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| From: | TSS (pool-71-248-147-42.dllstx.dsl-w.verizon.net)
|
| Subject: | BASE MAD COW USA (spontaneous NOT) |
|
Date: | February 14, 2007 at 8:50 am PST |
18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.
snip...
64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.
Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.
snip...
http://www.seac.gov.uk/minutes/95.pdf
3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse
Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University
Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.
***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***
6:30 Close of Day One
http://www.healthtech.com/2007/tse/day1.asp
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...
http://www.cjdsurveillance.com/resources-casereport.html
There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.
He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
Subject: SEAC 96th MEETING ON TUESDAY 20 FEBRUARY 2007 AGENDA (HIGH SUSCEPTIBILITY OF A PRIMATE SPECIES TO THE BASE)
Date: February 13, 2007 at 2:46 pm PST
Agenda
96th meeting on Tuesday 20 February 2007
http://www.seac.gov.uk/minutes/95.pdf
CONFERENCE ON PRION DISEASES OF NEUROPRION, NETWORK OF EXCELLENCE, TURIN, ITALY, 3-6 OCTOBER 2006
BASE
OUR OBSERVATIONS UNDERLINE THE HIGH SUSCEPTIBILITY OF A PRIMATE SPECIES TO THE BASE PRION STRAIN AND PROVIDE A BIOCHEMICAL BASIS FOR THE IDENTIFICATION OF A POTENTIAL OCCURRENCE IN MAN. ...page 9...tss
http://www.seac.gov.uk/papers/96-2.pdf
UPDATE ATYPICAL SCRAPIE IN A TSE RESEARCH FLOCK
http://www.seac.gov.uk/papers/96-4.pdf
> Some unofficial information from a source on the inside looking out -
>
> Confidential!!!!
>
> As early as 1992-3 there had been long studies conducted on small
> pastures containing scrapie infected sheep at the sheep research station
> associated with the Neuropathogenesis Unit in Edinburgh, Scotland.
> Whether these are documented...I don't know. But personal recounts both
> heard and recorded in a daily journal indicate that leaving the pastures
> free and replacing the topsoil completely at least 2 feet of thickness
> each year for SEVEN years....and then when very clean (proven scrapie
> free) sheep were placed on these small pastures.... the new sheep also
> broke out with scrapie and passed it to offspring. I am not sure that TSE
> contaminated ground could ever be free of the agent!!
> A very frightening revelation!!!
>
http://www.microbes.info/forums/index.php?showtopic=306
Science 24 September 2004:
Vol. 305. no. 5692, pp. 1918 - 1921
DOI: 10.1126/science.1103581
Perspectives
BIOMEDICINE:
A Fresh Look at BSE
Bruce Chesebro*
Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle
form of a family of progressive brain diseases. These diseases include
scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic
wasting disease (CWD) in deer and elk. They are also known as either "prion
diseases" because of the association of a misfolded cellular prion protein
in pathogenesis or "transmissible spongiform encephalopathies" (TSEs)
because of the spongelike nature of the damaged brain tissue (1).
The recent discovery of two BSE-infected cows, one in Canada and one in the
United States, has dramatically increased concern in North America among
meat producers and consumers alike over the extent to which BSE poses a
threat to humans as well as to domestic and wild animals. The European BSE
epidemic of the late-1980s seems to have been initiated a decade earlier in
the United Kingdom by changes in the production of meat and bone meal (MBM)
from rendered livestock, which led to contamination of MBM with the BSE
infectious agent. Furthermore, the fact that UK farmers fed this rendered
MBM to younger animals and that this MBM was distributed to many countries
may have contributed to the ensuing BSE epidemic in the United Kingdom and
internationally (2).
Despite extensive knowledge about the spread of BSE through contaminated
MBM, the source of BSE in Europe remains an unsolved mystery (2). It has
been proposed that BSE could be derived from a cross-species infection,
perhaps through contamination of MBM by scrapie-infected sheep tissues (see
the figure). Alternatively, BSE may have been an endemic disease in cattle
that went unnoticed because of its low level of horizontal transmission.
Lastly, BSE might have originated by "spontaneous" misfolding of the normal
cellular prion protein into the disease-associated abnormal isoform (3),
which is postulated to be the infectious agent or "prion."
Five possible sources of BSE in North American cattle. Sheep, deer, and elk
could spread prion diseases (TSEs) to cattle through direct animal contact
or contamination of pastures. Endemic BSE has not been proven to exist
anywhere in the world, but it is difficult to exclude this possibility
because of the inefficient spread of BSE infectivity between individual
animals (2). BSE caused by spontaneous misfolding of the prion protein has
not been proven.
CREDIT: KATHARINE SUTLIFF/SCIENCE
Spontaneous protein misfolding is not a new phenomenon as proteins are known
to sometimes misfold after synthesis. Cells in turn have devised ingenious
ways to deal with this problem. These include molecular chaperone proteins
that bind to misfolded proteins and help them to unfold, and organelles
called proteosomes that degrade misfolded or unwanted proteins. However,
although misfolded prion proteins have been generated in test tubes as well
as in cultured cells, it has been difficult to demonstrate that such
misfolded abnormal prion proteins are infectious (4, 5). Even the most
recent data do not prove conclusively that infectivity has been generated in
vitro because misfolded synthetic prion proteins were not able to transfer
disease directly to wild-type mice (6). To obtain infectivity and subsequent
prion disease, the misfolded proteins had to be inoculated and incubated for
1 to 2 years in transgenic mice that overexpressed a mutant version of the
prion protein. Previous data from this group showed that transgenic mice
expressing high amounts of prion protein developed neurological disease
without inoculation of misfolded prion protein (7). Thus, at the biochemical
level, the critical attributes of the misfolded prion protein required for
infectivity are not known, and misfolding of prion protein alone may not be
sufficient to generate an infectious agent (.
Nevertheless, the idea that BSE might originate due to the spontaneous
misfolding of prion proteins has received renewed interest in the wake of
reports suggesting the occurrence of atypical BSE (9-11). These results
imply that new strains of cattle BSE might have originated separately from
the main UK outbreak. Where and how might such strains have originated?
Although such rare events cannot be studied directly, any number of sources
of the original BSE strain could also explain the discovery of additional
BSE strains in cattle (see the figure). However, it would be worrisome if
spontaneous BSE were really a valid etiology because such a mechanism would
be impossible to prevent--unlike other possible scenarios that could be
controlled by large-scale eradication of TSE-positive animals.
Another way to look at this problem is to examine evidence for possible
spontaneous TSE disease in other animals besides cattle. Spontaneous BSE
would be extremely difficult to detect in cattle, where horizontal spread is
minimal. However, in the case of the sheep TSE disease, scrapie, which
spreads from ewes to lambs at birth as well as between adults, spontaneous
disease should be detectable as new foci of clinical infection. In the early
1950s scrapie was eradicated in both Australia and New Zealand, and the
mainland of both these countries has remained scrapie-free ever since. This
scrapie-free status is not the result of selection of sheep resistant to
scrapie because sheep from New Zealand are as susceptible as their UK
counterparts to experimental scrapie infection (12). These experiments of
man and nature appear to indicate that spontaneous clinical scrapie does not
occur in sheep. Similarly, because CWD is known to spread horizontally, the
lack of CWD in the deer or elk of eastern North America but its presence in
western regions would also argue against a spontaneous disease mechanism.
This is particularly noteworthy in New Zealand, where there are large
numbers of deer and elk farms and yet no evidence of spontaneous CWD. If
spontaneous scrapie does not occur in sheep or deer, this would suggest that
spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are
unlikely to be found in cattle or humans. The main caveat to this notion is
that spontaneous disease may arise in some animal species but not others. In
humans, sCJD--which is considered by some researchers to begin by
spontaneous misfolding of the prion protein--usually takes more than 50
years to appear. Thus, in animals with a shorter life-span, such as sheep,
deer, and cattle, an analogous disease mechanism might not have time to
develop.
What can we conclude so far about BSE in North America? Is the BSE detected
in two North American cows sporadic or spontaneous or both? "Sporadic"
pertains to the rarity of disease occurrence. "Spontaneous" pertains to a
possible mechanism of origin of the disease. These are not equivalent terms.
The rarity of BSE in North America qualifies it as a sporadic disease, but
this low incidence does not provide information about cause. For the two
reported North American BSE cases, exposure to contaminated MBM remains the
most likely culprit. However, other mechanisms are still possible, including
cross-infection by sheep with scrapie or cervids with CWD, horizontal
transmission from cattle with endemic BSE, and spontaneous disease in
individual cattle. Based on our understanding of other TSEs, the spontaneous
mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE
of unknown etiology--might be a better term to describe the origin of this
malady.
What does all this imply about testing cattle for BSE in North America?
Current testing in the United States indicates that BSE is rare (one
positive result in 40,000 cattle tested). However, additional testing of
200,000 head of slaughtered cattle over the next 1 to 2 years, as recently
proposed by the U.S. Department of Agriculture (USDA), should tell us the
incidence more precisely. Nevertheless, if any rare cases are detected, we
may still not know their origin. If evidence arises of a focal occurrence of
BSE, we might gain important insight into unexpected sources of
contamination. However, because current tests do not seem to be able to
detect BSE in infected animals less than 30 months of age, even more
extensive testing will not completely guarantee the negative status of
younger animals in the food chain. Therefore, the alternative option of
testing all slaughtered cattle, as implemented in some countries such as
Japan, would appear to provide little additional benefit. This fact has been
acknowledged as the basis for a new agreement between the United States and
Japan aimed at reestablishing the beef trade between the two countries.
One problem with the current U.S. testing program was the announcement a few
months ago of unconfirmed positive BSE tests in two additional North
American animals that were subsequently found to be negative when tested
with the more accurate method of Western blotting. The public release of
information about unconfirmed positive tests detected by the rapid test used
for mass screening may be a good idea in the interest of openness, but it ha
s the potential to create unwarranted anxiety. If unconfirmed positives are
a frequent occurrence, it would seem reasonable to follow a more cautious
approach and wait until confirmatory testing is complete before publicly
announcing the details.
Based on the experience of many European countries, the mainstays of
controlling BSE in cattle and avoiding spread to humans are threefold:
first, eliminate feeding of ruminant tissues to ruminants; second, remove
high-risk cattle tissues from human food; and third, continue to test for
BSE in cattle in order to monitor progress with the elimination of the
disease on a local and national basis. In the next 12 months, after
extensive USDA test results are available, the extent of any possible BSE
spread in the United States will be better documented. But, in fact, the
United States and Canada have already instituted the most important steps to
prevent the spread of cattle BSE in advance of the results--that is, a ban
on feeding ruminant MBM to other ruminants and removal of high-risk tissues
from meat for human consumption. It is hoped that the new data will not
deviate enough from previous predictions to require further measures for
management of this problem. The most important line of defense against any
possible spread of BSE will be to maintain strict vigilance in the
implementation of the current regulations.
References
S. B. Prusiner, Proc. Natl. Acad. Sci. U.S.A 95, 13363 (1998) [Medline].
P. G. Smith, R. Bradley, Br. Med. Bull. 66, 185 (2003) [Medline].
C. Weissmann, A. Aguzzi, Curr. Opin. Neurobiol. 7, 695 (1997) [Medline].
A. F. Hill et al., J. Gen. Virol. 80, 11 (1999) [Medline].
R. Chiesa et al., J. Virol. 77, 7611 (2003) [Medline].
G. Legname et al., Science 305, 673 (2004).
D. Westaway et al., Cell 76, 117 (1994) [Medline].
B. Chesebro, Science 279, 42 (1998).
A. G. Biacabe et al., EMBO Rep. 5, 110 (2004) [Medline].
Y. Yamakawa et al., Jpn. J. Infect. Dis. 56, 221 (2003) [Medline].
C. Casalone et al., Proc. Natl. Acad. Sci. U.S.A. 101, 3065 (2004)
[Medline].
E. F. Houston et al., J. Gen. Virol. 83, 1247 (2002) [Medline].
http://www.sciencemag.org/cgi/content/full/305/5692/1918
However, Phillips did not have an explanation of how the first cow got BSE and other
explanations continue to be put forward. One journalist commented on the idea favoured
by the Phillips Committee that BSE started with a spontaneous mutation:
However, apart from there being little evidence for the idea, a random mutation
could not explain why Britain alone has suffered the problem. America, for
instance, has 10 times the number of cattle, and so must in theory run ten times
the risk of a similar random event leading to BSE and so being passed on in
recycled meat and bone meal.13
http://www.parliament.uk/commons/lib/research/rp2001/rp01-089.pdf
Evaluation of the Potential for Bovine Spongiform
Encephalopathy in the United States
Joshua T. Cohen
Keith Duggar
George M. Gray
Silvia Kreindel
Harvard Center for Risk Analysis
Harvard School of Public Health
Hatim Abdelrahman
Tsegaye HabteMariam
David Oryang
Berhanu Tameru
Center for Computational Epidemiology
College of Veterinary Medicine
Tuskegee University
November 26, 2001
snip...
2.3.1 Spontaneous BSE
A potential way in which BSE could be introduced into the United States is the
development of a spontaneous case of a BSE in a native animal. A “spontaneous case” is one that
occurs in an animal with no known risk factors for development of BSE. The presumed
mechanism by which a BSE could occur spontaneously is by the mutation of the PrP gene to a
Section 2
- 20 -
form that codes for PrPsc, and subsequent recruitment of PrPc until disease is manifest (Prusiner,
1989); (for review see: (Chesebro, 1999). There is no direct evidence of this mechanism,
although some argue that all mammals might have a low spontaneous rate of TSE (Hueston,
1997). In addition, a transgenic animal over-expressing the PrP gene has apparently replicated
the human TSE GSS (Hsiao et al., 1991). Recent results, in which mice expressing the same
point mutation but at normal levels failed to develop disease (Manson et al., 1999), suggest the
mutations may increase susceptibility rather than directly cause the disease. Although at this time
there is no scientific evidence suggesting that spontaneous BSE exists, the BSE Inquiry suggested
that TSEs could possibly develop sporadically in other species, as they do in humans (BSE
Inquiry, 2000). In contrast, the Review of the origin of BSE (Horn et al., 2001) concluded that
although the spontaneous case hypothesis cannot be excluded, there is no evidence supporting the
presence of sporadic form prion disease in cattle or sheep.
snip...
http://www.aphis.usda.gov/lpa/issues/bse/risk_assessment/mainreporttext.pdf
http://www.aphis.usda.gov/lpa/issues/bse/madcow.pdf
WHY would several strains of TSE in feed not be a plausible theory rather than a theory never proven, the spontaneous theory $$$
WHY is it not plausible to think that BASE might have come from feed too ???
WHY WOULD ONE STRAIN AMPLIFY AND TRANSMIT, AND THE OTHER NOT ???
WHY would one strain of TSE in cattle transmit orally via feed i.e. BSE, and the other i.e. BASE not transmit orally ???
answer =
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
snip...
To minimise the risk of farmers' claims for compensation from feed
compounders.
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.
snip...
THE FUTURE
4..........
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 ;
http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
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
Jan 4, 2007 USDA Proposes to Allow Additional Imports From BSE Minimal-Risk Countries
http://www.usda.gov/wps/portal/ut/p/_s.7_0_A/7_0_1OBcontentidonly=true&contentid=2007/01/0001.xml
• Transcript
http://www.usda.gov/wps/portal/ut/p/_s.7_0_A/7_0_1OBcontentidonly=true&contentid=2007/01/0002.xml
• Docket
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/Docket2006-0041.pdf
• Risk Assessment
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/RiskAssessment06-041-1%20.pdf
– Estimation of BSE Prevalence in Canada
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/BSE_Prevalence.pdf
– Harvard Model of BSE Implications
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/HarvardModel06-041-1.pdf
Suppressed peer review of Harvard study October 31, 2002.
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
• Environmental Assessment
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EnvironmentalAssessment10-27-2006.pdf
• Economic Analysis
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EconomicAnalysisAPHIS-2006-0041.pdf
Jan 4, 2007 MEDIA ADVISORY: USDA Chief Veterinarian Proposes Expansion Of BSE Minimal-Risk Rule
http://www.aphis.usda.gov/newsroom/content/2007/01/med-adv_bse_mrr.shtml
Nov 13, 2006 Statement By Deputy Under Secretary Of Marketing & Regulatory Programs Chuck Lambert Regarding Status Of Beef Trade With South Korea
http://www.usda.gov/wps/portal/ut/p/_s.7_0_A/7_0_1OBcontentidonly=true&contentid=2006/11/0444.xml
BSE MRR 2
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/RiskAssessment06-041-1%20.pdf
REVIEW OF THE USDA’S RULE
PROVIDING FOR CANADIAN BEEF AND
CATTLE IMPORTS
CONGRESS
MARCH 1, 2005
99 PAGES ...TSS
http://agriculture.house.gov/hearings/109/1091.pdf
FOR IMMEDIATE RELEASE
March 1, 2005
Committee Examines USDA Canadian Beef Rule
Hears Testimony from Agriculture Secretary Johanns
http://agriculture.house.gov/republicans/press/109/pr050301.html
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS
DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01
FULL TEXT URL @
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=8374
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&P=3381
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA
https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9dOpenDocument&AutoFramed
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle 03-025IFA 03-025IFA-2 9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
THE SEVEN SCIENTIST REPORT ***
http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf
PAUL BROWN M.D.
http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf
9 December 2005
Division of Dockets Management (RFA-305)
SEROLOGICALS CORPORATION
James J. Kramer, Ph.D.
Vice President, Corporate Operations
http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf
Embassy of Japan
http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm
Dockets Entered on December 22, 2005
2005D-0330, Guidance for Industry and FDA Review Staff on Collection of
Platelets
by Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ...
http://www.fda.gov/ohrms/dockets/dailys/05/Dec05/122205/122205.htm
03-025IF 03-025IF-631 Linda A. Detwiler [PDF]
Page 1. 03-025IF 03-025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4.
Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12.
http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-631.pdf
03-025IF 03-025IF-634 Linda A. Detwiler [PDF]
Page 1. 03-025IF 03-025IF-634 Linda A. Detwiler Page 2.
Page 3. Page 4. Page 5. Page 6. Page 7. Page 8.
http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-634.pdf
Page 1 of 17 9/13/2005 [PDF]
... 2005 6:17 PM To: fsis.regulationscomments@fsis.usda.gov Subject: [Docket
No. 03-025IFA]
FSIS Prohibition of the Use of Specified Risk Materials for Human Food ...
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
03-025IFA 03-025IFA-6 Jason Frost [PDF]
... Zealand Embassy COMMENTS ON FEDERAL REGISTER 9 CFR Parts 309 et al
[Docket No. 03-
025IF] Prohibition of the Use of Specified Risk Materials for Human Food and
...
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-6.pdf
In its opinion of 7-8 December 2000 (EC 2000), the SSC ... [PDF]
Page 1. Linda A. Detwiler, DVM 225 Hwy 35 Red Bank, New Jersey 07701 Phone:
732-741-2290
Cell: 732-580-9391 Fax: 732-741-7751 June 22, 2005 FSIS Docket Clerk US ...
http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf
3. Mad Cow Disease: FDA's Management of the Feed Ban Has Improved,
but Oversight Weaknesses Continue to Limit Program Effectiveness.
GAO-05-101, Feb. 25.
www.gao.gov/cgi-bin/getrpt?GAO-05-101
Highlights - www.gao.gov/highlights/d05101high.pdf
OUTLOOK 07: US Pins Hope Of MAD COW Beef Trade On Safety
Status from OIE (GOD HELP US)
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&T=0&P=20678
NATURE NEWS BLOG
http://blogs.nature.com/news/blog/2006/06/cjdrelated_disease_can_incubat.html
4th CASE VCJD VIA BLOOD TRANSFUSION, BSE, BASE, AND SPORADIC CJD
By Terry S Singeltary PART I
http://bloodindex.org/view_news_zone.php?id=206
4th CASE VCJD VIA BLOOD TRANSFUSION, BSE, BASE, AND SPORADIC CJD
By Terry S Singeltary PART II
http://bloodindex.org/view_news_zone.php?id=207
THE WAY IT WAS BEFORE GWs BSE MRR POLICY, before the USA had documented BSE ;
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.
####
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
TEXAS BOVINE DISEASE CARCASS DISPOSAL METHOD
“Anthrax is under-reported, because many ranchers in this area automatically
dispose
of carcasses and vaccinate livestock when they find dead animals that are
bloated or
bloody--common signs of the disease,” said Dr. Fancher.
http://www.tahc.state.tx.us/news/pr/2005/2005Jul_Anthrax_Confirmed_in_SuttonCty.pdf
REMINDER, CATTLE ON FEED IN TEXAS
IN TEXAS, cattle on feed for decades, fda says 5.5 grams ruminant protein,
if tainted with TSE, is not enough to kill a cow. actually, it's enough to
kill 100+ cows ;-)
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
U. S. Department of Health and Human Services
U. S. Food and Drug Administration
Office of Regulatory Affairs
May 20, 2003
Summary of ORA BSE Import Bulletin 99B-14
The Food and Drug Administration (FDA) has alerted its import field offices
to the potential importation of human food products and nutritional
supplements containing ruminant material from BSE-affected or at-risk
countries as determined by United States Department of Agriculture
(USDA)/Animal, Plant Health and Inspection Service (APHIS). The current
action is a followup to an earlier FDA alert issued in January 2000
regarding bulk shipments of high risk bovine tissues from these same
countries. An expanded list of products at issue and a list of the current
BSE-affected countries is set out below.
USDA/APHIS has prohibited the importation into the United States of all
edible ruminant products from Europe, Oman, and other BSE-affected
countries. The Import Bulletin will facilitate FDA's careful review of all
imports of FDA-regulated products to ensure coordination with APHIS on the
prohibitions. FDA's review will include evaluation of product ingredient
lists to determine whether the products offered for import contain certain
ruminant materials. Products that appear to contain ruminant material from
the identified countries will be referred to APHIS for disposition.
PRODUCTS
Any products containing ruminant material such as (but not limited to):
Cheese products containing meat of ruminant origin
Ruminant meat products
Poultry products containing or processed with ruminant products
Rennet from ruminant animals
Pie fillings containing or processed with ruminant products
Multiple ingredient food products (soups, stews, sandwiches, mixed dinners,
etc.) containing or processed with ruminant products
Baby foods, geriatric foods, and dietary foods containing or processed with
ruminant products
Vitamins, minerals, proteins, and other dietary supplements that contain or
have been processed with ruminant material
Food additives (emulsifiers, enzymes, flavor enhancers, etc.) containing or
processed with ruminant materials
Botanicals containing or processed with ruminant materials
Animal by-products and extracts for human use
BSE-AFFECTED OR AT-RISK COUNTRIES
ALBANIA (AL)
ANDORRA (AD)
AUSTRIA (AT)
BELGIUM (BE)
BOSNIA-HERZEGOVINA (BA)
BULGARIA (BG)
CANADA (CA)
CROATIA (HR)
CZECH REPUBLIC (CS)
DENMARK (DK)
FEDERAL REPUBLIC OF YUGOSLAVIA (YU)
FINLAND (FI)
FRANCE (FR)
GERMANY (DE)
GREECE (GR)
HUNGARY (HU)
IRELAND, REPUBLIC of (IE)
ISRAEL (IL)
ITALY (IT)
JAPAN (JP)
LIECHTENSTEIN
LUXEMBOURG (LU)
MACEDONIA, the former YUGOSLAV REPUBLIC of (MK)
MONACO (MC)
NETHERLANDS (NL)
NORWAY (NO)
OMAN (OM)
POLAND (PL)
PORTUGAL (PT)
ROMANIA (RO)
SAN MARINO (SM)
SLOVAK REPUBLIC (SLOVAKIA) (SK)
SLOVENIA (SI)
SPAIN (ES)
SWEDEN (SE)
SWITZERLAND (CH)
UNITED KINGDOM (Great Britain including Northern Ireland, and Falkland
Islands) (GB)
http://www.cfsan.fda.gov/~comm/bseimpor.html
TSS
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