U.S. Considers Additional Mad Cow Regulations

According to the Atlanta Journal-Constitution, the Food and Drug Administration is considering additional regulations of animal feed to strengthen the country’s protection from a breakout of mad cow disease.

The FDA is currently seeking comments on the difficulty and costs that would be imposed to remove the brains and spinal cords of animals before they are rendered. After the public comment period, the FDA will consider drafting a rule to require the removal of such organs from animals rendered for animal feed.

Existing regulations already ban the inclusion of rendered parts of ruminants and minks from begin included in feed given to other ruminants, but feed manufacturers are allowed to include chicken and pig parts in ruminant feed, and ruminants can be included in chicken and pig feed.

The new regulations would require the removal of brains and spinal cords from all rendered products.

Source:

Creutzfeldt-Jakob Disease: U.S. may ban more animal parts from feed. Jeff Nesmith, The Atlanta Journal and Constitution, January 12, 2003.

World Health Organization Presents BSE Report

The World Health Organization’s Maura Ricketts presented her organization’s October 2002 report on Mad Cow disease in late January. The report warns that Eastern European and Asian countries are still vulnerable to possible outbreaks of the disease.

The report notes that the key to preventing BSE is to ensure that meat and bone meal from ruminants is not be fed back to ruminants. A few countries have gone further and enacted laws banning the use of meat and bone meal from ruminants in animal feed altogether.

The report also finds that other than Europe, Australia, New Zealand and some countries in the Pacific Rim and Americas, much of the world lacks any sort of active surveillance system to detect BSE.

On the other hand, all of the available evidence — including from the WHO report — is that BSE is far less of a threat to human health than most existing foodborne illnesses and diseases. According to WHO, worldwide from 1994 to 2001, there were a total of 122 deaths either confirmed or probably caused by vCJD which is believed to be caused from exposure to BSE. There are a total of 11 other individuals who are still alive but have conditionally been diagnosed with vCJD (an accurate diagnosis of vCJD is impossible, at the moment, before death of an individual afflicted with the disease).

Source:

Understanding the BSE Threat. World Health Organization, October 2002.

World health body warns that mad cow still a risk. Reuters, Richard Waddington, January 30, 2003.

First Direct Estimate of Extent of British vCJD Toll

Research published in the British Medical Journal offers the first direct estimate of the extent of vCJD in Great Britain.

Researchers examined 8,318 appendix and tonsil samples removed from patients between 1995 and 1999. Seventy percent of the samples came from individuals aged 20 to 29 — the group believed to be most vulnerable to vCJD.

The results? Only one person’s appendix showed signs of the vCJD prion. This would translate to an infection rate of 120 cases per one million people.

Peter Smith, chairman of the Spongiform Encephalopathy Advisory Committee, told Reuters,

It [the results] offers some limited reassurance, the findings could have been a lot worse than this.

. . .

This is the first time that anybody has been able to get any sort of handle on the level of exposure. But it is a small sample and what is needed now is larger-scale studies.

Efforts to create such larger-scale studies are in the works. This particular study will continue until a total of 15,000 tissue samples are checked. The British Department of Health plans to create a tonsil archive to collect tens of thousands of tonsil samples for analysis (tonsils are believed to be more likely to accumulate the deviant prions than is the appendix).

But certainly a rate in the 120 cases per million population rate fits with the relatively small number of vCJD cases documented so far.

Source:

First direct estimate of hidden vCJD cases. NewScientist.Com, September 19, 2002.

British ‘Mad Cow’ Toll May Be Lower than Feared. Richard Woodman, Reuters, September 19, 2002.

The Chronic Wasting Disease Controversy

ConsumerFreedom.Com published a review of concerns about chronic wasting disease in deer and elk (often referred to as “mad deer disease.”) Like Mad Cow Disease and Cruetzefeld-Jakobs, CWD involves prions that cause lesions to form in the brain of deer and elk. The current debate is centered around what, if any, risk the disease poses to human beings.

In deer and elk, the disease was first identified in the late 1970s in deer that were held in captivity. The perception, however, is that the disease has spread rapidly with some studies suggesting that as many as 3 percent of deer in some areas may be suffer from CWD.

A major problem in assessing the extent of the risk to human beings is that no one knows how CWD is transmitted. The Mad Cow epidemic was caused when tissues from the central nervous system and brains from cows were fed back to other cows after the rending process. But CWD is clearly infectious in the wild without requiring such an elaborate transmission method, and has also jumped to elk.

As The Center for Consumer Freedom noted, groups such as the Organic Consumers Association and people like John Stauber, author of Mad Cow USA, are claiming that CWD has already killed humans. They point to four cases of young people who died from CJD.

CJD generally kills people in their 60s and 70s, so several cases of the disease among young adults certainly calls for investigation. The Center for Disease Control ruled out Mad Cow Disease as a possible culprit, at which point Stauber and others pointed out that two of the men who died were hunters and a third victim was the daughter of a hunter.

Stauber told The Wall Street Journal back in May that, “I think that we have to assume the worst of CWD — that it could be even more dangerous and costly than mad cow because of its unique ability to spread through the environment and animal to animal.”

This ignores a couple of salient points. First, Stauber never bothers to mention that the CDC also investigated whether or not exposure to CWD might have caused these individuals’ disease, and concluded that there was “no strong evidence for a causal link” between CWD and the deaths of the four people from CJD.

Moreover, Stauber’s claim that CWD can spread quickly from “animal to animal” is a distortion. Obviously it spreads among deer and elk, but there is apparently a species barrier that keeps it from jumping to other mammals. Cows penned in with deer suffering from CWD, for example, do not contract any sort of prion disease from the deer. Besides, the important issue for human beings is whether or not the disease can spread easily from deer/elk to human beings. So far the answer is no.

Even with Mad Cow Disease there is clearly a high species barrier that makes transmission to humans very difficult. Despite all of the claims that potentially tens of thousands of people would die in Great Britain, the number of actual cases of vCJD in the UK has been very small. Traditional food poisoning is a far higher risk to human beings than Mad Cow Disease.

Second, although researchers at the National Institutes of Health’s Rocky Mountain Laboratory were able to use CWD prions to transform healthy human prions into a deadly diseased form, this transformation turned out to be surprisingly difficult to do even under laboratory conditions.

Rather than the sort of hysteria that Stauber and his ilk promote, a better course is that already adopted by state and federal authorities who are proceeding on numerous fronts to find out once and for all how CWD is spread among deer and elk and what, if any, risk of infection it poses to human beings.

Of course, don’t look for animal rights activists to line up behind such research since it largely involves laboratory research with mice and other animals. In fact, it is fascinating to look at animal rights sites that mention Nobel Prize winner Stanley Prusiner’s ongoing research into prions without even a hint that Prusiner is working with laboratory animals.

Sources:

‘Mad deer’ plague baffles scientists. Antonio Regalado, Wall Street Journal, May 24, 2002.

“Mad Cow”: A Review. Center for Consumer Freedom, July 10, 2002.

Study adds to ‘mad cow’ worries. Lou Kilzer, Rocky Mountain News, March 19, 2002.

Study: Deer with CWD considered edible. Larry Porter, The Omaha World-Herald, April 8, 2002.

The Prion Diseases. Stanley B. Prusiner.

Oral Polio Vaccine Poses No Mad Cow Disease Risk

Back in October 2000 the British government forced the withdrawal of an oral polio vaccine manufactured by Medeva out of concerns that it might be able to transmit Mad Cow Disease. This week, the government announced that the vaccine was safe and admitted the withdrawal was prompted by the government’s misunderstanding of its own regulations.

Many vaccines, including Medeva’s oral polio vaccine, use bovine serum as a growth medium. Hundreds of thousands of people received that vaccine and there was some concern and confusion within the British government as to whether or not Medeva had complied with laws designed to ensure the safety of medicines.

Back in 2000, the UK’s Medicines Control Agency claimed that chemicals derived from cattle tissue had been used in the production of the oral vaccine. Medeva told the government that no beef cattle tissue was used and its production process includes a step designed to eliminate cattle proteins, but the Health Minister ordered the withdrawal anyway.

In announcing that the vaccine was safe, British Health Minister Hazel Bears admitted that the Medicines Control Agency had given inaccurate advice because it misinterpreted the guidelines governing the use of animal products in vaccines.

The upshot of the withdrawal, of course, was simply to further feed anti-vaccination hysteria in Great Britain.

One side note. After claims about Mad Cow Disease and the polio vaccine surfaced, animal rights activists jumped all over this claim. Fascinating, isn’t it, that as soon as they think they might have a wedge issue they completely forget their “animal research never helped nobody” nonsense?

Source:

Polio vaccine ‘safe’. The BBC, July 5, 2002.

No risk to humans from recalled polio vaccine, government says. Associated Press, July 5, 2002.

Polio vaccine link to vCJD dismissed. The BBC, December 18, 2001.

Animal Tests for Prion Disease Move Closer

The Scientist published an article this month reporting on advances made by Stanley Prusiner in understanding — and hopefully treating — prion diseases such as CJD, vCJD, and BSE.

In the article, Prusiner — who won the 1997 Nobel Prize for his work on prions — notes that there is still much that researchers do not understand about prion diseases. “We though the number of cases of the disease [vCJD] would increase two to three times,” Prusiner told scientists at the University of Pennsylvania, “but the number of cases in 2001 was similar to the number in 2000.”

That seems to be due to an oddity with vCJD. Whereas CJD generally affects older people, vCJD seems to affect mainly younger people.

The good news is that Prusiner believes there is enough known about prion diseases to start looking at trials to test therapies for the diseases. Some compounds used to treat other diseases also appear to have the ability to prevent normal prions from degenerating into diseased prions that cause CJD.

Prusiner is currently working to develop a mouse model to test such compounds. His plan appears to involve a drug discovery compound to examine 11,000 compounds that might have some effect on prion disease and then test the promising ones in a mouse model before proceeding to human clinical trials.

Source:

Prion-Disease trials on the horizon?. Jennifer Fisher Wilson, The Scientist, 16[6]:28, Mar. 18, 2002.