A personal message to the Board from Mark Purdey!

[mark purdey]

Mark sent this message for the Board to me today. Apparently, for whatever computer glitch reason, he is unable to post it himself.
*******************************************************
(from Mark Purdey, Somerset, UK)

I was greatly saddened to read some of the wildly irrelevant and impertinent comments that have been posted about my research data and hypotheses on the origins of TSE.

I feel that my critics need to do their homework first, before launching into their tirade of speculative and misguided comments about the authenticity of my first hand research into TSEs.
...

In this respect, I feel that it is totally unfair that my work is being subjected to this misappropriated assault on your pages.



I also feel that your readers should be aware of the personal and financial hardship that entrepreneurial researchers such as myself have had to endure for the 'crime' of launching fresh observations and ideas into the public arena ...

Whilst many reputable scientific establishments are currently making a small fortune out of the fruits of my own pioneering work, my own life has ironically degenerated into a state of total collapse. All I ask is for a bit of basic human respect, and not for the accolades of acidity that are sent my way nearly everyday. Thank you Kathy, for being the only intelligent and open minded contributor to ranchers.com

Yours,

Mark Purdey

Look, Mark Purdey, I applaud you for your perserverance, your bravery in taking on the establishment, and your creativity. It may well be that you were instrumental in bringing the familial and other genetic clusters in Slovenia to the attention of science.

I acknowledge that you suffered but your suffering sir is NOTHING compared to the suffering of the families afflicted with CJD and variant CJD and to the extent that your writings are used to ignore public health threats and to avoid taking public health measures that may well protect humans from CJD, then your writings are being ill used. You should acknowledge that and if you do not, I will pay no further attention to you.

Your supporters use your writings to (1) deny that CJD is transmissable from person to person, e.g., via contaminated surgical instruments or tissue or blood donations; (2) reject totally the strong hypothesis that variant CJD is due to the BSE epidemic in the UK being "pushed" over the species barrier. They claim that all cases of human CJD are due to metal contamination. It is they who are perverting your theories and therefore subjecting you to ridicule. Unless you deny these things as well and in which case, you should be ignored since in the case of (1) you deny fact and in the case of (2) you reject a hypothesis that must be accepted for the time being and must lead our public health measures given its strength.

NO ONE has denied that the ultimate cause of TSEs is unknown. However TSEs ARE transmissable between species, albeit not easily, and they are certainly transmissable among the same species. The suffering of the individual and his/her family who contracts CJD or variant CJD is hideous beyond description. If TSEs are your life work, you had better be taking that into consideration.

I am well aware of how devastating CJD is for families , having spent many hours interviewing the surviving relatives of CJD victims for a book that I am currently writing. furthermore, i have also experienced the terror in the faces of cattle which i had purchased into my farm and later found to be suffering from BSE. God knows how i would have felt if i had been observing this in my children. So I sympathise with you.

In this respect, we are not at war with each other. We should be all working together for the sake of a safer healthier world for our children to grow up in. This is why i try my hardest to be completely impartial in my research, basing everything on the hard data amassed from my environmental analyses that are processed at London Uni.

However, you still seem to totally misunderstand the basis of my work and you ought to read my many publications in the academic literature before you pass erroneous judgement. I am NOT denying the well proven fact that the TSE agent is transmissible and pathogenic . But what I am saying that is new is that the transmissible agent is not a microbiological agent, but it is a metal microcrystal with a piezoelectric pathogenic capacity . Once the metal microcrystal has successfully traversed the brain barrier and implanted itself into the neuronal membranes, it binds up with the prion and ferritin proteins and multireplicates itself ( eg; grows ) into the substantial fibril crystalline structure that hallmarks the TSE diseased brain. This fibril silicaceous structure is piezoelectric - eg it will convert incoming sonic / tactile pressure waves into electrical shocks , and it is these shocks which 'burn out' the so called spongiform holes in the brains of CJD victims - by inducing a chain reaction of free radical mediated neurodegeneration every time the crystal contaminated victim is exposed to a sonic challenge from the external environment. This is why you observe the so called spongiform halo effect around each fibril plaque ( eg the crystal ) in the neuropathology of the TSE diseased brain

The metal microcrystal is therefore heat resistant , transmissible and pathogenic ; therefore fulfills all of the idiosyncratic prerequisites of the TSE causal agent . So why has there been so much resistance to accepting the need to research this idea ?

I have identified the consistent presence of these piezoelectric metal microcrystal pollutants / sonic challenges in every single TSE cluster environment. Furthermore, assuming that it can be shown that these microcrystals are present in the TSE diseased brain inoculum that is utilised in all of these TSE transmission lab experiments, then it could be argued that the success of these transmission trials is a result of the microcrystal being transmitted across by injection into the fresh animal on each occasion, which, in turn, will initiate a multireplication of metal-protein crystals and a TSE all over again - So what is the sticking point here ? I cannot understand it - academic egos ? prejudice ? reputation ?

 

[Mike]

Mark, Have you read this gentleman's findings in research? It seems you have something in common. It might behoove you and the cattle industry to hook up with him. The sooner we find the origination of BSE, the better off we will all be.

Vitaly Vodyanoy
541 Summertrees Drive
Auburn, Alabama (AL)
36832-6766

Telephone:
(334)826-9894 Home
e-mail: vodyavi@vetmed.auburn.edu

 

[mark purdey]

Mark, Have you read this gentleman's findings in research? It seems you have something in common. It might behoove you and the cattle industry to hook up with him. The sooner we find the origination of BSE, the better off we will all be.

Vitaly Vodyanoy
541 Summertrees Drive
Auburn, Alabama (AL)
36832-6766

Telephone:
(334)826-9894 Home
e-mail: vodyavi@vetmed.auburn.edu

Yes, I have heard of the Auburn research , and currently have a paper in press which draws attention to the precise correlation between the conclusion of their lab studies and my field research.

This is very , very important research , and , as you say, the sooner we can unravel the origins of this grotesque disease the better for us all. If you can understand disease cause , then you are almost full way towards unravelling the best means of preventing, controlling and even curing these diseases.

This is why I remain totally bewildered by the resistance of governments towards getting to the truth, and even more bewildered by the resistance of the CJD support groups towards my work - I know that if one of my kids had died of this tagic illness, then I would be more than eager to pinpoint the original cause.

Despite having spent hundreds of hours over the years emailing with the rlatives of CJD victims , discussing cures - re the use of the anti-crystallisation proteoglycan polysulphates - (heparan molecules) , I have only ever found myself being criminalised and subjected to total mockery by their support groups here in the UK . they should appreciate the fact that somebody is having the guts to go against the grain and look for the truths under the cover story. Of course, governments are going to evade issues that involve their former chemical munition programmes causing vCJD !!!! A kindergarten child is going to realise this . I think people need to realise that I am not paid to carry out my research. It is totally voluntary and virtually fulltime now.

If it wasn't for generous donations from the likes of kathy Czar, then my research would have totally dried up

It is time that critique over the failure of our society to unearth the origins of TSEs was directed at those who are paid vast amounts of our taxes to undertake this research , and not at voluntary workers such as myself . It is these researchers who are failing to come up with the answers.

A Professor called Roy Anderson recieved 4 million UK pounds to predict the future incidence curve of vCJD and BSE . What real benefits did this quesstimated data provide for anyone ???? Despite predicting everything wrong, this guy is still an academic hero !! My own research remains unfunded despite my repeated attempts to acquire funding . In light of the fact that several of my environmental observations in the TSE cluster zones have lead on to substantial break throughs in our understanding of the origins of these diseases, then i find this whole rejection is quite ironic and counterproductive .

 

[rkaiser]

Thanks for coming on board here on the good ship "rancher.net" Mark.

Our goals here on ranchers are similar, our tactics simply sway. A good bunch of people trying to uncover truth, and help those who do not research, but simply follow.

Go easy on good old reader the second, she also has great intentions.

Randy Kaiser working for the ranchers of the world. :wink:

 

[bse-tester]

Mark Purdey wrote:

Whilst many reputable scientific establishments are currently making a small fortune out of the fruits of my own pioneering work, my own life has ironically degenerated into a state of total collapse. All I ask is for a bit of basic human respect, and not for the accolades of acidity that are sent my way nearly everyday. Thank you Kathy, for being the only intelligent and open minded contributor to ranchers.com

It has to be said that we here on this board accept, or at least try to accept all points of view and offerings that provide good and intelligent discussion that may or may not provide us all a greater understanding of what is going on in the world of ranching and prion dieseases. The last thing we need here is to be unceremoniously catagorized as being unintelligent, closed minded individuals whose input is to be considered either worthless or the rantings of those who know nothing. I take exception to the manner in which Mark Purdey does in fact label those of us who are trying to conduct ourselves in an acceptable manner and he should realize that we are simply here to share info and ideas and not to engage in useless rhetoric. So Mark, before you hand out your own version of acidic labels, please remember and consider the fact that you are not the only researcher in the world of prion disease who has had a rough go of it, and that Kathy is certainly not the only intelligent person making contributions here!! There are many of us who have shared the trials and the long hard roads to nowhere hoping sometimes against all hope to finally make a difference!!!

 

[mark purdey]

Thanks for coming on board here on the good ship "rancher.net" Mark.

Our goals here on ranchers are similar, our tactics simply sway. A good bunch of people trying to uncover truth, and help those who do not research, but simply follow.

Go easy on good old reader the second, she also has great intentions.

Randy Kaiser working for the ranchers of the world. :wink:

Thanks Randy. I appreciate your consideration a lot.
You probably would be better off telling me to go easy on Mark Purdey :wink:

I was direct with Purdey about what is objectionable about his theories -- when they are used as smokescreens to help big business kill public health measures.

TSEs are transmissable and amplification is a demonstrated danger to human health. Mark can search for the ORIGINAL cause all he wants with my blessing, as long as he acknowledges that TSEs transmit -- including BSE -- and therefore we need to have measures and funding for surveillance, for testing, and for keeping SRMs, surgical instruments, blood and tissue out of blood/food/medical chain.

I can well understand the UK families' opposition to Mark if his theories are being used to deny the BSE - vCJD link and to avoid taking the measures needed to avoid any further ripples of the BSE epidemic. We do not know how many are asymptomatic carriers in the UK but we know there are such people and it is likely to be in the thousands at least. We need funding for research to detect TSEs early, to clean blood, etc. Anyone who denies this is my foe, as I have said. Regardless of how lofty they claim their goals to be, their actions speak louder.

Come on R2. why don't you read what I have just said - THAT THE TSE AGENT IS A TRANSMISSIBLE AGENT. you go on and on as though I am trying to deny this well established fact. what is your game ?

If you wish to delude yourself that meat and bone meal and / or beef were the vectors that transmitted the TSE agent then you remain in total denial of the true epidemiological facts .

How do you explain why no BSE broke out in the middle eastern dairy herds despite recieving boatloads of UK meat and bone meal as feed throughout the BSE era ?

How do you explain the emergence of 43, 000 cases of BSE in UK cattle that were born after the 1988 ban of meat and bone going into ruminant feeds in the UK?

How do you explain the emergence of BSE farms that never fed any meat and bone meal in any of its various guises ? I could take you to many such farms around me .


These and many other flaws that have been cited in the official feed theory and recorded in my publications, clearly indicate that the meat and bone meal theory is discredited.

Here in the UK , honest vets and farmers will openly admit that the meat and bone meal theory served as a convenient cover story that was exploited in order to show the world that British beef was now safe because the feed that was supposedly responsible had been banned.

So the theory was used as a politically and commercially convenient cover story . However, once other countries were forced into the BSE battlefield because of BSE breakdowns in their own herds, the momentum of this myth simply kept on rolling to such an extent that the bureaucracies and government depts could never back out of it .

So, in respect of my own first hand experience of BSE here in the UK, I have to say that anybody who promotes this THEORY on the cause of TSEs is merely thwarting the healthy and productive evolution of TSE science.

Why can't we admit to the flaws and the political lies, and simply get on with looking for the truth .

My research may well be objectionable to certain people or vested interests because it does not suit their particular agenda or whatever, but, the bottom line is that I am in pursuit of the truth. Whether I am talking about nerve agent dumping in the UK seas, or crashed japanese bombers in the territories of the New Quinea Fore tribe , or scrapie clusters in sheep grazing former military controlled firing ranges, I am speaking from first hand experience , having personally visited these areas, interviewed the people involved , collected analytical evidence . I have photos , documentation, data , video as proof. Nobody can take these first hand experiences away from me. Whether you listen, that's up to you. I am just carrying on with my research.

 

[mark purdey]

I can see why the vCJD families don't embrace you.

How do you explain the new cases of vCJD in 26 year olds in European countries that received high amounts of UK MBM -- France now has 13 cases, Ireland several cases, Portugal 1, the Netherlands 1? How do you explain the coincidence of a new human TSE primarily in young people -- pathologically similar to BSE -- occurring subsequent to a massive epidemic of BSE in the UK? And how do you discount the transmission studies which have been done all over the world for the past 10 years or so showing that BSE and CJD are transmissable to other species?

How nice that you have traveled widely. I have too. But nothing I have seen or done in my life prepared me to witness what CJD does to a young human being. I suggest you stop bothering to try to convince me that you are both compassionate and right. It's obvious that your crusade has no room for compassion or concern for public health.

Go ahead and post. I did bother to read your website from cover to cover some months ago because Kathy and Randy recommended it. But I don't recommend that you and I continue a dialogue since it is pointless. I will read what you post here and I keep an open mind about the ORIGINAL aetiology of BSE. But I think you're ignoring a massive amount of evidence and more troubling, your ego or whatever is getting in the way of your AT THE VERY LEAST accepting that the BSE as the link to vCJD has to be taken very seriously from a public health standpoint.

And yes, how do you explain the fact that the feed ban drastically reduced the cases of BSE? I am well aware of BARB cases, some of which are explained through maternal transmission, others likely through gaps in the feed ban, still others by other forms of vertical transmission given recent evidence of prions in blood and urine, still others from scrapie which I believe is the original origin of BSE.

You have still failed to read my actual work !! I therefore reiterate that I agree that the TSE causal agent is transmissible under certain circumstances. And secondly, I agree that vCJD is the same disease as BSE. But my observations have lead me to conclude that vCJD and BSE are caused by a shared exposure to the same environmental factors , as opposed to being caused by ingestion of the one TSE affected species by another species.

It seems that you have some pathological problem about the nature of my work, and whatever I am saying about the true position of my work in my postings you are choosing to ignore in your follow up responses. In this respect , you are right, we are all wasting our time having dialogue since it is going round and round in circles.

Good luck with your research.

All the best ,

Mark

 

[rkaiser]

More horrible deaths will occur R2 if the world fails to recognise the true cause of BSE and vCJD. You have used the guilt trip approach from the day I started reading your posts R2, but continue to ignore that more harm could come to humanity, not to mention the animal kingdom, if heed is not paid to metal contamination and other environmental disturbances brought on by human greed and neglect.

 

[mark purdey]

I read several of the published papers on your website.
You have not answered a single one of my questions.
You do like words like "pathological," don't you?

Good luck with your research and on the way to the ultimate explanation for TSEs, please remember to support each and every precautionary measure that there is current scientific and public health support for, regardless of our immature state of knowledge. Do you really want to be in the position in 20 years of having rejected precautionary measures and seeing fellow humans die horribly? That's the position that the medical field and the governments are in today.

Dear R2,

your questions are very important and broad ranging, and to give them fair justice would involve me in providing a book's worth of answers, which I would be happy to provide at a time when I am not so busy writing a book to a tight deadline.

In fact , I have even travelled out to Sicily to investigate the environmental circumstances surrounding the 2 vCJD cases out there, so I have covered this ground and can only reiterate my answer to you , that all of these cases of new variant strain TSEs - whether in cows, cats, humans , zoo animals , can ALL be related back to a common exposure to the same unique package of environmental factors - a primary exposure to heat resistant , acid resistant, silicaceous microcrystals ( be it barium , strontium, silver, manganese, plutonium or uranium silicate species ) followed by a secondary exposure to acoustic shock waves which activate the dormant pathogenic capacity retained in these crystal contaminants that have become successfully implanted ( as metal-protein complexes ) in the brains of exposed individuals .

It is completely back to front and impractical for us to attempt to screen and cleanse the entire foodchain of the TSE causal factors eg; the metal microcrystals, whilst our governments continue to permit the wholesale unrestricted application of these corporate nanotechnologies into the open environment. The only way we can nip this problem in the bud is to prevent the open release of these nanotox nasties at the point where they first enter the foodchain ; eg; where corporations have been marketing highly efficient systemic acting microcrystal based insecticides or war gases which are deliberately designed for their active ingredients to taverse body membrane barriers with ease and penetrate the central nerves for the purpose of killing mammalian 'pests' as efficiently as possible .

What annoys me is that despite independent funded trials at the dept of neuroscience at the Institute of Psychiatry in London producing pathogenic prion protein as a result of exposing prion protein neuroblastoma cells to phosmet ( containing phosphorous microcrystals as active ingredient ), the whole result was squashed by the British government , and , to my horror, the canisters of phosmet ( ICI held the patent !! ) were still for sale on the shop shelves thereafter, despite these positive results of the trial. This is highly , highly irresponsible criminal behaviour in my view, and this is why I have dedicated my life to researching and uncovering the truths of these dispicable government funded crimes of humanity. I will carry on regardless of whether I get support from any CJD group or not.

And finally , If you have only read my website , R2, then you have not read my published academic peer reviewed journal articles, which provide some of the evidence that explains the spatial / temporal emergence of the vTSE clusters to which you refer.

If you are prepared to loose your anonymous status and betray your true identity, and email me at TSEPurdey@aol.com , then I am more than happy to email you pdf files of the papers that may interest you. If not, then you can view the abstracts of most of my academic papers free of charge on the Pub Med database under Mark Purdey. .

Best,


mark

 

[mark purdey]

Mark Purdey wrote:

Whilst many reputable scientific establishments are currently making a small fortune out of the fruits of my own pioneering work, my own life has ironically degenerated into a state of total collapse. All I ask is for a bit of basic human respect, and not for the accolades of acidity that are sent my way nearly everyday. Thank you Kathy, for being the only intelligent and open minded contributor to ranchers.com

It has to be said that we here on this board accept, or at least try to accept all points of view and offerings that provide good and intelligent discussion that may or may not provide us all a greater understanding of what is going on in the world of ranching and prion dieseases. The last thing we need here is to be unceremoniously catagorized as being unintelligent, closed minded individuals whose input is to be considered either worthless or the rantings of those who know nothing. I take exception to the manner in which Mark Purdey does in fact label those of us who are trying to conduct ourselves in an acceptable manner and he should realize that we are simply here to share info and ideas and not to engage in useless rhetoric. So Mark, before you hand out your own version of acidic labels, please remember and consider the fact that you are not the only researcher in the world of prion disease who has had a rough go of it, and that Kathy is certainly not the only intelligent person making contributions here!! There are many of us who have shared the trials and the long hard roads to nowhere hoping sometimes against all hope to finally make a difference!!!

Sure, I take your point here and accept that I have made an overstatement !! It was just quite a shock for me when I suddenly came across this whole hornet's nest of unfair critique of my work on these pages for the first time - where two commentators had implied that my work had been refuted without actually supplying any references of the research studies involved - plus there was a heap of other unsubstantiated critique. I am sure if you had come across a similar batch of unjust critique over your own work ( which you could easily rectify had you known about it ) you would have felt as frustrated as me !!! Its human nature.

Its abit of a case of once bitten , twice shy with me . I have recieved this type of unjustified sterotype infectious second hand critique so frequently , that I have developed my own style of Pavlovian response to it.

Since my work is international and involved with many neurodegenerative disorders, this kind of critique is continually raised over my work, and I cannot physically and mentally cope with it during peak periods. I only have one body, plus have to make a living like all of us for my family. On the other hand , I am extremely appreciative of rational critique of my work , which has proved most helpful in the past in enabling my work to evolve and stand up to new challenges as fresh data from TSE research studies has come to light.

So I do apologise for overreacting, and now that I have had time to read more of the pages involved with the TSE debate on ranchers.net, I have a better idea of who is who ( despite the anonymous status of most participants - which i find weird !! ) and why people have been responding to postings in the way that they have been. And, as you rightly point out, the majority of you are making some very rationa, intelligent comments in relation to some of the other Agri-eco-health chat sites that abound .

So please do not allow my premature irrational comments to tarnish the good integrity of those that post on ranchers.net

I appreciate your objectivity, and can also say that I know many others who deserve research funding on the TSE front. But all i can say is that the despicable way in which my own personal invites for funding were mishandled would have been sufficient to have driven anyone insane . Thats a long boring story ! I have to get that anger out of my system some times.

 

[bse-tester]

Mark, welcome aboard. I too am finding the funding side of life to be a challenge and those who would willingly provide funding to some truly ridiculous projects, fail to see the importance of what may well affect the lives of millions of people. Perhaps we should all instead of seeking funding for individual projects, group together and seek a major player with extremely deep pockets to fund a group of projects in one foul swoop? Who can say what tomorrow may bring?

 

[rkaiser]

Well R2, I'm sorry I upset you ----- again.

When have I ever talked of ignoring precaution?In fact I am an advocate, here in Canada, of BSE testing for export marketing purposes and have never once suggested that we step back down from movement toward SRM removal and feed bans. Who knows what kind of metal contaminated body parts we could be passing on to the next unfortunate animal.

Do you understand the part of Mark's theory that involves transmission?

It is not transmission of an infective prion agent but transmission of the contaminant that caused the animal to become ill.

Smokescreen is exactly the word. And the smokescreen is the infectious prion crap.

I am sorry R2, but you are the one person on this board who is ignoring. Ignoring the fact that while you and your kind continue on the infectious prion mission, time is lost. Lives are lost - some human, but mostly animal. While the true cause is right before your nose.

Push for testing if you must, push for protection from SRM's (if you understand why you are removing them), and keep the idea of TSE's in the forefront. But at the same time R2, help us push to find the cause. The metalic imbalance cause that you cannot refute. The cause that will once and for all stop the madness.

 

[mark purdey]

Mark, welcome aboard. I too am finding the funding side of life to be a challenge and those who would willingly provide funding to some truly ridiculous projects, fail to see the importance of what may well affect the lives of millions of people. Perhaps we should all instead of seeking funding for individual projects, group together and seek a major player with extremely deep pockets to fund a group of projects in one foul swoop? Who can say what tomorrow may bring?

Well, exactly, I was thinking the same when i Started to read down your posting. I guess any collaboration would pivot upon how similar your line of research is to my own , and whether they could be batched together as a single unified project,

I have some protocols in mind for live tests ( looking at the crystalline structures of hard tissues - antlers, etc ) which are relatively easily accessible in a practical sense , plus I have some pilot data which I have amassed at a Uni in the UK, also some potential molecules in mind that could cross b/b/ barrier and arrest the growth of the fibril crystals in the early stages of TSEs. So my input would be coming from further environmental surveillance of clusters, potential live tests and cures that are designed upon the environmental data .

I understand that funding is being offered by the Albertan prion research group ( do i have the name right ? ) which puts out a call for funding projects every six months.

I have found the gov officials / gov scientists involved with TSEs in Alberta to be much more open minded and intelligent than any where else I have visited in the world !! I suppose they have not had long enough yet to get rooted into the sterotype paradigms that exist in countries like the UK where scrapie research got bogged down into reductionist cul de sacs about 40 years ago . Well, in truth, I find myself getting bogged down into my own paradigms at times, until someone kicks me up the ........ Its human nature

The intensity of CWD that exists / has existed in Alberta / saskatchewan also offers a good sized population group with CWD positives and CWD negatives for any study.

I am seriously booked up with my book until the New Year, but should be free next Spring , apart from a quick field study on MS with kasan Uni in Russia.


Best,

mark

 

[mark purdey]

More horrible deaths will occur R2 if the world fails to recognise the true cause of BSE and vCJD. You have used the guilt trip approach from the day I started reading your posts R2, but continue to ignore that more harm could come to humanity, not to mention the animal kingdom, if heed is not paid to metal contamination and other environmental disturbances brought on by human greed and neglect.

BS Randy and you know what that means. I had the misfortune to personally see what not taking precautions in our medical practices leads to. Because of my personal situation I read about the many other similar cases of iatrogenic CJD. I choose to share this knowledge with you because you are among the few Americans who understand and care about these diseases and you can make a difference. In addition, you are unfairly impacted by our governments not openly and quickly taking measures against these diseases.

Thankfully some of you understand this better than I do. But several of you are into denial and smokescreen behavior.

Smokescreen is all you are about - status quo, ignore the BSE epidemic, ignore the non coincidental deaths of 150+ young people from a brand new TSE which occurred shortly after the height of the BSE epidemic and which now follows exports of MBM to the EU, killing 26 year olds in Portugal, Netherlands, Ireland, and France -- especially France where the bulk of the exports were. Ignore the 99+ % of researchers and scientists and find a silly reason to reject their research -- research founded on exactly the same practices that are making major breakthroughs in the biological sciences and medical research.

I have publications too but that does not make me a celebrity whose every word must be instantly given total credibility on Ranchers.Net. Mark Purdey has to convince us of the worth of his ideas, just like everyone else. Smearing me as he tried to do and as you have just done , much to my disappointment, and making sweeping generalizations, is not going to cut it.

I am exactly what my name implies -- a well read person whose personal tragedy caused her to pay attention. Mark needs to accept personal responsibility for his activities, that's life, that's not guilt. I do not blame the surgeon who operated on my husband and I don't blame the public health establishment since less was known 25 years ago. Now that we have a strong hypothesis about TSEs crossing species barriers and being potentially transmissable in blood and tissue donations, we need to take precautions to not amplify the cases of CJD and vCJD. As well as look for the cause, as well as look for treatments and cures.

hey, reader 2, I have just seen where you are from in the USA. I am actually giving several lectures in your neck of the woods in early febuary, so why don't you come along to one of the public one's and take me to task ? In that forum, we can work through all of your challenges , and sort out a happy medium. It will do us both good and we could learn alot from each other's perspectives no doubt . let me know if you are happy to come along .

Best,

mark

 

[mark purdey]

Mark,

Let me know where you are speaking. There is a world in which you come to accept my views partially and some of your views are broadly accepted by me and others and you see that some have to be discarded.

I think on the metals as a trigger, your views may have merit. However I have no doubt that TSEs are actually a neurodegenerative disease, like cancer is a disease, but one which can be triggered by environmental factors AND one unlike cancer and Alzheimer's which can be both genetic and transmissable. Much more like SARS, AIDS, and avian flu and quite possibly originally a zoonotic disease like them but affecting the CNS. A disease that we have immunities to normally that are somehow broken down with age or due to genetic mutation or under certain probably inflammatory conditions in the case of the disease entering the immature
digestive track.

I suppose my travels to cluster areas around the world have provided me with an insight into any unique environmental features that are common to the cluster areas, and when you continually witness the precise correlation with the TSE foci and sonic shocks, it is impossible to let go of that observation and discard it as irrelevant. Of course, people are going to think that I am mad to raise this, but when you study the interactive science of metals , proteins and sonic challenge further, the whole damn puzzle of TSE cause is solved - well in my view.

I have just returned from investigating a cluster of vCJD that erupted in 1996 in a few remote kent villages, and the sonic shock element was very clear cut ( like all clusters I have investigated ). Sadly, the girlfriend of the trainer pilot of a squadron of tornadoes had lived in the village of Smarden, and when training was intense during the gulf war period, the trainer would always fly his squadron on the low flightpath over his girlfriend's house - presumably to show off abit. The low flights eventually ceased as did the outbreaks of CJD.

But this area of kent was also seriously polluted with piezoelectric silicate microcrystals ( from a major brick works ) , which make the local populations vulnerable to the sonic challenge . So you need the microcrystal poisoning first, and then the sonic shocks as a secondary activator . The protein-silicate crystals then burst into a state of hyper multireplication, and the TSE disease process is set in train.

Personally, from my studies, I think the acoustic wave prerequisite is very relevant. The sonication and centrifugal treatments of the TSE brain homogenate probably provide that agitation prerequisite in the lab transmission experiments , but its subtle pathogenic role has gone unnoticed . But of course,you do need the microcrystal seeded prion crystal ( The TSE agent ) as a starter before any transmission experiment is going to work .

I thought when Soto et al's work was published on sound waves pinpointing the presence of rogue prions in blood, then people would connect this in vitro observation to my environmental in vivo observations of sound from low fly jets , etc, creating the final formation of rogue prion protein , but sadly no !!

Obviously I have had to become multidisciplinary in my resesarch, but most TSE researchers are not going to be aware of the physico-chemistry of crystals and how it is well proven that the vibration from sound can cause crystal structures to proliferate, etc, which is very much what could be going on in TSEs where piezoelectric metal protein crystals have formed and any incoming sound of a select frequency will invoke a deadly chain reaction of pathogenicity in the crystal contaminated brain .

This is perfectly easily testable , and could be done very cheaply using BSE brainstem tissues and BSE-free brainstems . But nobody will even entertain the ideaof running such a simple challenge , which is outrageous.

Pine needles are piezoelectric metal silicates too - that is where they fit in.They will form metal protein crystals that render animalS susceptible to the sonic cHALLENGE.

must rush

 

[flounder]

Greetings,

A kind greetings from Texas!


mark purdey wrote;


Come on R2. why don't you read what I have just said - THAT THE TSE AGENT IS A TRANSMISSIBLE AGENT. you go on and on as though I am trying to deny this well established fact. what is your game ?

If you wish to delude yourself that meat and bone meal and / or beef were the vectors that transmitted the TSE agent then you remain in total denial of the true epidemiological facts .

How do you explain why no BSE broke out in the middle eastern dairy herds despite recieving boatloads of UK meat and bone meal as feed throughout the BSE era ?


TSS WRITES;


comparing apples to oranges, these middle eastern dairy herds recieved far less MBM i.e. flours and meals, and or greaves, than those of documented BSE countries. ...



http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf


mark purdey wrote;


How do you explain the emergence of 43, 000 cases of BSE in UK cattle that were born after the 1988 ban of meat and bone going into ruminant feeds in the UK?


TSS WRITES;


very easily, non-compliance to feed ban and cross contaminations. pre-clincal
animals still going into the feed chain, even to this date. the partial compliance of the
feed ban is the cause of the sharp decline of BSE over the years.


http://www.bseinquiry.gov.uk/files/yb/1995/01/05003001.pdf


of course the ruminant feed ban was working against the grain anyway, so
compliance was going to be a joke;


STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

To minimise the risk of farmers' claims for compensation from feed
compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by
maintaining the availability of meat and bone meal as a raw
material in animal feeds, and ensuring time is available to make any
changes which may be required.

snip...

THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at
handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which
contain illegal traces of ruminant protein. More likely, a few positive
test results will turn up but proof that a particular feed mill knowingly
supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct
linkage between feed milling _practices_ and actual BSE cases,
the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf


http://www.bseinquiry.gov.uk/files/yb/1995/01/11001001.pdf


MR PURDEY'S LETTER IN FARMERS WEEKLY 1996

http://www.bseinquiry.gov.uk/files/yb/1996/03/12006001.pdf


CURRENT STATUS OF SE TRANSMISSIBILITY/BIOASSAY STUDIES
27 FEBRUARY 1996

http://www.bseinquiry.gov.uk/files/yb/1996/02/27001001.pdf

http://www.bseinquiry.gov.uk/files/yb/1996/02/29001001.pdf


PROGRESS REPORT-BSE CATTLE TRANSMISSIONS

http://www.bseinquiry.gov.uk/files/yb/1995/01/03003001.pdf

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradley's answer (that it would take less than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise that it

could take as little of 1 gram of brain to cause BSE by the oral route within the

same species. This information did not become available until the "attack rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to ensure

that the actual result was within both a lower and an upper limit within the study

and the designing scientists would not have expected all the dose levels to trigger

infection. The dose ranges chosen by the most informed scientists at that time

ranged from 1 gram to three times one hundred grams. It is clear that the designing

scientists must have also shared Mr Bradley's surprise at the results because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf

Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml


HERE is a doozy, the oral dose of BSE in primates--look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE. NOW that is a small dose for sure;


Published online
January 27, 2005
http://image.thelancet.com/
extras/05let1056web.pdf
Commissariat à l'Energie
Atomique/Direction des
Sciences du Vivant/Départment
de Recherche Médicale,
18 Route du Panorama, 92265
Fontenay-aux-Roses, France
(C I Lasmézas DrMedVet,
E Comoy DrMedVet,
Risk of oral infection with bovine spongiform
encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,
Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant
Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the efficiency of oral infection
and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral
transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a
BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the
other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a
preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public
health measures can prevent transmission of BSE to man....

snip...end...tss


NEW MAD COW STRAIN CALLED BASE, VERY SIMILAR TO SPORADIC CJD IN HUMANS;


Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease

Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli *

*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy


Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.


--------------------------------------------------------------------------------

C.C. and G.Z. contributed equally to this work.

||To whom correspondence should be addressed.

E-mail: salvatore.monaco@mail.univr.it. .

www.pnas.org/cgi/doi/10.1073/pnas.0305777101


http://www.pnas.org/cgi/content/abstract/0305777101v1


>> Differences in tissue distribution could require new regulations
>> regarding specific risk material (SRM) removal.
>
>
>
>

snip...end

full text ;

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE.


For personal use. Only reproduce with permission from Elsevier Ltd

Up to 400 000 cows with undiagnosed bovine spongiform

encephalopathy (BSE) infection are estimated to

have been slaughtered for food before brain and spinal

cord were banned from human consumption in 1989.

More restricted exposure to BSE could have continued

through 1995 from consumption of processed meat

products containing mechanically recovered meat

contaminated with central nervous system (CNS) tissue

and spinal ganglia.1 The discovery of BSE in Canada and

the USA, where consumption of brain and other viscera

was allowed until 2003, and of secondary cases of variant

Creutzfeldt-Jakob disease (vCJD) in the UK, possibly

attributable to contaminated blood donated by people

with pre-clinical primary infection, reinforces the need

for an experimental assessment of the risk of oral

exposure to BSE. We therefore investigated oral

transmission of BSE to non-human primates.

We chose cynomolgus macaques for the study because

these old-world monkeys have a digestive physiology

similar to that of human beings, are methionine

homozygous at codon 129 of the PRNP gene, and have a

BSE neuropathology similar to that of vCJD.2,3 We gave

two 4-year-old adult macaques a 5 g oral dose of brain

homogenate from a BSE-affected cow. We tested for

proteinase-resistant prion protein (PrPres) in this

homogenate with a commercial BSE-testing ELISA kit

(Bio-Rad, Marnes-la-Coquette, France). A sample of the

100% homogenate brain paste inoculum that was fed to

the primates was rehomogenised at 20% weight-pervolume

in the kit buffer. Serial dilutions were made with

a pool of 20% weight-per-volume BSE-negative brain

homogenate in the same buffer. Testing was done

according to the manufacturer's instructions and results

were con.rmed by a western blot test (Bio-Rad) with a

similar process of PrPres dilution. With both methods,

dilutions of up to 1 in 300 provided a positive signal

(.gure A).

One macaque developed neurological disease

60 months after exposure and was killed at 63 months

because of recumbency. Histopathological examination

of the brain of this animal showed the typical pathology

of vCJD (.gure B) and an accumulation of PrPres

associated with the follicular dendritic cells in tonsils

(.gure C), spleen, and intestine. A western blot showed

similar patterns of PrPres in a brain sample from the

macaque and the BSE-infected bovine inoculum

(.gure D). The other macaque remained free of clinical

signs 76 months after exposure, and a tonsil biopsy done

at 72 months was negative (.gure E).

In a previous study, two macaques orally dosed with

5 g of brain from a macaque with terminal clinical BSE

became ill after 44 and 47 months.4 The results of the

present study suggest that the incubation period for

interspecies transmission of BSE can be considerably

Published online

January 27, 2005

http://image.thelancet.com/

extras/05let1056web.pdf

Commissariat à l'Energie

Atomique/Direction des

Sciences du Vivant/Départment

de Recherche Médicale,

18 Route du Panorama, 92265

Fontenay-aux-Roses, France

(C I Lasmézas DrMedVet,

E Comoy DrMedVet,

C Herzog DipBiol,

F Mouthon DipBiol, F Auvré,

E Correia,

N Lescoutra-Etchegaray DipBiol,

Prof N Salès PhD, J-P Deslys MD);

Veterinary Laboratories

Agency, New Haw, Addlestone,

UK (S Hawkins MIBiol,

T Konold DrMedVet,

G Wells BVetMed); and 7815

Exeter Road, Bethesda, MD

20814, USA (P Brown PhD)

Correspondence to:

Dr Jean-Philippe Deslys

e-mail: jpdeslys@cea.fr

www.thelancet.com Published online January 27, 2005 http://image.thelancet.com/extras/05let1056web.pdf 1

Risk of oral infection with bovine spongiform

encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,

Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys

The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant

Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the ef.ciency of oral infection

and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral

transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a

BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the

other remained free of disease at 76 months. On the basis of these .ndings and data from other studies, we made a

preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public

health measures can prevent transmission of BSE to man.

B

C

E

A

Dilution

D

3·215

1·989

0·984

0·302

0·131

0·065

0·052

1/10

1/30

1/100

1/300

1/1000

1/3000

Neg

36 kDa

36 kDa

22 kDa

22 kDa

16 kDa

1 2 3 4

ELISA detection of PrPres (absorbance units)

Figure: PrPres content of brain homogenate and histopathological assessment of macaque tissues

(A) Results of in-vitro testing for PrPres in BSE-infected inoculum by ELISA and western blot. Neg=normal bovine

brain material. (B) Typical .orid plaque in the occipital cortex of the macaque that developed disease.

PrPres detected by proteinase K treatment with SAF32 anti PrP monoclonal antibody (kindly provided by Jacques

Grassi, CEA Saclay). The dense core of PrPres is surrounded by several vacuoles in a .brillar proteinaceous corona;

bar=10 m. (C) Positive PrPres staining in tonsil (80% of follicules stained positive) of the macaque that developed

disease; bar=50 m. (E) Negative PrPres staining in tonsil of the macaque that did not develop disease; bar=50 m.

(D) Western blot showing similar PrPres patterns in samples from a patient with vCJD (lane 1), the macaque that

developed disease (lane 3), and the bovine BSE inoculum (lane 4). By contrast, a macaque inoculated intracerebrally

with material from a patient with sporadic CJD showed a different PrPres pattern (lane 2).

For personal use. Only reproduce with permission from Elsevier Ltd

Research Letters

longer than that of intraspecies transmission (60 months

vs 44 and 47 months, representing 36% and 28%

increases, respectively). The interval between the period of

peak exposure to infectious BSE tissue and the hitherto

peak incidence of vCJD is about 10–15 years, but

incubation periods of up to 40 years have followed oral

infection with kuru between human beings.5 Therefore,

maximum incubation periods might exceed 50 years in

cases of oral transmission of BSE from cattle to man.

The present data do not provide a de.nitive minimum

infective dose for transmission of cattle BSE to primates,

but they do give enough information for a preliminary

assessment of the adequacy of existing measures to

protect the human food chain. Results of ongoing

experiments provide a rough estimation of the intraspecies

transmission rates in cattle. The BSE brain

inoculum to which the cattle were exposed had an

infectivity titre of 103·5 mouse infectious (intracerebral

and intraperitoneal) units ID50 per g (ID50 is the dose at

which 50% of animals become infected). Interim results

at 6 years after exposure suggest that the oral ID50 in

cattle may be between 100 mg and 1 g (table 1; S A C

Hawkins, T Konold, G A H Wells, unpublished data).

Since the brain of a cow weighs 500 g and a spinal cord

200 g, CNS tissues from a cow with clinical signs of BSE

could contain enough infective agent to transmit disease

orally to 490–1400 cows (70% of 700 g if 1g is needed, or

20% of 700 g if 100 mg is suf.cient), or to 70 primates

(50% of 700 g if 5 g represents the oral ID50).

The accuracy of estimates of the oral ID50 for man will

not be improved until completion, several years from

now, of a large dose-response European study (QLK1-

2002-01096) in macaques, in which the minimum dose

is 50 mg. However, because similar inocula were used in

both the cattle and macaque studies,6 a tentative comparison

can be made between the ef.ciency of oral infection

in cattle and that in primates. On this basis, a factor of

7–20 could be considered as the range of magnitude of a

bovine-to-primate species barrier for oral BSE infection

(70 primates infected compared with 490 or 1400 cows,

with a similar dose).

Elimination from the human food chain of CNS

tissues from cows with clinical BSE is estimated to have

reduced the risk of human exposure to the disease by

about 90%.7 Risk was further reduced in continental

Europe by systematic screening for the diagnostic

presence of PrPres in the brainstem of all cattle older than

30 months, and in the UK by the total interdiction of

cows older than 30 months. In an oral exposure study to

assess the pathogenesis of BSE in cattle, in which the

same European Union-evaluated test as we used in the

present study was applied to CNS tissues, some

preclinical cases of the disease were diagnosed.8

Using the same test, pooled brainstem from cows with

clinical BSE has yielded a endpoint titre of PrPres

corresponding to a 1-in-300 to 1-in-1000 dilution of

positive brainstem.6,9 If people were to eat CNS tissues

from a cow with preclinical BSE with a concentration of

PrPres just below the test detection limit of 1 in 300, they

would need to ingest at least 1·5 kg to reach the degree

of exposure equivalent to that in the 5 g of brain used for

oral transmission to the macaque in the present study. If

the oral ID50 for man was one log below this dose (ie,

similar to that in cattle, and not accounting for any

species barrier between cattle and man; see table), 150 g

of CNS tissue that tested falsely negative could represent

an infective dose. Because use of cattle brain and spinal

cord for human consumption is prohibited, and in view

of the existing mechanically recovered meat regulations,

a person would be very unlikely to ingest this amount of

cattle CNS tissue.

The minimum sensitivity of screening tests to detect

100% of BSE-infected animals has yet to be ascertained.

However, our results provide reassurance that BSE

screening procedures combined with CNS removal are

effective measures to protect the human food chain.

Contributors

J-P Deslys, C Lasmézas, and E Comoy were responsible for design and

management of this study. G Wells, S Hawkins, and T Konold were

responsible for the pathogenesis study in ruminants. C Lasmézas,

C Herzog, and N Lescoutra-Etchegaray were in charge of the primate

experiments. F Auvré undertook the biochemical analyses. N Salès was

responsible for the immunohistochemical analyses, which were done

by E Correia. C Lasmézas, E Comoy, F Mouthon, G Wells, P Brown, and

J-P Deslys drafted the manuscript.

Con.ict of interest statement

Commissariat à l'Energie Atomique owns a patent covering the BSE

diagnostic test commercialised by Bio-Rad. All authors had full access to

all data and had responsibility to submit for publication. The funding

sources had no role in the collection, analysis, and interpretation of

data, writing of the report, or decision to submit the paper for

publication.

2 www.thelancet.com Published online January 27, 2005 http://image.thelancet.com/extras/05let1056web.pdf

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the .rst positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Research Letters

Acknowledgments

We gratefully acknowledge the expert care of the primate animals

provided by René Rioux, Sébastien Jacquin, and Anthony Fort, and the

technical expertise of Dominique Marcé, Capucine Dehen,

Sophie Freire, and Aurore Jolit Charbonnier. This work has received

.nancial support from the French Ministry of Research (GIS Prion). It is

now continued within the framework of the EU consortium QLK1-2002-

01096 and the European network of Excellence NeuroPrion. Ongoing

studies by the Veterinary Laboratories Agency in cattle are funded by the

UK Department for Environment, Food, and Rural Affairs.

References

1Anderson RM, Donnelly CA, Ferguson NM, et al. Transmission

dynamics and epidemiology of BSE in British cattle. Nature 1996;

382: 779–88.

2 Lasmézas CI, Deslys JP, Demaimay R, et al. BSE transmission to

macaques. Nature 1996; 381: 743–44.

3 Lasmézas CI, Fournier JG, Nouvel V, et al. Adaptation of the bovine

spongiform encephalopathy agent to primates and comparison with

Creutzfeldt-Jakob disease: implications for human health. Proc Natl

Acad Sci USA 2001; 98: 4142–47.

4 Herzog C, Salès N, Etchegaray N, et al. Tissue distribution of bovine

spongiform encephalopathy agent in primates after intravenous or

oral infection. Lancet 2004; 363: 422–28.

5 Klitzman RL, Alpers MP, Gajdusek DC. The natural incubation

period of kuru and the episodes of transmission in three clusters of

patients. Neuroepidemiol 1984; 3: 3–20.

6 Deslys JP, Comoy E, Hawkins S, et al. Screening slaughtered cattle

for BSE. Nature 2001; 409: 476–78.

7 European Commission. Opinion of the Scienti.c Steering

Committee on the Human Exposure Risk via food with respect to

BSE. Adopted on 10 December 1999. http://europa.eu.int./comm/

food/fs/sc/ssc/out67_en.pdf (accessed Jan 17, 2004).

8 Grassi J, Comoy E, Simon S, et al. Rapid test for the preclinical

postmortem diagnosis of BSE in central nervous system tissue.

Vet Rec 2001; 149: 577–82.

9 Moynagh J, Schimmel H. Tests for BSE evaluated. Bovine

spongiform encephalopathy. Nature 1999; 400: 105.

www.thelancet.com Published online January 27, 2005 http://image.thelancet.com/extras/05let1056web.pdf 3



mark purdey wrote;


How do you explain the emergence of BSE farms that never fed any meat and bone meal in any of its various guises ? I could take you to many such farms around me .


TSS WRITES;

please do. show us the data. were there ever sheep and goats there?
was there ever tainted feed there? history of these cattle from birth to date?
history of these farm feeding practices please? please show us the data?


mark purdey wrote;


These and many other flaws that have been cited in the official feed theory and recorded in my publications, clearly indicate that the meat and bone meal theory is discredited.


TSS WRITES;

this is totally false. the many transmission studies do not lie.
amplification and transmission. the feed theory as you call it is NOT a theory.
it is fact, proven time and time again. the 44 tons or so of UK mbm the USA
imported into the USA was a small amount compared to other BSE docoumented
countries. but this does not really matter if you consider the USAs own history
of TSE and the feeding of TSE tainted rendered products back to animals for
human consumption. ...TSS


mark purdey wrote;



Here in the UK , honest vets and farmers will openly admit that the meat and bone meal theory served as a convenient cover story that was exploited in order to show the world that British beef was now safe because the feed that was supposedly responsible had been banned.

So the theory was used as a politically and commercially convenient cover story . However, once other countries were forced into the BSE battlefield because of BSE breakdowns in their own herds, the momentum of this myth simply kept on rolling to such an extent that the bureaucracies and government depts could never back out of it .

So, in respect of my own first hand experience of BSE here in the UK, I have to say that anybody who promotes this THEORY on the cause of TSEs is merely thwarting the healthy and productive evolution of TSE science.

Why can't we admit to the flaws and the political lies, and simply get on with looking for the truth .

My research may well be objectionable to certain people or vested interests because it does not suit their particular agenda or whatever, but, the bottom line is that I am in pursuit of the truth. Whether I am talking about nerve agent dumping in the UK seas, or crashed japanese bombers in the territories of the New Quinea Fore tribe , or scrapie clusters in sheep grazing former military controlled firing ranges, I am speaking from first hand experience , having personally visited these areas, interviewed the people involved , collected analytical evidence . I have photos , documentation, data , video as proof. Nobody can take these first hand experiences away from me. Whether you listen, that's up to you. I am just carrying on with my research.


TSS wrote;

transmission, transmission, transmission, and your OP theory does not transmit. amplification and transmission! this has well been proven via MBM time and time again. good luck on the origin of TSE anyway. i wish you the best, but in finding the origin, this will NOT stop the agent from spreading. you have to stop it at its source i.e. the feeding of tainted ruminant protein to animals for human/animal consumption for one. secondary transmission via the surgical and medical arenas, and other modes of transmission will also play a crutial roll in the spreading of TSEs. these must be stopped in there tracks too. these early transmission studies are but a few of many more. the later transmission studies (posted here on this list for those interested in the transmission of these TSEs) the more recent ones are from much less tainted materials than originally thought to infect a species. science is still in the very early days of TSE research. there are many unanswered questions still left to answer. but to flagrantly ignore the transmission studies, will only allow this agent to further spread, expose, and kill. ... TSS


EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Scientific Steering Committee
OPINION ON
ORGANOPHOSPHATE (OP) POISONING AND
HYPOTHETICAL INVOLVEMENT IN THE ORIGIN OF BSE
Background
In its opinion on possible links between BSE and Organophosphates adopted on 25-26 June
1998 and in its opinion on Hypotheses on the origin and transmission of BSE adopted on 29-
30 November 2001 the SSC concluded that there is no scientific evidence in support of the
hypothesis of an OP origin of BSE.
The issue of organophosphate poisoning has not been dealt with by the SSC so far. The
concerns expressed in the enquiries cover mainly intoxication by occupational exposure of
shepherds and farmers to OPs upon use against ecto-parasites, especially in sheep dipping and
treatment of cattle against Warble Fly infestation. Risks from residues are addressed to a
lesser extend.
In early 2003, a large number of additional enquiries on the issue have been addressed to
European Commission's Health and Consumer Directorate General. Four of these with
substantial enclosures were by one person. Most of them are addressing both issues: chronic
organophosphate (OP) poisoning and the origin of BSE.
Information provided with the enquiries
In addition to numerous newspaper and magazine articles the enclosures to the enquiries
provide the Material Safety Data Sheet on diazinon, the OHSA Occupational Safety and
Health Guideline for Tetraethylpyrophosphate (TEPP), an US agency Hazardous Substances
Fact Sheet on crufomate, company safety information sheets, some correspondence with UK
authorities including their activities to improve safe use of these chemicals. The information
regarding claimed OP chronic poisoning of cases presented does not provide evidence, neither
for OPs being the cause for diseases nor for their exclusion (i.e., "very low" bloodcholinesterase
levels, provided without data or comparison with the normal distribution of
values; successful treatment of a patient for OP clearance without giving any OP data). It
C:\WINNT\Temporary Internet Files\SSC_Last_OP_Final.doc 2
seems however, that due to insufficient, non-prudent use of the safety requirements undue
exposures of shepherds and farmers have occurred.
There is no additional information on the claimed involvement of OPs in the origin of BSE.
This applies for both, the hypotheses on the direct effect of OPs as well as on their
hypothetical role for Cu-deficiency to be involved in the origin of BSE (Cu binding of prion
protein is known). New publications are mentioned in one enquiry but they have not yet been
provided. In an Internet search no recent scientifically valid publications were traceable. The
SSC had been informed that research would be launched on this hypothesis, but no
information has been provided so far on its status or on results.
Conclusions
a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines – addressed in the enquiries – provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf


TSS

 

[flounder]

Sunday, October 16, 2005 10:48 AM


Also, what is your take on this theory?


i have always tried to stay neutral, because i just do not know, nor does anyone else, the 'origin' of the 'agent'. this is what i have most always called 'tse agent' as opposed to the 'prion disease'. i have never concentrated my efforts on the origin. my efforts have always been ''amplification and transmission'', this we know and have known for decades. its been well documented, but corporate interests have kept any substantial strict regulations/guidelines/enforcement from coming about. from the cattle industry, sheep, deer and elk industry, feed industry, pharmaceutical industry, surgical/medical industry, cosmetic industry, nutritional supplements industry, etc. they all are and have been involved with this campaign to make the regulations the most 'industry friendly' as possible. the incubation period of this agent is what has allowed this to happen, and the fact that very few are documented (human TSE), due to lack of credible surveillance and very few elderly demented are autopsied. the cards are and have been stacked heavily against us. i bench about GW alot, and this administration _has_ been more blatant about secrecy and have been _caught_ more about lying about feed bans and triple firewalls etc, but let us face the facts, it's been going on for decades. The harvest that you reap depends on the kind of seeds you sow. If you sow corn, you reap a bountiful harvest, if you sow mad cow disease (i.e. human/animal TSEs) via a multitude of routes, sources and strains, due to nothing more than greed, and through that greed you go against all of Gods giving's from an industry so fraught with greed i.e. the rendering industry and factory farming (hence, i am still a meat eater, kinda) then you reap Gods wrath. This is the basic nature of God's Justice: "YOU REAP WHAT YOU SOW" ! it's been around for thousands of years. amen.

hallelujah, it's Sunday morning and i'm sounding like a preacher now. frightening isn't it ;-) ... with kindest regards, terry/TSS