British scientists discovered in 1995 that what had been feared for six years was becoming reality. A mysterious infectious agent associated with BSE appeared to have crossed the species divide and triggered an aggressive form of the brain-wasting disease CJD.
No longer were older people the most susceptible. New-variant CJD (nvCJD) had also smashed an age barrier and was affecting young people who had eaten BSE-contaminated beef.
The link between BSE and nvCJD has centred since then on the role of an abnormal protein - a rogue prion - found only in diseased animals with BSE, which was believed to set off a chain reaction in humans.
Normal prion protein is coathanger-shaped with about 230 basic units, known as amino acids. Rogue prion protein has identical amino acid sequences but adopts a different molecular shape. Normal prion protein is made in a cell and moves to its surface membrane. It is believed to strengthen the cover of nerve cells. The rogue form causes normal prions to change shape and to become abnormal. These abnormal prions cannot be digested by enzymes.
As a consequence, cell membranes literally pop like a soap bubble, releasing the rogue prion protein. They leave a small hole where nerve cells are usually located. Multiple holes give brain tissue a spongy appearance. This process starts a lethal chain reaction which culminates in death.
Research by the Institute of Animal Health in Edinburgh, published in the journal Nature last October, confirmed that nvCJD and BSE were caused by the same prion agent.
The medical director of the British National Blood Service, Dr Angela Robinson, explained yesterday why a distinction needed to be made between classical CJD and nvCJD in terms of precautions. Over 20 years, the classical form of CJD had "never ever been shown to transmit through any sort of transfusion, blood or blood product, despite looking hard for it". However, it was not known if the new variant would behave in the same way.
She added: "The indications are that the risks are negligible, if any at all. But, until such time as we know more, we are taking extra precautionary measures to minimise the risk, if there is any."
In reality, it is not possible to say definitively if there is a risk. The rogue prion responsible for CJD has to have cells present for transmission to occur. Some Irish CJD specialists say that the bloodproduct risk is zero because the withdrawn agent was in the form of a basic protein and was not used with the cells necessary for infectivity.
On this issue Dr Robinson said: "We still don't know enough of how this disease does transmit. There is a suggestion that white blood cells may be involved, but we really don't have enough evidence yet. Until such time as we have a reliable diagnostic test, which we don't have at the moment, we have to behave in this way, to eliminate as far as possible any product that may or may not have been contaminated with a donation from a (nvCJD) case in the past."
Of the 22 British nvCJD cases found since the end of 1995, four were found to be blood donors, but only two of these donations found their way into the blood product pool. Risks for the 268 Irish people who received the potentially contaminated protein product - used as a radiological dye in lung scans - are so negligible, she said, that they should not even worry about it. The risk of not having a blood transfusion or not receiving a blood product far outweighed this.
BSE may be eliminated from cattle within a few years, yet with nvCJD a great imponderable remains: the question of its incubation period. It is feared that, with a possible period of up to 20 years applying, a sharp rise in cases may occur. Given this possibility, extreme caution is needed to reduce the risk of transmission. Caution will have to be applied in equal measure with blood products.