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From: TSS ()
Subject: BSE CANADA/USA Latest Information (as of May 8, 2006 - 16:00 EST)
Date: May 8, 2006 at 2:36 pm PST

Latest Information (as of May 8, 2006 - 16:00 EST)
The Canadian Food Inspection Agency (CFIA) has tested 12 cattle potentially exposed to the same feed as the affected animal. All tests were negative.
The remaining 11 cattle from the feed cohort are being evaluated for compensation purposes and will be tested shortly.
The investigation of animals of interest has been concluded. This includes 146 cattle from the affected animal’s feed cohort and its two most recently born offspring.
Of these groups, 74 cattle had previously died, 34 cattle were deemed untraceable due to lack of information, 23 live cattle were located and 15 cattle were exported to the United States. Thirty-four untraceable animals out of 146 is not an unusual rate for investigations of this type.
The findings of the feed investigation are being reviewed and will be posted to the CFIA’s Web site in a final report.

Jim Rogers (202) 690-4755

Statement by USDA Chief Veterinary Officer John Clifford Regarding Canada’s BSE Epidemiological Investigation
April 28, 2006

"The U.S. Department of Agriculture continues to work closely with our counterparts in Canada on animal tracebacks in regards to their most recent case of BSE. Canada has informed us that 15 feed cohorts of the BSE-positive animal entered the United States. USDA has located one of these animals, and it will be euthanized and tested. The disposition of the remaining 14 animals is still being determined. "Experience worldwide has shown us that it is highly unusual to find BSE in more than one animal in a herd or in an affected animal's offspring. However, we will continue to work with Canada to locate as many animals of interest in this case as possible. It is important to remember that the United States maintains a series of interlocking safeguards which are what protect animal and public health. These safeguards include the removal of specified risk materials from the food supply and the Food and Drug Administration's 1997 ruminant-to-ruminant feed ban."

May 2, 2006 Statement by USDA Chief Veterinary Officer John Clifford Regarding the Conclusion of the Epidemiological Investigation Into a Bovine Spongiform Encephalopathy (BSE)-Positive Cow Found in Alabama
• Alabama BSE Investigation Final Epidemiology Report

no comment, its disgustingly hopeless, but reminds me of ;


.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 directions:

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 affected.

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 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.




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 ;

Like lambs to the slaughter
31 March 2001
Debora MacKenzie
Magazine issue 2284
What if you can catch old-fashioned CJD by eating meat from a sheep infected
with scrapie?
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but
Singeltary was suspicious. The diagnosis didn't fit her violent symptoms,
and he demanded an autopsy. It showed she had died of sporadic
Creutzfeldt-Jakob disease.

Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number
of campaigners who say that some sCJD, like the variant CJD related to BSE,
is caused by eating meat from infected animals. Their suspicions have
focused on sheep carrying scrapie, a BSE-like disease that is widespread in
flocks across Europe and North America.

Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in ...

The complete article is 889 words long.

full text;

Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*,
Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James
Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys*
* Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction
des Sciences du Vivant/Département de Recherche Medicale, Centre de
Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc,
BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre
Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de
Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital,
75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western
General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and
Institute for Animal Health, Neuropathogenesis Unit, West Mains Road,
Edinburgh EH9 3JF, United Kingdom

Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)


There is substantial scientific evidence to support the notion that bovine
spongiform encephalopathy (BSE) has contaminated human beings, causing
variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns
about the possibility of an iatrogenic secondary transmission to humans,
because the biological properties of the primate-adapted BSE agent are
unknown. We show that (i) BSE can be transmitted from primate to primate by
intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD
to humans could be readily recognized pathologically, whether it occurs by
the central or peripheral route. Strain typing in mice demonstrates that the
BSE agent adapts to macaques in the same way as it does to humans and
confirms that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. The agent responsible for French iatrogenic
growth hormone-linked CJD taken as a control is very different from vCJD but
is similar to that found in one case of sporadic CJD and one sheep scrapie
isolate. These data will be key in identifying the origin of human cases of
prion disease, including accidental vCJD transmission, and could provide
bases for vCJD risk assessment.

60. ARC funding of scrapie research was never adequate but at least it was appropriately

long-term. As a result of the USA Department of Agriculture’s scrapie eradication

programme, both MRI and IRAD received 5-10 year grants for sheep experiments under

US Public Law 480. This was an Act ‘to increase the consumption of US agricultural

commodities in foreign countries, to improve the foreign relations of the US, and for other

purposes’. At IRAD, at this time, it had become the practice to economise by taking

lamb crops from the scrapie-injected ewes, for sale locally for human consumption.

Subject: SCRAPIE USA UPDATE AS of March 31, 2006 2 NEW CASES IN GOAT, 82

Date: April 30, 2006 at 4:49 pm PST
SCRAPIE USA UPDATE AS of March 31, 2006


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 costs_''...

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
and Burger who demonstrated that the disease was transmissible with a long
period, and that affected mink had a spongiform encephalopathy similar to
that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough,
Because of the similarity between TME and scrapie, and the subsequent
finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it
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
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,
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
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
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
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
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
with a brain suspension from affected mink. Each developed a fatal
encephalopathy after incubation periods of 18 and 19 months.

These findings suggest that TME may result from feeding mink infected cattle
we have alerted bovine practitioners that there may exist an as yet
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
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
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
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The
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
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
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.



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