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Ongoing BSE cases linked to dirty feed bins

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rkaiser

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:lol: :lol: :lol: :lol: :lol:

Good one R2.

They forgot to mention that these feed bins had been brought down from Mars the previous year. Prions were actually placed in the bins by Martians planning to take over the world once humans have been eradicated by their biological warfare techniques.
 

TimH

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reader (the Second) said:
Ongoing BSE cases linked to dirty feed bins
FORDYCE MAXWELL
VETERINARY scientists now believe that dirty feed bins are the most likely cause of cattle born after the end of July 1996 developing BSE.

That was when a ban was introduced on the use of bonemeal, identified as the source of the BSE epidemic of the early 1990s, in ruminant rations.


But a number of cattle born after the ban started - known as BARB (born after the reinforced ban) cases - have developed the brain disease BSE, linked since March 1996 with the fatal human condition CJD.

Yesterday Charles Milne, Scotland's chief state vet, said nine herds in south-west England, the West Midlands and south-west Wales have produced 20 BARB cases.

Investigations on these farms have revealed a possible source of infection as the BSE agent - still never identified precisely - existing inside feed bins that had not been thoroughly cleaned for years.

Milnes said: "In experiments, as little as one milligram of BSE-infected brain tissue has been enough to infect a calf. In some of these herds, feed was stored in feed bins that were in use before August 1996, and had never been cleaned."

Similarly, he said, recent 2001 and 2002 BARB cases from a single herd in south-west Wales might have been infected by old feed dislodged when a bin was moved in 2002.

He said: "We believe that the current risk of BSE infection as a result of the persistence of the BSE agent in feed bins, from feed produced prior to the feed ban, is extremely low. Nevertheless, we strongly recommend feed bins are cleaned routinely and very thoroughly, particularly those in use before August 1996 and not cleaned out since."

Public health risks from BARB cases are negligible, Milnes said, because of strict controls that take specified risk materials from cattle carcases out of the human food chain. But he added: "Our aim is total eradication of BSE from the national herd by the end of 2010. To do this we need the continued help of farmers and veterinary surgeons throughout the UK."

BSE cases reached a peak in the early 1990s with more than 200,000 cases a year. Fewer than 200 a year are now being found and no cattle born since July 1996 and found to be developing BSE originated in Scotland.

This article: http://business.scotsman.com/agriculture.cfm?id=2402752005

Last updated: 14-Dec-05 01:20 GMT

http://business.scotsman.com/agriculture.cfm?id=2402752005


So BSE has now been "linked" to CJD and not only vCJD?? Ya, OK. :roll:

If the BSE agent is "still never identified precisely" how can they make any definitive claims about the source of this "agent" and what it may or may not be capable of?? :roll:

Great article, R2. :wink:
 

rkaiser

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vCJD - CJD - MAD COW - Whichever term best keeps the fear boiling.

R2 was a martian wasn't she?
 

rkaiser

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I always have fun R2.


although we have not had an epidemic so our feed was likely never infectious to the extent that it was in the UK.

You know darn well that I will never agree to a statement like this R2.

Feed is not infectious, unless you possibly consider the rouge metals floating in the feed, potential for future problems.
 

TimH

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reader (the Second)- "TimH - I believe in the UK, they often use CJD where they mean vCJD. The family of diseases are extremely similar with the age of the vCJD victims being the primary differentiator, besides the pathology at autopsy. And presumably the route of infection."

Thanks for clearing that up, R2. No big deal when scientists fail to use the correct terms,right? After all, what's the worst thing that could happen?? So what if people get the impression that classic CJD is somehow linked to beef consumption!!! No big deal, right R2??

So, other than having different pathology at autopsy, vCJD and CJD are extremely similar diseases. I see. :roll:

reader (the Second)- "I didn't even pay attn to the "CJD" quote.... Get a life"

The last time you didn't pay attention to what you were posting you ended up telling a big fat "mistake" on this forum, R2. Remember the "prions in milk" thing??? :roll:

And just what is the supposed link between vCJD and beef consumption, anyway??? Is there any more to it , other than BSE and vCJD seemed to emerge at roughly the same time?? Some would argue that that evidence is circumstancial, at best. Are you aware of any definite linkage between the two diseases R2???
 

Kathy

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For 20 some years, the science behind BSE has been slopped across the news paper pages, like a mop on a dirty floor. Spreading the dirt, and never cleaning things up entirely.

While statements such as those made by VLA, and Scotlands head vet, eg: "In experiments, as little as one milligram of BSE-infected brain tissue has been enough to infect a calf" are regurgitated over and over again with no debate.

If it were so darn easy to infect these cattle, why on Earth were they unable to infect ANY cattle in their experiments at High Mowbray. "...no cases of BSE have developed in the feeding studies involving 1000 cows that were experimentally challenged with high doses of MBM feed/innoculant on a Dept of Agriculture farm at High Mowbray in Yorkshire, UK." quote Mark Purdey article, Aug. 2003. Why, to this day, are researchers, like those in Lethbridge Alberta, having to inject concentrated, sonicated PrPSc directly into the brains of cattle, in order to transmit the disease agent?

All the scientists working on this disease have never infected a cow by feeding that animal "spiked (artificially poisoned)" Meat and bone meal, or milk replacer. They have had 20 plus years to do this, and still, we are basing our science on injecting and or drenching concentrated PrPSc homogenated tissue.

I am beginning to believe man did evolve from apes!
 

flounder

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TEXAS
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

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

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

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

snip...

THE FUTURE

4..........

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

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

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

SEE full text ;

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




pigs & pharmaceuticals


http://www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf





Terry S. Singeltary SR.
P.O. Box 42
Bacliff, Texas USA 77518



http://neurology.thelancet.com Published online October 31, 2005


Coexistence of multiple PrPSc types in individuals with

Creutzfeldt-Jakob disease

Magdalini Polymenidou, Katharina Stoeck, Markus Glatzel, Martin Vey, Anne Bellon, and Adriano Aguzzi

Summary

Background The molecular typing of sporadic Creutzfeldt-Jakob disease (CJD) is based on the size and glycoform

ratio of protease-resistant prion protein (PrPSc), and on PRNP haplotype. On digestion with proteinase K, type 1 and

type 2 PrPSc display unglycosylated core fragments of 21 kDa and 19 kDa, resulting from cleavage around amino

acids 82 and 97, respectively.

Methods We generated anti-PrP monoclonal antibodies to epitopes immediately preceding the differential proteinase

K cleavage sites. These antibodies, which were designated POM2 and POM12, recognise type 1, but not type 2, PrPSc.

Findings We studied 114 brain samples from 70 patients with sporadic CJD and three patients with variant CJD.

Every patient classified as CJD type 2, and all variant CJD patients, showed POM2/POM12 reactivity in the

cerebellum and other PrPSc-rich brain areas, with a typical PrPSc type 1 migration pattern.

Interpretation The regular coexistence of multiple PrPSc types in patients with CJD casts doubts on the validity of

electrophoretic PrPSc mobilities as surrogates for prion strains, and questions the rational basis of current CJD

classifications.


snip...


The above results set the existing CJD classifications

into debate and introduce interesting questions about

human CJD types. For example, do human prion types

exist in a dynamic equilibrium in the brains of affected

individuals? Do they coexist in most or even all CJD

cases? Is the biochemically identified PrPSc type simply

the dominant type, and not the only PrPSc species?


http://neurology.thelancet.com Published online October 31, 2005




what i been saying for years, that the diagnostic criteria differentiating between the nvCJD (i.e. 'the chosen ones') and the sCJD (i.e. 'the forgotten ones') has been terribly flawed from the beginning. .... full text html at bottom of this email, if you want the full text pdf with all the bells and whistles, please email me and i will send pdf....tss
 

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