Monday, January 28, 2013

U.S. Trade Representative Ron Kirk and Agriculture Secretary Tom Vilsack Announce Agreement to Further Open Japan’s Market to U.S. Beef

Press Release No.: PENDING




Contact: USDA Office of Communications




(202) 720-4623




U.S. Trade Representative Ron Kirk and Agriculture Secretary Tom Vilsack Announce Agreement to Further Open Japan’s Market to U.S. Beef




Washington, D.C. – United States Trade Representative Ron Kirk and United States Agriculture Secretary Tom Vilsack today announced that the United States and Japan have agreed on new terms and conditions which pave the way for expanded exports of U.S. beef and beef products to Japan. Under these new terms, which enter into effect on February 1, 2013, Japan will now permit the import of beef from cattle less than 30 months of age, compared to the previous limit of 20 months, among other steps. It is estimated that these important changes will result in hundreds of millions of dollars in exports of U.S. beef to Japan in the coming years. This agreement also goes a long way toward normalizing trade with Japan by addressing long-standing restrictions that Japan introduced in response to bovine spongiform encephalopathy (BSE).




“This is great news for American ranchers and beef companies, who can now – as a result of this agreement – increase their exports of U.S. beef to their largest market for beef in Asia,” said Ambassador Kirk. “This represents a significant and historic step in expanding U.S. beef trade with Japan and growing American exports and jobs here at home. We welcome Japan’s action.”




“Today’s announcement reflects another successful effort by the Obama Administration that boosts the bottom line for America’s agriculture. We are in the most successful period in history for America’s agriculture sector, with agricultural exports this year expected to set yet another record,” said Secretary Vilsack. “We will continue our efforts to break down barriers and expand access for high-quality, safe and wholesome U.S. food and agricultural products to Japan and around the world.”




The two governments also agreed to regular and ad hoc consultations to review progress under the agreement and address any issues that may arise. In an accompanying letter exchange, Japan also confirms its ongoing BSE risk assessment by its Food Safety Commission (FSC), which includes a consideration of raising the age limit above 30 months for beef and beef product imports from the United States, taking into account international standards. To view the letter from Ambassador Kirk and Secretary Vilsack to Ambassador Sasae, click here. To view the letter from Ambassador Sasae to Ambassador Kirk and Secretary Vilsack, click here.




Background




In December 2003, Japan banned U.S. beef and beef products following the detection of a bovine spongiform encephalopathy (BSE)-positive animal in the United States. In July 2006, Japan partially reopened its market to allow imports of some U.S. beef from animals aged 20 months or younger produced under a special program for Japan.




In December 2011, at the request of Japan’s Ministry of Health, Labor and Welfare (MHLW), Japan’s independent Food Safety Commission (FSC) initiated a risk assessment to examine raising the maximum age of the cattle from which U.S. and certain other foreign beef and beef products could be exported to Japan, as well as revising the definition of specified risk materials (SRMs). (SRMs are certain cattle tissues that can carry the BSE agent.) Based on an FSC risk assessment released last October, Japan entered into consultations with the United States to revise the import requirements, including raising the age limit for U.S. cattle and adopting a revised definition of SRMs for U.S. beef and beef product imports that is closely aligned with international standards of the World Organization for Animal Health (OIE).




# # #










now, for the rest of the story ;






THE TRUTH





Friday, January 25, 2013



Japan may relax US Mad Cow BSE beef import rules in Feb 2013










Saturday, August 4, 2012


Final Feed Investigation Summary - California BSE Case - July 2012








Tuesday, July 17, 2012


O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012









Wednesday, May 25, 2011


O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011


----- Original Message -----


From: Terry S. Singeltary Sr.


To: BSE-L@LISTS.AEGEE.ORG


Cc: trade@oie.int ; oie@oie.int ; f.diaz@oie.int ; scientific.dept@oie.int ; cjdvoice@yahoogroups.com ; BLOODCJD@YAHOOGROUPS.COM


Sent: Tuesday, May 24, 2011 2:24 PM


Subject: O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011








Saturday, December 18, 2010


OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011








Monday, November 23, 2009


BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E. COMMISSION DECISION of 11 November 2009 amending the Annex to Decision 2007/453/EC as regards the BSE status of Chile, Colombia and Japan (notified under document C(2009) 8590)









Tuesday, January 1, 2008


BSE OIE USDA


Subject: OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local cattle dealers i.e. USDA


Date: May 14, 2007 at 9:00 am PST


OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local cattle dealers i.e. USDA


STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION


March 9, 2007










Tuesday, November 02, 2010


IN CONFIDENCE


The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".


BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992









2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006









Comments on technical aspects of the risk assessment were then submitted to FSIS.


Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.


This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:









Owens, Julie


From: Terry S. Singeltary Sr. [flounder9@verizon.net]


Sent: Monday, July 24, 2006 1:09 PM


To: FSIS RegulationsComments


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)


Page 1 of 98









FSIS, USDA, REPLY TO SINGELTARY









U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001













Thursday, January 17, 2013



Canada, U.S. agree on animal-disease measures to protect trade, while reducing human and animal health protection











Monday, December 31, 2012





Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012















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














TSS

Saturday, November 10, 2012

Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials

Nov 9, 2012 WI Firm Recalls Beef Tongues


Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials


Recall Release CLASS II RECALL FSIS-RC-073-2012 HEALTH RISK: LOW


Congressional and Public Affairs Adam Tarr (202) 720-9113


WASHINGTON, Nov. 9, 2012 – Black Earth Meat Market Inc., a Black Earth, Wis. establishment, is recalling approximately 99 pounds of beef tongue products because they 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.


The products subject to recall are: [View Labels (PDF Only)]


Various size cases of Black Earth Meats Natural Beef Tongues and Black Earth Meats Local Beef Tongues produced on October 8, 11, 17 and 18, 2012.


The products bear Est. 34379 inside the USDA mark of inspection and were distributed to a restaurant in Wisconsin and a distributor in Illinois.


The problem was discovered during a routine Food Safety Assessment at the establishment. 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. There is no indication that any of the cattle slaughtered displayed any signs of BSE.


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.


Consumers and media with questions about the recall should contact Bartlett Durand, Managing Member, at (608)767-3940.


Consumers with food safety questions can "Ask Karen," the FSIS virtual representative available 24 hours a day at AskKaren.gov or via smartphone at m.askkaren.gov. "Ask Karen" live chat services are available Monday through Friday from 10 a.m. to 4 p.m. ET. 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. #






Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU


Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation






Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>


Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)






Saturday, July 23, 2011


CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE







Sunday, February 5, 2012


February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE







Tuesday, April 24, 2012


MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA







Wednesday, April 25, 2012


4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012







Thursday, April 26, 2012


Update from USDA Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States WASHINGTON bulletin at 04/26/2012 10:11 PM EDT








Tuesday, May 1, 2012


BSE MAD COW LETTERS TO USDA (Tom Vilsack, Secretary of Agriculture) and FDA (Magaret Hamburg, Commissioner of FDA) May 1, 2012







Wednesday, May 2, 2012


ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH







Friday, May 4, 2012


May 2, 2012: Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States






Sunday, May 6, 2012


Bovine Spongiform Encephalopathy Mad Cow Disease, BSE May 2, 2012 IOWA State University OIE







Wednesday, May 16, 2012


OIE UPDATE BOVINE SPONGIFORM ENCEPHALOPATHY UNITED STATES OF AMERICA MAY 15, 2012







Friday, May 18, 2012


Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012







Thursday, June 14, 2012


R-CALF USA Calls USDA Dishonest and Corrupt; Submits Fourth Request for Extension


R-CALF United Stockgrowers of America







Monday, June 18, 2012


R-CALF Submits Incomplete Comments Under Protest in Bizarre Rulemaking “Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products”







Wednesday, June 27, 2012


First US BSE Case Since 2006 Underscores Need for Vigilance


Neurology Today 21 June 2012







Tuesday, July 17, 2012


O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 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







Saturday, August 4, 2012


***Final Feed Investigation Summary - California BSE Case - July 2012







Monday, August 06, 2012


Atypical neuropathological sCJD-MM phenotype with abundant white matter Kuru-type plaques sparing the cerebellar cortex







USDA TRIPLE BSE MAD COW FIREWALL, SRM, FEED, AND SURVEILLANCE

















2012




***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...








MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...


***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model







***Infectivity in skeletal muscle of BASE-infected cattle







***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.







***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.







The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.


In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.







Friday, May 11, 2012


Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits


***support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE






Thursday, June 21, 2012



Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism



Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M. Nicholson1


1 National Animal Disease Center, United States Department of Agriculture, Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa State University, Ames, Iowa, United States of America


Abstract


The majority of bovine spongiform encephalopathy (BSE) cases have been ascribed to the classical form of the disease. Htype and L-type BSE cases have atypical molecular profiles compared to classical BSE and are thought to arise spontaneously. However, one case of H-type BSE was associated with a heritable E211K mutation in the prion protein gene. The purpose of this study was to describe transmission of this unique isolate of H-type BSE when inoculated into a calf of the same genotype by the intracranial route. Electroretinograms were used to demonstrate preclinical deficits in retinal function, and optical coherence tomography was used to demonstrate an antemortem decrease in retinal thickness. The calf rapidly progressed to clinical disease (9.4 months) and was necropsied. Widespread distribution of abnormal prion protein was demonstrated within neural tissues by western blot and immunohistochemistry. While this isolate is categorized as BSE-H due to a higher molecular mass of the unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with monoclonal antibodies 6H4 and P4, and a second unglycosylated band at approximately 14 kDa when developed with antibodies that bind in the C-terminal region, it is unique from other described cases of BSE-H because of an additional band 23 kDa demonstrated on western blots of the cerebellum. This work demonstrates that this isolate is transmissible, has a BSE-H phenotype when transmitted to cattle with the K211 polymorphism, and has molecular features that distinguish it from other cases of BSE-H described in the literature.



snip...



Most significantly it must be determined if the molecular phenotype of this cattle TSE remains stable when transmitted to cattle without the E211K polymorphism as several other isolates of atypical BSE have been shown to adopt a molecular profile consistent with classical BSE after passage in transgenic mice expressing bovine PrPC [40] or multiple passages in wild type mice [23]. Results of ongoing studies, namely passage of the E211K Htype isolate into wild-type cattle, will lend further insight into what role, if any, genetic and sporadic forms of BSE may have played in the origins of classical BSE. Atypical cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins highlight that it may not be possible to eradicate BSE entirely and that it would be hazardous to remove disease control measures such as prohibiting the feeding of meat and bone meal to ruminants.








P.4.23



Transmission of atypical BSE in humanized mouse models



Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA



Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.



Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.



Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.



Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.



Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.










P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS



Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA



Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.



III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)














I ask Professor Kong ;



Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment


''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''


Professor Kong reply ;


.....snip


''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''


Best regards,


Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA




END...TSS




Thursday, December 04, 2008 2:37 PM


"we have found that H-BSE can infect humans."


personal communication with Professor Kong. ...TSS




BSE-H is also transmissible in our humanized Tg mice.


The possibility of more than two atypical BSE strains will be discussed.


Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.













let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.




please see history of infamous atypical ghBSE Alabama style. the second Texas mad cow that was finally documented, was the ‘typical’ atypical h-BSE, not genetic. ...tss




Tuesday, November 6, 2012


Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and Sporadic CJD, November-December 2012 update







TSS

Tuesday, September 11, 2012

Japan Moves Closer To Raising 20-Month Age Limit For Beef Imports, and further risk consumer to CJD

Japan Moves Closer To Raising 20-Month Age Limit For Beef Imports


The Japanese government this week took a new step toward relaxing its current restrictions on imports of beef from the U.S. and three other countries when a panel of experts from the country's Food Safety Commission found that allowing the sale of beef from cattle up to 30 months of age from those countries instead of the current 20 months poses a "negligible" risk to human health, according to a Japanese official.1082 words







Japan Moves Closer To Raising 20-Month Age Limit For Beef Imports


The Japanese government this week took a new step toward relaxing its current restrictions on imports of beef from the U.S. and three other countries when a panel of experts from the country’s Food Safety Commission found that allowing the sale of beef from cattle up to 30 months of age from those countries instead of the current 20 months poses a “negligible” risk to human health, according to a Japanese official.


The experts also recommended that the Japanese government loosen its definition of specified risk materials (SRMs) that must be removed from beef before they can be sold in Japan, a move that would also facilitate U.S. beef exports to the country, according to the official.


For instance, U.S. exporters cannot currently ship T-bone steaks from cattle 20 months or under to Japan because that cut of meat includes a portion of the cow’s spinal column. Japan’s current import rules consider the head, spinal cord and spinal column from cattle of all ages to be SRMs. The experts recommended that Japan relax this definition so that these parts of the animal would only be considered SRMs if they are from cattle older than 30 months. This is the same definition used by the U.S.


Both of these recommendations were part of a draft risk assessment approved on Sept. 5 by a subcommittee of the Food Safety Commission that would apply to imports of beef from U.S., Canada, France and the Netherlands. All of these countries are considered by the World Organization for Animal Health to pose a “controlled risk” for bovine spongiform encephalopathy (BSE), also known as mad cow disease.


A separate risk assessment would be required for other countries looking to have the BSE age restrictions relaxed for their exports, the official added. But the draft risk assessment contains recommendations for relaxing BSE restrictions both for domestic Japanese and imported beef.


For example, the draft risk assessment recommended that the looser definition of specified risk materials would also apply domestically as well as for imports.


In addition, while Japan currently requires that domestic cattle over 20 months of age undergo mandatory “blanket” BSE testing at the time of slaughter, the draft risk assessment recommends that this testing be limited to cattle over 30 months, the official said.


The draft risk assessment still needs to be approved by the entire Food Safety Commission, which could happen this month, either at its Sept. 10 meeting or a subsequent one on Sept. 24. This would be followed by a round of public comments to be submitted within 30 days, which would be analyzed before the commission would consider a final risk assessment. Once that is approved, the commission would turn over the issue to the Ministry of Health.


The Office of the U.S. Trade Representative and Sen. Max Baucus (D-MT) on Sept. 5 praised the action by Japan as a positive step toward greater market access for U.S. beef exporters.


“We welcome the important step taken by Japan’s risk assessment body and we look forward to an expeditious conclusion to the risk assessment process,” a USTR spokeswoman said in an e-mail.


Baucus, who last month met with Japanese officials in Tokyo to discuss the beef restrictions and other trade issues, said in a statement he was encouraged by the steps taken today by the Japanese government. “We’re headed in the right direction,” Baucus said. “U.S. beef — from cattle of all ages — is the safest in the world and I am confident we will continue to expand exports on the global market.”


The U.S. Meat Export Federation (USMEF) also praised the subcommittee’s approval of the draft risk assessment in a separate statement, calling it an “important step in Japan’s process of bringing its import regimen into conformance with international standards.” In a Sept. 5 interview, USMEF spokesman Joe Schuele said it will likely take until late 2012 or early 2013 for Japan to complete its regulatory process and formally amend its import rules.


The Japanese government first announced in December that it would request a risk assessment from Food Safety Commission to determine whether the risk of consuming beef from U.S. cattle up to 30 months in age is higher than the risk of consuming beef from cattle no older than 20 months (Inside U.S. Trade, Dec. 23). The commission is an independent body under the purview of the Japanese prime minister’s cabinet.


The U.S. has pushed for Japan to relax its restrictions on U.S. beef exports as one confidence-building measure that would facilitate Japan’s entry into the Trans-Pacific Partnership talks (Inside U.S. Trade, June 15). While Japan has expressed an interest in joining TPP talks and held consultations with the U.S. and other TPP partners about that possibility, it has not yet made an internal decision about whether to join.


After approving a final risk assessment, the Food Safety Commission would forward it to Japan’s Ministry of Health, which would open negotiations with the four affected trading partners to discuss import inspection protocols and other technical measures.


Those negotiations would touch upon issues such as ensuring that each trading partner has a verification system in place to determine that cattle slaughtered for shipment to Japan are 30 months or younger. They would also likely determine what procedure Japan would follow in the event it discovers a shipment that does not comply with the new age requirements.


After Japan has completed those negotiations with the U.S. and other trading partners, Japan’s Health Ministry would have to make a final decision on changing the import rules. It would then inform the general public and an advisory council of the decision, the official said.


Subsequently, the health and agriculture ministries would formally amend the import requirements by sending out updated instructions to customs authorities and posting the changes on their websites, according to the official.


Sources have said they do not expect eventual U.S.-Japan negotiations over the new import protocol to be a major challenge given that the U.S. already has a verification system in place to ensure beef exports to Japan come from cattle 20 months and younger, and has similar system for verifying that beef sent to South Korea is from cattle 30 months and younger.










Alternative BSE Risk Assessment Methodology for Beef and Beef Offal Imported into Japan



Yasuhiro YOSHIKAWA1)*, Motohiro HORIUCHI2), Naotaka ISHIGURO3), Mutsuyo KADOHIRA4), Satoshi KAI5), Hidehiro MIZUSAWA6), Chisato NAGATA7), Takashi ONODERA8), Tetsutaro SATA9), Toshiyuki TSUTSUI10), Masahito YAMADA11) and Shigeki YAMAMOTO12)



1)School of Veterinary Medicine, Kitasato University, 23–35–1 Higashi, Towada, Aomori 034–8628, Japan



2)Laboratory of Veterinary Hygiene, Department of Applied Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido 060–0818, Japan



3)Laboratory of Food and Environmental Hygiene, Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu 501–1193, Japan



4)Department of Life Science and Agriculture, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido 080–8555, Japan



5)Faculty of Business, Marketing and Distribution, Nakamura Gakuen University, Fukuoka, Fukuoka 814–0198, Japan



6)Department of Neurology and Neurological Science, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo 113–8619, Japan



7)Department of Epidemiology & Preventive Medicine, Graduate School of Medicine, Gifu University, Gifu 501–1193, Japan



8)Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1–1–1 Yayoi, Bunkyo-ku, Tokyo 113–8657, Japan



9)Department of Pathology, National Institute of Infectious Diseases, Toyama, Shinjuku-ku, Tokyo 162–8640, Japan



10)Epidemiological Research Team, National Institute of Animal Health, Tsukuba, Ibaraki 305–0856, Japan



11)Department of Neurology and Neurobiology of Aging, Graduate School of Medical Science, Kanazawa University, Kanazawa 920–8640, Japan



12)Division of Biomedical Food Research, National Institute of Health, Yoga, Setagaya-ku, Tokyo 158–8501, Japan



(Received 11 September 2010/Accepted 31 October 2011/Published online in J-STAGE 14 November 2011)





snip...




Recently, there have been a few cases of irregular forms of BSE (atypical BSE) reported apart from classical BSE in Europe, Japan and the U.S.A. These reports of atypical BSE indicated variation in molecular sizes of abnormal prion proteins (PrPSc) among cases, and eventually two major sizes of proteins were designated as the H and L types. Most of the atypical BSE cases were found in aged cattle over 8 years old, but a remarkable exception exists in Japan, where a steer only 23 months old was reported to have been infected with atypical BSE (the 8th BSE case in Japan). When this exception was excluded, the detection ages of atypical BSE cases ranged from 6.3 to 18 years old. The average detection ages for the H and L types were 11.8 and 11.6 years old, respectively [3].




To the best of the authors’ knowledge, there have been about 40 cases of atypical BSE reported worldwide, yet the OIE does not require distinction between classical and atypical BSE cases in member countries for their reports, while the EFSA only recently referred to case reporting by classical/atypical recognition in its 2009 scientific opinion. These situations seem to further obscure the clear number of atypical BSE cases occurring in the world.




The origin of atypical BSE has not yet been determined. According to EFSA’s scientific opinion published in 2008, all the cases of atypical BSE were reported with birth dates before the real feed ban in January 2001 in Europe. Therefore, the possibility of these atypical cases being attributed to contaminated feeds, just as in classical BSE, cannot be completely denied. On the other hand, data of atypical BSE cases (both the H and L types) in France did not show any reasonable correlation between birth year and frequency of occurrence, as was indicated in classical BSE cases, thus raising the possible interpretation of atypical BSE being sporadic isolated cases of prion disease [3].




Based on the data accumulated in France, the frequencies of atypical BSE cases per 1 million tested adult cattle were estimated to be 0.41 and 0.35 cases for the H and L types, respectively (1.9 and 1.7 cases for the H and L-types, respectively, when limiting the sampling to tested cattle over 8 years old). In Japan, a total of 10 million cattle including fallen stock and slaughtered cattle were tested for BSE, and the results showed no positive cases of the H type and 2 positive cases (case 8, a 23-month-old steer; case 24, a 169-month-old Japanese black cow) of the L type of atypical BSE. These data indicate that Japan has prevalence frequencies of 0 and 0.2 cases of the H and L types of atypical BSE per 1 million cattle including tested fallen stock and slaughtered cattle (zero and approximately 1.5 cases of the H and L types respectively, when limiting the sampling to tested slaughtered cattle over 8 years old).




Atypical BSE of both the H and L types was confirmed to be transmissible by intracerebral inoculation in transgenic mice expressing alleles of bovine or ovine PrP genes and of inbred mice. However, for transgenic mice expressing human prion protein, the L type but not the H type could be transmitted according to the previously published reports (recently, it was reported that H type also transmissible to the humanized transgenic mice). There have also been reports of glycosylation pattern transformation from L-type BASE3 PrPSc-like type to more of the classical BSE PrPSc type. This phenomenon was observed during passage using inbred and transgenic TgVR2 mice. As for the atypical cases of BSE confirmed in Japan, the 24th case of BSE was determined to have had the atypical L type at the detection age of 169 months old, and its sample was successfully transmitted to transgenic mice expressing bovine prion protein. However, transmission of a sample from the other case of atypical L-type BSE confirmed in Japan (the 8th case; detected at the age of 23-month-old) was reported to be unsuccessful in transgenic mice expressing bovine prion protein. The reason for this inconsistency is not clear at this time, although the possible presence of a limitation in the amount of prion protein accumulated in the subject’s brain sample or that the inoculated volume was too low to reach the detection limit cannot be excluded.




A recent report has shown that the atypical L type of BSE has a higher degree of potential for pathogenicity than that its classical counterpart because incubation periods are shorter in atypical BSE transmitted to transgenic mice expressing human prion protein, suggesting that atypical BSE possibly has a higher degree of pathogenicity when compared to its classical counterpart [7].




In contrast to classical BSE, the systemic distribution of abnormal prion protein in atypical BSE cases is barely known. Therefore, it is unclear whether the brainstem is truly the optimal part for sampling and testing in H/L type detection. Likewise, information regarding the infectivity distribution of atypical BSE is scarce in bovine peripheral tissues and body fluid. All together, the lack of essential data hinders, to a certain extent, evaluation of the relative risk-reducing effects of various SRM removal measures for cattle.




Based on the currently available data concerning the potential risks for humans of atypical BSE and prevalence of atypical BSE, it may be too extreme to deny the risk of MRM, especially in MRM derived from aged cattle. However, the degree of influence of the presence of atypical BSE on our concept of the MRM risk will be limited to a low level under the circumstances with presently available knowledge and our discussion. In the meantime, one must also be reminded of the fact that only a limited amount of data is currently available concerning atypical BSE. A proper amount of dis cretion should be used when interpreting these data to avoid unnecessary confusion. Further research and accumulation of data will bring additional insight into the mechanism, pathogenicity and transmission potential of atypical BSE, for which further assessment may become necessary in the future.




To gain the final result of this assessment, the periodic BSE risk status of a country (the sum of invasive BSE risk and domestic stability) and efficacy of present BSE riskreducing measures at meat processing lines were combined and used as an indicator of comprehensive likelihood of BSE prion contamination in beef and beef offal imported into Japan. Surveillance data were used to verify reliability of the assessment. Finally, a summary of each country was expressed in schematic figures (an example is shown in Fig. 4). In Fig. 4, a model country’s invasive risk was ranked as high (from 1986–2005) but was reduced to the middle level from 2006 onwards. The efficacy of feed ban (domestic stability) was unstable during 1986–1989 but improved to the middle level (1990–1996), to the stable level (1997–2000) and then to the very stable level (2001-until now). Current risk reduction efficacy at meat processing lines, determined by factors such as the definition of SRM, compulsory removal of SRM by law, and HACCP/SSOP procedures were good and verified and were therefore rated as ◎. BSE testing at slaughterhouse (>30 months), proper slaughtering procedures such as avoidance of air stunning and pithing were verified as ◎. All together, the overall risk reduction was extremely effective.




The final assessment for this model country was as follows: the domestic BSE exposure/propagation risk was low, and risk reduction at meat processing lines was extremely effective; therefore, the risk of BSE contamination of beef and beef offal imported from this assessed country was considered to be negligible.




RISK ASSESSMENT OF BEEF AND BEEF OFFAL IMPORTED INTO JAPAN









Tuesday, July 17, 2012


O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012







Monday, September 3, 2012


2012 JAPAN BANS DEER AND ELK MEAT AND ALLOWS SOME BEEF PRODUCTS, what about TSE prion concerns ?






We can confirm that of the 100 cases, 49 were under 30 months of age, of these the youngest case was 20 months old.


BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS


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


Information released on 2 February 2005 Summary of information requested What statistics are available on cattle less than 30 months of age found to have BSE? Information released VLA has recorded approximately 100 cases of BSE in cattle of 30 months of age or under during the entire period of the BSE epidemic (1986 - 2005). The figure is approximate as for 51 of these the age is only estimated. This is because farmers did not have accurate documentation to confirm birth date. This was not a requirement at the time. We can confirm that of the 100 cases, 49 were under 30 months of age, of these the youngest case was 20 months old.


Information released on 2 February 2005 Summary of information requested What statistics are available on cattle less than 30 months of age found to have BSE?


Information released VLA has recorded approximately 100 cases of BSE in cattle of 30 months of age or under during the entire period of the BSE epidemic (1986 - 2005). The figure is approximate as for 51 of these the age is only estimated. This is because farmers did not have accurate documentation to confirm birth date. This was not a requirement at the time.


We can confirm that of the 100 cases, 49 were under 30 months of age, of these the youngest case was 20 months old.









Youngest confirmed case 20 Months, Oldest confirmed case 22 Years, Data valid to 01 April 2008







BSE Youngest and oldest cases by year of onset - GB 20 months, 21 months, (8) 24 months, see complete list of younger than 30 month ;







BSE Youngest Japan 21 months, 23 months







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







Feed borne infection (31-34) a) Recent unpublished experiments at the VLA have shown that feeding exceptionally low doses (0.001g) of infected neural tissue can cause BSE. b) The working hypothesis of Defra that the major cause of BSE in BARBs cases has been through the ingestion of contaminated feed, most likely by young animals, is strongly supported. Thus control of the disease requires, as it has always required, completely eliminating the agent from the cattle feed chain. a) There has been a fall in the underlying incidence of BSE by birth cohort 1996/97 to 99/00 in GB, but the 2001/2 case leaves doubt subsequently. There has also been a fall in other countries except where feed controls were introduced later. 34. In view of the exceedingly low doses of brain material required to infect young cattle, the reductions in incidence consequent on the feed bans in the UK and elsewhere and the lack of evidence that other causes are responsible, the strongest hypothesis for BARBs is infection of animals via ingestion of BSE contaminated material.







url changed to ;













Detection of PrPSc in peripheral tissues of clinically affected cattle after oral challenge with BSE




Martin Franz1, Martin Eiden1, Anne Balkema-Buschmann1, Justin Greenlee2, Hermann M Schaetzl3, Christine Fast1, Juergen Richt4, Jan-Peter Hildebrandt5 and Martin Groschup1,6


+ Author Affiliations


1 Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany; 2 National Animal Disease Center, ARS-USDA, Ames, IA, USA; 3 Depts of Veterinary Sciences and Molecular Biology, University of Wyoming, Laramie, WY, USA; 4 Kansas State University, College of Veterinary Medicine, Manhattan, KS, USA; 5 University Greifswald, Germany


↵6 E-mail: martin.groschup@fli.bund.de


Received 6 June 2012. Accepted 20 August 2012.



Abstract



Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative prion disease that mainly affects cattle. Transmission of BSE to humans caused a variant form of Creutzfeldt-Jakob disease (vCJD). Following infection the protease-resistant, disease-associated isoform of prion protein (PrPSc) accumulates in the central nervous system and in other tissues. Many countries have defined bovine tissues that may contain prions as specified risk materials (SRMs), which must not enter the human or animal food chains and therefore must be discarded. Ultrasensitive techniques such as the protein misfolding cyclic amplification (PMCA) have been developed to detect PrPSc when present in miniscule amounts that are not readily detected by other diagnostic methods such as immunohistochemistry or western blot. This study was conducted to determine when and where PrPSc can be found by PMCA in cattle orally challenged with BSE. A total of 48 different tissue samples from 4 orally BSE-infected cattle at clinical stages of disease were examined using a standardized PMCA protocol. The protocol used brain homogenate from bovine PrP transgenic mice (Tgbov XV) as substrate and three consecutive rounds of PMCA. Using this protocol PrPSc was found in brain, spinal cord, nerve ganglia, optic nerve, and Peyer’s patches. We could confirm the presence of PrPSc in adrenal gland as well as in mesenteric lymph node – a finding, which was recently reported by another group. Interestingly, additional positive results were obtained for the first time in oesophagus, abomasum, rumen, and rectum of clinically affected cattle.








Wednesday, May 2, 2012


ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH






Wednesday, July 28, 2010


re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010


Sent: Wednesday, July 28, 2010 11:42 AM


Subject: re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE


Greetings again Ms Williams et al at FOIA USDA,


Thank You again for your kind reply on this important information. However, I am concerned that you may not be aware of new transmission studies. You (USDA et al) state Ma'am ;




================================================


The SCA with Italy was mainly to confirm our respective country’s diagnostic tests would detect the various atypical BSE cases as seen in each country), in the meantime, the Italians have published their transmissibility and pathogenesis work on their BASE cases in the following article:


Lombardi G, Casalone C, A DA, Gelmetti D, Torcoli G, Barbieri I, Corona C, Fasoli E, Farinazzo A, Fiorini M, Gelati M, Iulini B, Tagliavini F, Ferrari S, Caramelli M, Monaco S, Capucci L, Zanusso G (2008) Intraspecies transmission of BASE induces clinical dullness and amyotrophic changes. PLoS Pathog 4:e1000075


The above mentioned paper concludes, “In all experimentally infected animals, no PrP**TSE was detected in peripheral tissues, including cervical and mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves and forelimb and limb muscles, either by standard Western blot analysis or following phosphotungstic acid precipitation.“


It is not necessary to change SRM removal due to any different tissue infectivity distribution between classical BSE and atypical BSE. At this time, there is no scientific evidence to suggest a need for expanding the list of tissues included in the Specified Risk Material (SRM) ban as a result of published studies on atypical BSE.


snip...


Moreover, in the paper by Buschmann A, Groschup MH (2005,) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192:934-942; the authors, when speaking about the classical BSE food-borne epidemic in Europe, concluded their “results provide further indication that the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system.”


end...




================================================


Again, in my opinion, the USDA is cherry picking the science they want to use, and in doing so, I believe they are putting human lives at risk.


I disagree for the following reasons. New studies indeed show that ;




July 10, 2010


see full text ;


Wednesday, July 28, 2010


re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010






USDA TRIPLE BSE MAD COW FIREWALL, SRM, FEED, AND SURVEILLANCE


2012



***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...






MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...



***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model







***Infectivity in skeletal muscle of BASE-infected cattle







***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.







***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.







The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission.


In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.






Friday, May 11, 2012


Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits



***support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE






Thursday, June 21, 2012



Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism



Justin J. Greenlee1*, Jodi D. Smith1, M. Heather West Greenlee2, Eric M. Nicholson1


1 National Animal Disease Center, United States Department of Agriculture, Agricultural Research Service, Ames, Iowa, United States of America, 2 Iowa State University, Ames, Iowa, United States of America



Abstract



The majority of bovine spongiform encephalopathy (BSE) cases have been ascribed to the classical form of the disease. Htype and L-type BSE cases have atypical molecular profiles compared to classical BSE and are thought to arise spontaneously. However, one case of H-type BSE was associated with a heritable E211K mutation in the prion protein gene. The purpose of this study was to describe transmission of this unique isolate of H-type BSE when inoculated into a calf of the same genotype by the intracranial route. Electroretinograms were used to demonstrate preclinical deficits in retinal function, and optical coherence tomography was used to demonstrate an antemortem decrease in retinal thickness. The calf rapidly progressed to clinical disease (9.4 months) and was necropsied. Widespread distribution of abnormal prion protein was demonstrated within neural tissues by western blot and immunohistochemistry. While this isolate is categorized as BSE-H due to a higher molecular mass of the unglycosylated PrPSc isoform, a strong labeling of all 3 PrPSc bands with monoclonal antibodies 6H4 and P4, and a second unglycosylated band at approximately 14 kDa when developed with antibodies that bind in the C-terminal region, it is unique from other described cases of BSE-H because of an additional band 23 kDa demonstrated on western blots of the cerebellum. This work demonstrates that this isolate is transmissible, has a BSE-H phenotype when transmitted to cattle with the K211 polymorphism, and has molecular features that distinguish it from other cases of BSE-H described in the literature.



snip...


Most significantly it must be determined if the molecular phenotype of this cattle TSE remains stable when transmitted to cattle without the E211K polymorphism as several other isolates of atypical BSE have been shown to adopt a molecular profile consistent with classical BSE after passage in transgenic mice expressing bovine PrPC [40] or multiple passages in wild type mice [23]. Results of ongoing studies, namely passage of the E211K Htype isolate into wild-type cattle, will lend further insight into what role, if any, genetic and sporadic forms of BSE may have played in the origins of classical BSE. Atypical cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins highlight that it may not be possible to eradicate BSE entirely and that it would be hazardous to remove disease control measures such as prohibiting the feeding of meat and bone meal to ruminants.








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...








October 2009


O.11.3


Infectivity in skeletal muscle of BASE-infected cattle


Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy


Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.


Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.


Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.


Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.







Sunday, August 26, 2012


Detection of PrPSc in peripheral tissues of clinically affected cattle after oral challenge with BSE






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...






==============================================




*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS


THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007


Date: March 21, 2007 at 2:27 pm PST


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II


___________________________________


PRODUCT


Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007


CODE


Cattle feed delivered between 01/12/2007 and 01/26/2007


RECALLING FIRM/MANUFACTURER


Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.


Firm initiated recall is ongoing.


REASON


Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.


VOLUME OF PRODUCT IN COMMERCE


42,090 lbs.


DISTRIBUTION


WI


___________________________________


PRODUCT


Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007


CODE


The firm does not utilize a code - only shipping documentation with commodity and weights identified.


RECALLING FIRM/MANUFACTURER


Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.


REASON


Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.


VOLUME OF PRODUCT IN COMMERCE


9,997,976 lbs.


DISTRIBUTION


ID and NV


END OF ENFORCEMENT REPORT FOR MARCH 21, 2007







Saturday, August 14, 2010


BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY


*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)


BANNED MAD COW FEED IN COMMERCE IN ALABAMA


Date: September 6, 2006 at 7:58 am PST PRODUCT


a) EVSRC Custom dairy feed, Recall # V-130-6;


b) Performance Chick Starter, Recall # V-131-6;


c) Performance Quail Grower, Recall # V-132-6;


d) Performance Pheasant Finisher, Recall # V-133-6.


CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.


REASON


Dairy and poultry feeds were possibly contaminated with ruminant based protein.


VOLUME OF PRODUCT IN COMMERCE 477.72 tons


DISTRIBUTION AL


______________________________







PRODUCT Bulk custom dairy pre-mixes,


Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE 350 tons


DISTRIBUTION AL and MS


______________________________


PRODUCT


a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;


b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;


c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;


d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;


e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;


f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;


g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6


CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.


REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".


VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags


DISTRIBUTION AL, GA, MS, and TN


END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006


###







Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006


Date: August 6, 2006 at 6:16 pm PST PRODUCT


a) CO-OP 32% Sinking Catfish, Recall # V-100-6;


b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;


c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;


d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;


e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;


f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;


g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;


h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;


i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;


j) CO-OP LAYING CRUMBLES, Recall # V-109-6;


k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;


l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;


m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE


Product manufactured from 02/01/2005 until 06/06/2006


RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.


REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".


VOLUME OF PRODUCT IN COMMERCE 125 tons


DISTRIBUTION AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006


###







MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II


______________________________


PRODUCT


a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;


b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;


c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;


d) Feather Meal, Recall # V-082-6 CODE


a) Bulk


b) None


c) Bulk


d) Bulk


RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.


REASON


Possible contamination of animal feeds with ruminent derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons


DISTRIBUTION Nationwide


END OF ENFORCEMENT REPORT FOR July 12, 2006


###







please see full text ;




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






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







Monday, September 3, 2012


Sale of misbranded and/or non-inspected meat and meat products to Omaha Public Schools indicted








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...






EFSA Journal 2011 The European Response to BSE: A Success Story


This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;


Monday, October 10, 2011


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...








see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;







2011 Monday, September 26, 2011


L-BSE BASE prion and atypical sporadic CJD






Saturday, March 5, 2011


MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA






Wednesday, August 01, 2012


Behavioural and Psychiatric Features of the Human Prion Diseases: Experience in 368 Prospectively Studied Patients






Monday, August 06, 2012


Atypical neuropathological sCJD-MM phenotype with abundant white matter Kuru-type plaques sparing the cerebellar cortex






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






Friday, August 24, 2012


Iatrogenic prion diseases in humans: an update






Monday, July 23, 2012


The National Prion Disease Pathology Surveillance Center July 2012







TSS