeldt-Jakob disease" -- after another rare brain disorder in humans -- and appears identical to BSE. Scientists still don't know the origin of mad cow, which was first confirmed in Britain in 1986. But they are convinced it spread among cattle because diseased animals were recycled -- infected parts were ground up and processed into animal feed. To date, there have been more than 175,000 confirmed cases in British cattle, and much smaller numbers in 14 other countries. There haven't been any in the U.S.
Researchers have demonstrated with experimental mice that the same infectious agent that causes BSE -- believed to be a rogue protein called a prion -- also causes the human disease. Yet there remains no definitive proof that infected beef was the source of the outbreak in humans, although this notion is now very widely accepted. "We can't do the obvious experiment, which is to actually feed BSE brain material to a human," notes Moira Bruce, a biologist in Edinburgh, Scotland, who did the mouse experiments.
Many Unknowns
Still other critical questions remain unanswered: How much exposure to the infectious agent does it take for a person to contract the disease? How long does it take for symptoms to appear? Why has the disease targeted mainly young people (the average age of victims was 29)? And, the greatest mystery: How many people walking around today might be infected?
What is clear is that the disease is dreadful. After lying essentially dormant for years, it suddenly attacks and decimates the brain. "There's no cure, there's no treatment, there's nothing you can do," says Dorothy Churchill of Wiltshire in southwest England, whose son, Stephen, was the first confirmed case. A fit young man who had passed tests to be a pilot in the Royal Air Force, he suddenly grew depressed in 1994, suffered hallucinations and soon couldn't bathe or eat. Within a year, he was dead at the age of 19.
The concern about human blood grew last year following research conducted in Britain and Switzerland. In London, a team led by John Collinge at Imperial College School of Medicine discovered traces of the disease in victims' tonsils, a lymphatic organ where white blood cells known as B lymphocytes circulate. The research also suggested that new-variant CJD behaves differently from the classical form of Creutzfeldt-Jakob disease, which isn't found in the tonsils (and has never been linked to transfusions).
Meanwhile, a team in Zurich led by Adriano Aguzzi conducted mouse experiments that indicated B lymphocytes may play a role in transporting the disease agent to the brain. The researchers found that mice with defective B lymphocytes didn't contract scrapie -- a related prion disease seen in sheep -- when injected with infected tissue in the abdominal cavity. Other mice with normal B lymphocytes did develop the disease.
The findings prompted Britain's health department last year to establish a policy to recall and destroy any plasma products made from blood donations from the people diagnosed with new-variant CJD. That is no easy task. Cases usually aren't confirmed until after death, and blood donations may have been made years before. Users of blood products also often aren't tracked. In fact, at least four of the 31 people who have died of the disease were blood donors, and in two cases, their blood was used in products given to patients.
An individual's blood may end up in thousands of products. To make plasma products in quantity, manufacturers pool many blood donations -- in Britain, as many as 62,000.
Dr. Rawlins, the advisory-board chief, says the recall policy adopted last year "meant that we were seriously going to interfere with the availability of blood products generally." So the next step, to import all plasma used in pools, was logical, he says. The decision, made in May, doesn't affect fresh-frozen plasma, which isn't pooled and is used in life-threatening situations. It also doesn't affect red blood cells, which are used in transfusions, or clotting agents called platelets, which are used in cancer therapies.
White Cells
Dr. Aguzzi, a professor at Zurich University, serves on another scientific panel that advises the British government on new-variant CJD and related diseases. After much debate, the panel recommended in June the removal of white blood cells from all blood donated in Britain, a process known as leukocyte reduction. The government accepted the advice in July.
"It was a difficult decision to take, and we still don't know whether it was the correct one," Dr. Aguzzi says. He supported leukocyte reduction even though he agrees that his own research "has certainly not proven that blood is infectious." He notes that his experiments involved mice, not people, and that the disease studied was scrapie, not BSE or new-variant CJD.
"I would say this was rather indirect evidence," he says, "On its own, it certainly would not suffice to justify measures of public health." In fact, his latest research, to be published next week in the journal Nature Medicine, shows that the role played by B lymphocytes in prion diseases remains unclear.
Still, he believes the decision was prudent in view of the tonsil research, plus recent findings of traces of the infectious agent in the human appendix as well. He also notes that there are other advantages to the removal of white blood cells, a practice that is already in use in several countries, including France and Portugal, and is under consideration by the U.S. Food and Drug Administration. Dr. Davey, of the American Red Cross, explains that the process can reduce bad reactions to transfusions, such as high fever, and eliminate the risk of transmitting viral diseases.
AIDS Experience
In weighing their decisions, Dr. Aguzzi and other scientists say they are particularly mindful of the early years of the AIDS epidemic, when thousands of people who had transfusions became infected before blood-screening tests existed. "The AIDS blood scandal was a catastrophe," he says, and with no screening test available for this disease, the situation may be "not totally dissimilar."
Whether the moves are warranted won't be known for years. The first step is to find out whether the disease can even be spread through blood. In addition, scientists must determine how many people have been infected. "The magnitude of the risk will depend ... on the number of blood donors who are incubating new-variant CJD, and this is not known," Dr. Aguzzi's committee noted.
At its suggestion, Britain's Health Department commissioned a London risk-management firm, Det Norske Veritas Ltd., to make an educated guess. In the first draft of its report, never made public, the firm estimated that as many as 100,000 people in Britain might be harboring new-variant CJD, based on estimates of infected animals that entered the food chain and other factors. The calculation was criticized by other researchers as unscientific, and was withdrawn. The firm has changed its focus to one of assessing ways to minimize any blood risk.
Roy Anderson, an Oxford University epidemiologist, says the question of how many people eventually will get the disease can't be answered, "depressingly, for another five years." His latest research suggests it takes on average at least nine years, and possibly much longer, for the symptoms of new-variant CJD to emerge. Until more time has passed, he says, it won't be known whether the number of future cases will be few, or in the thousands.
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