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From: TSS ()
Subject: Japan won't ease U.S. beef ban terms
Date: November 4, 2005 at 6:46 pm PST

Posted on Fri, Nov. 04, 2005


Japan won't ease U.S. beef ban terms

Associated Press


TOKYO - Japan on Friday rebuffed Washington's demands that Tokyo ease its terms for lifting a ban on U.S. beef imports, imposed two years ago because of fears of mad cow disease.

U.S. Agriculture Secretary Mike Johanns had earlier insisted that cows younger than 30 months are considered safe from mad cow disease, and can be imported. Japan wants to set the limit at 21 months.

"We have received no formal request (from Washington), and even if we did receive one, we're not in a position to say yes," Japan's Agriculture Minister Shoichi Nakagawa said Friday.

He said Japan would study the issue.

"Our focus is on ensuring safety and gaining public consent," he said.

Tokyo banned American beef in December 2003 after the discovery of the first U.S. case of mad cow disease.

Japan was then the most lucrative overseas market for U.S. beef, and an increasingly impatient Washington has pushed hard for the ban to be lifted.

Earlier this week, Japan's food safety commission approved a report saying the mad cow disease risk in U.S. beef was minuscule as long as imports were limited to meat from cows under 21 months, and all brain and spinal cord matter was removed.

Japan is expected to reach a decision on the matter by the end of the year, after monthlong public hearings that began this week.

Johanns has criticized the commission's report, saying the conditions are too stringent.

"The science is very, very clear that in animals under 30 months, you just don't have a (mad cow disease) problem," Johanns said Thursday. "So obviously we hope to continue to open up the marketplace."

Many scientists believe that beef from cattle infected with mad cow disease, or bovine spongiform encephalopathy, can cause a fatal brain disorder in humans.

Japanese consumers remain deeply wary of U.S. beef, with recent polls showing that nearly 70 percent opposed lifting the ban.

http://www.dfw.com/mld/dfw/news/breaking_news/13085547.htm

i don't believe johanns could tell the truth if the world depended on it.

this is par the course for this administration. ...

"Terry S. Singeltary Sr."
11/03/2003 01:19 PM

To:
regulations@aphis.usda.gov


cc:


bcc:


Subject:
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA


I would like to kindly comment on Docket No. 03-080-1

USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA ;

>Under this proposal, ruminant and ruminant products eligible for entry into
>the United States from a BSE minimal risk region would include:
>
>1) bovine
>animals less than 30 months of age for immediate slaughter;
>
>2) bovine
>animals for feeding to be moved to a designated feedlot and then to
>slaughter at less than 30 months of age;
>
snip...

>6) fresh (chilled or frozen)
>meat from bovines less than 30 months of age; 7) fresh (chilled or frozen)
>whole or half carcasses of bovines less than 30 months of age; 8) fresh
>(chilled or frozen) bovine liver; 9) fresh (chilled or frozen) bovine
>tongues;


the myth that cattle under 30 months of age are free from BSE/TSE is
just that, a myth,
and it's a false myth !

the youngest age of BSE case to date is 20 months old; As at: 31 May
2003 Year of onset Age youngest case (mnths) Age 2nd youngest case
(mnths) Age 2nd oldest case (yrs.mnths) Age oldest case (yrs.mnths) 1986
30 33 5.03 5.07 1987 30 31 9.09 10.00 1988 24 27 10.02 11.01(2) 1989 21
24(4) 12.00(2) 15.04 1990 24(2) 26 13.03 14.00 1991 24 26(3) 14.02 17.05
1992 20 26 15.02 16.02 1993 29 30(3) 14.10 18.10 1994 30(2) 31(2) 14.05
16.07 1995 24 32 14.09 15.05 1996 29 30 15.07 17.02 1997 37(7) 38(3)
14.09 15.01 1998 34 36 14.07 15.05 1999 39(2) 41 13.07 13.10 2000 40 42
17.08 19.09 2001 48(2) 56 14.10 14.11 2002 51 52 15.08 15.09(2) 2003 50
62 11.11 14.11

http://www.defra.gov.uk/animalh/bse/bse-statistics/bse/yng-old.html

http://www.defra.gov.uk/animalh/bse/index.html

The implications of the Swiss result for Britain, which has had the most
BSE, are complex. Only cattle aged 30 months or younger are eaten in
Britain, on the assumption, based on feeding trials, that cattle of that
age, even if they were infected as calves, have not yet accumulated
enough prions to be infectious. But the youngest cow to develop BSE on
record in Britain was 20 months old, showing some are fast incubators.
Models predict that 200-300 cattle under 30 months per year are infected
with BSE and enter the food chain currently in Britain. Of these 3-5
could be fast incubators and carrying detectable quantities of prion.

http://www.sare.org/htdocs/hypermail/html-home/28-html/0359.html


https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed

With the 100% cattle testing under this new system,
Japan has found another 10 BSE cases
(as of April 2004).
BSE Cases in Japan


8

October 7, 2003

23 months

No Clinical Signs

9

November 4, 2003

21 months

No Clinical Signs

http://www.us.emb-japan.go.jp/english/html/fafacts/bse/bse.htm

oral dose of BSE in primates--look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE.

Published online

January 27, 2005

Risk of oral infection with bovine spongiform

encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,

Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys

The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)—which can lead to variant

Creutzfeldt-Jakob disease (vCJD)—is compounded by incomplete knowledge about the ef.ciency of oral infection

and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral

transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a

BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the

other remained free of disease at 76 months. On the basis of these .ndings and data from other studies, we made a

preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public

health measures can prevent transmission of BSE to man.

snip...

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection   

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the .rst positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

snip...end

www.thelancet.com Published online January 27, 2005

FOR IMMEDIATE RELEASE
P01-05
January 30, 2001
Print Media: 301-827-6242
Consumer Inquiries: 888-INFO-FDA

--------------------------------------------------------------------------------

Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT


Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise
that it

could take as little of 1 gram of brain to cause BSE by the oral route
within the

same species. This information did not become available until the "attack
rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to
ensure

that the actual result was within both a lower and an upper limit within the
study

and the designing scientists would not have expected all the dose levels to
trigger

infection. The dose ranges chosen by the most informed scientists at that
time

ranged from 1 gram to three times one hundred grams. It is clear that the
designing

scientists must have also shared Mr Bradley's surprise at the results
because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml


NEW MAD COW STRAIN CALLED BASE, VERY SIMILAR TO SPORADIC CJD IN HUMANS;


Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy:
Molecular similarities with sporadic Creutzfeldt-Jakob disease

Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari
, Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria
Caramelli *

*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto
Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via
Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual
Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale
L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale
della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and
¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan,
Italy


Edited by Stanley B. Prusiner, University of California, San Francisco, CA,
and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are
mammalian neurodegenerative disorders characterized by a posttranslational
conversion and brain accumulation of an insoluble, protease-resistant
isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and
animal TSE agents exist as different phenotypes that can be biochemically
differentiated on the basis of the molecular mass of the protease-resistant
PrPSc fragments and the degree of glycosylation. Epidemiological, molecular,
and transmission studies strongly suggest that the single strain of agent
responsible for bovine spongiform encephalopathy (BSE) has infected humans,
causing variant Creutzfeldt-Jakob disease. The unprecedented biological
properties of the BSE agent, which circumvents the so-called "species
barrier" between cattle and humans and adapts to different mammalian
species, has raised considerable concern for human health. To date, it is
unknown whether more than one strain might be responsible for cattle TSE or
whether the BSE agent undergoes phenotypic variation after natural
transmission. Here we provide evidence of a second cattle TSE. The disorder
was pathologically characterized by the presence of PrP-immunopositive
amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE
cases, and by a different pattern of regional distribution and topology of
brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc
type with predominance of the low molecular mass glycoform and a
protease-resistant fragment of lower molecular mass than BSE-PrPSc.
Strikingly, the molecular signature of this previously undescribed bovine
PrPSc was similar to that encountered in a distinct subtype of sporadic
Creutzfeldt-Jakob disease.


----------------------------------------------------------------------------
----

C.C. and G.Z. contributed equally to this work.

||To whom correspondence should be addressed.

E-mail: salvatore.monaco@mail.univr.it .

www.pnas.org/cgi/doi/10.1073/pnas.0305777101


http://www.pnas.org/cgi/content/abstract/0305777101v1


1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of
known infectious tissues. The asymptomatic incubation period in the one
monkey exposed to the virus of kuru was 36 months; that in the two monkeys
exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months,
respectively; and that in the two monkeys exposed to the virus of scrapie
was 25 and 32 months, respectively. Careful physical examination of the
buccal cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has remained
asymptomatic during the 39 months that it has been under observation.

PMID: 6997404


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=6997404&dopt=Abstract

TSS

TSS




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