FDA believes current regulation protects the public from
BSE but reopens comment period due to new studies
March 4, 2013
The Food and Drug Administration (FDA) is reopening the
comment period for the interim final rule entitled “Use of Materials Derived
From Cattle in Human Food and Cosmetics.” The interim final rule protects
consumers from exposure to bovine spongiform encephalopathy (BSE) by prohibiting
the use of certain cattle parts in human food, including dietary supplements,
and cosmetics. Under the interim final rule amended in 2005, the small intestine
of cattle can be used in human food, dietary supplements, and cosmetics if the
portion of the small intestine known as the distal ileum has been properly
removed.
Since 2005, there have been scientific studies that found
trace levels of infectivity in parts of cattle small intestine, other than the
distal ileum, from animals with BSE. However, FDA believes that the levels of
infectivity are so low that they do not pose a significant health risk to humans
or ruminants in the U.S. Consistent with FDA’s position, the World Organization
for Animal Health has not changed its definition of “specified risk material” to
include any part of the small intestine other than the distal ileum.
Further, FDA does not believe there would be a measurable
reduction in the risk from BSE to the American public by removing additional
parts of the cattle small intestine and, as such, it would be appropriate to
finalize the interim final rule without changing any provisions related to the small intestine.
Nonetheless, FDA is reopening the comment period to give interested parties an
opportunity to comment on the studies and on FDA’s tentative
conclusion.
Additional information:
Use of Materials
Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment
Period
This article has a comment period that ends in 60 days
(05/03/2013)
Action
Interim Final Rule; Reopening Of The Comment
Period.
Summary
The Food
and Drug Administration (FDA or “we”) is reopening the comment period for the
interim final rule entitled “Use of Materials Derived From Cattle in Human Food
and Cosmetics” that published in the Federal Register of
July 14, 2004 (69 FR 42256). The
interim final rule prohibited the use of certain cattle material to address the
potential risk of bovine spongiform encephalopathy (BSE) in human food,
including dietary supplements, and cosmetics. In the Federal
Register of September 7, 2005 (70 FR 53063), we
amended the interim final rule to make changes, including providing that the
small intestine of cattle, formerly prohibited cattle material, could be used in
human food and cosmetics if the distal ileum was removed by a specified
procedure or one that the establishment could demonstrate is equally effective
in ensuring complete removal of the distal ileum. Since 2005, peer-reviewed
studies have been published showing the presence of infectivity in the proximal
ileum, jejunum, ileocecal junction, and colon of cattle with BSE. Therefore, we
are reopening the comment period for the interim final rule to give interested
parties an opportunity to comment on the new studies concerning infectivity in
parts of the small intestine other than the distal ileum.
Unified Agenda
Use of Materials Derived From Cattle in Human Food and Cosmetics
10 actions from July 14th,
2004 to September 2011
DATES:
Submit either
electronic or written comments by May 3, 2013.
ADDRESSES:
Submit electronic
comments to http://www.regulations.gov. Submit
written comments to the Division of Dockets Management (HFA-305), Food and Drug
Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852.
FOR FURTHER INFORMATION CONTACT:
Johnny
Braddy,Center for Food Safety and Applied Nutrition (HFS-316),Food and Drug
Administration,5100 Paint Branch Pkwy.,College Park, MD
20740,240-402-2131.
SUPPLEMENTARY INFORMATION:
I. Background
In the Federal Register of July 14, 2004 (69 FR 42256), FDA
published an interim final rule entitled “Use of Materials Derived From Cattle
in Human Food and Cosmetics.” The interim final rule prohibited the use of
certain cattle material to address the potential risk of BSE in human food and
cosmetics. The interim final rule designated the small intestine as prohibited
cattle material and prohibited its use in human food or cosmetics. In the Federal Register of September 7, 2005 (70 FR 53063), we
amended the interim final rule to allow the use of the small intestine if the
distal ileum is removed by a procedure that removes at least 80 inches of
uncoiled and trimmed small intestine as measured from the ceco-colic junction
and progressing proximally towards the jejunum or by a procedure that the
establishment can demonstrate is equally effective in ensuring complete removal
of the distal ileum.
On January 12, 2004,
the U.S. Department of Agriculture, Food Safety and Inspection Service (FSIS),
issued an interim final rule to designate materials that could potentially
contain BSE infectivity as specified risk materials (SRMs) and prohibit their
use for human food (see “Prohibition of the Use of Specified Risk Materials for
Human Food and Requirements for the Disposition of Non-Ambulatory Disabled
Cattle”; 69 FR 1862;
January 12, 2004). FSIS's interim final rule designated the distal ileum as an
SRM but required that the entire small intestine be removed and disposed of as
inedible to ensure the effective removal of the distal ileum. On September 7,
2005, FSIS, like FDA, amended its interim final rule to permit the use of the
entire small intestine for human food if the distal ileum is removed by a
procedure that removes at least 80 inches of the uncoiled and trimmed small
intestine as measured from the ceco-colic junction and progressing proximally
towards the jejunum or by a procedure that the establishment demonstrates is
effective in ensuring complete removal of the distal ileum.
When the FDA and FSIS
amendments to the interim final rules were published in 2005, BSE infectivity
had been demonstrated in lymphoid tissue of the distal ileum. In naturally
occurring cases, sparse immunostaining had also been observed in the myenteric
plexus of the distal ileum indicating the presence of PrPSc [,] a TSE-specific protein (Ref. 1). Because the
myenteric plexus extends throughout the small intestine, both FDA and FSIS
considered that it was possible that infectivity might also exist in the
myenteric plexus of the jejunum or the duodenum. We stated in our 2005 amendment
to our interim final rule that if we became aware of data indicating that other
portions of the small intestine harbored BSE infectivity, we would take action
appropriate to the public health risk. FSIS stated in its 2005 amendment to its
interim final rule that while it believed that the primary tissues of concern
for spreading the BSE agent had been identified, FSIS would use the results of
future studies on BSE to further refine its policies with regard to BSE
(70 FR 53043 at
53047; September 7, 2005). In 2007, FSIS issued a final rule to make permanent
the interim measures implemented in 2004 and amended in 2005 (72 FR 38700; July
13, 2007).
Since we amended our
interim final rule in 2005 and FSIS issued its final rule in 2007, peer-reviewed
studies have been published showing the presence of some infectivity in the
proximal ileum, jejunum, ileocecal junction, and colon of cattle with
BSE. The new scientific data confirms the presence of limited amounts of BSE
infectivity in the small intestine outside of the distal ileum of classical BSE
infected cattle under experimental inoculation and field conditions. The
infectivity levels reported in these studies were much lower than the
infectivity levels that were previously demonstrated in the distal
ileum.
We have added several
peer-reviewed studies (Refs. 2 to 6) to the administrative record. We invite
comment on those studies.
Additionally, the
European Food Safety authority (EFSA) Panel on Biological Hazards (BIOHAZ) has
reviewed and evaluated new data as it relates to the BSE epidemiological
situation in the European Union. We have added the EFSA documents to the
administrative record as well (Refs. 7 and 8). We have evaluated the data from
the studies. Only trace amounts of infectivity have been found in the proximal
ileum, jejunum, ileocecal junction, and colon of cattle with naturally occurring
cases of BSE. We tentatively conclude that the effect of these traces of
infectivity on the risk of human or ruminant exposure to BSE in the United
States is negligible. The very low levels of infectivity in parts of the
intestine other than the distal ileum, the sharp decline in the prevalence of
BSE worldwide, FDA's BSE-related restrictions on the contents of animal food and
feed (see 21 CFR 589.2000
and 589.2001), and the extremely low prevalence of BSE within cattle in the
United States due to the presence of effective mitigations and compliance with
international standards suggest that the risk from parts of the intestine other
than the distal ileum is extremely low. We also note that the World Organization
for Animal Health (formerly known as the Office International des Epizooties or
“OIE”) has not changed its definition of SRMs to include any part of the small
intestine in addition to the distal ileum. Based on this assessment, we
tentatively conclude that requiring the removal of additional parts of the small
intestine would not provide a measurable risk reduction compared to that already
being achieved by removal of the distal ileum in all cattle and that it would be
appropriate to finalize our interim final rule without changing any provisions
related to the small intestine. We invite comment on this tentative
conclusion.
II. Comments
Interested persons may
submit either electronic comments regarding this document to http://www.regulations.gov or written
comments to the Division of Dockets Management (see ADDRESSES). It is only necessary to send one set of comments.
Identify comments with the docket number found in brackets in the heading of
this document. Received comments may be seen in the Division of Dockets
Management between 9 a.m. and 4 p.m., Monday through Friday, and will be posted
to the docket at http://www.regulations.gov.
III. References
The following
references have been placed on display in the Division of Dockets Management
(see ADDRESSES) and may be seen by interested persons
between 9 a.m. and 4 p.m., Monday through Friday, and are available
electronically at http://www.regulations.gov.
1. Terry, L.A., S.
March, S.J. Ryder, et al., “Detection of Disease Specific PrP in the Distal
Ileum of Cattle Exposed Orally to the Agent of Bovine Spongiform
Encephalopathy,”Veterinary Record, vol. 152, pp. 387-392,
2003.
2. Balkema-Buschmann,
A., C. Fast, M. Kaatz, et al., “Pathogenesis of Classical and Atypical BSE in
Cattle.”Preventive Veterinary Medicine, vol. 102, pp. 112-117,
2011.
3. Hoffmann, C., M.
Eiden, M. Kaatz, et al., “BSE Infectivity in Jejunum, Ileum and Ileocaecal
Junction of Incubating Cattle,”Veterinary Research, vol. 42,
p. 21, 2011.
4. Kimura K. and M.
Haritani, “Distribution of Accumulated Prion Protein in a Cow With Bovine
Spongiform Encephalopathy,”The Veterinary Record, vol. 162,
pp. 822-825, 2008.
5. Okada H., Y.
Iwamaru, M. Imamura, et al. “Detection of Disease-Associated Prion Protein in
the Posterior Portion of the Small Intestine Involving the Continuous Peyer's
Patch in Cattle Orally Infected With Bovine Spongiform Encephalopathy Agent,”Transboundary and Emerging Diseases, vol. 58(4), pp. 333-343,
Aug. 2011.
6. Stack M., S.J.
Moore, A. Vidal-Diez, et al. “Experimental Bovine Spongiform Encephalopathy:
Detection of PrP(SC) in the Small Intestine Relative to Exposure Dose and
Age,”Journal of Comparative Pathology, vol. 145, pp. 289-301,
2011.
7. “European Food
Safety Authority (EFSA) Panel on Biological Hazards (BIOHAZ),”EFSA
Journal, vol. 1317, pp. 1-9, 2009.
8. “European Food
Safety Authority (EFSA) Panel on Biological Hazards (BIOHAZ),”EFSA
Journal, vol. 9(3), p. 2104, 2011.
Dated: February 26,
2013.
Leslie Kux,
Assistant Commissioner for
Policy.
[FR
Doc. 2013-04869 Filed
3-1-13; 8:45 am]
BILLING
CODE 4160-01-P
SUBMIT A FORMAL COMMENT ;
Use
of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the
Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
Greetings again FDA et al,
I
once again would like to make a comment submission on the same topic BSE aka mad
cow disease FDA-2004-N-0188-0051, renewed March 4,
2013 due to new scientific concerns for human health, the same ones of which I
have been trying to warn you of since December 14, 1997, when I lost my mother
to the hvCJD i.e. the Heidenhain Variant of CJD.
I
told myself I was not going to do this anymore, because I don’t believe that you
care, and that you already have your mind made up, and that no matter how much
documented evidence that is brought forth, trade and the almighty dollar will
win out again, over a disease that is 100% fatal, once clinical. a disease that
has mutated into many strains and variants in many different species, all of
which have been fed back livestock producing animals for feed. it’s a vicious
cycle of greed, one of which they have already started to repeal and bring back
into commerce, i.e. mad cow feed for some species, and if left up to the OIE and
the USDA, they will have all these safe guards for the TSE prion disease
repealed, because it hurts their bottom dollar.
The
USDA, FSIS, APHIS, FDA, CDC, mad cow follies, or mad cow debacle, as it is known
around the world, has and will continue to exist, simply because of the greed
and ignorance there from it all. This new science, and other new science in the
TSE prion world now, some of which has been around for some time, but yet
ignored by the USDA et al, to a point now, where the amplification of the TSE
prion agent in the USA and North America is at it’s worst ever, and continues to
mount via many species.
The
USDA et al TRIPLE BSE FIREWALL, as they claim it to be, is and was a farce. ALL
of it, the SURVEILLANCE, the TESTING, the FEED BAN, and the SRM removal. 10
years post partial and voluntary mad cow feed ban of August 4, 1997 i.e.
2007 (one decade), 10 MILLION POUNDS OF BLOOD LACED, BANNED MEAT AND BONE MEAL
WENT INTO COMMERCE IN THE USA, never to be returned, fed out. The year before
that, 2006, was a banner years as well for banned mad cow feed in commerce in
the USA. please see the FDA recalls below in source reference. The surveillance
and testing for BSE aka mad cow disease in the USA was also hampered with much
fraud, from the least likely BSE test to find mad cow disease being used, to
only BSE testing the OBEX area of the brain for BSE, to the sad, sad, reality of
USDA testing cattle brains that they new were BSE free.
until
you get the corporate and political science policy making out of the way, you
will never stop the TSE prion aka mad cow type disease.
the
USA must test every cow for the TSE Prion disease.
the
USA must stop all feeding to all species of ruminant and non ruminant
protein.
the
USA must extend and enhance the mad cow feed ban. this is what was said they
would do long ago, if science shows change in tissue infectivity, but they went
back on their word, in my opinion.
Wednesday, May 2, 2012
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND
ANIMAL HEALTH
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of
Atypical BSE UPDATE July 28, 2010
Sent: Wednesday, July 28, 2010 11:42 AM
Subject: re-Freedom of Information Act Project Number 3625-32000-086-05,
Study of Atypical BSE UPDATE
Greetings again Ms Williams et al at FOIA USDA,
Thank You again for your kind reply on this important information. However,
I am concerned that you may not be aware of new transmission studies. You (USDA
et al) state Ma'am ;
================================================
The SCA with Italy was mainly to confirm our respective country’s
diagnostic tests would detect the various atypical BSE cases as seen in each
country), in the meantime, the Italians have published their transmissibility
and pathogenesis work on their BASE cases in the following article:
Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C,
Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S,
Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of
BASE induces clinical dullness and amyotrophic changes. PLoS Pathog 4:e1000075
The above mentioned paper concludes, “In all experimentally infected
animals, no PrP**TSE was detected in peripheral tissues, including cervical and
mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and
forelimb and limb muscles, either by standard Western blot analysis or following
phosphotungstic acid precipitation.“
It is not necessary to change SRM removal due to any different tissue
infectivity distribution between classical BSE and atypical BSE. At this time,
there is no scientific evidence to suggest a need for expanding the list of
tissues included in the Specified Risk Material (SRM) ban as a result of
published studies on atypical BSE.
snip...
Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine
spongiform encephalopathy-sensitive transgenic mice confirm the essential
restriction of infectivity to the nervous system in clinically diseased cattle.
J Infect Dis 192:934-942; the authors, when speaking about the classical BSE
food-borne epidemic in Europe, concluded their “results provide further
indication that the pathogenesis of BSE in cattle is fundamentally different
from that in sheep and mice, due to an exclusive intraneuronal spread of
infectivity from the gut to the central nervous system.”
end...
================================================
Again, in my opinion, the USDA is cherry picking the science they want to
use, and in doing so, I believe they are putting human lives at risk.
I disagree for the following reasons. New studies indeed show that ;
July 10, 2010
see full text ;
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of
Atypical BSE UPDATE July 28, 2010
Monday, December 26, 2011
*** Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE
in these countries.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
The present study demonstrated successful intraspecies transmission of
H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc
in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be
minimally defined by oral transmission of different TSE agents (C-type, L-type,
and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected
cattle have been initiated and are underway to provide information regarding the
extent of similarity in the immunohistochemical and molecular features before
and after transmission.
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
Friday, May 11, 2012
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits
***support risk assessments in some peripheral tissues derived from cattle
affected with H-type BSE
Thursday, June 21, 2012
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy
Associated with E211K Prion Protein Polymorphism
Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M.
Nicholson1
1 National Animal Disease Center, United States Department of Agriculture,
Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa
State University, Ames, Iowa, United States of America
Abstract
The majority of bovine spongiform encephalopathy (BSE) cases have been
ascribed to the classical form of the disease. Htype and L-type BSE cases have
atypical molecular profiles compared to classical BSE and are thought to arise
spontaneously. However, one case of H-type BSE was associated with a heritable
E211K mutation in the prion protein gene. The purpose of this study was to
describe transmission of this unique isolate of H-type BSE when inoculated into
a calf of the same genotype by the intracranial route. Electroretinograms were
used to demonstrate preclinical deficits in retinal function, and optical
coherence tomography was used to demonstrate an antemortem decrease in retinal
thickness. The calf rapidly progressed to clinical disease (9.4 months) and was
necropsied. Widespread distribution of abnormal prion protein was demonstrated
within neural tissues by western blot and immunohistochemistry. While this
isolate is categorized as BSE-H due to a higher molecular mass of the
unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with
monoclonal antibodies 6H4 and P4, and a second unglycosylated band at
approximately 14 kDa when developed with antibodies that bind in the C-terminal
region, it is unique from other described cases of BSE-H because of an
additional band 23 kDa demonstrated on western blots of the cerebellum. This
work demonstrates that this isolate is transmissible, has a BSE-H phenotype when
transmitted to cattle with the K211 polymorphism, and has molecular features
that distinguish it from other cases of BSE-H described in the literature.
snip...
Most significantly it must be determined if the molecular phenotype of this
cattle TSE remains stable when transmitted to cattle without the E211K
polymorphism as several other isolates of atypical BSE have been shown to adopt
a molecular profile consistent with classical BSE after passage in transgenic
mice expressing bovine PrPC [40] or multiple passages in wild type mice [23].
Results of ongoing studies, namely passage of the E211K Htype isolate into
wild-type cattle, will lend further insight into what role, if any, genetic and
sporadic forms of BSE may have played in the origins of classical BSE. Atypical
cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins
highlight that it may not be possible to eradicate BSE entirely and that it
would be hazardous to remove disease control measures such as prohibiting the
feeding of meat and bone meal to ruminants.
the
USA BSE GBR risk assessment, from the evidence I put forth below, in my opinion,
should be BSE GBR IV.
The
only thing that matters to the USDA and the OIE is trade, nothing else matters.
just ask Stanley Prusiner, who won the Nobel prize for the PRION, he said it
himself.
US
SENATOR AND PROFESSOR STANLEY PRUSINER ''DAMNING TESTIMONY''
Senator Michael Machado from California
''USDA does not know what's going on''.
''USDA is protecting the industry''.
''SHOULD the state of California step in''
Stanley Prusiner
''nobody has ever ask us to comment''
''they don't want us to comment''
''they never ask''
i
tried to see Venemon, after Candian cow was discovered with BSE. went to see
lyle. after talking with him...
absolute ignorance...
then thought I should see Venemon...
it
was clear his entire policy was to get cattle bonless beef prods across the
border...
nothing else mattered...
his
aids confirmed this...
5
times i tried to see Venemon, never worked...
eventually met with carl rove the political...
he
is the one that arranged meeting with Venemon...
just trying to give you a sense of the distance...
healh public safety...
was
never contacted...
yes
i believe that prions are bad to eat and you can die from them...
END
PLEASE NOTE THESE VIDEOS HAVE BEEN REMOVED FROM THE INTERNET $$$
Dr.
Stan bashing Ann Veneman - 3 minutes
Recall Authority and Mad Cow Disease: Is the Current System Good for
Californians?
Tuesday, February 24, 2004
JOINT HEARING
AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND
SELECT
COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER,
Chairs
please see ;
Thursday, January 17, 2013
Canada, U.S. agree on animal-disease measures to protect trade, while
reducing human and animal health protection
Sunday, May 6, 2012
***
BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
THIS is just ONE month report, of TWO recalls of prohibited banned MBM,
which is illegal, mixed with 85% blood meal, which is still legal, but yet we
know the TSE/BSE agent will transmit blood. we have this l-BSE in North America
that is much more virulent and there is much concern with blood issue and l-BSE
as there is with nvCJD in humans. some are even starting to be concerned with
sporadic CJD and blood, and there are studies showing transmission there as
well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD
COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that
reaches commerce is ever returned via recall, very, very little. this was 2007,
TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN
THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow
feed that was in ALABAMA in one of the links too, this is where the infamous
g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the
USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM
IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash
Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The
firm does not utilize a code - only shipping documentation with commodity and
weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was
cross contaminated with prohibited meat and bone meal and the labeling did not
bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID
and NV
END
OF ENFORCEMENT REPORT FOR MARCH 21, 2007
Saturday, August 14, 2010
BSE
Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr
PRIONPATHY
***
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a)
EVSRC Custom dairy feed, Recall # V-130-6;
b)
Performance Chick Starter, Recall # V-131-6;
c)
Performance Quail Grower, Recall # V-132-6;
d)
Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba
J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by
letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based
protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling
Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is
complete. REASON Possible contamination of dairy animal feeds with ruminant
derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a)
Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags,
Recall # V-121-6;
b)
Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall #
V-122-6;
c)
Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d)
Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags,
Recall # V-124-6;
e)
Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f)
Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g)
Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville,
AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall
is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with
ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END
OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a)
CO-OP 32% Sinking Catfish, Recall # V-100-6;
b)
Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c)
Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d)
CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e)
"Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f)
CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag,
Recall # V-105-6;
g)
Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall #
V-106-6;
h)
CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20
Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall #
V-107-6;
i)
CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j)
CO-OP LAYING CRUMBLES, Recall # V-109-6;
k)
CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l)
CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m)
CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur,
AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is
complete.
REASON Animal and fish feeds which were possibly contaminated with
ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END
OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD
COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22
71.248.128.67
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.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END
OF ENFORCEMENT REPORT FOR July 12, 2006
###
SPECIFIED RISK MATERIAL SRM BREACHES USA
----- Original Message -----
From: Terry S. Singeltary Sr. To: AgRepublicanPress@mail.house.gov
Sent: Friday, July 22, 2011 4:23 PM
Subject: Fw: Valley Farm Meats (DBA Strasburg Provision, Inc) Issues
Precautionary Recall for Beef Products Due to Possible Contamination with
Prohibited Materials SRM
Greetings USDA et al,
I
have not seen this on the USDA site yet ???
have i missed it ???
thank you, kind regards, terry
Ohio Department of Agriculture and Ohio Department of Health
Governor
John R. Kasich
Lieutenant Governor
Mary Taylor
ODA
Director
James Zehringer
ODH
Director
Theodore E. Wymyslo, M.D.
DT:
July 14, 2011
TO:
Health Commissioners, Directors of Environmental Health and Interested
Parties
RE:
Recall Announcement (ODA/ODH) 2011-076
Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary
Recall for Beef Products Due to Possible Contamination with Prohibited
Materials
snip...end...TSS
=========================================
Ohio Department of Agriculture and Ohio Department of Health
Governor
John R. Kasich
Lieutenant Governor
Mary Taylor
ODA
Director
James Zehringer
ODH
Director
Theodore E. Wymyslo, M.D.
DT:
July 14, 2011
TO:
Health Commissioners, Directors of Environmental Health and Interested
Parties
RE:
Recall Announcement (ODA/ODH) 2011-076
Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary
Recall for Beef Products Due to Possible Contamination with Prohibited
Materials
[STRASBURG, Ohio] – Valley Farm Meats (DBA Strasburg Provision, Inc) of
Strasburg, OH announces a voluntary recall of an unknown amount of beef products
that may contain the spinal cord and vertebral column, which are considered
specified risk materials (SRMs). SRMs must be removed from cattle over 30 months
of age in accordance with federal and state regulations. SRMs are tissues that
are known to contain the infective agent in cattle infected with Bovine
Spongiform Encephalopathy (BSE), as well as materials that are closely
associated with these potentially infective tissues. Therefore, federal and
state regulations prohibit SRMs from use as human food to minimize potential
human exposure to the BSE agent.
The
products subject to recall include all beef products slaughtered and processed
by or purchased from Valley Farm Meats retail store, 1317 N. Wooster Ave NW,
Strasburg, OH 44680 or purchased from Ed Lind Livestock and Poultry, 3333 Church
Rd B, Medina, Ohio 44256. These products were produced between 01/28/2011 and
07/05/2011 and offered for sale from 01/28/2011 through 07/11/2011.
The
package labels or beef carcasses may bear the Ohio mark of inspection and “Est.
80”, however products processed through Ed Lind Livestock and Poultry may not
contain such markings. The problem was discovered through routine inspection
activities by the Ohio Department of Agriculture’s Division of Meat Inspection.
The Department has received no reports of illnesses associated with consumption
of this product.
The
United States Department of Agriculture’s Food Safety and Inspection Service
classifies this type of potential contamination as a low health risk, however
individuals concerned about an illness should contact a health care
provider.
Because of potential product contamination, Valley Farm Meats urges its
customers who have purchased the suspect product(s) not to eat them and to
return them to the company. Customers may bring those designated packages to
Valley Farm Meats, 1317 N Wooster Avenue NW, Strasburg, OH 44680 during regular
business hours or call the company’s owner, Paul Berry at 330-878-5557.
Valley Farm Meats issues beef recall
TimesReporter.com staff report
Posted Jul 13, 2011 @ 03:18 PM
see
old FSIS example of SRM recalls from the past ;
North Dakota Firm Recalls Whole Beef Head Products That Contain
Prohibited Materials
Recall Release CLASS II RECALL FSIS-RC-023-2010 HEALTH RISK: LOW
Congressional and Public Affairs (202) 720-9113 Catherine Cochran
WASHINGTON, April 5, 2010 - North American Bison Co-Op, a New Rockford,
N.D., establishment is recalling approximately 25,000 pounds of whole beef heads
containing tongues that may not have had the tonsils completely removed, which
is not compliant with regulations that require the removal of tonsils from
cattle of all ages, the U.S. Department of Agriculture's Food Safety and
Inspection Service (FSIS) announced today.
Tonsils are considered a specified risk material (SRM) and must be
removed from cattle of all ages in accordance with FSIS regulations. SRMs are
tissues that are known to contain the infective agent in cattle infected with
Bovine Spongiform Encephalopathy (BSE), as well as materials that are closely
associated with these potentially infective tissues. Therefore, FSIS prohibits
SRMs from use as human food to minimize potential human exposure to the BSE
agent.
The
product subject to recall includes: Various weight cases of "Beef Heads KEEP
FROZEN." Each case bears the establishment number "EST. 18859" inside the USDA
mark of inspection and a case code number "16999." "North Dakota Natural Beef"
is printed in the bottom left-hand corner of each label.
The
recalled products were produced between June 25, 2009, and February 19, 2010.
These products were shipped to distribution centers in Md., Mich., and Minn. for
further sale.
The
problem was discovered during FSIS inspection activities at the establishment.
FSIS routinely conducts recall effectiveness checks to verify recalling firms
notify their customers of the recall and that steps are taken to make certain
that the product is no longer available to consumers.
Media with questions about the recall should contact Philip Wicke, Vice
President of Operations, at (701) 356-7723. Consumers with questions about the
recall should contact Jeremy Anderson, Director of Customer Service, at (952)
545-2495
Consumers with food safety questions can "Ask Karen," the FSIS virtual
representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat
and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and
Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through
Friday. Recorded food safety messages are available 24 hours a day. #
Missouri Firm Recalls Cattle Heads That Contain Prohibited
Materials
Recall Release CLASS II RECALL FSIS-RC-021-2008 HEALTH RISK: LOW
Congressional and Public Affairs (202) 720-9113 Amanda Eamich
WASHINGTON, June 26, 2008 – Paradise Locker Meats, a Trimble, Mo.,
establishment, is voluntarily recalling approximately 120 pounds of fresh cattle
heads with tonsils not completely removed, which is not compliant with
regulations that require the removal of tonsils from cattle of all ages, the
U.S. Department of Agriculture’s Food Safety and Inspection Service announced
today.
Tonsils are considered a specified risk material (SRM) and must be
removed from cattle of all ages in accordance with FSIS regulations. SRMs are
tissues that are known to contain the infective agent in cattle infected with
BSE, as well as materials that are closely associated with these potentially
infective tissues. Therefore, FSIS prohibits SRMs from use as human food to
minimize potential human exposure to the BSE agent.
The
products subject to recall include: Boxes of “BEEF HEAD, PARADISE LOCKER MEATS.”
Each shipping package bears the establishment numbers “EST. 31865” inside the
USDA mark of inspection.
These products were sent to retail establishments and restaurants in the
Kansas City, Kansas, area.
The
problem was discovered through routine FSIS inspection that verified there had
been incomplete removal of the tonsils by the recalling establishment.
Media and consumers with questions about the recall should contact
company Production Supervisor Louis Fantasma at (816) 370-6328.
Consumers with food safety questions can “Ask Karen,” the FSIS virtual
representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat
and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and
Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through
Friday. Recorded food safety messages are available 24 hours a day. #
HAS
the greed and money gotten so bad that the FSIS, USDA, APHIS, OIE et al, just
decided that not only to exempt the atypical Scrapies and apparently now the
BSE's, exempt them all, and just agreed to choose to not even speak about it
anymore. i mean...really, the USDA and OIE have systematically covered up mad
cow disease i.e. they call it SSS policy. where is USA burying them all at ? i
do not accept the star trek like cloaking device that appears to be the only
thing left that could be protecting the USA from mad cow disease....really.
sadly, Canada has now taken the same low road as the USA in regards to
discussing and making public documents on there mad cow cases. all this, 2011,
with the science mounting, still follow the global myth of the UKBSEnvCJD only
theory, and that all the sporadic CJDs (85%+ of all human TSE) are a mear
happenstance of bad luck, when North America is plum full of different strains
of the Transmissible Spongiform Encephalopathy in different species, all of
which over a period of time, decades, were rendered and fed to food producing
animals for human and animal food...really. i really just don't buy it...tss
some history on SRM's IN COMMERCE ;
SEE
FULL TEXT HERE ;
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials
SRMs
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials
SRM WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM
MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE
infectivity in the absence of detectable PrPSc accumulation in the tongue and
nasal mucosa of terminally diseased cattle
SPECIFIED RISK MATERIALS SRMs
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject
PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in
the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a
non-profit Swiss Foundation
USA
BSE AKA MAD COW SURVEILLANCE AND TESTING BREACHES
2004, highly suspect stumbling and staggering mad cow reported, however,
NO TESTING DONE, ON ORDERS FROM AUSTIN $
May
4, 2004
Statement on Texas Cow With Central Nervous System Symptoms
On
Friday, April 30th, 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)...
USDA regulations, any cow that exhibits signs of central nervous system
(CNS)
According to a 1997 Animal and Plant Health Inspection Service (NHIS)
Memorandum, brain samples all of such animals should be sent for BSE testing.2
The memorandum notes that "it is essential that brain specimens be collected
from adult cattle condemned for CNS signs as part of our national surveillance
of BSE."
The
cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and
fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from
APHIS personnel at the plant to conduct BSE testing, however, an APHIS
supervisor in Austin reportedly refused the test and instructed the plant to
send the carcass for rendering.5
May
13,2004
Page 2
snip...
The
cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and
fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from
APHIS personnel at the plant to conduct BSE testing, however, an APHIS
supervisor in Austin reportedly refused the test and instructed the plant to
send the carcass for rendering.5
This sequence of events is troubling, and it raises the question of
whether this is an isolated incident. In 1997, USDA noted a major gap between
the number of cattle condemned for CNS symptoms and the number of these cows
actually tested for mad cow disease. The Department found:
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To:
paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at
OIG, ...............
snip...
There will be several more emails of my research to follow. I
respectfully request a full inquiry into the cover-up of TSEs in the United
States of America over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff,
Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST In
Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John
Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by
TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days
later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary
for Marketing and Regulatory Programs resigns. Three days later same mad cow
found in November turns out to be positive. Both resignation are unexpected.
just pondering... TSS
MAD
COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To:
Carla Everett References: <[log in to unmask]> <[log in to unmask]
us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and
i see the TEXAS department of animal health is ramping up forsomething, but they
forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
terry
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 –0600
From: Carla Everett
To:
"Terry S. Singeltary Sr." References: <[log in to unmask]>
The
USDA has made a statement, and we are referring all callers to the USDA web
site. We have no information about the animal being in Texas. Carla At 09:44 AM
11/19/2004, you wrote:>Greetings Carla,>>i am getting unsubstantiated
claims of this BSE 'inconclusive' cow is from>TEXAS. can you comment on this
either way please?>>thank you,>Terry S. Singeltary Sr.>>
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
To:
"Terry S. Singeltary Sr."
References: ...sniptss
our
computer department was working on a place holder we could post USDA's
announcement of any results. There are no results to be announced tonight by
NVSL, so we are back in a waiting mode and will post the USDA announcement when
we hear something. At 06:05 PM 11/22/2004,
you
wrote:
>why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of animal.>>>>>>
==========================
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
Greetings Carla,
still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
terry
==============================
USDA did not test possible mad cows
By
Steve Mitchell
United Press International
Published 6/8/2004 9:30 PM
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims
ittested 500 cows with signs of a brain disorder for mad cow disease last year,
but agency documents obtained by United Press International show the agency
tested only half that number.
""These 9,200 cases were different because brain tissue samples were
preserved with formalin, which makes them suitable for only one type of
test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE
IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine,
and these were probably from the most high risk cattle pool, the ones the USDA
et al, SHOULD have been testing. ...TSS
TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND
CALLS FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS
CONFIRMED
THE
USDA MAD COW FOLLIES POSITIVE TEST COVER UP
JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED
OIG
AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7 MONTHS
LATER
TEXAS MAD COW
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE
THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i
confirmed this case 7 months earlier to the TAHC, and then, only after i
contacted the Honorable Phyllis Fong and after an act of Congress, this animal
was finally confirmed ;
During the course of the investigation, USDA removed and tested a total
of 67 animals of interest from the farm where the index animal's herd
originated. All of these animals tested negative for BSE. 200 adult animals of
interest were determined to have left the index farm. Of these 200, APHIS
officials determined that 143 had gone to slaughter, two were found alive (one
was determined not to be of interest because of its age and the other tested
negative), 34 are presumed dead, one is known dead and 20 have been classified
as untraceable. In addition to the adult animals, APHIS was looking for two
calves born to the index animal. Due to record keeping and identification
issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding
and slaughter channels, four are presumed to have entered feeding and slaughter
channels and one calf was untraceable.
Executive Summary In June 2005, an inconclusive bovine spongiform
encephalopathy (BSE) sample from November 2004, that had originally been
classified as negative on the immunohistochemistry test, was confirmed positive
on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA)
identified the herd of origin for the index cow in Texas; that identification
was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal
Health Commission (TAHC), established an incident command post (ICP) and began
response activities according to USDA’s BSE Response Plan of September 2004.
Response personnel removed at-risk cattle and cattle of interest (COI) from the
index herd, euthanized them, and tested them for BSE; all were negative. USDA
and the State extensively traced all at-risk cattle and COI that left the index
herd. The majority of these animals entered rendering and/or slaughter channels
well before the investigation began. USDA’s response to the Texas finding was
thorough and effective.
snip...
Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having
received an animal of interest. The herd was placed under hold order on 7/27/05.
The herd inventory was conducted on 7/28/05. The animal of interest was not
present within the herd, and the hold order was released on 7/28/05. The person
who thought he sold the animal to the owner of Trace Herd 3 had no records and
could not remember who else he might have sold the cow to. Additionally, a
search of GDB for all cattle sold through the markets by that individual did not
result in a match to the animal of interest. The animal of interest traced to
this herd was classified as untraceable because all leads were exhausted.
Trace Herd 4 The owner of Trace Herd 4 was identified as having received
one of the COI through an order buyer. Trace Herd 4 was placed under hold order
on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05.
There were 233 head of cattle that were examined individually by both State and
Federal personnel for all man-made identification and brands. The animal of
interest was not present within the herd. Several animals were reported to have
died in the herd sometime after they arrived on the premises in April 2005. A
final search of GDB records yielded no further results on the eartag of interest
at either subsequent market sale or slaughter. With all leads having been
exhausted, this animal of interest has been classified as untraceable. The hold
order on Trace Herd 4 was released on 8/23/05.
Trace Herd 5 The owner of Trace Herd 5 was identified as having received
two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67
head of cattle in multiple pastures. During the course of the herd inventory,
the owner located records that indicated that one of the COI, a known birth
cohort, had been sold to Trace Herd 8 where she was subsequently found alive.
Upon completion of the herd inventory, the other animal of interest was not
found within the herd. A GDB search of all recorded herd tests conducted on
Trace Herd 5 and all market sales by the owner failed to locate the
identification tag of the animal of interest and she was subsequently classified
as untraceable due to all leads having been exhausted. The hold order on Trace
Herd 5 was released on 8/8/05.
Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having
received an animal of interest and was placed under hold order on 8/1/05. This
herd is made up of 58 head of cattle on two pastures. A herd inventory was
conducted and the animal of interest was not present within the herd. The owner
of Trace Herd 6 had very limited records and was unable to provide further
information on where the cow might have gone after he purchased her from the
livestock market. A search of GDB for all cattle sold through the markets by
that individual did not result in a match to the animal of interest.
Additionally, many of the animals presented for sale by the owner of the herd
had been re-tagged at the market effectually losing the traceability of the
history of that animal prior to re-tagging. The animal of interest traced to
this herd was classified as untraceable due to all leads having been exhausted.
The hold order on Trace Herd 6 was released on 8/3/05.
Trace Herd 7 The owner of Trace Herd 7 was identified as having received
an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7
contains 487 head of cattle on multiple pastures in multiple parts of the State,
including a unit kept on an island. The island location is a particularly rough
place to keep cattle and the owner claimed to have lost 22 head on the island in
2004 due to liver flukes. Upon completion of the herd inventory, the animal of
interest was not found present within Trace Herd 7. A GDB search of all recorded
herd tests conducted on Trace Herd 7 and all market sales by the owner failed to
locate the identification tag of the animal of interest. The cow was
subsequently classified as untraceable. It is quite possible though that she may
have died within the herd, especially if she belonged to the island unit. The
hold order on Trace Herd 7 was released on 8/8/05.
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An
Arizona meat processing company and its owner pled guilty in February 2007 to
charges of theft of Government funds, mail fraud, and wire fraud. The owner and
his company defrauded the BSE Surveillance Program when they falsified BSE
Surveillance Data Collection Forms and then submitted payment requests to USDA
for the services. In addition to the targeted sample population (those cattle
that were more than 30 months old or had other risk factors for BSE), the owner
submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from
healthy USDA-inspected cattle. As a result, the owner fraudulently received
approximately $390,000. Sentencing is scheduled for May 2007.
snip...
4
USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad
cow issue for some years, and with Linda Detwiler and others sent lengthy
detailed critiques and recommendations to both the USDA and the Canadian Food
Agency."
end...tss
Saturday, May 26, 2012
Are
USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
What irks many scientists is the USDA’s April 25 statement that the rare
disease is “not generally associated with an animal consuming infected feed.”
The
USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of
the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
“We
can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with
the USDA during the Clinton Administration now at Mississippi State.
In
the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins
of atypical cases of BSE,” she said
The
argument about feed is critical because if feed is the cause, not a spontaneous
mutation, the California cow could be part of a larger outbreak.
SNIP...
Saturday, August 4, 2012
***
Final Feed Investigation Summary - California BSE Case - July 2012
in
the url that follows, I have posted
SRM
breaches first, as late as 2011.
then
MAD
COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007,
when they ceased posting them.
then,
MAD
COW SURVEILLANCE BREACHES.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform
Encephalopathy (BSE) in the United States Friday May 18, 2012
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY
2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON
92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS
GUILTY"
Wednesday, December 22, 2010
Manitoba veterinarian has been fined $10,000 for falsifying
certification documents for U.S. bound cattle and what about mad cow disease
?
USDA ET AL SECRET TEST THEY USE ON HOW NOT TO FIND MAD COW DISEASE IN
USA
Tuesday, November 02, 2010
IN
CONFIDENCE
The
information contained herein should not be disseminated further except on the
basis of "NEED TO KNOW".
BSE
- ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic
criteria CVL 1992
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Comments on technical aspects of the risk assessment were then submitted
to FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received
on the 2005 updated Harvard BSE risk assessment. Please bear the following
points in mind:
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
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
***
FSIS, USDA, REPLY TO SINGELTARY
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
2012 atypical L-type BSE BASE California reports
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
MAD
COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in
Primate Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical
BSE in these countries.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
The
present study demonstrated successful intraspecies transmission of H-type BSE to
cattle and the distribution and immunolabeling patterns of PrPSc in the brain of
the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined
by oral transmission of different TSE agents (C-type, L-type, and H-type BSE
agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been
initiated and are underway to provide information regarding the extent of
similarity in the immunohistochemical and molecular features before and after
transmission.
In
addition, the present data will support risk assessments in some peripheral
tissues derived from cattle affected with H-type BSE.
Thursday, June 21, 2012
Clinical and Pathologic Features of H-Type Bovine Spongiform
Encephalopathy Associated with E211K Prion Protein Polymorphism
Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M.
Nicholson1
1
National Animal Disease Center, United States Department of Agriculture,
Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa
State University, Ames, Iowa, United States of America
Abstract
The
majority of bovine spongiform encephalopathy (BSE) cases have been ascribed to
the classical form of the disease. Htype and L-type BSE cases have atypical
molecular profiles compared to classical BSE and are thought to arise
spontaneously. However, one case of H-type BSE was associated with a heritable
E211K mutation in the prion protein gene. The purpose of this study was to
describe transmission of this unique isolate of H-type BSE when inoculated into
a calf of the same genotype by the intracranial route. Electroretinograms were
used to demonstrate preclinical deficits in retinal function, and optical
coherence tomography was used to demonstrate an antemortem decrease in retinal
thickness. The calf rapidly progressed to clinical disease (9.4 months) and was
necropsied. Widespread distribution of abnormal prion protein was demonstrated
within neural tissues by western blot and immunohistochemistry. While this
isolate is categorized as BSE-H due to a higher molecular mass of the
unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with
monoclonal antibodies 6H4 and P4, and a second unglycosylated band at
approximately 14 kDa when developed with antibodies that bind in the C-terminal
region, it is unique from other described cases of BSE-H because of an
additional band 23 kDa demonstrated on western blots of the cerebellum. This
work demonstrates that this isolate is transmissible, has a BSE-H phenotype when
transmitted to cattle with the K211 polymorphism, and has molecular features
that distinguish it from other cases of BSE-H described in the literature.
snip...
Most significantly it must be determined if the molecular phenotype of
this cattle TSE remains stable when transmitted to cattle without the E211K
polymorphism as several other isolates of atypical BSE have been shown to adopt
a molecular profile consistent with classical BSE after passage in transgenic
mice expressing bovine PrPC [40] or multiple passages in wild type mice [23].
Results of ongoing studies, namely passage of the E211K Htype isolate into
wild-type cattle, will lend further insight into what role, if any, genetic and
sporadic forms of BSE may have played in the origins of classical BSE. Atypical
cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins
highlight that it may not be possible to eradicate BSE entirely and that it
would be hazardous to remove disease control measures such as prohibiting the
feeding of meat and bone meal to ruminants.
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
Thursday, July 22, 2010
BSE
INQUIRY DFA 18 COSMETICS
From:
TSS
Subject: Use of Materials Derived From Cattle in Human Food and
Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
Date: April 17, 2008 at 2:41 pm PST
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN
VACCINES
Sunday, May 18, 2008
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
1999
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
2001
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To:
Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l
3:03 PM freas ...
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 Subject:
BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To:
BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Greetings List Members,
I
was lucky enough to sit in on this BSE conference call today and even managed to
ask a question. that is when the trouble started.
I
submitted a version of my notes to Sandra Blakeslee of the New York Times, whom
seemed very upset, and rightly so.
"They tell me it is a closed meeting and they will release whatever
information they deem fit. Rather infuriating."
and
i would have been doing just fine, until i asked my question. i was surprised my
time to ask a question so quick.
(understand, these are taken from my notes for now. the spelling of
names and such could be off.)
[host Richard Barns] and now a question from Terry S. Singeltary of CJD
Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give
for serum or tissue donor herds?
[no
answer, you could hear in the back ground, mumbling and 'we can't. have him ask
the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or
tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD
world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
from this point, i was still connected, got to listen and tape the whole
conference. at one point someone came on, a woman, and ask again;
[unknown woman] what group are you with?
[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down
CJD and other human TSE's world wide. i was invited to sit in on this from
someone inside the USDA/APHIS and that is why i am here. do you intend on
banning me from this conference now?
at
this point the conference was turned back up, and i got to finish listening.
They never answered or even addressed my one question, or even addressed the
issue. BUT, i will try and give you a run-down for now, of the conference.
IF
i were another Country, I would take heed to my notes, BUT PLEASE do not depend
on them. ask for transcript from;
RBARNS@ORA.FDA.GOV 301-827-6906
he
would be glad to give you one ;-)
Rockville Maryland, Richard Barns Host
BSE
issues in the U.S., How they were labelling ruminant feed? Revising issues.
The
conference opened up with the explaining of the U.K. BSE epidemic winding down
with about 30 cases a week.
although new cases in other countries were now appearing.
Look at Germany whom said NO BSE and now have BSE.
BSE
increasing across Europe.
Because of Temporary Ban on certain rendered product, heightened
interest in U.S.
A
recent statement in Washington Post, said the New Administration (old GW) has a
list of issues. BSE is one of the issues.
BSE
Risk is still low, minimal in U.S. with a greater interest in MBM not to enter
U.S.
HOWEVER, if BSE were to enter the U.S. it would be economically
disastrous to the render, feed, cattle, industries, and for human health.
(human health-they just threw that in cause i was listening. I will now
jot down some figures in which they told you, 'no need to write them down'. just
hope i have them correct. hmmm, maybe i hope i don't ???)
80%
inspection of rendering
*Problem-Complete coverage of rendering HAS NOT occurred.
sizeable number of 1st time FAILED INITIAL INSPECTION, have not been
reinspected (70% to 80%).
Compliance critical, Compliance poor in U.K. and other European Firms.
Gloria Dunason Major Assignment 1998 goal TOTAL compliance. This _did
not_ occur. Mixed level of compliance, depending on firm.
Rendering FDA license and NON FDA license
system in place for home rendering & feed 76% in compliance 79%
cross contamination 21% DID NOT have system 92% record keeping less than 60%
total compliance
279
inspectors 185 handling prohibited materials
Renderer at top of pyramid, significant part of compliance. 84%
compliance
failed to have caution statement render 72% compliance & cross
contamination caution statement on feed, 'DO NOT FEED TO CATTLE'
56
FIRMS NEVER INSPECTED
1240 FDA license feed mills 846 inspected
"close to 400 feed mills have not been inspected"
80%
compliance for feed.
10%
don't have system.
NON-FDA licensed mills There is NO inventory on non licensed mills.
approximately 6000 to 8000 Firms ??? 4,344 ever inspected. "FDA does not have a
lot of experience with"
40%
do NOT have caution statement 'DO NOT FEED'.
74%
Commingling compliance
"This industry needs a lot of work and only half gotten to"
"700 Firms that were falitive, and need to be re-inspected, in addition
to the 8,000 Firms."
Quote to do BSE inspection in 19 states by end of January or 30 days,
and other states 60 days. to change feed status??? Contract check and ask
questions and pass info.
At
this time, we will take questions.
[I
was about the third or fourth to ask question. then all B.S.eee broke loose, and
i lost my train of thought for a few minutes. picked back up here]
someone asking about nutritional supplements and sourcing, did not get
name. something about inspectors not knowing of BSE risk??? the conference
person assuring that Steve Follum? and the TSE advisory Committee were handling
that.
Some other Dr. Vet, whom were asking questions that did not know what to
do???
[Dennis Wilson] California Food Agr. Imports, are they looking at
imports?
[Conference person] they are looking at imports, FDA issued imports
Bulletin.
[Linda Singeltary ??? this was a another phone in question, not related
i don't think] Why do we have non-licensed facilities?
(conference person) other feed mills do not handle as potent drugs???
Dennis Blank, Ken Jackson licensed 400 non FDA 4400 inspected of a total
of 6000 to 8000, (they really don't know how many non licensed Firms in U.S.
they guess 6000 to 8000??? TSS)
Linda Detwiler asking everyone (me) not to use emergency BSE number,
unless last resort. (i thought of calling them today, and reporting the whole
damn U.S. cattle herd ;-) 'not'
Warren-Maryland Dept. Agr. Prudent to re-inspect after 3 years.
concerned of Firms that have changed owners.
THE
END
TSS
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############
snip...
see
full text and more here on tissue donor herds and the TSE Prion disease ;
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
http://jama.jamanetwork.com/article.aspx?articleid=1031186
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
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/content/60/2/176/reply#neurology_el_535
2009
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
re-Human Prion Diseases in the United States Posted by flounder on 01 Jan 2010 at 18:11 GMT
I kindly disagree with your synopsis for the following reasons ;
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Proposal ID: 29403
Wednesday, August 24, 2011
*** There Is No Safe Dose of Prions
Monday, December 26, 2011
*** Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites
Thursday, February 14, 2013
***
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE
prion disease
Wednesday, February 20, 2013
***
World Organization for Animal Health Recommends United States' BSE Risk Status
Be Upgraded
Statement from Agriculture Secretary Tom Vilsack:
Monday, January 14, 2013
*** Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe
Thursday, February 21, 2013
***
National Prion Disease Pathology Surveillance Center Cases Examined January 16,
2013
Monday, May 30, 2011
***
CEPs for gelatin and impact of the revised EU Note for Guidance on the TSE risk
EMEA/410/01 Rev.3) will come into force in July 2011
Monday, February 01, 2010
Import Alert 17-04 BSE CJD HIGH RISK TISSUES, Nutritional Supplements
and Cosmetics
snip...
1998 MY SUBMISSION TO THE BSE INQUIRY ENGLAND
Sender: "Patricia Cantos"
To: "Terry S Singeltary Sr. (E-mail)"
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100
3 July 1998 Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref:
E2979
Dear Mr Singeltary,
Thank you for your E-mail message of the 30th of June 1998 providing the
Inquiry with your further comments. Thank you for offering to provide the
Inquiry with any test results on the nutritional supplements your mother was
taking before she died.
As requested I am sending you our general Information Pack and a copy of
the Chairman's letter. Please contact me if your system cannot read the
attachments.
Regarding your question, the Inquiry is looking into many aspects of the
scientific evidence on BSE and nvCJD. I would refer you to the transcripts of
evidence we have already heard which are found on our internet site at http://www.bse.org.uk. Could you please provide
the Inquiry with a copy of the press article you refer to in your e-mail? If not
an approximate date for the article so that we can locate it? In the meantime,
thank you for you comments. Please do not hesitate to contact me on 0171 261
8332 should you have any queries.
Yours sincerely Patricia Cantos Families Team Leader Attachments TSS
==============
My neighbors Mom also died from CJD. She had been taking a nutritional
supplement which contained the following; vacuum dried bovine BRAIN, bone meal,
bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine
kidney, and vacuum dried porcine stomach. As I said, this woman taking these
nutritional supplements, died from CJD. The particular batch of pills that was
located, in which she was taking, was tested. From what I have heard, they came
up negative, for the prion protein. But, in the same breath, they said their
testing, may not have been strong enough to pick up the infectivity. Plus, she
had been taking these type pills for years, so, could it have come from another
batch?
IPLEX, mad by standard process;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal Bone, bovine liver
powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine
stomach.
also;
i will only list animal ingredients of the following Nutritional
Supplements by only ONE company;
Standard Process Co.
IPLEX; bovine EYE PMG Extract, veal bone PMG Extract, bovine liver powder,
vaccuum dried porcine stomach, vacuum dried bovine adrenal, vacuum dried bovine
kidney, bovine adrenal, vacuum dried BOVINE BRAIN, bone meal, vacuum dried veal
bone.
A-FBetafood R vacuum dried bovine prostate, bovine liver powder, vacuum
dried bovine kidney, bovine orchic glandular extract, bovine liver fat
extract.
Arginex R bovine liver powder.
Adrenal, Desiccated TM Vacuum dried bovine adrenal.
Albaplex R bovine liver PMG Extract, vacuum dried bovine adrenal, bovine
kidney PMF Extract, bovine thymus Cytosol Extract, bovine liver powder, bone
meal, vacuum dried bovine kidney, veal bone meal.
Allerplex TM bovine lung PMF Extract, bovine adrenal PMF Extract, bovine
liver fat extract (yakriton), bone meal, vacuum dried bovine kidney, vacuum
dried veal bone.
Immuplex R Bovine liver PMG Extract, bovine liver powder, veal bone PMF
Extract, bovine spleen PMF Extract, vacuum dried bovine and ovine spleen, bovine
thymus PMF Extract, bovine thymus Cytosol Extract.
Vasculin R Bovine Heart PMG Extract, veal bone PMF Extract, bovine liver
powder, vacuum dried porcine duodenum, bovine adrenal Cytosol Extract, vacuum
dried bovine and ovine spleen.
Zypan R bovine pancreas Cytosol Extract, vacuum dried bovine and ovine
spleen.
last i heard, they were getting sued;
Suit Filed Over Mad Cow Disclaimer
By Jason Hoppin The Recorder March 23, 2001
snip...see full text ;
Volume 15, Number 5—May 2009
Research
Chronic Wasting Disease Prions in Elk Antler Velvet
Thursday, January 31, 2008
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 99th
meeting held on 14th December 2007
snip...
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION
40. The Chair explained that the purpose of the question and answer session
was to give members of the public an opportunity to ask questions related to the
work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to
the meeting, asking: “With the Nor-98 now documented in five different states so
far in the USA in 2007, and with the two atypical BSE H-base
13 © SEAC 2007
cases in Texas and Alabama, with both scrapie and chronic wasting disease
(CWD) running rampant in the USA, is there any concern from SEAC with the rise
of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any,
in relations to blood donations, surgery, optical, and dental treatment, do you
have with these unknown atypical phenotypes in both humans and animals in the
USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA
animal and human health officials?”
41. A member considered that this question ............
Comment from Terry S Singletary Sr
| Document ID: APHIS-2006-0041-0006 | Document Type: Public Submission |
This is comment on
Proposed Rule: Bovine Spongiform Encephalopathy; Minimal-Risk
Regions; Importation of Live Bovines and Products Derived From
Bovines
Docket ID:
|
RIN:0579-AC01 |
Topics: No Topics associated with this
document
----- Original Message -----
From: Terry S. Singeltary
Sr.
Sent: Wednesday, November 29, 2006 1:24
PM
Subject: TSE advisory committee for
the meeting December 15, 2006 [TSS SUBMISSION]
November 29, 2006
Greetings FDA, DHH, Dr.
Freas, and Dr. Harvey et al,
a kind and warm Holiday Greetings to you
all.
i kindly wish to submit the following to the TSE
advisory committee for the meeting December 15, 2006,
about the assessment for potential exposure to vCJD in
human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related
communication material ;
i see the media picked up
on this as a 'low risk', from what the gov. agency perceived to be to
them;
however, i seem to disagree. from my primitive ciphering,
i see it another way. this is a huge catastrophic risk. 3 in 160 is 1.9%. so
call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million.
also, what about the mixed genotypes/mixed susceptibility? what about the silent
carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN
strain or phenotype? this risk assessment is just more BSe to me. Just another
in a long line of industry fed crap. i pray that my assessment is the one that
is wrong. but it is THEY who roll the dice with your life. It is THEY who refuse
to regulate an industry that has run amok. just from a recall aspect of potentially tainted blood,
and these are just recent recalls ;
Attachment to Singletary comment
SNIP...SEE FULL TEXT IN THE
ATTACHMENT SOURCE REFERENCES AT THE BOTTOM OF THIS SUBMISSION
;
Attachment to Singletary
comment
Response to Public Comments
on
the
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update,
October 31, 2005
INTRODUCTION
The
United States Department of Agriculture’s Food Safety and Inspection Service
(FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present
findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy
Update, October 31, 2005 (report and model located on the FSIS website: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).
Comments on technical aspects of the risk assessment were then submitted
to FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received
on the 2005 updated Harvard BSE risk assessment. Please bear the following
points in mind:
Suppressed peer review of Harvard study October 31, 2002.
October 31, 2002 Review of the Evaluation of the Potential for Bovine
Spongiform Encephalopathy in the United States Conducted by the Harvard Center
for Risk Analysis, Harvard School of Public Health and Center for Computational
Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report
Prepared for U.S. Department of Agriculture Food Safety and Inspection Service
Office of Public Health and Science Prepared by RTI Health, Social, and
Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024
2005
----- Original Message -----
From: Terry S. Singeltary Sr.
Sent: Wednesday, September 07, 2005 9:44 PM
Subject: Use of Materials Derived From Cattle in Human Food and
Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
-------- Original Message --------
Subject: Docket No, 04-047-l Regulatory Identification No. (RIN)
091O-AF46 NEW BSE SAFEGUARDS (comment submission)
Date: Sun, 11 Jul 2004 21:34:22 –0500
From: "Terry S. Singeltary Sr."
CC:
regulations@aphis.usda.gov, burt.pritchett@fda.gov
Docket No. 04-047-l No. 04-021ANPR No. 2004N-0264 NEW BSE SAFEGUARDS
Federal Measures to Mitigate BSE Risks: Considerations for Further Action
Greetings FDA,
USDA and APHIS et al, I would kindly like to comment on the continued
delay of the regulations that have been proposed for years to reduce the risk of
BSE/TSE in the USA. Each day that is wasted debating this issue allows this
agent to spread, and many many more humans and animals become needlessly exposed
to this agent via a multitude of potential routes and sources right here in the
USA. TO continue to ignore the new findings from several scientists about the
fact that BSE is not the only strain of TSE in cattle, the fact that new
atypical strains of TSE are showing up in not only cattle, but sheep and the
fact that the new strain of TSE in cattle seems to be more similar to sporadic
CJD as opposed to the nv/v CJD, to continue to ignore these findings will only
further spread this agent. CWD and Scrapie have been running rampant in the USA
for decades. BOTH of which have been rendered and fed back to animals for
human/animal consumption for decades. All of which transmits to primates by the
natural and non-forced oral consumption of TSE scrapie, CJD, Kuru agent (and CWD
by inoculation). Strong Scientific evidence discovered back in the 80s support
the fact that a TSE has been prevalent in the USA bovine for decades, either
undetected or ignored. IF you consider the recent stumbling and staggering TEXAS
cow that was showing all signs of a CNS/TSE disorder that was ordered to be
rendered without BSE/TSE test, brains, spinal cord, head and all (as to no
possible evidence left of TSE), I would think the 'ignored' or 'covered up' to
be the better terminology. Then you have the Downer in Washington state that was
actually a good walker and then all the banned Canadian products that some how
found it's way across the border into the USA, considering all this, it is very
difficult for me to believe that the FDA/USDA/APHIS et al are doing everything
possible to protect the 'consumer'. Hardly the case;
Congressman Henry Waxmans Letter to the Honorable Ann Veneman
(updated links 2013...tss)
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2004/ucm108292.htm
http://oversight-archive.waxman.house.gov/documents/20040608105007-72922.pdf
http://oversight-archive.waxman.house.gov/documents/20040607142914-86912.pdf
http://oversight-archive.waxman.house.gov/documents/20040817120642-85052.pdf
http://oversight-archive.waxman.house.gov/documents/20040817120805-51929.pdf
http://www.usda.gov/oig/webdocs/Testimony7-2004.pdf
http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/bse_final_epi_report8-05.pdf
http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0235.xml
http://www.cidrap.umn.edu/cidrap/content/other/bse/news/june3005bse.html
http://www.fda.gov/downloads/ICECI/EnforcementActions/EnforcementStory/EnforcementStoryArchive/UCM091074.pdf
http://www.fda.gov/ICECI/EnforcementActions/EnforcementStory/EnforcementStoryArchive/ucm107472.htm
snip...
From: TSS Subject:
Re:
Docket No. 2004N-0081 Use of Materials Derived From Cattle in Human Food and
Cosmetics [TSS SUBMISSION]
Date: September 7, 2005 at 7:35 pm PST
In
Reply to:
Docket No. 2004N-0081 Use of Materials Derived From Cattle in Human Food
and Cosmetics posted by TSS on September 7, 2005 at 7:07 am:
----- Original Message -----
From: Terry S. Singeltary Sr.
Subject: Use of Materials Derived From Cattle in Human Food and
Cosmetics [Docket No. 2004N-0081] RIN 0910-AF47
Greetings FDA,
I
would kindly like to comment on ;
Use
of Materials Derived From Cattle in Human Food and Cosmetics [Docket No.
2004N-0081] RIN 0910-AF47
SUMMARY: The Food and Drug Administration (FDA) is amending the interim
final rule on use of materials derived from cattle in human food and cosmetics
published in the Federal Register of July 14, 2004. In the July 14, 2004,
interim final rule, FDA designated certain materials from cattle, including the
entire small intestine, as ``prohibited cattle materials'' and banned the use of
such materials in human food, including dietary supplements, and in cosmetics.
FDA is taking this action in response to comments received on the interim final
rule. Information was provided in comments that persuaded the agency that the
distal ileum, one of three portions of the small intestine, could be
consistently and effectively removed from the small intestine, such that the
remainder of the small intestine, formerly a prohibited cattle material, could
be used for human food or cosmetics. We (FDA) are also clarifying that milk and
milk products, hide and hide-derived products, and tallow derivatives are not
prohibited cattle materials. Comments also led the agency to reconsider the
method cited in the interim final rule for determining insoluble impurities in
tallow and to cite instead a method that is less costly to use and requires less
specialized equipment. FDA issued the interim final rule to minimize human
exposure to materials that scientific studies have demonstrated are highly
likely to contain the bovine spongiform encephalopathy (BSE) agent in cattle
infected with the disease. FDA believes that the amended provisions of the
interim final rule provide the same level of protection from human exposure to
the agent that causes BSE as the original provisions. ...
I
would kindly like to submit the following ;
I
find it very very disturbing that FDA now takes the position;
>>>Information was provided in comments that persuaded the
agency that the distal ileum, one of three portions of the small intestine,
could be consistently and effectively removed from the small intestine, such
that the remainder of the small intestine, formerly a prohibited cattle
material, could be used for human food or cosmetics. <<<
TSE
science is emerging and the old testing techniques for TSEs are becoming much
more sensitive than when some of these old BSE tissue bio-assays were done in
the distant past. I urge once again for the FDA and the USDA to put forth sound
science instead of the political and corporate science they have floundered with
for the last 3 decades. THERE is much new data out that dispute the position the
FDA/USDA have taken on SRMs.
STATEMENT ON INFECTIVITY IN BOVINE TONSIL
Background
1.
The views of the Committee were sought on unpublished results from an
ongoing long-term study of the pathogenesis of BSE in cattle. This study
is
being carried out by the Veterinary Laboratory Agency and is funded by
the
Food Standards Agency (FSA).
2.
In this study, cattle were orally dosed with 100g of BSE-infected bovine
brain material. At various times after oral dosing, cattle were killed
and
different tissues tested for infectivity. In the first instance, the
presence of
infectivity was assessed by injection of various tissues into inbred
mice
("mouse bioassay "). In this research infectivity was detected in:
•
distal ileum (the earliest infectivity was detected at 6 months after
inoculation.)
•
brain and spinal cord and closely associated nervous tissue
(infectivity was detected in the months just prior to the clinical onset
of
BSE in cattle)
•
at a single time point (around the time of clinical onset) bone marrow
was
also found to contain infectivity. ...snip
UPDATE OF THE OPINION ON
TSE
INFECTIVITY DISTRIBUTION IN RUMINANT TISSUES
INITIALLY ADOPTED BY
THE
SCIENTIFIC STEERING COMMITTEE
AT
ITS MEETING OF 10-11 JANUARY 2002
AND
AMENDED AT ITS MEETING OF 7-8 NOVEMBER 2002
following the submission of (1) a risk assessment by the German Federal
Ministry of
Consumer Protection, food and Agriculture and (2) new scientific
evidence
regarding BSE infectivity distribution in tonsils
3.
New work, work still in progress and future work
The
infectivity of neural and non-neural tissues by intracerebral inoculation of
cattle is being
assayed in projects M03006 and M03007. These studies are important since
it is possible
that some tissues may not yet have been found to be infective, due to
the fact that
infectivity in these tissues is below the detection limits of the tests
applied so far. To date,
this study has shown infectivity in CNS tissues, the distal ileum,
tonsil tissue and the
nictitating membrane (the nictitating membrane is also known as the
third eyelid). Other
challenged and control cattle continue to be closely monitored for
clinical signs of BSE.
Research is ongoing to determine the susceptibility of other food animal
species to TSEs.
These include a project to determine the susceptibility of pigs to
scrapie through oral
exposure (M03005) and a project to further study the transmission of BSE
to pigs (M03010).
Project M03024 aims to determine whether UK red deer are susceptible to
BSE by oral
exposure. These studies are important since it is highly probable that
pigs and deer were
historically exposed to ruminant derived meat and bone meal (MBM). ...
TSEs And The Environment
The
LANCET Volume 351, Number 9110 18 April 1998
BSE: the final resting place
snip...
The
first matter to consider is the distribution of infectivity in the bodies of
infected animals. The brain (and more generally, the central nervous system) is
the primary target in all transmissible spongiform encephalopathies (TSE), and
it contains by far the highest concentration of the infectious agent. In
naturally occuring disease, infectivity may reach levels of up to about one
million lethal doses per gram of brain tissue, whether the disease be kuru, CJD,
scrapie, or BSE. The infectious agent in BSE-infected cattle has so far been
found only in brain, spinal cord, cervical and thoracic dorsal root ganglia,
trigeminal ganglia, distal ileum, and bone marrow.4 However, the much more
widespread distribution of low levels of infectivity in human beings with kuru
or CJD, and in sheep and goats with scrapie, suggests that caution is advisable
in prematurely dismissing as harmless other tissues of BSE-infected cattle.
snip...end...TSS
snip...
BY
reducing or weakening the SRM list due to the Economic Impact of BSE on the U.S.
Beef Industry and while doing so, ignoring all 'sound science', again the
FDA/USDA et al are willing to put every human and animal out there at risk to
further exposure to this TSE agent, all for a buck. this is not 'sound science'
this is what i call 'corporate science', and it is and will continue to expose
people. some of these people will die from this agent either directly or
indirectly via a multitude of scientific proven routes and sources. WE must
remove all political and corporate science from TSE research.
I
find it disturbing that products that carry SRMs are still on the market for
humans such as nutritional supplements ;
ODD, I just picked up a catalog from STANDARD PROCESS INC. 2003 - 2004
Product Catalog (a chiropractor had just left this catalog in my wife's foot
doctors office 4/5/05) and it's full of THOSE SRMS FOR HUMANS. I wonder how much
is still left on the market, and how much is still in production, how much
crosses the borders? 5 pages of products full of SRMs for humans. THIS is a
really fine catalog, i am just now going over. LOADED with SRMs for humans. NO
wonder my neighbors mom died from CJD while taking these damn mad cow pills.
THEY even have a candy bars loaded with SRMs. HERE is one ;
NATURAL COCOA STANDARDBAR (mad cow candy bar) (i will just list animal
organs)
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine
kidney...
NATURAL PEANUT BUTTER STANDARDBAR
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine
kidney...
USF
(MAD COW) OINTMENT (RUB A DUB DUB, KURU ETC) ;
bovine orhic glandular extract
UTROPHIN PMG
bovine uterus PMG
VASCULIN
bovine heart PMG extract, veal bone PMG extract, bovine liever, porcine
duodenum, bovine adrenal Cytosol extract, bovine spleen, ovine spleen (some
yummy stuff)
IPLEX (neighbors mom died from CJD while taking these pills for years)
bovine eye PMG extract, veal bone PMG, bovine liver, porcine stomach,
bovine adrenal, bovine kidney, bovine adrenal Cytosol extract, BOVINE BRAIN,
bovine bone, veal bone meal
MYO-PLUS
bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract,
bovine spleen, ovine spleen, bovine adrenal Cytosol extract, BOVINE BRAIN
NEUROPLEX
bovine orchic Cytosol extract, bovine spleen, BOVINE BRAIN PMG EXTRACT,
BOVINE ANTERIOR PITUITARY, bovine liver, BOVINE PITUITARY PMG EXTRACT, AND MORE
BOVINE BRAIN... HOLY MAD COW IN A PILL !!!
NEUROTROPHIN PMG
BOVINE BRAIN PMG
NIACINAMIDE B6 VM
bovine liver, porcine stomach, bovine spleen ovine spleen, BOVINE BRAIN
OCULOTROPHIN PMG BOVINE EYE PMG
ORCHEX
bovine liver, bovine orchic Cytosol extract, porcine stomch, bovine
spleen, ovine spleen, BOVINE BRAIN
OSTARPLEX
veal bone PMG extract, veal bone PMG extract, bovine liver, porcine
stomach, bovine adrenal, bovine spleen, ovine spleen, BOVINE BRAIN
PARAPLEX
bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG,
BOVINE PITUITARY PMG EXTRACT, bovine thyroid PMG extract
PITUITROPHIN PMG
RUMAPLEX
BOVINE BRAIN, veal bone PMG extract, bovine adrenal, bovine prostate
Cytosol extract, veal bone meal, bovine liver PMG extract, bovine spleen, ovine
spleen, bovine liver
SENAPLEX
bovine liver PMG extract, bovine adrenal, BOVNE BRAIN, veal bone meal,
bovine kidney, bovine orchic extract, bovine spleen, ovine spleen ..........
THESE are just a few of MANY of just this ONE COMPANY.
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC
-2 Accepted - Volume 7
253
1 DR. BOLTON:
I
have an additional question about 2 that. What is the assurance that additional
locally sourced 3 tracheas are not added into that manufacturing process, thus 4
boosting the yield, if you will, but being returned to the 5 U.S. as being
produced from U.S.-sourced raw material? 6 DR. McCURDY: Are there data to
indicate how many 7 grams, or whatever, of infected brain are likely to infect 8
an organism, either animal or man, when taken orally? 9 DR. BROWN: If I am not
mistaken, and I can be 10 corrected, I think a half a gram is enough in a cow,
orally; 11 in other words, one good dietary-supplement pill. 12 DR. McCURDY:
What I am driving at is the question 13 we are asked is really not do we wish to
regulate these 14 things coming in. I think the statements about difficulties 15
in regulating things in the future or near future for new 16 regulations were
probably accurate. 17 But I think that we could exhibit some quite 18 reasonable
concern about blood donors who are taking dietary 19 supplements that contain a
certain amount of unspecified- 20 origin brain, brain-related, brain and
pituitary material. 21 If they have done this for more than a sniff or something
22 like that, then, perhaps, they should be deferred as blood 23 donors. 24 That
is probably worse than spending six months in 25 the U.K. 254 1 DR. BROWN: That
is exactly right. I think that 2 is why the discussion has apparently been on
things that are 3 not directly related to these questions because, in order to 4
think about deferrals for blood donors who are taking 5 dietary supplements with
things like bovine brain in them, 6 it is very important that we know that those
products are 7 safe. 8 I think we have heard enough to suggest that they 9 may
not be. 10 DR. McCURDY: There is one other item that needs 11 to be considered
and that is what proportion of blood donors 12 are doing this; that is, how many
blood donors would you 13 lose, and I don't know what the demographics--there is
14 fairly good information on the demography of blood donors. 15 I have no idea
what the demography of people who take these 16 supplements is. Maybe they are
old men like me and aren't 17 going to be blood donors anymore. 18 DR. BROWN:
The wording of the question is not as 19 demanding as the wording of other
deferral questions; that 20 is, the question here is consider recommending. We
are 21 not even recommending at this point. We are saying to the 22 FDA, please
think about this. It is worth thinking about. 23 DR. DETWILER: One point about
brain from Europe, 24 and Jean Philippe is still here, those are considered 25
specified risk material and it is not correct to be 255 1 incinerated; correct?
Or destroyed? Brain and spinal cord 2 and other high-risk tissues in Europe? 3
DR. NORTON: In tomorrow morning's British Medical 4 Journal, which has appeared
on-line today, there is an 5 article called U.S. Takes Precautions against BSE.
One 6 paragraph says, Even though the U.S. and U.K. governments 7 ban the
practice of feeding cattle products to cows, in the 8 early 1990s, some U.K.
renderers continued to manufacture 9 and ship contaminated meat and bonemeal
around the world. 10 British export statistics show that thirty-seven tons of 11
meal made from offal was sent to the United States in 1997, 12 well after the
U.S. government banned imports of such risky 13 meat. The ultimate use of these
imports has not been 14 identified. 15 That will appear tomorrow morning. 16 DR.
DETWILER: That actually was in The New York 17 Times. That is a direct quote out
of The New York Times 18 article. We called the reporter on that. That
statement, 19 the thirty-seven tons, was taken out of the U.S. 20 Geographical
BSE Risk Assessment. What they didn't put in 21 there, in the statement, was the
remainder of the GBR is at 22 that time, the big labeling for that category in
the U.K., 23 because it was illegal for them to ship it to us from their 24 own
regs. It is illegal for us to get that. 25 We did go and try and trace that so
that wasn't [FULL TEXT ABOUT 600 PAGES] 3681t2.rtf
IN
fact, we are now finding 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 (ic ip 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.
ic ip=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
THEN you must consider cross contamination at feed mills and such. this
has been well proven in both the UK and the USA to date via r-to-r feed ban
violations. IT was proven in the UK that they indeed put profits before human
health;
[PDF] The BSE Inquiry / Statement No. 14 Issued 20 March 1998 THE ...
The
BSE Inquiry / Statement No. 14. Issued 20 March 1998 ... number of feed
compounders and it became clear that cross contamination of feeds could occur.
...
[PDF] The BSE Inquiry / Statement No 76F (Supplementary) Mr Alan ...
But
the mainbut the main problem was probably cross-contamination. ...
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 ;
snip...
From: TSS
Subject: Inspector to file charges against USDA for them charging him
with misconduct on telling the truth about SRM mad cow violations
Date: September 7, 2005 at 1:37 pm PST
Consumer Health
Inspector to file charges against USDA By Steve Mitchell Sep 6, 2005,
22:46 GMT
WASHINGTON, DC, United States (UPI) -- The federal meat inspector who
was charged with misconduct by the U.S. Department of Agriculture after he
claimed mad cow disease safeguards were being violated at slaughterhouses told
United Press International he plans to file charges against the agency.
Stan Painter, a USDA inspector and chair of the National Joint Council
of Food Inspection Locals, the inspectors union, notified the agency`s
management in a letter last December he was aware of instances where the
riskiest parts of older cows were not being marked or removed from processing.
Painter worried these risky parts -- known as specified risk materials,
or SRMs -- could enter the food supply and infect people, causing a fatal brain
illness called variant Creutzfeldt Jakob disease.
Two
cases of mad cow have been detected in U.S. herds, and some suspect there are
more. The USDA put the SRM safeguards in place in 2004 to protect the public
from mad cow disease -- also known as bovine spongiform encephalopathy or BSE --
if more cases are detected.
The
USDA did not respond to Painter`s concerns until he made his letter known to
news outlets.
On
Dec. 28, 2004, the agency charged Painter with personal misconduct for not
revealing the names of the inspectors who told him of the SRM violations.
Officials also told him he was under a formal investigation, which was dropped
last month after the release of internal documents revealing more than 1,000
violations of the USDA`s SRM regulations.
Painter said he thinks the USDA was attempting 'to harass and intimidate
him (and) to have a chilling effect' on other inspectors.
'I
plan to file charges against the agency,' he told UPI, adding he has not yet
decided if he will go through the legal system, through internal USDA procedures
or another avenue.
Asked about Painter`s intent to bring charges, agency spokesman Steven
Cohen told UPI the documents -- called noncompliance reports, or NRs --
demonstrate 'that BSE safeguard regulations are being enforced and prohibited
materials did not reach the public.'
Mad
cow disease remains a sensitive topic for the USDA because it can have
significant economic ramifications. The U.S. beef industry lost billions of
dollars because more than 60 nations closed their borders in 2003 to American
beef after the report of the first detected case in U.S. herds. Japan, formerly
the largest importer of American beef, still has not reopened its borders.
For
months, USDA officials denied Painter`s allegations in media reports, saying
they had investigated and found no evidence to substantiate his claims. The NRs
released last month under the Freedom of Information Act, however, showed 1,036
violations of SRM regulations in at least 35 states, Puerto Rico and the Virgin
Islands, with some plants being cited repeatedly for infractions. The USDA
delayed releasing the documents for eight months despite a federal law mandating
a response within 30 days.
Patty Lovera, of the watchdog group Public Citizen, which requested the
USDA documents, said some of the violations cited in the NRs are egregious. In
one, an employee at a plant in Michigan was not properly marking older cows to
have their SRMs removed because he did not have a pencil. In another, an
employee in a Missouri plant was loading cow heads onto his pickup truck to take
home to feed to his dog.
Lovera charged the USDA with attempting to silence Painter and failing
to address problems with the SRM ban.
'Their behavior through this whole thing is appalling,' she told UPI.
'Stan brought them concerns about a policy and instead of investigating the
policy, they investigated him.'
Last December, after Painter made his letter known publicly, the USDA
sent an officer to Painter`s house while he was on leave to question him about
the allegations in his letter. Later, USDA officials interrogated Painter twice,
asking him for the names of the inspectors who told him about the violations.
Painter said he intentionally was kept ignorant of the inspectors` names
because he feared the agency would retaliate against them. Painter also said
USDA officials did not need the inspectors` names because they could determine
where the infractions were occurring by looking at their database of NRs.
Sometime around June the U.S. Embassy in Japan posted a notice on its
Web site stating USDA officials had found no evidence to substantiate Painter`s
claims and had requested a criminal investigation into his actions. The notice
was removed in July after UPI reported its existence.
Although Cohen acknowledged more than 1,000 NRs were written by USDA
inspectors, he minimized their significance, saying they 'amount to less than
one-half of one percent of the total written for all reasons by (USDA)
inspection program personnel.'
Lovera said any infraction of mad cow safeguards should be of concern,
because this disease always is fatal in humans and cooking does not destroy the
pathogen.
'You have very little margin of error for something you don`t want to
get because you can`t cook it away and you can`t disinfect it,' she said.
Painter said his concern now is what the agency will do to fix what he
sees as shortcomings in the SRM policy.
'It`s a failed policy,' he said. 'It doesn`t protect the consumer.'
Cohen did not respond to whether the USDA planned to change the SRM
regulations.
The
USDA`s Office of Inspector General has launched an investigation to determine
whether the regulations are being implemented effectively, and results are due
out soon.
E-mail: sciencemail@upi.com
Copyright 2005 by United Press International
makes no difference, GW will change the SRM rules like he has the BSE
GBR risk assessment to the terribly flawed BSE MRR policy, the legal trading of
all strains of TSE, the 'gold card'. ...TSS
IN
a time when FDA/USDA et al should be strengthening the TSE regulations, it seems
corporate interest has won out again over sound science and consumer protection
from an agent that is 100% fatal for the ones that go clinical. With the many
different atypical TSEs showing up in different parts of the world, and with GWs
BSE MRR policy (the legal policy of trading all strains of TSEs), the battle
that has waged for the last 25 years to eradicate this agent from this planet
will be set back decades, if not lost for good. ...TSS
snip...
APHIS-2006-0041-0006 TSE advisory committee for the meeting December 15,
2006
Thursday, April 17, 2008
Use
of Materials Derived From Cattle in Human Food and Cosmetics [Docket No.
2004N-0081] RIN 0910-AF47
[Federal Register: April 17, 2008 (Volume 73, Number 75)] [Rules and
Regulations] [Page 20785-20794] From the Federal Register Online via GPO Access
[wais.access.gpo.gov] [DOCID:fr17ap08-7]
Scientific Opinion on BSE Risk in Bovine Intestines Question number:
EFSA-Q-2009-00226
Adopted: 10 September 2009 Summary (0.1Mb)
Opinion (0.1Mb)
Summary
Following a request from the European Commission (EC), the Panel on
Biological Hazards (BIOHAZ) was asked to deliver a scientific opinion on the BSE
related risk of bovine intestines used for casings. Regulation (EC) No 999/2001
of the European Parliament and of the Council stipulates that certain tissues
from bovine, ovine and caprine animals must be considered as Specified Risk
Material (SRM) and must be removed from the food and feed chain to protect the
health of consumers against the risk of bovine transmissible spongiform
encephalopathies (BSE). The intestines, from the duodenum to the rectum, of
bovine animals of all ages are currently included in the list of SRM. The "TSE
roadmap" prepared by the EC details the short, middle and long term actions on
TSE measures such as SRM removal and sets the objectives to ensure and maintain
the existing high level of consumer protection. It allows for amendments of the
current SRM list based on new evolving scientific knowledge while ensuring and
maintaining a high level of consumer protection.
Specifically, the mandate asked the BIOHAZ panel to evaluate the
scientific validity of a report prepared by Det Norske Veritas Ltd" (DNV) for
the Swiss Cervelas task force. This report provides an assessment of the current
potential human exposure to BSE infectivity that could result from eating
sausages made with EU bovine casings. The BIOHAZ panel was further requested to
evaluate the conclusions of the DNV report and, if it was considered necessary
based on the report and any other new relevant scientific information, to
provide a re-assessment of the BSE related risk of bovine intestines after
processing into natural sausage casings.
The
BIOHAZ panel evaluated the risk assessment as described in the DNV report, and
took into account the relevant previous EFSA opinions as well as new scientific
data on the same subject.
New
but limited experimental scientific data demonstrate that in addition to ileum,
also jejunum may harbour infectivity when a large BSE inoculum dose was used to
experimentally infect cattle. With regard to the DNV Report, the BIOHAZ Panel
considers its approach (concept and methodology) scientifically sound, whereas
the interpretation of the results as obtained is not shared by the Panel. Its
assumptions were based on limited scientific data obtained from a single
morphometric study (which was already found to be inadequate in the previous
EFSA Opinion on bovine casings) and on limited and earlier data on the presence
of PrPsc/infectivity in bovine gut after experimental oral BSE inoculation.
There is uncertainty about the relative BSE risk of neural and lymphoid tissues
in casings compared to CNS that might have significant impact on the calculated
results of the DNV Report. The Panel notes that the DNV Report considers the
individual human BSE exposure risk from bovine casings, excluding ileum, to be
"very low". However, when the upper confidence limits are taken into account,
along with the uncertainties in key parameter assumptions, the calculated total
human exposure per year in the EU from bovine casings, even when ileum is
excluded (based on the calculated BSE prevalence in 2007) is 11.000 cattle oral
ID50 units per year (when all casings would have been sourced in the UK) and
about 1.000 cattle oral ID50 units per year (when all casings would have been
sourced in the Netherlands) and therefore cannot be considered negligible. Thus
the conclusion in the DNV report that sausage casings sourced from intestines of
cattle in EU Member States would lead to a negligible risk for human consumption
cannot be considered valid. Moreover, when considering other new relevant
scientific information it is concluded that the previous EFSA assessment of the
BSE related risk of bovine intestines after processing into natural sausage
casings remains valid. The Panel recommends that future considerations on the
risk in bovine casings should take into account the BSE prevalence in cattle at
that time.
Published: 22 September 2009
SUMMARY
OPINION
snip...
6.
Overview of current scientific knowledge on BSE risk in Bovine Intestines. The
previous EFSA Opinion on BSE risk from bovine intestine summarised the
scientific knowledge that was available until early 2007. Since then, additional
publications have become available on a natural BSE case in Japan (Kimura and
Haritani, 2008) and two experimental studies that examined
presence of PrPsc and/or infectivity in the intestines of cattle
challenged orally with 100g (Espinosa et al., 2007; Hoffmann et al., 2007).
Moreover, a new study performed by the VLA in the UK on PrPsc in BSE-infected
cattle (Stack, 2009) and preliminary results from the German BSE pathogenesis
study have recently be made available to EFSA and were also taken into account.
6.1. New experimental studies on intestines of BSE infected cattle
Espinosa et al. (2007) examined pooled tissues from 13 cattle inoculated
at ages between 4 and 6 months and culled at ages between 24 and 39 months.
Infectivity in Tgbov mice but not PrPsc by ELISA/WB was found in Peyer's patches
dissected from distal ileum at all ages. Hoffmann et al (2007) demonstrated
PrPsc by IHC in Peyer's patches of distal ileum in one of two preclinical
animals sacrificed at 24 and 28 months post inoculation (mpi). Most recently,
Arnold et al. (2009) estimated the titre of infectivity in the distal ileum from
the incubation time found by bioassay in wild type mice. Over time, the
infectivity in the distal ileum showed an initial increase up to 14-18 months
post exposure, followed by a decrease, which was likely to be highly variable
between animals. However, these estimates were based on mouse titration of brain
material, while the incubation period to dose relationship may differ between
brain and intestines (Robinson et al., 1990).
6.2. Infectivity of intestines in cattle with natural BSE infection
Data on presence of PrPsc or infectivity in intestines of natural BSE
cases are sparse. The immunohistochemistry (IHC) and Western blot examinations
of three BSE infected cattle detected in Japan in the course of active
surveillance (but showing locomotor deficits) found PrPsc in distal ileum of two
(by IHC confined to the myenteric plexus) (Iwata et al., 2006). No PrPsc was
detected in Peyer's patches of distal ileum, or in samples of other regions of
small and large intestine, or in a range of other lymphoid tissues. Labelling of
myenteric plexus was also detected in 9/29 confirmed field cases of BSE examined
in the UK (Terry et al., 2003). Infectivity by wild-type mouse assay or the
presence of PrPsc has not been found in the distal ileum, or other levels of
intestine in a total of some six natural BSE cases studied (Fraser and Foster,
1994; Buschmann and Groschup 2005; Iwata et al., 2006). In one of these cases in
Germany, however, infectivity was detected in the distal ileum by bioassay in
TgBov XV mice (Buschmann and Groschup, 2005). More recently, another BSE case
(94 months of age) in Japan showed definite or equivocal immunoreactivity in
nerve cells of the myenteric plexus in ileum, caecum and colon, and in Schwann
cells of the myenteric plexus in duodenum, jejunum, ileum, caecum and colon
(Kimura and Haritani, 2008).
6.3. Study commissioned by ENSCA
This ENSCA commissioned study investigated the presence of BSE PrPsc in
small intestines of cattle that had been orally challenged at 4-6 months of age
with 100g or 1 g doses of BSE affected brain tissue. These animals were culled
and examined 18-30 months post inoculation (p.i.). Three methods to identify
PrPsc were applied: a commercial ELISA test, Western immunoblotting, and IHC.
Results confirmed previous observations that PrPsc was mainly confined to
lymphoid tissue of the ileum, whereas the duodenum was negative and no part of
the enteric nervous system tested positive. The lymphoid tissue of the jejunum
of one high-dosed animal tested positive. As expected, the low-dosed animals had
a much lower frequency of positive ileum samples (1/18 vs. 15/18 in the
high-dose group) and some longer incubation times (24 months in the one animal
with positive ileum), whereas the high-dose group included animals positive at
all ages examined.
As
the ENSCA commissioned study was performed retrospectively on archival tissue,
sampling was limited by availability, and the study authors themselves concede
that "it is possible tissue sampling was not optimal" for duodenum and jejunum
of low-dosed animals. The 1g-dosed group included 6 animals sampled at 18 months
p.i., 6 at 24 months, and 6 at 30 months. The 100g-dosed group included 6
animals sampled for ileum at 18 months p.i., 6 at 24 months, and 6 at 30 months;
duodenum and jejunum, however, were sampled only in 2 animals each at
18, 24 and 30 months p.i., respectively. From each level of the intestine, three
sections were examined by IHC per case. While at least two of the three sections
of the ileum per case contained lymphoid follicles, in 36% of the duodenum
cases, and in 39% of the jejunum cases lymphoid follicles were absent in any of
the examined sections. The frequency of positive follicles per section ranged
between 1% and 14% in ileum of the high-dose group, and 0,7% in the one positive
ileum of the low-dose group, and was 6,7% and 11,1% in the two positive jejunum
sections of one high-dosed animal.
Conclusions on the ENSCA commissioned study:
.
This study confirms that detectable PrPsc is mainly confined to lymphoid tissue
of the ileum in cattle orally challenged with 100g of BSE brain and culled at
18, 24 and 30 months postinoculation (p.i.)
.
One out of 18 animals challenged orally with 1g of BSE brain was positive in
ileum.
.
One out of 18 animals challenged orally with 100g of BSE brain was positive in
jejunum.
.
The duodenum was always negative.
.
However, the sampling in particular of duodenum and jejunum was limited and
contained lymphoid tissue only in a part of sections examined.
.
In contrast to previous reports on natural BSE cases in older animals, the
enteric nervous system was always negative.
.
In consideration of the previous EFSA opinion on bovine intestine that gives
detailed advice for future studies, in particular concerning the lower frequency
of lymphoid follicles in parts of the intestine other than the distal ileum, the
present ENSCA commissioned study meets some but not all recommendations; in
particular the mostly negative results obtained for jejunum and duodenum should
not be over-interpreted when tissue sampling was limited.
6.4. New preliminary data on bovine intestine from the German BSE
Pathogenesis study
In
the German BSE pathogenesis study performed at the Friedrich-Loeffler-Institute
(FLI), 56 Simmental cross-breed calves aged about four months were challenged
orally with 100g brainstemhomogenate pooled out of clinically BSE diseased
cattle. The infectivity load in the homogenate was about 106.1 ID50 (grams of
tissue)-1 as determined by end-point titration in Tgbov XV mice (Buschmann &
Groschup, 2005, Hoffmann et al., 2007). Furthermore, as controls, 18 calves were
inoculated orally with a BSE-negative brainstem homogenate. Four to five animals
were selected randomly and euthanised every four months. More than 150 tissue
and body fluid samples were sampled at subsequent necropsies from each animal
under TSE-sterile conditions.
After oral exposure with the TSE agent, previous studies had
demonstrated consistently early prion accumulation in the gut associated
lymphatic tissue, about six months post infection (mpi) in cattle (Terry et al.,
2003), and at two mpi in scrapie infected sheep (van Keulen et al., 2002) and in
21 days old lambs (Andreoletti et al., 2002). In contrast to scrapie, the
accumulation of PrPd in the distal ileum of BSE-infected cattle was confined to
an only minor proportion of follicles respectively neurons/glial cells of the
enteric nervous system (Terry et al., 2003).
Normally when performing IHC, a three micrometer section per paraffin
block is used, reflecting a very small proportion of the tissue sample.
Therefore a serial section procedure was newly established at the FLI to
increase the total amounts of tissue structures examined per sample and
consequently increasing the probability of detecting PrPsc accumulation.
Thereby, five sections per paraffin block with a plane distance of about 25-30
µm were examined. Hence, a tissue depth of about 150-200 µm per block was
screened for positive immunosignals. Additionally two different PrP-specific
monoclonal antibodies, highly sensitive for the detection of bovine PrPsc were
used.
According to this method, representative samples of the small intestine,
in particular Peyer's patches of the distal ileum but also the ileo-caecal
junction from most of the infected animals of the German BSE Pathogenesis study
were examined by IHC. From 4 mpi until 44 mpi in most animals (38/43), PrPsc was
detectable, initially in the follicles of the Peyer's patches and at later
stages of the incubation period in the enteric nervous system too.
Conclusions on the German pathogenesis study
.
With improved sampling, nearly all animals dosed with 100 g of BSE brain tissue
showed PrPsc in distal ileum between 4 and 44 mpi, first in lymphoid tissue and
later in enteric nervous system.
7.
Review of the DNV report
7.1. Summary of the report
DNV
makes an attempt to quantify the amount of BSE infectious load in bovine sausage
casings. This is then extrapolated to the risk carried in an individual sausage,
a normal persons risk per year and the overall exposure within the EU in a year.
The key points of the DNV Report are as follows:
.
The DNV Report assumes that the ileum is not used for the production of casings
and is removed and discarded.
.
The DNV Report is based on the assumption that potential infectivity in bovine
intestine used for sausage casing production would be 2 logs less than in the
ileum. Based on experimental data, the infectivity in the distal ileum was
considered to be at a titre equivalent to that in the CNS at the late stage of
infection. Thus infectivity in non-ileal parts of the intestines used for
casings production was assumed to be 100 fold less than in the CNS.
.
The DNV Report uses a value of 0.43g/m (obtained from Wijnker et al.) of casing
to quantify the amount of lymphoid and neural tissue that might harbour
infectivity in a sausage casing,
.
The results of the DNV Report calculate that an exposure per person per year
from bovine casings produced in the Netherlands "would be very low" even when a
high consumption pattern like in Germany is assumed (upper range 7 x 10-6 cattle
oral (CO) ID50 units). For casings sourced in the UK, the exposure would be
about one log higher.
.
When the calculated total amount of cumulative human exposure per year in the EU
is considered, the following scenario emerges: 11.000 CO ID50 units per year
when all casings would have been sourced in the UK, and about 1.000 CO ID50
units when all casings would have been sourced in the Netherlands, a country
with an about average prevalence of BSE in the EU4.
4
How can the output of the DNV calculations be interpreted in terms of potential
human infections? If we follow, as in the previously adopted EFSA Opinions on
Tallow and MBM (EFSA 2005 a and b) the cautionary advice of the original QRA WG
and assume the species barrier is 1 as a worst case scenario, then there would
be up to 5500 infected person in the EU per year in the first scenario, and up
to about 500 in the second. This would have to assume a linear dose-response
curve of infectivity at very low doses. If the species barrier was given a more
realistic value obtained from the analysis carried out on the exposure of the
British population to the BSE agent (EFSA, 2006) of around 1000 - 4000, this
would mean that there might be up to around 1 to 5 infected person in the EU per
year in the first scenario, and less than 1 in the second.
snip... see full text ;
Meeting of the Transmissible Spongiform Encephalopathies Committee On
June 12, 2009 (Singeltary submission)
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of
Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of
Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
Monday, May 30, 2011
CEPs for gelatin and impact of the revised EU Note for Guidance on the
TSE risk EMEA/410/01 Rev.3) will come into force in July 2011
Note concerning CEPs for gelatin and impact of the revised EU Note for
Guidance on the TSE risk
Thursday, December 22, 2011
Risk of Prion Disease Transmission through Bovine-Derived Bone
Substitutes: A Systematic Review Clin Implant Dent Relat Res. 2011 Dec 15. doi:
10.1111/j.1708-8208.2011.00407.x. [Epub ahead of print]
Volume 18, Number 1—January 2012 Dispatch
Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
Nadine Mestre-Francés , Simon Nicot, Sylvie Rouland, Anne-Gaëlle
Biacabe, Isabelle Quadrio, Armand Perret-Liaudet, Thierry Baron, and Jean-Michel
Verdier Author affiliations: Institut National de la Santé et de la Recherche
Médicale (INSERM) U710, Montpellier, France (N. Mestre-Francés, S. Rouland,
J.-M. Verdier); Université Montpellier 2, Montpellier (N. Mestre-Francés, S.
Rouland, J.-M. Verdier); École Pratique des Hautes Etudes, Paris, France (N.
Mestre-Francés, S. Rouland, J.-M. Verdier); Agence Nationale de Sécurité
Sanitaire, Lyon, France (S. Nicot, A.-G. Biacabe, T. Baron); Hopitaux Civils de
Lyon, Lyon, France (I. Quadrio, A. Perret-Liaudet); Université Lyon 1, Lyon (I.
Quadrio, A. Perret-Liaudet); INSERM U1028, Lyon (I. Quadrio, A. Perret-Liaudet);
Centre National de la Recherche Scientifique, Lyon (I. Quadrio, A.
Perret-Liaudet)
Abstract
We
report transmission of atypical L-type bovine spongiform encephalopathy to mouse
lemurs after oral or intracerebral inoculation with infected bovine brain
tissue. After neurologic symptoms appeared, transmissibility of the disease by
both inoculation routes was confirmed by detection of disease-associated prion
protein in samples of brain tissue.
SNIP...
The
Study A total of 12 mouse lemurs of both sexes (Center for Breeding and
Experimental Conditioning of Animal Models, University Montpellier 2,
Montpellier, France) were maintained in animal Biosafety Level 3 facilities,
according to requirements of the French ethics committee (authorization
CE-LR-0810). Young and adult lemurs were fed (8 animals) or IC inoculated (4
animals) with 5 or 50 mg of L-BSE–infected brain tissue (10% homogenate in 5%
glucose) (Table). The isolate for the L-BSE agent (02–2528) was derived from
cattle in France (11). When progression of prion disease was evident, the lemurs
were euthanized and their brains were isolated. Brains were processed for
Western blot analysis with SHa31 monoclonal antibody against PrP for PrPres
detection, as described in mice (11); for histologic examination by using
hematoxylin and eosin staining; and for disease-associated prion protein (PrPd)
immunochemical detection by using the paraffin-embedded tissue blot method or
immunohistochemical analysis with monoclonal antibody 3F4 against PrP.
Beginning ≈3 months before the terminal stage of the disease (19–22
months after inoculation), neurologic symptoms developed in the 4 mouse lemurs
that received IC inoculations (Table). In all 4 animals, initial clinical signs
and symptoms were blindness, thigmotaxic behavior, and poor appearance of the
fur. Appetite and general fitness were maintained; anxiety and aggressiveness
were not observed. Next, locomotion became slower, followed by incoordination
and loss of balance in the last month of life. Ipsilateral circling behavior was
reported, indicating unilateral degeneration of the striatum. This behavior
stopped 15 days after onset, suggesting damage to the contralateral striatum.
Disequilibrium, with frequent falls, became more noticeable. At the terminal
stage of the disease, the animals were prostrate.
One
orally inoculated lemur, which was fed 5 mg of infected brain and euthanized 27
months later, had signs and symptoms of disease similar to those in
IC-inoculated animals, except for the ipsilateral circling behavior. In 2 lemurs
fed 50 mg and 2 others fed 5 mg of L-BSE–infected brain, clinical signs and
symptoms of prion disease developed just a few weeks before the animals were
euthanized (18 and 32 months and 33 and 34 months after inoculation,
respectively). Disease was characterized by progressive prostration, loss of
appetite, and poor appearance of the fur, without incoordination or
disequilibrium. The 3 remaining lemurs were orally inoculated at 2 years of age
and were still alive and healthy 28 months after inoculation (Table).
snip...
Conclusions
We
demonstrated that the agent of L-BSE can be transmitted by the oral route from
cattle to mouse lemurs. As expected, orally inoculated animals survived longer
than IC-inoculated animals. Orally inoculated lemurs had less severe clinical
signs and symptoms, with no evidence of motor dysfunction. It was previously
suggested that the agent of L-BSE might be involved in the foodborne
transmission of a prion disease in mink (11,12), a species in which several
outbreaks of transmissible mink encephalopathy had been identified, notably in
the United States (13).
Our
study clearly confirms, experimentally, the potential risk for interspecies oral
transmission of the agent of L-BSE. In our model, this risk appears higher than
that for the agent of classical BSE, which could only be transmitted to mouse
lemurs after a first passage in macaques (14). We report oral transmission of
the L-BSE agent in young and adult primates. Transmission by the IC route has
also been reported in young macaques (6,7). A previous study of L-BSE in
transgenic mice expressing human PrP suggested an absence of any transmission
barrier between cattle and humans for this particular strain of the agent of
BSE, in contrast to findings for the agent of classical BSE (9). Thus, it is
imperative to maintain measures that prevent the entry of tissues from cattle
possibly infected with the agent of L-BSE into the food chain.
Dr
Mestre-Francés is an assistant professor at the École Pratique des Hautes
Études. Her research focuses on neurodegenerative diseases (Alzheimer disease,
prion diseases) in the nonhuman primate model Microcebus murinus.
October 2009 O.11.3 Infectivity in skeletal muscle of BASE-infected
cattle
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1,
Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3,
Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5,
Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological
Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS
Torino, Italy; 5University of Verona, Italy
Background: BASE is an atypical form of bovine spongiform encephalopathy
caused by a prion strain distinct from that of BSE. Upon experimental
transmission to cattle, BASE induces a previously unrecognized disease phenotype
marked by mental dullness and progressive atrophy of hind limb musculature.
Whether affected muscles contain infectivity is unknown. This is a critical
issue since the BASE strain is readily transmissible to a variety of hosts
including primates, suggesting that humans may be susceptible.
Objectives: To investigate the distribution of infectivity in peripheral
tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice
expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and
i.p. with 10% homogenates of a variety of tissues including brain, spleen,
cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from
cattle intracerebrally infected with BASE. No PrPres was detectable in the
peripheral tissues used for inoculation either by immunohistochemistry or
Western blot.
Results: Mice inoculated with BASE-brain homogenates showed clinical
signs of disease with incubation and survival times of 175±15 and 207±12 days.
Five out of seven mice challenged with skeletal muscle developed a similar
neurological disorder, with incubation and survival times of 380±11 and 410±12
days. At present (700 days after inoculation) mice challenged with the other
peripheral tissues are still healthy. The neuropathological phenotype and PrPres
type of the affected mice inoculated either with brain or muscle were
indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
Discussion: Our data indicate that the skeletal muscle of cattle
experimentally infected with BASE contains significant amount of infectivity, at
variance with BSE-affected cattle, raising the issue of intraspecies
transmission and the potential risk for humans. Experiments are in progress to
assess the presence of infectivity in skeletal muscles of natural BASE.
see
much more here ;
Friday, December 23, 2011
Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
Volume 18, Number 1—January 2012 Dispatch
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to
Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The
rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy
cattle...
2010-2011
When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material
(SRM) in atypical BSE. The incumbent of this position will develop new and
transfer existing, ultra-sensitive methods for the detection of atypical BSE in
tissue of experimentally infected cattle.
Wednesday, March 31, 2010
Atypical BSE in Cattle
To
date the OIE/WAHO assumes that the human and animal health standards set out in
the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which
include the H-type and L-type atypical forms. This assumption is scientifically
not completely justified and accumulating evidence suggests that this may in
fact not be the case. Molecular characterization and the spatial distribution
pattern of histopathologic lesions and immunohistochemistry (IHC) signals are
used to identify and characterize atypical BSE. Both the L-type and H-type
atypical cases display significant differences in the conformation and spatial
accumulation of the disease associated prion protein (PrPSc) in brains of
afflicted cattle. Transmission studies in bovine transgenic and wild type mouse
models support that the atypical BSE types might be unique strains because they
have different incubation times and lesion profiles when compared to C-type BSE.
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the
resulting molecular fingerprint had changed, either in the first or a subsequent
passage, from L-type into C-type BSE. In addition, non-human primates are
specifically susceptible for atypical BSE as demonstrated by an approximately
50% shortened incubation time for L-type BSE as compared to C-type. Considering
the current scientific information available, it cannot be assumed that these
different BSE types pose the same human health risks as C-type BSE or that these
risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The
TSE road map defining the evolution of European policy for protection against
prion diseases is based on a certain numbers of hypotheses some of which may
turn out to be erroneous. In particular, a form of BSE (called atypical Bovine
Spongiform Encephalopathy), recently identified by systematic testing in aged
cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
P.9.21 Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim
McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre,
Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of
Calgary, Canada
Background: Three BSE types (classical and two atypical) have been
identified on the basis of molecular characteristics of the misfolded protein
associated with the disease. To date, each of these three types have been
detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16
Canadian BSE cases based on the biochemical properties of there associated
PrPres.
Methods: Immuno-reactivity, molecular weight, glycoform profiles and
relative proteinase K sensitivity of the PrPres from each of the 16 confirmed
Canadian BSE cases was determined using modified Western blot analysis. Results:
Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L
type. The Canadian H and L-type BSE cases exhibited size shifts and changes in
glycosylation similar to other atypical BSE cases. PK digestion under mild and
stringent conditions revealed a reduced protease resistance of the atypical
cases compared to the C-type cases. N terminal- specific antibodies bound to
PrPres from H type but not from C or L type. The C-terminal-specific antibodies
resulted in a shift in the glycoform profile and detected a fourth band in the
Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *** It also
suggests a similar cause or source for atypical BSE in these countries.
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in
the EU
Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES
AND FOOD SAFETY a non-profit Swiss Foundation
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject
PRO/AH/EDR>
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
P.4.23
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3,
Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5,
Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto
Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany;
4National Veterinary Research Institute, Poland; 5Kansas State University
(Previously at USDA National Animal Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and
the classical BSE strain (BSE-C) has led to over 200 cases of clinical human
infection (variant CJD). Atypical BSE cases have been discovered in three
continents since 2004; they include the L-type (also named BASE), the H-type,
and the first reported case of naturally occurring BSE with mutated bovine PRNP
(termed BSE-M). The public health risks posed by atypical BSE were largely
undefined.
Objectives: To investigate these atypical BSE types in terms of their
transmissibility and phenotypes in humanized mice. Methods: Transgenic mice
expressing human PrP were inoculated with several classical (C-type) and
atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation
time, characteristics and distribution of PrPSc, symptoms, and histopathology
were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected
with minimal spongiosis and an average incubation time of 20-22 months, whereas
only one of the C-type BSE-inoculated mice developed prion disease after more
than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse
brains was biochemically different from bovine BASE or sCJD. PrPSc was also
detected in the spleen of 22% of BASE-infected humanized mice, but not in those
infected with sCJD. Secondary transmission of BASE in the humanized mice led to
a small reduction in incubation time.*** The atypical BSE-H strain is also
transmissible with distinct phenotypes in the humanized mice, but no BSE-M
transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than
classical BSE, has a lymphotropic phenotype, and displays a modest transmission
barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg
mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
P26
TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED
MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina
Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi
Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case
Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto
Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany;
4National Veterinary Research Institute, Poland; 5Kansas State University,
Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous
address: USDA National Animal Disease Center, Ames, IA 50010, USA
Classical BSE is a world-wide prion disease in cattle, and the classical
BSE strain (BSE-C) has led to over 200 cases of clinical human infection
(variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have
been discovered in three continents since 2004. The first case of naturally
occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006
in the USA. The transmissibility and phenotypes of these atypical BSE
strains/isolates in humans were unknown. We have inoculated humanized transgenic
mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M
isolate. We have found that the atypical BSE-L strain is much more virulent than
the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the
humanized transgenic mice with distinct phenotype, but no transmission has been
observed for the BSE-M isolate so far.
III
International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND
THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
I
ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform
Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as
cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or
another, but we have found that H-BSE can infect humans. I hope we could publish
these data once the study is complete. Thanks for your interest.''
Best regards,
Qingzhong Kong,
PhD
Associate Professor Department of Pathology Case Western Reserve University
Cleveland, OH 44106 USA
END...TSS
Tuesday, November 02, 2010
BSE
- ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic
criteria CVL 1992
Thursday, December 04, 2008 2:37 PM
"we
have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
BSE-H is also transmissible in our humanized Tg mice.
The
possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits
Thursday, December 22, 2011
Risk of Prion Disease Transmission through Bovine-Derived Bone
Substitutes: A Systematic Review
Clin Implant Dent Relat Res. 2011 Dec 15. doi:
10.1111/j.1708-8208.2011.00407.x. [Epub ahead of print]
Friday, December 16, 2011
Creutzfeldt-Jacob Disease Question Asked by Lord Walton of Detchant
P-Capt filter
Saturday, December 3, 2011
Candidate Cell Substrates, Vaccine Production, and Transmissible
Spongiform Encephalopathies
Volume 17, Number 12—December 2011
Wednesday, August 24, 2011
All
Clinically-Relevant Blood Components Transmit Prion Disease following a Single
Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
2011
Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic
CJD
Tuesday, November 08, 2011
Can
Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease
Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011
Original Paper
Conclusions:These findings raise doubt about the possibility of a
reliable CJD surveillance only based on mortality data.
Editorial: The European Response to BSE: A Success Story
EFSA Journal 2011; 9(9):e991 [3 pp.]. doi:10.2903/j.efsa.2011.e991
Author Herbert Budka, Member and Vice-Chair of EFSA's Panel on Biological
Hazards (BIOHAZ)Contact
Type: Editorial Published: 02 September 2011 Affiliation: European Food
Safety Authority (EFSA), Parma, Italy Article
Editorial Bovine spongiform encephalopathy (BSE, "mad cow disease") was
officially first reported in November 1986 in the UK. It became quickly
interpreted as likely counterpart in bovines of scrapie, the paramount
transmissible spongiform encephalopathy (TSE, prion disease) in sheep and goats.
A landmark epidemiological study by John Wilesmith and co-workers (Wilesmith et
al., 1988) identified in 1988 cattle feedstuffs containing ruminant-derived
protein (meat-bone meal, MBM) as source for the evolving epidemic that numbered
almost 185.000 diagnosed cases in total in the UK and a further 5.500 elsewhere
in the EU, with some 2 million infected bovines estimated to have entered the
human food chain in the UK. The first UK response was a ban on feeding MBM to
ruminants, as a measure that significantly curbed but did not eliminate the
epidemic.
A
likely link between BSE and the human disease variant Creutzfeldt-Jakob disease
(vCJD) was published in early April 1996 (Will et al., 1996), followed by a
media outbreak of apocalyptic scenarios sketching a man-made disaster of then
unpredictable proportions. Health authorities were frantically acting to limit
damage from BSE not only to human health, but also to agriculture, economies,
political credibility and public confidence. In the UK, the Phillips Inquiry
(Lord Phillips et al., 2000) took two and a half years to accrue insight into
why and how the BSE saga developed. The key conclusions depicted BSE as a
consequence of intense farming practices, with significant shortcomings in the
way things were done, with sensible measures taken that were not always timely
and adequately implemented and enforced, and implicitly guided by the belief
that BSE was not a real threat to human health. Moreover, there was too much
secrecy and unjustified reassurance by governmental bodies in order to protect
the agricultural industry.
Almost simultaneously with publication of the Phillips Report, the
second public BSE crisis started in 2000 when first results of active BSE
surveillance on the European continent confirmed scientists' opinion that
political claims of "freedom from BSE" in several countries were wishful
thinking rather than reality. As a result, the EU TSE Regulation of 2001[1] laid
down a comprehensive set of harmonised rules for the prevention, control and
eradication of TSEs, including an EU-wide total ban on the feeding of animal
proteins to farmed animals. More or less independent national food safety
authorities were now established in most EU countries, and the need to separate
risk assessment from risk management could no longer be ignored.
Since the first BSE crisis of 1996, the European Commission (EC) has
embarked on a science-guided response, establishing a TSE/BSE ad hoc Group of
their Scientific Steering Committee (SSC) that provided up to 2003 a plethora of
opinions on all aspects of BSE and other TSEs (SSC, 1997-2003). The SSC was a
risk assessment and risk advisory body, separated from risk management which
remained with the EC Directorate General for Health & Consumers (DG SANCO).
From December 1997, the SSC adopted their first important documents on the
scientific basis to protect human health from BSE, such as the definition of
tissues containing most of infectious TSE agents (prions), termed Specific Risk
Materials (SRM). Regrettably, politicians in several EU Member States (MS) were
then unwilling to translate this into legislation, still sticking to their
"freedom from BSE" illusion. It was only after a delay of almost 3 years that
the EU-wide SRM ban, the most important measure to protect public health from
BSE, became implemented.
Since 2003, EFSA has taken over the role of science-based advice to the
EC on BSE/TSE-related matters, with the BIOHAZ Panel producing an equally
impressive amount of opinions and reports (EFSA, 2003-2011) as the former SSC.
As a whole, these scientific risk assessments - first by the SCC, then by EFSA -
and their translation into adequate measures by national and EC risk managers
were the basis of the European response to BSE, which has been a spectacular
success story. This is evident from quantitative data on both the animal and
human disease. First, the prevalence of BSE as detected by current surveillance
has come down steadily in the EU to a trickle, from several thousands of cases
in the early 2000s, to 44 in 2010 in the EU (11 in the UK) (OIE, 2011). Second,
surveillance of vCJD in the UK indicates that the epidemic, having reached a
peak in the year 2000 when there were 28 deaths, has declined to a current
incidence of about one diagnosis/death per year (Andrews, 2011). Clearly, it is
now time to be re-assured but still too early for complacency (Budka et al.,
2008).
Given the quantitative indicators of what seems, in the EU, to be the
near-extinction of the animal epidemic and control of cattle-to-human
transmission, is there anything left for concern? Unfortunately, there is. With
BSE, the global disease burden is far from clear in countries with less
well-developed surveillance. In humans, the potential continuing person to
person spread by blood and blood products remains a problem as seen with the
four cases of transfusion-associated vCJD infection to date (Andrews, 2011).
With BSE and other TSEs in animals, the recognition of the wide diversity of
prion strains in the field, including three new forms of animal TSEs (L-type
Atypical BSE, H-type Atypical BSE and Atypical scrapie), has complicated disease
diagnosis and surveillance, as well as scientific assessment of their potential
risks to humans. EFSA and the European Centre for Disease Prevention and Control
(ECDC) recently delivered a scientific opinion on any possible epidemiological
or molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential. In particular the
L-type Atypical BSE agent might be similarly or even more virulent to humans
than the Classical BSE agent. While mankind has been in contact with the major
TSE of small ruminants for centuries, there is no epidemiological evidence to
suggest that classical scrapie is zoonotic; however, experimental transmission
data on humanised mice and non-human primates have been very scarce so
far.
What does this mean for the future? The decline of the BSE epidemic seen
by 2005 led to consideration of some relaxation of costly BSE control measures
as depicted in the EU TSE Roadmap (EC, 2005), and will inevitably be followed by
further relaxation as already outlined in another EU TSE Roadmap 2 of 2010 (EC,
2010). It remains critical that current levels of consumer protection are
maintained and all future changes from well established and highly effective
current risk management measures are based upon sound scientific advice that
EFSA will continue to provide.
Which old issues will remain, and which new issues will become relevant?
For Atypical BSE, the most widely accepted hypothesis is that of a spontaneously
arising ("sporadic") disease in relatively old bovines. If this holds true, it
will be impossible to eradicate such a disease which originates de novo;
probably we then have to live forever with a ban on SRMs, in particular the
central nervous system (CNS), of older cattle. Given our insufficient knowledge
about the true prevalence of atypical animal prion strains in the field, it will
be important to continue and improve the systematic surveillance of animal TSEs,
and to refine our diagnostic and laboratory methods and experiments. As some
scientific data suggest that there is probably no absolute molecular barrier to
transmission of TSE agents between mammalian species (EFSA Panel on Biological
Hazards (BIOHAZ) and ECDC, 2011), the issue of a zoonotic potential of prions is
likely to remain with us a time. For human TSEs including sporadic CJD, it will
be important to continue systematic surveillance that should be able, as clearly
shown with vCJD in the past, eventually to identify emerging new phenotypes or
new prion strains. In sum, at a time when many scientists and most decision
makers are no longer interested in prions and their risk, it will be prudent to
stay vigilant, although this must be in a way that is balanced with other risks
to human and animal health. In the risk assessment area, this will continue to
be a challenge for EFSA in the years to come.
--------------------------------------------------------------------------------
[1]
Regulation (EC) No 999/2001 of the European Parliament and of the Council of 22
May 2001 laying down rules for the prevention, control and eradication of
certain transmissible spongiform encephalopathies. OJ L 147, 31.05.2001, p.
1-40.
see
full text and more here ;
Tuesday, October 4, 2011
De
novo induction of amyloid-ß deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi:
10.1038/mp.2011.120
Molecular Psychiatry advance online publication 4 October 2011; doi:
10.1038/mp.2011.120
De
novo induction of amyloid-ß deposition in vivo
R
Morales1,2, C Duran-Aniotz1,3, J Castilla2,4, L D Estrada2,5 and C Soto1,2
1Mitchell Center for Alzheimer's Disease and Related Brain Disorders,
Department of Neurology, University of Texas Houston Medical School, Houston,
TX, USA 2University of Texas Medical Branch at Galveston, Galveston, TX, USA
3Universidad de Los Andes, Facultad de Medicina. Av. San Carlos de Apoquindo
2200, Las Condes, Santiago, Chile 4CIC bioGUNE, Parque Tecnologico de Biskaia,
Ed 800, 48160 Derio and IKERBASQUE, Basque Foundation for Science, 48011 Bilbao,
Spain
Correspondence: Dr C Soto, Mitchell Center for Alzheimer's Disease and
Related Brain Disorders, Department of Neurology, University of Texas Houston
Medical School, 6431 Fannin St, Houston, TX 77030, USA. E-mail:
Claudio.Soto@uth.tmc.edu
5Current address: Laboratorio de Señalización Celular, Centro de
Envejecimiento y Regeneración. P. Universidad Catolica de Chile, Santiago,
Chile.
Received 8 March 2011; Revised 15 August 2011; Accepted 25 August 2011;
Published online 4 October 2011.
Abstract
Alzheimer's disease (AD), the most common type of senile dementia, is
associated to the build-up of misfolded amyloid-ß (Aß) in the brain. Although
compelling evidences indicate that the misfolding and oligomerization of Aß is
the triggering event in AD, the mechanisms responsible for the initiation of Aß
accumulation are unknown. In this study, we show that Aß deposition can be
induced by injection of AD brain extracts into animals, which, without exposure
to this material, will never develop these alterations. The accumulation of Aß
deposits increased progressively with the time after inoculation, and the Aß
lesions were observed in brain areas far from the injection site. Our results
suggest that some of the typical brain abnormalities associated with AD can be
induced by a prion-like mechanism of disease transmission through propagation of
protein misfolding. These findings may have broad implications for understanding
the molecular mechanisms responsible for the initiation of AD, and may
contribute to the development of new strategies for disease prevention and
intervention.
Keywords:
amyloid; prion; protein misfolding; disease transmission
see
more here ;
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in
Amyotrophic Lateral Sclerosis (ALS)
Monday, September 26, 2011
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI,
GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011
Friday, November 23, 2012
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA,
AND CANADA
Monday, January 14, 2013
Gambetti et al USA Prion Unit change another highly suspect USA mad cow
victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes
along with this BSe
Thursday, February 21, 2013
National Prion Disease Pathology Surveillance Center Cases Examined January
16, 2013
Sunday, February 10, 2013
Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection
report/CJD
Mad
Cow Scaremongers
Mad
Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent
2003-2011
re-2003
"he
also blindly insists upon a mad-cow with Alzheimer's, Parkinson's, and Lou
Gehrig's disease."
SNIP...SEE FULL TEXT ;
layperson
TSS
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
-------- Original Message --------
Subject: [Docket No. 04-116-1] USE of veterinary biological products on
the topic of Transmissible Spongiform Encephalopathies (TSS SUBMISSION)
Date: Fri, 05 Nov 2004 11:49:49 -0600
From: "Terry S. Singeltary Sr."
CC:
Nicole.L.Ruffcorn@aphis.usda.gov, Questa.R.Glenn@aphis.usda.gov, BSE-L
> Meeting topics and proposed presentation titles should be submitted
> to Steven A. Karli, director, CVB, APHIS, Veterinary Services, 510
> South 17 St., Suite 104, Ames, IA 50010-8197; phone (515) 232-5785,
> fax (515) 232-7120 or e-mail CVB@aphis.usda.gov. For registration
> information contact Nicole Ruffcorn at the same address and fax
number
> or via phone dial (515) 232-5785 extension 127 or e-mail
I wish to kindly submit the following to Mr. Steven A. Karli for the 13th
public meeting to discuss regulatory and policy issues related to the
manufacture, distribution, and use of veterinary biological products on the
topic of Transmissible Spongiform Encephalopathies (all of them).
[Docket No. 04-116-1]
Greetings APHIS/USDA et al,
INOCULATION of the TSE agent is the most effected mode of transmission, or
so it seems.
MOST people have forgotten the medicines act of 1968 where they state not
to use scrapie associated fibers SAF for any pharmaceuticals for animals in vet
products;
June 1983 MEDICINES ACT 1968
''Unless there is a risk from a heat-resistant pathogen such as the scrapie
agent, no restrictions are placed on substances sterilized by autoclaving
provided that the complete mass is held at a minimum of 115°C for at least 15
minutes''...
PLEASE do not forget the infamous 'Louping-ill vaccine' incident;
SNIP...END
-------- Original Message --------
Subject: Bovine-derived Products Used in the Manufacture and Formulation
of Vaccines: Current Policies and Issues for the Future
Date: Fri, 5 Nov 2004 15:06:53 –0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
##################### Bovine Spongiform Encephalopathy
#####################
2004 PDA/FDA Joint Regulatory Conference - 9/20-22/2004
SNIP...END
layperson
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
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