Tuesday, June 4, 2013

INTERPRETING RESULTS OF FSIS VERIFICATION SAMPLING OF DOMESTIC BEEF PRODUCT DERIVED FROM ADVANCED MEAT RECOVERY SYSTEMS (AMR01/FAMR01) FSIS Notice 38-12

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.


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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


__________________________________________________










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.


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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


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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


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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.




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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


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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


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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.


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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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