OR SHOULD WE HOLD OPS RESPONSIBLE?
IF you shout long enough and loud enough you will eventually be heard. At least, thats what a Somerset organic dairy farmer who feels he has been ignored by the government for over a decade is hoping.
Mark Purdey, who now labels himself an "independent scientist", wrote to farmers weekly as long ago as 1987 revealing he had observed a link between the incidence of BSE and the use of Phosmet, an organophosphate used to treat warble fly.
Yet vigorous efforts to persuade MAFF, which has allocated £76.4m on around 200 BSE research projects, to support his research since then have come to nothing. This has left him seething at the governments "negligence."
He recently met MAFF officials to discuss a further application for funding and is hoping the government will finally be spurred into action.
He and a Cambridge scientist have just had research published supporting his view that Phosmets effect in reducing copper levels in cattle is compounded by an excess of manganese to cause BSE.
Mr Purdey, who farms Jersey cows at Halse, near Taunton, became suspicious of Phosmet when he noted high BSE incidence in areas of the country, including much of the south east and south west, where from 1982 farmers were required by MAFF to use the OP.
He also claims there is no record of cows dying from BSE that were born and raised on organic farms, where high doses of the OP are generally avoided. He has also listed similarities between BSE and chronic low dose OP poisoning.
Role of Manganese
He first became aware of the possible role of manganese in the BSE story during a tour of the world that took in Canada, Iceland and Slovakia in the mid-1990s. Investigating environmental factors in isolated clusters of TSE diseases, the group that includes BSE and vCJD, he found soil and vegetation samples contained manganese levels around 2.5 times higher than normal and low copper levels.
He also became aware that human CJD-type diseases were sometimes connected to high levels of manganese oxide in the environment, notably in Chile where mine workers were affected by what is locally referred to as "manganese madness".
David Brown, a scientist specialising in prion research at the department of biotechnology at Cambridge University, read of Mr Purdeys findings and became interested. Now he has now shown that, when added to cell cultures, manganese bonds to normal protein to create the "rogue" form of prion protein found in large quantities in TSE victims.
US scientist Stanley Prusiner first proposed that a "rogue" prion, PrPsc, kills animals and humans by converting normal prion protein molecules into dangerous ones that cause degenerative diseases of the brain. This is widely accepted within the scientific community, but how normal prion proteins, which do not contain genetic material, are turned into the dangerous "rogue" form is the subject of much debate.
"It appears to be a double whammy effect," Mr Purdey explained. "Phosmet used to treat adult cows results in lower copper levels in their brains and in those of their calves. If the animal then consumes large quantities of manganese in feed or from mineral blocks, it bonds to the prions in the place of copper and rogue prions are created," he said.
The rogue prions continue to turn normal prion protein into the rogue form in a "self-perpetuating" process called auto-oxidation that gradually destroys the brain cells, he explained.
Mr Purdey believes some animals are more genetically susceptible to this process than others and attributes the culling of this genotype, alongside reduced use of Phosmet, to the falling number of BSE cases.
In 1997 he put his proposals to SEAC, MAFFs advisory body on BSE, which concluded that more evidence would be required to justify further research into a possible role for OPs in causing BSE. It decided that OPs did not accumulate in cattle, which they would need to for them to cause disease, and noted that the BSE epidemic is better explained by the use of BSE-contaminated feedstuffs.
Same feed as victims
But Mr Purdey points out that many animals in this country have eaten the same feed as BSE victims and not contracted the disease, while British meat and bonemeal has been sold all over the world without BSE epidemics ensuing. Cattle born after the introduction of strict new feed controls in the 1990s have continued to contract BSE, he added.
He also disagrees with SEACs contention that vCJD is caused by eating cattle. In March 1999, it noted that two pieces of research involving mice had shown the link to be more certain.
Mr Purdey thinks the most likely cause is through vaccinations in doctors surgeries.
Dr Brown is also sceptical. He points to the lack of statistical correlation between the incidence of BSE, which has fluctuated considerably over the years, and of vCJD, which has remained very stable, as an indicator that the two are not directly linked.
"This could be down to the long incubation of CJD which means the peak could come much later, in 10 years or more," he admitted. "But if there is a link between BSE and vCJD it is very difficult to prove."