From: Terry S. Singeltary Sr. [
[email protected]]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Page 1 of 98
8/3/2006
Greetings FSIS,
I would kindly like to comment on the following ;
From: Terry S. Singeltary Sr. [
[email protected]]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Page 1 of 98
8/3/2006
Greetings FSIS,
I would kindly like to comment on the following ;
[Federal Register: July 12, 2006 (Volume 71, Number 133)]
[Notices]
[Page 39282-39283]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr12jy06-35]
-----------------------------------------------------------------------
DEPARTMENT OF AGRICULTURE
Food Safety and Inspection Service
[Docket No. FSIS-2006-0011]
Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Update; Notice of Availability and Technical Meeting
AGENCY: Food Safety and Inspection Service, USDA.
ACTION: Notice of availability and announcement of technical meeting.
-----------------------------------------------------------------------
SUMMARY: The Food Safety and Inspection Service (FSIS) is announcing
the availability of an updated risk assessment model and report for
BSE. The previous risk assessment, released in October 2003, was
revised to incorporate information available through December 2003,
including the discovery of a BSE-infected cow in Washington State. The
revised risk assessment model evaluates the impact of measures
implemented after the discovery of the BSE-positive cow and
recommendations made by an international BSE panel. FSIS will also hold
a technical meeting to discuss the updated risk assessment model and
report.
DATES: The public meeting will be held on July 25, 2006, from 1 p.m. to
4 p.m. Comments on the updated Harvard Risk Assessment must be received
by August 11, 2006.
snip...END
http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-10928.htm
MY comments/questions are as follows ;
1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught with error after the PEER REVIEW
assessment assessed this fact, how do you plan on stopping this from happening again, will there be another peer
review with top TSE Scientist, an impartial jury so-to-speak, to assess this new and updated Harvard BSE/TSE risk
assessment and will this assessment include the Atypical TSE and SRM issues ?
*** Suppressed peer review of Harvard study October 31, 2002 ***
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
2. WITH A RECENT NATION WIDE MAD COW FEED BAN RECALL in the past few months that consisted of
some 10,878.06 TONS, then another Mad Cow feed ban warning letter in May, IT should seem prudent to ask why our
feed bans continue to fail in 2006, and continue to fail today ?
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL
FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER
H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm
initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
Page 2 of 98
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VOLUME OF PRODUCT IN COMMERCE
10,878.06 tons
DISTRIBUTION
Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006
Date: June 27, 2006 at 7:42 am PST
Public Health Service
Food and Drug Administration
New Orleans District
297 Plus Park Blvd.
Nashville, TN 37217
Telephone: 615-781-5380
Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS
OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner
Louisiana.DBA Riegel By-Products
2621 State Street
Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your
rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations
from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal
Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of
Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being
manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)
(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).
Page 3 of 98
8/3/2006
Our investigation found you failed to provide measures, including sufficient written procedures, to prevent
commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from
mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the
same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers
between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after
processing mammalian tissues.
You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of
protein derived from mammalian tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in
ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from
mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product
which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is
misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended
for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and
distribute are in compliance with the law. You should take prompt action to correct these violations, and you should
establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory
action, such as seizure and/or injunction, without further notice.
You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you
have taken to bring your firm into compliance with the law. Your response should include an explanation of each step
taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working
days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any
available documentation demonstrating corrections have been made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424
Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please
contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez
Acting District Director
New Orleans District
http://www.fda.gov/foi/warning_letters/g5883d.htm
3. WHY still now only partial ruminant feed ban, with the fact that now we seem to have 3 cases of nvCJD to humans
i.e. humanbovineTSE that were responsible from blood, and the fact the last 2 mad cows documented in the USA were
that of an Atypical strain, would it not seem prudent to remove blood as well from ruminant feed ?
Page 4 of 98
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WOULD it not seem prudent to improve and expand the SRM list now? as per your own thinking ;
> If transmission occurs, tissue distribution comparisons will be made between cattle
> infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in
> tissue distribution could require new regulations regarding specific risk material
> (SRM) removal.
FULL text ;
Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
Project Number: 3625-32000-073-07
Project Type: Specific C/A
Start Date: Sep 15, 2004
End Date: Sep 14, 2007
Objective:
The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to
conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy.
The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2.
Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue
distribution of atypical BSE isolates in cattle and other species.
Approach:
This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto
Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to
analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of
the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate.
Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and
sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of
transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between
cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require
new regulations regarding specific risk material (SRM) removal.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490
Page 5 of 98
8/3/2006
HOWEVER, JAPAN has already shown infectivity in tissues other than CNS in there atypical TSE in cattle, so why should we wait,
and expose many to this agent needlessly, since the last two mad cows in the USA were also atypical TSE ?
PrPSc distribution of a natural case of bovine spongiform encephalopathy
Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa
Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Kannondai, Tsukuba 305-0856 Japan
[email protected]
Abstract
Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes progressive neurodegeneration of the central nervous system. Infectivity of BSE agent is
accompanied with an abnormal isoform of prion protein (PrPSc).
The specified risk materials (SRM) are tissues potentially carrying BSE infectivity. The following tissues are designated as SRM in Japan: the skull including the brain and
eyes but excluding the glossa and the masse- ter muscle, the vertebral column excluding the vertebrae of the tail, spinal cord, distal illeum. For a risk management step, the
use of SRM in both animal feed or human food has been prohibited. However, detailed PrPSc distribution remains obscure in BSE cattle and it has caused controversies
about definitions of SRM. Therefore we have examined PrPSc distribution in a BSE cattle by Western blotting to reassess definitions of SRM.
The 11th BSE case in Japan was detected in fallen stock surveillance. The carcass was stocked in the refrigerator. For the detection of PrPSc, 200 mg of tissue samples
were homogenized. Following collagenase treatment, samples were digested with proteinase K. After digestion, PrPSc was precipitated by sodium phosphotungstate (PTA).
The pellets were subjected to Western blotting using the standard procedure. Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish peroxidase was used
for the detection of PrPSc.
PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected in the peripheral nerves
(sciatic nerve, tibial nerve, vagus nerve).
Our results suggest that the currently accepted definitions of SRM in BSE cattle may need to be reexamined.
T. Kitamoto (Ed.)PRIONSFood and Drug Safety================
ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004;
Bovine spongiform encephalopathy (BSE) in Japan
snip...
"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to
amplify the BSE prion"
NO. Date conf. Farm Birth place and Date Age at diagnosis
1. 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23
2. 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21
Test results
# 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative
b = atypical BSE case
c = case of BSE in a young animal
b,c, No PrPSc on IHC, and no spongiform change on histology
International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004.
Page 6 of 98
8/3/2006
Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1
SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail;
[email protected]
Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail:
[email protected]
=================================
Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer
Jpn. J. Infect. Dis., 56, 221-222, 2003
Laboratory and Epidemiology Communications
Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer
Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1,
Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2
Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-
8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916
Communicated by Tetsutaro Sata
(Accepted December 2, 2003)
*Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases,
Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640, Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail:
[email protected]
Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the
country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad
Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in
the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and
immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is
detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE
Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A
hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC,
all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the
distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus.
An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki
case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was
slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed
no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex
region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSEassociated
PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster
migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with
an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative
amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot
shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band
intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane
2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the
Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These
findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case.
The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank
accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-
monthold Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect
positive signals of PrPSc (data not shown).
Page 7 of 98
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Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has
been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype,
have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein
(PrP) coding region as in our case (5,6).
The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal
(MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF
report, the previous seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed.
However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present
cases remains to be investigated.
REFERENCES
Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the
aetiology of 'new variant' CJD. Nature, 383, 685
690. Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett,
C., Cousens, S., Fraser, H. and Bostock, C. J. (1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE
agent. Nature, 389, 498-501. Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same
prion strain causes vCJD and BSE. Nature, 389, 448-450. Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE
Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK. Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona,
C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel molecular and
neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention
concepts. Gasreig, Munhen, October 8-10. Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of
bovine spongiform encephalopatie. International Conference on Prion Disease: from basic research to intervention concepts.
Gasreig, Munhen, October 8-10. Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J.,
Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE prions propagate as either variant CJD-like or sporadic
CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366.
9/13/2005
Page 12 of 17
SEE SLIDES IN PDF FILE;
http://www.nih.go.jp/JJID/56/221.pdf
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
4. WHAT does USDA/FDA ET AL intend to do about the risks of atypical BSE/TSE in cattle now that infectivity
shows in tissue samples other than CNS in Japan, the fact now that the last Texas mad cow and that last mad cow in
Alabama were indeed of the atypical strain, the fact that the studies long ago in Mission, Texas of USA sheep scrapie
transmission to the USA bovine, which proved an 'atypical tse' in the USA bovine, the fact also that USDA/FDA are
still floundering on the last SRM regulations, but with the BASE strain now in cattle that is not similar to nvCJD, but
very similar to the sporadic CJD, and sporadic CJD has tripled in the last few years in the USA. WHAT do you plan to
do to protect human health from these atypical strains of TSE, in relations to SRMs ?
5. THE 2004 Enhanced BSE surveillance program, that tested all those cows, but then we found just how terribly
flawed the program was, from testing protocols, to testing the most likely to have BSE i.e. high risk, to the
geographical distribution of the testing and high risk areas, to letting the tissue samples of one mad cow sit on a shelf
Page 8 of 98
8/3/2006
for 7+ months and then having to have an act of Congress to ever get that cow finally confirmed, to that other Texas
mad cow they decided to not even bother testing at all, just rendered that very suspect cow, to suspect to test evidently,
back to that Alabama mad cow that they could only give a guess as to age with dentition where we all know that the
age of that cow was so close to 10 years it could have been 9 years 7 months to 10 years 3 months, thus possibly being
an BAPB i.e. USA 'born after partial ban', to all those rabies suspect cows that did not have rabies, and DID NOT get
tested for BSE/TSE in that June 2004 enhanced surveillance program, even though the common lay person knows the
suspect rabies negative cows are suppose to be BSE/TSE tested, how does one correct all these blatant failures and will
they be corrected?
snip...
6. WHAT happened to the test results and MOUSE BIO-ASSAYS of those imported sheep from Belgium
confiscated and slaughtered from the Faillace's, what sort of TSE did these animals have ?
snip...
7. WHY is it that the Farm of the Mad Sheep of Mad River Valley were quarantined for 5 years, but none of these
farms from Texas and Alabama with Atypical TSE in the Bovine, they have not been quarantined for 5 years, why
not, with the real risk of BSE to sheep, whom is to say this was not BSE ?
snip...
8. Scrapie in sheep and goat, CWD in deer and elk, are both running rampant and have been for decades, you cannot
and have not controled it, what do you plan to do about that, anything different since everything else has failed so far ?
snip...
WITH ANIMAL TSE in the USA rampant (the USA is the most documented Nation in the world with the most species
with TSE, all of which have been rendered and fed back to animals for human and animal consumption for decades),
with atypical TSE now in the USA, when will you start testing all animals susceptible to a TSE ?
I find it deeply disturbing that now USDA et al in fact are cutting BSE/TSE testing in the USA bovine down to 40,000 a year for the
following reasons ;
BSE monitoring in bovine animals EU Jan 1 to June 6 2006 COMPARED to USA (how not to find BSE)
COMPARING APPLES TO ORANGES I.E. USA TESTING FIGURES FOR BSE TO CATTLE RATIO
before June 2004 Enhanced BSE surveillance, during June 2004 Enhanced BSE cover-up, and
Page 25 of 98
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AFTER, which was proposed this week to be around 40,000 annually from here on out, in a cattle
population for USA of about 100 million every year.
THEN COMPARE TO E.U. COUNTRIES TESTING FIGURES FOR BSE TO CATTLE RATIO.
PLEASE note besides the total tests *** country, I have added total cattle population along
with some additional information on some countries below. While you are analyzing the additional
information, check out some of the imports to USA from documented BSE countries and please note,
among other things, the infamous, non-species coding system for feed, mbm, and such.
Seems those USA BSE triple firewalls have been seeping all along.
AFTER analyzing for yourself, then ask yourself, who is fooling whom? ...TSS
snip...
SEE FAILURES ;
PLEASE NOTE, while your are analyzing this information, please note just how terribly flawed
the June 2004 Enhanced BSE surveillance program was in the USA, all those cattle tested are
meaningless. 1st off, the following does not make any sense to me and even at that, why so
many ?
It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200
routine
IHC tests on samples that did not first undergo rapid testing. This was done to ensure that samples inappropriate for the
rapid screen
test were still tested, and also to monitor and improve upon IHC testing protocols. Of those 9,200 routine tests, one test
returned a
non-definitive result on July 27, 2005.
http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html
CAN you imagine how many might have been positive, IF proper BSE testing protocols were used.
WE know the infamous IHC gold standard for BSE the USDA et al boast about so much, is not as
gold as they claim. COME to find out, it is the least likely to find BSE, and maybe that is why it was
so gold to the USDA. IT also reminds me of the other infamous 'gold standard' the USDA preach about
all the time ;
*** Suppressed peer review of Harvard study October 31, 2002 ***
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
WE found out just how inept the program was from the TEXAS mad cow that
USDA et al tried to cover-up, but got caught by the Honorable Phyllis Fong of the OIG.
SEE FAILURES ;
Page 72 of 98
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snip...
TO REDUCE TESTING OF BSE IN THE USA TO ONLY 40,000 A YEAR, is simply not scientific regardless of
what the OIE BSE testing protocol calls for. ALL one has
to do is look at the countries above that all went down with BSE, that all went by the infamous OIE BSE testing
protocols. THEN and only then, after the USA finally fumbled the 'BSE FREE' golden egg and accidently had to
document a case or two of mad cow, low and behold, what next? yep, you guessed it, time to move the goal post in the
middle of the football game, GWs and his sleeping partners at the OIE, gave birth to the BSE MRR policy, the legal
trading of all strains of TSE globally was born. ...
BILLING CODE: 3410-34-P
DEPARTMENT OF AGRICULTURE
Animal and Plant Health Inspection Service
9 CFR Parts 93, 94, 95, and 96
[Docket No. 03-080-3]
RIN 0579-AB73
Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities
AGENCY: Animal and Plant Health Inspection Service, USDA.
ACTION: Final rule.
snip...full text 98 pages ;
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
TSS