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From: TSS (216-119-132-20.ipset12.wt.net)
Subject: Re: DAILY COMMODITY MARKET COMMENTARY Tuesday, October 12, 2004 15:26 GMT ''Oprah should be looking into the cattle industry again''
Date: October 13, 2004 at 12:19 pm PST

In Reply to: DAILY COMMODITY MARKET COMMENTARY Tuesday, October 12, 2004 15:26 GMT ''Oprah should be looking into the cattle industry again'' posted by TSS on October 12, 2004 at 1:11 pm:

Two-two-twos-day! · 31 August 04
in News

So it turns out that there is a group of major US beef companies and Japanese food service companies who are fed up with the continuing Japanese ban on US beef. They’ve apparently decided to break out their copies of Outlook Express, since they’re on an email campaign directed at governmental officials from both countries. (This, BTW, is often referred to as “astroturfing.”

The High Plains Journal has a short blurb about the whole thing:
“We cannot wait for the U.S. and Japanese government bureaucrats to solve the problem,” one of the Japanese organizers of the campaign told DTN. “Bureaucrats don’t do anything.”

Last December 24, American beef trade with Japan and most other markets came to a halt as the U.S. announced its first case of bovine spongiform encephalopathy.

In public, the U.S. and Japanese officials continue to volley over the state of the talks. On Monday, for example, a senior Japanese official denied any progress in beef talks.

And, while this is going on there’s a company out of Ft. Lauderdale called The Trader’s Exchange Corporation that’s complaining that the USDA isn’t doing enough to prevent mad cow disease from spreading in the US cattle population, and that it’s having a negative effect on cattle futures:
Both Cattle markets are still trading near historical highs and traders should be building long term Put positions or selling futures on rallies. The USDA is not doing anything to help detect and prevent Mad Cow disease and if the media where to focus on this Cattle prices would be near historical lows.

Comment
http://madcowering.com/?c=News

commenting closed for this article
http://madcowering.com/?c=News

I find it most disturbing that the
thread below is closed;

And, while this is going on there’s a company out of Ft. Lauderdale called The Trader’s Exchange Corporation that’s complaining that the USDA isn’t doing enough to prevent mad cow disease from spreading in the US cattle population, and that it’s having a negative effect on cattle futures:
Both Cattle markets are still trading near historical highs and traders should be building long term Put positions or selling futures on rallies. The USDA is not doing anything to help detect and prevent Mad Cow disease and if the media where to focus on this Cattle prices would be near historical lows.

Comment

commenting closed for this article

SEEMS THIS company out of Ft. Lauderdale called The Trader’s Exchange Corporation that’s complaining that the USDA isn’t doing enough to prevent mad cow disease, seems they are very much
up on this topic and are not taking
the lies that the Bush administration has been telling them. I APPLAUD THEM! THEY HAVE BALLS where most media just prints
what the feds want them to.

MY MOTHER AND MANY MORE ARE DEAD
FROM THIS AGENT AND THE DEATHS ARE
MOUNTING. PLEASE ALLOW ME TO TELL
YOU THE TRUTH. YES, I AM ANGRY!
WE HAVE BEEN LIED TO, JUST TO SAVE
THERE PRECIOUS COMMODITIY.
NO MORE!!!

lets see, where do i start;

1st, let me tell you something.
TSE has been in the USA bovine for
decades, just a differenct strain.
daaaaaaaaaaaaaaaa;

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

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

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

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

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

INTRODUCTION

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

OBSERVATIONS AND RESULTS

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

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

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

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

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

MARSH

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

THE most disturbing factor of this topic are the new atypical TSEs
showing up in not only cattle, but also sheep, and no one knows yet
about how many different strains of cwdTSE in deer/elk. WITH evidence of
sporadic CJD being very similar to these atypical TSEs in cattle and sheep,
and the findings from Asante, Collinge et al that BSE prions propagate
as either nvCJD or sporadic CJD, the ramifications of these findings are very very worrisome and should not go ignored any further. WITH
the fact that there are over 20 documented strains of scrapie, and the
most logical hypothesis is scrapie to BSE, why would one believe in
only one phenotype of TSE in the bovine. IN fact, we have a new study
of two distinct prion strains derived from BSE in mice. YOU must not
continue to ignore these studies;

BSE prions propagate as either variant CJD-like or sporadic CJD-like
prion strains in transgenic mice expressing human prion protein

http://embojournal.npgjournals.com/cgi/content/full/21/23/6358

THE new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic Creutzfeldt-Jakob disease

http://www.pnas.org/cgi/content/abstract/0305777101v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt-Jakob disease: Implications for
human health

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

In an experimental study of the transmissibility of BSE to the pig,
seven of 10 pigs, infected at 1-2 weeks of age by multiple-route
parenteral inoculation with a homogenate of bovine brain from
natural BSE cases developed lesions typical of spongiform
encephalopathy…

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract
THE recent discoveries of previously unidentified strains of
Scrapie such as 221C44 and the Nor9845;

FULL TEXT APPRX. 91 PAGES

UK Strategy for Research and
Development on Human and Animal
Health Aspects of Transmissible
Spongiform Encephalopathies

2004-2007

http://www.mrc.ac.uk/pdf-uk_strategy_v5.2.pdf

WHEN in fact, the findings from Marsh and the findings at
MISSION, TEXAS support even further evidence that there
are further strains of TSE in the USA besides that one
accidentally documented BSE case in Washington on
Dec. 23, 2003;

In Confidence – Perceptions of unconventional slow virus diseases of animals in the USA – Report of a visit to the USA – April-May 1989 – G A H
Wells [head of England’s main veterinary lab]

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

YEP, THAT company out of Ft. Lauderdale called The Trader’s Exchange Corporation that’s complaining that the USDA isn’t doing enough to prevent mad cow disease from spreading in the US cattle population, IS JUST TELLING
THE DAMN TRUTH, and folks such as
yourself are just ignoring it.

TRANSMISSIONS STUDIES DO NOT LIE,
ONLY POLITICIANS AND THE CORPORATIONS THAT PUT THEM IN OFFICE DO….........

4.5 MILLION WITH ALZHEIMERS AND
BY 2050 WILL BE 19 MILLION.

4 UNIVERSITY STUDIES SHOW THAT
FROM 3 TO 33 % OF PEOPLE DIAGNOSED
WITH ALZHEIMERS AFTER AUTOPSY,
ACTUALLY HAD CJD (YALE, DUKE, PA
AND A MEXICAN STUDY).........

IT’S ALL BEEN DOCUMENTED…..

TSS

FULL TEXT;

http://madcowering.com/article/63/#comment

TSS




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