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A few words for flounder to ponder

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rkaiser

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A Comment from Mark Purdey on the latest press release on BSE origins
A Lyddite or Luddite's view on the origins of mad cow?

I was appalled to see such sensationalist mass media hype scare=mongering the world still further adrift from the truth about the origins of BSE. This time, it centres upon the same old scientific clique of un-intelligentsia and how their tale of a few odd human bones from the Indian out-backs had leaked into UK cattle feed, thereby causing BSE. Yet, there is no scientific data to support this hypothesis. The one time astute BBC science reporter, Susan Watts, who has launched this latest scandal, should be ashamed of herself.

At the centre of this BSE melodrama is Dr Colchester, renowned for his earlier attempts to pin a cluster of five cases of vCJD in the Kent countryside onto a supply of drinking water that had allegedly become contaminated by waste water from a meat rendering factory. But in a balanced and rational scientific forum, you would have thought that this expert would have been instantly discredited on the basis that only one of the five vCJD cases involved had actually lived in this water catchments area and therefore been drinking water from the particular supply under the spotlight. Furthermore the whole assertion of water contamination by this rendering plant has never been substantiated , since the company involved had merely been draining their run off water into a ditch which had no linkage to the relevant water course.

On the BBC News-Night piece last night, Prof John Collinge was the only expert to make a sensible comment on this latest issue. "How could BSE have been transmitted from India to the UK through cattle feed when there have never been any cases of new strain TSE recorded on the Indian continent?"

Even more mysterious was the fact that nobody has picked up on the true relevance of the other press release put out by Texas Uni last week - that the use of sound waves on living tissues will determine whether a person's prion protein is primed for BSE or not. Although widely aired on the BBC news, nobody had connected this lab observation to my 4x published field research studies carried out in every cluster zone of TSE across the world - which concluded that exposures to sonic shock waves will activate the metal micro-crystallised piezoelectic prion contaminants in mammalian brain, unleashing a deadly cascade of electric shocks into surrounding tissues - literally burning out the so called spongiform holes in the brain. This is founded upon the elementary laws of physics and the properties of piezoelectric materials such as lyddite; the common component of the chemical detonators found in the TSE cluster areas Funnily enough, it was 'lyddite' that was first developed at the UK's military test ranges at Lydd in Kent - a mere five miles upwind from where the previously aforementioned Kent cluster of vCJD erupted. (See: Table Fig:2)

The fact that every cluster of TSE in the world is located around sites where piezoelectric micro-crystal contaminants {used as detonators} have leaked as a result of local activities with military munitions should not be ignored. Since TSE clusters and Munition sites are both rare phenomena, then the persistent occurrence of these two phenomena in the precise same region has got to offer more than a mere coincidence.

Thousands of tons of chemical munitions and detonators were mass manufactured at Ordnance factories like the Queniborough depot in Leicestershire - half a mile distant from the world's largest cluster of vCJD. Since these bombs were never dropped on Germany during world war two, boatloads of the unused munition were dumped into the North and Irish seas around the UK coastline . Decades later the metal canisters corroded , contaminating the whole marine food chain . It was the fish meal sourced from these metal micro-crystal contaminated seas which was fed to the British dairy herd, causing the massive epidemic of BSE.

Furthermore, These micro-crystals are heat resistant, transmissible and will produce a progressive pathogenesis once implanted into living tissue . They therefore fulfil all of the idiosyncratic prerequisites of the mysterious TSE causal agent, which no other bacterial (tuberculosis, etc.) or protein only causal theory has previously achieved.

And it's not only the lab work from Texas Uni that has lent strong support to my research data and hypothesis . Auburn Uni have shown that once these metal micro-crystals contaminate tissues, they do indeed seed the growth of the rogue metal prion protein crystal fibrils which cause BSE.

I find it absolutely incredible that our UK government and scientific Institutions are prepared to put the full force of public money behind a full scale funding of this 'kitched-up' kindergarten scare story on human remains causing BSE, whilst they continue to blindly ignore the well proven, widely published true cause of TSEs. We live in retrograde times.



Table - Fig:2

Ref.
Location
Date
TSE type
Munitions connection
Sonic Source

USA

[92]
Tucson, AZ.
1978
CJD cluster
Missile factory workers
Workshop tests

[93]
Fort Collins, CO.
1968
CWD cluster in wild/ captive deer
Missile silos, Rocky Flats nuclear munitions factory leak, munition incineration in Lyons cement kiln and 11 million galls of nerve agent at Rocky Mountain Arsenal
Quarry explosions,

Rifle shooting, LF jets, Front range tectonic fault line.

[94]
Mt Horeb, WI
2000
CWD cluster in wild deer
Clean up/incineration of munitions at Badger Ammunition Plant in 1999 [97], Hercules flight path
Explosions for new road, Rifle shooting, Quake epicentre, LF jets

[95]
Kimball, NE.
2000
CWD cluster in wild deer
Incineration of Badger Munitions at Kimball incinerator in 1999 [97],

Missile silos.
LF jets, rifle shooting.

[94]
White Sands Missile Range, NM.
2000
CWD cluster in wild deer
Missile and bomb testing range.
Missile explosions.

[98]
Mission, TX.
1960s
Scrapie cluster
Former military airbase (WW2). Bomb storage.
Under former take off flight path.

[27]
Garden State, NJ
1990s
sCJD cluster
Fort Dix military Camp, MacGuire airbase.
LF jets, Gun and shell explosions

[27]
Mabton, WA
2004
1st US BSE
Hanford Nuclear weapons Plant, Yakima Military training camp, Othello airbase.
LF jets, Shell explosions.

[27]
Spokane, WA.
2004
1st US vCJD
Hanford Nuclear weapons Plant, Yakima Military training camp, Othello airbase.
LF jets, Shell explosions

CANADA

[27]
Nameo, AL
2001
1st Canadian CWD captive deer
Nameo Military airbase
Under take off flight path

[27]
Leduc, AL
2003
1st US BSE cow reared here
Leduc International Airport – mainly civilian
Under take off flight path

[27]
Tulliby Lake, AL
2003
1st Canadian BSE
Cold Lake Airbase and air weapons / cruise missile test range.
Under LF jet practise circuit/ Hercules flight path

[27]
Hillmond, SA
2002
CWD cluster in farmed elk
Fall out from Cold Lake air weapons test range.
Under Lloydminster airport take off path / Hercules Flight path. Gas well pumping.

[27]
Manitou, SA
2002
CWD cluster in wild deer
Camp wainwright tank shelling range. Detonation / incineration of waste munitions , chemical munitions [99]
Tank shelling, Manitou rifle shooting range.

[27]
Between Lloydminster and Saskatoon, SA.
2002
1st vCJD
Fall out from Camp Wainwright / Cold Lake air weapons range
LF jets, Munition explosions.

United Kingdom

[3]
Burnham-on-Sea, Somerset
2000
vCJD cases
Puriton Ordnance Factory,

Former WW2 airbase.
LF military jets

[3]
Armthorpe, nr Doncaster

2000
vCJD cluster
RAF Finningley
LF military jets [101] flight path, Concorde visits

[54]
Queniborough, Leicestershire
1996
vCJD cluster
Queniborough ordnance depot [55], WW2 Bomber crash [100]
LF military jets, Kegworth International airport flightpath, Concorde visits

[3]
Villages north of Tenby, South Wales.
2000
vCJD cluster
Castlemartin and Pendine Sands tank shelling / bomb test ranges
LF military jets

[3]
SW Lancashire
1999
vCJD cases
Chorley Ordnance Factory / munition incinerator [63]
LF military jets

[3]
Sunderland area
1998
vCJD cases
Cokeworks munition incinerator.[63]
?

[3]
Lympstone, Devon
2000
vCJD cases
Lympstone marine camp
LF aircraft flight path (Exeter airport), Concorde visits.

[3]
Eastleigh, Southampton.
1998
vCJD cases
Eastleigh works Munition factory,.
LF aircraft flightpath, (Southampton airport).

[3]
E Chinnock / Stoke, Somerset
1992
sCJD cluster
Yeovilton Naval airbase
LF military jets

[7]
Villages west of Ashford, Kent.
1996
vCJD cluster
Local woodlands used as chemical / conventional bomb depots in WW2. Lydd military explosive range.

WW2 Bomber /USAF airbases at Headcorn / High Halden. WW2 Bomb Alley [65]
Lydd military explosive range,

LF military jets,

Flightpaths into Heathrow airport and local Headcorn airport [66]

[102]
Villages north of Woodbridge, Suffolk.
1975
sCJD cluster
Orfordness nuclear / conventional bomb factories.

Bomber airbase and crash landing in Parham village
LF military jet flightpath

Weston Longeville
1998
vCJD case
W Longeville US bomber base / bomber crash site [67]

WW2 munition stores
LF military jets

FAR EAST

[96]
Guam
2002
CJD case
WW2 chemical munitions buried in victim’s land
LF military jets, tropical storms, earthquake tectonic fault lines

[74]
Highlands of New Guinea
1950s
Kuru cluster
WW2 US Bomber crashes / exploding bombs
Bomb explosions, thunderstorm belt, earthquake tectonic fault line


[3]
Obhiro, Hokkaido, Japan
1950s
Scrapie cluster
WW2 army weapons test range
?

[50]
Fuji valley, Japan
1950s
s/familial CJD cluster
Munitions / film factories, aluminum alloy factories,
Volcanic / earthquake belt

ITALY

[103]
Parma region, Italy
1975
sCJD cluster
Munitions factory
?

[53]
Ragusa, Sicily
2000
BSE cases
Comiso USAF airbase. Nuclear cruise missile base [76]
LF jet flight path

[53]
Trapani , Sicily
1998
BSE cases
Trapani Bergi NATO airbase [76]
LF jet / stealth jet flight path

[53]
Menfi , Sicily
2001
vCJD case
Sciacca WW2 Bomber Airbase. Intense bombing.
LF jets / Quarry explosions.

[52]
Aspromonte, Calabria
1990
S/familial CJD clusters
Ordnance / nuclear waste dumping. Explosions.
LF jets, Explosions, Earthquake tectonic fault line

[48]
Barbagia Monte,

Sardinia.
1995
Scrapie clusters
Ordnance / toxic waste dumping
LF jets, Quarry explosions

[48]
Assemini, Sardinia
1999
Scrapie cluster
Decimmannu NATO airbase
LF military and civilian jet flight paths

[53]
Arborea, Sardinia
2001
1st BSE case
Capo de Frasco air weapons test range
LF jet practice circuit / explosions


FIGURE 2; KEY TSE CLUSTERS AROUND THE WORLD AND THEIR SPATIAL-TEMPORAL ASSOCIATION WITH LOCATIONS WHERE MILITARY MUNITIONS HAVE BEEN MANUFACTURED, TESTED, STORED, INCINERATED, DUMPED, etc.
(LF jets = low fly jets )
 

adventureman

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bse tester, reader the second, any comments on this? Anyone else, got something to say about it?

Personally I don't think prions are the real cause of TSE's just an effect. Some erie coincidences shown though.
________
GM LS engine history
 

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R2, I see you're back. Hope you didn't work too hard while you where gone.

Your attempts, once again, to discredit the honorable work of Mark Purdey, never ceases to amaze me.

You stated:
Relating this to the Concorde and BSE is silly silly silly.

Dr. Soto's cyclical amplification procedure:
"In this procedure, conceptually analogous to polymerase chain reaction cycling, aggregates formed when PrPSc is incubated with PrPC are disrupted by sonication to generate multiple smaller units for the continued formation of new PrPSc. "

This directly links to the Rocky Mountain Labs/NIH "Most Infectious Prions" paper which showed that prion aggregates of a very specific size were required to scavenge or induce other proteins into their aggregates.

It also exemplifies Dr. H. Kretschmar's paper which states:

"We achieved approximately 200,000-fold PrPres amplification by PMCA. In contrast, although initial amplification was comparable to PMCA reactions, PrPres levels quickly dropped below detection limit when samples were not subjected to ultrasound. These results indicate that aggregate breakage is essential for efficient autocatalytic amplification of misfolded prion protein and suggest an important role of aggregate breakage in prion propagation."

Mark Purdey's hypothesis has many aspects to it which may influence the formation of prions, and also which may cause prion plaques, (which many scientists now view as our brain's protection mechanism), to break apart into the fragments which are capable of inducing further malformation of proteins (altering of their tertiary structure).

Dr. Vodyanoy has gone that one step further, and analysed healthy blood samples from various mammals and sharks. He has shown in his newly released paper "Novel Metal Clusters Isolated from Blood are Lethal to Cancer Cells" - that proteon nucleating centers (PNCs) consisting of metallic nanoparticles capture hemoglobin, or fragments thereof, in the absence of haptoglobulin which normally does this job. In Vodyanoy's study, he exposed healthy blood PNCs to various cultured cancer cells. They killed 90% of the R98 glioma cells and 75% of the RG2 glioma cells, while having only a small affect on non-cancerous cells (25%).

The important thing now is to look at the blood of the individuals and animals that are ill with these neurological diseases, and determine what kinds of PNCs are present within their blood. It is highly possible that other metals which form these nanoclusters are also scavenging hemoglobin but because they are capable of being ferromagnetic; these PNCs when combined with the iron in hemoglobin produce a catalyst/seed which inititates various prion formations.

To say that Mark Purdey's work is laughable, truely shows your bias against him. Your inability to have an open mind to his and other's findings which have not been tested, or not yet fully tested, reveals your true motive, which is to discredit his work at all costs, even when it makes you look laughable.

However, this is no laughing matter! It is about time the papered doctors/researchers give credit where credit is due.

Dr. Stanley Prusiner has been patenting methods of isolating prions using the principles first brought forth by Mark Purdey. Using phosphotungstate acid on magnetic beads to bind prion aggregates from blood, and brain homogenate samples. Mark is aware of Dr. Prusiner's requests to the medical journals in which he (Mark) has been published, for reprints of Mark's articles.

Laugh all you want R2. While you are busy giggling about how to discredit Purdey's work, hundreds of scientists are taking it very seriously and utilizing the data put forth in his multiple peer-reviewed publications, including Dr. S.B. Prusiner (check out "Selective Precipitation of Prions by Polyoxometalate Complexes, by Prusiner, JR Long and JG Safar, University of California, Berkeley).
 

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Reader (the Second) wrote:

I agree that there are environmental triggers involved but as I have said before, Purdey adds more variables to his theory of BSE / vCJD causitivity each time his theory fails to fit the facts. First insecticides, then manganese, then all heavy metals, then supersonic jets, and so on. It becomes laughable at some point as the pursuance of a scientific hypothesis.


The work being done by Purdey is still somewhat in its infancy relative to conclusive evidence, but that is not a reason to dismiss it out of hand. His hypothesis regarding metals and their effect on cells and to the formation of rogue prions is intersting and may have some serious grounds for further study. My position is simply this - I do not dismiss the work of anyone who is dedicated to their field. Mark Purdey is certainly dedicated to the quest with respect to prion disease, as is Prusiner and others. I take all studies as a potentially viable source of research and until such times as it is proven either factual, workable and reasonable it should be regarded as something that may or may not hold valuable potential, regardless of who is behind it. Even the crackpots of our time have prven that the world was indeed not flat and that where the map read "there be monsters here," only peacocks and rainbows were to be found. All I am saying is, keep an open mind because if it is even slightly closed, that most precious ideas which often come from the ramblings of those we consider to be unworthy of our attention, may not be allowed to enter in and that in itself would be a shame because they may hold the key to our future understanding of this disease.
 

rkaiser

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Welcome back reader, we missed you!

It was I who talked of veterinarians clapping their hands to distinguish initial POTENTIAL BSE cases in the UK. It happened, but it certainly was not any kind of difinitive experiment. Lots of BSE cases in the UK reader, and the vets used some unorthadox methods when they first walked on to the farms.

Your explaination of hypersensation in a neurological problematic brain is right on the money. Is BSE not a neurological problem?
 

bse-tester

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Thousands of tons of chemical munitions and detonators were mass manufactured at Ordnance factories like the Queniborough depot in Leicestershire - half a mile distant from the world's largest cluster of vCJD. Since these bombs were never dropped on Germany during world war two, boatloads of the unused munition were dumped into the North and Irish seas around the UK coastline . Decades later the metal canisters corroded , contaminating the whole marine food chain . It was the fish meal sourced from these metal micro-crystal contaminated seas which was fed to the British dairy herd, causing the massive epidemic of BSE.

Can you prove this hypothesis? It is one thing to state or quote something that someone has thought up and then attempt to show it as being true, but to actually suggest that the cause of the UK epidemic was fish meal relating to the coastal areas of the North and Irish seas is a bit of a stretch Randy. The British Government was one of the few wartime Governments that did not actively engage in bombing others with chemical weapons, let alone fill their fisheries with unexploded chemical weapons. Also, as a young lad who grew up in England right after the end of the second war, and one having a Father who served in the Royal Navy and myself in the Royal Engineers, I can tell you that the entire southern coast of England, the entire southern section of the coastline of the North Sea and the French and Dutch coastlines are still considered to be somewhat dangerous due to the immense amounts of unexploded ordnance that can be found at low tide throughout those areas. At Selsey Bill, in southern UK, we used to collect everything imaginable up to and including 4" cannon shells and more hand-grenades than I care to mention. Also, huge quantities of bullets can still be harvested at low tide there to this day in the mud-flats. But to relate all of this to being the cause of BSE is any way is one giant leap into the world of fantasy unless, and I stress - unless, it has been shown to be possible by virtue of studies that indicate a connection. Can you advise as to how many people make up that so-called "world's largest cluster of vCJD?" Also, can you catagorically state that you know this information to be true or are you simply retelling that which was suggested to have happened? Please do not take this as anything other than a simple request for facts to back up your statements, I am not engaging you in combat here, just asking for clarification. By the way, in my discussions with Prof. John Collinge, National Hospital, London, we are hopeful he may join us in conducting a British-based validation of our test protocol for CJD.
 

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I think that Mark sometimes emphasizes a point too strongly, without conclusive evidence. However, I do believe he is trying to point out that this Lyddite/and other explosive detonators are a common denominator found in every cluster of vCJD.

The fact that he hasn't the cash to prove his hypothesis, should not stop us from trying to understand the possible connection.

I believe there is no doubt that the use of Phosmet in the UK dramatically increased the incidence of BSE - did it cause it? If the cause of a disease is dependent upon several situations coming together at the same time, how can you say any one thing alone caused it.

If Mark has printed info. regarding the dumping of lyddite, or other ammunitions sites, I assure you, he has the evidence to support his comments. If you want to discuss this evidence, then I suggest you contact him directly through his webpage www.markpurdey.com or www.purdeyenvironment.com, where you'll find his email address.

The beginnings of this "infectious" hypothesis came from one man, Stanley Prusiner, yet when he was questioned for his still unproven hypothesis, the scientific community was put in their place and the train headed down this new road, pouring billions into the infectious theory.

The answer to these neurological diseases will only come from people with open minds, who are willing to look at all of the evidence presented. Expressing your concern over someone adding to his hypothesis, frightens me. I would hope that when the evidence becomes more clear, no matter what the scientific field, that the researchers will be willing to change their positions and expand their views. Narrow tunnel vision will not bring us to the truth.

Some people would say that the absence of testing some of Purdey's theories, is evidence in itself. Research can be done more than one way. You don't just go out to prove something, sometimes you have to disprove it. With all the billions of dollars spent on prion science, no one is working to directly disprove Purdey.
 

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Funny R2 should mention ulcers being caused by bacteria.

This is what we are now told. And when my neighbor almost died this July of a perforated ulcer, he stated, this same thing - the bad bacteria in his gut ate several holes in his stomach. He also admits to taking massive amounts of anti-inflammatories. Did the anti-inflammatories contribute to the rapid growth of the bad bacteria?

The docs want us to believe they don't; yet this is what Vioxx was produced for - to be less damaging on the stomach.

The chicken or the egg question? But common sense would tell us not to abuse anti-inflammatories.
 

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It is explained huh! Jeez TimH, I thought you had left us for some other board? But I see you are back here so, welcome, and hey, try to play nice in the pool with the rest of the children. Ever been to England TimH? I somehow doubt it.
 

bse-tester

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The beginnings of this "infectious" hypothesis came from one man, Stanley Prusiner, yet when he was questioned for his still unproven hypothesis, the scientific community was put in their place and the train headed down this new road, pouring billions into the infectious theory.


Kathy, Prusiner is not the origin of the "Infectious Theory." This was given credence back in the mid-70's by a young man working for the Ministry of Food and Fisheries [MAFF], UK,. A man by the name of Dr. Harash Narang. Records will support the fact that he identified PrPsc as an infectious agent that Prusiner later referred to as being a disease of some interest that is devoid of any nucleic acid due to its small size and that it contains only protease-resistant protein as its sole content [Prusiner et al 1982].
 

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bse-tester, Narang may have had earlier remarked on it, but so did Gadjusek. I shall clarify - Prusiner is the American who created hysteria, in the USA.

A quote from his speech to the Food Safety Caucus of the House of Representatives of the United States Congress, January 27, 2004, Prusiner stated:

"Only 25 years ago, I discovered prions and named these unprecedented infectious agents.
"

Maybe we should put Narang and Prusiner in a boxing ring, and see who comes out alive.
 

bse-tester

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Kathy, please do not think that I am one who is pushing Narang to the forefront. The fact that I know Harash very well is not important here, but it is important to note that when he first started with MAFF, way back before Prusiner even thought of giving speeches and patenting this and that at the blink of an eye, Narang had already began his theories regarding prion disease and infectivity of same while he was working with an electron microscope studying fibrils and the effects of the scrapie prion on other tissues. Prusiner came along some years later with his hypothesis and claims and the fact that he was one who liked to publish and speak louder than most in those days doesn't make him the "all-seeing eye" when it comes to prion research. One could argue that Prusiner took many beads of sweat from others who did the work and then glued them all together to form HIS hypothesis. Narang and others who were working for government agencies in the early days were still regarded as humble scientists simply doing that which they were paid to do and along the way, if they made ground-breaking discoveries, it was all part of the daily routine and simply logged with all the other stuff until a later date. I still find it amazing that nobody has publicly challenged Prusiner for his proclaiming himself to be the discoverer of prions.
 

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bse-tester said:
It is explained huh! Jeez TimH, I thought you had left us for some other board? But I see you are back here so, welcome, and hey, try to play nice in the pool with the rest of the children. Ever been to England TimH? I somehow doubt it.

"........ with the rest of the children"???? :???: :???:

There "IT" is again!!!(rearing "IT'S" ugly head) :roll: :roll:

Just WHY would you "somehow doubt" that I have ever been to England??? :???:
 

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Greetings,

a kind greetings from bacliff, Texas, where we dodged a bullet.
90 to100 mph winds here (backyard Galveston bay), but Rita spared us the worst.
i lost most of my shingles on the north side of the house facing the bay.
my and jr stayed here to fend off looters and the wife and another boy and there family
took off to east Texas on 59, and that was another nightmare in itself. highway to hell
more like it. but everybody o.k. here, but just to the east, they were not so lucky and we
pray for them. ...


> A few words for flounder to ponder


nothing to ponder here. transmission studies do not lie and no OPs were used during transmission studies. the feeding of scrapie infected sheep and goats, the feeding of CWD infected deer and elk, the feeding of TSE infected cattle, ALL fed back and forth amongst one another over decades, is what has caused this. you can dream all you want about OPs, but there is no credence in this hypothesis. it is old news, that has been disproven time and time again. show me OPs in these studies? fact is, there were no OPs here, and OPs were not the cause of the amplification and the spreading of this agent. ...


1: J Infect Dis 1980 Aug;142(2):205-8



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



Published online before print March 20, 2001, 10.1073/pnas.041490898
Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,dagger, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas KoppDagger , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce||, Dominique Dormont*, and Jean-Philippe Deslys*

snip...


Discussion

One aim of this study was to determine the risk of secondary transmission to humans of vCJD, which is caused not by a primarily human strain of TSE agent but by the BSE strain having passed the species barrier to humans. This risk is tightly linked to the capacity of the BSE agent to adapt to primates and harbor enhanced virulence (i.e., induce disease after a short incubation period and provoke disease even if highly diluted) and to its pathogenicity after inoculation by the peripheral route. With respect to the latter, there are huge variations between different TSE agent strains and hosts. For example, the BSE agent is pathogenic to pigs after i.c. inoculation but not after oral administration (23). Thus, we wanted to know to what extent the BSE/vCJD agent is pathogenic to humans by the i.c. and i.v. routes. To achieve this, we used the macaque model. To monitor the evolution of the BSE agent in primates, but also to verify the identity of French vCJD, we conducted parallel transmission to C57BL/6 mice, allowing strain-typing. The experimental scheme is depicted in Fig. 1.

Characterization of the BSE Agent in Primates. The identity of the lesion profiles obtained from the brains of the French patient with vCJD, two British patients with vCJD, and nonhuman primates infected with BSE provides experimental demonstration of the fact that the BSE agent strain has been transmitted to humans both in the U.K. and in France. Further, it lends support to the validity of the macaque model as a powerful tool for the study of vCJD. As far as the evolution of the BSE agent in primates is concerned, we observed an interesting phenomenon: at first passage of BSE in macaques and with vCJD, there was a polymorphism of the lesion profile in mice in the hippocampal region, with about half of them harboring much more severe vacuolation than the mice inoculated with cattle BSE. At second passage, the polymorphism tended to disappear, with all mice showing higher vacuolation scores in the hippocampus than cattle BSE mice. This observation suggests the appearance of a variant of the BSE agent at first passage in primates and its clonal selection during second passage in primates. The lesion profiles showed that it was still the BSE agent, but the progressive appearance of a "hippocampal signature" hallmarked the evolution toward a variant by essence more virulent to primates.

Characterization of the CJD and Scrapie Strains. Controls were set up by transmitting one French and one U.S. scrapie isolate from ruminants as well as French sCJD and iCJD cases from humans. None of these revealed a lesion profile or transmission characteristics similar or close to those of BSE or vCJD, respectively, thus extending to the present French scrapie isolate the previous observation that the BSE agent was different from all known natural scrapie strains (4, 24).
The lesion profiles of sCJD and iCJD differed only slightly in severity of the lesions, but not in shape of the profile, revealing the identity of the causative agents. One of us reported the absence of similarity between sCJD (six cases) and U.K. scrapie (eight cases) in transmission characteristics in mice (4). Herein, we made the striking observation that the French natural scrapie strain (but not the U.S. scrapie strain) has the same lesion profile and transmission times in C57BL/6 mice as do the two human TSE strains studied. This strain "affiliation" was confirmed biochemically. There is no epidemiological evidence for a link between sheep scrapie and the occurrence of CJD in humans (25). However, such a link, if it is not a general rule, would be extremely difficult to establish because of the very low incidence of CJD as well as the existence of different isolates in humans and multiple strains in scrapie. Moreover, scrapie is transmissible to nonhuman primates (26). Thus, there is still a possibility that in some instances TSE strains infecting humans do share a common origin with scrapie, as pointed out by our findings.

Transmission of vCJD and BSE to Nonhuman Primates. vCJD transmitted readily to the cynomolgus macaque after 2 years of incubation, which was comparable to the transmission obtained from first-passaged macaque BSE and much shorter than the interspecies transmission of BSE. Starting with 100 mg of BSE-macaque brain material, dilutions up to 4 µg still provoked disease. These data suggest that the BSE agent rapidly adapts to primates accompanied by enhanced virulence.
Examination of macaque brain inoculated with vCJD revealed a similar pathology to that with second-passage BSE. The distribution of vacuolation and gliosis, as well as the pattern of PrP deposition, including the dense, sometimes florid plaques, were similar to the human vCJD and the BSE hallmarks of the first passage (1, 2). These data show that the phenotype of BSE in primates is conserved over two passages. Moreover, they confirm that the BSE agent behaves similarly in humans and macaques, a precious finding that will prove useful in the near future for the design of pathogenesis or therapeutic studies. Because of the number of macaques examined in this study, we can now reliably state that the pathology, in particular the PrP deposition pattern provoked by BSE, is similar in older and very young animals. However, plaque deposition is greater, and mature florid plaques were more numerous, in the young, which may be correlated with a longer duration of the clinical phase observed in this animal (2). This is important with regard to the fact that vCJD has been diagnosed mainly in teenagers and young adults, which raises the concern that older patients may have been misdiagnosed because of an alternative phenotype of the disease. One should bear in mind, however, that cynomolgus macaques are all homozygotes for methionine at codon 129 of the PrP gene. Thus, our observations may not be relevant to humans carrying one or both valine alleles; however, all patients with vCJD reported to date have been M/M at this position (27).

Intravenous Transmissions to Nonhuman Primates. Brain pathology was identical in macaques inoculated i.c. and i.v. The i.v. route proved to be very efficient for the transmission of BSE, as shown by the 2-year survival of the animals, which is only 5 months longer than that obtained after inoculating the same amount of agent i.c. As the i.v. injection of the infectious agent implies per se a delayed neuroinvasion compared with a direct inoculation in the brain, this slight lengthening of the incubation period cannot, at this stage, be interpreted as a lower efficiency of infection as regards the i.c. route.
These data should be taken into account in the risk assessment of iatrogenic vCJD transmission by i.v. administration of biological products of human origin. They also constitute an incentive for a complete i.v. titration.
Conclusions

From BSE and vCJD transmissions in nonhuman primates, a number of conclusions can be drawn that are of major importance for human health: (i) human-adapted BSE appears to be a variant of the BSE agent that is more virulent for humans than cattle BSE and is efficiently transmitted by the peripheral route; (ii) the detection of vCJD in unusually young patients is probably not because of a lack of diagnosis of cases in older patients, thus raising the question of the source of human contamination with BSE early in life; and (iii) iatrogenic transmissions from patients with vCJD would be readily recognized by using the same diagnostic criteria as those applied to vCJD [clinical and pathological criteria (27) comprising neuronal loss and gliosis in the thalamus correlated with high MRI signal (28, 29)], whether such contaminations had occurred by the central or i.v. route. Primary and iatrogenic cases of vCJD could be distinguished on the basis of the patient's clinical history.

The risk assessment of biological products of human origin, notably those derived from blood, has been deeply modified by the appearance of vCJD. We confirm that the BSE agent has contaminated humans not only in the U.K. and the Republic of Ireland but also in France, and we show that its pathogenic properties for primates are being enhanced by a primary passage in humans. Considering the flow of potentially contaminated bovine-derived products between 1980 and 1996, it is obvious that further vCJD cases may occur outside the U.K. Thus, and in the light of the present study, it is necessary to sustain worldwide CJD surveillance regardless of national BSE incidence and to take all precautionary measures to avoid iatrogenic transmissions from vCJD.

snip...




http://www.pnas.org/cgi/content/full/041490898v1






Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
[email protected]

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757
===================================

now, just what is in that deer feed? _ANIMAL PROTEIN_

Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L
To: BSE-L

8420-20.5% Antler Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50 POUNDS
22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,
Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline
Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine
Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

http://www.bodefeed.com/prod6.htm
===================================

MORE ANIMAL PROTEIN PRODUCTS FOR DEER

Bode's #1 Game Pellets
A RATION FOR DEER
F3153

GUARANTEED ANALYSIS
Crude Protein (Min) 16%
Crude Fat (Min) 2.0%
Crude Fiber (Max) 19%
Calcium (Ca) (Min) 1.25%
Calcium (Ca) (Max) 1.75%
Phosphorus (P) (Min) 1.0%
Salt (Min) .30%
Salt (Max) .70%


Ingredients

Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,
Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline
Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine
Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

FEEDING DIRECTIONS
Feed as Creep Feed with Normal Diet

http://www.bodefeed.com/prod8.htm

INGREDIENTS

Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__,
L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium
Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic
Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,
Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,
Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate

DIRECTIONS FOR USE

Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================

DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box 117
Sandy Lake, PA 16145
PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:

Food and Drug Administration Investigator Gregory E. Beichner conducted
an inspection of your animal feed manufacturing operation, located in
Sandy Lake, Pennsylvania, on March 23,
2001, and determined that your firm manufactures animal feeds including
feeds containing prohibited materials. The inspection found significant
deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE) . Such deviations cause products being manufactured at this
facility to be misbranded within the meaning of Section 403(f), of the
Federal Food, Drug, and Cosmetic
Act (the Act).

Our investigation found failure to label your
swine feed with the required cautionary statement "Do Not Feed to cattle
or other Ruminants" The FDA suggests that the statement be
distinguished
by different type-size or color or other means of highlighting the
statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal
feeds containing prohibited material. This
flushed material is fed to wild game including deer, a ruminant animal.
Feed material which may potentially contain prohibited material should
not be fed to ruminant animals which may become part of the food chain.

The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...

http://www.fda.gov/foi/warning_letters/g1115d.pdf


DO you not think that MAFF would have not jumped on the bandwagon of the OP theory,
as opposed to the mad cow theory if they could have found any credence to it?


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



In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells


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




Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...

snip...

It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...

snip...

3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...

snip...

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

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf




and even the UK BSE mad cow farmers themselves don't believe it;


1) None of our animals that contracted BSE were treated with OP's, even
in utero.
2) My kids were treated with OP's as infants to control head lice. This
seems to be endemic as infection waves in UK primary schools (and
possibly elsewhere).
3) One might argue if the continued use of british beef in the UK was
ethical, none the less it happened. We have a duty to learn from it, not
least a duty to learn on behalf of those people who died so horribly....

you can ignore the transmission studies all you want, but they will never change.
you can ignore the fact that the feeding of TSE infected ruminants to ruminants was
common practice for decades. but it's not going to go away. blame it on the martians,
it's as about as likely as the OP theory. but it still will NOT change the transmission studies,
no matter what you say or do. ...


TSS
 

bse-tester

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TimH, if you have ever been to England, you would know the answer ?Needless to say, you will have to figure it out yourself. You associate something with me being a "...young lad in England," and yet you do not explain yourself. Rather, you leave subtle comment. So, explain your initial comment and I shall do the same.
 

TimH

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bse-tester said:
TimH, if you have ever been to England, you would know the answer ?Needless to say, you will have to figure it out yourself. You associate something with me being a "...young lad in England," and yet you do not explain yourself. Rather, you leave subtle comment. So, explain your initial comment and I shall do the same.

Soooooo..... Which way is it, bse tester???? :???:

Is it... I'll have to "figure it out" for myself??.......or ....you will explain your initial comment if I tell you what "IT" is????

By the way, how is that 'trying to create demand for your BSE test' thing going??? Have you scared anybody into cracking their wallet open yet?? :roll: :roll: :D
 

flounder

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THE ROYAL SOCIETY: LIVESTOCK INFECTIONS

Submission by Dr Harash K Narang

18/12/01



http://www.royalsoc.ac.uk/inquiry/index/288.pdf



Experimental Biology and Medicine 226:629-639 (2001)
© 2001 Society for Experimental Biology and Medicine



--------------------------------------------------------------------------------
MINIREVIEW
A Critical Review of Atypical Cerebellum-Type Creutzfeldt-Jakob Disease: Its Relationship to ``New Variant'' CJD and Bovine Spongiform Encephalopathy
Harash K. Narang,1

Ken Bell International, Newcastle-upon-Tyne NE2 3DH,United Kingdom


Abstract
Top
Abstract
Introduction
Protein Versus Virus Hypotheses
Role of PrP
Role of Mutation in...
CJD
History of CJD
Odd Cases of Sporadic...
The Link between BSE...
Plaques
Selected Case Historie
J.D. and E.B.
K.H.
Histopathological Studies
CJD and Blood Transfusion
In Conclusion
References


Shortly after the appearance of bovine spongiform encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD) was identified in young patients with nonclassical presentation such as difficulty in balancing and ataxia. The classical CJD in older patients starts with dementia. To distinguish between the two types, CJD in young persons has been termed ``new variant'' (nvCJD). The distinguishing features of classical CJD include initial presentation with dementia, confluent spongiform changes are very unusual in the cerebellum, and PrP plaques are rarely observed. For nvCJD, initially, difficulty with balancing and ataxia occurs, confluent spongiform changes are seen in the cerebellum, and a large number of PrP plaques are seen. The Icelandic observation of sheep scrapie revealed a predominantly ataxic form of scrapie, termed Type II, rather than the itchy form termed Type I. Both types have been known to exist in Europe. Since the clinical signs of Type II scrapie in sheep with trembling and ataxia are similar to those seen in BSE and nvCJD, this suggests that Type II is the cause of BSE and nvCJD. Over 8 years, from 1989 to 1996, I examined the clinical histories of 33 CJD cases aged between the ages of 18 and 84. Six under the age of 40 and 15 over the age of 40 had leading clinical features such as difficulty in balancing and ataxia similar to those seen in the young cases classified as ``nvCJD.'' Brains were examined from the six of 15 cases over the age of 40, which revealed similar pathology to that seen in young patients classified as ``nvCJD.'' These findings suggest that all age groups are susceptible to the strain of the agent derived from BSE cattle.


Key Words: bovine spongiform encephalopathy . Creutzfeldt-Jakob disease . nemavirus . protease-resistant protein (PrP) . scrapie . scrapie-associated fibril . spongiform encephalopathy



SNIP...





In Conclusion
Top
Abstract
Introduction
Protein Versus Virus Hypotheses
Role of PrP
Role of Mutation in...
CJD
History of CJD
Odd Cases of Sporadic...
The Link between BSE...
Plaques
Selected Case Historie
J.D. and E.B.
K.H.
Histopathological Studies
CJD and Blood Transfusion
In Conclusion
References


Since the first appearance of BSE, CJD has been identified in young patients. However, based on the three main distinguishing features described above and on a literature review, it has been revealed that patients of all age groups have died of CJD, but have not been recorded as such; older patients have been disqualified by age. The term ``new variant'' (nvCJD) was introduced because it was thought to be a new strain. However, realizing that the disease pre-existed, the term ``variant'' CJD (vCJD) has recently been introduced. A study of Icelandic sheep scrapie and review of the European scientific literature has demonstrated the existence of two strains of scrapie in sheep: Type I, ``itchy'' and Type II, the ataxic ``trembly'' type. Cases of the ataxic-cerebellar form of CJD were described 20 to 30 years before BSE appeared. These clinical signs, trembling and ataxia, are similar in BSE, vCJD, kuru, and in sheep inoculated with brain tissues from cows. Since the clinical signs of Type II scrapie in sheep with trembling and ataxia are similar to those seen in BSE and nvCJD, this suggests that Type II is the cause of BSE and vCJD. Many ``atypical'' cases, with all the unusual leading clinical features such as difficulty in balancing and ataxia, have been reported in patients. Because PrP immunostaining techniques were unavailable in the past, these patients' brains should be re-examined for PrP plaques, along with CJD patients who have received a blood transfusion. The pattern and distribution of PrP plaques should be used as a guide to determine the strain and source of infection and confirm that the name nvCJD is misleading.


snip...



http://www.ebmonline.org/cgi/content/full/226/7/629



H. Narang
A Critical Review of the Nature of the Spongiform Encephalopathy Agent: Protein Theory Versus Virus Theory
Experimental Biology and Medicine, January 1, 2002; 227(1): 4 - 19.

http://www.ebmonline.org/cgi/content/full/227/1/4



H. K. Narang
Lingering Doubts about Spongiform Encephalopathy and Creutzfeldt-Jakob Disease
Experimental Biology and Medicine, July 1, 2001; 226(7): 640 - 652.



http://www.ebmonline.org/cgi/content/full/226/7/640



TSS
 

Kathy

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Terry, there can be no reason for you to protest so vehemetly to the possiblity that OPs caused animals to be more susceptible to TSEs, other than some connection to the manufacturer of OPs.

Certainly, this is as possible as any other unproven theory.

Transmission experiments such as the mink one, did not track what chemicals these mink were treated with. What animals are treated most with chemicals to protect their coats? Mink, sheep.....

Your precious transmission experiments are using brain homogenate, and all kinds of iatrogenic transmission.

I don't want to waste my precious time convincing you about the harmful affects of OPs. Why don't you just get off your high horse and accept some facts, that OPs chelate copper, causing imbalances in enzymes and other bodily functions.

Jesh.
 

Kathy

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bse tester, I am just messing with Prusiner's huge ego. I do not wish to dismiss the hard work of others such as Narang. I am sure there have been many scientist working very hard at their everyday jobs, to find answers to all kinds of questions.

I just finished a book by Robert F. Kennedy Jr., called, "Crimes against Nature", in which he unveils how GW Bush has slashed and demolished any past steps/laws taken to protect the environment/ and the People, of the USA. You should pick it up and read it. It gives glaring evidence of patronage appointments which have lead to big business, running all aspects of the US government.

A comment which caught my attention, was how the government scientists are disheartened and quiting, left and right. They work hard to put together the research and some bureaucrat modifies the findings, to fit their agenda. Does this sound familiar?

Our Canadian CFIA has been busy, local papers say they have iatrogenically "infected" some calves with BSE, and deer with CWD, in a facility near Lethbridge, AB.

I also found this new report done by the CFIA, which confirms what Stan, the man, has been patenting which is that phosphotungstic acid (PTA) used to precipitate PrPSc from samples, is indeed useful.

Evaluation of Western blotting methods using samples with or without sodium phosphotungstic acid precipitation for diagnosis of scrapie and chronic wasting disease.

Huang H, Rendulich J, Stevenson D, O'Rourke K, Balachandran A.

Ottawa Laboratory Fallowfield, Animal Diseases Research Institute, Canadian Food Inspection Agency, 3851 Fallowfield Road, Ottawa, Ontario. [email protected]

The purpose of this study was to enhance the sensitivity of the Western blot (WB) test for use as an alternative and confirmatory method for the diagnosis of scrapie and chronic wasting disease (CWD) in Canada by comparing 2 sample preparation procedures: an abnormal prion protein (PrPSc) concentration procedure using sodium phosphotungstic acid (PTA) precipitation and a procedure using crude sample without precipitation. A total of 100 cerebrum samples (52 sheep and 48 elk), including 66 negative (31 sheep, 35 elk) and 34 positive (21 scrapie and 13 CWD positive) samples diagnosed by using immunohistochemistry (IHC) on retropharyngeal lymph node (RPLN) and medulla oblongata at obex, were tested by using WB with the 2 sample preparation procedures. The WB using non-PTA enriched sample (crude extract) detected, on average, only 71.7% (9 of 15, 60.0% for scrapie, 5 of 6, 83.3% for CWD) of the samples that tested positive by using WB with PTA enriched samples. No case was positive by WB using crude extract but negative by WB using PTA enriched sample. No false positive was found. Serial dilution of PTA precipitated samples demonstrated that the technique increases the detection limit approximately 100 fold. Additionally, the comparison of the WB and IHC on cerebrum from all the positive cases demonstrated that WB following PTA precipitation and IHC had 100% agreement by detecting 6 positive for CWD on cerebrum; while IHC detected scrapie in only 14 out of 15 positive cerebrum samples by using WB following PTA precipitation. Phosphotungstic acid precipitation is therefore a useful adjunct to WB analysis of scrapie and CWD and tissues.
 

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