BSE disposal of specied risk material nightmare

[Kathy]

Last December 2007, I sent a copy of Mark Purdey's new book "Animal Pharm" along with a couple of DVD documentaries Mark and on "depleted uranium" to my AB Agriculture Minister (G. Groenveld).

I also included a letter which expressed my deep concerns about how Specified Risk Material is being mixed with contaminated soil from the Oil and Gas industry, and buried in a landfill at Coronation, AB. The plans are to build an incinerator (or so a news article stated) that will later burn this stored SRM/waste in a high temperature incinerator (like Swann Hills). Nobody asked the neighborhood if we wanted it!

I recently spoke with an owner of a small butcher shop, who informed me that only the SRMs from Cargill and Tyson are going to Coronation. That all the rest of the SRMs from AB and SK are being sent to Saskatoon to be incinerated. After incineration, the "ash" is then trucked to Rimbey and buried in a landfill there, where (he said) it is guarded 24/7.

Why the need to protect, or prevent, access to the "SRM ash"? Certainly, after burning this material at high temperatures, there would be NO PROTEIN material left. Only the metals and minerals would remain.

After sending a letter to Groenveld, the CFIA and AB Veterinary Department in June 07, the book 'Animal Pharm"/DVDs to GG in December 07, and a follow up email to GG in April 08 (as I had not heard from GG to know if he had received the package in Dec)...... I got my own package in the mail from the Hon. GG - RETURNING Mark Purdey's book and the DVDs.

Here is what the Hon. Minister of Agriculture stated:

"May 12, 2008

Dear Mrs. Czar:

Thank you for your April 20, 2008 email regarding a package you sent to my constituency office in December 2007. I apologize for the delay in responding to you. The package has now been located and I have reviewed and shared the enclosed material with the Office of the Chief Provincial Veterinarian.

The true origin of transmissible spongiform encephalopathies is unknown at this time. Many different theories about the cause and pathogenesis of these diseases have been advanced, and it is possible that many factors interact to result in disease development.

Current scientific evidence strongly supports the theory that the infectious agent for bovine spongiform encephalopathy (BSE) is composed largely of a prion transmitted through the consumption of BSE-contaminated food products. This consensus is the basis for removing and destroying specified risk material (the prion containing tissues) at the source, thus alleveating any possibility of cross-contamination of animal feed products. However, Agriculture and Rural Development will continue to monitor the scientific literature related to BSE and other issues impacting agriculture, and adjust our policies and regulations accordingly as theories are validated by further study and research.

Please find enclosed your copy of Mark Purdey's "Animal Pharm" and the two DVD documentaries. I appreciate the opportunity to review this material and I commend your initiative in investigating issues which may impact your livestock operation. Agriculture and Rural Development will continue to support BSE research and other animal health initiatives as key elements of growing sustainable agriculture in Alberta.

Sincerely,
George Groenveld
Minister
enclosures"


So there you have it!

The true origin of transmissible spongiform encephalopathies is unknown at this time.

And it will never be "known" because the people/docs heading up the Alberta Prion Institute (Dr. David Westaway) refuse to admit the importance of copper to the well-being and proper formation of the healthy prion protein. Dr. Westaway was very rude at a recent CWD meeting, where-in I attempted to bring forward the work of Dr. Vitaly Vodyanoy of Auburn University in Alabama (see USA patent application 20070122799) for an example.

Dr. Westaway declared copper "unrelated to prion disorders" and then insulted the integrity of any research/researcher coming from Alabama.

CWD in wild deer and elk "in Alberta" have been diagnosed based on positive tests of the lymph glands in the neck - for the "most part", according to Dr. Margo Pybus. There is a problem here, as CWD positive animals should also show "pos" in the brain tissue - but many cervids (in AB) have not. So tell me, do they actually have CWD, or are they battling against an "environmental toxin" such as "depleted uranium" or "tungsten" particulate that is causing their immune system and lymph system to work overtime to eliminate subsequent "malformed proteins".

As the Hon. Minister states, "...it is possible that many factors interact to result in disease development."

But, because the reknown BSE/prion researchers of the UK have told us that the "infectious agent" was in the feed we are dealing with a very costly SRM removal and disposal system. Even though their "transmission experiments" absolutely fail to imitate real-life situations; and "contaminated MBM" feeding trials in the UK failed to induce BSE in any animals. (read Animal Pharm) I've donated a couple dozen to Alberta libraries.

Small butcher shops across this country are being forced out of business because of the costs they must pay to "ensure the safety of our food". Is not this cost in the interest of the public good? Are not the procedures they must follow, IMPOSED by a government/CFIA that ADMITS - "The true origin of TSEs is unknown at this time."

So tell me, why are the small butcher shops paying for this "safety measure", for that matter why force Cargill and Tyson too? Wouldn't it be cheaper to test the animals? (Using the BIO-RAD test kit developed by the French Atomic Energy Commission: BIO-RAD stands for "Radiation-Biology" in french - so its flipped around).

Disposal of SRMs in the manner which is presently taking place is a FARCE. As one butcher stated, "Its basically saying you can eat the inside of a piece of bread but all the crust is poison."

For all my efforts (and Mark Purdey's) to investigate the TRUE multifactor cause of BSE, I am given a pat on the head and a door slammed in my face. The two DVDs I sent to GG were:

"Mad Cows and an Englishman" (a doc. about the early findings of Mark Purdey), and

"The Doctor, The DU and the Dying Children" a doc. about how depleted uranium from conventional weapons (bullets, bombs and bunker busters) used in Iraq and Afganistan have polluted the environment and are causing the death and disease of those unfortunate enough to be exposed to the depleted uranium (inhaled nanoparticles, consumed in food and water, or adsorbed via the skin).

I note, Minister GG did NOT mention "depleted uranium" in his response. Neither has he offered to investigate the use of depleted uranium weapons at CFB Suffield, Wainwright, or Cold Lake.

Also, why did it take my follow-up e-mail of April 20, 2008 for GG to "locate" my package sent in December 2007?

I have to wonder who actually reviewed this information (the book and the DVD documentaries).

This information is posted here so that you can make some of your own conclusions. When valid scientific data is brought forward to our government, CFIA and the Office of the Chief Provincial Veterinarian (of AB)... their response is thus.

They continue to "inject brain homogenate" into the cranium of animals to determine the cause of BSE and other TSEs. This is NOT based on the feeding of MBM. Direct injection into the brain, reflects "inhalation" (especially directly through the olfactory system/nose) not "consumption".

If anyone cares for more information on this subject, I will gladly supply it to you (ie: how the inhalation of rogue metal nanoparticles is contaminating the prion protein and causing its malformation, thus its inability to function properly causes a cascade of oxidative damage that destroys the viability of the cell)... You can also search the "Entrez Pubmed" medical search engine for Oxidative Stress, metals, Mark Purdey, David R. Brown, F. Paquet and prions.

Our government has left us to the whims of a CFIA that bases its BSE prevention criteria on the findings of researchers that have corrupted the science - to protect whom?

[wilagro]

I will believe the CFIA findings UNTIL there is a more plausible scenario.

Contaminated bone meal from Great Britain sold all over the world (including North America), was a common vector for spreading the causative agent of BSE. The processing of bovine waste into material added to feed concentrate to provide cheap protein, compounded the problem by mixing and distributing contaminated feed. This practice should never have been allowed at any time.

Depleted Uranium...stretching the bounds of plausibility in my opinion.

Heavy metals...I would like to see more research as to their place in this puzzle, if any.

My opinion on the BSE phenomena, others may disagree.

[per]

You won't find anyone who thinks it is OK to feed animal protein to animals but how do you explain CWD in wild deer. Not too many of them were fed by anyone anything other than what is natural and existing in the environment. Notwithstanding, Kathy's point of testing would be cheaper than hauling the SRM's back and forth is quite valid.

[wilagro]

per: From what I read CWD is similar but not quite the same as BSE.

One possibility in the spread of CWD are common natural salt licks where saliva (fresh or dried) from one animal could be picked up by another animal. That is probably a long shot although someone suggested that the same thing could happen with grass. Nobody really knows. So far there have not been many whitetail deer infected here (east-central AB), although a few were found last fall in Alberta along the border with Sask. More deer infected in Sask. so far...but that could change also.

Testing for BSE would be a good thing if the tests could be proven to be accurate for young as well as older animals and less costly than disposal of SRMs.

[tman]

The one specific question that I have never seen come up is "how did BSE originate?" Now lets assume that the whole contaminated feed thing is true and accurate. How did these prions form initially? At some point the very first infected animal that was ground up and fed back to its pen mates had to have been "infected" by some other form. All that CFIA etc has theories on is the spread, NOT the cause.

[wilagro]

I presume that conditions were right for the first "mutation" or abnormal formation of prions. Somewhat like the flu virus does.

Anyway the abnormal prions seem able to replicate themselves when introduced to another animal (or human).

This is science way above my understanding and we can only hope that researchers will solve this puzzle.

[rkaiser]

Thanks again Kathy for all of your effort.

Can't really expect much more out of poor old GG. He is taking lead form many people in his position as he cannot possibly learn everything about everything. Sometimes the lead person has his / her own agenda and that is painfully obvious in this case.

[farmers_son]

From Animalnet:

ONTARIO: U of O research examines risks of mad cow disease
21.may.08
Ottawa Business Journal
Julie Fortier
http://www.ottawabusinessjournal.com/2976772642041.php
It may be hard to believe that although bovine spongiform encephalopathy (BSE), or 'mad cow disease,' has cost the Canadian economy around $10 billion in lost trade and compensation, little is known about the disease.
This month, PrioNet Canada, a federally funded network that studies prion-based diseases like BSE, moved to change that by announcing $590,000 in funding for two related projects at the University of Ottawa.
The funding is part of an $8-million injection into 19 projects across the country examining prion diseases and their effects, and will fuel research conducted by U of O's Dr. Daniel Krewski and Dr. Michael Tyshenko.

See PrioNet at:
http://www.prionetcanada.ca/

The Canadian Cattlemen's Association is one of Prionet's partners as well as universities across Canada, The Alberta Prion Institute and the Canadian Food Inspection Agency.

[grassfarmer]

Thanks Kathy for keeping up the battle! I'm interested (and horrified)that the BSE ash is being hauled to Rimbey - i'll try and dig up where it's really going.
Tman - the original "theory" in the UK was that BSE originated by a cross species contamination of feeding remains of scrapie infected sheep to cattle. They seem to have dropped that story of late.
As you say the feed theory needs to have had an original cause and this has never been proven. Where I would disagree with Kathy, and Mark, was that there was no transmission of BSE through feed in the UK. I think that Mark did some sterling work on the causes of BSE and probably got closer to the truth than anyone else has but having lived through BSE in the UK and seeing the spread/speed factor of it I am firmly convinced that it was spread for a period through the calf milk replacer. How else do you explain that it was virtually confined to dairy farm reared stock - several beef breeds never had a case. The first case in the Galloway breed was on a farm close to me - a farm that also had a dairy herd and the cow in question had been orphaned as a calf and reared on milk powder with the dairy replacements.

[Kathy]

The milk replacer has high levels of manganese.

The feed, MBM, (especially in UK and other EU countries) at the time of the huge BSE situation, was contaminated with chemicals from the Organophosphate treatment of cattle.

As for the prion causing the disease, and replicating on its own? Don't believe everything you hear. Next time old Bessy injects homogenized brain tissue into her little brain, then the CFIA's transmission theory might be considered plausible.

The Blood Brain Barrier protects the brain. However, inhalation of extremely small particulate can bypass the BBB and go directly to the brain via the olfactory system.

The cattle/deer et al. that are feeding will inhale alot of particulate fromt the feed or soil due to their anatomy.

I wish I could show everyone hear all the research I have dug up on the subject. I can only express to you that I have seen enough to be convinced this is a metal/mineral contamination problem - and absolutely not an infectious disease.

The feeding trials that are claimed to show transmission of prions do not. They show that something that was in brain material of diseased animals, when specially treated and highly concentrated, then drenched into the stomachs of a few bovine calves - caused some but NOT all the calves to have a positive test, which identifies specific amino acid sequences that are NOT specific to only malformed prion proteins. In the Terry, Wells study, the researchers had to pool tissue samples in order to get this positive.

If feed were the agent of tranmission, there would be millions of cases throughout the world, as Mark pointed out, especially in the Arab Emerits - as they imported the most of this feed.

By tricking people that they are getting this disease from a mysterious prion protein in feed, the real cause is being ignored - but thankfully NOT by everyone.

Meanwhile at the AB Prion Institute, we have Dr. Westaway telling people that copper and the prion protein have no relationship with each other. This is a flat out lie!

These researhers (abstract below) have shown that a "ferritin" (iron) based molecule/metal nanoparticle-based, was capable of distinguishing/separating man-made prion peptides via the region which is supposed to bind copper.

Copper is not magnetic, and in order for the columns to capture the peptides, other metals must be bound to this region - which are paramagnetic.

Uranium and other heavy metals, when lodged in the body (usually attached to proteins) cause much damage from what's called the "chemical effect" (not radiation).

Dr. Chris Busby of the UK, has shown how this effect is happening. He has demonstrated the "photo-electron effect" where the various metals/minerals absorb and amplify back-ground radiation (being everything from sound, light, UV - gamma et al.).

In a study in 2007 by Elsaesser et al. the researchers used a "CERN Monte Carlo model" to pattern the effect of predicted enhancement of gamma and x-rays with various metals vs. H20

They demonstrated that the absorption of gamma and x-ray was proportional to the 4th power of the atomic number. With a water molecule (H20) having an atomic weight of 3.33 it had an enhancement effect of 1 (one).
Calcium effect = 1220
Strontium effect = 17,073
Barium effect = 79,675
Gold effect = 308,943
Uranium effect = 585,365

In this model, when water was exposed to 100,000 photons there were 4 tracks of electrons shooting off of it.

With Gold and Uranium, under exposure to ONLY 1,000 photons there were SIGNIFICANTLY more electron tracks shooting out of the metal nucleus.

This demonstrates how these heavy metals are capable of releasing electron energy in a form which is directly related to energy input. This is a CASCADE EFFECT!

Also, for decades it has been known that uranyl ions (the most common form of uranium in human blood) have an affinity for DNA. Depleted uranium (uranyl acetate, for example) is used as a laboratory stain for DNA. Under very, very low concentrations, uranium will saturate DNA. This has an effect on the ability of the cell to produce healthy proteins, including repair proteins.

An example of exposure to LEAD in dogs, (abstract below) demonstrates how this heavy metal was capable of causing spongiform in the brain. Dr. Amir Hamir did this study in 1984. He is presently working on CWD, in the US. The low calcium died, allowed the lead to take the place of calcium in the dogs body.

I'm not saying only depleted uranium can cause these diseases; tungsten and lead, barium, strontium - all these other rogue metals which enter the body and "stick" are causing problems, (not just TSEs). However, the thing with "burned" or "incinerated" metals, is that they vapourize with specific temperatures/metal and recondense into "insoluble" metal nanoparticles.

DU weapons and bombs create unfathonable amounts of these insoluble metal/metal alloy particles. When they stick in the body, they cannot be eliminated the same as natural/non-fired metals. Our bodies don't know how to handle them very well. They stay lodged where-ever they are and they very very slowly, release metal ions from the particle. They ALSO absorb and enhance background radiation in an "atomic weight" and "particle size" relationship. The smaller the insoluble particle, the more trouble as it can float through the body unimpeded, and lodge anywhere. Having an affinity for DNA, uranium is EXTREMELY dangerous - thus it should be left in the ground, undisturbed.


J Comp Pathol. 1984 Apr;94(2):215-31. Links
Neuropathological lesions in experimental lead toxicosis of dogs.Hamir AN, Sullivan ND, Handson PD.
Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.

PMID: 6736309



Chem Res Toxicol. 2007 May;20(5):784-9. Epub 2007 Apr 14. Links
Uranyl acetate as a direct inhibitor of DNA-binding proteins.Hartsock WJ, Cohen JD, Segal DJ.
Department of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona 85721, USA.

Zinc finger proteins, one of the largest families of DNA-binding proteins in higher eukaryotes, are so named because they require zinc ions for appropriate structure and function. Dysregulation of zinc finger-containing DNA transcription and repair proteins has been proposed as a potential mechanism for the toxic effects of some metal ions. Uranium metal has been reported to be both a cytotoxic and a genotoxic agent. We hypothesized that these toxic effects of uranium might be due to its ability to directly disrupt zinc finger activity. To test this hypothesis, two purified zinc finger proteins, Aart and Sp1, were analyzed by electrophoretic mobility shift in the presence of uranyl acetate. Inhibition of binding was apparent at 10 microM uranyl acetate, while no inhibition was observed with up to 2000 microM the cytotoxic metalloid sodium arsenite. Preincubation of the DNA with uranyl acetate did not inhibit zinc finger protein binding, suggesting that the inhibition was due to direct uranyl interaction with the protein. Surprisingly, uranyl acetate inhibited two nonzinc finger DNA-binding proteins, AP1 and NF-kappaB, to a similar extent, and zinc finger inhibition was reduced in the presence of bovine serum albumin. These results suggest that uranium can directly inhibit the function of DNA-binding proteins, most likely via a nonspecific protein interaction.

PMID: 17432879



Anal Biochem. 2007 Jul 1;366(1):1-8. Epub 2007 Mar 13. Links
Nanoengineered analytical immobilized metal affinity chromatography stationary phase by atom transfer radical polymerization: separation of synthetic prion peptides.McCarthy P, Chattopadhyay M, Millhauser GL, Tsarevsky NV, Bombalski L, Matyjaszewski K, Shimmin D, Avdalovic N, Pohl C.
Research and Development, Dionex Corporation, Sunnyvale, CA 94088, USA.

Atom transfer radical polymerization (ATRP) was employed to create isolated, metal-containing nanoparticles on the surface of nonporous polymeric beads with the goal of developing a new immobilized metal affinity chromatography (IMAC) stationary phase for separating prion peptides and proteins. Transmission electron microscopy was used to visualize nanoparticles on the substrate surface. Individual "ferritin" molecules were also visualized as ferritin-nanoparticle complexes. The column's resolving power was tested by synthesizing peptide analogs to the copper binding region of prion protein and injecting mixtures of these analogs onto the column. As expected, the column was capable of separating prion-related peptides differing in number of octapeptide repeat units (PHGGGWGQ), (PHGGGWGQ)(2), and (PHGGGWGQ)(4). Unexpectedly, the column could also resolve peptides containing the same number of repeats but differing only in the presence of a hydrophilic tail, Q-->A substitution, or amide nitrogen methylation.

PMID: 17481564

[flounder]

Monday, June 23, 2008 Persistence of Pathogenic Prion Protein during Simulated Wastewater Treatment Processes

http://chronic-wasting-disease.blogspot.com/2008/06/persistence-of-pathogenic-prion-protein.html

Wednesday, June 11, 2008

Transmission and Detection of Prions in Feces

The Journal of Infectious Diseases 2008;198:81-89 © 2008 by the Infectious Diseases Society of America. All rights reserved. 0022-1899/2008/19801-0015$15.00 DOI: 10.1086/588193

snip...

P04.61 Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3 1University of Wisconsin, Soil Science/Civil and Environmental Engineering, USA; 2University of Wisconsin, Civil and Environmental Engineering, USA; 3University of Wisconsin, Comparative Biosciences, USA

Concern has been expressed that prions could enter wastewater treatment systems through sewer and/or septic systems (e.g., necropsy laboratories, rural meat processors, private game dressing) or through leachate from landfills that have received TSE-contaminated material. Prions are highly resistant to degradation and many disinfection procedures raising concern that they could survive conventional wastewater treatment. Here, we report the results of experiments examining the partitioning and survival of PrPSc during simulated wastewater treatment processes including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc can be efficiently extracted from activated and anaerobic digester sludges with 1% sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl sarcosinate. Activated sludge digestion does not result in significant degradation of PrPSc. The protein partitions strongly to the activated sludge solids and is expected to enter biosolids treatment processes. A large fraction of PrPSc survived simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions were to enter municipal waste water treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for excluding inputs of prions to municipal wastewater treatment facilities that would result in unacceptable risk of prion disease transmission via contaminated biosolids.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie McKenzie2, Judd M. Aiken1,2*

Soil may serve as an environmental reservoir for prion infectivity and contribute to the horizontal transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. .

In conclusion, our results provide compelling support for the hypothesis that soil serves as a biologically relevant reservoir of TSE infectivity. Our data are intriguing in light of reports that naïve animals can contract TSEs following exposure to presumably low doses of agent in the environment [5,79]. We find that Mte enhances the likelihood of TSE manifestation in cases that would otherwise remain subclinical (Figure 3B and 3C), and that prions bound to soil are orally infectious (Figure 5). Our results demonstrate that adsorption of TSE agent to inorganic microparticles and certain soils alter transmission efficiency via the oral route of exposure. full text is here:

http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030093

http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-L.pdf

http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-S.pdf

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&F=&S=&m=1742&P=7260

Science 14 October 2005:Vol. 310. no. 5746, pp. 324 - 326DOI: 10.1126/science.1118829 Reports

Coincident Scrapie Infection and Nephritis Lead to Urinary Prion Excretion

Harald Seeger,1* Mathias Heikenwalder,1* Nicolas Zeller,1 Jan Kranich,1 Petra Schwarz,1 Ariana Gaspert,2 Burkhardt Seifert,3 Gino Miele,1 Adriano Aguzzi1

Prion infectivity is typically restricted to the central nervous and lymphatic systems of infected hosts, but chronic inflammation can expand the distribution of prions. We tested whether chronic inflammatory kidney disorders would trigger excretion of prion infectivity into urine. Urinary proteins from scrapie-infected mice with lymphocytic nephritis induced scrapie upon inoculation into noninfected indicator mice. Prionuria was found in presymptomatic scrapie-infected and in sick mice, whereas neither prionuria nor urinary PrPSc was detectable in prion-infected wild-type or PrPC-overexpressing mice, or in nephritic mice inoculated with noninfectious brain. Thus, urine may provide a vector for horizontal prion transmission, and inflammation of excretory organs may influence prion spread.

snip...

SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2008/06/transmission-and-detection-of-prions-in.html

Thursday, April 03, 2008 A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html

P01.47

Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in vitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1 1University of British Columbia, Brain Research Centre, Canada; 2Public Health Agency of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases Research Institute, Canada Food Inspection Agency, National Reference Laboratory for Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical Biophysics, University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that can affect North American cervids (deer, elk, and moose). Although the risk of CWD crossing the species barrier and causing human disease is still unknown, however, definite bovine spongiform encephalopathy (BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit the exposure of humans to CWD.

Aim: In view of the fact that BSE can be readily transmitted to non-bovid species, it is important to establish the species susceptibility range of CWD.

Methods: In vitro conversion system was performed by incubation of prions with normal brain homogenates as described before, and protease K (PK) resistant PrP was determined by immunoblotting with 6H4 monoclonal prion antibody.

Results: Our results demonstrate that PrPC from cervids (including moose) can be efficiently converted to a protease-resistant form by incubation with elk CWD prions, presumably due to sequence and structural similarities between these species. Interestingly, hamster shows a high conversion ratio by PrPCWD. Moreover, partial denaturation of substrate PrPC can apparently overcome the structural barriers between more distant species.

Conclusions: Our work correctly predicted the transmission of CWD to a wild moose. We find a species barrier for prion protein conversion between cervids and other species, however, this barrier might be overcome if the PrPC substrate has been partially denatured in a cellular environment. Such an environment might also promote CWD transmission to non-cervid species, *** including humans. Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro conversion than PrPC treated at physiological pH. This has implications for the process by which the prion protein is converted in disease.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

SEWING THE SEEDS OF MAD COW (CWD) THROUGH ANIMAL PROTEIN $

[PDF]

BSE INQUIRY Statement of behalf of the Environment Agency ... File Format: PDF/Adobe Acrobat - View as HTML ... his Statement of March 1998 to the BSE Inquiry ... systems subject to regular or intermittent contamination by rapid movement of recharge water

BSE INQUIRY

Statement of behalf of the Environment Agency Concerning Thruxted Mill By Mr C. P. Young Principal Hydrogeologist, Soil Waste and Groundwater Group WRc plc; Medmenham, Bucks

http://www.bse.org.uk/files/ws/s490.pdf

http://www.michigan-sportsman.com/forum/showthread.php?t=23313

http://www.americansportsman.com/messageboard/hunting/smallgamehunting/deer/viewpost.asp?mb=deerhunting&post=642

http://www.biggamehunt.net/forums/viewtopic.php?t=14549&start=0


If only a proportion of infected cattle can be detected, does testing provide significant consumer protection?

The extent to which testing increases consumer protection is still open to question, especially if other protective measures are in place (see below).

It is conceivable that tissues not previously recognised as infected may still be found as research continues. Infectivity levels are expected to be extremely low, and undetectable with the tools used so far. If these tissues were otherwise consumed then the destruction of the carcase would afford the consumer a greater degree of protection. If the tissues are not sufficiently infectious to pose a health risk, and/or are not consumed, then the additional protection provided may be nil.

Recent results from Japan and Germany confirm this point(2,11,12,14), with positivity or infectivity being detected in some peripheral nerves that would not normally be removed as SRM. The amount of infectivity present is low, and considered be up to 1000-fold lower than the brain. Unpublished evidence suggests that these become positive only after the brain and spinal cord. This therefore confirms that testing and removal of positive animals does provide some additional, as yet unquantifiable, protection to consumers over and above that provided by removal of SRM. Given that detection of positivity or infectivity in some peripheral nerves coincides with the onset of clinical signs, it is probable that such animals would be detected before slaughter, and therefore excluded from the food chain.

http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_0 70516.pdf


please see SRMs i.e. SPECIFIED RISK MATERIALS ;

http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html


Copper deficiency in the young bovine results in dramatic decreases in brain copper concentration but does not alter brain prion protein biology

L. R. Legleiter, J. W. Spears and H. C. Liu Department of Animal Science and Interdepartmental Nutrition Program, North Carolina State University, Raleigh, NC

Jerry_Spears@ncsu.edu

Abstract

A manganese (Mn) for copper (Cu) substitution on cellular prion proteins (PrPc) in the brain that results in biochemical changes to PrPc has been implicated in the pathogenesis of transmissible spongiform encephalopathies. Recent research in the mature bovine does _NOT_ support this theory. The present study tested this hypothesis using progeny from gestating cows receiving Cu-deficient diets or Cu-deficient diets coupled with high dietary Mn. Copper-adequate cows (n = 39) were assigned randomly to treatments: 1) control (adequate in Cu and Mn), 2) Cu-deficient (-Cu), and 3) Cu-deficient plus high dietary Mn (-Cu Mn). Cows assigned to treatments -Cu and -Cu Mn received no supplemental Cu and were supplemented with molybdenum (Mo) to further induce Cu deficiency. The -Cu Mn treatment also received 500 mg supplemental Mn/kg dietary DM. Calves were weaned at 180 d and maintained on the same treatments as their respective dams for 260 d. Copper-deficient calves (-Cu and -Cu Mn) had decreased (P = 0.001) brain (obex) Cu and tended to have increased (P = 0.09) obex Mn relative to controls. Obex Mn/Cu ratios were substantially increased (P < 0.001) in calves receiving -Cu and -Cu Mn treatments compared to controls and were higher (P < 0.001) in -Cu Mn calves than in -Cu calves. Obex prion protein characteristics, including proteinase K degradability, superoxide dismutase (SOD)-like activity, and glycoform distributions, were largely unaffected. Obex tissue antioxidant capacity was not compromised by perturbations in brain metals, but Cu-deficient calves tended to have decreased (P = 0.06) Cu/Zn SOD activity and increased (P = 0.06) Mn SOD activity. Although obex copper was decreased due to Cu deficiency and Mn increased due to exposure to high dietary Mn, the obex metal imbalance had minimal effects on PrPc functional characteristics in the calves.

http://jas.fass.org/cgi/content/abstract/jas.2007-0403v1

Subject: FATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE Date: May 3, 2007 at 8:41 am PST

KEY FINDINGS

Organophosphate Studies

6. Studies using phosmet (an organophosphate pesticide) were carried out throughout the project. No relationship between this compound and the potential to cause a TSE were identified. In studies with oral dosing of rats, it was shown that PrP expression levels increased in the brain but there was no association between this and formation of proteinase K (PK) resistant PrP.

snip...

12. A model of seed protein aggregation and fibril formation was established using PrP charged with Mn2 . PrP-Mn2 was found to form small circular aggregates able to catalyse further protein aggregation and fibrilisation of PrP. This model unlike other published models (for example those of Baskakov et al.1) does not require the presence of denaturants and is not an autocatalytic process (i.e. the substrate of the reaction did not aggregate). The results suggest that Mn2 may play a role in the formation of prion seeds

__although further studies showed that this material was not infectious in mouse bioassay.__

snip...

24. The project also generated information concerning the relation of TSEs to environmental factors: . __Potentially no role for organophosphates in TSEs.__ . Increased Mn in the diet results in higher PrP levels in the brain. . No conclusion is yet possible in terms of the relationship between environmental trace element concentrations and the geographical occurrence of TSEs (classical scrapie or BSE). . Some confirmation was provided that in some specific farms occurrence of classical scrapie correlates with high Mn levels.

http://www.seac.gov.uk/papers/97-4.pdf

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

OP'S MEETING WITH PURDEY

http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf

P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfilment of the study "BSE in primates" supported by the EU (QLK1-2002-01096).

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.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;

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.

snip...

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 (ic ip 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 first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and int****ritoneal.

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

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

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

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500 From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov

snip...

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 ehoover@lamar.colostate.edu

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

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

J Infect Dis. 2004 Aug 1;190(3):653-60.

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.

http://www.ncbi.nlm.nih.gov/

10,000,000 LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II ___________________________________ PRODUCT Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing. REASON Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI

___________________________________ PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007 CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified. RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete. REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html

Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST

snip... see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ;

see full text ;

Friday, April 25, 2008

Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46

http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html

SPECIFIED RISK MATERIALS

http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html

PLEASE see full USA MAD COW FEED PROGRAM ;

http://madcowfeed.blogspot.com/

Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the United States of America (USA) Question number: EFSA-Q-2003-083

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1,0.pdf

TSS

-------------------- BSE-L@LISTS.AEGEE.ORG --------------------