EATING British beef is about a dangerous as breathing the air in an industrial city, according to a UCD scientist who has been studying scrapie and BSE for the past 10 years.
Dr Mark Rogers said there was no scientific evidence of a link between BSE in cattle and Creutzfeldt Jakob Disease (CJD) in humans. However, he said the British government may have evidence of which he was not aware.
Dr Rogers worked in the University of California with Prof Stan Prusiner, the first scientist to isolate a pure sample of the causative agent behind such diseases as scrapie, BSE and CJD. He moved to UCD four years ago and has continued to work on these causative agents, called prions. "I don't think there was ever any problem with Irish beef.
I wouldn't have any problem eating British beef today."
Since the British government, in the late 1980s, ended the inclusion of infectious parts of all animals, such as brain and nervous tissue, in cattle feeds, the risk has been "very, very low, about as big as breathing the air in an industrial city," he said.
Dr Rogers says he believes the BSE epidemic resulted from the change in Britain in the early 1980s in how sheep offal was processed before being fed to cattle, with the brains of infected cattle then being fed to other cattle. "That was asking for disaster. That's where you got the rapid epidemic. In hindsight, it was a crazy thing to do."
However, he says he "does not necessarily hold the view" that BSE has caused CJD in humans. If the 10 cases of CJD in Britain mentioned in the media were caused by eating beef, "then presumably they are due to eating meat during the 1980s."
The average incubation time for CJD can be 15-20 years. There is no way of knowing whether the 10 people were infected early or late in the 1980s, Dr Rogers said, or of knowing if more people are going to develop the disease as a result of eating infected meat then.
Prions, the causative agent of scrapie, BSE and CJD, are a type of protein found in all mammals, including humans. Scientists have not yet worked out their function. The proteins are found primarily in the brain.
In humans these proteins can spontaneously adopt an abnormal shape. An "abnormal" form of the protein can be ingested, say, by a cow eating an infected cow's brain tissue in its feed. Abnormal prions then "force" their shape on the normal prion proteins in healthy cells.
The body is unable to break down these abnormal proteins. They build up in a cell until they eventually kill it. They can also spread from cell to cell. The build up eventually leads to toxic effects in the brain.
"When you open up someone who has died from the disease, you literally find holes in the brain," Dr Rogers said.
When Prof Prusiner first isolated pure samples of the prion protein and said it was the causative agent behind CJD type diseases, a San Francisco newspaper ran a story headlined "SF scientists discover a new form of life." But Dr Rogers says that, although abnormal prions can move from one animal to another and "replicate" themselves, he wouldn't call them a form of life. "I don't like to use that sort of term. The arguments are technical, but they don't fulfil all the criteria."
CJD affects about one person in every million. In 90 per cent of cases, this is due to genetic mutation leading to production of abnormal prion proteins. In the remainder of cases, the disease is inherited. There has been no increase in the incidence of CJD in Britain, Dr Rogers points out.
In collaboration with Mr Owen Monks and Mr Eddie Weaver, of the Department of Agriculture's veterinary research laboratory in Abbotstown, Dublin, Dr Rogers has developed a diagnostic test for scrapie or BSE in slaughtered sheep and cattle. They are now hoping to develop it commercially.
