Tuesday, December 2, 2014

UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease

UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease
 
Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease
 
Subject: UK EXPORTS OF MBM TO WORLD
 
UK EXPORTS OF MBM TO WORLD
 
 
 
 
OTHERS
 
BEEF AND VEAL
 
 
 
 
LIVE CATTLE
 
 
FATS
 
 
EMBRYOS
 
 
GELATIN ETC
 
 
SEMEN
 
 
MEAT
 
 
Monday, December 1, 2014
 
Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014
 
 
Friday, November 28, 2014
 
BOVINE SPONGIFORM ENCEPHALOPATHY BSE AKA MAD COW DISEASE PORTUGAL CONFIRMED
 
 
nvCJD CONFIRMED TEXAS USA 2014
 
‘’The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.’’
 
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
 
Updated: October 7, 2014
 
CDC and the Texas Department of State Health Services (DSHS) have completed the investigation of the recently reported fourth vCJD case in the United States. It confirmed that the case was in a US citizen born outside the Americas and indicated that the patient's exposure to the BSE/vCJD agent most likely occurred before he moved to the United States; the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.
 
 
Sunday, November 23, 2014
 
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European
 
 
Monday, November 3, 2014
 
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
 
National Prion Disease Pathology Surveillance Center Cases Examined1 (October 7, 2014)
 
***6 Includes 11 cases in which the diagnosis is pending, and 19 inconclusive cases;
 
***7 Includes 12 (11 from 2014) cases with type determination pending in which the diagnosis of vCJD has been excluded.
 
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob disease (sCJD),
 
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
 
***and 21 cases of sporadic Fatal Insomnia (sFI).
 
 
Monday, November 3, 2014
 
The prion protein protease sensitivity, stability and seeding activity in variably protease sensitive prionopathy brain tissue suggests molecular overlaps with sporadic Creutzfeldt-Jakob disease
 
 
Tuesday, November 04, 2014
 
The pathological and molecular but not clinical phenotypes are maintained after second passage of experimental atypical bovine spongiform encephalopathy in cattle
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
Tuesday, August 12, 2014
 
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST 2014
 
 
Thursday, October 02, 2014
 
[Docket No. APHIS-2013-0064] Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy
 
 
Saturday, August 14, 2010
 
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
 
 
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
 
 
Sunday, December 15, 2013
 
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE ***
 
 
Tuesday, August 12, 2014
 
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST 2014
 
 
Thursday, June 23, 2011
 
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
 
 
Wednesday, April 25, 2012 4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
 
 
2012 ATYPICAL L-TYPE BSE BASE CALIFORNIA ‘confirmed’ Saturday, August 4, 2012
 
*** Final Feed Investigation Summary - California BSE Case - July 2012
 
 
Monday, November 3, 2014
 
Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination
 
 
*** why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
1: J Infect Dis 1980 Aug;142(2):205-8
 
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
 
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
 
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
 
snip...
 
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
 
PMID: 6997404
 
 
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
 
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
 
snip...
 
76/10.12/4.6
 
 
Nature. 1972 Mar 10;236(5341):73-4.
 
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
 
Gibbs CJ Jr, Gajdusek DC.
 
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
 
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
 
C. J. GIBBS jun. & D. C. GAJDUSEK
 
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
 
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
 
 
 
Thursday, July 31, 2014
 
*** EFSA Scrapie reduction unlikely without effective breeding programme
 
 
Tuesday, November 04, 2014
 
*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011
 
 
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis *video*
 
 
Jeff Schwan, sporadic cjd, clustering, and BSE aka mad cow type disease, is there a link ? *video*
 
 
1997-11-10: Panorama - The british disease *video*
 
 
Sunday, September 6, 2009
 
MAD COW USA 1997 *video*
 
 
Tuesday, November 04, 2014
 
*** Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease
 
 
IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe.
 
I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.
 
JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ...
 
Tuesday, July 17, 2012
 
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012
 
 
Thursday, December 20, 2012
 
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH BOVINE MAD COW DISEASE
 
 
Monday, November 30, 2009
 
*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE, DOES NOT SURPRISE ME $
 
 
Sunday, August 24, 2014
 
USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program Goals TSE PRION October 17 – 23, 2013
 
SNIP...
 
REPORT OF THE COMMITTEE 344 Ewes were experimentally inoculated with brain homogenate obtained from a U.S. sheep with clinical Nor98-like scrapie.
 
Recipient ewes are bred annually to examine the placenta for evidence of a transmissible agent. Placentas shed 2009-2013 were negative.
 
*** In 2013, one recipient ewe developed an unrelated disease. At postmortem examination, abundant accumulation of PrPSc was observed only in the cerebellum of this ewe with much less accumulation in the hindbrain obex. This confirms that initial inoculation of these ewes has been successful. Monitoring continues in the remaining ewes of this study.
 
Sunday, August 24, 2014
 
USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program Goals TSE PRION October 17 – 23, 2013
 
 
Sunday, June 29, 2014
 
Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014
 
 
USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE WORLD (?) [protected by the BSE MRR policy] $$$
 
IN my opinion, from the following risk factors i will post below, and the fact that the OIE and the USDA systematically did away with the BSE GBR system for the BSE MRR system, for the legal trading all strains of TSE globally, and the ramifications there from (BSE MRR), MY confidence level of any TSE regulatory risk assessment is 0...that is ZERO CONFIDENCE LEVEL IN ANY REGARDS TO THE TSE PRION DISEASES AKA MAD COW DISEASE. The BSE MRR regulations were set up to fail, and make legal the trading of all strains of TSE prion disease globally. the consumers were hung out to dry around the globe, and the ramifications there from will be long and costly thanks to the OIE and the USDA et al. ...TSS
 
================================
 
 
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE-Risk (GBR) of United States of America (USA)
 
Question N° EFSA-Q-2003-083
 
Adopted July 2004
 
Summary of scientific report The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003. The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties. A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries. EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
 
Key words: BSE, geographical risk assessment, GBR, USA, third countries
 
 
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 1 - European Food Safety Authority Scientific Expert Working Group on GBR Working Group Report on the Assessment of the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004
 
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA - 7 - 2.3
 
Overall assessment of the external challenge
 
The level of the external challenge that has to be met by the BSE/cattle system is estimated according to the guidance given by the SSC in its final opinion on the GBR of July 2000 (as updated in January 2002). Live cattle imports: In total the country imported 2038 (other sources) or 1128 (CD) live cattle from BSE risk countries other than Canada, of which 327 (other sources) or 323 (CD) came from the UK. From Canada the imports were >500,000 animals per year. The numbers shown in table 1 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5 year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow to assume that certain imported cattle did not enter the domestic BSE-cattle system, i.e. were not rendered into feed. In the case of the USA, all the animals for which tracing information showed that they were not rendered were excluded from the external challenge.
 
MBM imports:
 
In total the country imported 689 tons MBM (CD) or 2,230 tons MBM (other sources) from BSE risk countries other than Canada, of which 5 tons (CD) or 101 tons (other sources) were exported from the UK (UK export data). From Canada, the imports were about 30 000 tons per year. The numbers shown in table 2 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5 year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow to assume that certain imported MBM did not enter the domestic BSE/cattle system or did not represent an external challenge for other reasons. As it was illegal to export mammalian MBM from UK since 27/03/1996, exports indicated after that date should only have included non-mammalian MBM. In the case of the USA imported MBM from UK in 1989 and between 1997 and 1999 was not taken into account.
 
Feeding Use of MBM in cattle feed
 
• Until 1997 ruminant MBM (RMBM) could legally be included in cattle feed and was indeed commonly fed to cattle of different age and type. Prior to the feed ban the US authorities estimated that 10% of all MBM would deliberately have been fed to cattle. Feed bans
 
• A ban to feed (several types of) MMBM to ruminants was put in place in August 1997. Derogation from the ban was granted for pure porcine and equine protein (MBM) coming from designated (single species) rendering plants. This MMBM might still be fed to cattle. Therefore this feed ban is a ruminant to ruminant ban.
 
• It is planned to prohibit the use of all mammalian and poultry protein in ruminant feed and prohibiting materials from non-ambulatory disabled cattle and dead stock from use in all animal feed.
 
Conclusion on the ability to avoid recycling
 
• Before 1997, US system would not have been able to avoid recycling of the BSEagent to any measurable extent. If the BSE-agent was introduced into the feed chain, it could have reached cattle.
 
• After the introduction of the 1997 ban in August 1997, the ability to avoid recycling of BSE-infectivity was somewhat improved. However, the rendering of ruminant material (including SRM and fallen stock) is inadequate (non pressurized), and cross-contamination potentials of cattle feed with other feeds remain.
 
• Therefore, the system is still unable to avoid recycling of BSE-infectivity if already present in the system or incoming.
 
Feeding
 
Until August 1997, RMBM was legally fed to cattle. Feeding was therefore "not OK". In August 1997 an RMBM-ban was introduced but feeding of non-ruminant MBM to cattle remained legal as well as feeding of RMBM to non-ruminant animals (farm animals and pets). An RMBM ban is difficult to maintain, as only labels can distinguish the various MMBMs. This makes control of the feed ban very difficult because analytical differentiation between ruminant and non-ruminant MBM is difficult if not impossible.
 
Due to the highly specialised production system in the USA, various mammalian MBM streams can be separated. Such a feed ban would therefore be assessed as "reasonably OK", for all regions where this highly specialised system exists. However, several areas in the USA do have mixed farming and mixed feed mills, and in such regions an RMBM ban would not suffice. Additionally, official controls for cattle feeds to control for compliance with the ban started in 2002. Thus, for the whole country, the assessment of the feeding after 1997 remains "not OK", but improving.
 
Rendering
 
The rendering industry is operating with processes that are not known to reduce
 
infectivity. It is therefore concluded that rendering was and is "not OK".
 
SRM-removal
 
SRM were and are still rendered for feed, as are (parts of) the fallen stock. SRMremoval
 
is therefore regarded as "not OK".
 
BSE-surveillance
 
Before 1989, the ability of the system to identify (and eliminate) BSE-cases was
 
limited. Since 1990 this ability is improved, thanks to a specific (passive) BSE
 
surveillance. The initiated introduction of active surveillance in risk populations
 
should improve the system significantly.
 
On the basis of the available information, it has to be concluded that the country's
 
BSE/cattle system was extremely unstable until today, i.e., it would have recycled and
 
amplified BSE-infectivity very fast, should it have entered the system. The stability of
 
the BSE/cattle system in the USA overtime is as given in table 4.
 
The present assessment modifies the stability assessment of the previous GBR report
 
in 2000 mainly due to a different perception of the impact of BSE surveillance on
 
stability and of the efficiency of the RMBM feed ban.
 
Interaction of stability and external challenge in the USA
 
Period Stability External Challenge Internal challenge
 
1980 to
 
1985
 
1986 to
 
1990
 
Moderate Possibly present
 
1991 to 1995
 
Very high
 
1996 to
 
2000
 
2001 to
 
2003
 
Extremely unstable Extremely high Likely to be present and growing
 
5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK
 
5.1 The current GBR as function of the past stability and challenge
 
• The current geographical BSE risk (GBR) level is III, i.e. it is likely but not
 
confirmed that domestic cattle are (clinically or pre-clinically) infected with the
 
BSE-agent.
 
Note1: It is also worth noting that the current GBR conclusions are not dependent on
 
the large exchange of imports between USA and Canada. External challenge due to
 
exports to the USA from European countries varied from moderate to high. These
 
challenges indicate that it was likely that BSE infectivity was introduced into the
 
North American continent.
 
snip...please see full text ;
 
 
EFSA publishes Geographical BSE-Risk (GBR) assessments for Australia, Canada, Mexico, Norway, South Africa, Sweden and the United States of America
 
Communiqué de presse 20 août 2004
 
The European Food Safety Authority (EFSA) has issued today seven up-to-date scientific reports on the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) assessments for Australia, Canada, Mexico, Norway, South Africa Sweden and the United States of America. While Australia’s GBR level I (i.e. presence of BSE in domestic cattle is highly unlikely) is maintained, that of Norway has been raised to level II (presence of BSE unlikely but not excluded), Sweden remains at GBR level II and those of Canada and the United States have been raised to level III (presence of BSE likely but not confirmed, or confirmed at a lower level) following a new assessment taking into account the most recent evidence. EFSA’s Scientific Expert Working Group on geographic BSE risk assessment also evaluated the status of Mexico and South Africa which were classified as level III.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Terry S. Singeltary Sr.
 
Bacliff, TEXAS USA 77518 MOM DOD 12/14/97 confirmed hvCJD

Friday, April 4, 2014

China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures

Two More Countries Lift BSE-Related Bans On U.S. Beef

 

Apr 2, 2014

 

Joe Schuele,

 

U.S. Meat Export Federation

 

U.S. beef exports gain access to the promising protein markets of Ecuador and Sri Lanka, but China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures.

 

In March, two trading partners agreed to resume imports of U.S. beef for the first time since December 2003. Ecuador and Sri Lanka were among a handful of nations that had never reopened after the first U.S. case of BSE, but both are now accepting U.S. beef.

 

Ecuador offers strong potential for U.S. beef offal sales

 

Exports to Ecuador face very few restrictions, with muscle cuts and offal items from cattle of all ages now eligible.

 

“That’s a huge bonus in a market where we expect to export a significant volume of offal products,” says Cheyenne Dixon, U.S. Meat Export Federation (USMEF) technical services manager.

 

The only significant constraint involves beef derived from cattle imported from Canada, in which case the animal must be in the U.S. for 60 days prior to slaughter.

 

“We hope this restriction is temporary, and it is a point on which the U.S. and Ecuadorian governments continue to negotiate,” Dixon explains. “But products derived from all domestic cattle are eligible, as well as beef from cattle imported from Mexico.”

 

In addition to providing high-quality beef cuts for Ecuador’s hotel and restaurant sectors, USMEF expects U.S. exporters to find success with variety meat items such as beef tripe, livers and hearts. Two introductory seminars for Ecuadorian importers are planned later this month – one in the capital city of Quito and one in Ecuador’s largest city, Guayaquil.

 

According to the Global Trade Atlas, Ecuador imported 1,006 metric tons (mt) of beef last year at a value of $4.5 million – down about 10% from 2012. Chile was Ecuador’s leading beef supplier, followed by Uruguay.

 

Sri Lanka's tourism push offers potential for U.S. beef products

 

Located off the southeastern coast of India, Sri Lanka was plagued by civil war and ongoing political conflict until 2009. The country was also devastated by a deadly tsunami in 2004. But recently, Sri Lankans have enjoyed a much more peaceful existence, which has led to economic growth and a revitalized tourism sector.

 

“Sri Lanka has ambitious plans to make it onto the ‘A list’ of Asian tourist destinations, in line with Bali (Indonesia) and several locations in Thailand,” says Joel Haggard, USMEF senior vice president for the Asia Pacific.

 

Haggard also notes that the capital city of Colombo, which has a greater-metropolitan population of approximately 1.5 million people, has several modern supermarket chains that currently rely mostly on domestic products.

 

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“Sri Lanka’s retail sector is expanding rapidly and there are certainly growth opportunities there for U.S. beef,” Haggard says.

 

Recently a group of veterinary officials from Sri Lanka’s Central Department of Animal Production and Health received an in-depth look at the U.S. beef industry as part of the USDA Foreign Agriculture Service’s Cochran Fellowship Program. Tiskumarage Aruni Tiskumara, DVM, who headed the delegation, expressed confidence in the safety and quality of U.S. beef.

 

“We had good exposure to all of the systems the U.S. beef industry has adopted,” she explains. “We are quite satisfied with the processing regulations and with the biosecurity aspects as well.”

 

Tiskumara noted that the “negligible risk” designation for BSE from the World Organization for Animal Health, which the U.S. received in May 2013, was a key factor in Sri Lanka’s decision to reopen the market.

 

“Until the U.S. achieved negligible risk status, we were not interested in U.S. beef,” she said. “But now that you have the negligible risk designation, technically there is no reason why we should not import beef from the U.S.A.”

 

Sri Lanka is also open to U.S. beef from cattle of all ages. Last year, Sri Lanka imported 74 mt of beef – mostly from Australia – valued at about $400,000.

 

Markets that remain closed to U.S. beef due to BSE include China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel and South Africa. Saudi Arabia reopened to U.S. beef in 2004, but suspended imports after a BSE case was detected in California in April 2012.

 

Joe Schuele is communications director for the U.S. Meat Export Federation.

 


 

BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein

 

Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.

 


 

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

 

Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD

 

Date: Thu, 28 Nov 2002 10:23:43 -0000

 

From: "Asante, Emmanuel A" e.asante@ic.ac.uk

 

To: "'flounder@wt.net'" flounder@wt.net

 

Dear Terry,

 

I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.

 

Thank you for your interest in the paper.

 

In respect of your first question, the simple answer is, yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.

 

I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.

 

Emmanuel Asante

 

<>

 

____________________________________

 

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)

 

____________________________________

 


 

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...

 


 

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...

 


 


 

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.

 

***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

 


 

LAST MAD COW IN USA, IN CALIFORNIA, WAS ATYPICAL L-TYPE BASE BSE TSE PRION DISEASE Thursday, February 20, 2014

 

Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr. Linda Detwiler 2014

 


 

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

 


 

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

 


 

Tuesday, August 18, 2009

 

* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009

 


 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 


 

Friday, March 21, 2014

 

Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?

 

“As of March 20, 2014, FSIS has completed all checks (effectiveness checks and disposition verification checks) for recalls 002-2014 and 013-2014 regarding Rancho Feeding Corporation. FSIS has determined that based on the number of successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses were notified of the recall and removed affected products from commerce that the recall activities were effective.”

 


 

*** And Terry, I promised the editor you would respond so thanks for backing my prediction up. I have read your tripe before so did not reread the whole thing. but your point about the age of the cattle takes on the scientific regulatory bodies of every country but one that exports US beef. They all, but one, agree that meat from cattle under 30 months of age carries zero risk of BSE prions. 1 △ ▽ • Reply • Share ›

 

Terry S. Singeltary Sr. > doc raymond • a month ago

 

Dr. Richard Raymond Sir, I only reply when you are scientifically wrong. I commented today, because again, you were scientifically wrong, and I proved it again, with scientific facts to back it up. sorry if that upsets you. you can fool some of the folks some of the time, but not all of us all the time. you either blatantly lied in your editorial, or you are grossly uninformed, time and time again. I think the public can take their pick on that, and in both cases, and they would be correct in both cases, in my opinion. you have a nice day sir. ...kind regards, terry

 

kind regards, terry

 

What is a Downer Calf?

 

By Dr. Richard Raymond | February 21, 2014

 


 

see full text Dr. Richard Raymond vs Terry S. Singeltary Sr.

 


 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

Saturday, August 4, 2012

 

Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation

 


 

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

 

This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$

 

ALABAMA MAD COW g-h-BSEalabama

 

In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.

 


 


 

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)

 


 

Greetings,

 

I have been most interested to see IF the h-BSE (h-BSE or g-h-BSEalabama???), but i have been most interested to see if in fact this atypical h-BSE is more virulent than c-BSE, as is the L-BSE (Italian strain) has been documented to be. We know from the studies of Kong et al that h-BSE will transmit to TG human 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.

 


 

HOWEVER, as to the virulance of it one way or the other compared to c-BSE and or L-BSE, i don't think no one has said yet or not? interesting this debate of the h-BSE TEXAS (2nd mad cow finally confirmed 7 months after the fact, and an act of Congress), compared to the g-h-BSEalabama strain documented in Alabama, that is identicle to the new human CJD in the USA that is killing the young and old, with clinical long duration, and different symptoms in some cases too, but not related to this ??? ALSO, this IBNC BSE, might this be the g-h-BSEalabama strain?

 

THE last two mad cows documented in the USA were in Alabama and Texas, both of which were atypical h-BSE.

 

SINGE then, the surveillance for TSE in cattle in the USA has been reduced to a number of which detecting any TSE would almost impossible.

 

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

 

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

 

"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end

 


 

UPDATE

 

Thursday, December 04, 2008 2:37 PM

 

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

 

personal communication with Professor Kong. ...TSS

 

TEXAS ATYPICAL H-BSE MAD COW CASE

 

On June 24, 2005, the USDA announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas, died at approximately 12 years of age, and represented the first endemic case of BSE in the United States. (see Texas BSE Investigation, Final Epidemiology Report, August 2005 External Web Site Policy PDF Document Icon (PDF – 83 KB))

 

ALABAMA ATYPICAL H-TYPE GENETIC BSE

 

On March 15, 2006, the USDA announced the confirmation of BSE in a cow in Alabama. The case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10-years-old. It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation (see second featured item above and Alabama BSE Investigation, Final Epidemiology Report, May 2006 External Web Site PolicyPDF Document Icon (PDF – 104 KB)).

 

In August 2008, several ARS investigators reported that a rare, genetic abnormality that may persist within the cattle population "is considered to have caused" BSE in this atypical (H-type) BSE animal from Alabama. (See Identification of a Heritable Polymorphism in Bovine PRNP Associated with Genetic Transmissible Spongiform Encephalopathy: Evidence of Heritable BSE External Web Site Policy. Also see BSE Case Associated with Prion Protein Gene Mutation External Web Site Policy.)

 

On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of the first known case of BSE in the United States. It was in an adult Holstein cow from Washington State. This diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Trace-back based on an ear-tag identification number and subsequent genetic testing confirmed that the BSE-infected cow was imported into the United States from Canada in August 2001. Because the animal was non-ambulatory (a "downer cow") at slaughter, brain tissue samples were taken by USDA's Animal and Plant Health Inspection Service as part of its targeted surveillance for BSE. However the animal's condition was attributed to complications from calving. After the animal was examined by a USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both before and after slaughter, the carcass was released for use as food for human consumption. During slaughter, the tissues considered to be at high risk for the transmission of the BSE agent were removed. On December 24, 2003, FSIS recalled beef from cattle slaughtered in the same plant on the same day as the BSE positive cow. (see Bovine Spongiform Encephalopathy in a Dairy Cow - Washington State, 2003.)

 


 

Tuesday, August 22, 2006

 

BSE ATYPICAL TEXAS AND ALABAMA UPDATE JANUARY 20, 2007

 


 

 

ABOUT THAT USDA INC FDA TRIPLE MAD COW FIREWALL ...HA, HA, HA, jokes you, it was nothing but ink on paper...

 

*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE ***

 

OAI 2012-2013

 

OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation.

 

*** An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not co...ntaminated with prohibited material.

 

Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.

 

ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St. Newberry SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y

 

DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN 46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y

 

ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC 28163-7617 OPR FL, TH NP 7/17/2013 OAI N

 

NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007 OPR FR, OF NP 7/16/2013 OAI Y

 

DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N

 

CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y

 

DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N

 

Ruminant Feed Inspections Firms Inventory (excel format)

 


 

PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates posted, as in numerical order, you will have to sift through them for yourselves. ...tss

 

snip...see full text ;

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

 

ONE SUCH INCIDENT CAN CAUSE 10,000,000 MILLION POUNDS OF SUSPECT BANNED MAD COW PROTEIN GOING INTO COMMERCE TO BE FED OUT ;

 

2007

 

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 4, 2012

 

*** Final Feed Investigation Summary - California atypical L-TYPE BASE BSE Case - July 2012

 


 

The accumulation of PrPSc in the hamster tongue following i.c. inoculation of two hamster-adapted TME strains and four hamster-adapted scrapie strains indicates that the spread of prions to the tongue may be a common event in prion diseases. The detection of PrPSc in axons of the tongue after i.c. inoculation suggests that one possible route involved in the establishment of tongue infection is axonal transport of HY TME from the brain to the tongue. In this case, TME transport may be via the motor efferent or sensory afferent pathways of the tongue. Prion infection of the XII nucleus, the spinal trigeminal nucleus, or the nucleus of the solitary tract would be necessary for prions to have access to and be transported within the tongue-associated cranial nerves. In cases of both natural and experimental oral infection of ruminants with scrapie and BSE, as well as in infection of deer with the CWD agent, there is evidence for the infection of the tongue-associated brain stem nuclei (27, 48, 56, 57).

 

snip....

 

The findings of the present study, and the ability of BSE to target brain stem regions that are synaptically connected to the tongue, indicate that the Specified Risk Material Regulations (15), which do not completely exclude tongue from human consumption, need to be reevaluated in order to minimize human exposure to BSE and other prion diseases through ingestion of food products containing tongue.

 


 

Exposure of the tongue to the prion agent during oral ingestion makes it a potential site of agent entry and neuroinvasion, especially if lesions have disrupted the mucosal epithelium (4). Although there are no epidemiological data that indicate this is a common route of prion agent entry, the tongue is a highly innervated peripheral tissue that may be a relevant site of neuroinvasion for a subset of prion diseases of livestock in which evidence for LRS infection is lacking.

 


 

Progress 12/01/08 to 11/30/09

 

Therefore, saliva may be one source of prions that is shed from a host and can infect a naive host through direct or indirect contact. The spread of prions into skeletal muscle cells via nerve fibers suggest that muscle tissue, and not just nerves that transverse muscle, are a potential source of prion exposure upon ingestion of food products containing meat.

 

Progress 12/01/05 to 11/30/09

 

To determine if the prion agent can directly infect epithelial cells at the tongue mucosa we analyzed the keratin layer of the stratified squamous epithelium (SSE). PrP-res was detected in both the keratin layer of the SSE and the SSE of filiform papillae. PrP-res did not always colocalize with markers for nerve fibers in these locations suggesting infection was present in epithelial cells. These studies strongly suggest that epithelial cells in the oral mucosa can support prion infection and shedding of the mucosa may be a source of prion infection in saliva. We investigated infection of tongue and nasal turbinates in over 80 ruminants infected with prion diseases. In prion-infected sheep, deer, and elk greater than 85% of tongue and nasal turbinates were PrP-res positive. Tongue and nasal turbinates from CWD or TME-infected cattle were examined from over 25 animals, but we were unable to detect PrP-res in any of these samples. These findings indicate that prion infection is present in mucosal tissues in ruminant species in which there is horizontal transmission of prions, but not in cattle in which there is not an endemic prion infection.

 

Impacts The implication from these findings is that the prion agent can spread away from the brain into mucosa tissues in the head, specifically the tongue and nasal cavity. Since these tissues have a mucosal surface, it may be possible that the prion agent is shed from the tongue or nasal cavity. In the tongue, the epithelium is continually undergoing terminal differentiation and shedding, and is then sloughed into saliva. In the nasal mucosa, olfactory neurons continually mature and turnover during adult life and prions may be shed from this mucosa into nasal secretions. Therefore, saliva and nasal secretions may be a potential source of prions that are shed from a host and can infect a naive host through direct or indirect contact. Another implication of these findings is that prion infection of ruminant muscle is a potential threat to animal and human food safety. The head of ruminants is banned for human or ruminant consumption with the exception of the tongue. Our findings indicate that prions undergo centrifugal spread from the brainstem to the tongue and can enter skeletal muscle cells via the neuromuscular junction and further replicate in muscle cells. These studies suggest that tongue should also be included in the specified risk materials in order to minimize exposure to tongue products containing prion agent.

 


 

Class I Recall 013-2014 Health Risk: High Feb 8, 2014

 

30- and 60-lb. boxes of “Beef Tongue”

 


 

DISTRIBUTION LIST

 


 


 

*** Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012

 


 

Saturday, December 21, 2013

 

**** Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle ****

 


 

Saturday, November 10, 2012

 

Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials

 

Nov 9, 2012 WI Firm Recalls Beef Tongues

 


 

Saturday, July 23, 2011

 

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

 


 

Friday, October 15, 2010

 

BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle

 


 

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

 


 

Tuesday, July 1, 2008

 

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

 


 

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

 


 

Monday, March 3, 2014

 

*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers to eat dead stock downers and whatever else the industry decides

 

see updated Rancho CLASS 1 HIGH RISK dead stock cancer downer recall for IDAHO

 


 


 

 

Prion 6:1, 52-61; January/February/March 2012; © 2012 Landes Bioscience

 

Salivary prions in sheep and deer

 

Experiments in prion-infected rodents have shown that the oral and nasal mucosa, including the papillae in the tongue, can harbor prions and may act as potential sources for the horizontal transmission of animal prion diseases since these tissues may release prions during their normal turnover. 34,35 Equally, the tongue, and the oral and nasal mucosa can also act as routes for neuroinvasion.36-39 Although prions were reported previously in the saliva of CWD-infected mule deer,10 the titers were not determined. A pooled and concentrated (10- fold) saliva sample from five white-tailed deer with CWD was reported to transmit prion disease to 8 of 9 Tg(CerPrP+/-)1536 mice in 342 ± 102 dpi.11 Based on published titration results with a pooled elk CWD inoculum in Tg(CerPrP+/-)1536 mice,40 we estimated the equivalent titer for this pooled CWD saliva sample to be -0.7 log ID50 U, which is similar to our value of -0.9 log ID50 U for scrapie saliva sample 444 based on 30 μl of 10% saliva preparations (Table 1).

 

snip...

 

Our results indicate a similar magnitude of salivary prion shedding between sheep and deer. Although salivary prion titers are much lower in comparison to those measured in brain, spleen and lymph nodes of affected animals, the number of prions secreted in saliva over the incubation period may approach that found in the brains of terminally ill animals, assuming that, similar to fecal prion shedding, salivary prion shedding is not restricted to terminally sick animals (Table 4). Also, possible differences between prion strains and animal species used in titration studies may affect the estimated titers. Whether these assumptions are accurate requires additional studies. It remains to be determined at what quantities scrapie prions are shed in urine and feces of scrapie-infected sheep (Table 4) as well as when and to what level this shedding may occur in presymptomatic animals. Whether prions shed in saliva have different strain characteristics from prions shed in feces is also unknown. In light of the similarities in peripheral prion distribution patterns and shedding of infectious prions by small ruminants and cervids, it will be important to determine whether patients with variant Creutzfeldt-Jakob disease (vCJD) who harbor prions in their lymphoreticular tissues,43,44 also shed vCJD prions in saliva, urine or feces.

 


 

 

Sunday, March 23, 2014

 

APHIS USDA National Scrapie Eradication Program February 2014 Monthly Report Fiscal Year 2014

 


 

 

Thursday, November 21, 2013

 

*** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy

 

The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.

 


 

 

Friday, November 22, 2013

 

Wasting disease is threat to the entire UK deer population CWD TSE Prion disease Singeltary submission to Scottish Parliament

 


 

 

Saturday, March 15, 2014

 

Potential role of soil properties in the spread of CWD in western Canada

 


 

 

Saturday, March 29, 2014

 

Game Farm, CWD Concerns Rise at Boone and Crockett Club

 


 

 

this just out cdc...tss

 

Sunday, March 30, 2014

 

*** Chronic Wasting Disease Agents in Nonhuman Primates ***

 


 

 

Monday, August 6, 2012

 

TAFS BSE in USA August 6, 2012

 

BSE in USA

 


 

 

 

Saturday, November 2, 2013

 

Exploring the risks of a putative transmission of BSE to new species

 


 

 

Sunday, November 13, 2011

 

California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock

 


 

 

Saturday, May 2, 2009

 

APHIS AND WHO PLAN TO EXEMPT THE ATYPICAL SCRAPIE NOR-98 FROM REGULATIONS AT MEETING THIS MONTH

 


 

 

Monday, November 30, 2009

 

USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE

 


 

 

Thursday, December 20, 2012

 

OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH BOVINE MAD COW DISEASE

 


 

 

Tuesday, July 2, 2013

 

APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals Eliminating ALL remaining BSE barriers to export market

 


 

 

I lost my mother to the Heidenhain Variant of Creutzfeldt Jakob Disease DOD 12/14/97 ‘confirmed’, and never could except the science that the USDA et al brought forth to date i.e. the UKBSEnvCJD only theory. I simply made a promise to mom, NEVER FORGET, and so soon you all FORGOT $

 

Seems none of the officials remember, that went through the mad cow debacle, or mad cow follies as I have termed them, and they are ongoing, for anyone who thinks mad cow disease is gone, they are only fooling themselves, and at the same time, making fools out of everyone that goes along with this TSE prion mad cow junk science that the OIE has brought to every country around the globe, and we will ALL pay the price in the years and decades to come. ...

 

IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe.

 

I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.

 

JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ...

 

 

IN A NUT SHELL ;

 

(Adopted by the International Committee of the OIE on 23 May 2006)

 

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

 


 

 

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

 


 


 

 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***

 


 

 

Sunday, October 13, 2013

 

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

 


 

 

*** When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.

 


 

 

Tuesday, April 01, 2014

 

*** Questions linger in U.S. CJD cases 2005, and still do in 2014 ***

 


 

 

Wednesday, April 2, 2014

 

Do prions cause Parkinson disease?: The evidence accumulates (pages 331–333)

 


 

 

kind regards, ......terry