NOTICE 38-13 6/4/13
DISTRIBUTION: Electronic NOTICE EXPIRES: 6/1/14 OPI: OPPD
INTERPRETING RESULTS OF FSIS VERIFICATION SAMPLING OF
DOMESTIC BEEF PRODUCT DERIVED FROM ADVANCED MEAT RECOVERY SYSTEMS
(AMR01/FAMR01)
I. PURPOSE
This notice updates the instructions in FSIS Notice 25-10 to inspection
program personnel (IPP) using the Public Health Information System (PHIS). This
notice includes directions from FSIS Notice 25-10 on how to interpret laboratory
results for domestic beef advanced meat recovery (AMR) product that was tested
for the presence of central nervous system (CNS) tissue. This notice also
instructs IPP to verify that the average daily volume of AMR product recorded in
PHIS includes the volume of AMR product diverted for use in the manufacture of
other beef products produced within the same establishment. FSIS will
incorporate these directions and information in a future revision of FSIS
Directive 7160.3, Advanced Meat Recovery Using Beef Vertebral Raw
Materials.
KEY POINTS:
• This notice applies only to beef, which includes veal.
• Beef AMR product is “meat,” and such product may be labeled as
“beef.”
• CNS tissue is a meat byproduct that consists of brain, spinal cord, and
trigeminal or dorsal root ganglia.
• “Meat” or “beef” derived from an AMR system that contains CNS tissue and
labeled or used as “beef” is misbranded.
• Skulls and vertebral bones from cattle 30 months of age and older are
specified risk materials (SRMs) and are not eligible for use in AMR
processing.
• The average daily volume of AMR product recorded in PHIS now includes the
volume of AMR product diverted for use in the manufacture of other beef products
(e.g. ground beef) produced within the same establishment.
• FSIS will sample beef AMR product made from skulls and vertebral bones
(including spinous processes) of animals younger than 30 months of age for CNS
tissue.
• FSIS verifies that establishments hold or maintain control of AMR product
that FSIS tests for CNS tissue.
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II. BACKGROUND
A. On January 12, 2004, the Agency issued an interim final rule Meat
Produced by Advanced Meat/Bone Separation Machinery and Meat Recovery (AMR)
Systems (69 FR 1874). In the rule, the Agency noted that AMR systems imitate the
physical action of hand-held high-speed knives for the removal of skeletal
muscle tissue from bone using hydraulic pressure. Furthermore, AMR systems apply
pressure to detach the meat (skeletal muscle) tissue from the bones in a ‘‘hard
separation’’ process (e.g., piston driven). This hard separation process is
followed by a soft separation process, a desinewing step that typically involves
the use of belt pressure against a rotating perforated steel drum to separate
meat from connective tissue, sinews (e.g. tendons), and other non-meat
components. In contrast, beef that is only “mechanically separated” is inedible
under 9 CFR 319.5(b) and is not to be used for human food.
B. The definition of “meat” is found in 9 CFR 301.2. AMR product from beef
bones must meet requirements in 9 CFR 318.24 to be used as “beef” in a beef meat
food product.
C. The AMR regulation (9 CFR 318.24) limits what beef materials can be used
to make AMR product. The ingoing source material for beef AMR product
excludes:
1. Specified risk material (SRM) (e.g. the skull or vertebral column from
cattle 30 months of age and older);
2. Bones from cattle of any age with visible CNS tissue (e.g. spinal cord);
and
3. Recycled crushed or “spent” skulls and vertebral columns previously run
through the AMR system in accordance with 9 CFR 318.24(c)(2).
D. Finished beef AMR product is subject to standards in 9 CFR 318.24. Beef
AMR product that complies with 9 CFR 318.24 may be shipped as a beef product
with a descriptive name or used as “beef” (see 69 FR 1874, 1876) in the
production of ground beef or similar beef products. The descriptive names of AMR
product shipped in commerce includes ‘‘beef trimmings, finely textured,’’ “beef,
finely textured,” “finely ground beef,’’ or any other common or usual name (e.g.
beef) that accurately describes its form.
E. Per FSIS Directive 10,010.1, Verification Activities for Escherichia
coli O157:H7 in Raw Beef Products, AMR belongs to the class of ground beef
components known as “other than beef manufacturing trimmings” that includes raw
esophagus (weasand) meat, head meat, cheek meat, low temperature rendered lean
finely textured beef (LFTB), partially defatted chopped beef, partially defatted
beef fatty tissue, and heart meat. Beef processors typically add 5 to 12 percent
AMR product to make ground beef or similar non-intact product.
F. Imported AMR product is not subject to AMR01 or FAMR01 sampling.
Sampling of imported product is conducted under the AMR Panel-Beef, Veal
type-of-inspection (TOI), which is a laboratory pathology type sample. Import
inspection personnel are to refer to FSIS PHIS Directive 9900.6, Laboratory
Sampling Program for Imported Meat, Poultry, and Egg Products, which provides
direction on submitting samples for pathology analyses.
III. UPDATING THE ESTABLISHMENT PROFILE IN PHIS
A. AMR sampling requests are based on AMR product information in the PHIS
Establishment profile. IPP are to verify and update, if necessary, establishment
profile information in PHIS (See FSIS Directive 5300.1, Managing the
Establishment Profile in the Public Health Information System (PHIS)), to
include the average daily volume of non-intact AMR produced by the establishment
whenever:
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1. IPP perform the monthly Update Establishment Profile task in PHIS;
or
2. IPP learn the establishment has begun or resumed production of AMR
product.
B. IPP are to enter or update the Establishment Profile – Products Volume
in PHIS to include the total average daily volume of AMR product produced by the
establishment. The total average daily volume of AMR product includes the volume
used in the production of ground beef or shipped in commerce under various
product names.
NOTE: The Establishment Profile in PHIS does not distinguish between AMR
product made from long bones, shank bones, and briskets of cattle of any age and
AMR product derived from skull or vertebral column of cattle less than 30 months
of age.
IV. SAMPLING
A. IPP are to submit samples of beef AMR product likely to contain CNS
tissue to the FSIS Eastern Laboratory when they receive through PHIS a directed
laboratory sample request under project code AMR01.
B. When IPP receive an AMR01 or FAMR01 request, IPP are to:
1. Verify that the establishment produces AMR product and that such product
is made from eligible bones per 9 CFR 318.24. Examples of eligible beef bones
include the following:
a. Long bones, shank bones, brisket bones of cattle of any age; and
b. Skull and vertebral bones of cattle less than 30 months of age (i.e.
non-SRM bones)
2. Verify that the establishment produces AMR product eligible for AMR01 or
FAMR01 sampling. AMR product eligible for sampling includes AMR product derived
from non-SRM bones associated with CNS tissue (e.g. skull, vertebral bones, or
dorsal spinous process (“feather bones” of cattle less than 30 months of age)).
IPP need not sample AMR product from non-vertebral long bones, shank bones, or
brisket bones that are not likely to contain CNS tissue;
3. Verify prior to sampling when and on which equipment (lines) that the
establishment produces AMR product eligible for sampling;
4. Collect samples of AMR product eligible for sampling. IPP are to collect
from multiple locations approximately two (2) pounds of AMR product from one AMR
system (i.e. lot) for each sample request. If a single lot of AMR product
eligible for sampling is produced over multiple shifts or on multiple machines,
the IIC is to coordinate sampling and ensure IPP collect a representative
sample;
5. Notify the establishment a sample has been collected;
6. Notify the establishment that the entire lot of product represented by
the sample is to be held or controlled pending sample results. IPP are to verify
the establishment holds or maintains the sampled lot under its control until
sample results are available and disposition of product is made. See FSIS Notice
7-13, Control of Agency Tested Products for Adulterants;
7. Verify establishment records show how each lot of AMR product is defined
or identified; and
8. Complete sample forms and ship samples to the FSIS Eastern Laboratory.
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V. WHEN AMR PRODUCT IS NOT AVAILABLE FOR SAMPLING
A. IPP in establishments producing AMR product with no eligible product
available for sampling are to cancel the sampling task and indicate that
eligible product is “unavailable” during the sampling timeframe. See Fig. 1.0
below.
B. If the status of AMR production changes dramatically (e.g., production
ceases long term) during an AMR01 sampling set or before follow-up FAMR01 sample
requests are issued, IPP are to indicate in “Other” reasons (see Fig. 1.0) when
the establishment has ceased AMR production and that AMR product is no longer
being produced. IPP are to document the details in Inspector Notes (see Fig. 4.0
referenced in Section Part VII, Enforcement, Section G. below) using PHIS and
explain why IPP are not collecting AMR01 and FARM01 samples.
Fig. 1.0 Reasons for Cancelling a Sampling Task
snip...
VI. NOTIFICATION OF RESULTS AND PRODUCT DISPOSITION
A. IPP can access sample results from the FSIS Eastern Laboratory posted in
both PHIS and the Laboratory Electronic Application for Results Notification
(LEARN). LEARN will eventually be replaced by a system known as Laboratory
Information Management System (LIMS) Direct.
B. IPP can access the AMR testing results from:
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1. The PHIS homepage under “My Inspections and Samples” tab;
2. LEARN (LIMS Direct) via a link in the Lab Result Report (Fig. 2.0) in
PHIS; and
3. LEARN (LIMS Direct) via the FSIS Applications menu. From the “Start
menu,” IPP select FSIS Applications Internet-Intranet LEARN (LIMS Direct)
CSI-IIC.
C. The result recorded in LEARN (LIMS Direct) provides a brief summary of
the laboratory’s findings. To view the summary sample results window, IPP:
1. Log into LEARN (LIMS Direct);
2. Enter either the establishment number or the form number;
3. Click “submit;”
4. Select the form number or the word “Pathology” under “Sample Type”
column; and
5. Click on the underlined word “Pathology” to open the sample result
information.
D. LEARN (LIMS Direct) displays a “Tissue submission of ‘Comminuted Meat’”
within the AMR01/FAMR01 AMR Monitoring project.
Figure 2.0 View of AMR Laboratory Result Report in PHIS
snip...
E. AMR laboratory results may be reported as “adulterated” or
“unadulterated.” Adulterated product may include product that is “economically
adulterated” or misbranded. The Lab Result Report in PHIS (Fig. 2.0 shown above)
indicates the test result is “Acceptable” and that the product is “Unadulterated
product.” A test result that is “Not Acceptable” indicates the AMR product is
misbranded because of the presence of CNS-type tissue.
6
F. After receiving results, IPP are to verify the proper labeling and
disposition of noncomplying AMR product not eligible for use as “beef.” IPP are
not to take action solely based on LEARN (LIMS Direct) results. IPP are to
determine product disposition and take enforcement action based on the detailed
final pathology laboratory results and product labeling. See FSIS Directive
10,200.1, Accessing Laboratory Sampling Information via LEARN (LIMS Direct),
Part VIII. A. The FSIS Eastern Laboratory Pathology Section sends the more
detailed final report via email (see Fig. 3.0 shown below), fax, or U.S. Postal
Service. If IPP have access to a fax machine and have provided an office fax
number in PHIS, the detailed report is faxed. If the laboratory has the FSIS
office fax number, it will also fax the report to the inspection office. The
laboratory also emails the detailed report to the “FSIS - AMR Notification
List.”
Figure 3.0 Example of a Beef AMR Sample Pathology Laboratory Report
G. There are three (3) possible laboratory results for Beef AMR in the
“Diagnosis” column under ANALYSIS RESULT. Typical results and labeling
restrictions based on the results are posted in Table 1.0 below:
Table 1.0. Possible Beef AMR Laboratory Results and Disposition
Lab Diagnoses (Analysis Result)
Examples of Findings in the Detailed Pathology Report
Labeling Restrictions based on Results
Skeletal Muscle & Associated Meat Tissues
“…skeletal muscle, adipose tissue, blood vessels, streaming nuclear debris,
bone, and cartilage”
This product meets the definition of “meat” in 9 CFR 301.2 and can be
labeled as “beef” or other accurate term.
Skeletal Muscle & Associated Meat Tissues with Spinal Cord Tissue or
DRG Sensory Ganglia (CNS tissues)
“…the presence of sensory ganglion (DRG) or CNS-type tissue along with
skeletal muscle, associated tissues, bone fragments, cartilage, and streaming
nuclear debris …”
Product containing CNS-type tissue does not meet the definition of “meat”
as defined in 9 CFR 301.2 and cannot be labeled solely as “beef.” This product
is misbranded if labeled as “beef” and cannot be used as “beef” in any standard
beef product. Beef AMR product that contains CNS type tissue and complies with
the bone solids and bone marrow criteria in 9 CFR 318.24(c) may be descriptively
labeled e.g. “Beef with Spinal Cord” or “Beef with Central Nervous System
Tissue.” Such products can be used in rendering operations or be used to make
broths, extracts or process flavors. Since a standard of identity does not exist
for this type of product, the establishment must contact the Labeling and
Program Delivery Staff (LPDS) for labeling approval. See 9 CFR 318.24(c) for
additional restrictions or limitations on
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noncomplying beef product. AMR product from or containing ineligible SRMs
is “adulterated.”
Organ tissue (i.e. meat byproducts such as kidney, liver, spleen) or
foreign material (e.g., fibrous plant material)
“…organs or tissues other than meat (e.g. kidney; liver) along with
skeletal muscle, associated tissues, bone fragments, cartilage, and streaming
nuclear debris.”
Product containing organ tissue (meat byproduct) is not “meat” as defined
in 9 CFR 301.2 and cannot be labeled solely as “beef.” To enter commerce, this
product may be descriptively labeled (e.g. “beef with beef byproducts” (e.g.
with
kidney) and the label will need sketch label approval from LPDS for this
non-standardized product.
NOTE: The descriptive labeling of AMR product includes “beef,” ‘‘beef
trimmings, finely textured,’’ “beef, finely textured,” or “finely ground beef,’’
or any other common or usual name that accurately describes its form.
H. IPP are to share the detailed report information and LEARN (LIMS Direct)
results with establishment management once detailed laboratory results are
received. Positive CNS tissue findings in AMR beef product generate a follow-up
sample request in PHIS under the project code FAMR01.
VII. ENFORCEMENT ACTIONS
A. IPP are to continue to follow instructions provided in FSIS Directive
7160.3 and verify the disposition of product per the guidelines in this notice
for CNS and CNS-type tissue or other tissue not considered “meat” when a random
AMR01 or follow-up FAMR01 result is noncompliant (i.e. misbranded or
adulterated).
B. IPP are to retain the product, notify the establishment, and issue a
Noncompliance Record (NR) for the misbranded product using the MSS; MSP; PDBFT;
PDPFT; PDCB; PDCP; AMRS task in PHIS based on all information including the
results in PHIS and the detailed report from the FSIS Field Service Laboratory –
Eastern Laboratory.
NOTE: The key for the abbreviations in this PHIS task name is as follows:
MSS (Mechanically Separated Species other than beef including veal); MSP
(Mechanically Separated Poultry); PDBFT (Partially Defatted Beef Fatty Tissue);
PDPFT (Partially Defatted Pork Fatty Tissue); PDCB (Partially Defatted Chopped
Beef); PDCP (Partially Defatted Chopped Pork); AMRS (Advanced Meat Recovery
Systems).
1. IPP are to attach a US Retain tag in accordance with 9 CFR 500.2(a)(2)
to any noncompliant misbranded product produced by the AMR system and tested on
the designated day of sampling.
2. IPP are to attach a US Reject tag in accordance with 9 CFR 500.2(a)(3)
on the AMR equipment producing noncompliant misbranded product. If the
establishment operates more than one AMR machine, IPP are to evaluate
establishment HACCP or other records to determine whether the process and
product are the same (e.g. same lot). IPP may take regulatory control actions on
additional AMR machines until the establishment demonstrates that effective
corrective actions and preventive measures or controls are in place. See FSIS
Directive 7160.3.
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C. If the establishment ships into commerce noncomplying product that is
misbranded because of the presence of CNS type tissue and produced on the
designated day of sampling, IPP are to alert the District Recall Officer of the
situation per FSIS Directive 8080.1, Recall of Meat and Poultry Products.
Misbranded product shipped in commerce may be subject to a Class III (i.e.,
non-health hazard) recall.
D. Before completing the NR and lifting the regulatory control action, IPP
are to verify that all corrective actions proffered by the establishment have
brought the AMR process back under control, and that the establishment has made
the proper disposition on the product.
E. IPP are to follow instructions in FSIS Directive 7160.3 to verify that
the establishment has effectively implemented corrective actions as described in
the establishment’s response to the noncompliance notification.
F. When FSIS AMR01 testing reveals that AMR product is not in compliance,
IPP will receive eleven (11) follow-up (FAMR01) sample requests via PHIS. IPP
will use ten (10) of the eleven (11) forms to collect follow-up samples as
instructed in the above directive. If there is a positive finding in any of the
follow-up samples, IPP will use the eleventh and last form to collect a sample
after the establishment demonstrates process control according to the above FSIS
Directive 7160.3. The purpose of this eleventh sample is for FSIS to verify that
the establishment’s process is back in control. If all ten (10) composite
follow-up samples are negative, IPP are to cancel (i.e. not schedule or not
perform) the last PHIS sampling task.
G. In the event IPP are delayed in taking the follow up (FAMR01) samples
for any reason, IPP are to document details and the need to take the follow-up
samples in the “Inspector Notes” section in PHIS. These inspector notes are to
be incorporated in future weekly meeting agendas and updated as needed. IPP are
to access the “Inspector Notes” through the “Inspection Verification” menu in
the left side navigation menu on the PHIS “Home” page. IPP are to capture these
notes under the “Processing” category. See Fig. 4.0.
Fig. 4.0 Using Inspector Notes in PHIS.
H. If the IPP do not receive the FAMR01 sample requests in PHIS within
three (3) business days following the positive notification, IPP are to email
the FSIS - AMR Notification List mailbox and enter on the subject line: “FAMR01
Forms Not Received.” IPP are to include establishment information in
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the email and copy the Front-line Supervisor (FLS) and District Case
Specialist to make them aware of the situation. Risk, Innovations, and
Management Staff (RIMS) will return incomplete requests or forward to the above
mailbox the sample form request submitted via askFSIS. The Office of Data
Integration and Food Protection (ODIFP) – Data Analysis and Integration Group
(DAIG) representative on this distribution list will then follow-up with the IPP
to ensure that they receive the sample request via PHIS to collect the composite
samples.
VIII. DATA ANALYSIS
OPPD and ODIFP-DAIG will analyze the results of AMR01 and FAMR01 sampling
and associated noncompliance data from the advanced meat recovery systems on an
annual basis. Data will be reviewed to determine what trends exist by district
and establishment.
IX. QUESTIONS
Refer questions regarding this notice to the Policy Development Staff
through askFSIS or by telephone at 1-800-233-3935. When submitting a question,
use the Submit a Question tab, and enter the following information in the fields
provided:
Subject Field: Enter Notice 38-13
Question Field: Enter your question with as much detail as possible.
Product Field: Select General Inspection Policy from the drop-down
menu.
Category Field: Select Public Health Information System – General
Information from the drop- down menu.
Policy Arena: Select Domestic (U.S.) Only from the drop-down menu.
When all fields are complete, press Continue.
Assistant Administrator
Office of Policy and Program Development
amazing, all this, the listing of said diseases, and not a word on Bovine
Spongiform Encephalopathy BSE TSE prion disease with regards to risk factor for
AMRS. simply amazing $$$
Central nervous system tissue has been detected at low levels (μg/g) on
subprimal cuts, in ground meat, and in tissue derived from advanced
meat-recovery systems in U.S. commercial plants (Schmidt et al., 2001). Nervous
tissue also has been detected in whole muscle cuts from cattle harvested in
European Union commercial facilities (Prendergast et al., 2004).
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.
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
Subject: SV: SV: Changes to UK Rendering System?
From: Karin.Irgens@DYREHELSETILSYNET.NO
Reply-To: Bovine Spongiform Encephalopathy
Date: Fri, 1 Dec 2000 22:11:59 +0100 Content-Type: text/plain
Parts/Attachments: text/plain (58 lines)
######### Bovine Spongiform Encephalopathy #########
Hello John
Although MRM was probably one of the most important sources of
contamination of human foods until it was banned in 1995 in the UK, the MRM
problem has nothing to do with rendering and MBM for animal feed.
Besides, I doubt that it would be very practical to _extract_ brain and
spinal cord after "crushing and shattering" of heads and spines !
According to the BSE Inquiry's final report, MRM was produced by :
..." high pressure being applied to bones to separate them from anything
that was still adhering. The resultant slurry was used in a range of meat
products for human consumption, including lower grade sausages, burgers an pies.
The major source of MRM was the spinal column"...
The BSE Inquiry certainly drew attention to this process. I think they even
wrote a "draft factual account" on MRM last year.
Best regards, Karin
-----Opprinnelig melding-----
Fra: john hazelwood: j_hazelwood@YAHOO.COM]
Sendt: 1. desember 2000 18:17
BSE-L@UNI-KARLSRUHE.DE
Emne: Re: SV: Changes to UK Rendering System?
TRUE But The UK invented MRM in the mid-nineteen
seventies, that is the industrial processing of whole
heads of cows and sheep plus skeletal waste on a huge
scale. The process was made viable by the collection
of hundreds of heads etc. That were then crushed,
shattered and centrifuged to extract the brains,
tongues, eyes, and spinal chord from the bone matrix.
A material was made from this slurry that could be
added to pies, sausages, burgers and baby filler as
cheap filler. The balance was used as a protein
supplement in animal feed.
Could you have a better way of spreading infectivity?
Did the BSE Inquiry describe or draw attention to
this process? I understand there was a HMSO
publication on MRM in 1980 but as yet I have not been
able to obtain a copy.
Best regards john
__________________________________________________
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############
SNIP...
Subject: Re: SV: SV: Changes to UK Rendering System?
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Tue, 5 Dec 2000 11:39:50 -0800 Content-Type: text/plain
Parts/Attachments: text/plain (253 lines)
######### Bovine Spongiform Encephalopathy #########
Karin and John,
forgot to add this;
57. On 22 June 1990, the APS/Parliamentary Secretary (Mr Curry) sent a
minute to Dr Denner, copied to Mr Capstick, Mr Meldrum, Mr Crawford, Mr Baker,
Mr Griffiths, Mr Lawrence and others, in which he explained that at a
demonstration of the MRM process which Mr Curry had seen at a slaughterhouse,
traces of spinal tissue had been found in the product and as a result the
Parliamentary Secretary was ‘very unhappy about MRM’.[53] A suggestion had been
made to Mr Curry that an efficient method of removing the spinal tissue would be
to apply a suction pump to the spinal canal after the head had been removed and
before the carcase was split. The Parliamentary Secretary asked for a short note
on the feasibility of such a method.
58. On 25 June 1990, Mr Bremner sent a minute to Mr Meldrum, copied to Dr
Denner, Mr Crawford, Mr D Taylor and Mr Griffiths. Mr Bremner reported that he
was ‘very surprised’ that the Parliamentary Secretary had seen traces of spinal
tissue in MRM and that ‘it is so unlikely that I suspect he was
misinformed’.[54] Mr Bremner explained that what the slaughterhouse operators
had said was that ‘they were not happy to sell MRM because of the risk of
contamination of the vertebrae with the spinal cord. Unfortunately not all the
spinal cord was being removed by the meat inspectors although only small pieces
were left’. He went on to say that although the idea of using a suction pump was
being pushed by the operators, he found it difficult to imagine how it would
work, and that ‘my own view was that if the meat inspectors had done their job
correctly, there would have been little risk and if the vertebrae were excluded
from MRM, there should be no further risk’.
59. In a manuscript minute dated 28 June 1990, Mr Meldrum asked Mr Bremner
to find out from his trade contacts whether any suction pumps were actually
available on the market.[55]
60. Dr Denner wrote to APS/Mr Curry on 26 June 1990 regarding the visit to
Canvin International Ltd. His minute was copied to PS/Minister, Private Offices,
Mr Capstick, Mr Packer, Mr Meldrum, Mrs Attridge, Mr Wentworth, Mr Crawford, Mr
Baker, Mr Griffiths and Mr Lawrence amongst others.[56] Dr Denner explained
that:- ‘There are two separate issues arising from the Parliamentary Secretary’s
(Mr Curry) visit to the abattoir. The first is the efficacy of removing spinal
cord from the carcase, which is a mandatory requirement of the Bovine Offals
(Prohibition) Regulations 1989. This issue is related to other problems of
abattoir practice such as the removal of the head meat and brains from cattle
heads, and the prevention of cross contamination from spinal fluids and tissue
during carcase dressing. The second problem is the safety of MRM prepared from
spinal column bones. Since legislation already exists for the removal of spinal
cord, any further consideration must stem from the risk posed by using spinal
column with the spinal cord removed in MRM piston type machines. Any policy
decision on BSE must be based on the best technical evidence available to be
consistent with previous MAFF policy. The CVO is already organising a study to
improve abattoir practice of splitting carcases. The use of a suction tube for
removal of spinal cord after splitting the carcase is an effective technique
already in use in some plants producing MRM from lamb spinal column bones. This
may be one of several possible techniques that can be studied. I understand the
Tyrrell Committee will discuss the use of spinal column in the preparation of
MRM at their next meeting on 2 July. Subject to their recommendation, Food
Science Division would be prepared to commission a study into verifying whether
central nervous system fluid or tissue is extracted into MRM during the
preparation in piston type machines when spinal column with the cord removed is
used. The results of such a study would give Ministers the basis for any further
action.’
61. The APS/Mr Curry replied to Dr Denner on 2 July 1990[57]. She explained
that:- ‘The MRM [at Canvins] was produced using a machine which used a piston
under hydraulic pressure. The traces of spinal tissue were identified by eye by
Canvin’s vet. However, Mr Bremner - who accompanied the Parliamentary Secretary
on this visit - said that it was possible that the material in question could
have been cartilage tissue. Mr Bremner felt that the machine was not working
properly as the MRM it produced was in larger pieces than normal.’
MRMs
MECHANICALLY RECOVERED MEAT MRM
there is no legislation in the UK specifically controlling MRM...
snip...
The vertebral column of bovine carcases, excluding the spinal cord, which
must have been removed in the slaughterhouse, can therefore be used in the
manufacture of MRM...
8. Implications regarding BSE
Even before BSE became known, MRM did not enjoy a good public opinion. It’s
appearance is not attractive and the concept of salvaging meat from waste bones
is not acceptable, particularly in today’s climate. ...
Policy – IN CONFIDENCE
BSE: Mechanically Recovered Meat (MRM)
How to define MRM or MSM i.e. Mechanically Recovered, or Mechanically
Separated Meats, legally $$$...tss
please note West Germany – MRM no permitted to be used in ‘’minced meat
products’’ eg sausages and burgers. ...tss
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
Mad cow disease, or bovine spongiform encephalopathy (BSE), 1st emerged in
Britain in 1986 as a result of "cannibalism," when beef offal was fed to cattle,
which are natural grass-eaters. The proteins, called prions, that cause BSE were
found in large quantities in the brains, spinal cords and spleens of cattle
(although they were also subsequently discovered in meat tissue). When animal
carcasses were ground down to form feed stuff for other cattle, prions were
passed on. They then colonised the brains of the cattle which ate them, and were
passed to humans via cheap, mechanically recovered meat -- such as processed
sinews and offal that were used at the time in school dinners and baby food. In
humans, the prions triggered the development of a new form of fatal human
dementia called new variant CJD, which was 1st identified in 1996.
Mad cow disease, or bovine spongiform encephalopathy (BSE), 1st emerged in
Britain in 1986 as a result of "cannibalism," when beef offal was fed to cattle,
which are natural grass-eaters. The proteins,called prions, that cause BSE were
found in large quantities in the brains, spinal cords and spleens of cattle
(although they were alsosubsequently discovered in meat tissue). When animal
carcasses were ground down to form feed stuff for other cattle, prions were
passed on. They then colonised the brains of the cattle which ate them, and were
passed to humans via cheap, mechanically recovered meat – such as processed
sinews and offal that were used at the time in school dinners and baby food. In
humans, the prions triggered the development of a new form of fatal human
dementia called new variant CJD, which was 1st identified in 1996.
People who ate such products are thought to be at greater risk of
developing the fatal brain disease vCJD, the human form of BSE. This is because
mechanically recovered meat (MRM) from cows is scraped from the bone and is
likely to include tissue from the nervous system.
-------- Original Message --------
Subject: Re: American Beef Supply at Risk
Date: Fri, 23 May 2003 17:11:59 –0500
From: "Terry S. Singeltary Sr." flounder@wt.net
Reply-To: Bovine Spongiform Encephalopathy BSE-L@uni-karlsruhe.de
snip...
PLUS we must not let them forget about the real possibility of BSE going
back to sheep, even if you don't believe that some or all phenotypes of scrapie
do not transmit to man (without ever testing), even though they transmit to
primates.
In the UK, they had an SRM ban (not very well enforced) since 1989, and MRM
ban since 1995. In the USA they still have no adequate ban in 2003, no adequate
surveillance system in 2003.
WHEN will there be BSE/CJD-Inquiries in Canada and USA?
WHEN will they make CJD reportable Nationally and issue a CJD Questionnaire
to each victims family?
WHEN will they start rapid TSE/BSE testing cattle in numbers suffient to
find them (1 Million annually for 5 years)?
WHEN will the FDA reply to my FOIA request of _all_ ruminant-to-ruminant
feed ban violations as asked?
snip...end...tss
From - Tue Jan 09 13:46:44 2001
From: "Sandy Blakeslee" sblakeslee@mindspring.com
To: flounder@wt.net
Subject: fda conference Date: Tue, 9 Jan 2001 12:27:06 –0700
Terry -- I understand you taped and listened in on the FDA conference
today. I missed it. I'm writing an update on BSE in the US for my paper
(NYTimes) and would like to know what was discussed today. Might I call you?
Where can I reach you?
Sandy
Sandra Blakeslee
blakes@nytimes.com
505 982 xxxx
Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA
Posting of cut version...
Date: Thu, 11 Jan 2001 22:02:47 -0700 From:
"Sandy Blakeslee" sblakeslee@mindspring.com
To: "Terry S. Singeltary Sr." References: 1
Hi terry -- thanks for all your help. I know it made a difference with the
FDA getting out that release.
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder@wt.net
To:sblakeslee@mindspring.com
Sent: Thursday, January 11, 2001 2:06 PM
Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting
of cut version...
snip...see ;
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
WHAT MAD COW FEED BAN ??? THAT MAD COW TRIPLE FIRE WALL WAS NOTHING BUT INK
ON PAPER $$$
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
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH
ONGOING 12 YEARS OF DENIAL
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen
Inc 2/11/10 USA
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Monday, September 17, 2012
BPI and Pink Slime: An Updated Timeline Sep 17, 2012
PINK SLIME LFTB MSM MRM BSE TSE PRION
Saturday, April 21, 2012
HISD seeks refund on burgers with 'pink slime'
Wednesday, March 14, 2012
PINK SLIME, MRM’s, BSE AKA MAD COW DISEASE, AND THE USDA NSLP
Saturday, May 26, 2012
SLIMED WITH BSE USA
re-Blogger tackles consumer questions about LFTB, BSE
Monday, September 3, 2012
Sale of misbranded and/or non-inspected meat and meat products to Omaha
Public Schools indicted
> > > Ackerman says downed cattle are 50 times more likely to have
mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than
ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of
mad cow disease in North America since 1993, at least 16 have involved downer
cattle, he said. < < <
don’t forget the children...
PLEASE be aware, for 4 years, the USDA fed our children all across the
Nation (including TEXAS) dead stock downer cows, the most high risk cattle for
BSE aka mad cow disease and other dangerous pathogens. who will watch our
children for CJD for the next 5+ decades ???
WAS your child exposed to mad cow disease via the NSLP ???
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH
RISK FOR MAD COW DISEASE ???
you can check and see here ;
WHO WILL FOLLOW THE CHILDREN FOR CJD SYMPTOMS (aka mad cow disease) FOR THE
NEXT 50 YEARS ???
Saturday, May 2, 2009
U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK
DOWNER COW SCHOOL LUNCH PROGRAM
Monday, August 27, 2012
Central Valley Meat Company: USDA Did its Job, OK?
Opinion & Contributed Articles
by Dr. Richard Raymond | Aug 27, 2012 Opinion
Dr. Richard Raymond former Undersecretary for Food Safety, U.S. Department
of Agriculture (2005-2008)
In closing, I expect Terry to add his two cents worth and I will point out
that the risk of variant CJD from eating US beef is as close to zero as we can
make it. There are many interlocking steps to keep us safe, including:
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
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
=============================================
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
Sunday, August 26, 2012
Detection of PrPSc in peripheral tissues of clinically affected cattle
after oral challenge with BSE
please see history of the USDA, OIE, mad cow follies and cover up and fraud
there from here ;
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
Thursday, May 30, 2013
Statement from Agriculture Secretary Tom Vilsack Regarding World
Organization for Animal Health (OIE) Upgrade of United States' BSE Risk Status
Release No. 0106.13 Contact: USDA Office of Communications (202)
720-4623
Tuesday, May 21, 2013
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common
origin and why the SSS policy is in full force $$$
Tuesday, May 7, 2013
Feds want five-year paper trail for livestock NAIS COOL
Friday, April 19, 2013
APHIS 2013 Stakeholder Meeting (March 2013) BSE TSE PRION
Wednesday, February 20, 2013
World Organization for Animal Health Recommends United States' BSE Risk
Status Be Upgraded
Statement from Agriculture Secretary Tom Vilsack:
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and
TSE prion disease
Monday, June 3, 2013
Unsuccessful oral transmission of scrapie from British sheep to
cattle
2011 Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Monday, July 23, 2012
The National Prion Disease Pathology Surveillance Center July 2012
Thursday, September 13, 2012
ABC NEWS SLIMED BY BPI OVER LFTB SCAM
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
see steady increase of the sporadic CJD’s. ...
The Akron, Ohio-based CJD Foundation said the Center for Disease Control
revised that number in October of 2004 to about one in 9,000 CJD cases per year
in the population group age 55 and older.
Provider Details
Creutzfeldt-jakob Disease Foundation
Description:
CJD is a rare, fatal brain disorder. The statistical incidence of CJD cases
in the US has been revised to reflect that there is one case per 9000 in adults
age 55 and older. Eighty five percent of the cases are sporadic, meaning there
is no known cause at present.
Toll free in state: (800) 659-1991, Main: (330) 665-5590
Service Categories Brain Injury, Dementia/Alzheimer's, Donations, Mental
Health
Contact Information: Phone: (330) 665-5590
Last Update Date: 07/23/2010
UK SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss
CREUTZFELDT-JAKOB DISEASE IN THE UK (By Calendar Year)
1990 – 28 cases
(with steady increase in the years from 1990 to 2011. ...tss)
2011 – 90 cases
1 in addition, the NCJDRSU has identified a total of 9 cases of VPSPr. http://www.cjd.ed.ac.uk/documents/figs.pdf
Thursday, April 4, 2013
Variably protease-sensitive prionopathy in the UK: a retrospective review
1991–2008
Brain (2013) 136 (4): 1102-1115. doi: 10.1093/brain/aws366
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD)
in Canada is also on a steady increase.
please see ;
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
Deaths of Definite and Probable CJD
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
1994 2 0 0 1 0 0 3
1995 3 0 0 0 0 0 3
1996 13 0 0 0 0 0 13
1997 16 0 1 1 0 0 18
1998 22 1 0 1 0 0 24
1999 26 2 2 1 0 0 31
2000 32 0 0 3 0 0 35
2001 27 0 2 1 0 0 30
2002 31 0 2 2 0 1 36
2003 27 1 1 0 0 0 29
2004 42 0 1 0 0 0 43
2005 42 0 0 2 0 0 44
2006 39 0 1 3 1 0 44
2007 35 0 0 4 0 0 39
2008 48 0 1 0 0 0 49
2009 48 0 3 2 0 0 53
2010 34 0 3 0 0 0 37
2011 37 0 2 1 0 1 41
2012 1 0 0 0 0 0 1
Total 525 4 19 22 1 2 573
1. CJDSS began in 1998
2. Data before 1998 are retrospective and partial, data from 1998 to 2008
are complete, and data for 2009 - 2012 are provisional
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic
CJD’s). ...tss
National Prion Disease Pathology Surveillance Center
Cases Examined1
(May 18, 2012)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 50 32 28 4 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 123 74 65 8 1 0
2000 145 103 89 14 0 0
2001 210 120 110 10 0 0
2002 248 149 125 22 2 0
2003 266 168 137 31 0 0
2004 326 187 164 22 0 13
2005 344 194 157 36 1 0
2006 382 196 166 28 0 24
2007 377 213 185 28 0 0
2008 396 232 206 26 0 0
2009 423 256 212 43 1 0
2010 413 257 216 41 0 0
2011 410 257 213 43 0 0
2012 153 82 51 15 0 0
TOTAL 44685 26406 2227 387 6 3
1 Listed based on the year of death or, if not available, on year of
referral;
2 Cases with suspected prion disease for which brain tissue and/or blood
(in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi
Arabia in the other case;
5 Includes 14 cases in which the diagnosis is pending, and 18 inconclusive
cases;
6 Includes 17 (16 from 2012) cases with type determination pending in which
the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of
sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive
Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
Rev 5/18/2012
> 6 Includes
> 17 (16 from 2012) cases with type determination pending in which the
diagnosis of vCJD has been excluded.
> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI)
and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases
of sporadic Creutzfeldt-Jakob disease (sCJD).
WELL, it seems the USA mad cow strains in humans classified as type
determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased
over the years, and the same old song and dance continues with sporadic CJD
cases $$$
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases. In BvI109, 3 VPSPr cases (2 VV and 1
MM) showed positive transmission until now. Overall, 5 voles were positive with
survival time between 281 and 596 d.p.i.. In contrast to what observed in
BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern,
characterized by low molecular weight PrPres. These PrPres fragments were
positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84,
suggesting that they are cleaved at both the C-terminus and the N-terminus.
Second passages are in progress from these first successful transmissions.
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
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.
snip...
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...
Volume 33, Issue 3, Article first published online: 20 JAN 2013
Special Lecture
Human prion diseases: Molecular, cellular and population biology
Mark W. Head
National CJD Research & Surveillance Unit, Centre for Clinical Brain
Sciences, School of Clinical Sciences,
The University of Edinburgh, Edinburgh, UK
snip...
Potential future zoonoses
Scrapie is endemic in many countries around the world, yet there is no
evidence to suggest that it is pathogenic for humans. The intense investigations
of ruminant TSEs that followed the BSE epidemic have resulted in the
identification of several distinct animal prion diseases, atypical or Nor98
scrapie in sheep and H-type and L-type BSE in cattle.32 Moreover, BSE is
experimentally transmissible to sheep and there are concerns that if BSE were to
have infected the national flock in the UK its presence might be masked by
endemic scrapie, but it might retain its pathogenicity for humans.33,34 Another
concern, particularly for the North American countries, is the spread of chronic
wasting disease in farmed and free-ranging deer and elk.35 There is no known
epidemiological link between any of these animal prion diseases and human
disease, but there are active efforts to try to quantify strain-related species
barriers between the diseases known to be a risk (BSE/ vCJD), those thought not
to represent a risk (scrapie) and those for which data is lacking (atypical
scrapie, H- and L-type BSE and BSE in sheep).36 In assessing whether or not
human prion diseases might have an animal origin, it is important to have a
proper understanding of the clinicopathological heterogeneity of the sporadic
human prion diseases, because it is against this backdrop that any new acquired
forms of the disease will be seen and from which it will need to be
distinguished.
Sporadic CJD and variably protease-sensitive prionopathy
Sporadic CJD is the most commonly occurring human prion disease; it occurs
world-wide and it has long been known to be clinically and pathologically
heterogeneous. The molecular basis for this heterogeneity is currently thought
to reside in a combination of the PRNP codon 129 polymorphic status of the
patient (MM, MV, or VV) and the type (type 1 or type 2) of the
protease-resistant component of PrPSc determined by protease K digestion and
Western blotting (termed PrPres).37,38 The original sCJD sub-classification
system of Parchi et al. that recognized six sCJD subtypes (MM1/MV1, MM2c, MM2t,
MV2,VV2 and VV1) has had to be modified to accommodate the growing number of
cases recognized to contain both type 1 and type 2 PrPres in different or
sometimes the same regions of the brain.39,40 Moreover, intensive surveillance
and investigation of forms of human prion disease that lack PRNP mutation and
known risk factors has identified another sporadic human prion disease, termed
protease-sensitive prionopathy (VPSPr).41While intensively investigated, the
etiology and diversity of the sporadic human prion diseases remain poorly
understood.
snip...
There is also a potentially important practical corollary to the idea of
prion-like spread, which may affect future stem cell therapies for
neurodegenerative diseases. Presumably therapeutic stem cell-derived neurons
would be equally susceptible to “infection” (with misfolded protein aggregates)
as the patient’s own cells, unless steps were taken to prevent this,55 the most
obvious of which would be to prevent expression of the gene product that can be
converted to a pathological prion-like isoform.The suggestion that a prion-like
mechanism of spread of molecular pathology underlies diseases as diverse as
Alzheimer’s disease and Parkinson’s disease has led some researchers to explore
whether the molecular pathology of these diseases is transmissible in an
experimental setting56–58 and to suggest that perhaps some cases of these more
common neurodegenerative illnesses might, like CJD, be acquired.58,59
snip...
MOLECULAR BASIS OF HUMAN PRION DISEASES Molecular strain typing Molecular
strain typing in the form of classifying the mobility and glycoform ratio of
protease-resistant prion protein byWestern blotting is a remarkably useful
adjunct to neuropathological assessment during the post-mortem diagnosis of
human prion diseases (Fig. 1). The glycoform ratio difference between vCJD and
all forms of sCJD is a remarkably robust phenomenon, although the mechanism
underlying it remains obscure. All cases of vCJD examined show type 2B PrPres,
irrespective of brain region assayed and the PrPres type is also found in
lymphoreticular tissues, albeit with presumably tissue-specific minor
modification of mobility and an accentuation of the glycoform ratio. Similarly
sCJD cases are characterized by a narrow range of glycoform ratios, distinct
from vCJD, and the presence of either type 1 or type 2 PrPres (type 1A and type
2A).The PrPres types found in the brain in iCJD and kuru resemble those found in
sCJD (type 1A and type 2A), from which they were presumably derived. Individual
cases of gCJD, GSS and FFI usually have type 1 or type 2 PrPres, but with a
glycoform ratio in which the non-glycosylated component is under-represented
(which we have termed A/B). However, this is not always true and a broad
spectrum of glycoform ratios can be found in genetic prion diseases. Moreover,
some cases of GSS are characterized by an approximately 8 kDa (N- and
C-terminally truncated) PrPres fragment, and some cases of FFI have little
detectable PrPres at all. Despite the diagnostic utility, a simple one-to-one
correspondence between PrPres type and disease phenotype (and by implication to
agent strain) seems unlikely in principle and is complicated by the facts.
First, the choice of analyzing only that fraction of PrPSc which survives a
particular concentration of protease may seem arbitrary. Second, the
interpretation of a molecular population variable, such as glycosylation site
occupancy, as conforming to two or three discrete types, could be seen as
simplistic. Lastly, protease digestion may be considered to be a somewhat blunt
instrument to distinguish secondary and higherorder conformational differences
in PrPSc. Even when genotype (mutations and polymorphisms) is taken into
account, three major types (1, 2, 8 kDa) and three wild-type genotypes (MM,MV
and VV) provide insufficient molecular variation to account for all the
phenotypic variations observed. For example, two forms of sCJD share methione
homozygosity and type 2A PrPres but one form closely resembles FFI (without the
causative mutation) and the other is CJD-like.8 Two more substantial problems,
which may point toward a more subtle and perhaps informative approach to PrPSc
analysis, are discussed below. The co-occurrence of PrPres types 1 and 2 Once
controversial, the idea that PrPSc in individual cases might be composed of
mixtures (or different types co-occurring) is now well recognized and
accepted.40,70 There are probably two phenomena at play here. One is the finding
of different predominant types in individual samples from different parts of the
brain or more rarely approximately equal amounts of type 1A and type 2A in the
same sCJD brain samples.The other is the observation made using antibodies that
specifically recognize type 1 or type 2 PrPres, that a minority type always
accompanies a majority type in sCJD and vCJD, albeit at sub-detectable levels
when conventional antibodies are used.71–75 The former issue is more tractable
and a consensus is beginning to emerge that when multiple brain sampling and
sensitive co-detection is performed on cohorts of sCJD cases, a plateau is
reached at between 30–40% of cases showing co-occurrence. Our own data examining
four regions (temporal cortex, parietal cortex, occipital cortex and thalamus)
instead of frontal cortex only, shows a rise in detected co-occurrence from 3%
to 24% of cases.76 Interestingly, only very rarely did this re-analysis involve
a change in the predominant type found in the brain overall. Parchi et al. have
offered a revised version of their 1999 sporadic CJD classification system that
adds mixed type to the original “pure” types and have shown that the most common
of these 12 sCJD subtypes can be recognized on histological grounds, without
reference to biochemical analysis.39,40,77 It will be interesting to see in the
fullness of time whether this additional complexity reflects a more refined
series of discrete clinicopathological phenotypes or whether it is indicative of
a spectrum of phenotypes depending on the spacio-temporal accumulation of PrPSc
types set against the patient genotype.78
Variably protease-sensitive prionopathy The phenotypic complexity of the
sporadic forms of human prion disease has increased with the report of a new
sporadic human prion disease, termed variably proteasesensitive prionopathy
(VPSPr) that is distinct from previously recognized sub-types of sCJD.41,79
There are no mutations in the open reading frame of PRNP. The patients have no
known risk factors for the disease, but the disease is most common in theVV
genotype, as opposed to sCJD, which is most common in the MM genotype. The
neuropathology involves medium-sized vacuolation and characteristic
microplaques. Durations of illness can be very long and this coupled with
symptoms that do not conform well to CJD have prompted speculation that the
condition may be under-ascertained. The most interesting aspect of the disease
from a biochemical perspective is that although PrPSc is abundantly present in
the brain, PrPres is difficult to detect because of its sensitivity to
proteolysis and because what remains after proteinase K (PK) digestion is both
C- and N-terminally cleaved by PK digestion and seen as a faint 8 kDa band on
Western blots (Fig. 2). The degree of protease resistance is reported to reflect
the codon 129 genotype, withVV being least resistant andMM being most resistant,
despite having the same 8 kDa PrPres fragment predominating.79We have identified
two cases of VPSPr prospectively in the UK80,81 and recently completed a
retrospective review for such cases confirming many of the original observations
by Gambetti and colleagues.41,79 Our work has shown that some areas of the VPSPr
brain contain PrPres similar in appearance to that found in sCJD and conversely
that some cases of sCJD have a very minor PrPres band similar to the 8 kDa
PrPres band that typifies VPSPr.82
snip...
The biochemical basis of the strain phenomenon The results of transmission
of individual samples from single examples of the six different Parchi et al.39
sCJD subtypes (MM1/MV1, VV1, MM2c, MV2, VV2) into humanized transgenic mice
suggest the existence of four distinct sCJD agents, termed M1, M2, V1 and V2,
and a fifth strain corresponding to MM2t or sporadic fatal insomnia.99,100
Interestingly, when we performed formally analogous experiments in the cell-free
PMCA reaction, similar results were obtained: The PrPres type of the seed was
conserved in the PMCA product and the efficiency of conversion appeared to be
determined by compatibility at codon 129 of PRNP.101 The behavior of the seeds
from heterozygous patients were particularly interesting, in that MV1 sCJD seeds
selectively amplified in MM substrate producing type 1 PrPres and MV2 sCJD seeds
selectively amplified in VV substrate producing type 2 PrPres (Fig. 6). These
results reinforce the association between methionine at codon 129 and the
production of type 1 PrPres and valine at codon 129 and the production of type 2
PrPres.
EMERGING RISKS Zoonotic disease BSE is the only animal prion strain with
demonstrated pathogenicity for humans.While it is tempting to suggest that
scrapie might represent the animal reservoir that results in some cases of sCJD,
there is no epidemiological evidence to support this hypothesis. The
pathogenicity of new or newly described animal prion diseases for humans is
unclear and this is particularly true for H- and L-type BSE, atypical scrapie
and for chronic wasting disease (CWD), all of which are probably consumed. Human
susceptibility has been modeled by attempted transmission to (humanized)
transgenic mice with sometimes conflicting results, depending on the transgenic
model used and depending upon whether central or peripheral tissues are
examined.102–106 We have attempted to establish whether PMCA can model the
molecular component of these hypothetical cross-species transmission events.107
The existing data correspond well with the established facts. First, PrPSc in
vCJD brain samples amplifies most efficiently in humanized mouse MM substrate,
less efficiently in MV substrate and not at all in VV. Cattle BSE PrPres is less
efficient than vCJD, but shows the same substrate genotypic preference. Sheep
scrapie fails to amplify detectably in any of the three substrates; however,
sheep BSE PrPres does amplify, again with a codon 129 preference for methionine
(Fig. 7). We are currently extending this approach to encompass atypical
scrapie, H- and L-type BSE and CWD using human rather than humanized PMCA
substrates.
Secondary infection
In the same way that animal reservoirs cannot be completely excluded as
causes of individual sCJD cases, neither can other environmental sources, such
as medical procedures. The known routes of iatrogenic CJD acquisition are
historically growth hormone therapy, dura mater grafting, corneal grafting and
certain highly specialized neurosurgical procedures. The secondary transmission
of vCJD by blood transfusion and experimental evidence showing the efficiency of
the transfusion of viable blood cells between scrapie and BSE-infected and naive
sheep have prompted a reappraisal of transfusion-transmitted CJD, including
consideration being given to the possibility of prion blood testing or
filtration.25,26,108,109
Blood transfusion is the original and most extensively used cellular
therapy, but we may be on the threshold of a new era of cellular therapies based
on embryonic stem cell and induced pluripotent stem cell technologies. Although
the potential for stem cell therapy-mediated prion transmission might be judged
remote, this was also considered to be the case for transfusion transmission of
CJD before 2004.
snip...
SUMMARY AND PERSPECTIVE While the prospect of a major epidemic of vCJD in
the UK and elsewhere seems to be receding, there remain a series of
uncertainties surrounding the eventual numbers of individuals that will suffer
from this devastating condition.The issues include the effects of genotype on
susceptibility and the possible existence of substantial numbers of asymptomatic
infected individuals that may pose risks of onward transmission. sCJD remains
the most frequently occurring human prion disease and arguably the least well
understood. Other idiopathic forms of human prion disease (such as VPSPr),
characterized by protease-sensitive forms of the prion protein, also exist and
their true prevalence may be hard to ascertain. The possible risks from newly
described animal prion diseases and from emerging cellular therapies are
currently poorly quantified. On a more theoretic level the prion hypothesis has
provided a unifying conceptual framework for TSE research and provided a
paradigm to interrogate the similarities and differences between the diverse
neurodegenerative conditions involving prion-like mechanisms of molecular
pathology.
Thursday, February 21, 2013
National Prion Disease Pathology Surveillance Center Cases Examined January
16, 2013
16 YEAR OLD SPORADIC FFI ?
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
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25,
2012
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Wednesday, June 13, 2012
MEXICO IS UNDER or MIS DIAGNOSING CREUTZFELDT JAKOB DISEASE AND OTHER PRION
DISEASE SOME WITH POSSIBLE nvCJD
Thursday, April 4, 2013
Variably protease-sensitive prionopathy in the UK: a retrospective review
1991–2008
Brain (2013) 136 (4): 1102-1115. doi: 10.1093/brain/aws366
Sunday, March 31, 2013
Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years
old, shall we pray
Tuesday, March 05, 2013
A closer look at prion strains Characterization and important implications
Prion
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
Tuesday, May 28, 2013
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a
methodological outline for evidence-based guidance
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
Saturday, May 25, 2013
Brain homogenates from human tauopathies induce tau inclusions in mouse
brain
Tuesday, May 21, 2013
IS ALZHEIMER’S DISEASE A PRION DISEASE? the possible secondary transmission
by blood transfusion are posed
Tuesday, May 7, 2013
Proteinopathies, a core concept for understanding and ultimately treating
degenerative disorders?
Monday, September 26, 2011
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS,
gCJD, hvCJD, sCJD, TSE, PRION, update 2011
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids,
Prionpathy, Prionopathy, TSE
TSS
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