Univ. of Texas researchers find way to detect 'Mad Cow' in live humans

The discovery is expected to lead to a much more effective detection method for the infectious proteins responsible for brain-destroying disorders, such as bovine spongiform encephalopathy, or BSE in cattle and variant Creutzfeldt-Jakob disease, or vCJD in humans.

The blood test would make it much easier to keep BSE-infected beef out of the human food supply, ensure that blood transfusions and organ transplants do not transmit vCJD, and give researchers their first chance to figure out how many people may be incubating the disease, according to senior author Claudio Soto.

"The concentration of infectious prion protein in blood is far too small to be detected by the methods used to detect it in the brain, but we know it's still enough to spread the disease," said Soto. "The key to our success was developing a technique that would amplify the quantity of this protein more than 10 million-fold, raising it to a detectable level."

The findings appear online in Nature Medicine.


Human remains in cattle feed may have caused mad cow epidemic

The mad cow disease epidemic could have been caused by the feeding of material containing human remains to cattle, a scientist claimed yesterday.

Alan Colchester, a professor of neurology at the University of Kent, said the most likely origin of BSE and the subsequent deaths from variant Creutzfeldt-Jakob disease was the import from the Indian subcontinent of bone meal containing infected human remains.

Since the first case of BSE was reported in Britain in 1986, the original cause has remained unknown.

The most widely favoured candidate has been the transmission of sheep scrapie, a fatal degenerative disease that affects the nerve system, to cattle through feed.

The spontaneous mutation of a prion, a small protein found in the brain cell membrane, to create a new form of bovine transmissible spongiform encephalopathy (TSE) has also been suggested.

Writing in this week's issue of the Lancet, Prof Colchester said neither of these theories had been proved and that he had amassed substantial circumstantial evidence to support his new hypothesis that BSE originated from an earlier human form of the disease.

He said: "The existing theories of the origin of BSE all have significant weaknesses, and so we set out to look for something more plausible, which I think we have found. We propose… that human TSE-contaminated material was the cause of BSE, that this was transmitted orally via animal feed and that the infective material originated in the Indian subcontinent.

"Further investigations are needed into the sources of animal by-products used in animal feed manufacture, and into the transmittability of human TSEs to cattle." Britain imported substantial quantities of whole bones, crushed bones and carcass parts for use in the manufacture of fertilisers and animal feed during the 1960s and 1970s, with about half coming from Pakistan, India and Bangladesh.

Hindus believe that it is essential for their remains to be disposed of in a river, preferably the Ganges, and, while the ideal is for bodies to be burnt, often corpses are thrown in whole.

The collection of bones and carcasses has long been an important trade for peasants in India and Pakistan.

Media and eyewitness reports have described human remains being sold to processing mills along with animal material.

The Indian National CJD Registry recorded only 69 cases of CJD between 1968 and 1997. However, Prof Colchester believes that there was substantial under-reporting and estimates the true figure to be closer to 150 cases a year.

The BSE epidemic peaked in 1992 in Britain with a total of more than 180,000 cases recorded. Variant CJD, the human form of BSE, has killed about 150 people since the first case was recorded in 1995.

Prof Colchester questioned why BSE did not appear earlier given that scrapie has been endemic in Britain for at least 200 years, and that material from sheep has been fed to cattle for at least 70 years.

He also noted that all published attempts to transmit scrapie experimentally to cattle by the oral route had failed.

James Ironside, a professor of clinical neuropathology at the National CJD Surveillance Unit in Edinburgh, described Prof Colchester's theory as interesting and theoretically plausible but said more concrete evidence would be needed before it could be taken more seriously.