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From: TSS (216-119-143-36.ipset23.wt.net)
Subject: "EFSA publishes new report on the Geographical BSE Risk Assessment" (GAIN report E34050)
Date: August 31, 2004 at 9:43 am PST

-------- Original Message --------
Subject: "EFSA publishes new report on the Geographical BSE Risk Assessment" (GAIN report E34050)
Date: Tue, 31 Aug 2004 10:55:47 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE


######## Bovine Spongiform Encephalopathy #########

BSE Risk Assessment:
- "EFSA publishes new report on the Geographical BSE Risk Assessment"
(GAIN report E34050)
http://www.useu.be/agri/srm.html

Transmissible Spongiform Encephalopaties

On July 30, 1997, the European Commission adopted Commission Decision
97/534/EC, commonly known as the Specified Risk Materials (SRM) ban. The
goal of the ban was to avoid health risks related to transmissible
spongiform encephalopaties (TSEs), such as BSE (mad cow disease) which
is linked to new variant Creutzfeldt-Jakob disease in humans. The ban
prohibited the use of SRMs (defined as the skull, tonsils, ileum and
spinal cord of cattle, sheep and goats aged over one year, and spleens
of sheep and goats) in any products sold in the EU.

The original date of implementation was July 1, 1998, but this was
delayed due to controversy over product sector coverage. In addition to
food and feed, the ban would have significantly affected production of
pharmaceuticals, cosmetics, medical devices and fertilizers. In
September 1999, the EU implemented specific regulations for SRMs on
medical products for human use (Directive 99/820/EC). It also provided
guidelines on how companies would comply with this Directive. Thus far,
it appears U.S. companies have successfully complied with it.

In June 2000, Commission Decision 2000/148/EC was adopted, which
repealed Commission Decision 97/534/EC, but set new requirements for
handling SRMs. This new measure limited the scope of the ban to food,
feed and fertilizer and required slaughterhouses and authorized meat
cutting and processing plants in all EU member states, regardless of
their BSE status, to remove the SRMs mentioned above. The measure became
effective October 1, 2001 for all EU member states.

Initially the ban did not apply to third countries. However in March
2001, the EU published the results of their geographical BSE risk (GBR)
assessment of third countries exporting food , feed or fertilizer
products to the EU. The United States' BSE status is provisionally
recognized as "unlikely, but cannot be excluded (GBR-2)".

In late May 2001, the European Commission adopted Regulation 999/2001
,
which is eventually intended to supersede all existing TSE legislation,
including 2000/418. Among other things, it establishes criteria to
classify the BSE status of member states and third countries into one of
five classification categories. Certain requirements, including removal
of SRM's, would then be applied to a country depending on the
classification. Under Regulation 1326/2001

(amended by Commission Regulation 1234/2003

setting the conditions for use of fishmeal, hydrolized proteins and
dicalcium phosphates in feed for non-ruminant farmed animals), the
transitional measures passed in July 2001, only countries recognized as
provisionally BSE-free (GBR-1) are not required to remove SRM's in order
to export to the EU. The EU currently recognizes New Zealand, Australia,
Norway, Chile, Argentina, Paraguay, Nicaragua, Botswana, Namibia and
Swaziland as provisionally BSE-free.

The United States is required to remove SRM's and MRM (mechanically
recovered meat) from animal products to the EU. The United States fully
expects to be placed in Category I or II once the categorization is
completed and would not be required to remove SRM's and MRM once
Regulation 999/2001 is fully implemented. The scientific risk assessment
of all countries have not been fully concluded. For only one third of
the countries requesting the determination of the BSE status, the
Scientific Steering Committee
has adopted a
final opinion. On June 28, 2003, the European Parliament and the Council
adopted Regulation 1128/2003

prolonging the transitional measures with two years, until July 1, 2005.
The extension maintains the present level of public health protection as
the transitional measures on SRM's and slaughter methods are maintained
within the EU and in respect of third countries. The two year extension
is designed for the Commission to continue its attempt to reach an
agreement at international level (OIE) on the determination of BSE
status of countries on the basis of risk. The Commission would at the
same time conclude the scientific risk assessments. However, even the
application of transitional measures of Regulation 999/2001 is extremely
disruptive for the U.S. industry.

EFSA publishes new report on the Geographical BSE Risk Assessment (GAIN
report E34050):

In August 2004 the European Food Safety Agency (EFSA) published new
scientific reports on the GBR classifications for seven countries. The
U.S. was classified in level three which means "BSE is likely but not
confirmed or confirmed at a lower level". The risk assessment was based
on information submitted by the countries concerned, and relates in
particular to imports of bovines and meat and bone meal from the UK and
other BSE-risk countries.

http://www.useu.be/agri/srm.html

Released: Aug 26 2004 EU-25 | EFSA publishes new report on the
Geographical BSE Risk Assessment
E34050 Highlight: In August 2004 the European Food Safety Agency (EFSA)
published new scientific reports on the GBR classifications for seven
countries. The U.S. was classified in level three which means "BSE is
likely but not confirmed or confirmed at a lower level". The risk
assessment was based on information submitted by the countries
concerned, and relates in particular to imports of bovines and meat and
bone meal from the UK and other BSE-risk countries.

Voluntary Report - public distribution
Date: 8/26/2004
GAIN Report Number: E34050
E34050
EU-25
Livestock and Products
EFSA publishes new report on the Geographical BSE
Risk Assessment
2004
Approved by:
Stan Cohen
U.S. Mission to the EU
Prepared by:
Karin Bendz
Report Highlights:
In August 2004 the European Food Safety Agency (EFSA) published new
scientific reports on
the GBR classifications for seven countries. The U.S. was classified in
level three which
means "BSE is likely but not confirmed or confirmed at a lower level".
The risk assessment was based on information submitted by the countries
concerned, and
relates in particular to imports of bovines and meat and bone meal from
the UK and other
BSE-risk countries.
Includes PSD Changes: No
Includes Trade Matrix: No
Unscheduled Report
Brussels USEU [BE2]
[E3]
USDA Foreign Agricultural Service
GAIN Report
Global Agriculture Information Network
Template Version 2.09
GAIN Report - E34050 Page 2 of 4
UNCLASSIFIED USDA Foreign Agricultural Service
On August 20, 2004 the European Food Safety Authority (EFSA) published
up-to-date
scientific reports on the Geographical Bovine Spongiform Encephalopathy
(BSE) Risk (GBR)
for seven countries. The countries are Australia, Canada, Mexico,
Norway, South Africa,
Sweden and the United States.
The GBR evaluations are based on information submitted by the countries
concerned in
response to a European Commission recommendation in 1998, which set out
the information
requirements for such an assessment. The scientific reports address the
GBR in a number of
countries based on data covering the period 1980-2003.
The information concerns in particular imports of bovines and meat and
bone meal (MBM)
from the United Kingdom and other BSE-risk countries, rendering
standards for animal byproducts,
use specific risk materials (SRMs), and feeding of meat and bone meal
(MBM) to
ruminants.
Table of the classification of the countries
GBR of the country/Region
GBR
level
Presence of one or more cattle clinically or preclinically
infected with the BSE agent in a
geographical region/country
Status Before Status After
I Highly unlikely Australia (I)
Norway (I) Australia (I)
II Unlikely but not excluded
Sweden (II)
Canada (II)
USA (II)
Sweden (II)
Norway (II)
III Likely but not confirmed or confirmed at a lower level South Africa
(N/A)
Mexico (N/A),
Canada (III)
USA (III)
South Africa (III)
Mexico (III)
IV Confirmed at a higher level
The result of the report is that Australia and Sweden were kept at the
same level as before
the update, while Norway, Canada and the U.S. were classed at a higher
level.
The EFSA concludes that the BSE agent that was found in the U.S. was
probably imported
into the U.S. and could have reached domestic cattle in the middle of
the 1980s. Cattle
imported in the mid-1980s could have been rendered in the late 1980s and
therefore led to
an internal challenge in the early 1990s. EFSA concludes that it is
possible that MBMs
imported into the U.S. reached domestic cattle and posed a risk in the
early 1990s.
According to the EFSA, a processing risk developed in the late 1980s and
early 1990s when
cattle imports from BSE-risk countries were slaughtered or died, and
were processed (partly)
into feed, together with some imports of MBM. This risk continued to
exist, and grew
significantly in the mid-1990s when domestic cattle, infected by
imported MBM, reached
processing. Given the low stability of the system, the risk increased
over the years with
continued imports of cattle and MBM from BSE risk countries.
This assessment deviates from the previous assessment (Scientific
Steering Committee
(SSC) opinion, 2000) because at that time several exporting countries
were not considered a
potential risk.
GAIN Report - E34050 Page 3 of 4
UNCLASSIFIED USDA Foreign Agricultural Service
It is also worth noting that the current GBR conclusions are not
dependent on the large
exchange of imports between the U.S. and Canada. The threat from
European exports to the
U.S. varied from moderate to high. These challenges indicate that it was
likely that BSE
infectivity was introduced into the North American continent.
EFSA and its Scientific Expert Working group on GBR are concerned that
the inspection
missions of the Food and Veterinary office (FVO  DG SANCO) conducted in
member states
and third countries didnt assess the available information in light of
the risk posed by BSE.
They recommend including BSE-related aspects in future inspection missions.
Expected development of the GBR
As long as there are no significant changes in rendering or feeding, the
stability remains very
to extremely unstable. Thus, the probability of cattle to be
(pre-clinically or clinically)
infected with the BSE-agent persistently increases.
Canada
For Canada the EFSA evaluation concludes that the BSE agent was probably
imported to the
country in the 1980s and could have been rendered in the late 1980s and
therefore posed a
risk in the early 1990s. A certain risk that BSE-infected cattle entered
processing in Canada,
and were at least partly rendered for feed, occurred in the early 1990s
when cattle imported
from the UK in the mid-1980s could have been slaughtered. This risk grew
significantly in
the mid-1990s when domestic cattle, infected by imported MBM, reached
processing. This
risk increased over the years with continued imports of cattle and MBM
from BSE risk
countries.
Australia
The EFSA concludes that in the case of Australia, an extremely or very
unstable system was
exposed to a very low or negligible challenge through the import of
cattle. Given the
negligible level of external challenge through MBM it is highly unlikely
that any internal risk
occurred.
This report is drafted from the EFSA scientific report. The full report
can be found at:
www.efsa.eu.int
GAIN Report - E34050 Page 4 of 4
UNCLASSIFIED USDA Foreign Agricultural Service
Visit our website: our website www.useu.be/agri/usda.html provides a
broad range of
useful information on EU import rules and food laws and allows easy
access to USEU reports,
trade information and other practical information.
E-mail: AgUSEUBrussels@usda.gov
Related reports from USEU Brussels:
Report
Number
Title Date Released
E24047 Host Country BSE Response Questionnaire
2004
04/05/04
E24044 European Commissioner David Byrns first
regular BSE report of the year
04/04/04
E24006 BSE  Potential Concerns of the European
Commission
01/09/04
These reports can be accessed through our website www.useu.be/agri or
through
the FAS website http://www.fas.usda.gov/scriptsw/attacherep/default.asp.

http://www.fas.usda.gov/gainfiles/200408/146107318.pdf

http://www.fas.usda.gov/gainfiles/200408/146107318.wpd

USDA/APHIS/FDA still don't get it;

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

HOUND STUDY

AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf


Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States

Email Terry S. Singeltary:

flounder@wt.net


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


http://www.neurology.org/cgi/eletters/60/2/176#535

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama

BRITISH MEDICAL JOURNAL

SOMETHING TO CHEW ON


BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

BMJ

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


Terry S. Singeltary Sr.

######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########





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