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From: TSS ()
Subject: U.S. Agriculture Department denies allegation it's hiding mad-cow cases ;-)
Date: April 7, 2005 at 7:30 pm PST

-------- Original Message --------
Subject: U.S. Agriculture Department denies allegation it's hiding mad-cow cases
Date: Thu, 07 Apr 2005 21:38:56 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy
CC: CJDVOICE


U.S. Agriculture Department denies allegation it's hiding mad-cow cases

April 7, 2005 - 18:52

WASHINGTON (CP) - The U.S. Agriculture Department said Thursday there's
"no way" it would hide cases of mad-cow disease because that would hurt
the beef industry.

A former department veterinarian, Dr. Lester Friedlander, said this week
on a speaking tour in Edmonton that U.S. officials found new cases of
the disease and chose not to reveal them.

"That's just not the case," spokesman Ed Loyd said, adding officials
expected to discover more cases but haven't yet.

"There's no way we'd benefit by being anything less than completely
transparent. It would jeopardize the markets we're trying to open," said
Loyd.

"It would set the entire beef industry in this country back. We're not
going to do anything to jeopardize that."

Friedlander, who's been invited to speak to Parliament's agriculture
committee next week, couldn't be reached for comment Thursday.

He told the Edmonton Journal newspaper Wednesday it's not credible the
United States has found just one case out of 120 million cattle.

The department revealed in December 2003 a Washington state cow
originally from Alberta tested positive for the disease.

Canada has announced three other cases. The first, in May 2003, sparked
an industry crisis when the United States shut the border to Canadian beef.

Last June, the United States launched a wider surveillance program and
has conducted 280,000 tests since.

"We expected to find additional cases," said Loyd.

"We still may but that has not occurred. All the results have been
negative."

Friedlander, a USDA veterinarian from 1985 to 1995 and chief inspector
at the largest hamburger plant in the U.S., said he was fired for
speaking out about safety issues.

He said former colleagues have told him about new cases of mad cow, or
bovine spongiform encephalopathy but they're near retirement age and
risk losing their pensions if they speak out.

The border was supposed to reopen to Canadian cattle March 7 but that
was temporarily delayed by a court challenge from R-CALF Stockgrowers of
America, a protectionist ranchers' group based in Montana that insists
Canadian meat is unsafe.

U.S. officials have appealed the ruling in an effort to resume trade
until a hearing on the long-term future of the border can be heard in July.

http://www.680news.com/news/international/article.jsp?content=w040755A

right...............

I had acquired the transcript of the Oprah trial yeas ago,
I still have the news clippings about this, my favorite part ;


CHIP -

exhibit 280, ... According to this US Department of Agriculture report,
encephalitis caused by unknown reasons could be a warning sign for
bovine spongiform encephalopathy, or mad cow disease. Is that your
understanding?

MIKE - Well, that's one of the things they told us to look for.

CHIP - Yeah, that's my point. Now, would you pull out Exhibit 358,
please. Could you tell us what those documents are?

MIKE - Those are dead slips from Cactus Feeders.

CHIP - Your fathers company.

MIKE ENGLER - Yes.

CHIP - and these show that the cause of death was encephalitis, correct?

Mike studies Exhibit 358.

MIKE ENGLER

Encephalitis, yes.

CHIP

And that was one of the neurological diseases that we just saw the
United States Department of Agriculture was saying was a possible cause
(Chris, you put case, but probably meant cause) of suspected BSE,
correct?

MIKE - Correct.

CHIP - There's something else stamped on here.
It says ''picked up by your local used cow dealer''.
Do you see that?

MIKE - Yes

CHIP - And that stamp means that these cows had died of encephalitis
before being taken to the rendering plant where they were ground
up, or rendered, in to feed for other cattle, correct?

MIKE - That's a possibility. .....snip....end
==============================


FDA Statement

FOR IMMEDIATE RELEASE
Statement
May 4, 2004

Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA


Statement on Texas Cow With Central Nervous System Symptoms

On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to
a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately
began an investigation. On Friday and throughout the weekend, FDA
investigators inspected the slaughterhouse, the rendering facility, the
farm where the animal came from, and the processor that initially
received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over
the weekend FDA was able to track down all the implicated material. That
material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known
as "mad cow disease," can exhibit such symptoms. In this case, there is
no way now to test for BSE. But even if the cow had BSE, FDA's animal
feed rule would prohibit the feeding of its rendered protein to other
ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and
informing the firm that FDA will not object to use of this material in
swine feed only. If it is not used in swine feed, this material will be
destroyed. Pigs have been shown not to be susceptible to BSE. If the
firm agrees to use the material for swine feed only, FDA will track the
material all the way through the supply chain from the processor to the
farm to ensure that the feed is properly monitored and used only as feed
for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the
U.K. showed that the disease spreads by feeding infected ruminant
protein to cattle.

Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action
specifying that the material go only into swine feed means also that it
will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates
closely with the U.S. Department of Agriculture on all BSE issues. The
animal feed rule provides crucial protection against the spread of BSE,
but it is only one of several such firewalls. FDA will soon be improving
the animal feed rule, to make this strong system even stronger.

####

rule

http://www.fda.gov/bbs/topics/news/2004/NEW01061.html


Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...

snip...

It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...

snip...

3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...

snip...

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

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


TSS






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