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"Atypical" BSE Found in USA

Mike

Well-known member
Atypical' strain of BSE found in U.S. cattle
By Chris Clayton, DTN Staff Reporter, and Journal staff

The two cases of bovine spongiform encephalopathy found in U.S. cattle over the past year came from a rare strain of BSE found largely in Europe that scientists are only beginning to identify, according to research by a French scientist.

Researchers in France and Italy who presented their work at an international conference in London reported two rare strains of bovine spongiform encephalopathy that are harder to detect and affect mainly older cattle.

Thierry Baron of the French Food Safety Agency presented research indicating that a 12-year-old Texas cow testing positive for BSE last June, and the 10-year-old Alabama cow that tested positive in March, showed identical testing patterns to a small number of BSE cases in France, Sweden and Poland.

Animal scientists are calling such strains "atypical" BSE, which is different from the "typical" BSE caused by cattle eating feed with ruminant offal contaminated with a BSE protein.

They don't know whether the atypical strains are caused by something else or simply appear spontaneously in older, susceptible cattle.

Art Davis, a U.S. Department of Agriculture scientist for the Animal and Plant Health Inspection Service at the National Veterinary Services Laboratory in Ames, Iowa, said in his presentation Sunday at the London conference that the Texas and Alabama test results showed completely different prion patterns than the Washington state case discovered in December 2003.

"The classical lesions were not there," Davis said of the cases. The Washington state cow originated in Alberta, Canada, near where several other BSE cases have been found.

The "typical" BSE strain caused a mad cow disease epidemic in Great Britain beginning in the mid-1980s that killed 184,000 cattle and more than 100 people who contracted a human form of the disease caused by eating contaminated beef products.

The scientific evidence shows that in almost all cattle cases, the fatal neurological disorder was contracted through contaminated meat and bone meal fed to the cow, typically at a young age.

However, scientists finding atypical cases of BSE are beginning to question if there has been a change in the abnormal protein that causes BSE or if cattle might be susceptible to a sporadic BSE affecting older cattle.

Danny Matthews, head of transmissible spongiform encephalopathies at England's Veterinary Laboratories Agency, said recent research on atypical cases of BSE raises questions over whether older cattle can sporadically get the disease or if there are more strains of BSE than previously understood. Scientists might also be facing something new, such as "son of BSE," he said.

"We don't fully understand what atypical BSE means," Matthews said. "Is it spontaneous or another source causing it? Time will tell."

Although the test patterns in the U.S. cases and atypical cases in Europe closely matched, Baron said there were no known links among any of the positive animals. The French Food Safety Agency sent a researcher to the United States to study the positive Texas case and compare its results to known cases in France that did not match the typical BSE positive tests.

"You could place them side-by-side and not tell the difference," Baron said.

Baron also raised the prospect that the disease could be sporadic in at least a small number of older cattle. He said, however, such a conclusion would be hard to determine because of the small number of cattle with this atypical strain globally.

Dr. Sam Holland, South Dakota's state veterinarian, said there are many strains of BSE and varying degrees of infectiousness of the agent.

"What if the scenario is there is an atypical prion out there that is much less infective, has a longer incubation period and has not been recognized as part of the Great Britain BSE experience identified in 1985 and '86?" Holland said. "There could be others out there that we haven't recognized yet."

He said it is possible the atypical strains are not caused by contaminated feed.

He said it still makes sense to continue the ban on ruminant offal in cattle feed to prevent the spread of typical BSE and eventually to eliminate that disease.

"Based on what we know about BSE, it makes good sense to, number one, keep some surveillance in place; number two, watch what we import and restrict shipments and movements from places that have had those syndromes; and, number three, with what we know about BSE, it seems to be very prudent to keep our ruminant offal ban in place," Holland said. "At least for typical BSE's, it seems to be very effective. It's probably reasonable to continue the ruminant offal ban even after the last typical BSE case has been eliminated."

Editor's note: DTN, a private company based in Omaha, Neb., provides information to agriculture, energy trading markets and other weather-sensitive industries. The Rapid City Journal received a copy of DTN's story and expanded on it.

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flounder

Well-known member
Research Project: Study of Atypical Bse

Location:


Virus and Prion Diseases of Livestock

Project Number: 3625-32000-073-07
Project Type: Specific C/A

Start Date: Sep 15, 2004
End Date: Sep 14, 2007




http://disc.server.com/discussion.cgi?disc=167318;article=2213;title=CJD%20WATCH




NEW STRAIN OF TSE USA CATTLE OR JUST INCOMPETENCE IN TESTING???




http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf




http://www.google.com/search?num=30&hl=en&lr=&edition=us&ie=UTF-8&search=search&tab=wn&scoring=d&q=Research+Project%3A+Study+of+Atypical+Bse+Project+Number%3A+tss&btnmeta%3Dsearch%3Dsearch=Search+the+Web



TSS
 

Kathy

Well-known member
My opinion:

Spontaneous BSE:

resulting from long term, low level exposure to metals which do not replace copper on the PrPC protein, but are used in the manufacturing of new PrPC proteins from their inception. Exposure could be sporadic and therefore, takes years and years before the disease manifests itself, if ever.

Classical BSE:

resulting from exposure to copper chelating agents which yanked the copper from the animals existing PrPC proteins, and also robbed copper (chelated it) preventing its utilization by newly manufactured PrPC proteins - causing a sped-up version of BSE. Metals attached to classical BSE prions probably radio-active.

Excessive exposure to organophosphates, sulfur and molybdenum could bind the bio-available copper causing copper deficiency.

Exposure to crushed bones, could introduce heavy metals which are concentrated there (as well as in certain organs, including brain tissue).


Stanley Prusiner's webpage makes these statements:
Recent investigations argue that the length of the incubation time specified by prion strains is determined by the rate of PrPSc clearance

During prion replication, an as yet to be identified factor that we have provisionally designated protein X binds to PrPC. The PrPC/protein X complex then binds PrPSc; by an unknown process, PrPC is transformed into a second molecule of PrPSc.

It is an interesting opinion that clearance of the PrPSc determines the strain. The body's ability to clear PrPSc molecules would depend upon other mechanisms not prions. Special attention should be given to why some metals are more readily expelled from the body than others.

I must disagree with the second statement entirely, Prusiner's fellow researchers at U of California, (Davis) have demonstrated that the PrPC prion with copper loaded within the back-bone could not possibly form the PrPSc molecule.

More and more evidence is coming forward which demonstrates the anti-oxidant properties of the healthy PrPC prion. The healthy PrPC prion has copper attached to it in at least 5 places including the octarepeat region, and within the back-bone (center).

Spontaneous BSE is a reality; but, truely nothing is spontaneous! There is always a cause and effect mechanism. Stopping the recycling of bone meal (including MBM) has eliminated a very potent source of toxins and metals within the food chain.



Factor X, is not necessarily a protein or protein fragment. It could be a multi-valent metal by itself (or attached to a metalloprotein chaperone).

For PrPC protein conversion to PrPSc to take place, a powerful copper chelating agent must first somehow steal the copper from the existing PrPC molecule. It appears that TSE transmission experiments are not using copper chelating agents, therefore, the formation of PrPSc plaques, in the experimental animals, must be derived from newly manufactured prion proteins which are screwed up from the very beginning.
 
A

Anonymous

Guest
Thanks Mike- I had heard this on the radio yesterday and thought it was quite interesting - but was unable to find it in print this morning....

This finding by these French scientists may play a large role in the future if the US has to argue the effectiveness of their feedban so far...This shows that this "Type" has connections to Europe - and is not a continuation of the strain found in Canada and was not regenerated from Canadian imports- yet...Further reason we need to strengthen our BSE safeguards and feedban to keep it out of the country....

This also gives a little bit of an answer to why USDA had such a tough time recognizing it in their testing- being that it is an atypical strain....Altho it doesn't excuse many of their blunderings with the handling of it...

And it also brings up the question of how many other undiscovered TSE's there are out there ........And what causes this "Atypical" strain?
 

Manitoba_Rancher

Well-known member
Oldtimer, your jsut looking for some sort of reason to try and keep Canadian cattle out of the US to try and boost your prices to record highs. Guess what I dont think your protectionist butt is going to have a hope of succeeding. :yeah:
 

flounder

Well-known member
Reader (the second) wrote;


>>>The thing that struck me was that the U.S. public health establishment funds surveillance for CJD, to be on the look out for VARIANT CJD in the U.S. However the criteria that they have been using are that the pathology of the tissue will be identical to that of BSE and vCJD in the UK (florid plaques). They claim that U.S. CJD cases can't be related to ingestion of infected food because the pathology is different from the 160 UK/EU cases. ...<


Deja-Moo i.e. same old bull from USDA i.e. BSe Bull Sh!t Encephalopathy.
THIS is how it is suppose to work$$$


Singeltary et al UKBSEnvCJD only theory 2006


http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13



Received September 26, 2005
Accepted February 24, 2006

Long-duration sCJD with PRNP codon 129 methionine homozygosity and cerebral cortical plaques
Raymond Yen-Yu Lo MD, Woei Cherng Shyu MD, PhD, and Hung Li PhD*

From the Department of Neurology (R.Y.-Y.L., W.C.S.), Neuro-Medical Scientific Center, Buddhist Tzu-Chi General Hospital, Tzu-Chi University, Hualien, Taiwan; and Institute of Molecular Biology (H.L.), Academia Sinica, Taipei, Taiwan; Institute of Biochemistry (H.L.), National Yang-Ming University, Taipei, Taiwan.




* To whom correspondence should be addressed. E-mail: [email protected]


Abstract-- The authors investigated a 40-year-old woman who presented with ataxia and dementia with little progression for over 40 months. The results of a CSF 14-3-3 protein and EEG study did not reveal major abnormalities. Brain MRI showed increased signal intensity over the occipital cortex in diffusion-weighted imaging. To our knowledge, this is the longest MM-type sporadic Creutzfeldt-Jakob disease case with cortical kuru-type plaques.


...snip


further into this study i find interesting ;

Discussion. Only 5 to 10% of patients with CJD
are reported to have duration of illness longer than 2
years. A clinicopathologic study conducted over 20
years found that only 15 of 225 patients with CJD
(7%) had clinical disease duration of 2 or more years,
and four of these were familial cases.2 Genetic study
for mutation was not yet available, so the true incidence
of long-duration sCJD was not known. The
PRPN gene of familial spongiform encephalopathy
presents with a point mutation, octapeptide repeat
insertion or deletion. These pathogenic mutations
may produce a 5- to 10-year history of slowly evolv-

ing dementia. However, our patient did not have positive
family history and the genetic analysis of her
PRPN gene proved normal without pathogenic
mutation.
It has been demonstrated that both the haplotype
at codon 129 of the PRNP gene and the type of
protease-resistant prion protein correlate well with
clinical and pathologic features of sCJD,3 and a phenotypic
classification with six groups (MM1, MM2,
MV1, MV2, VV1, VV2) has also been developed.5 Although
some consider the codon 129 genotype only
one factor in determining sCJD phenotype,6 it is generally
concluded that survival is shorter in patients
who are MM at codon 129 of the PRNP gene compared
with that seen in MV and VV cases.1 Among
sCJD MM1 and MM2 cases in a previous study,5 the
longest disease duration was 36 months. However,
our patient was MM at codon 129 without typing of
protease-resistant prion protein and still not confined
to wheelchair or bed after 40-month disease
progression.
The pathologic study demonstrated the prion protein
within spongiform changes and the accumulation
of amyloid or kuru plaques, consistent with the
findings for patients with CJD of long survival.7
Kuru-type plaques are associated with MV24 sCJD
subgroups but were not found in MM cases until one
recent case report.8 However, this patient presented
with a rapid progression to death in an 11-month
clinical duration, much shorter than in our case.
Despite the codon 129 methionine homozygosity,
our patient shared many clinical manifestations with
MV2 subgroup including signs of cognitive decline
and ataxia, long disease duration, and kuru-type
plaque formation (table). Nevertheless, proteaseresistant
prion protein typing was not characterized
in our patient due to limited tissue biopsy. According
to a previous study,5 we believe that Western blot
analysis of the prion protein would help to further
clarify this contradiction in classification. ...end
2 NEUROLOGY 66 June (2 of 2) 2006

===============================

NOVEMBER 15, 1999


Re: vCJD in the USA * BSE in U.S. 15 November 1999
Previous Rapid Response Next Rapid Response Top Terry S Singeltary,
NA
medically retired

Send response to journal:
Re: Re: vCJD in the USA * BSE in U.S.

In reading the recent article in the BMJ about the potential BSE tests being
developed in the U.S. and Bart Van Everbroeck reply. It does not surprize
me, that the U.S. has been concealing vCJD. There have been people dying
from CJD, with all the symptoms and pathological findings that resemble U.K.
vCJD for some time. It just seems that when there is one found, they seem to
change the clarical classification of the disease, to fit their agenda. I
have several autopsies, stating kuru type amyloid plaques, one of the
victims was 41 years of age. ...


snip...FULL TEXT;


http://bmj.bmjjournals.com/cgi/eletters/319/7220/1312/b#5406



U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
well... 2 January 2000
Top Terry S Singeltary
retired



http://bmj.bmjjournals.com/cgi/eletters/320/7226/8/b#EL1



TSS





http://www.neurology.org/cgi/content/abstract/01.wnl.0000217913.37108.94v1
 

Kathy

Well-known member
Murgen,

As far as I know, sheep have fewer locations on the prion protein for copper to attach, than cattle.

For example: if sheep have 3 locations and cattle have 6, then the sheep would require a lower concentration of copper to fill these three spots (in competition with other metals). If other metals bind in the sheep prion locations where copper should have, they will more readily manufacture a defective prion. Cattle with more copper binding sites, would be less susceptible to defective prions when only a few metals, besides copper, bind to the prion. In other words, there is more wiggle room for cattle prions because they have more binding locations.

All mammals still require copper!

A report on Oil and Gas Emissions came out in May (WISSA - Western Interprovincial Science Studies Association). Forage analysis of 501 samples in Alberta and Saskatchewan showed dietary deficiency in these forage samples:

95% were deficient in Zinc
93% were deficient in copper
64% were deficient in phosphorous
60% were deficient in selenium


The report also stated, that "higher than recommended concentrations of molybdenum, sulfur or nitrates" were found.

The study also stated, that most ranchers/dairies were aware of the deficiencies and supplemented their cattles' diets.

I'd bet that most ranchers are not aware that their feed is deficient in this many minerals. I'd like to get a mineral that supplements the copper and selenium but ALL the trace metal salt blocks sold here contain very high levels of manganese, and their cobalt levels are almost nothing.
 

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