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From: TSS ()
Subject: Mad cow testing dispute or cover-up ???
Date: May 10, 2006 at 7:17 am PST

Mad cow testing dispute featuressome crazy bureaucratic logic

Last Updated: May 8, 2006, 05:00:10 AM PDT

A ranching and meat-processing company in Kansas wants to test all its cattle for mad cow disease at its own expense.
The Bush administration won't let the firm do it. Oh, but that's not all. If the company tries to buy the $20 testing kits, the feds will treat such a transaction as an illegal purchase of a controlled substance.

We wish we were making this up, but we're not. Talk about mad cow, this is crazy people. It's also an intrusive government abusing an old law.

In 1913, when cholera was decimating hog herds, scam artists were selling fake serums to farmers. Congress responded with the Viruses, Serums, Toxins, Anti-Toxins and Analogous Products Act. It gave the federal government authority to regulate diagnostic testing devices for farm animals.

The Bush administration rediscovered this law when the Kansas company, Creekstone Farms, announced plans to test its entire herd for mad cow disease. The company was willing to go far and beyond the government's test regimen to reassure its customers in places such as Japan.

Private companies make these test kits and there is nothing dangerous about them. Still, the U.S. Department of Agriculture says ranchers such as Creekstone Farms can't buy them.

Creekstone Farms is a victim of a much larger debate over the nation's limited testing of its beef supply. The USDA tests about 1 percent of the nation's beef cattle for mad cow disease. That sampling, the government and large meatpacking companies say, is plenty. Many other nations, especially those that import our beef, test a far greater percentage of their herds. Japan requires 100percent testing.

Creekstone Farms once sold its high-end Angus beef (no growth hormones, no antibiotics) to Japan. Now it can't because of this mad cow disease testing dispute between Japan and the Bush administration. Nor can Creekstone Farms voluntarily test 100percent of its cattle, because the USDA has cut off the supply of thetest kits.

In business, the customer is always right. The Bush administration is wrong to deny Creekstone's customers — whether in Topeka or in Tokyo — access to tested beef. So, Creekstone is suing the USDA.

The administration likes to tout "free market" solutions to big problems. Creekstone came up with a good one. It's crazy not to let the firm pursue it.

BOTTOM line, the USDA and GW et al know exactly what will happen if they 'test to find' mad cow i.e. BSE in the USA, they will find many many cases. THIS is the only reason why they dug this old 1913 law. THE june 2004 enhanced BSE surveillance program was designed 'not to find' BSE, but they accident found a few cases. i cannot imagine how many cases would actually have been found if they would have used proper BSE testing protocols and used proper testing on the 9,200 they refused to use rapid test or WB. with the terribly flawed IHC test that were used on those 9,200 animals, all 9,200 could very well have been positive BSE. AS the CDC's Prion expert said, all those tests before 2005 are meaningless...

Paul Brown CDC

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

'The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases,' Dr. Paul Brown, former medical director of the National Institutes of Health`s Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. 'The question was, `How many?` and we still can`t answer that.'

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has 'absolutely no confidence in USDA tests before one year ago' because of the agency`s reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency`s inspector general.

'Everything they did on the Texas cow makes everything they did before 2005 suspect,' Brown said....

I can show you documents from the USDA and the UK and much more, showing where they lied,
distorted, twisted the facts over the years, put off and put off just to be an 'industry friendly'
policeman, and here we are, with a country that has more documented TSE in more species
than any other country, with who knows how many exposed, with a proven terribly flawed and
or inept TSE surveillance system for humans and animals, a broke down feed ban, and a bunch
of dead beats in the white house, sitting in a cloak of fear and under the guise of DHS. ...

yee haw !


.42 On 15 May Mr Bradley sent a minute to Dr Watson, Dr Shreeve, Dr Roberts,
Mr Wells and Mr Mike Dawson noting that, 'by agreement with the Director',
the proposed Vision article would now be circulated as a separate Directive
to VICs in England and Wales only.


It has been agreed that a joint/co-ordinated CVL-VIS publication will be
produced in due course. Meanwhile, because of the nature of the disorder,
its political implications and possible effects on exports it is essential
that VIS staff must not, at this stage, discuss it with or consult workers
at Research Institutes and University Departments. Furthermore, any
statements for publication or discussions at meetings must be cleared by the
respective Directors of the Services.

2.44 On 27 May Dr Peter Dawson succeeded Dr Williams as the ACVO and Head of
the VI Service, and Dr Richard Cawthorne succeeded Dr Peter Dawson as Head
of the Veterinary Investigation Section (VI Section) at Tolworth.

2.45 The final version of Mr Wells's article, entitled 'A Novel Bovine
Neurological Disorder?', was eventually circulated on 8 June 1987 to
Superintending Veterinary Investigation Officers in England and Wales. The
document was headed 'urgent' and 'in confidence'. It described the nature,
symptoms and pathology of the new disease and gave instructions for the
submission of pathological material to the CVL. It included the following

Similar clinical cases are of interest to VI Section, Tolworth, and the
Pathology and Virology Departments at CVL. Such cases must be notified
initially only to SVO(HQ), VI Section, Tolworth and Neuropathology Section,
Pathology Department, CVO. At this stage VI staff should not consult workers
at Research Institutes or University Departments . . .
A co-ordinated VIS/CVL publication on this subject is proposed. All
statements for publication, or discussion at meetings MUST BE CLEARED by
respective Directors of Services.

It is essential not to refer to the condition as bovine scrapie. While the
clinical and pathological changes may provide evidence of its similarity to
diseases caused by unconventional infectious agents such as scrapie in
sheep, it is important to emphasise that the aetiological basis of BSE
remains unknown and no connection with encephalopathies in other species,
including scrapie in sheep, has been established.

. . . the fact that it so far appears to be a uniquely British disorder
could prejudice our cattle exports if it is publicised in inaccurate or
exaggerated terms. It would be particularly misleading if it were to be
described as 'scrapie in cattle'. Scrapie is a disease of sheep, the
existence of which in British flocks is an impediment to our export trade,
but although it is also an encephalopathy there is no evidence that BSE is
attributable to the same cause as scrapie and it is important to distinguish
between the two conditions . . .
A point to emphasise, if you are pressed on numbers of cases, is that while
it may be suspected in over 100 herds and distributed over a wide area, it
has been confirmed in only 25 animals, out of a total UK cattle population
of just over 12.5 million. Moreover, cases tend to be in individual animals
rather than whole herds being affected. There is no evidence that it is
transmissible to humans or that the meat or milk from animals with BSE are

Office Note


A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer





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

To minimise the potential damage to compound feed markets through adverse

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.




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 ;

and what did the USDA say when all this was going on ;

''this was a fanatical incident to be _avoided_ in the US _at all

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


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...


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


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_...


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

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


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

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.


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.


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.

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

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
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
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
diseases of the nervous system. Vol. 1, Academic Press, New York, pp
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in
Proceedings of the Seventh Annual Western Conference for Food Animal
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
in cattle. Vet. Rec. 121:419-420.


and then the BSE MRR policy of the legal trading of all strains of TSE globally was born $$$,
thanks to GW and the OIE. ...

my Mom died 12/14/97 confirmed Heidenhain Variant Creutzfeldt Jakob Disease

the ukbsenvcjd only theory is total BSe, Bull Sh!t Encephalopathy (i can send the long version to explain that)




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