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Prions: testable? traceable?

BTox said:

Just a IMO, but I would put NO credibility to any article on Mercola's site.

I should have said that in my post from the get-go, but I forgot.

He's re-printing an article that showed up on the web, and in many newspapers, back in 2000. I had scanned the article, but it's back at home on my computer.

I was looking for a better site, but eventually gave up ("www.christianparents.com" anyone?).
 
Suezoled said:

Also, he himself is trying to sell something, and that make me wonder about favoritism in articles.

Exactly, he is trying to sell medical/health quackery. I have seen him spin the results of clinical trials 180 degrees from the truth.
 
Does anybody know if cattle in the US are still being fed animal remains?

It seems like the first time around with the mad cow scare feeding cattle pig remains was stopped. But what about other animal remains? What's the situation in Canada?
 
The opinions from public health vets are that so long as one doesn't use feeds containing cattle as a source of protein that includes the spinal cord and brain, then you are okay. But can these people say so with absolute certainty? No. If I recall correctly, in the Kuru outbreaks in the South Fore tribal area of Papua New Guinea, the mourners would eat the brains of their deceased relatives. Once this type of cannibalism was stamped out the disease dissapeared. And the prion has only been identified in brain and spinal cord tissue.

I posted the key words you can use to search Google or any other search engine above:

1. KURU
2. Chronic Wasting Disease or CWD
3. Bovine spongiform encephalopathy or BSE
4. Scrapie,
5. CJD or v-CJD or nv-CJD where v=variant or nv=new variant of CJD which is the prion disease of concern in people and which is evidently transmitted by ingestion of beef contaminated by traces of brain and spinal cord tissue.CJD=Creutzfeldt-Jakob Disease.

Before BSE appeared on the scene this prion disease (CJD) was most commonly linked to corneal transplants and tissue grafts between infected and non-infected people. Surgical instruments,
probes and electrodes used in brain and spinal surgery even if properly sterilized were also cited as transmitters of CJD since prions are not theoretically subject to sterilization.
 
Should I stop eating the bit of spinal cord in my chops?

CJD has also been transmitted by intake of pituitary gland extract in the treatment of infertility (sorry, perhaps this has laready been mentioned)

(Don't tell Rustler2 though)
 
BillyJoe said:
Should I stop eating the bit of spinal cord in my chops?

CJD has also been transmitted by intake of pituitary gland extract in the treatment of infertility (sorry, perhaps this has laready been mentioned)


Good question about "chops," whether lamb or veal (calf) chops. If we had a big BSE problem to begin with veal shops with possible bits of the cord attached would be a bad idea. Sheep carry a prion disease called scrapie and while there is no evidence it is transmittable to humans, it may be. Recently when a new snakebite (for North American snakebite) antiserum maker (a British Co: Protherics) switched from horse (equine) to sheep (ovine) based donor animals, the question arose as to which sheep to use: the Welsh flocks they already had, donor sheep in the U.S. where, in fact the anti-serum will be used the most or in Australian or New Zealand sheep. The decision was to use the large, certifiably prion-free Aussie sheep. The Australian sheep were not only prion free but because they are larger than U.S. and British sheep, they could produce more antiserum per animal. This created an amusing problem for the FDA in approving the product. So, for absolute safety's sake the
venom to provoke the antibodies which came from U.S. snakes, was exported to Australia, injected into Australian sheep, the serum of the inoculated sheep was collected, and then shipped to the U.K. where it was purified in the laboratory and then packaged and sent to the U.S. for sale and use. It was a logistical nightmare for the FDA to inspect this operation but they did... in three different countries: U.S., England and Australia.

Scrapie has shown up from time to time in U.S. flocks and sheep flocks have to be destroyed when that happens.

So if you are eating imported New Zealand or Australian lamb then you should be pretty safe.....and there is no proof scrapie is a danger to people but there are some who say it is and with this disease there is no taking any chances apparently.
 
Interesting post Steve, but...er....we don't need to import Australian sheep down here, they are already here :)
 
Yup. Didnt notice your location.

You guys and New Zealand have the best sheep in the world. The tight control Australia imposes on animal imports is responsible, no doubt.
 
SteveGrenard said:
The opinions from public health vets are that so long as one doesn't use feeds containing cattle as a source of protein that includes the spinal cord and brain, then you are okay.

The FDA called a halt to the feeding of most mammalian protein to cattle. IIRC, earlier they had ruled against feeding ruminants to ruminants. This dates back to at least 1997.
 
Yes, mammalian proteins were banned from this feed in Aug, 1997 but there has been some backsliding potential from these regs which is implied in the following article from 4H Clubs of America published in 2001. The infected cow in question was also born a few months before the FDA ban went into effect. It has not been made clear even if the regs had existed at the time this cow was born whether or not they applied in Canada. ?? Which of course brings up another major problem re importing Canadian beef into the U.S. or to anywhere.

http://www.ianr.unl.edu/pubs/animaldisease/nf482.htm






Here is the original release from the FDA concerning the ban. This article ties in sheep scrapie as a possible agent causing BSE in cattle as well. We have had outbreaks of scrapie in the U.S. as recently as a year ago.



http://vm.cfsan.fda.gov/~lrd/tpprotei.html

T97-20 - June 3, 1997

FDA PROHIBITS MAMMALIAN PROTEIN IN SHEEP AND CATTLE FEED

The Food and Drug Administration today announced publication of a final regulation that
prohibits the use of mammalian protein (with certain exceptions) in the manufacture of animal
feeds given to ruminant animals such as cows, sheep and goats. The rule will take effect 60 days
after its publication June 5. The following may be used to answer questions.

This prohibition is a preventive measure designed to protect animals from transmissible
degenerative neurological diseases such as bovine spongiform encephalopathy (BSE) and to
minimize any potential risk to humans. No case of BSE has ever been documented in cattle in the
U.S. But if a case of BSE were ever found here, these measures would prevent the spread of
BSE through feeds by precluding amplification of BSE in U.S. cattle.

In January, FDA proposed a regulation that would have prohibited the feeding of
ruminant protein to other ruminant animals. In a draft rule published April 17, FDA expanded
that prohibition to include nearly all mammalian protein. Like the proposal, however, the final
rule allows the use of products believed to pose a minimal risk of BSE transmission. These
products include blood, blood products, gelatin, milk, milk products, protein derived solely from
swine and equine sources, and inspected meat products which have been offered for human food
and further heat processed for food, such as plate waste from restaurants and other institutions.

By prohibiting nearly all mammalian protein from being used in ruminant feed, FDA
believes it has made the final regulation more practical and effective. Pure pork and pure equine
protein are excluded because these animals are not known to have transmissible spongiform
encephalopathies (TSEs), and because the protein is processed so that it is not contaminated by
potentially infective proteins.

In addition to prohibiting tissues with the potential to spread TSEs such as BSE, the final
regulation also requires process and control systems to ensure that feed for ruminants does not
contain the prohibited mammalian tissue.

The first case of BSE was reported in the United Kingdom in 1986. Epidemiological
evidence gathered in the U.K. suggests an association between the outbreak there and the feeding
to cattle of protein derived from sheep infected with scrapie, another TSE.

Today's final rule caps a period of intense discussion about the most appropriate way to
provide an additional layer of protection against the potential risk from BSE in this country. In
the last year, FDA has sought comment on the best course of action by publishing an Advance
Notice of Proposed Rulemaking, a Proposed Rule and a Draft Rule. The agency has received
more than 1460 formal comments on this issue, and has held two open public meetings to discuss
the most appropriate course of action.

The current state of knowledge concerning TSEs is far from complete. FDA will continue
its close collaboration with the scientific community and with
public health officials, at home and
abroad, on measures to reduce the potential risk of these diseases.
 
Here are updates from the USDA on the situation:

USDA News <oc.news@usda.gov> [edited]
<http://www.usda.gov/news/releases/2003/12/0448.htm

USDA Statement: BSE Update 29 Dec 2003
Release No. 0448.03
BSE Update
29 Dec 2003


USDA continues to work with the Canadian officials to verify traceback of the
index animal. Records obtained from the owner correspond with Canada's
records indicating that this animal was approximately 6-1/2 years old at the
time of slaughter. USDA is working with Canada to conduct DNA testing to
verify that the correct animal has been identified. The age of the animal is
significant. She would have been born before feed bans were implemented in
North America in August 1997.

The feed bans prohibit the inclusion of ruminant protein in feed intended for
other ruminants to eat. That practice has been identified time and time again
as the primary means by which BSE spread.

On the morning of 25 Dec 2003, the BSE world reference lab in Weybridge,
England, confirmed USDA's 23 Dec 2003 preliminary diagnosis of BSE in a
single nonambulatory dairy cow that had been slaughtered on 9 Dec 2003 at
Vern's Moses Lake Meats in Washington State.

At the time of USDA's preliminary diagnosis on 23 Dec 2003, USDA's Food
Safety and Inspection Service (FSIS) issued a Class II recall for the
facility's entire day's production. The recall was classified as Class II due
to the extremely low likelihood that the beef being recalled contains the
infectious agent that causes BSE.

The herd the affected animal came from is under a State quarantine in
Washington. While USDA has not made any decisions on the dispositions of this
herd, any cattle that die on the farm will be tested for BSE.

USDA's Animal and Plant Health Inspection Service (APHIS) has determined the
following additional information through its traceback investigation:

-- USDA is continuing to trace the other 73 head of cattle that came in the
same shipment. Furthermore, USDA has identified another shipment of 8 cows
from the same herd in Canada which USDA is also tracing.

-- The cow had 3 calves while she was in the United States. One of them died
shortly after birth. One of them remains in the herd in Washington State
where the index cow had most recently lived. That herd is under a "hold
order" placed by the State of Washington -- again, not to stop the spread of
disease, because BSE is not contagious, but rather to prevent further
complications to traceback and traceforward investigations. USDA is
continuing to consider the appropriate disposition of these animals.

-- A 3rd calf from the index cow -- her most recently born bull calf -- is
currently commingled in a herd of about 460 young bull calves, all around 30
days of age. That group of calves remains under a "hold order" pending
completion of USDA's epidemiological investigation. Maternal transmission of
BSE from mother to calf is very rare, if it occurs at all, but the animals
are being held out of an abundance of caution, to preserve public and
international confidence in the health of the U.S. cattle herd.

USDA's Food Safety Inspection Service (FSIS) has determined the following
additional information:

-- Since the discovery of BSE, FSIS has been working around the clock to
protect the public health. A recall was initiated out of an abundance of
caution following the report of one cow testing presumptive positive for
BSE. Even though USDA remains confident in the safety of these beef
products, USDA is and will continue to verify distribution and control of all
products related to this recall.

-- To briefly summarize the current situation on the beef products related to
the 23 Dec 2003 BSE recall. The beef products were distributed from Vern's
Moses Lake to Midway Meats on 11 Dec 2003. All of the central nervous system
related tissue, brain, spinal cord and distal ileum, were removed at the
Vern's facility during the slaughter that occurred on 9 Dec 2003. Those are
the tissues that are most likely to contain the BSE agent. Because the meat
leaving Vern's did not contain these high-risk materials, the recalled beef
presents an essentially zero risk to consumers.

-- FSIS is verifying that the customers have been notified of the recalled
products and know how to handle the product.

-- FSIS has found that the products were distributed to 42 locations from
Interstate Meats and Willamette Valley Meats. The vast majority of these
products -- at least 80 percent -- were distributed to stores in Oregon and
Washington.

-- FSIS is verifying that these 42 distributors are complying with their
requirement to notify their customers.

-- In overseeing this process, FSIS has found that all of the companies that
have received these products have been proactively notifying their customers.

APHIS and FSIS continue to work closely with our colleagues in State and
other Federal agencies as part of this investigation. Information will be
posted to <http://www.usda.gov> as it becomes available.

Consumers with other food safety questions can phone the toll-free USDA Meat
and Poultry Hotline at 1-888-MPHotline. The hotline is available in English
and Spanish and can be reached from 10 a.m. to 4 p.m. (Eastern Time), Monday
through Friday. Recorded food safety messages are available 24 hours a day.
 
The Institute of Medicine of the National Academies has recently completed a
2-year study on "Transmissible Spnongiform Encephalopathies: Assessment of
Relevant Science" and the final report entitled "Advancing Prion Science"
although not yet published, is available online at <http://www.nap.edu>; then
search on prion.

Much of the science relative to the present discussions of mad cow disease
and human threat are covered in that volume.

--
Richard T. Johnson, MD
Distinguished Service Professor of Neurology, Microbiology & Neuroscience
The Johns Hopkins University School of Medicine & Bloomberg School of Public
Health
The Johns Hopkins Hospital
600 North Wolfe Street
Baltimore, MD 21287
 
As far as I was told, prions are not full proteins, much the way viruses are not full DNA strands, but bits that invade a cell and force its own type of DNA to be replicated. Since it's only bits, the type of DNA that is replicated is dependent on the cell it invades and what DNA is available and what it uses.

Although, I do find it curious how strong a prion is, able to survive outside a host body for so long.... however, I don't find it "impossible" that 2 mutations could support each other to make a disease.
 
zakur said:
This guy claims the idea that prions cause BSE/TSE/CJD is junk science. He points the finger at Spiroplasma.
I've met a guy (actually he was Professor of Immunology at Imperial College, London, so not just your common or garden nut) who was convinced that spongiform encephalopathies are autoimmune reactions triggered by exposure to a soil bacterium called Acinetobacter calcoaceticus.

There were a lot of holes in his logic, though.

Point is, it's all very unclear. The apparent certainties displayed in the texts Steve cuts and pastes (I don't think he knows anything about TSEs, it looks to me as if he just does a Google search and posts the results to make himself look knowledgeable) really crumble when you examine the actual facts. Basically, a whole lot of "nobody really knows".

Rolfe.
 
Actually Rolfe what I know about prions comes mostly from concerns over scrapie as I was involved down the line in seconding a decision to use prion free Australian sheep to harvest anti-bodies to manufacture a specialized monoclonal polyclonal serum. This was instead of using potentially prion infected sheep in the UK (where the initial research was done) or sheep in the U.S. which also has scrapie outbreaks from time to time.

But beyond that, like everyone else I know what I have learned through reading and discussion. I assume you learn and know things the same way or does knowledge just pop into your head by some mysterious force making you so much smarter and wiser than the rest of us?

The NAS volume (on-line) on TSE's pretty much will sum up the current state of knowledge on this subject. This field has been evolving for decades. The only certainties thru that time were seen at post mortem. If your friend has a theory that some soil bacterium triggers a reaction that causes SEs, I am sure the whole world looks forward to him proving it.

Thanks also for the ad hominems.
Why don't you ask Hoyt if you can borrow his giant proctoscope and try it on yourself. ?
 
SteveGrenard said:
If your friend has a theory that some soil bacterium triggers a reaction that causes SEs, I am sure the whole world looks forward to him proving it.
I didn't say that Professor Ebringer was a friend, I said I'd met him. In fact I attended a lecture by him, and followed up by corresponding with him about the subject matter.

I believe he has quit the field, which is probably little loss: as I said, there were many holes in his theory which he was very reluctant to face up to. However, he did highlight some very real holes in the prion theory which don't go away.

Perhaps if you discussed matters intelligently, in your own words, people might believe you had some real knowledge and understanding to offer. Simply posting chunks of other people's pre-digested platitudes doesn't really foster a terribly good impression.

Rolfe.
 
Rolfe: Perhaps if you discussed matters intelligently, in your own words, people might believe you had some real knowledge and understanding to offer. Simply posting chunks of other people's pre-digested platitudes doesn't really foster a terribly good impression.


I said already I have limited knowledge on prions and that is based on an assesment of the published research and some limited experience looking at the scrapie problem when using sheep as antibody donors. There was absolutely no evidence the highly purified antibodies harvested from potentially scrapie infected sheep would transmit the disease but in an abundance of caution the manufacturer, the FDA and everyone involved agreed it would be best to harvest the antibodies from down-under prion-free sheep since prion diseases have never ever been found in Oz. If you were your buddy Larsen, you would be calling for references and URLS if they weren't offered; and, if they were offered, pedictably like I remember Flodin used to do, you would be calling for original thought. Are you falling prey to these deceptive skeptical mind-games or are you just one of them?

At the outset, in case you missed it Rolfe, I was BEING HELPFUL to someone who only knew this problem by the popular press name "Mad Cow Disease" and who was asking for more info they obviously couldn't find. LOL. I pointed them to searching such terms as Kuru, Scrapie, CJD, n-CJD and nv-CJD, Chronic Wasting Disease, BSE and a testing update because they are not apt to see any of these terms in the tabloids or dream them up themselves. Now they also know the USDA publishes regular, almost daily updates on this as well.

If your contact is right about his theory, science would have to find a new reason for the existence of prions in brain and spinal cord tissue. Wouldn't that be fun?
 
SteveGrenard said:
If your contact is right about his theory, science would have to find a new reason for the existence of prions in brain and spinal cord tissue. Wouldn't that be fun?
Oh, he covered all that in the lecture. That wasn't the problem. He believed that the prions were a consequence of the auto-immune process which was underway - produced by the pathology, rather than causing it.

However, there were lots of other problems with his theory. His erroneous information on the extent of the studies MAFF had done, for a start, and his refusal to face the fact that some of these studies had thrown up results which simply couldn't be explained by his hypothesis.

He never answered one simple question: if A. calcoaceticus is ubiquitious in the bovine intestine, why does it cause BSE when introduced back into that intestine by consuming intestinal contents? And what was it about the change in the rendering process which sparked the problem?

I spent some time trying to reformulate his theory to take account of the studies he was ignoring, and my more realistic assessment of the ubiquity (or lack of it) of A. calcoaceticus, because the start of the thought process had some merit. However, I came to the conclusion that there were far more problems with this hypothesis than the prion one.

As I said, I found out recently that he has given up in the huff, because he wasn't being taken seriously. Quel surprise. However, we mustn't forget that even the prion theory is only a theory, currently the least worst. There are still aspects of it which fly in the face of some very fundamental tenets of molecular biology.

Maybe as more is revealed we'll discover why the prion thing isn't impossible after all, and reconcile all the contradications. Probably this is the most likely outcome. But it's also possible that a completely novel approach might come up with a better model than any we currently have, and throw it all into the melting pot.

Rolfe.
 

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