I wish to send this old interview from bbc radio 4 back in 1999 i believe. but most importantly is some of the late Dr. Joe Gibbs and sporadic CJD, and pathology and links of illness, young people with CJD, all right here in the USA. there is much misspelling, which i left the way it was, i am not too good at spelling either :-)
1999
BSE-The Untold Story
Richard Uridge investigates reports that a new version of the brain disease CJD is taking hold in young people across the Atlantic, and asks whether American Scientists are right to question Britain's strategy for dealing with Mad Cow Disease, and it's equivalent in humans.
Richard Uridge : Mad Cow Disease.Three simple words with an almost humorous ring, but there's nothing remotely funny about Bovine Spungiform Encephelopathy, so far it's claimed 40 lives in Britain,and no one's sure how many more people will die.
[Compare the 40 dead people to the thousands who die of lung cancer from smoking,or the number involved in drink driving accidents or from alcohol damage to the brain or liver and, purely in terms of numbers and risk,one wonders why. Perhaps because it was perceived that it would permeate the human food chain? BSE is such a scare story -LB]
"I think we were in real difficulty with these diseases, they're biologically obscure, they have very long incubation periods and we simply didn't have some of the information that people would have liked us to have and we still don't."
Richard Uridge : BSE has cost British tax payers a staggering 4 billion pounds.More than 3 million cattle have been slaughtered, and British farming ears to recover. Yet there's the possibility that our whole response to the disease is will take many ybased on an incorrect hypothesis. This programme investigates the challenges to the pillars of conventional wisdom on BSE, and its human equivalent new variant Creuzfeld-Jacob disease.
"If we're wrong, and the route of transmission is not through eating beef, then we have decimated an industry, and we have frightened millions of people totally unnecessarily"
Richard Uridge : In fact, there's a serious body of scientific opinion that believes BSE got into people through the blood stream, not the stomach. Right or wrong, last week the British government started importing one blood product, plasma from the US, where officially there is no BSE, and no new variant of CJD. But American experts have told us that Britain could be making a big mistake because there's mounting concern that a new strain of CJD is taking hold on the other side of the Atlantic. "We have our own BSE problem here.You know we're facing what the UK faced a few years ago."
"Is it a time bomb, is it just something that a few people seem susceptible to, it makes for a very bad science-fiction movie."
Richard Uridge : So our story begins in America. Older people have been sporadically and apparently spontaneously contracting CJD for may years, but now younger Americans are being affected, and bearing in mind that it was young people getting CJD here that alerted Britain to a possible link with mad cows, the trend is worrying an increasing number of people across the Atlantic. Andrew Kimbrel is a lawyer in Washington DC, and Director of the Centre for Food Safety. His particular concern is that the picture is confused, because no one is monitoring the disease properly, as the case of Douglas McKewan suggests.
Andrew Kimbrel : He was one of 7 cases in a cluster in Utah, in the past year. Now when I spoke to Tracy McKewan, his wonderful wife, the story that she told, what it took for her to get this disease diagnosed was extra ordinary, and they put them through every test you can imagine. He was a man in his 30s, young kids, good job, just a regular guy. Comes home feeling sick, feeling disorientated, not sure what's going on with him. They decide that he's mentally ill. Well she doesn't believe it. She thinks something's terribly wrong. So she happens to see a guy on TV talking about one of the other CJD cases in their area, and she says "That's what my husband has, that's what he has". So she calls her doctor,a nd he says, you know, "Darling if I had to listen to everybody who sees things on TV, and says "That's what I have" or "My husband has"...".She says "No,that's what he has", and she then has to go to another hospital, they won't do it, she then has to go to Washington here, where she finally gets some NIH people to do the proper tests, and of course she has the variant CJD, and he died. For all we know there could be 50 or 100, but 7 who had enough courage, enough, to get the special test, to go the next step, to figure out what's going on. This is a very fast .....people are dying in months, they waste away in months.
[It sounds like Roy Neary in Close Encounters -LB]
Richard Uridge : Jay Whitlock is wasting away from CJD in Oklahoma.doctors say it's a sporadic case. His wife Julie is not so sure. One - because he's just 27 years old. Two - because the symptoms she describes are almost identical to those who've suffered from new variant CJD in this country. It's a critical distinction, and one which she outlined for us in this, her first ever media interview.
Julie Whitlock : Right now, he's in a field nursing facility. He's uncomprehensive [I think she means incomprehensible -LB], having some hallucinations, incontinent. He still does, know me, he will hug me and hold me, use names. He started having memory trouble in January of this year 1999. He was forgetting phone numbers, and then when we would be heading somewhere to go eat, he'd go past the restaurant,a nd I'd say "What are you doing?" and he'd say "Well where are we going?", and I'd tell him again, and we'd be heading home and he'd take different routes to get home, and I'd say "What are you doing?" and he'd say, "If you want to drive, you get over here and drive". So you know, the next time he'd take different directions somewhere, I would think "Okay, he's testing me", you know? I'd think it was just a man thing, he was... you know, just doing that on purpose,and then... that was through January, and it was February 1st, his employer talked to me, and said, "You know, he's forgetting... are you having trouble?", Jay said, "Well he's forgetting some stuff", he said "Well he's doing it at work too", and I didn't have any idea about that. So that's when I got him to the doctor the next day. Most times, I feel like we're living a nightmare, and, you know, the children, Zachary, he's... the youngest is 3, and he knows daddy's sick, he doesn't understand any more. But the oldest, he knows there's no medicine to make daddy better, and he will pray to God to find the medicine [A lot of good that will do -LB] to make his daddy better. You know, so the kids are.. you know it's just continuous stress, worry and heartache.
Richard Uridge : Sadly there is no cure for CJD, and proof of whether Mr Whitlock does indeed have the new variant will have to wait until after his death. Only then can tests be conclusive. But if the tests are positive, how might he and the other American victims have contracted the disease? One theory is that it comes from eating deer or elk meat infected with a Spungiform Encephelopathy, similar to Mad Cow Disease, but it is only a theory. Even in Britain there is still no absolute proof, that eating mad cows gave humans CJD, and that's something that bothers June Goodfield, a zoologist, and campaigner for the public understanding of science.
June Goodfield : It isn't enough just to say, "In the absence of any other viable hypothesis, this is the best one". It isn't enough, because we have a number of things, including the fact that we have not reproduced it experimentally in non-hum, an primates, weighing against it. It is vitally important we find out why. It's important because, if we're wrong, and the route of transmission is not through eating beef, then we have decimated an industry, and we have frightened millions of people totally unnecessarily, and I believe we could nail it down.
Richard Uridge : She says that there are experiments that could establish this one way or another, and she argues that if eating meat was the cause, we should have seen many more cases by now.
June Goodfield : If you think of the tons of BSE infected hamburgers that have been fed, probably, to British children, if eating BSE infected meat was the cause of new variant CJD in human beings, we would would be expecting to see evidence of this in that age group and we are not seeing it. [Not if it has very long incubation periods-LB] That is a very significant epidemiological fact.
Richard Uridge : The mainstream consensus among British experts that is despite the lack of absolute proof, the government had to act on what remains a very probable explanation. Alan Dickinson, carried out much of the ground breaking work on Scrapie, the sheep brain disease, which many people believe was the cause of BSE in cows. He thinks eating infected material from mad cows is almost certainly the way humans got new variant CJD. His careful not to blame per se, he says the more likely culprit is infected brains, spinal chord or offal, which then got into pies, sausages and burgers.
[If this is true why aren't dogs and cats suffering from CJD or BSE as, those products are more likely to end up in dog and cat food? -LB]
Alan Dickinson : The fact that 20-30 people have got BSE, I think is indisputable.The fact that they have got it from something that you would be likely to buy in a supermarket or a butchers shop, I think is a very,very high, probability. Alternative probabilities, I see no reasonable ones for accepting. If you have a hit-and-run accident, and the car is never found, you are in a reasonable position to conclude that it was a car that did it, for a variety of reasons. I think we're in this same position, of saying, a bovine product of some sort..... a bovine food product of some sort, has been the origin of these cases in humans.
Richard Uridge : Our search for clues now takes us back to the late 1950s, when the American Nobel Prize winner Carlton Gadusek, was working with the Foray people in Papua New Guinea. He was intrigued by a brain disease called "kuru". Why, he wanted to know, did only the women and children of the tribe suffer from it. June Goodfield is one of Dr Gadusek's contemporaries.
June Goodfield : The men of the Foray were the ones who were responsible for going hunting, and they went off, and they would sort of kill a few wild pig or what have you. But they kept the spoils of the hunting for themselves. On the whole, the women of the Foray ate vegetables, roots and tubers and what have you, the occasional rodent. But often had very little meat, and they would from time to time, as they prepared the bodies for burial, put slivers of the meat from the flesh, and eat them and give them to the children, or they would put the brain tissue into a little bamboo and steam it and eat it. But anybody who says that Carlton Gadusek believes that cannibalism was the route, is misrepresenting what Carlton Gadusek thinks, and I know because I've asked him, and I've quoted it in my book, and I know because I've asked Joe Gibbs, and I've quoted it in my book.
[There was a TV programme that claimed that a tribe, maybe the same one, had the women and children eat the brains of the dead males, maybe this was the misrepresentation -LB]
Richard Uridge : Gibbs worked with Dr Gadusek, so we spoke to him in his office in Maryland, and asked him about his experiments with chimpanzees to test the theory that eating brains spread kuru in the Foray tribe.
Joe Gibbs : The first experiments we did were to put stomach tubes into the animals, as you would for a gastric analysis, and through those tubes, we introduced copious amounts of highly infectious, known to be transmissible kuru, CJD, and nothing has ever happened to those animals.
June Goodfield : Faced with the fact that experimentally they could not reproduce this route of transmission, that is eating, in the laboratory, they were faced with the fact, "How on Earth did the young children and the women of the Foray get the infected agent?". The only way that Gadusek and Gibbs could experimentally reproduce this,was by inoculation in some form.
Joe Gibbs : Somewhat later, in the course of our studies, I designed an experiment, in which I took squirrel monkeys and starved them for two or three days, then allowed them to handle the infected tissues, from other primates that had developed the diseases, kuru, CJD and Scrapie and in doing so, they consumed the infected tissues. I think in most cases it was upwards of around 80 grams of tissue and all of these squirrel monkeys, both, for kuru, CJD and Scrapie, all developed disease.They have positive pathology and we extracted the prion protein from their brain. So it was, yes we transmitted orally, but letting the animals handle the tissue and consume the tissue, rather than putting it directly into the stomach of chimpanzees and other small monkeys.
June Goodfield : And they finally came to the conclusion that if you looked at the kids and the women, you know they're not living in antiseptic, sterile conditions, they're living in close contact with the Earth, where they have cuts and sores on their hands, where if they are scrabbling with their hands in the bodies or the brain tissue, their inoculating themselves through open wounds or they've been handling a bit of material and they rub their eyes, and it's coming in through the mucus membrane, or they're picking their noses and and it's going in through the mucus membrane there. They believe it was self inoculation. it's inoculation through some way getting into the blood stream.
Joe Gibbs : And they had multiple, multiple, multiple, routes of inoculation. Lesions on their skin, in their eyes, in their mouths, and other lesions caused by puni grass cuts and by leeches on their bodies and so forth, mosquito bites. All these provided a ample means of infectivity.
Richard Uridge : Put simply, these experiments suggest that primates are infected while eating, but not by eating. In other words by inoculation rather than by ingestion. But "so what if it does?", says Dr Ros Ridley, of the School of Vetinary Medicine in Cambridge.
Ros Ridley : Whether the infectious material got in through cuts in the skin, cuts in the mouth, perhaps with bad teeth or whatever, or whether it was because they swallowed it, is, in a sense, immaterial. They contaminated each other with the brains of their dead relatives by handling that material. Now if we look across now to the new variant CJD and we look at those people who have become infected, they are absolutely, perfectly normal people leading perfectly normal lives in Britain.They have not inoculated themselves with some strange material. They don't have strange professions. They don't work in abattoirs, or they don't dissect animals up, or anything of that sort. They're just ordinary people. What they have done,o f course,i s to eat beef in many forms, not just the recognisable meat form, but prepared foods of various types, everything from sausages onwards, potentially contains beef from various parts of the carcass, and so in their case, the likelihood that it is eating, rather than some other means of introducing bovine material into the body, seems overwhelming, because they are such ordinary people.
Richard Uridge : In the course of making this programme, we discovered that despite the proclaimed ordinariness of its victims, an abattoir worker, Jason Keat, has died of new variant CJD, and if transmission is through blood, as we have already heard that some scientists believe, could vaccines or or other medicines containing things like calf serum, have played a part? The year long BSE enquiry which was due to have reported its findings next month, has looked into that possibility, and sections of the food industry have perhaps naturally, been keen to cast doubt on the infected meat theory. So could it have been vaccines? Professor Robert Will heads Britain's CJD Surveillance unit based in Edinburgh.
Robert Will : I personally believe that's highly unlikely, because if there was any infectivity in calf serum, it will have been at a very,very low level.
[People are worried about the very very low level of microwaves in cell phones which may be producing brain tumours. Level is not the question. In principle is the question. As Chaos theory shows, small things can have big effects. So how low the level is may not be relevant. Although longer time exposure and power level may be relevant in cell phones, so maybe level is important - LB]
Whereas I think that we know there probably was a high level of exposure orally to BSE infection through the food chain.T he other issue is that when vaccines are given, they are only given in a very tiny dosage, once, and so the level of exposure, as far as I'm concerned is likely to be minute, compared to other types of exposure that almost certainly did take place. There is further concern, however, about the issue of blood and perhaps surgical instruments. As far as I'm concerned from the evidence we have on classical CJD, I don't think there is any good evidence that this form of CJD has been transmitted through blood or blood products. We can't be absolutely certain about that, which is why more work is being done, epidemiologically, and also to do with transmission studies. However, new variant CJD might be different, and the reason for that is that I believe it's due to a different infectious agent, and we have evidence from Dr Ironside's work that the tissue distribution of infectivity in the body foe example, in the lymph nodes and spleen, is likely to be much higher in new variant CJD than it is in the ordinary form of CJD, and that does raise legitimate concerns about the possibility of blood or blood products resulting in on ward transmission of new variant CJD from an individual who is incubating it to someone who receives the product, and for that reason, although there are enormous uncertainties about the type of risk
[Ref:Video:BB14:RI 3; N30:The Numbers Game;OB4 Equinox {Living Dangerously}; Protext Files; Green File Mindfld.wri;Red File: Reith992.wri],
that's involved, or the level of risk, a number of actions have been taken, for example in the UK plasma products, that are derived from blood, will be sourced from plasma... derived from outside the UK, from the middle of this year, and there's also plans to remove the white cells from all blood donations throughout the UK. So, I think, although this is a theoretical risk of onward transmission, it's something that has been taken very seriously, and action has been taken.
Room for a Moo?
Rural crisis: Broadbottom farmer David Gould says life is near to impossible for dairy farmers in the wake of the BSE problems. Economics dictate he can't keep calfs like this one.
A FARMER hit hard by the rural crisis is giving away his cows to anyone who can offer them a good home. Broadbottom farmer David Gould says plummeting market prices are making life near impossible for dairy farmers. Prices have dropped so low that some farmers routinely shoot calves dead just after birth in an attempt to stem spiralling losses. Farmer Gould refuses to do this but says such a 'hand to mouth existence' cannot go on without the help of some Good Samaritans. So he's now calling on anyone with enough spare land to give him a helping hand and adopt 'a farm-yard friend'. Economics "The economics of the situation leads to some farmers shooting them - but I can't do that," he said. "If there are any readers out there who can take one or more off my hands and give them a good home I would be willing to do it. "You don't necessarily have to be a farmer to look after a cow but someone with a smallholding with a couple of acres of land." The Little Hill Farm owner says the number of farms with cows has dropped to a paltry 10 locally. But such a situation - which sees a farmer collect less than nine pence per pint of milk - has arisen due to the strength of the pound and the BSE crisis. "The powers that be say the prices are to do with the strength of the pound," he said. "But as far as I know we don't export milk, or if we do it must be very little." Betrayed He added: "The BSE crisis has been the main factor though and we do feel betrayed by the way the government handled the whole issue. "It's the government's fault in the first place for relaxing the sterilisation process. "Through all the years we were punished but the farmers themselves never let their standards slip." If you have the resources to 'home a cow', contact The Advertiser on 0161 339 7611 and we will pass on your details. Mark Travis [It's nice to know that some of our "countryside guardians" look after their animals so well that they don't shoot them in cold blood because they don't turn a profit. Well done farmer Gould for putting life before money -LB]
A FARMER who will give away bull calves to a caring home has had several offers to" help - including sponsorship from the Hindu community. The Advertiser reported how Broadbottom farmer David Gould is offering to take a novel approach to falling market prices. Farmers countrywide face prices which have dropped so low that some consider shooting calves dead just after birth in attempt to stem spiralling losses Farmer Gould won't do that and instead is proposing to hand over any bull calf to someone who can offer a suitable home. We have already had a number of offers for help from a few unlikely sources. A proposed urban farm and a land owner have said they wish to help by taking them off David's hands. David is especially grateful to those offering help because another imminent calving spell is set to signal new additions in Broadbottom. "We have none left now but we will start calving next week and if it's practical for them we hope to do something soon in the coming weeks," he said. "We will have to think through what is best for the cows but we are definitely keen for others to come forward if they wish." Sponsor Ashton man Vishnu Mohandas proposed sponsoring the calves, a scheme which he and his friends have already done at a Sanctuary in Watford. "I read this in the paper and was very pleased with how Mr Gould is handling the situation Mr Mohandas said . "I have sent money to India for a similar scheme while I, and many others nearby, have contributed money to a sponsorship scheme in Watford. Anyone interested in adopting a bull calf must have plenty of land. [The Advertiser 27/9/2000]
MP speaks out
MP Andrew Bennett has slammed farmers involved in recent petrol protests - saying "they've got a cheek". Mr Bennett described last week's crisis as very sad, adding that farmers got their fuel virtually for free. The MP went on to reveal his thoughts about the haulage industry and how, in order for the majority of lorry drivers to he satisfied, there would have to he cuts. "We've got a third more lorry drivers than we need - there should be some restructuring,"he said. "I appreciate many are self-employed and buy vehicles by mortgaging their houses, but they shouldn't take it out on the general public,it doesn't help." Mr Bennett says motorists should consider smaller cars and recommended working and shopping locally.
[Whilst I agree with Andrew,and the Farmers and hauliers have no right to break the rule of law "for the benefit of the country" we've probably got a third too many politicians too,and they're probably paid a third too much -LB]
Richard Uridge : The process of leuko - depletion - filtering out white cells, in which the infective agent is thought to be more concentrated, won't start until November. But the Department of Health told us that the decision to source plasma from countries without BSE came into effect just last week. Then they told us that the imports are coming from the US, where as we've been hearing, there are growing concerns that CJD is spreading to much younger people than normal, 27 in at least one case. but Professor Will says there's no evidence of a new variant of CJD that can't be traced to Britain, and anyway these are only precautions against a theoretical risk. Alan Dickinson agrees, although he did find the infective agent of the sheep brain disease Scrapie, in blood during his research.
Alan Dickinson : You're not dealing with solid tissues, you're dealing with serum and blood which can have small amounts of infectivity. I think I was the first person to show that. I regarded finding it on a small proportion of occasions , in heart, blood, as really an index that my crude method of extracting blood from a heart, was sufficient to incorporate quite a lot of heart tissue and blood cell lining tissue. I'm sure I was doing it far more crudely, and one would hope that more is known now about this..... you can hear me perhaps doubting this, more is recognised and appreciated about the ease of cross contamination of these kinds of products when people think they are dealing in clean room situations with safety cabinets. These words are dangerous in their own right.
Richard Uridge : There are other doubts about the official British position on CJD, and again they arise from the investigations into kuru, in the Foray tribe of Papua New Guinea, and later work by Joe Gibbs. Essentially the question boils down to how new is new variant CJD? Twenty years ago a neurosurgeon died in Boston, apparently of sporadic CJD, but as Joe Gibbs explains, later examination of his brain, revealed the classic symptoms of the new variant.
Joe Gibbs : I maintain that the so-called florid or daisy plaques that they refer to in new variant, occurs outside of the UK in cases, and I've shown them in kuru, chronic wasting disease of deer and elk are massive plaques with vaccules around them, and then the paediatric neurosurgeon in Boston who died. he was first diagnosed has having a very rare skin disease called Almeyer Dago's Disease, and that disease he did have, but then he started to develop neurological signs, and ultimately died and we received the autopsy tissues on him. We demonstrated that he had the prion protein in brain and in lung tissue and it turned out to be the very clear sporadic type of CJD. Now my argument here is that, I'm not sure what are the restrictive clinical and pathological characteristics of so-called new variant, because I can show a number of these things in sporadic cases. I can show people that have gone for psychiatric evaluation, then they developed ataxia and had an extended period of clinical progressive disease over a period of 18 months - 2 years, but they turned out not to have new variant,according to the UK description.
Richard Uridge : British CJD experts have also examined the Boston neurosurgeon's brain tissue. Professor Robert Will believes Joe Gibb's theory's based on a misunderstanding.
Robert Will : Well I think there's a whole wealth of evidence now, that suggest that new variant CJD is a new disease. For example, when the original paper was published in April 1996, one of the things we put in that paper, was the importance of reviewing other neuropathological information from the past, in other countries, to see whether this disease had been seen before elsewhere, and since then we have not been informed or been able to identify, any other case which fulfils the neuropathological appearances of new variant CJD. Now I think there's a slight misunderstanding here, because although florid plaques are a very important component of the diagnosis, neuropathologically, the fact that there is a single or one or two, florid plaques,i s not the issue. The issue is that these plaques are widely distributed throughout the brain. So it is true that occasionally, a type of florid plaque has been seen other cases, you know single or one or two florid plaques, for example, in the case you mentioned, of the neurosurgeon, and also in another case, with dura mater related CJD, but these cases have been reviewed by Dr Ironside and by other neuropathologists, and the view I think, is clearly that the occasional florid plaque does happen sometimes, but the overall neuropathological appearances do not look at all like new variant CJD, and the general consensus among the neuropathological community is, according to my understanding, that new variant CJD is indeed a new disease.
Richard Uridge : Another of the commonly held beliefs about BSE concerns the role played by the animal feed industry. However unsavoury it sounds, renderers turned animals carcasses into animal feed. Sheep were fed to cows, and cows were fed to cows.
[Then if the farming community was decimated they have only their greedy exploitative selves to blame -LB]
Everything went into the pot and was cooked to produce meat and bone meal, then the temperature of the whole process was reduced, ostensibly to save on fuel, and the assumption is it was no longer hot enough to kill off the infective agent. More recent experiments have shown that's probably not true, because even the higher temperature doesn't work. Only one condition does. It's called "pressure cooking", and is now widely used in mainland Europe. Paul Foxcroft is Sales Director of the rendering company Prospa de Molder. He doesn't dispute that BSE was spread by infected feed, but now thinks a combination of things caused BSE to explode in Britain and only in Britain.
Paul Foxcroft : You've got more, unknown to anybody, more active Scrapie agent in the meat and bone meal, year upon year, as more and more sheep are slaughtered. Perhaps a sudden boost of active Scrapie agents within the meat and bone meal again as if there was an increase in the incidence of Scrapie within the sheep flock. You have more meat and bone meal, more then of that meat and bone meal going into the dairy feed, you then have more of that dairy feed being put into the cow. Now I don't believe that combination of circumstances has existed anywhere else in the world, at that same time. We could be perhaps a little mischievous and raise the possibility of organophosphates as maybe a predisposing factor. There certainly could will be genetic factors in terms of genetic susceptibility, as the gene pool is narrowed if you like, with artificial insemination over the last several decades, where we've perhaps used bulls with a susceptibility, or lack of resistance, whichever way you want to term it, into the herd... national herd. Therefore, it's almost a lottery, we've hit this horrendous jackpot, at least we got all the numbers. There are plenty of other countries out there that have perhaps only got 1, 2, or 3, or 4 of the numbers and for that they get nothing.
Richard Uridge : So why are the numbers coming up in America now? What special combination of circumstances exists across the Atlantic? Michael Hanson of the US Consumers Association believes his governments rules about what goes into animal feed are far too lax, and that they just aren't looking hard enough into the problem of CJD.
Michael Hanson : There is the problem of "if you don't look, you don't find". They tend to be concentrating on supposedly looking for a British style BSE case, they're not focusing on intensively sampling animals that might be at risk. So the brain chemistry, the neuropathology that they're looking at, they're looking for the very obvious signs, like you see in BSE cattle in Britain. They're not looking for more subtle signs, and even though there is a quotes "surveillance system", we think it's highly flawed, and while there's no direct evidence, I think there's indirect evidence that there might be a TSE existing in food animals, in the US.
Richard Uridge : Andrew Kimbrel, the lawyer from the Centre for Food Safety, who told us that America was having its own BSE crisis has a shopping list for his government.
Andrew Kimbrel : We just filed a formal legal petition saying "make CJD a reportable disease" which it is not in this country,e ven though we've seen explosions of cases, for goodness sake "stop feeding ruminants to ruminants". We're asking exactly for the UK regulations on feeding animals to animals, which we don't have in this country. "Blood Supply", and an investigation on why in the world our wildlife is coming down with TSEs, at such an alarming rate.
Richard Uridge : So what are we to make of the developments in America? And what can they tell Britain about its pillars of conventional wisdom on mad cows and CJD? I went to see the man who advises the British government on these issues, the chairman of the Spungiform Encephelopathy Advisory Committee or CEAC, Professor Sir John Patterson. I asked him first about the cases of CJD in younger people, and the claims that America now has a new variant of the disease.
John Patterson : It's very difficult to comment on that usefully. All my experience on the UK CEAC tells me that you really need to know all the details of any cases or any problems that are being posed before commenting on them. But if it's true that there are some cases of human Spungiform Encephelopathy in unusually young people, then I think now we have some clear definitions of the clinical state of those patients, we have some modern imaging techniques, for doing MRI scans, and most particularly we have some laboratory based biochemical tests that can be applied to material from these patients which should be able to define the situation much more clearly, and I think you need to get all those details first, before judging what the significance might be.
Richard Uridge : But it wouldn't surprise you, or perhaps it would, if there were 40 cases eventually, in America over the next 2-3 years?
John Patterson : Oh I think it would surprise me enormously if that were the case, and that's why one would want to know all the details of any such case, let alone 40, before commenting on it.
Richard Uridge : One of the conventions, with BSE is that it was caused by people ingesting the infected agent... infected meat, yet some experiments carried out by Carlton Gadusek in he 1950 showed that it might actually be through blood contact. Has his work been disregarded in building the current hypothesis?
John Patterson : No, not at all, I mean it's clearly recognised that there are a number of ways of transmitting Spungiform Encephelopathies.You refer of course, to the peripheral route of inoculation, blood to blood, and you would have to say that in that context, the most vulnerable people would be those that are occupationally exposed because they work in abattoirs, and to date, there have been no cases of variant CJD in abattoir workers which would link the occupation with the exposure.
Richard Uridge : What about the death of Jason Keat? He was an abattoir worker in his 20s, on his death certificate it says that he died from new variant CJD?
John Patterson : You, you... I mean I .... It may surprise you to know of course that I can't relate individual names to individual cases. It is true that there are one or two people that who've classical CJD who've worked in abattoirs, and if you tell me that Jason Keat was one of those with variant CJD who also worked in an abattoir, then I accept that, but then there 39 other cases, who didn't and it's very difficult to unify those 39 cases with a hypothesis about blood to blood transmission. Whatever his occupation he probably, like the other 39 cases, was a consumer of beef products, which would be the most likely hypothesis for the way in which BSE was contracted.
Richard Uridge : You don't think 1 in 40 or 1 in 41 is significant then?
John Patterson : Er no, I don't think it is, in the same way that one of the cases we know had been a vegetarian for many years, but if you trace back the history of that individual, to the point at which she became a very strict vegetarian, then it's most likely we think, that she was exposed to beef products before she became a strict vegetarian and the occurrence of one case we don't feel necessitates altering our proposal about the most likely route of transmission.
Richard Uridge : But it is just a hypothesis, at this stage. Is it possible that another hypothesis would explain transmission and that is that is that vaccines have somehow played a role?
John Patterson : I think that the CJD surveillance unit and Professor Will in quite a long and extensive questionnaire to the families of each of these cases, and looking all the time for occupational exposure, geographic clustering, medical histories, histories of operations which might unify all these 40 cases, then you cannot find such evidence.
Richard Uridge : And in the absence of any other evidence, the current hypothesis is the best one, in your view?
John Patterson : I think it is, yes.
Richard Uridge : If I can turn to the use of blood and blood products. Is there a concern that BSE or new variant CJD should I say, could be spread through blood products?
John Patterson : Yes, and this is going back a little while now, but of course CEAC made some recommendations to the government about that, particularly in relation to removing the white cells from blood transfusion, and the technique which is called leuko-depletion is being extended to become comprehensive in the UK blood transfusion service as soon as possible.
Richard Uridge : Because the white cells actually carry a greater proportion of the infective agent?
John Patterson : Again the evidence is very incomplete in this, but if you think about it intuitively, and you say "we must apply the precautionary principle", then it seems logical to remove the white cells, as the most likely component of blood which would transmit the infection.
Richard Uridge : Why is it that precautionary measures are being taken only now?
John Patterson : Well it takes quite a long time of course to set some of these processes in train....
Richard Uridge : That's 3 years potentially in which people could have been infected person to person.
John Patterson : There is a possibility that if variant CJD is transmissible by blood or blood products, and that some of the cases we know have been blood donors, that it might have been transfused from one individual to another, that's exactly the sort of eventuality that one is trying to prevent, from people who are currently incubating variant CJD, but haven't actually manifested it, yet. That's why those precautions are being taken.
Richard Uridge : Might it not have been more sensible to take that precautionary measure at the outset? It didn't seem that it was a problem taking precautionary measures as far as the beef industry was concerned quickly, so why not the medical industry?
John Patterson : I think that's exactly right, because of course the proposition was that the source of cases of variant CJD was oral exposure to beef products which contained some of the specified offals, most notably brain and spinal chord. So it was important really to shut that door as quickly as possible. There was then a need to look at the evidence about the transmission of classical CJD via blood transfusion,and there the evidence is conflicting, and by and large there, the conclusion has to be that classical sporadic CJD is only very rarely transmitted by blood transfusion, if at all. However, it then became clear that variant CJD was behaving differently, particularly in relation to the phase of the infection in humans, in the lymphoid tissues. You can find the agent of variant CJD in the spleen and in the tonsils and in the lymphoid tissue in the appendix,and so one had to recognise that it was possible that circulating lymphocytes also contained this agent. There was also a developing body of knowledge about animal experimentation using mice, which led one, taking all this into account, to recommend to the government that leuko-depletion would be a sensible precautionary measure. Now that all took time to develop, time to think about and then of course, once you've made the decision, time to implement. So that's where you get the apparent delay from.
Richard Uridge : Finally, are we now any nearer to breaking the deafening silence on the crucial question? How many more people will die from variant CJD in Britain? We've seen estimates prepared for the Royal Society, based on the number of cases so far. Depending on how you interpret them, the projections are either good news or chilling reading. They indicate there could be as few as a dozen or so more deaths,or as many as 13 million.
John Patterson : That was one of the major questions that was asked immediately on March 20th 1996, and the answer then was that there was a very broad range of possibilities. Three years later and fortunately the range of possibilities still remains very wide, and so, to be honest I think the only that we will tell, is to wait for another 2 or 3 or 5 years before we can answer... we can narrow down that range usefully for you.
http://www.fortunecity.com/emachines/e11/86/bse.html
http://www.radiolistings.co.uk/candc/uridge_richard.html
http://www.radiolistings.co.uk/programmes/bse___the_untold_story.html
Wednesday, May 19, 1999 Published at 06:45 GMT 07:45 UK
Sci/Tech
BSE fears over US blood imports
But a BBC programme says some experts fear a new kind of Creutzfeld-Jakob Disease (CJD), the human equivalent of BSE, is killing young Americans.
The programme, "BSE - The Untold Story", was broadcast on Radio 4.
CJD is normally a disease of elderly people, but the type linked to eating the meat of BSE cattle - new variant CJD - attacks young patients.
CJD is not a notifiable disease in the USA, so there are no accurate figures on the number of cases or the ages of patients.
A Washington lawyer, Andrew Kimbrell, told the programme: " We've seen explosions of cases.We're facing what the UK faced a few years ago".
"Is it a time bomb? Is it just something that a few people seem susceptible to?"
http://news.bbc.co.uk/2/hi/science/nature/347137.stm
MADCOW USDA the untold story
http://madcowusda.blogspot.com/
NOW, remember what was said about the FIRST TEN, i.e., what i call the chosen ones ;
Lancet 1996; 347: 921- 25
A new variant of Creutzfeldt-Jakob disease in the UK
R G Will, J W Ironside, M Zeidler, S N Cousens, K Estibeiro, A Alperovitch, S Poser, M Pocchiari, A Hofman, P G Smith
Summary
snip...
Discussion
The ten cases of CJD in this report are remarkable in that they have a specific neuropathological profile which, to our knowledge, has not been described previously[6,8] and which is so consistent that neuropathological samples from the cases are virtually indistinguishable. The cases are further characterised by having remarkably low ages at onset for CJD and other atypical features, including a generally protracted and unusual clinical course and absence of EEG changes typical of CJD. These findings raise the possibility that the cases represent a new clinicopathological variant of CJD.
Effect of age
It is possible that the unusual neuropathological profile of these cases is due to their young age. Review of published reports on previous young patients worldwide did not reveal any descriptions of neuropathology similar to these UK cases. In 14 cases of CJD aged less than 30 years previously reported outside the UK, plaques are described in only one, and in this report the possible diagnosis of Gerstmann- Straussler- Scheinker syndrome was raised. In four of these cases,[9-12] pathological reports have been reviewed and there was no evidence of PrP plaques (Paul Brown, personal communication). We did immunocytochemical staining on another of these cases of CJD aged 27 years from Poland (courtesy of Professor Kulczycki) and on a 16- year- old patient from the UK dying of CJD in 1980, and there was no evidence of plaque formation in either case. We also did immunocytochemical staining on 11 cases of CJD developing after administration of human growth hormone (mean age 27.5 years) and although PrP plaques were present predominantly in the cerebellum, the neuropathological features in these cases'3 were otherwise quite distinct from the young patients in this report. We emphasise that plaque distribution and spongiform change in these ten young cases were clearly apparent on routine light microscopy. Current evidence suggests, therefore, that the pathological profile in these cases is unlikely to be simply an age- related feature.
CJD has been described previously in young patients, but these are usually isolated case reports[9-12] and in systematic surveys the identification of CJD in patients aged less than 30 years old is exceptional. In the UK, only one such case was identified between 1970 and 1989. In France, between 1968 and 1982[14], only two patients aged less than 30 years old were identified; only one was identified in Japan between 1975 and 1977; and none at all in Israel between 1963 and 1987. Additional cases aged less than 40 years have been identified through the European surveillance project on CJD (1993- 95); two cases aged 22 and 34 years old were found in the Netherlands; two aged 31 and 33 years old in Germany; two aged 26 and 37 years old in France; and one aged 37 years old in Italy. Six of these cases are judged on clinical evidence not to be similar to the cases described in this report. Neuropathological information is available on two of these six cases, neither of which showed the characteristic changes. In the remaining case, full neuropathological information will be available shortly.
Case ascertainment
The overall incidence of CJD has risen in the UK in the 1990s[15], although this is due mainly to an increase in the incidence of CJD in those aged over 75 years (these cases have a typical clinicopathological profile). The most likely explanation for this is improved ascertainment of CJD in the elderly, with the possible implication that the identification of young cases of CJD may be due to similar improved case ascertainment due in part to the publicity surrounding the BSE epidemic. It is noteworthy that three of the ten cases in this report were notified to the CJD Surveillance Unit as suspect cases of CJD only after biopsy samples had been examined. In the absence of neuropathological examination, these cases might not have come to the attention of the CJD Surveillance Unit. It seems likely, however, that patients of this age dying of a progressive neurological condition would have undergone necropsy in the past. Two cases came to the attention of the CJD Surveillance Unit through unconventional means (through a newspaper report and after a clinical presentation of other cases) which led to their notification earlier than would otherwise have been the case. All of the ten cases were identified over 10 months and although there was extensive publicity surrounding two young cases in late 1995, there has been considerable publicity regarding CJD and BSE since 1990. Other European countries have undertaken systematic surveillance of CJD over a similar period and there has been no obvious increase in the incidence of CJD in young patients despite detailed investigation.
There is a possibility that the diagnosis of such atypical cases may previously have been previously missed. Three of the 14 cases discussed above were from Poland, aged 19, 23, and 27 years, and were identified in the course of a study of subacute sclerosing panencephalitis (SSPE)[16] A recent review of the clinical details of suspect but unconfirmed cases of SSPE held by the SSPE register in the UK has provided no evidence that cases of CJD were misdiagnosed as SSPE in the UK. Although improved ascertainment remains a potential explanation for the identification of the young patients we report, such information as is available does not support this interpretation.
Possible link with BSE
The first aim of the CJD Surveillance Unit has been to identify any changes in CJD that might be attributable to the transmission of BSE to the human population. Although the small number of cases in this report cannot be regarded as proof, the observation of a potentially new form of CJD in the UK is consistent with such a link. The common neuropathological picture may indicate infection by a common strain of the causative agent, as in sheep scrapie in which strains of the disease have been identified which can be distinguished on the basis of diseaseincubation period and distinctive neuropathological profile in mouse models[17]. Exposure of the human population to the BSE agent is likely to have been greatest in the 1980s, and especially towards the end of that decade, before the ban on the use of specified bovine offal was introduced. This would be consistent with an incubation period of between 5 and 10 years for these cases.
If the present cases are due to exposure to the BSE agent and this accounts for the distinctive neuropathological appearance, it is not clear why this previously unrecognised variant of the disease has been found only in persons under the age of 45 years. The absence of this variant in older persons could be due to age- related exposure to the agent; to reduced susceptibility among older persons; or to misdiagnosis of this variant of the disease in older age- groups, especially in those in which dementia is more common.
We were alerted earlier to a possible link between CJD and BSE by our finding of an apparent excess of CJD among cattle farmers[15]. Our interpretation of this was tempered by observations of high rates among cattle farmers in other European countries in which BSE was either very rare or had not been reported. None of the four farmers showed the neuropathological features described here, and all were consistent with previous experience of sporadic cases of CJD.
Conclusions
We believe that our observation of a previously unrecognised variant of CJD occurring, to date, only in persons under the age of 45 years is a cause for great concern. That it is due to exposure to the BSE agent is perhaps the most plausible interpretation of our findings. However, we emphasise that we do not have direct evidence of such a link and other explanations are possible. That these cases have been observed now because of improved ascertainment cannot be completely dismissed. It seems unlikely, however, that such a distinctive neuropathological pattern would have been missed previously, especially among persons dying at a young age. It is essential to obtain information on the clinical and neuropathological characteristics of young patients with CJD in Europe and elsewhere, and historically in the UK, but proof of an association between BSE and CJD may depend on animal transmission studies and continued epidemiological vigilance. If there is a causal link then, given the potentially long and widespread exposure to the BSE agent, further cases of this new variant of CJD are likely to arise.
We thank J Mackenzie for data management, P Brown for reviewing an early version of the manuscript, J Collinge for assistance with the molecular analysis, and W B Matthews who initiated CJD surveillance in the UK in the 1980 for advice. The CJD Surveillance Unit is funded by the Department of Health and the Scottish Home and Health Department and suported by BBSRC (grant no 15/BS204814). The Concerted Action on CJD Surveillance in Europe was funded through the EC Biomed I Programme. The epidemiological surveillance of CJD would not be possible without the collaboration of neurologists and neuropathologists throughout the UK and Europe.
References
snip.....
http://www.cjd.ed.ac.uk/lancet.htm
sporadic CJD, the big lie
Subject: Sporadic creutzfeldt-jakob disease in two adolescents (see sCJD, the big lie) Date: May 28, 2007 at 7:58 am PST
J Neurol Neurosurg Psychiatry. Published Online First: 23 May 2007. doi:10.1136/jnnp.2006.104570 © 2007 by BMJ Publishing Group Ltd
Original articles
Sporadic creutzfeldt-jakob disease in two adolescents
K Murray 1, D L Ritchie 1, M Bruce 2, C A Young 3, M Doran 3, J W Ironside 4 and R G Will 4* 1 NationalCJD Surveillance Unit, United Kingdom 2 Neuropathogenesis Unit, United Kingdom 3 Walton Centre for Neurology and Neurosurgery, United Kingdom 4 National CJD Surveillance Unit, United Kingdom
* To whom correspondence should be addressed. E-mail: r.g.will@ed.ac.uk.
Accepted 15 April 2007
Abstract
Background: Sporadic Creutzfeldt-Jakob disease (CJD) is a condition predominantly affecting older age groups, with cases aged less than 45 years rare and an age at onset or death of less than 20 years exceptional.
Methods: Data from the systematic study of sporadic CJD in the UK are available from 1970 onwards. Clinical and pathological data are reviewed in order to identify atypical cases, including those at the extremes of the age range of sporadic CJD. Detailed analysis of atypical cases is undertaken and in selected cases laboratory transmission studies are carried out in order to provide information on the characteristics of the infectious agent.
Results: In the UK two cases of sporadic CJD in adolescents have been identified, dying aged 16 and 20 years. The first case predated the epidemic of bovine spongiform encephalopathy and the characteristics of the second case, including laboratory transmission studies, are consistent with a diagnosis of sporadic rather than variant CJD.
Conclusion: The cases in this report indicate that sporadic CJD can develop at a very young age, that variant CJD is not the only form of CJD occurring in this age group and that neuropathological examination is essential to accurate diagnosis of human prion disease.
http://jnnp.bmj.com/cgi/content/abstract/jnnp.2006.104570v1
Sent: Monday May 28, 2007
Subject: THE BIG LIE SPORADIC CJD AND MAD COW DISEASEs i.e. TSE
Terry S. Singeltary Sr.
POLICY IN CONFIDENCE; CONFIDENTIAL; CJD IN FARMER WITH BSE COW ie OCCUPATIONAL EXPOSURE
Subject: POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW
POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW
LIKELY TO ATRACT MEDIA ATTENTION
snip...
DOES ANYONE BESIDES ME SEE A PATTERN YET ???
Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic CJD, whatever the hell that is. and there have been 16 year old die from sporadic CJD in the USA as well.
SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly are expendable, pets and kids are not.
Science was dictated by 'big buisness' after the Vickey Rimmer case with the ukbsenvcjd only myth.
snip...
see full text sporadic CJD the big lie;
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&T=0&P=25276
Thursday, July 10, 2008
A New Prionopathy, or the same old BSe
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Saturday, July, 18, 2009
Greetings,
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena’s. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date. But, while sub-clinical, how many can one exposed human infect? Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas? why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved? would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite? The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.
The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
please see history, and the ever evolving TSE science to date ;
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
SEE THE DAMNING VIDEO NOW AT THE BOTTOM OF THE BLOG BELOW ;
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html
Transmissible mink encephalopathy - review of the etiology
http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html
Wednesday, July 1, 2009
Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)
http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html
Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE
SOMETHING TO PONDER ???
O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???
OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$
IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???
http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html
Tuesday, August 04, 2009
Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
http://chronic-wasting-disease.blogspot.com/2009/08/susceptibilities-of-nonhuman-primates.html
Thursday, July 23, 2009
UW Hospital warning 53 patients about possible exposure to rare brain disease
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/uw-hospital-warning-53-patients-about.html
Wednesday, August 05, 2009 Rate of CWD infection increases in core area WISCONSIN
http://chronic-wasting-disease.blogspot.com/2009/08/rate-of-cwd-infection-increases-in-core.html
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
2009
NOW, let's analyze some data since 1999. ...TSS
Sunday, August 3, 2008 The conference celebrating ‘The end of kuru: 50 years of research into an extraordinary disease’
1: Related Articles Collinge J, Alpers MP.
Introduction. Philos Trans R Soc Lond B Biol Sci. 2008 Jul 31. [Epub ahead of print] No abstract available. PMID: 18672464 [PubMed - as supplied by publisher]
http://journals.royalsociety.org/content/j104810238060l8w/fulltext.pdf
In our field studies, we have interviewed many individuals who participated in traditional mortuary feasting or who described the participation of family members from the preceding generation. These detailed descriptions will be published elsewhere but have reaffirmed the oral histories of endocannibalism in the Fore recorded previously12,22–24 and that this practice ceased abruptly at the time of Australian administrative control over the kuru areas. Although isolated events might have occurred for a few years after this prohibition, we are confident that new exposures of individuals to kuru at mortuary feasts would not have occurred after 1960. Not only have no cases of kuru been recorded in people born after 1959 (and only nine were recorded in those born after 1956); but also all the 11 last recorded cases of kuru that we report here were born before 1950. If any source of infection remained, whether from surreptitious cannibalism, possible ground contam-ination with human prions at sites where food was prepared, or other lateral routes, we would expect individuals born after this period to have kuru—especially since children are thought to have had shorter incubation periods than adults. However, no such cases have been observed. Additionally, although a fraction of hamster-adapted scrapie prions have been shown to survive in soil for at least 3 years,25 the mortuary feast practices (during which the entire body would be consumed) were undertaken so that any substantial contamination of soil would not have occurred, and traditional bamboo knives and leaf plates were burned after the feast.
snip...see full text ;
http://kuru-tse.blogspot.com/2008/08/conference-celebrating-end-of-kuru-50.html
Oral transmission of KURU, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY
snip...
A The Present Position with respect to Scrapie
A1 The Problem
Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries.
The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep.
It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible.
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf
Epidemiology of Scrapie in the United States 1977
http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
http://scrapie-usa.blogspot.com/
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284
FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in ...
http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html
Nor98 scrapie identified in the United States
J Vet Diagn Invest 21:454-463 (2009)
Christie M. Loiacono,1 Bruce V. Thomsen, S. Mark Hall, Matti Kiupel, Diane Sutton, Katherine O'Rourke, Bradd Barr, Lucy Anthenill, Delwyn Keane
Abstract.
A distinct strain of scrapie identified in sheep of Norway in 1998 has since been identified in numerous countries throughout Europe. The disease is known as Nor98 or Nor98-like scrapie, among other names. Distinctions between classic scrapie and Nor98 scrapie are made based on histopathology and immunodiagnostic results. There are also differences in the epidemiology, typical signalment, and likelihood of clinical signs being observed. In addition, sheep that have genotypes associated with resistance to classic scrapie are not spared from Nor98 disease. The various differences between classic and Nor98 scrapie have been consistently reported in the vast majority of cases described across Europe. The current study describes in detail the pathologic changes and diagnostic results of the first 6 cases of Nor98 scrapie disease diagnosed in sheep of the United States.
Key words: Histopathology; Nor98; PrP immunolabeling; scrapie; sheep.
snip...
The current study describes the diagnostic findings of the first 6 cases of Nor98 scrapie in sheep of the United States.
snip...
Results
Case 1
snip...see full text ;
Wednesday, July 1, 2009
Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)
http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html
http://nor-98.blogspot.com/
http://scrapie-usa.blogspot.com/
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN VACCINES
http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html
Monday, August 17, 2009 Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/transmissible-spongiform-encephalopathy.html
Monday, May 19, 2008 S
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.html
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
http://bseinquiry.blogspot.com/2008/05/bse-cjd-and-baby-foods-great-debate.html
Sunday, May 18, 2008
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
http://bseinquiry.blogspot.com/2008/05/bse-inquiry-draft-factual-account-dfa.html
Monday, August 17, 2009
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/transmissible-spongiform-encephalopathy.html
PRODUCT Red Blood Cells Leukocytes Reduced. Recall # B-1148-09 CODE Unit: 3291680 RECALLING FIRM/MANUFACTURER Florida's Blood Centers, Inc, Orlando, FL, by telephone on January 12, 2009 and by letter dated January 13, 2009. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION FL
___________________________________
PRODUCT 1) Recovered Plasma. Recall # B-1151-09; 2) Red Blood Cells Leukocytes Reduced. Recall # B-1152-09 CODE 1) and 2) Unit: 6585642 RECALLING FIRM/MANUFACTURER Carter BloodCare/ WE & Lela I Stewart Blood Center, Inc, Tyler, TX, by fax on April 23, 2007 and March 11, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX and Switzerland
___________________________________
END OF ENFORCEMENT REPORT FOR JULY 1, 2009
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm170185.htm
PRODUCT 1) Red Blood Cells, Leukocytes Reduced. Recall B-1180-09; 2) Recovered Plasma. Recall # B-1181-09 CODE 1) and 2) Unit: 27LT64128 RECALLING FIRM/MANUFACTURER ARC Greater Alleghenies, Johnstown, PA, by telephone or electronic notification on December 1, 2008 and by letter dated December 3, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor who may have been at risk for Creutzfeldt-Jakob disease (CJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION CA, WV
___________________________________
PRODUCT 1) Recovered Plasma. Recall # B-1214-09; 2) Red Blood Cells. Recall # B-1215-09 CODE 1) and 2) Unit: KS25920 RECALLING FIRM/MANUFACTURER Inova Health Care Services, Blood Donor Services, Sterling, VA, by letter dated November 23, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION VA, NJ
___________________________________
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm170893.htm
PRODUCT Source Plasma. Recall # B-1206-09 CODE Units: 07YARF0702, 07YARE9866, 07YARE9175, 07YARE8806, 07YARE6013, 07YARE6743, 07YARE7284, 07YARE3054, 07YARE1421, 07YARE1044, 07YARE0168, 07YARD9701, 07YARD8977, 07YARD8152, 07YARD7695, 07YARD6945, 07YARD6722, 07YARD5923, 06YARE3812, 06YARE4248, 06YARE4943, 06YARE5522, 06YARE6898, 06YARE7196, 07YARA0218, 07YARA0575, 07YARA1157, 07YARA1574, 07YARA2145, 07YARA2571, 07YARA5682, 07YARA8317, 07YARA9272, 07YARA9637, 07YARB0583, 07YARB1028, 07YARB1861, 07YARB2231, 07YARB2855, 07YARB3489, 07YARB4656, 07YARB5193, 07YARB5849, 07YARB6358, 07YARB7036, 07YARB7618, 07YARB8311, 07YARB8853, 07YARB9492, 07YARC0024, 07YARC0639, 07YARC1138, 07YARC1799, 07YARC2236, 07YARC3313, 07YARC4218, 07YARC4928, 07YARC5294, 07YARC5924, 07YARC7298, 07YARC8991, 07YARC9252, 07YARD3794, 07YARD4519, 07YARD5590, 07YARF3027
RECALLING FIRM/MANUFACTURER BioLife Plasma Services LP, Fayetteville, AR, by fax on January 14, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 66 units DISTRIBUTION CA
PRODUCT 1) Red Blood Cells. Recall # B-1250-09; 2) Fresh Frozen Plasma. Recall # B-1251-09 CODE 1) and 2) Unit: 4054709 RECALLING FIRM/MANUFACTURER Wellmont Health System dba Marsh Regional Blood Center, Kingsport, TN, by letter dated October 4, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TN
___________________________________
PRODUCT Source Plasma. Recall # B-1254-09 CODE Units: 363035924, 363035761, 363034642, 363034463, 363034153, 363033965, 363033670, 363033509, 363033093, 363032543, 363032383, 363032099, 363031873, 363031593, 363031321, 363031001, 363030738, 363030235, 363030057, 363029728, 363028978, 363028657, 363028438, 363028031, 363027863, 363027492, 363027314, 363026918, 363026688, 363026356, 363026123, 363025728, 363025483, 363025047, 363024873, 363024318, 363023960, 363023655, 363023279, 363022828, 363022612, 363020673, 363020392, 363021363, 363021144, 363019633, 363019419, 363018827, 363018647, 363016935, 363016561, 363016170, 363015723, 363014906, 363014413, 363014104, 363013235, 363012843, 363012402, 363011999, 363011601, 363011195, 363008854, 363008420, 363008054, 363007611, 363007268, 363006814, 363006486, 363006074, 363005753, 363005310, 363004961, 363004496, 363004188, 363003610, 363000147, I74029391, I74028830, I74028628, I74025361, I74024797, I74024560, I74024220, I74024002, I74023653, I74023404, I74023044, I74022854, I74022445, I74022288, I74021933, I74021763, I74021452, I74021274, I74020724, I74019586, I74025147, 363015212 RECALLING FIRM/MANUFACTURER Talecris Plasma Resources Inc, Fort Worth, TX, by facsimile on March 13, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for Creutzfeldt-Jakob Disease (CJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 99 units DISTRIBUTION NC
___________________________________
END OF ENFORCEMENT REPORT FOR JULY 22, 2009
###
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm173256.htm
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-1281-09; 2) Platelets Leukocytes Reduced. Recall # B-1282-09; 3) Recovered Plasma. Recall # B-1283-09 CODE 1) Units: 1974540, W044108025910; 2) Unit: W044108025910; 3) Units: W044108025910, 1974540 RECALLING FIRM/MANUFACTURER Siouxland Community Blood Bank, Sioux City, IA, by letter and email on February 3, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 5 units DISTRIBUTION Austria, IA
___________________________________
END OF ENFORCEMENT REPORT FOR JULY 29, 2009
###
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm174738.htm
2008
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
note that some states only make cjd reportable in <> THAT HAVE THOSE PROCEDURES............sorry, i get angry at all the stupidity, and greed, because all the ignorance is born from the fear of $$$ with TSEs and ramifications of a link with livestock producing animals. for petes sake, to date, all iCJD cases have been from sporadic CJD strains. that's all iCJD is, is sporadic CJD, until a route and source found, but the pathology is the same. except for those 4 from nvCJD blood.
vCJD-related abnormal prion protein in a person with haemophilia - an update
Following the finding of evidence of the abnormal prion protein that causes variant Creutzfeldt-Jakob Disease (vCJD) in a haemophilia patient at post mortem, a risk assessment of the possible routes of exposure for this individual has been published by the Department of Health [1].
The vCJD-related abnormal prion protein was detected only in the individual's spleen but the finding was the first of the agent in a haemophilia patient [2].
To date, no haemophilia or bleeding disorder patients have been diagnosed with or died from clinical vCJD.
The investigations into the possible routes of infection considered, assuming that the abnormal prion protein did indicate vCJD infection, four possible infection routes: dietary exposure to BSE; surgical procedures; transfusions with several units of red cells; and treatment with large amounts of UK sourced Factor VIII. This included two batches of Factor VIII 8Y that were sourced from plasma pools which included plasma from a single donor who later developed clinical vCJD.
The calculations involved in this risk assessment depend on the likely prevalence of subclinical vCJD infections among the UK population, the infectivity of plasma products and blood components - both of which are subject to great uncertainties - and the number of donors contributing to the plasma pools. The risk assessment concludes that in scenarios based on current evidence, the most likely source of this patient's infection was treatment with UK sourced clotting factors.
This haemophilia patient had been treated in the 1990s with over 390,000 units of UK-sourced Factor VIII, including over 9,000 units from two implicated batches of Factor VIII 8Y (linked to a donor who later developed clinical vCJD).
The risk assessment concluded that, based on plausible assumptions, the patient was more likely to have been infected by a batch of Factor VIII that was not sourced from a pool containing plasma from the donor known to have vCJD (a non-implicated batch), than by one of the two implicated batches that were linked to this donor.
This is because far more units of non-implicated than implicated batches were administered to this patient. Each batch of plasma product is sourced from many thousands of donors (around 20,000), any one of whom could have had an asymptomatic abnormal prion protein infection. The relative risks from implicated and non-implicated batches will only be clarified further by long-term follow-up of patients.
The CJD Incidents Panel considered the risk assessment, together with other information, and concluded that this evidence confirms its existing advice to patients already notified as at increased risk of vCJD. There is therefore currently no reason to change that advice, nor to notify any new groups of patients. There is no change in the public health vCJD "at risk" status of any patients with bleeding disorders.
All patients with bleeding disorders [3] who have been treated with UK-sourced pooled factor concentrates or antithrombin [4] between 1980 and 2001 [5] are classified as "at risk of vCJD for public health purposes". Special infection control precautions and other safety measures apply to these patients.
All haemophilia centre doctors were informed of the Panel's decision on Tuesday, 9 June, 2009 and were asked to send a letter to their patients who have been notified as at increased risk of vCJD. Further information is available at http://www.hpa.org.uk/vcjdplasmaproducts.
Notes
1. vCJD risk assessment calculations for a patient with multiple routes of exposure. Department of Health, 9 June 2009. Available at:
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_100357
2. HPA. Post mortem finding of asymptomatic variant Creutzfeldt-Jakob Disease abnormal prion protein in a person with haemophilia, Health Protection Report [serial online] 2009; 3 (10): news. Available at:
http://www.hpa.org.uk/hpr/archives/2009/news0709.htm#vcjd
3. Defined here as congenital and acquired haemophilia (Haemophilia A and Haemophilia B), Von Willebrand Disease, other congenital bleeding disorders and congenital antithrombin III deficiency.
4. ie clotting factors and antithrombin made from pooled plasma. These include factor VIII, factor IX, factor VII, factor XI, factor XIII and prothrombin complex concentrates as well as antithrombin.
5. The start date of 1980 is when BSE is thought to have entered the human food chain. The end date of 2001 is the last possible expiry date of any product manufactured by the UK fractionators that was sourced from UK donors until 1998.
http://www.hpa.org.uk/hpr/archives/2009/news2309.htm#cjd
Variant CJD and plasma products Introduction
Earlier notification of patients who had received implicated plasma products
Asymptomatic vCJD abnormal prion protein in a haemophilia patient
Introduction Certain plasma products, manufactured using plasma from donors who later developed vCJD, may have exposed people who received them to infectivity and an increased risk of developing vCJD. The level of risk is unknown, and likely to be very low. The risk in such circumstances is in addition to a general risk for many people in the UK from past exposure to the BSE agent from eating beef and beef products.
The conclusions of a vCJD Blood Risk Assessment carried out by Det Norske Vertis Consulting have been accepted by the Spongiform Encephalopathy Advisory Committee (SEAC), the Committee on the Microbiological Safety of Blood and Tissue (now the Advisory Committee on the Safety of Blood Tissues and Organs - SaBTO), and by the Committee on Safety of Medicines.
As a consequence, all patients with bleeding disorders 1 who have been treated with UK-sourced pooled factor concentrates or antithrombin 2 between 1980 and 2001 3 are classified as at risk of vCJD for public health purposes. These patients should follow advice to reduce the risk of spreading vCJD to other patients.
Please also see Information leaflets for patients and healthcare professionals.
Earlier notification of patients who had received implicated plasma products In 2004 the HPA, the UK Haemophilia Centre Doctors' Organisation (UKHCDO) and colleagues notified patients who had received plasma products manufactured using plasma from donors who had subsequently developed vCJD. That notification dealt with plasma donations which had been used to manufacture factor VIII, factor IX, antithrombin, intravenous immunoglobulin G, albumin, intramuscular human normal immunoglobulin and anti-D.
Patients treated with these plasma products were managed according to an assessment of potential vCJD infectivity carried out by the Health Protection Agency with the CJD Incidents Panel.
The UKHCDO and patient representatives, the CJD Incidents Panel and UK Health Departments agreed that it was likely that many patients with bleeding disorders would have had sufficient exposure to these implicated plasma products to put them 'at risk of vCJD for public health purposes'. It was also thought likely that further batches of UK-sourced plasma products would be implicated in the future as more cases of vCJD arose.
In 2004 all patients with bleeding disorders were told whether they had received UK-sourced pooled factor concentrate or antithrombin between 1980 and 2001. Those who had were informed that special precautions needed to be taken to reduce the chance of any further spread of vCJD and were asked to follow public health advice.
Asymptomatic vCJD abnormal prion protein in a haemophilia patient A person with haemophilia was recently found to have evidence of the agent (abnormal prion protein) that causes vCJD only in his spleen at post mortem.
The post mortem was carried out as part of a study jointly co-ordinated by the UK Haemophilia Centre Doctors Organisation and the National CJD Surveillance Unit. This was the first time that vCJD abnormal prion protein had been found in a patient with haemophilia.
Up to the present, no haemophilia or bleeding disorder patient has been diagnosed with or died from clinical vCJD This haemophilia patient had been treated with several batches of UK-sourced clotting factor Factor VIII. This includes two batches of Factor VIII manufactured using plasma from a single donor who developed clinical vCJD 6 months after donating the plasma. These batches are called 'implicated' batches because they are linked to a donor who subsequently developed vCJD.
The haemophilia patient was in his 70s when he died of a condition unrelated to vCJD, 11 years and one month after receiving the second batch of implicated Factor VIII. He had no signs or symptoms of vCJD or other neurological disease when alive.
The patient had also received several transfusions of red cells, and had undergone surgical procedures in the past. A recent statistical assessment of the available information has concluded that the most likely source of vCJD infection was treatment with UK plasma-sourced clotting factors.
The risk assessment, together with other information, has been considered by the CJD Incidents Panel. The Panel has concluded that this evidence confirms its existing advice to patients already notified as at increased risk of vCJD. There is therefore currently no reason to change that advice, or to notify any new groups of patients.
There is no change in the pubic health vCJD 'at risk' status of any patients with bleeding disorders.
The CJD Incidents Panel keeps all new information about potentially infected products under close and regular review and advises doctors and their patients about the implications of all new evidence as it emerges.
Patients who are unsure about their vCJD at risk status, or who would like more information, should contact their haemophilia centre.
1. Defined here as congenital and acquired haemophilia (Haemophilia A and Haemophilia B), Von Willebrand Disease, other congenital bleeding disorders and congenital antithrombin III deficiency. 2. ie. clotting factors and antithrombin made from pooled plasma. These include factor VIII, factor IX, factor VII, factor XI, factor XIII and prothrombin complex concentrates as well as antithrombin. 3. The start date of 1980 is when BSE is thought to have entered the human food chain. The end date of 2001 is the last possible expiry date of any product manufactured by the UK fractionators that was sourced from UK donors until 1998.
Last reviewed: 10 June 2009
http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1195733818681
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Saturday, July, 18, 2009
Greetings,
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena’s. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date. But, while sub-clinical, how many can one exposed human infect? Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas? why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved? would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite? The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.
The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
please see history, and the ever evolving TSE science to date ;
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
2003
Neurology 2003;60:176-181 © 2003 American Academy of Neurology
-------------------------------------------------------------------------------- Views & Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.
http://www.neurology.org/cgi/content/abstract/60/2/176
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176
Reply to Singletary 26 March 2003
Ryan A. Maddox, MPH
Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g., vCJD, iatrogenic CJD, unusual CJD clusters).
As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.
Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication).
References
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.
2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.
3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.
4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.
5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: http://www.cjd.ed.ac.uk/figures.htm. Accessed February 18, 2003.
http://www.neurology.org/cgi/eletters/60/2/176
http://www.neurology.org/cgi/eletters/60/2/176#535
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/%20fulltext
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
Brian S. Appleby, MD; Kristin K. Appleby, MD; Barbara J. Crain, MD, PhD; Chiadi U. Onyike, MD, MHS; Mitchell T. Wallin, MD, MPH; Peter V. Rabins, MD, MPH
Background: The classic Creutzfeldt-Jakob disease (CJD), Heidenhain, and Oppenheimer-Brownell variants are sporadic CJD (sCJD) phenotypes frequently described in the literature, but many cases present with neuropsychiatric symptoms, suggesting that there may be additional sCJD phenotypes.
Objective: To characterize clinical, diagnostic, and molecular features of 5 sCJD variants.
Design: Retrospective analysis.
Setting: The Johns Hopkins and Veterans Administration health care systems.
Participants: Eighty-eight patients with definite or probable sCJD.
Main Outcome Measures: Differences in age at onset, illness progression, diagnostic test results, and molecular subtype.
Results: The age at onset differed among sCJD variants (P=.03); the affective variant had the youngest mean age at onset (59.7 years). Survival time (P.001) and the time to clinical presentation (P=.003) differed among groups. Patients with the classic CJD phenotype had the shortest median survival time from symptom onset (66 days) and those who met criteria for the affective sCJD variant had the longest (421 days) and presented to clinicians significantly later (median time from onset to presentation, 92 days; P=.004). Cerebrospinal fluid analyses were positive for 14-3-3 protein in all of the affective variants, regardless of illness duration. Periodic sharp-wave complexes were not detected on any of the electroencephalography tracings in the Oppenheimer-Brownell group; basal ganglia hyperintensity was not detected on brain magnetic resonance imaging in this group either. All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.
Conclusions: The classic CJD phenotype and the Heidenhain, Oppenheimer-Brownell, cognitive, and affective sCJD variants differ by age at disease onset, survival time, and diagnostic test results. Characteristics of these 5 phenotypes are provided to facilitate further clinicopathologic investigation that may lead to more reliable and timely diagnoses of sCJD.
Arch Neurol. 2009;66(2):208-215
snip...
COMMENT
snip...see full text ;
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE
SOMETHING TO PONDER ???
O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???
OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$
IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???
http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html
Saturday, August 01, 2009
Cases of Early-Onset Sporadic Creutzfeld-Jakob Disease in Michigan
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cases-of-early-onset-sporadic.html
Monday, July 27, 2009
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Monday, August 17, 2009
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/transmissible-spongiform-encephalopathy.html
WE must make all human TSE reportable in every state, and internationally, of ALL age groups, and this must be mandatory.
WE must test all livestock producing animals for animal and human consumption for Transmissible Spongiform Encephalopathy, and let the chips fall where they may. This masquerade of BSE testing in the USA, and the mad cow feed ban that never was must stop. ...
My Mother autopsy as follows ;
Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: "Bonnie L. Singeltary"
Sunday, August 12, 2007 3:29 PM
Subject: Re: Hello Dr. Gibbs...........
Wed, 29 Nov 2000 14:14:18 -0500
a private email from the late Dr. Gibbs, a true pioneer in the research of human/animal TSEs and one that never wavered on helping the families and victims of this horrible disease, and one that helped me many times in trying to seek out the truth;
Subject: Re: Hello Dr. Gibbs...........
Date: Wed, 29 Nov 2000 14:14:18 -0500
From: "Clarence J. Gibbs, Jr., Ph.D."
To: "Terry S. Singeltary Sr." References: <3a254430.9fb97284@wt.net>
Hi Terry:
326 E Stret N.E., Washington, D. C. 20002.
Better shrimp and oysters than cards!!!!
Have a happy holiday and thanks for all the information you bring to the screen.
Joe Gibbs
==========
with kindest regards,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
