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CWD: deer-to-human transmission data released
John Stauber: Could 'mad cow type epidemics happen in the US
Lancet appendix study appears
House of Lords: the questions continue
Secret Keele meeting: bizarre details emerge
'Mad cow' rule cuts Tucson blood donations
Britain dismisses new BSE transmission fears
French Ban On British Beef Could Be Lifted In 2002
Parkinson's and pesticides: home bug spray may increase Parkinson's risk
Human BSE Foundation update

Mad deer disease can infect normal human brains in laboratory tests

Monday, May 8, 2000 has further information and facts on CJD.
Jennifer Kelly or Amy Leska, EMS 202/463-6670 Washington, D.C. 
Public health advocates are demanding that the Food and Drug Administration close loopholes in animal feed regulations to prevent the spread of U.S. mad cow-type diseases now at epidemic levels in Western deer and elk that might infect people who eat meat.

In a letter sent today to the FDA, the Center for Food Safety (CFS), the Humane Farming Association, and families of U.S. victims of the human version of mad cow disease, Creutzfeldt-Jakob disease (CJD) are demanding new efforts to protect public health and food safety. The FDA was asked to respond to a legal petition filed in January 1999 that would change U.S. animal feed regulations to prevent the spread of U.S. mad cow-type diseases already occurring in deer, elk, sheep and humans, and suspected in pigs and cattle.

Under current FDA regulations animals known to be infected with mad cow-type disease such as deer and elk infected with 'chronic wasting disease' and scrapie-infected sheep, can be legally fed to pigs, chickens and pets, which in turn can be rendered and fed to cows. Billions of pounds of slaughterhouse waste in the form of rendered animal by-products are fed to US livestock every year as fat and protein supplements, despite this practice being the known route of transmission of British mad cow disease.

A fatal 'mad deer' disease called chronic wasting disease or CWD is occurring at epidemic levels in deer and elk in Western states and on game farms, CFS legal director Joseph Mendelson wrote in the letter to the FDA. This may already be claiming human lives as is suggested by the alarming appearance of unusually young victims of Creutzfeldt-Jakob disease.

Today at the first CJD Foundation conference in Miami, government researcher Byron W. Caughey, Ph.D., announced that in laboratory tests CWD from deer can infect human brain tissue at rate similar to British mad cow disease. In Britain 56 people have died of human mad cow disease, the death toll is climbing and some scientists suspect it will claim hundreds of thousands of lives in the decades ahead. Caughey's research on US mad deer disese was conducted at the National Institutes of Health Rocky Mountain Laboratories in Hamilton, Montana, and has not yet been published.

The most recent suspected victim of US mad deer disease is Jay Dee Whitlock II of Oklahoma, who died of CJD on April 7, 2000. Whitlock, 28, was an avid deer hunter and venison consumer. He is the second young hunter to die of CJD in the past year.

John Stauber, co-author of Mad Cow USA and a speaker at the CJD Foundation conference, said, "The announcement that US mad deer disease can infect the human brain, and that it happens at a rate similar to British mad cow disease, is extremely disturbing. A deadly human dementia might be already spreading from deer and elk into hunters in Western states, and the policies of the FDA and other agencies are completely inadequate to protect public health.

Could 'mad cow type epidemics happen in the US

John Stauber, talk given 7 May 00 CJD Foundation conference  Miami
Center for Media & Democracy
520 University Avenue,  Suite #310 Madison, WI 53703
"Three years ago Sheldon Rampton and I were finishing our book Mad Cow USA published in November of 97. In our introduction we wrote that ours is not a biology book nor a diet guide, but a "book about politics and how it operates in the real world. It explains how government officials have placed concerns for the food industry over human health and welfare. In addition to telling the story of an exotic, mysterious and frightening disease, we have written this book to report on equally dangerous legal and political trends which threaten not only our physical health, but also our fundamental democratic rights..."

The title of this session asks a question: "Could 'mad cow type epidemics happen in the US.?" My answer is not only could they, but they are. Sheep scrapie arrived in the US a half century ago and thanks to government bungling is now widely spread throughout the US, with dozens of different strains. Chronic wasting disease may have begun as sheep scrapie but now it is spreading through deer and elk in western states and on game farms.

In the past two years two western state hunters under the age of 30 have died of CJD, and some of us suspect they may be human victims of a new strain of TSE in sheep, deer or elk that has begun claiming young human victims in the US.

Since 1964 researchers have suspected that transmissible mink encephalopathy TME in the US is from a hidden TSE in cattle, and the late Dr. Richard Marsh, to whom we dedicate our book, believed that he isolated that TSE in mink in Wisconsin in 1985, a year before the British strain of TSE dubbed mad cow disease was observed.

As our book was going to completion, we discovered that USDA inspectors felt they had identified a TSE in pigs way back in the the 1970s, when few researchers other than a small group in what Paul Brown calls the Club were very concerned or aware of TSE diseases.

Of course, British mad cow disease and the looming specter of hundreds of thousands of people condemned to death in the decades ahead has changed everything. Everything, that is, except public policy here in the US. For despite the fact that two Nobel prize winners in this area of research are from the US, there is a public relations cover-up of massive proportions in this country that is preventing us from effectively establishing public policies that can monitor, prevent and eventually treat TSE diseases.

Please note that I said a public relations cover-up; that's important. I suspect that if TSE diseases were spread by mosquitoes, we'd be spraying pesticides all over the US to try and irradiate sheep scrapie and chronic wasting disease. But these diseases are spread by agribusiness through animal livestock products fed to people and animals, and thus instead of putting the concerns of people first, we have see that consistently governments have put the concerns of industry first.

We've heard eminent and hard working scientists talk about TSE diseases in terms that dizzy the head of even other scientists. This is a very contentious and mysterious area of research because TSE diseases break many rules.

Luckily, my co-author and I are not experts or scientists. However, we did have the benefit of being able to interview top TSE researchers like Richard Marsh and Dr. Gajdusek, have them review parts of our manuscript, and thus deliver a book that is based on solid, sound science regarding what is known, and what is unknown, what is proven, and what is not.

From my perspective, this is the most important point and perspective to keep in mind:

For the past thirty years a massive unregulated experiment in creating new strains of TSE disease has been undertaken by the livestock industry, and we're the guinea pigs. The experiment is ongoing. The experiment began as a really neat idea: lets take the billions and billions of pounds of slaughterhouse waste, blood and offal that is produced every year from cattle and pigs and sheep and roadkill and pets and zoo animals, and let's recycle it. Let's turn it into protein fat supplements, and let's feed it back to the livestock we eat.

It seemed like a good idea. Unfortunately, what it didn't take into account was the infectious prion agent. As Dr. Gibbs has pointed out, probably every mammalian species has a TSE disease at some minute level: people, pigs, cows, sheep, mink, cats and dogs, deer, elk. Grind up the most infectious parts of millions and millions of animals, concentrate them into feed supplements, and you are creating an environment not only for spreading and amplifying existing agents such as scrapie in sheep, but also for creating an untold number of new strains of TSE.

This is especially important to grasp. In laboratory experiments, when TME or scrapie or CJD is injected into new animal species, whole new strains of TSE are created, and they can have different potential to infect new host species. The process of rendering animal waste into animal feed has been a massive and ongoing experiment in the creation of new TSEs, one of which emerged in Britain in the mid 1980s as mad cow disease, has clearly spread into humans claiming over fifty so far, and in my guess will in the years ahead be founded to have infected hundreds of thousands of Britons.

I said that this outbreak of BSE in Britain changed everything, but what really changed everything was what caused that outbreak: feeding rendered animal by-products back to animals as food.

I wish I could tell you that this practice has been stopped, but it has not. I wish I could tell you that well informed and courageous officials in the FDA, the USDA and the CDC have taken the mad bull by the horns, and are right now executing a precautionary policy to insure that what has happened in Britain does not happen in the US. Unfortunately, that is not the case.

Dr. Hansen will shortly explain why the much heralded FDA feed regulations on rendered animal by-products announced in 1997 are in many ways a farce. For instance, in the US calves are literally being weaned on cattle blood protein, and scrapie infected sheep can be used as feed for pigs which can be used as feed for cattle.

But the problem is beyond just the poor US animal feed regulations. You need look no further than your favorite vitamin and nutritional supplement stores. Right now, with the full knowledge of the FDA, the NIH, the CDC, millions of Americans are popping over the counter as glandular supplements. These unregulated products contain the most infectious parts of slaughtered animals, the very parts that make up the so-called Specified Bovine Offal that should be banned from cattle feed, such as the brain, pituitary, and glandular system. These pills are pooled, collected from hundreds of thousands of animals and taken daily by untold numbers of Americans, probably millions given the popularity of supplements.

Again, this amounts to an unregulated human experiment, minus laboratory controls or knowledgeable consent, feeding humans the most infectious parts of animals, possible creating new TSEs by passaging animal TSE from pooled glandular products.

I've brought along four different bottles of the pills I'm talking about, and I've asked that they be pass around so you can look at them yourself and read the label.

Some would say that FDA's hands are tied, that thanks to lobbying by the nutritional supplement industry the FDA lacks the power to prevent sales of these glandular. Actually this points to another frightening disease rampant among otherwise good people who populate government agencies which I call BCD for Bureaucratic Cowardice Disease. FDAs hands might be tied and they can't yank these products from the market, but their mouths are not gagged and concerned officials should be speaking out loudly warning the American public that they are consuming animal brains and glands and might want to consider the potential risks.

There is a reason why scientists in agencies and universities, not to mention corporations, avoid sticking their necks out, and we need look no further than Richard Marsh, a dedicated and conservative scientist who took it upon himself to speak up in 1993 in an interview in Wisconsin's largest farm paper. Richard Marsh warned Wisconsin farmers, thousands of whom were feeding rendered cow by-products back to their cows, that given the mad cow outbreak in Britain they should, despite the reassurances from USDA that such feeding was safe, stop.

The day after that article appeared Dr. Marsh was literally called on the carpet in the office of the dean of the school of agriculture at the University of Wisconsin, and read the riot act. he was told that industry funders were threaten to sue him, sue the school, cut off money for research, and who did he think he was?

Within months the school scrambled and pulled together a symposium on the subject, which served to dismiss and marginalize Dr. Marsh's views. When Dr. Marsh died of cancer in 1997, after the British announcement that mad cow disease was killing young people, the same University had the gall to praise Dr. Marsh and his work as in the best tradition of the University. Some of us feel that the stress and abuse heaped on Dr. Marsh >from 1993 to 1997 had an impact on his health that contributed to his demise.

This is what happens to scientists who break ranks and speak out, and it is a great loss to us today because I think if Dick Marsh was still alive he would be leading the charge to confront the ignorance and the cow-towing to industry that typifies this issue.

Dr. Marsh was a colleague and contemporary of many of the researchers in this room. As Paul Brown whom he once worked with might say, he was a member of the club. But Dr. Marsh was able to make realizations that I'm afraid most of the club members haven't yet come to, and he was able to put his sense of scientific obligation to society in front of concerns about his funding, or even his personal and professional safety.

I first began investigating mad cow type diseases in the early 1990s when I was working in Wisconsin organizing farmers and consumers opposed to Monsanto's genetically engineered bovine growth hormone, the cattle equivalent of human growth hormone which when injected into cattle forced them to produce more milk. Well, its not quite that biologically simple as I'm sure any woman here who has had children can imagine.

It was brought to my attention by a retired industry veterinary researcher that in order to make the hormone work, cows need to be fed additional fat and protein supplements, and that the cheapest supplements were rendered byproducts from other cows. This veterinarian told me this was very bad because it was exactly what had cause the outbreak of BSE in Britain.

I investigated and found this was true - massive feeding of cows to cows was going on in the US, despite the fact that as early as the Fall of 1987 British epidemiology had shown that is was this practice that spread mad cow disease.

I remember one of my first meetings with Dr. Marsh. We talked about his believe that a US BSE agent, different than the British strain, was in cattle at low levels and was the cause of occasional outbreaks of TME. I know that eminent researchers in this room dispute that, but frankly Dr. Marsh never doubted it and I think the evidence and commons sense remains in his favor.

I had just been to a holistic chiropractor for my chronically bad lower back, and had been sold a bottle of adrenal gland extract which I showed to Dr. Marsh - he practically fell out of his chair and I immediately stopped taking them.

He was shocked to learn that such glandular were sold. Imagine what he might think today, that at this late stage of the game with kids in their 20s in the US dying of CJD, that these glandulars are sold without warning.

Of course, I may be taking a risk myself in saying this. After all, we are in Florida, one of 13 states in the US in which the Animal Feed Industry Association members have succeeded in lobbying into law a food product disparagement bill. I could end up like Oprah Winfrey and her guest Howard Lyman, forced to spend millions and millions of dollars (which in my case would be thousands and thousands and then bankruptcy) to convince a jury that my remarks today are based on sound science.

Having written two books in the past five years, one on political PR and the other on the politics of food, I can tell you that a major reason why there has not been more news media coverage of this issue is the multi-million dollar PR campaign and litigation threats of the food industry which we document extensively in our book.

I find it ironic that this weekend as we're meeting here President Clinton announced Saturday a new initiative to address the safety of hot dogs. Philip Brasher of the Associated Press speculates that as he is leaving office the President wants to burnish his image with food safety initiatives.

The irony is that it is under this administration that the food industry has launched an all out attack on our first amendment rights by lobbying food libel laws onto the books, and the administration has remained silent. Despite knowing of the risks of cow cannibalism since the beginning of his presidency, his administration did nothing until 1997, and as we reveal in our book and Dr. Hansen will explain, the regulations are severely inadequate.

I am circulating a letter being delivered by the Center for Food Safety urging the agency to respond to the petition filed by that group and many of the families in this room that calls on FDA to severely tighten its regulations. Yet, probably to avoid publicity, the FDA stonewalls.

A couple weeks ago I was in Washington and I attended a conference that was paid for in part by the lobbyists responsible for putting food censorships laws on the books, the Animal Feed Industry Association and the law firm of Ollsen Frank and Weeda that drafted the model bill that was then lobbied for at the state level by the American Farm Bureau. I picked up this glossy brochure in which the FDA is slapping itself on the back for its food safety initiatives. In it I read that the FDA's BSE Educational Activities have Gained an award from the vice president:

The US feed regulations and the FDA were honored with VP Al Gore's Hammer Award. Dr. Stephen F. Sundlof, the directory of FDA's Center for Veterinary Medicine, the man who since January 1999 has been unable to respond to the legal petition to close gaping loopholes in the FDA regulations stated: "thanks to the development of the BSE regulation, we can continue to say that there has not been a single case of BSE reported in the United States. Educational efforts ... will help assure that we can continue to make that claim."

In researching our books we had access to documents obtained through the Freedom on Information Act. One 1991 document of the USDA was titled "BSE Public Relations," and if someday attorneys in a class action lawsuit on behalf of CJD patients in the US are looking for a smoking gun demonstrating that concerns for industry were place over concerns for people, this is it.

(p.148-149) According to this document, the mere perception that BSE might exist in the United States could have devastating effects on our domestic markets for beef and dairy products." The report examined how the British handled their PR, and it fretted over a story in the British magazine The Economist which, quote, "could potentially create alarm among US consumers," unquote, because it reported that, quote,"many veterinarians and medical experts have come around to the belief that humans could catch the mystery brain disease."

This USDA PR document approvingly noted a quote in the Washington Post by Dr. Joseph Gibbs at NIH in 1990 saying "I don't think there is any danger in consuming British beef." Remember, this was in 1991. It had known for four years that it was feeding cows to cows that was spreading BSE in Britain. More and more were fearing that humans would die. Meanwhile, in the US, billions of pounds of cow by-products were still being fed, in fact the amount was increasing each year.

Was there no one inside the USDA or FDA who saw the lunacy, indeed the criminality, in knowing this and letting cannibalistic feeding go one in the US? Some did. The report notes that "some (USDA APHIS) staff members... argue that because there is evidence that pigs, cats, mink, deer and a variety of experimental animals may b e susceptible to trans. spongiform. encephalopathy, the only prudent policy is to not feed products that contain these agents to ANY SPECIES OF ANIMAL."

That's it. That's what we should have done then, and that's what we should be doing now, but are not. Instead we are still exposing ourselves and US livestock to a massive TSE experiment.

So, in 1991 the USDA and FDA rejected this advice by some anonymous staffers, as they do today. This 1991 USDA PR report admitted that a more cautious policy would be, quote, "to prohibit the feeding of sheep and cattle-origin protein products to all ruminants, regardless of age. The advantage of this option is that it minimized the risk of BSE. The disadvantage is that the cost to the livestock and rendering industries would be substantial."

In fact, absolutely nothing of substance was done until August of 1997, when FDA announced its sham feed regulation, winner of the coveted Al Gore hammer award, designed as a PR fig leaf so that FDA can say 'we are keeping British mad cow disease out of our livestock."

Let me say that the only bright spot in this story of corporate and government collusion, irresponsibility and censorship has been a few brave souls like Richard Marsh, Richard Lacey in England, others who have bucked the tide and spoken out, and those of you who are the families and loved ones of CJD victims.

Through CJD Foundation and CJD Voice you have found each other, and you will eventually force responsibility onto government and industry because if you don't no one else will.

In conculusion, we need a massive commitment in the United States to address TSE diseases. We need to start by admitting the shortcomings of our failed federal feed policies and change them. We need to dedicate hundreds of millions of research dollars, if necessary, to try to eradicate scrapie in sheep, eradicate CWD in deer and in elk, and investigate, research, test and monitor for TSEs in humans and animals. We need money for research to develop treatments, because while this disease used to be rare disease, I suspect we are about to see it emerge full blown in Britain with hundreds of thousands of victims, and more and younger victims appearing in the United States, as a result of our thirty year experiment in animal cannibalism.

The leadership for this will not come from politicians in bed with the agribusiness industry. It will not come from researchers who while brilliant are stuck back in pre-BSE days, still viewing this as a rare unusual disorder. It will come from average citizens who husbands and mothers and children are dying of this bizarre class of dementia diseases in increasing numbers, and who are not afraid to demand that the right policies be implemented and funded. It is upon your shoulders that leadership falls, and so far you are doing admirably."

Britain dismisses new BSE transmission fears

Mon, May 8, 2000 Reuters World Report
Britain's Ministry of Agriculture said on Monday there was no evidence to indicate that a hitherto unknown "third way" of mad cow disease transmission existed. The ministry comments followed reports that cattle could contract mad cow disease -- Bovine Spongiform Encephalopathy (BSE) -- through soil contaminated by cow dung.

French Farm Minister Jean Glavany said in April BSE may be passed in a mysterious third way, which he did not detail.

Transmission is currently thought to occur through contaminated feed and in a smaller number of cases from cow to calf. "Currently there is no evidence that a third way of BSE transmission exists," the ministry said in a statement. Britain has said the last cows were infected through contaminated feed in 1996.

But the Agriculture Ministry said it would examine the likely route of exposure in all cases of BSE in animals born in 1996 or later to ensure that a third way of transmission had not been missed. Maternal transmission means that a small number of infected calves may still be born but culling measures should ensure that the numbers are very small, the ministry added.

Germany in March overturned a four-year import ban on British beef imposed after the mad cow disease scare. However, France still maintains a ban on British beef. BSE is a fatal brain-wasting disease which scientists believe can spread to people via infected beef. It emerges as a new variant of Creutzfeldt-Jakob Disease (vCJD), for which there is no known cure. More than 50 people have died in Britain from vCJD. Despite a recent study showing no evidence of CJD in 3,000 specimens of human tissue, scientists say the final epidemic could affect hundreds or hundreds of thousands of people.

BSE expert raises new fears

Mon, May 8, 2000 By Nick Mead, PA News
The BSE epidemic may last longer than previously thought because of a "real risk" that the disease was spread by cow pats from infected cattle, a leading scientist said today. BSE expert Dr Alan Dickenson told Radio Four's Farming Today programme that his research suggested cattle continued to catch BSE long after the date the Government believed was possible. The new findings sparked fears that Britain was risking another trade war with France and Germany over the spread of the disease.

Microbiologist Dr Stephen Dealler told the programme that unless urgent action was taken to curb the spread of the disease, the French and Germans would impose new restrictions on British beef.

The Government has insisted that the last cattle were infected in August 1996, either through contaminated feed or, in a small number of cases, from mother to calf. But Dr Dickenson, the founding director of the Neuropathogenisis Unit in Edinburgh which researches BSE, warned that animals born after August 1996 may have caught the disease a "third way", through infected soil. His research shows that cow pats excreted on to grazing land by cattle at the height of the epidemic posed a "real risk" of infection.

If cattle born after August 1996 caught BSE through infected soil, the epidemic would last longer than the Government predicted. The disease's five-year incubation period means it will not be possible to tell whether Dr Dickenson is right until 2001.

Dr Dealler said he feared France and Germany would extend their bans on the import of British beef unless the Government takes action to stop the spread of the disease. He added that the future spread of BSE could be "drastically reduced" if cattle and sheep were injected with the drug pentosan polysulphate. The compound, used in the United States to treat cystitis, has been shown to drastically reduce BSE infectivity in laboratory mice, Dr Dealler said.

A spokesman for the Ministry of Agriculture, Fisheries and Food, said: "Currently there is no evidence that a third way of BSE transmission exists. MAFF is alive to the possibility that a different route of exposure may have been masked by food borne transmission. MAFF will examine the likely route of exposure in all cases of BSE in animals born in 1996 or later to ensure that any third way of transmission is not missed. Measures introduced in 1996 should ensure that no cases born after August 1996 were infected from contaminated feed. Maternal transmission of BSE means that there will still continue to be a limited number of cases born after August 1996. However because of the offspring cull, these numbers are likely to be very small."

Opinion (webmaster): Yes, but how has scrapie persisted for centuries despite a feed ban and culls and why should BSE be any different? And both species have questionable inbred alleles. MAFF research over many decades has never been able to pinpoint the underlying mechanism of scrapie persistence.

COMTEX Newswire Tue, May 9, 2000

UK govt says no evidence of BSE spread from slurry London. An official from the UK Agriculture Ministry said Monday there is no scientific evidence, so far, showing the horizontal transfer of Bovine spongiform Encephalopathy (BSE), or mad cow disease, from [cow excrement] slurry in fields. The official was responding to research by BSE expert Dr Alan Dickenson, who said earlier that cow excrement on grazing land at the height of the epidemic posed a "real risk" of infection.

The French Agriculture Ministry has announced the 17th case of bovine spongiform encephalopathy (BSE), or mad cow disease, in France so far this year. It said the cow was born in the North-West France district of La Manche in November 1994. The cow was destroyed along with the rest of the herd of 142 cows.

Secret Keele meeting: bizarre details emerge

12 May 00
The Minister of State, Ministry of Agriculture, Fisheries and Food (Baroness Hayman) responded to a House of Lords question as follows:

"Almost 300 people attended the workshop including the grant holders and their assistants and students, some members of SEAC and representatives of the Funders. There were formal presentations of the research projects and two poster sessions. There were 125 posters; 26 of these were selected and the researchers invited to give short oral presentations. Essentially this is an exercise in research management. After the meeting, the funders discussed the format and the quality of the science and results. Some future directions for research were identified." Elsewhere it was said that 2 researchers from the international research community were present.

Comment (webmaster): This gets ever more bizarre. In other words, the Keele meeting was a rather large and vigorous conventional scientific meeting with tons of posters etc, oaths of secrecy being a ludicrous concept with 300 attendees -- it would take everybody in the UK CJD line plus their dental hygenist to get to this number.

The main features of the secrecy was exclusion of non-British researchers who are outside the reach of the heavy arm of the Official Secrets Act. Of course the press was also kept in the dark, not to mention the public who paid for MRC and MAFF research with their taxes.

Earlier it was said the reason for secrecy was so work in progress could be safely discussed -- of course, people are hardly shy about presenting such poster material at open scientific meetings such as the one in Iceland. But to _never_ release the contents of the poster sessions!!!

The secrecy shuts out hundreds of foreign researchers who in the past have competed too effectively for research honors. Edinburgh, for decades the center of TSE research in the UK, has long been a sore loser over virus vs protein-only and indeed some researchers there still cling to it. Finally, without the secrecy, information might have gotten out to the public domain without spinmeisters having first controlled it .

A pitched battle is raging now over who shall monopolize nvCJD research, the Surveillance Unit or Collinge. The American experience favors a much more broadly based distribution of grants over centralized control of empires, but since that doesn't seem to be an option, it would be better if London MRC and Collinge prevail, since molecular biology and medicine are the core subjects for further characterization and understanding of prion diseases, not agricultural interests or pathology (which retains a role in diagnosis).

The main fretting at open sessions at the Keele meeting focused on surgical intruments as the current most worrisome development so there must have been some news on that. An irritating aspect of the meeting was reportedly the "overexposure of well known prima donnas who were given two major lecture slots while most mere mortals were given one if they were lucky or more likely a poster slot! " Sounds all too familiar.

In the webmaster's opinion, private sessions took place after scientists had presented their news and left. These discussed the status of the epidemic and how news would be managed. The real purpose of the conference was to bring together the scientists wto inform the ministers and have the Civil Servants decide on the way forward after the scientists had left. Emergency planning committees weren formed and spin doctors are trying to figure out the least damaging way and time for breaking the news.

Meanwhile, the latest UK suicide study flatly contradicts the 'ethics' committee pretext for holding up the prospective fresh tonsil test:

Suicidal ideation among outpatients at general neurology clinics: prospective study

BMJ 2000;320:1311-1312 ( 13 May 2000)
Alan J Carson,  Steven Best,  Charles Warlow,  Michael Sharpe
Suicide is one of the ten most common causes of death for both men and women in Great Britain.1 Psychiatric disorders are the main risk factor, but numerous studies have also identified physical illness as an important contributory factor.... As part of the interview all patients were asked: "In the last two weeks, have you had thoughts that you would be better off dead or of hurting yourself in some way?"

Patients who answered yes were asked to describe the nature of these thoughts. To be classed as experiencing suicidal ideation the patient had to have thought about active plans for committing suicidesuch as buying tabletsnearly every day for the previous two weeks.

The clinical characteristics of the patients attending the clinics are shown in the table. One in 11 patients (26/300) seen at the general neurology clinics had given serious thought to committing suicide in the past two weeks. Almost all of these patients (23/26) had major depression.

It might be assumed that suicidal ideation would be more likely to occur in patients with progressive, debilitating neurological conditions. However, this was not the case. Twelve of the 26 patients who had experienced suicidal ideation had medically unexplained symptoms, and most of the remainder had non-progressive conditions.

Our findings do not support the view that suicidal ideation occurring in neurology patients is largely a rational response to progressive physical illness. Instead, the findings underscore the importance of major depressive disorder in influencing the ways that medically ill patients think about their illnesses and themselves.

Parkinson's and pesticides: home bug spray may increase Parkinson's risk

May 8, 2000 Reuters
Opinion (webmaster): Related ideas surfaced as causes of the BSE epidemic, notably required use of Phosmet, a neuroactive insecticide. A small but non-decisive amount of experimental data is consistent with such an enhancing role.

People exposed to bug sprays in the home and garden may have a higher risk of Parkinson's disease, an incurable and fatal deterioration of the brain, researchers said on Friday.

The study, which is sure to cause controversy, is the first to show that exposure to pesticides in the home may lead to Parkinson's, although other studies have suggested that exposure to the chemicals at work is a risk. Lorene Nelson, a neuroepidemiologist at Stanford University School of Medicine, and colleagues studied 500 people newly diagnosed with the disease which is characterised by shaking and a freezing of the muscles.

They told a meeting of the American Academy of Neurology in San Diego that people who had been exposed to pesticides were twice as likely to develop Parkinson's disease as people not exposed to pesticides.

"This study is the largest yet of newly diagnosed individuals with Parkinson's disease and it is the first study to show a significant association between home pesticide use and the risk of developing Parkinson's disease," Nelson said in a statement.

For their study they questioned 496 people who had been diagnosed with Parkinson's disease. Each patient was asked if they had used or been exposed to insecticides, herbicides, weed killers or fungicides in the home or garden.

They compared these surveys to those done by 541 people without Parkinson's. Parkinson's patients were more than two times as likely to have been exposed to insecticides in the home. People exposed to herbicides also had a higher risk, but exposure to insecticides in the garden and to fungicides did not seem to be associated with the disease. Parkinson's is caused when brain cells that produce an important neurotransmitter, or message-carrying chemical, are destroyed.

"Certain chemicals that an individual is exposed to in the environment may cause selective death of brain cells or neurons," Nelson said. "If we could understand why these neurons are being killed in certain circumstances, we can then try and prevent it."

She said much more study was needed before anyone could draw any conclusions about pesticides and Parkinson's. "No specific guidelines regarding avoidance of pesticides can be given at this time but, in general, this is an area of public health importance that needs to be pursued," she said.

French Ban On British Beef Could Be Lifted In 2002, Official Says

Tue, 09 May 2000  BridgeNews
Louis Orenga, President of the French Meat Information Center, told BridgeNews Tuesday the ban on British beef could be lifted in 2002 when compulsory labeling is enforced and as long as French scientists consider the product safe.

The official was reacting to the news of a new Bovine Spongiform Encephalopathy (mad cow disease) transmission hypothesis from British BSE expert Dr Alan Dickenson, who said Monday cow excrement on grazing land at the height of the epidemic posed a "real risk" of infection.

"The fact that BSE cases are still appearing is one thing, and exposing consumers to that risk is another," he stressed.

He said even though BSE cases will continue to appear well after 2001, the consumers have to be protected as well as possible. He also insisted the precautionary principle was crucial in the crisis. "It's impossible to eliminate all risk so we need the best control systems," he added. He also urged all EU countries to withdraw risk materials from animals.

"It's crucial to have a normalized system in Europe," he said. He added the day the French government will lift the ban on British beef will be good news because it will mean that the epidemic has been mastered. EU Delays Decision On BSE Risk Materials Until M... Wire Service: DJ () Date: DJ

EU Delays Decision On BSE Risk Materials Until May 23

Thu, May 11, 2000  Dow Jones By Eric R. Drosin
The European Union Commission Thursday delayed a decision on banning certain animal tissues in food and feed products in an effort to prevent mad cow disease until May 23. The Commission said in a statement that wanted to give member states "some more time" to consider the Commission's proposal.

The proposal says that all E.U. member states will be obliged to remove the skull, the tonsils and the spinal cord of cattle, sheep and goats above 12 months of age before processing the animals for human or animal consumption.

In high-risk countries such as Portugal and the U.K., the proposal says the entire head of the animal, the thymus, spleen, intestines and the vertebral column of animals over 6 months of age will also have to be removed.

According to the Commission, the removal of Specified Risk Materials - brain and spinal cord tissue, which are infected when certain animals contract BSE - is the single biggest contribution that can be made to reducing the risk to humans from BSE. The proposal will replace the previous Commission's plan, which hasn't yet been accepted by member states.

'Mad cow' rule cuts city blood donations

Thursday, 11 May 2000 By Carla McClain Arizona Daily Star 
More than 50 critically needed blood donors have been turned away from Tucson's Red Cross this spring because of fears of "mad cow disease" infection, officials have confirmed. Ordered by the federal government in March, the controversial nationwide ban on potentially infected donors is expected to significantly reduce blood donations in this country ‹ worsening already severe shortages.

The ban specifically targets anyone who has spent six or more months in Great Britain in the past 20 years ‹ during the outbreak of mad cow disease there. No outbreaks of the rapidly fatal, brain-destroying disease have been reported in the United States.

Red Cross officials and Tucson infectious disease experts believe the donor ban is premature and unnecessary. They say the risk of human transmission of mad- cow-type infection is extremely small and still unproven.

"I think it's crazy to screen these people out," said Dr. Eskild Petersen, University of Arizona infectious disease specialist. "Even if we could confirm a risk of infection ‹ and we absolutely cannot yet ‹ the numbers of people possibly infected by mad cow are incredibly small. Human cases are still very, very rare. "But I understand the very major concern about the safety of our blood supply. You want it to be as safe as possible, so you tend to go to extremes to assure that. All this is happening partly because of the lessons learned from HIV (the AIDS virus)."

During the mid-1980s, thousands of Americans were infected by the deadly AIDS-causing virus after getting infected donor blood. Despite compelling evidence that blood carried the virus and that blood contact could transmit it, officials delayed screening donor blood for it, with devastating consequences.

But the facts surrounding mad cow disease are far less clear, with much about it still a mystery ‹ though a frightening one ‹ to medical scientists. Known scientifically as bovine spongiform encephalopathy (BSE), mad cow disease hit epidemic proportions in cattle herds in Great Britain during the 1980s, peaking in 1993.

Nearly 200,000 infected cattle were slaughtered to try to stop the spread of the disease ‹ and because of fear the deadly disease would be transmitted to humans through infected meat. And indeed, unusual clusters of what is suspected to be the human form of mad cow disease ‹ a new variant of the very rare and incurable Creutzfeldt-Jakob disease ‹ have since appeared in Great Britain, killing 53 people.

Although it has not been proved with scientific certainty, scientists nevertheless strongly suspect the new form of Creutzfeldt-Jakob ‹ which also kills quickly by attacking the brain ‹ is in fact transmitted to humans through the infected meat of "mad" cows.

That is because the infectious agents that cause mad cow disease and variant Creutzfeldt-Jakob ‹ extremely small abnormal proteins known as a prions ‹ have been analyzed and found to be similar. But the prion is so small that it cannot be detected in blood, so there is no way to screen blood for either infection. As a result, it is not known if humans can infect one another through blood contact, including donated blood.

And that is why Red Cross officials are protesting the ban ‹ ordered for an indefinite period by the federal Food and Drug Administration ‹on any blood donor who has spent a total of six cumulative months in the United Kingdom between 1980 and 1996.

"There is very little science supporting this policy," Jacquelyn Fredrick, chief operating officer for the American Red Cross Biomedical Services, recently told a congressional subcommittee in Washington, D.C. "Yet it has been estimated the nation could lose at least 2.2 percent of donations . . . at a time when the blood supply is marginal."

The impact on Southern Arizona's blood supply will be "very significant," said Kay Donohoe, director of donor services for the Red Cross in Tucson. "This is yet another blow to blood donation ‹ when we're facing a critical shortage of blood in Arizona this summer. And it's happening even though there is no medical proof of blood-to-blood transmission. We're very concerned about it. We're struggling with how we're going to get enough blood for Memorial Day and the rest of the summer."

Since the ban went into effect two months ago, about 50 Tucson donors have been refused at the Red Cross, though Donohoe suspects twice that many have stayed away, after hearing of it. She fears the agency may lose up to 5 percent of donations in the coming year. Most of the affected donors come from Davis-Monthan Air Force Base ‹ where regular blood drives are held ‹ because so many in the military have been stationed in parts of Great Britain.

"This took us completely by surprise. When I heard I couldn't donate blood, I said, 'What is this?' " said Carol Watkins, who is stationed at DM with her husband, Richard. Both are longtime Air Force blood donors who were based in England from 1983 to 1986. "One day you can donate, and the next day you can't. It's been a shock. People are very confused about it," she said.

Realizing she is considered to be at risk for infection with the deadly mad cow disease, Watkins insisted she is not worried. "I kind of laugh when people say I'm going to fall over and die laughing hysterically," she said, referring to the disease's rapid dementia. I was there 14 years ago. I think I'd probably know by now if I was going to get it."

Petersen, at the UA, fully agreed she faces almost no risk. "There is absolutely no reason to panic. None," he said. "Even with the outbreaks (in England), the numbers are still too small. Human cases are still unbelievably rare."

House of Lords: the questions continue

last updated 16 May 00 Lord Lucas questions 
[Earlier questions and answers are found elsewhere]
Question 44 Whether they will ask the Spongiform Encephalopathy Advisory Committee if, in the light of current research and the actions taken to protect human health with reference to human blood, they still consider it appropriate to allow blood, gelatin and tallow to be fed to calves. (HL1930)

Answer: The Minister of State, Ministry of Agriculture, Fisheries and Food (Baroness Hayman):

SEAC last looked at the safety of gelatin and tallow in October 1997. The Committee concluded that no further measures were necessary. Following their recommendations on precautionary measures in relation to human blood in October 1997, they reviewed the use of bovine blood in animal feed in March 1998 and saw no need to go beyond existing controls.

In February 2000 SEAC considered preliminary evidence suggesting infectivity could be demonstrated in the blood plasma of mice experimentally infected with a mouse adapted BSE agent. The Committee noted that the pathogenesis of the disease caused by BSE in mice was different to the pathogenesis of BSE in cattle but more similar to that of TSEs in sheep and humans. Given the difference in the pathogenesis of the disease in cattle and this mouse model, and taking account of the results of bioassays of cattle tissues in both mice and cattle, the Committee concluded that there were no implications for the safety of the food chain from these findings. SEAC will continue to review these areas in the light of new scientific evidence.

Question 45: Why the recent meeting of Transmissible Spongiform Encephalopathy researchers in Keele was held in private; who was invited to it; what confidentiality agreements they were required to sign; and whether the minutes of that meeting will now be published. (HL2032)

Answer: The Minister of State, Ministry of Agriculture, Fisheries and Food (Baroness Hayman):

A Joint Funders Workshop on TSE Research in the UK was held in Keele (4-6 April 2000). This comprised a meeting of funded scientists working in the field of TSEs, Department/Research Council Officials and five members of SEAC (Spongiform Encephalopathy Advisory Committee). Meetings of this type have been held annually by the BBSRC (Biotechnology and Biological Sciences Research Council) for a number of years. The first joint meeting with the participation of other funders was held in 1998.

The purpose of these meetings is to inform the funding bodies of the progress being made in the work they are supporting, to share results and encourage collaboration and networking between the scientists. The researchers present were funded by one or more of the following funding bodies: BBSRC, Department of Health, Medical Research Council and MAFF. Two international guest speakers were also invited.

This was a closed meeting as interim results were presented, and most of the research work discussed was pre-publication. For this reason, a confidentiality agreement was signed by conference delegates. Written reports covering all sessions of the workshop will be circulated to the Funders, however the proceedings will not be published.

A workshop of this kind has been held annually for a number of years. There was nothing unusual or secretive about this one. The purpose is to inform the UK public sector funders of TSE research of the progress of the research they are currently funding. Specifically it keeps the Funders up to date with the aims and progress of the work; allows the Funders to meet researchers in the field, and gives an overview of the UK funded research effort so that any areas of common interest or missing areas can be identified. It also encourages networking and interaction between researchers, which strengthens the science.

The purpose of the confidentiality agreement was to satisfy the researchers that they could openly talk about any interim results or future directions of research. Many of the results presented were just emerging and in several cases the researchers discussed ideas for future research. It would not be appropriate to publish these results before they have been properly analysed and interpreted. To do so would open the researchers up to potential criticism for the quality of their work. Interim results may also be misleading, pointing to conclusions that cannot later be sustained.

The researchers are encouraged to publish their results once they will stand up to peer review which will place the results in the public domain. This workshop was organised by the BBSRC. TSE research is also funded by MAFF, DH and MRC. To present a complete picture of the TSE research effort, projects from all four Funders are now included.

Almost 300 people attended the workshop including the grant holders and their assistants and students, some members of SEAC and representatives of the Funders. There were formal presentations of the research projects and two poster sessions. There were 125 posters; 26 of these were selected and the researchers invited to give short oral presentations.

Essentially this is an exercise in research management. After the meeting, the funders discussed the format and the quality of the science and results. Some future directions for research were identified. The answer to the PQ was cleared with all of the Funders.

Question 46: What were the Veterinary Laboratories Agency's and the Wellcome Trust Centre for Epidemiology of Infectious Disease's forecasts for United Kingdom BSE cases in 2000 and 2001 (a) in 1997; (b) in 1998; (c) in 1999; and (d) at the latest date available; and to what factors any changes are ascribed. (HL2062)

Answer: The Minister of State, Ministry of Agriculture, Fisheries and Food (Baroness Hayman):

The Veterinary Laboratories Agency (VLA) provide estimates of future BSE cases in Great Britain for the current year and the following two years. These forecasts do not include Northern Ireland.

At any point in time there is insufficient data on current cases, such as results of all brain examinations, to extrapolate accurate estimates beyond that point. They did not therefore produce forecasts for 2000 or 2001 during 1997. Forecasts for 2000 and 2001 which have been produced by the VLA model are shown in the following table. Predictions of the number of confirmed BSE cases expected in 2000 and 2001 (VLA)

                                Year 2000                Year 2001
Date of prediction                 Lower Central Upper      Lower Central Upper
September 1998                      451    618   784
January 1999                        548    729   911
April 1999                          743    951  1159
June 1999                           763    973  1183          260  393   526
October 1999                        883   1107  1331          323  468   613
January 2000                        889   1114  1339          325  470   615
April 2000                          887   1112  1337          325  470   615
The Wellcome Trust Centre for Epidemiology of Infectious Disease (WTCEID) published forecasts of future BSE cases in 1997. If 10% maternal transmission for the last six months of the incubation period is assumed, the number of BSE cases in 2000 and 2001 were estimated to be between 198-280 and 76-105 respectively.

In 1999, the group presented revised estimates to the Spongiform Encephalopathy Advisory Committee (SEAC). In 2000, it was estimated that there will be 1527-2202 BSE cases and in 2001, between 733-1283 cases. With the acquisition of additional data since 1996 and 1997, the confidence intervals surrounding the central estimates for cases in 2000 and 2001 have narrowed considerably.

Predictions of future BSE cases are based upon existing case data, knowledge of mechanisms of transmission and assumptions about the rate of decline of exposure. The models used by VLA and WTCEID outlined above are different. Each model will generate variations in the predictions depending on the set of criteria used and the process is continually refined to take account of the progress of the epidemic and improved understanding of the disease. The epidemic still continues to decline in line with the current, and therefore most accurate, predictions.

Question 47: Whether they are aware of any experimental results that show that, when cattle infected with BSE are used in the preparation of substances used in making human vaccines and injectible medicines, no infectious material reaches the final product; and, if not, whether they propose to sponsor any such research. (HL2368)

Answer: The Parliamentary Under-Secretary of State, Department of Health (Lord Hunt of Kings Heath):

Research into the pathogenicity and epidemiology of Bovine Spongiform Encephalopathy has been extensive. Last year this Government spent over £26 million on research on Transmissible Spongiform Encephalopathies. There has been no specific research to detect these agents in medicines. However when bovine materials are used in the manufacture of some human vaccines and some injectable medicines, manufacturers are required to comply with the European Note for Guidance on Minimising the Risk of Transmitting Animal Spongiform Encephalopathy Agents via Medicinal Products. This requires:

i.  careful sourcing of the bovine materials such as from countries where
       there have no reported cases of BSE,
ii. nature of the animal tissue used in the manufacture and
iii.production process and its control.
For injectable products that do not include bovine material as an ingredient in the finished product, purification processes designed to remove the material are used. The manufacturers of such products are required to provide validation of those processes to the Medicines Control Agency. For products that include bovine material in the finished product, compliance with the guidance minimises any risk of the presence of BSE infected material at any stage of the manufacturing process.

Question 48: Further to the Written Answer by Lord Hunt of Kings Heath on 2 May (WA 162), whether they would ask the permission of the individual concerned to release the information in question, since that individual has stated publicly that she would be happy for the information to be released.[HL2314]

Answer: Lord Hunt of Kings Heath:

It remains inappropriate for the Government to publish details about individual cases.

Retrospective study of prion protein accumulation in tonsil and appendix tissue

Lancet 2000; 355: 1693 - 1694  13 May 2000
ames W Ironside, David A Hilton, Azra Ghani, Nicola J Johnston, Lisa Conyers, Linda M McCardl
Comment (webmaster): The reason why 26% of the tonsils were discarded turns out not to be the quality of preserved tissue per se but that they lacked sufficient numbers of lymphocytes or follicular dendritic cells ['cases with fewer than five lymphoid follicles were excluded'].

This turned out to be mainly an appendix study (only 95 tonsils were studied out of 4166 samples, for 2.2%). This allocation of emphasis is thrown into doubt by the statement that a second appendix examined in a nvCJD case, taken out 9 years prior to disease onset, was found negative (3rd paragraph from end). This unpublished factoid probably accounts for the lack of enthusiasm seen in announcing null results.

On the other hand, further positive lymphoid tissues are said been found at necropsy in nvCJD though no details are given in this Lancet article. Also, the age range of tissues reflected the age range of victims rather than being drawn from childhood surgeries.

"...Prion-protein accumulation has been detected by western blot and immunocytochemistry in several lymphoid tissues (including the tonsil and appendix) sampled at necropsy (JWI, unpublished), and during life in tonsil biopsy specimens from individuals with clinically evident nvCJD.1 Lymphoid tissue involvement has been shown in scrapie in sheep and in several experimental scrapie models, usually from an early stage in the disease incubation period. In view of the likely lengthy incubation period for nvCJD in human beings, estimation of future numbers of cases is difficult, with wide ranges published.

We investigated the presence of prion protein in surgically resected appendix and tonsil specimens as an indicator of numbers of individuals in the UK population who could be at high risk of developing nvCJD. Since all cases of confirmed nvCJD to date have been between the ages of 15 and 54 years, we only examined tissue samples from individuals aged between 10 and 50 years at operation.

Furthermore, only samples taken from 1995 onwards were examined because these will have had a longer time from possible BSE exposure than earlier samples, with therefore a greater likelihood of prion protein being detectable. Examination of the first batches of samples from individuals aged 10-30 years is now complete.

Paraffin-embedded tissue blocks from 4166 appendix and tonsil specimens were retrieved from archives of pathology departments in the Lothian and southwest regions of the UK (table)... Prion protein was detected by the well characterised and widely used mono-clonal antibodies 3F4 and KG9 and visualised with the catalysed signal amplification system , which gives superior results, in terms of sensitivity, to most other immunohistochemical visualisation systems.

Haematoxylin and eosin-stained sections were assessed to ensure that at least five lymphoid follicles were present; sections were recorded as positive if prion-protein staining was detected in follicular dendritic cells or tingible body macro-phages in lymphoid follicles.

Cases with fewer than five lymphoid follicles were excluded because in a previously reported case, and in those examined at necropsy, prion protein could only be shown in 25% of follicles. The average number of follicles in those samples included in the study was 20 per case, giving a 96% chance of a positive sample being declared.

Necropsy tonsil tissues from confirmed cases of nvCJD were used as a positive control for each group of slides stained by immuno-histochemistry for prion protein. Negative controls were done by omitting the primary antiserum. 30 cases from each batch of 1000 were exchanged between study centres for quality control and validation of results. No tonsil or appendix sample was found to be positive for prion protein ...

Prion protein has been previously detected by immunohistochemistry in the tonsils of all sheep who subsequently went on to develop scrapie by 8 months in those homozygous for a susceptibility prion-protein polymorphism, and by 15 months in heterozygotes at that locus, but was not detected in those who remained free of symptoms.

However, few data are available on nvCJD; in one patient prion protein was detected in an appendix removed in 1995, 8 months before onset of symptoms, and in another case prion protein was not detected in an appendicectomy specimen removed in 1990, 9 years before onset of symptoms (unpublished).

The mean incubation period for nvCJD is unknown, although peak exposure of the UK population to the BSE agent is likely to have been between 1988 and 1992. By use of a mathematical model to generate epidemic scenarios that are consistent with age-stratified disease incidence to the end of 1998, if we assume that tests are able to detect infection in the last 75% of the nvCJD incubation period (with 100% sensitivity and specificity), then the upper bound on epidemic size is reduced from several million cases to about 150 000 cases. However, if tests are only able to detect infection in the last 50% of the incubation period, these results do not reduce the previously reported uncertainty in epidemic size.

Clearly, larger studies are required, some of which are already underway. Studies with unfixed tissue samples are also planned, allowing western blotting for prion protein to be undertaken (which might be more sensitive than immunohistochemistry), with verification of positive samples by transmission studies. Further data might also become available from animal studies and from future cases of nvCJD in the next few years, which detail how long after exposure prion protein can be detected in lymphoid tissues with these techniques, and will aid interpretation of negative findings."

Human BSE Foundation update

Thu, 11 May 2000 Sion Jones 
Updated contact information for the Human BSE Foundation (which is focused on helping British families affected by nvCJD) is as follows:  

Helpline: 0191 3894157  

Human BSE Foundation 
99 Warkworth Drive 
Deneside View Chester-le-street 
Co.Durham DH2 3TW UK   
Contact: Francis Hall     
The group is currently in the process of updating its web site. For the time being please use Sion Jones. [Sion lost a partner in 1998 to nvCJD and is currently on the committee of the HBSEF. -- webmaster]

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