Sent: Saturday, August 22, 2009 3:18 PM
Subject: FREE Kim Min-sun, she is correct about mad cow fears from USDA BEEF
Kim Min-sun is correct about mad cow fears from USDA BEEF
WHOM is to say, whether or not, one would rather die fast from cyanide, or slow from mad cow disease. some would rather die in a fast mode, than say slowly, an agonizing death, from Creutzfeldt Jakob Disease ??? IN a free society, would one not have the right of free speech to voice that opinion ???
WHOM is to say, that some sub-types of the CJD in the USA, is not from the atypical mad cow disease in the USA ???
WHAT DID ONE OF THE TOP USA SCIENTIST ON PRIONS AND TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY SAY ABOUT USA BEEF ???
Kim Min-sun, who allegedly "misled the public to boycott U.S. beef consumption", did NOT mislead anyone. the fact of the matter is, the Korean Government, and it's people, are being mislead by the USA government i.e. USDA. the proof is here, you only need to watch this video and you will see whom has mislead whom...
SEE THE DAMNING VIDEO NOW AT THE BOTTOM OF THE BLOG BELOW ;
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN
''nobody has ever ask''
''they dont want our comment''
''they don't want to know, the don't care''
''i have tried repeatedly''
''level of absolute ignorance''
''Entire policy was driven...heard from mr. laycraft, so now, after time has passed, it's ok for Canada, cattle under 30 month, to the USA, THAT'S ALL THAT MATTERED!
PRUSINER ASKED : IF FROM YOUR TESTIMONY, A DEMONSTRATED THREAT TO PUBLIC HEATH ?
''yes, i think prions are bad to eat, and you can die from them''
http://maddeer.org/video/embedded/prusinerclip.html
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Atypical BSE North America Update February 2009
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
Sunday, December 28, 2008
MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html
Transmissible mink encephalopathy - review of the etiology
http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html
Wednesday, July 1, 2009
Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)
http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE
SOMETHING TO PONDER ???
O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???
OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$
IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???
http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html
WHAT ABOUT THOSE USDA FDA MAD COW FEED FIREWALLS, THAT PREVENTS MAD COW DISEASE IN THE USA $$$
THE AUGUST 4, 1997 MAD COW FEED BAN IN THE USA WAS NOTHING MORE THAN INK ON PAPER, THE PARTIAL AND VOLUNTARY FEED BAN WAS NOT ENFORCED !!! see for yourself ;
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
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Thursday, March 19, 2009 MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Tuesday, July 28, 2009 MAD COW COVER-UP USA MASKED AS SPORADIC CJD
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
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
http://www.upi.com/
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
see full text ;
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html
Research article Mutations at codons 178, 200-129, and 232 contributed to the inherited prion diseases in Korean patients
Bo-Yeong Choi , Su Yeon Kim , So-Young Seo , Seong Soo A An , SangYun Kim , Sang-Eun Park , Seung-Han Lee , Yun-Ju Choi , Sang-Jin Kim , Chi-Kyeong Kim , Jun-Sun Park and Young-Ran Ju
BMC Infectious Diseases 2009, 9:132doi:10.1186/1471-2334-9-132
Published: 22 August 2009
Abstract (provisional) Background Polymorphisms of the human prion protein gene (PRNP) contribute to the genetic determinants of Creutzfeldt-Jakob disease (CJD). Numerous polymorphisms in the promoter regions as well as the open reading frame of PRNP were investigated. Greater than 90% of Koreans, Chinese, and Japanese carry the homozygote 129MM codon. In Korea, polymorphisms have not been comprehensively studied, except codons 129 and 219 in PRNP among Korean CJD cases. Although polymorphisms at codons 129 and 219 play an important role in susceptibility to sporadic CJD, patients with other polymorphisms in PRNP exhibited critical distinctions of clinical symptoms.
Methods The genetic analyses of PRNP were carried out among probable CJD patients in comparison with the results from magnetic resonance imaging (MRI) and electroencephalogram (EEG).
Results The molecular analysis revealed that three mutations at codons D178N, E200K, and M232R in heterozygosity. Patients with the D178N and M232R mutations had a 129MM codon, whereas the patient with the E200K mutation showed 129MV heterozygosity. They all revealed strong 14-3-3 positive signals. The 67-year-old patient with the D178N-129M mutation showed progressive gait disturbance and dysarthria was in progress. The 58-year-old patient with the E200K mutation coupled to the 129MV codon had gait disturbance, dysarthria, agitation, and ataxic gait, and progressed rapidly to death 3 months from the first onset of symptoms. The 65-year-old patient with the M232R mutation showed rapidly progressive memory decline and gait disturbance, and died within 16 months after onset of symptoms.
Conclusions Despite differences in ethnicity, the clinical and pathological outcomes were similar to the respective mutations around the world, except absence of insomnia in D178N-129M subject.
http://www.biomedcentral.com/1471-2334/9/132/abstract
Monday, May 12, 2008
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.
http://www.defra.gov.uk/vla/vla/vla_ati_020205.htm
Youngest confirmed case 20 Months, Oldest confirmed case 22 Years, Data valid to 01 April 2008
http://www.defra.gov.uk/vla/science/docs/sci_tse_stats_gen.pdf
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 ;
http://www.food.gov.uk/multimedia/pdfs/otmbsestatistics.pdf
BSE Youngest Japan 21 months, 23 months
http://www.jstage.jst.go.jp/article/ehpm/10/3/130/_pdf
Why Americans, As Well as Koreans, Should Be Worried About Mad Cow Tainted USA Beef
By Terry S. Singeltary Sr. May 15, 2008
Straight to the Source
Web Note: This is an important commentary by Terry S. Singeltary Sr., on a recent Business Week story on the controversy in South Korea over their government's lifting on the ban on conventional (non-organic) beef, despite the fact that the USDA is still allowing slaughterhouse waste and blood and manure to be fed to cows, and refusing to test all cows at slaughter. See the Mad Cow section of the OCA website for in-depth information. Terry is a regular blogger on the OCA website on Mad Cow issues.
Ronnie Cummins
One Korean official says the probability of a human being catching a mad cow disease by eating U.S. beef is like the one of a golf player scoring a hole-in-one and then being killed by lightning.
this is typical BSe. you here industry groups comment 'your more likely to get hit by a car than die from CJD'. well, maybe so, but my mother and many more did not die from getting hit by a car, they died from CJD, my mothers being the hvCJD (confirmed), and my neighbors mother died from CJD (confirmed). the UKBSEnvCJD _only_ theory is incorrect. there are more strains of mad cow than the UK BSE in beef to nvCJD in humans in the UK. The deception by the USDA, FDA, and the Bush administration about mad cow disease, CJD, and all Transmissible Spongiform Encephalopathy over the past 8 years have been outrageous, to a point of being criminal. I am vested in nothing, but the truth.
snip...see full text ;
http://www.grassrootsnetroots.org/articles/article_12387.cfm
USDA VS KOREA typical or atypical BSe
http://usdavskorea.blogspot.com/
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Saturday, August 22, 2009
Tuesday, April 14, 2009
Tons of USA Beef Suspected of Mad Cow Disease Sold KOREA
04-14-2009 19:43
Tons of Beef Suspected of Mad Cow Disease Sold
By Kim Rahn Staff Reporter
About 13 tons of American beef were falsely sold as Australian products five years ago in defiance of a disposal order issued after a case of mad cow disease, or bovine spongiform encephalopathy (BSE), was reported in the United States.
The prosecution indicted two men, identified as Seon and Kim, Monday, for having hoarded the American beef from a discount store where Seon worked and having supplied it to big discount store chains and department stores.
In December 2003, when cows suspected of having the disease were found in the U.S. and Seon's company was ordered to dispose of all American beef, he allegedly destroyed seven tons and falsely reported to the company that he had destroyed the entire 29 tons in the store.
Among the remaining 22 tons, Seon delivered 12.7 tons to discount stores and department stores between August and December 2004. The two fabricated expiration dates of the products and labeled them as ``Australian beef,'' raking in 280 million won in revenue. The products sold out.
Seon claimed that they did not distribute about 10 tons of the remaining products, but prosecutors suspect they did, requesting a tax agency audit Kim's company.
The prosecution is considering expanding the investigation into other meat distributors to search for similar cases.
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000162/!x-usc:mailto:rahnita@koreatimes.co.kr
http://www.koreatimes.co.kr/www/news/nation/2009/04/117_43177.html
Why Americans, As Well as Koreans, Should Be Worried About Mad Cow Tainted USA Beef By Terry S. Singeltary Sr. May 15, 2008 Straight to the Source
Web Note: This is an important commentary by Terry S. Singeltary Sr., on a recent Business Week story on the controversy in South Korea over their government's lifting on the ban on conventional (non-organic) beef, despite the fact that the USDA is still allowing slaughterhouse waste and blood and manure to be fed to cows, and refusing to test all cows at slaughter. See the Mad Cow section of the OCA website for in-depth information. Terry is a regular blogger on the OCA website on Mad Cow issues.
Ronnie Cummins
http://www.organicconsumers.org/articles/article_12387.cfm
http://www.fpif.org/fpiftxt/3940
http://www.testcowsnow.com/export-of-beef-and-beef-products-to-korea-usda-fsis-notice-expires-7109-opi-oppd
http://usdavskorea.blogspot.com/2008/05/usda-vs-korea-typical-or-atypical-bse.html
*** 2009 ***
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)
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf
Research Project: GENETIC AND BIOLOGICAL DETERMINANTS OF RESPIRATORY DISEASE SUSCEPTIBILITY Location: Animal Health Systems Research
Title: Association of a bovine prion gene haplotype with atypical BSE
Author
Clawson, Michael
Submitted to: Meeting Abstract Publication Type: Abstract Publication Acceptance Date: December 2, 2008 Publication Date: January 1, 2009 Citation: Clawson, M.L. 2009. Association of a bovine prion gene haplotype with atypical BSE [abstract]. Plant and Animal Genomes XVII Conference. Abstract No. W091. Available:
http://www.intl-pag.org/17/abstracts/
Technical Abstract: Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a class of fatal neurodegenerative disorders that occur in humans, ruminants, cats, and mink. Three distinct TSEs afflict cattle: classical bovine spongiform encephalopathy (BSE), atypical H-type BSE, and atypical L-type BSE. Classical BSE was identified in the 1980s and is acquired by cattle through the consumption of feed contaminated with the infectious prion agent. Atypical BSEs have only recently been recognized as distinct cattle prion diseases and are extremely rare. The full extent of genetic susceptibilities to atypical BSEs is unknown; however, one atypical H-type case identified in the United States (2006) was most likely caused by a genetic mutation in the prion gene, E211K. We have identified an association of a bovine prion DNA haplotype with atypical BSE that is independent of E211K. The haplotype spans a portion of the prion gene that includes part of intron 2, the entire coding region of exon 3, and part of the three prime untranslated region of exon 3 (13 kb). Despite the low frequency of this haplotype among general cattle populations, it was present in a majority of H- and L-type atypical BSE cases from Canada, France, and the United States. This result indicates that there is a genetic component to atypical BSE susceptibility in addition to E211K.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=234699
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
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
P02.35
Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf
Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock
Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement
Start Date: Sep 15, 2004 End Date: Sep 14, 2009
Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490
Wednesday, February 11, 2009
Atypical BSE North America Update February 2009
Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198
snip...end
source :
Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72
Bovine spongiform encephalopathy
Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD
http://avmajournals.avma.org/doi/ref/10.2460/javma.234.1.59
Atypical BSE North America Update February 2009
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
Thursday, April 9, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed
http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html
full text ;
Sunday, April 12, 2009 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
http://bse-atypical.blogspot.com/2009/04/transmission-of-atypical-bovine.html
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Tons of Beef Suspected of Mad Cow Disease Sold
By Kim Rahn Staff Reporter
About 13 tons of American beef were falsely sold as Australian products five years ago in defiance of a disposal order issued after a case of mad cow disease, or bovine spongiform encephalopathy (BSE), was reported in the United States.
The prosecution indicted two men, identified as Seon and Kim, Monday, for having hoarded the American beef from a discount store where Seon worked and having supplied it to big discount store chains and department stores.
In December 2003, when cows suspected of having the disease were found in the U.S. and Seon's company was ordered to dispose of all American beef, he allegedly destroyed seven tons and falsely reported to the company that he had destroyed the entire 29 tons in the store.
Among the remaining 22 tons, Seon delivered 12.7 tons to discount stores and department stores between August and December 2004. The two fabricated expiration dates of the products and labeled them as ``Australian beef,'' raking in 280 million won in revenue. The products sold out.
Seon claimed that they did not distribute about 10 tons of the remaining products, but prosecutors suspect they did, requesting a tax agency audit Kim's company.
The prosecution is considering expanding the investigation into other meat distributors to search for similar cases.
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000162/!x-usc:mailto:rahnita@koreatimes.co.kr
http://www.koreatimes.co.kr/www/news/nation/2009/04/117_43177.html
Why Americans, As Well as Koreans, Should Be Worried About Mad Cow Tainted USA Beef By Terry S. Singeltary Sr. May 15, 2008 Straight to the Source
Web Note: This is an important commentary by Terry S. Singeltary Sr., on a recent Business Week story on the controversy in South Korea over their government's lifting on the ban on conventional (non-organic) beef, despite the fact that the USDA is still allowing slaughterhouse waste and blood and manure to be fed to cows, and refusing to test all cows at slaughter. See the Mad Cow section of the OCA website for in-depth information. Terry is a regular blogger on the OCA website on Mad Cow issues.
Ronnie Cummins
http://www.organicconsumers.org/articles/article_12387.cfm
http://www.fpif.org/fpiftxt/3940
http://www.testcowsnow.com/export-of-beef-and-beef-products-to-korea-usda-fsis-notice-expires-7109-opi-oppd
http://usdavskorea.blogspot.com/2008/05/usda-vs-korea-typical-or-atypical-bse.html
*** 2009 ***
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)
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf
Research Project: GENETIC AND BIOLOGICAL DETERMINANTS OF RESPIRATORY DISEASE SUSCEPTIBILITY Location: Animal Health Systems Research
Title: Association of a bovine prion gene haplotype with atypical BSE
Author
Clawson, Michael
Submitted to: Meeting Abstract Publication Type: Abstract Publication Acceptance Date: December 2, 2008 Publication Date: January 1, 2009 Citation: Clawson, M.L. 2009. Association of a bovine prion gene haplotype with atypical BSE [abstract]. Plant and Animal Genomes XVII Conference. Abstract No. W091. Available:
http://www.intl-pag.org/17/abstracts/
Technical Abstract: Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a class of fatal neurodegenerative disorders that occur in humans, ruminants, cats, and mink. Three distinct TSEs afflict cattle: classical bovine spongiform encephalopathy (BSE), atypical H-type BSE, and atypical L-type BSE. Classical BSE was identified in the 1980s and is acquired by cattle through the consumption of feed contaminated with the infectious prion agent. Atypical BSEs have only recently been recognized as distinct cattle prion diseases and are extremely rare. The full extent of genetic susceptibilities to atypical BSEs is unknown; however, one atypical H-type case identified in the United States (2006) was most likely caused by a genetic mutation in the prion gene, E211K. We have identified an association of a bovine prion DNA haplotype with atypical BSE that is independent of E211K. The haplotype spans a portion of the prion gene that includes part of intron 2, the entire coding region of exon 3, and part of the three prime untranslated region of exon 3 (13 kb). Despite the low frequency of this haplotype among general cattle populations, it was present in a majority of H- and L-type atypical BSE cases from Canada, France, and the United States. This result indicates that there is a genetic component to atypical BSE susceptibility in addition to E211K.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=234699
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
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
P02.35
Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf
Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock
Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement
Start Date: Sep 15, 2004 End Date: Sep 14, 2009
Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490
Wednesday, February 11, 2009
Atypical BSE North America Update February 2009
Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198
snip...end
source :
Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72
Bovine spongiform encephalopathy
Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD
http://avmajournals.avma.org/doi/ref/10.2460/javma.234.1.59
Atypical BSE North America Update February 2009
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
Thursday, April 9, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed
http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html
full text ;
Sunday, April 12, 2009 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
http://bse-atypical.blogspot.com/2009/04/transmission-of-atypical-bovine.html
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Saturday, December 27, 2008
Disappointing decision on U.S. beef petition i.e. FORCE FEEDING KOREANS USDA MAD COW BEEF
[Editorial] Disappointing decision on U.S. beef petition
The Constitutional Court has ruled against a constitutional petition by 96,000 citizens claiming that the “process by which the Lee Myung-bak administration resumed imports of American beef by formalizing the move with an official announcement (gosi) in the daily government gazette (Gwanbo) was unconstitutional.” The Gwanbo is equivalent to the Federal Register in the United States. Its decision is a big disappointment for the Koreans who had hoped the court would stand in defense of the people’s safety and quarantine inspection sovereignty, because if the gosi was declared unconstitutional in accordance with the petition, which had more signatories than any in history, it would have been automatically invalidated and the Korean government would then have had the justification to renegotiate the beef deal with the United States.
The constitutional petition put before the Constitutional Court asserted that the administration’s move “significantly increases the possibility of bovine spongiform encephalopathy in humans and therefore infringes on constitutionally-guaranteed dignity and worth as humans, the right to pursue happiness, the right to life, and the right to health.” Negotiations with the United States on beef made it so that Korea accepts American beef without limits to age or parts, and that Korea cannot halt beef imports even if there is an outbreak of mad cow disease in the United States. Additional negotiations allowed for restrictions on beef from cows older than 30 months of age and on specified risk material, or SRM, but that was not a fundamental solution. It wrongly assumed that the United States had strengthened prohibitions on animal-based feed that had been relaxed, and another mistake was permitting the importation of some SRM, believing it to be parts that are safe.
Even the current head of the Ministry of Government Legislation said that the process was constitutionally flawed and that he, too, would have taken the issue to the Constitutional Court had he been in the opposition. He said that it is highly problematic, in a constitutional way, to implement something with a directive announcement (gosi) from the relevant Cabinet minister without legislation-drafting procedures, when the issue directly relates to the country’s health.
“While the gosi’s protection measures may not be perfect,” the court said it its decision, “one cannot conclude that this was wholly, or very much, an action that violated the state's constitutional duty to protect the safety of lives and bodies.” It is hard to understand how surrendering quarantine inspection sovereignty and exposing the country to the risk of mad cow disease cannot be concluded to be in inconsistent with or inadequate as far as the duty to the state. It is also disappointing that the court never even had an open oral debate that included expert testimony about a case that was the subject of intense national interest.
The mission of the Constitutional Court is to defend the basic rights of the people and weed out laws that are unconstitutional for violating those rights. The minority opinion was right in stating that the gosi “violates the petitioners’ basic rights because it inadequately carries out the state’s duty to protect basic rights regarding (the safety) of life and body.”
Please direct questions or comments to [englishhani@hani.co.kr]
http://english.hani.co.kr/arti/english_edition/e_editorial/329968.html
Tuesday, May 13, 2008 Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008
snip...
Re..Korea vs USDA beef (the truth)
Greetings KIWA et al and all Koreans,
A kind greetings from Bacliff, Texas.
I submit this data with great concern, sincerity, and in peace.
President Lee Myung-bak states ;
Greetings KIWA et al and all Koreans,
A kind greetings from Bacliff, Texas.
I submit this data with great concern, sincerity, and in peace.
President Lee Myung-bak states ;
"halt imports if another case of bovine spongiform encephalopathy turned up in the United States." now that is funny. a mad cow with BSE would have to drop from the sky onto the white house lawn and run around jerking, trembling, stumbling and staggering uncontrollably for months before anyone would every confirm a mad cow case with BSE, and then it would take an act of congress to confirm it, and President Lee Myung-bak knows this. it's all about commodities and futures $$$
Monday, May 5, 2008
STATEMENT OF DR. RICHARD RAYMOND USDA UNDERSECRETARY FOR FOOD SAFETY Regarding the Safety of the U.S. Food Supply please see full text with some additional information the good Dr. Raymond seems to have forgotten about ;
http://usdameatexport.blogspot.com/2008/05/statement-of-dr-richard-raymond-usda.html
USDA BEEF DEAL WITH KOREA AND the truth, what the usda et al are not telling you...
http://flounder068.vox.com/library/post/usda-beef-deal-with-korea-and-the-truth-what-the-usda-et-al-are-not-telling-you.html
DOWNER CATTLE SCHOOL LUNCH PROGRAM
http://downercattle.blogspot.com/
http://downercattle.blogspot.com/2008/05/humane-society-releases-new-video-of.html
"Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD."
Sincerely, Pierluigi Gambetti, MD Director, National Prion Disease Pathology Surveillance Center Stephen M. Sergay, MB, BCh President, American Academy of Neurology
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
THE LAST TWO MAD COWS documentED IN TEXAS AND ALABAMA WERE ATYPICAL BSE. then GW, USDA et al shut the testing down $$$ (new they would find more. ...tss)
please see full text with additional comments and links @ ;
http://prionunitusaupdate2008.blogspot.com/
Sunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html
==============================
THE only fool is one who fools himself, and GW and his administration and their junk science will fool humans for just so long, then the incubation will catch up. none of this was about science, it was all about commodities and futures and the exporting of beef. nothing else mattered, literally, just ask old stanley prusiner the nobel prize winner for the PRION, what did old stan say ;
STANLEY PRUSINER NOBEL PEACE PRIZE WINNER ON THE PRION
US AG SEC AND LAYCRAFT
"nothing matters, except beef from Canada under 30 months bone in beef product, that's ALL THAT MATTERS!" US SENATOR AND STAN THE MAN SLAM USDA "DAMNING TESTIMONY"
Senator Michael Machado from California
"USDA does not know what's going on". "USDA is protecting the industry". " SHOULD the state of California step in"
Stanley Prusiner
"nobody has ever ask us to comment"
"they don't want us to comment"
"they never ask"
i tried to see Venemon, after Canadian cow was discovered with BSE. went to see lyle. after talking with him.
absolute ignorance.
then thought i should see Venemon.
it was clear his entire policy was to get cattle boneless beef prods across the border.
nothing else mattered.
his aids confirmed this.
5 times i tried to see Venemon, never worked.
eventually met with carl rove the political.
he is the one that arranged meeting with Venemon.
just trying to give you a sense of the distance.
threat to health public safety.
was never contacted.
yes i believe that prions are bad to eat and you can die from them.END
Dr. Stan bashing Ann Veneman - 3 minutes - Damning testimony
http://maddeer.org/video/embedded/08snip.ram
File Name: USDA DON'T ASK DON'T TELL POLICY 02snip.rpm DAMNING testimony of consumer consumption of Washington mad cow in California
http://www.maddeer.org/video/embedded/02snip.rm
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
see full text ;
http://sciencebushwhacked.blogspot.com/
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST 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
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
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
snip...
see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ; Friday, April 25, 2008
Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46
http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html
2006 was a banner year too for mad cow protein fed out into commerce. those were just one of many ; Specified Risk Materials
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
http://nor-98.blogspot.com/
http://www.yacomitservice.com/php/eng/board.php?board=kkkqna&command=body&no=84
snip...
http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.html
USDA VS KOREA typical or atypical BSe
http://usdavskorea.blogspot.com/
Friday, May 9, 2008 USDA VS KOREA typical or atypical BSe Honorable people of Korea,
a kind and warm greetings from Texas.
snip...
http://usdavskorea.blogspot.com/2008/05/usda-vs-korea-typical-or-atypical-bse.html
Why Americans, As Well as Koreans, Should Be Worried About Mad Cow Tainted USA Beef
By Terry S. Singeltary Sr. May 15, 2008
Straight to the Source
Web Note: This is an important commentary by Terry S. Singeltary Sr., on a recent Business Week story on the controversy in South Korea over their government's lifting on the ban on conventional (non-organic) beef, despite the fact that the USDA is still allowing slaughterhouse waste and blood and manure to be fed to cows, and refusing to test all cows at slaughter. See the Mad Cow section of the OCA website for in-depth information. Terry is a regular blogger on the OCA website on Mad Cow issues.
Ronnie Cummins
One Korean official says the probability of a human being catching a mad cow disease by eating U.S. beef is like the one of a golf player scoring a hole-in-one and then being killed by lightning.
this is typical BSe. you here industry groups comment 'your more likely to get hit by a car than die from CJD'. well, maybe so, but my mother and many more did not die from getting hit by a car, they died from CJD, my mothers being the hvCJD (confirmed), and my neighbors mother died from CJD (confirmed). the UKBSEnvCJD _only_ theory is incorrect. there are more strains of mad cow than the UK BSE in beef to nvCJD in humans in the UK. The deception by the USDA, FDA, and the Bush administration about mad cow disease, CJD, and all Transmissible Spongiform Encephalopathy over the past 8 years have been outrageous, to a point of being criminal. I am vested in nothing, but the truth.
snip...see full text ;
http://www.grassrootsnetroots.org/articles/article_12387.cfm
Tuesday, May 13, 2008
Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008
http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.html
http://flounder068.vox.com/library/post/concerned-americans-against-mad-cow-disease-statement-of-solidarity-with-koreans-may-13-2008.html
http://www.koreantopnews.com/story.php?title=USDA_VS_KOREA_typical_or_atypical_BSe_Concerned_Americans_against_Mad_Cow_Disease_STATEMENT_OF_SOLIDARITY_with_Koreans_May_13_2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
http://flounder068.vox.com/library/post/bse-youngest-age-statistics-under-30-months.html
Friday, June 20, 2008
USDA TO KOREA AND THE WORLD, EAT THAT AND LIKE IT
http://usdavskorea.blogspot.com/2008/06/usda-to-korea-and-world-eat-that-and.html
Wednesday, June 11, 2008
OIE Recognition of the BSE Status of Members RESOLUTION No. XXI (Adopted by the International Committee of the OIE on 27 May 2008)
snip...
http://usdavskorea.blogspot.com/2008/06/oie-recognition-of-bse-status-of.html
http://organicconsumers.org/forum/index.php?showtopic=1566
U.S. slams door on revising S. Korea beef import pact
June 11, 2008, 10:14PM
http://usdavskorea.blogspot.com/2008/06/us-slams-door-on-revising-s-korea-beef.html
Saturday, June 7, 2008
Export Requirements for the Republic of Korea IMPORT HEALTH REQUIREMENTS FOR U.S. BEEF AND BEEF PRODUCTS
http://usdavskorea.blogspot.com/2008/06/export-requirements-for-republic-of.html
Wednesday, July 23, 2008
Audit says USDA lost track of imported cattle Report No. 50601-0012-Ch March 2008 Audit says USDA lost track of imported cattle Canada has reported 13 cases of mad cow
http://usdameatexport.blogspot.com/
UPDATE DECEMBER 2008
Monday, December 22, 2008
[Docket No. FDA–2008–D–0597] Draft Guidance for Industry: Small Entities Compliance Guide for Renderers—Substances Prohibited From Use in Animal Food
Greetings,
I kindly wish to submit the following to [Docket No. FDA–2008–D–0597] ;
I would kindly like to once again comment on the failed attempts of the FDA et al to stop the spread of animal TSEs, including BSE, through the legal, and illegal feeding practices, of feeding animal protein to livestock for human and animal consumption. Since the terribly flawed, partial, and voluntary August 4, 1997 ruminant to ruminant feed ban was put into place, literally 100s of thousands of tons of banned animal protein has been fed out into commerce, even as late as 2007, when some 10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. 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. NOW, how much of that product that went out into commerce was fed out to cattle, and how much was ever recovered ? AND to think that feeding blood to livestock producing animals is still legal, when scientific study after study shows that TSEs are easily transmitted via blood. IT is absolutely unacceptable that still in 2008, the USA is still feeding highly suspect mad cow feed to USA cattle, and other livestock producing animals. Especially when the last two cases of BSE that were allowed to be tested and reported were of the atypical BSE category, of which we now know the atypical BSE is more virulent than that of the typical BSE, and when ARS research on the atypical BSE said long ago the SRM rules may need to be changed, IF the atypical BSE were to be proven to be more virulent. Why do we continue to flounder? I have submitted to these BSE feed dockets until I am blue in the face, and still to date, they still debate an issue that should have been settled long ago. IT's a fine example of how big ag, big industry, have a stranglehold on sound science and policy making thereof. How many millions of animals and humans have been needlessly exposed to this TSE agent, due to nothing more than ignorance and greed, simply because of a disease that is 100% fatal, but one that has such a long incubation period. For the government and industry as a whole, to continue to flagrantly violate said rules and regulations, in my opinion, should be regarded as criminal, and treated as such. People are dying. ...
Please see references ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
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
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
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
2006 WAS A BANNER YEAR ALSO FOR MAD COW FEED BAN VIOLATIONS ''IN COMMERCE''
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
snip...
see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ;
see full text ;
Friday, April 25, 2008
Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46
http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html
SPECIFIED RISK MATERIALS
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
0C3.01
Transmission of atypical BSE to Microcebus murinus, a non-human primate: Development of clinical symptoms and tissue distribution of PrPres
Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L -type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).
Objectives and Methods: In order to see if the atypical BSE cases were transmissible to primates, either animals (were intracerebrally inoculated with 50 ul of a 10% brain homogenates of two atypical French BSE case, a H-type (2 males and 2 females) and a L-type (2 males and 2 females).
Results: Only one of the four lemurs challenged with H-type BSE died without clinical signs after 19 months post inoculation (mpi), whereas all the 4 animals inoculated with L -type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms got worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-type, spongiform changes without PrPres accumulation were observed in the brainstem. However Western blot analysis did not allow to detect PrPres into the brain. For the L-type, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem. whereas into the cortex the spongiosis was evidenced, but the Vacuolisation was weaker. Strong deposits of PrPres were detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis also readily confirmed the presence of protease-resistant prion protein.
Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain in a model of non human primate.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum 100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg Primate (oral route)* 1/2 (50%) Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%) RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%) PrPres biochemical detection The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal. Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........
http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose
It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s145d.pdf
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
snip... full text ;
http://madcowfeed.blogspot.com/2008/12/docket-no-fda2008d0597-draft-guidance.html
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain
Qingzhong Kong,1* Mengjie Zheng,1 Cristina Casalone,2 Liuting Qing,1 Shenghai Huang,1? Bikram Chakraborty,1 Ping Wang,1 Fusong Chen,1 Ignazio Cali,1 Cristiano Corona,2 Francesca Martucci,2 Barbara Iulini,2 Pierluigi Acutis,2 Lan Wang,1 Jingjing Liang,1 Meiling Wang,1 Xinyi Li,1 Salvatore Monaco,3 Gianluigi Zanusso,3 Wen-Quan Zou,1 Maria Caramelli,2 and Pierluigi Gambetti1* Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106,1 CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy,2 Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy3 *Corresponding author. Mailing address: Department of Pathology, Case Western Reserve University, Cleveland, OH 44106. Phone for Pierluigi Gambetti: (216) 368-0586. Fax: (216) 368-2546. E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000025/!x-usc:mailto:pxg13@case.edu . Phone for Qingzhong Kong: (216) 368-1756. Fax: (216) 368-2546. E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000025/!x-usc:mailto:qxk2@case.edu ?Present address: Department of Patient Education and Health Information, Cleveland Clinic Foundation, Cleveland, OH 44195. Received November 30, 2007; Accepted January 16, 2008.
Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to be caused by only one strain, BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE strains by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE strain-infected cattle. Sixty percent of the inoculated Tg mice became infected after 20 to 22 months of incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE strain-infected Tg mice, but none of the Tg mice infected with prions causing a sporadic human prion disease, showed the presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE strain-infected humanized Tg mouse brains are different from those from the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation times are observed for the BASE strain-infected Tg mice. These results suggest that in humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2268471
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." ... interesting. ... TSS
Thursday, June 05, 2008
Review on the epidemiology and dynamics of BSE epidemics
Vet. Res. (2008) 39:15 www.vetres.org DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article
snip...
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
snip...
Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
full text 18 pages ;
http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf
please see full text ;
http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html
***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***
Progress Report from the National Prion Disease Pathology Surveillance Center
An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD
April 3, 2008
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
A New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html
Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
sporadic Fatal Familial Insomnia
http://sporadicffi.blogspot.com/
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
mailto:flounder9@verizon.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
2 January 2000 British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999 British Medical Journal vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
Creutzfeldt Jakob Disease
http://creutzfeldt-jakob-disease.blogspot.com/
USA PRION UNIT BLOG
http://prionunitusaupdate2008.blogspot.com/
Sunday, April 20, 2008 Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008
Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.
see full text ;
http://prionunitusaupdate2008.blogspot.com/2008/04/progress-report-from-national-prion.html
CJD TEXAS (cjd clusters)
http://cjdtexas.blogspot.com/
USA WRITTEN CJD QUESTIONNAIRE ???
http://cjdquestionnaire.blogspot.com/
Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html
2007
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
Friday, August 29, 2008
CREEKSTONE VS USDA COURT OF APPEALS, BUSH SAYS, NO WAY, NO HOW
http://madcowtesting.blogspot.com/2008/08/creekstone-vs-usda-court-of-appeals.html
Sunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
0C3.01
Transmission of atypical BSE to Microcebus murinus, a non-human primate: Development of clinical symptoms and tissue distribution of PrPres
Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L -type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).
Objectives and Methods: In order to see if the atypical BSE cases were transmissible to primates, either animals (were intracerebrally inoculated with 50 ul of a 10% brain homogenates of two atypical French BSE case, a H-type (2 males and 2 females) and a L-type (2 males and 2 females).
Results: Only one of the four lemurs challenged with H-type BSE died without clinical signs after 19 months post inoculation (mpi), whereas all the 4 animals inoculated with L -type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms got worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-type, spongiform changes without PrPres accumulation were observed in the brainstem. However Western blot analysis did not allow to detect PrPres into the brain. For the L-type, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem. whereas into the cortex the spongiosis was evidenced, but the Vacuolisation was weaker. Strong deposits of PrPres were detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis also readily confirmed the presence of protease-resistant prion protein.
Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain in a model of non human primate.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
P7.09
Biochemical screening for identification of atypical bse in belgium, 1999-present
Authors
Alexandre DobIy: Caroline Rodeghiero, Riet Geeroms; Stephanie Durand, Jessica De Sloovere, Emanuel Yanopdenbosch, Stefan Roels,
Content
Background: Recently atypical forms of BSE have been described. Western blot analyses showed that, in comparison to the classic BSE (C-type), they are demonstrable by a higher or lower molecular weight of the unglycosylated PrPres. They Viere thus named H-type and L-type BSE (L-type is also called BASE). In addition they show a lower proportion of diglycosylated PrPres than C-type. These emerging types represent different strains of BSE. They show unique incubation periods and histological lesions. Such types have been described on different continents. Indeed they might correspond to "sporadic" forms of BSE. In 2004 we already described one L-type in Belgium.
Objective: We retrospectively analysed the bovines at least 7-year-old in the Belgian archive of BSE diagnosed cattle in order to determine the prevalence of the two types of atypical BSE in Belgium.
Methods: We analysed homogenates from 39 bovines of 93 months old in median (min: 84, max: 181 months). The most recent one was diagnosed in 2006. We used Western blot with a panel of anti-PrP antibodies (Ab). They detect different regions of the PrP protein, from N-terminal to C-terminal: 12B2, 9A2, Sha31. SAFB4, 94B4. Their combination is aimed at an efficient typing diagnostic. We detected bound Ab with SuperSignal West Dura (Pierce) and analysed PrPres, signals with an image-analysis software (Quantity One, Bio-Rad).
Results: The results are still under analysis. We will detail the most crucial characteristics for typing PrPres. These include 1) the apparent molecular mass of the an-, mono- and diglycosylated bands, 2) the binding affinity to the five Ab (e.g.12B2 for H-type), 3) the presence of a fourth (unglycosylated) band and 4) the glycoprofile based on the relative proportions of the visible bands.
Discussion: The emergence of atypical types of BSE is partially due to a better knowledge of prion strains and more efficient diagnostic techniques. As the area in the brain where the PrPres is deposited can differ drastically between the types, it is essential to ascertain that the sampling techniques and analyses are adapted to these new types. As these new strains seem more virulent than classic types, they represent one of the next challenges in the field of prions.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
http://www.prion2008.com/
Tuesday, November 11, 2008
Transmission of atypical bovine prions to mice transgenic for human prion protein
DOI: 10.3201/eid1412.080941
http://bse-atypical.blogspot.com/2008/11/transmission-of-atypical-bovine-prions.html
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Tuesday, June 3, 2008
SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html
SCRAPIE USA
http://scrapie-usa.blogspot.com/
Sunday, September 07, 2008
CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA
http://chronic-wasting-disease.blogspot.com/2008/09/cwd-live-test-and-political-aspects-or.html
Saturday, October 18, 2008
WYOMING STAR VALLEY MOOSE TESTS POSITIVE FOR CWD
http://chronic-wasting-disease.blogspot.com/2008/10/wyoming-star-valley-moose-tests.html
http://chronic-wasting-disease.blogspot.com/
Friday, December 12, 2008
The prion strain phenomenon: Molecular basis and unprecedented features
http://bse-atypical.blogspot.com/2008/12/prion-strain-phenomenon-molecular-basis.html
Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC -254 Accepted - Volume 11
http://www.fda.gov/OHRMS/DOCKETS/DOCKETS/02n0276/02N-0276-EC-254.htm
http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
PART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
Monday, December 08, 2008
vCJD & dental treatment
http://creutzfeldt-jakob-disease.blogspot.com/2008/12/vcjd-dental-treatment.html
Friday, December 12, 2008
Prions in Milk from Ewes Incubating Natural Scrapie
http://scrapie-usa.blogspot.com/2008/12/prions-in-milk-from-ewes-incubating.html
Friday, December 05, 2008
Detection of Prion Infectivity in Fat Tissues of Scrapie-Infected Mice
http://scrapie-usa.blogspot.com/2008/12/detection-of-prion-infectivity-in-fat.html
REPORT ON CURRENT & FUTURE SURVEILLANCE FOR BOVINE SPONGIFORM ENCEPHALOPATHY
http://madcowtesting.blogspot.com/2008/11/report-on-current-future-surveillance.html
November 25, 2008
Update On Feed Enforcement Activities To Limit The Spread Of BSE
http://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.html
Plasma & Serum Proteins Receive Continued FDA Approval
4/25/2008 APC, Inc. is pleased to advise our customers and industry partners that as anticipated, the Food and Drug Administration (FDA) will continue to allow the use of bovine blood, plasma and serum proteins in ruminant feeds.
In April 2008 FDA announced the publication of its Final Rule for 21 CFR Part 589.2001 - Substances Prohibited From Use in Animal Food or Feed. FDA specifically stated in their opinion that, "FDA is not prohibiting the use of blood and blood products in animal feed because we believe such a prohibition would do very little to reduce the risk of BSE transmission."
Known as a leader in developing nutritional products for the swine industry, where 95% of pig starter diets in the United States contain functional proteins, APC has more recently developed their line of colostrum replacers, supplements, feed additives and milk replacer ingredients for calves. Products include plasma, serum and immunoglobulin concentrate based Acquire®, Lifeline®, Gammulin® and Nutrapro® used to optimize the health and performance of calves.
To view the full report for Final Rule 21 CFR Part 589.2001 visit:
http://www.fda.gov/OHRMS/DOCKETS/98fr/FDA-2002-N-0031-nfr.pdf
To view the complete Feed Rule 21 CFR Part 589 visit:
http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=589&showFR=1
Friday, November 21, 2008
Plasma & Serum Proteins Receive Continued FDA Approval
http://madcowfeed.blogspot.com/2008/11/plasma-serum-proteins-receive-continued.html
http://madcowfeed.blogspot.com/
Thursday, November 27, 2008
Prion diseases are efficiently transmitted by blood transfusion in sheep
http://vcjdblood.blogspot.com/2008/11/prion-diseases-are-efficiently.html
stupid is, as stupid does. (forest gump)
Thank You,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
The Constitutional Court has ruled against a constitutional petition by 96,000 citizens claiming that the “process by which the Lee Myung-bak administration resumed imports of American beef by formalizing the move with an official announcement (gosi) in the daily government gazette (Gwanbo) was unconstitutional.” The Gwanbo is equivalent to the Federal Register in the United States. Its decision is a big disappointment for the Koreans who had hoped the court would stand in defense of the people’s safety and quarantine inspection sovereignty, because if the gosi was declared unconstitutional in accordance with the petition, which had more signatories than any in history, it would have been automatically invalidated and the Korean government would then have had the justification to renegotiate the beef deal with the United States.
The constitutional petition put before the Constitutional Court asserted that the administration’s move “significantly increases the possibility of bovine spongiform encephalopathy in humans and therefore infringes on constitutionally-guaranteed dignity and worth as humans, the right to pursue happiness, the right to life, and the right to health.” Negotiations with the United States on beef made it so that Korea accepts American beef without limits to age or parts, and that Korea cannot halt beef imports even if there is an outbreak of mad cow disease in the United States. Additional negotiations allowed for restrictions on beef from cows older than 30 months of age and on specified risk material, or SRM, but that was not a fundamental solution. It wrongly assumed that the United States had strengthened prohibitions on animal-based feed that had been relaxed, and another mistake was permitting the importation of some SRM, believing it to be parts that are safe.
Even the current head of the Ministry of Government Legislation said that the process was constitutionally flawed and that he, too, would have taken the issue to the Constitutional Court had he been in the opposition. He said that it is highly problematic, in a constitutional way, to implement something with a directive announcement (gosi) from the relevant Cabinet minister without legislation-drafting procedures, when the issue directly relates to the country’s health.
“While the gosi’s protection measures may not be perfect,” the court said it its decision, “one cannot conclude that this was wholly, or very much, an action that violated the state's constitutional duty to protect the safety of lives and bodies.” It is hard to understand how surrendering quarantine inspection sovereignty and exposing the country to the risk of mad cow disease cannot be concluded to be in inconsistent with or inadequate as far as the duty to the state. It is also disappointing that the court never even had an open oral debate that included expert testimony about a case that was the subject of intense national interest.
The mission of the Constitutional Court is to defend the basic rights of the people and weed out laws that are unconstitutional for violating those rights. The minority opinion was right in stating that the gosi “violates the petitioners’ basic rights because it inadequately carries out the state’s duty to protect basic rights regarding (the safety) of life and body.”
Please direct questions or comments to [englishhani@hani.co.kr]
http://english.hani.co.kr/arti/english_edition/e_editorial/329968.html
Tuesday, May 13, 2008 Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008
snip...
Re..Korea vs USDA beef (the truth)
Greetings KIWA et al and all Koreans,
A kind greetings from Bacliff, Texas.
I submit this data with great concern, sincerity, and in peace.
President Lee Myung-bak states ;
Greetings KIWA et al and all Koreans,
A kind greetings from Bacliff, Texas.
I submit this data with great concern, sincerity, and in peace.
President Lee Myung-bak states ;
"halt imports if another case of bovine spongiform encephalopathy turned up in the United States." now that is funny. a mad cow with BSE would have to drop from the sky onto the white house lawn and run around jerking, trembling, stumbling and staggering uncontrollably for months before anyone would every confirm a mad cow case with BSE, and then it would take an act of congress to confirm it, and President Lee Myung-bak knows this. it's all about commodities and futures $$$
Monday, May 5, 2008
STATEMENT OF DR. RICHARD RAYMOND USDA UNDERSECRETARY FOR FOOD SAFETY Regarding the Safety of the U.S. Food Supply please see full text with some additional information the good Dr. Raymond seems to have forgotten about ;
http://usdameatexport.blogspot.com/2008/05/statement-of-dr-richard-raymond-usda.html
USDA BEEF DEAL WITH KOREA AND the truth, what the usda et al are not telling you...
http://flounder068.vox.com/library/post/usda-beef-deal-with-korea-and-the-truth-what-the-usda-et-al-are-not-telling-you.html
DOWNER CATTLE SCHOOL LUNCH PROGRAM
http://downercattle.blogspot.com/
http://downercattle.blogspot.com/2008/05/humane-society-releases-new-video-of.html
"Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD."
Sincerely, Pierluigi Gambetti, MD Director, National Prion Disease Pathology Surveillance Center Stephen M. Sergay, MB, BCh President, American Academy of Neurology
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
THE LAST TWO MAD COWS documentED IN TEXAS AND ALABAMA WERE ATYPICAL BSE. then GW, USDA et al shut the testing down $$$ (new they would find more. ...tss)
please see full text with additional comments and links @ ;
http://prionunitusaupdate2008.blogspot.com/
Sunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html
==============================
THE only fool is one who fools himself, and GW and his administration and their junk science will fool humans for just so long, then the incubation will catch up. none of this was about science, it was all about commodities and futures and the exporting of beef. nothing else mattered, literally, just ask old stanley prusiner the nobel prize winner for the PRION, what did old stan say ;
STANLEY PRUSINER NOBEL PEACE PRIZE WINNER ON THE PRION
US AG SEC AND LAYCRAFT
"nothing matters, except beef from Canada under 30 months bone in beef product, that's ALL THAT MATTERS!" US SENATOR AND STAN THE MAN SLAM USDA "DAMNING TESTIMONY"
Senator Michael Machado from California
"USDA does not know what's going on". "USDA is protecting the industry". " SHOULD the state of California step in"
Stanley Prusiner
"nobody has ever ask us to comment"
"they don't want us to comment"
"they never ask"
i tried to see Venemon, after Canadian cow was discovered with BSE. went to see lyle. after talking with him.
absolute ignorance.
then thought i should see Venemon.
it was clear his entire policy was to get cattle boneless beef prods across the border.
nothing else mattered.
his aids confirmed this.
5 times i tried to see Venemon, never worked.
eventually met with carl rove the political.
he is the one that arranged meeting with Venemon.
just trying to give you a sense of the distance.
threat to health public safety.
was never contacted.
yes i believe that prions are bad to eat and you can die from them.END
Dr. Stan bashing Ann Veneman - 3 minutes - Damning testimony
http://maddeer.org/video/embedded/08snip.ram
File Name: USDA DON'T ASK DON'T TELL POLICY 02snip.rpm DAMNING testimony of consumer consumption of Washington mad cow in California
http://www.maddeer.org/video/embedded/02snip.rm
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
see full text ;
http://sciencebushwhacked.blogspot.com/
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST 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
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
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
snip...
see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ; Friday, April 25, 2008
Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46
http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html
2006 was a banner year too for mad cow protein fed out into commerce. those were just one of many ; Specified Risk Materials
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
http://nor-98.blogspot.com/
http://www.yacomitservice.com/php/eng/board.php?board=kkkqna&command=body&no=84
snip...
http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.html
USDA VS KOREA typical or atypical BSe
http://usdavskorea.blogspot.com/
Friday, May 9, 2008 USDA VS KOREA typical or atypical BSe Honorable people of Korea,
a kind and warm greetings from Texas.
snip...
http://usdavskorea.blogspot.com/2008/05/usda-vs-korea-typical-or-atypical-bse.html
Why Americans, As Well as Koreans, Should Be Worried About Mad Cow Tainted USA Beef
By Terry S. Singeltary Sr. May 15, 2008
Straight to the Source
Web Note: This is an important commentary by Terry S. Singeltary Sr., on a recent Business Week story on the controversy in South Korea over their government's lifting on the ban on conventional (non-organic) beef, despite the fact that the USDA is still allowing slaughterhouse waste and blood and manure to be fed to cows, and refusing to test all cows at slaughter. See the Mad Cow section of the OCA website for in-depth information. Terry is a regular blogger on the OCA website on Mad Cow issues.
Ronnie Cummins
One Korean official says the probability of a human being catching a mad cow disease by eating U.S. beef is like the one of a golf player scoring a hole-in-one and then being killed by lightning.
this is typical BSe. you here industry groups comment 'your more likely to get hit by a car than die from CJD'. well, maybe so, but my mother and many more did not die from getting hit by a car, they died from CJD, my mothers being the hvCJD (confirmed), and my neighbors mother died from CJD (confirmed). the UKBSEnvCJD _only_ theory is incorrect. there are more strains of mad cow than the UK BSE in beef to nvCJD in humans in the UK. The deception by the USDA, FDA, and the Bush administration about mad cow disease, CJD, and all Transmissible Spongiform Encephalopathy over the past 8 years have been outrageous, to a point of being criminal. I am vested in nothing, but the truth.
snip...see full text ;
http://www.grassrootsnetroots.org/articles/article_12387.cfm
Tuesday, May 13, 2008
Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008
http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.html
http://flounder068.vox.com/library/post/concerned-americans-against-mad-cow-disease-statement-of-solidarity-with-koreans-may-13-2008.html
http://www.koreantopnews.com/story.php?title=USDA_VS_KOREA_typical_or_atypical_BSe_Concerned_Americans_against_Mad_Cow_Disease_STATEMENT_OF_SOLIDARITY_with_Koreans_May_13_2008
BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS
http://bseyoungestage.blogspot.com/
http://flounder068.vox.com/library/post/bse-youngest-age-statistics-under-30-months.html
Friday, June 20, 2008
USDA TO KOREA AND THE WORLD, EAT THAT AND LIKE IT
http://usdavskorea.blogspot.com/2008/06/usda-to-korea-and-world-eat-that-and.html
Wednesday, June 11, 2008
OIE Recognition of the BSE Status of Members RESOLUTION No. XXI (Adopted by the International Committee of the OIE on 27 May 2008)
snip...
http://usdavskorea.blogspot.com/2008/06/oie-recognition-of-bse-status-of.html
http://organicconsumers.org/forum/index.php?showtopic=1566
U.S. slams door on revising S. Korea beef import pact
June 11, 2008, 10:14PM
http://usdavskorea.blogspot.com/2008/06/us-slams-door-on-revising-s-korea-beef.html
Saturday, June 7, 2008
Export Requirements for the Republic of Korea IMPORT HEALTH REQUIREMENTS FOR U.S. BEEF AND BEEF PRODUCTS
http://usdavskorea.blogspot.com/2008/06/export-requirements-for-republic-of.html
Wednesday, July 23, 2008
Audit says USDA lost track of imported cattle Report No. 50601-0012-Ch March 2008 Audit says USDA lost track of imported cattle Canada has reported 13 cases of mad cow
http://usdameatexport.blogspot.com/
UPDATE DECEMBER 2008
Monday, December 22, 2008
[Docket No. FDA–2008–D–0597] Draft Guidance for Industry: Small Entities Compliance Guide for Renderers—Substances Prohibited From Use in Animal Food
Greetings,
I kindly wish to submit the following to [Docket No. FDA–2008–D–0597] ;
I would kindly like to once again comment on the failed attempts of the FDA et al to stop the spread of animal TSEs, including BSE, through the legal, and illegal feeding practices, of feeding animal protein to livestock for human and animal consumption. Since the terribly flawed, partial, and voluntary August 4, 1997 ruminant to ruminant feed ban was put into place, literally 100s of thousands of tons of banned animal protein has been fed out into commerce, even as late as 2007, when some 10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. 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. NOW, how much of that product that went out into commerce was fed out to cattle, and how much was ever recovered ? AND to think that feeding blood to livestock producing animals is still legal, when scientific study after study shows that TSEs are easily transmitted via blood. IT is absolutely unacceptable that still in 2008, the USA is still feeding highly suspect mad cow feed to USA cattle, and other livestock producing animals. Especially when the last two cases of BSE that were allowed to be tested and reported were of the atypical BSE category, of which we now know the atypical BSE is more virulent than that of the typical BSE, and when ARS research on the atypical BSE said long ago the SRM rules may need to be changed, IF the atypical BSE were to be proven to be more virulent. Why do we continue to flounder? I have submitted to these BSE feed dockets until I am blue in the face, and still to date, they still debate an issue that should have been settled long ago. IT's a fine example of how big ag, big industry, have a stranglehold on sound science and policy making thereof. How many millions of animals and humans have been needlessly exposed to this TSE agent, due to nothing more than ignorance and greed, simply because of a disease that is 100% fatal, but one that has such a long incubation period. For the government and industry as a whole, to continue to flagrantly violate said rules and regulations, in my opinion, should be regarded as criminal, and treated as such. People are dying. ...
Please see references ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
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
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
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
2006 WAS A BANNER YEAR ALSO FOR MAD COW FEED BAN VIOLATIONS ''IN COMMERCE''
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
snip...
see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ;
see full text ;
Friday, April 25, 2008
Substances Prohibited From Use in Animal Food or Feed [Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46
http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html
SPECIFIED RISK MATERIALS
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
0C3.01
Transmission of atypical BSE to Microcebus murinus, a non-human primate: Development of clinical symptoms and tissue distribution of PrPres
Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L -type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).
Objectives and Methods: In order to see if the atypical BSE cases were transmissible to primates, either animals (were intracerebrally inoculated with 50 ul of a 10% brain homogenates of two atypical French BSE case, a H-type (2 males and 2 females) and a L-type (2 males and 2 females).
Results: Only one of the four lemurs challenged with H-type BSE died without clinical signs after 19 months post inoculation (mpi), whereas all the 4 animals inoculated with L -type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms got worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-type, spongiform changes without PrPres accumulation were observed in the brainstem. However Western blot analysis did not allow to detect PrPres into the brain. For the L-type, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem. whereas into the cortex the spongiosis was evidenced, but the Vacuolisation was weaker. Strong deposits of PrPres were detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis also readily confirmed the presence of protease-resistant prion protein.
Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain in a model of non human primate.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum 100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg Primate (oral route)* 1/2 (50%) Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%) RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%) PrPres biochemical detection The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal. Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. .........
http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose
It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s145d.pdf
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
snip... full text ;
http://madcowfeed.blogspot.com/2008/12/docket-no-fda2008d0597-draft-guidance.html
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain
Qingzhong Kong,1* Mengjie Zheng,1 Cristina Casalone,2 Liuting Qing,1 Shenghai Huang,1? Bikram Chakraborty,1 Ping Wang,1 Fusong Chen,1 Ignazio Cali,1 Cristiano Corona,2 Francesca Martucci,2 Barbara Iulini,2 Pierluigi Acutis,2 Lan Wang,1 Jingjing Liang,1 Meiling Wang,1 Xinyi Li,1 Salvatore Monaco,3 Gianluigi Zanusso,3 Wen-Quan Zou,1 Maria Caramelli,2 and Pierluigi Gambetti1* Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106,1 CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy,2 Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy3 *Corresponding author. Mailing address: Department of Pathology, Case Western Reserve University, Cleveland, OH 44106. Phone for Pierluigi Gambetti: (216) 368-0586. Fax: (216) 368-2546. E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000025/!x-usc:mailto:pxg13@case.edu . Phone for Qingzhong Kong: (216) 368-1756. Fax: (216) 368-2546. E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000025/!x-usc:mailto:qxk2@case.edu ?Present address: Department of Patient Education and Health Information, Cleveland Clinic Foundation, Cleveland, OH 44195. Received November 30, 2007; Accepted January 16, 2008.
Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to be caused by only one strain, BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE strains by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE strain-infected cattle. Sixty percent of the inoculated Tg mice became infected after 20 to 22 months of incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE strain-infected Tg mice, but none of the Tg mice infected with prions causing a sporadic human prion disease, showed the presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE strain-infected humanized Tg mouse brains are different from those from the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation times are observed for the BASE strain-infected Tg mice. These results suggest that in humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2268471
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." ... interesting. ... TSS
Thursday, June 05, 2008
Review on the epidemiology and dynamics of BSE epidemics
Vet. Res. (2008) 39:15 www.vetres.org DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article
snip...
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
snip...
Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
full text 18 pages ;
http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf
please see full text ;
http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html
***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***
Progress Report from the National Prion Disease Pathology Surveillance Center
An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD
April 3, 2008
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
A New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html
Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html
http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
sporadic Fatal Familial Insomnia
http://sporadicffi.blogspot.com/
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
mailto:flounder9@verizon.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
2 January 2000 British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999 British Medical Journal vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
Creutzfeldt Jakob Disease
http://creutzfeldt-jakob-disease.blogspot.com/
USA PRION UNIT BLOG
http://prionunitusaupdate2008.blogspot.com/
Sunday, April 20, 2008 Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008
Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.
see full text ;
http://prionunitusaupdate2008.blogspot.com/2008/04/progress-report-from-national-prion.html
CJD TEXAS (cjd clusters)
http://cjdtexas.blogspot.com/
USA WRITTEN CJD QUESTIONNAIRE ???
http://cjdquestionnaire.blogspot.com/
Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html
2007
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
Friday, August 29, 2008
CREEKSTONE VS USDA COURT OF APPEALS, BUSH SAYS, NO WAY, NO HOW
http://madcowtesting.blogspot.com/2008/08/creekstone-vs-usda-court-of-appeals.html
Sunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
0C3.01
Transmission of atypical BSE to Microcebus murinus, a non-human primate: Development of clinical symptoms and tissue distribution of PrPres
Background: Atypical BSE cases have been observed in Europe, Japan and North America. They differ in their PrPres profiles from those found in classical BSE. These atypical cases fall into 2 types, depending on the molecular mass of the unglycosylated PrPres band observed by Western blot: the L -type (lower molecular mass than the typical BSE cases) and H-type (higher molecular mass than the typical BSE cases).
Objectives and Methods: In order to see if the atypical BSE cases were transmissible to primates, either animals (were intracerebrally inoculated with 50 ul of a 10% brain homogenates of two atypical French BSE case, a H-type (2 males and 2 females) and a L-type (2 males and 2 females).
Results: Only one of the four lemurs challenged with H-type BSE died without clinical signs after 19 months post inoculation (mpi), whereas all the 4 animals inoculated with L -type BSE died at 19 mpi (2 males) and 22 mpi (2 females). Three months before their sacrifice, they developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms got worse according to the disease progression, until severe ataxia. The brain tissue were biochemically and immunocytochemically investigated for PrPres. For the H-type, spongiform changes without PrPres accumulation were observed in the brainstem. However Western blot analysis did not allow to detect PrPres into the brain. For the L-type, severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem. whereas into the cortex the spongiosis was evidenced, but the Vacuolisation was weaker. Strong deposits of PrPres were detected by western blot, PET-blot and immunocytochemistry in the CNS: dense accumulation was observed into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques. Western blot analysis also readily confirmed the presence of protease-resistant prion protein.
Conclusions: L-type infected lemurs showed survival times considerably shorter than for classical BSE strain, indicating that the disease is caused by a very virulent distinct prion strain in a model of non human primate.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
P7.09
Biochemical screening for identification of atypical bse in belgium, 1999-present
Authors
Alexandre DobIy: Caroline Rodeghiero, Riet Geeroms; Stephanie Durand, Jessica De Sloovere, Emanuel Yanopdenbosch, Stefan Roels,
Content
Background: Recently atypical forms of BSE have been described. Western blot analyses showed that, in comparison to the classic BSE (C-type), they are demonstrable by a higher or lower molecular weight of the unglycosylated PrPres. They Viere thus named H-type and L-type BSE (L-type is also called BASE). In addition they show a lower proportion of diglycosylated PrPres than C-type. These emerging types represent different strains of BSE. They show unique incubation periods and histological lesions. Such types have been described on different continents. Indeed they might correspond to "sporadic" forms of BSE. In 2004 we already described one L-type in Belgium.
Objective: We retrospectively analysed the bovines at least 7-year-old in the Belgian archive of BSE diagnosed cattle in order to determine the prevalence of the two types of atypical BSE in Belgium.
Methods: We analysed homogenates from 39 bovines of 93 months old in median (min: 84, max: 181 months). The most recent one was diagnosed in 2006. We used Western blot with a panel of anti-PrP antibodies (Ab). They detect different regions of the PrP protein, from N-terminal to C-terminal: 12B2, 9A2, Sha31. SAFB4, 94B4. Their combination is aimed at an efficient typing diagnostic. We detected bound Ab with SuperSignal West Dura (Pierce) and analysed PrPres, signals with an image-analysis software (Quantity One, Bio-Rad).
Results: The results are still under analysis. We will detail the most crucial characteristics for typing PrPres. These include 1) the apparent molecular mass of the an-, mono- and diglycosylated bands, 2) the binding affinity to the five Ab (e.g.12B2 for H-type), 3) the presence of a fourth (unglycosylated) band and 4) the glycoprofile based on the relative proportions of the visible bands.
Discussion: The emergence of atypical types of BSE is partially due to a better knowledge of prion strains and more efficient diagnostic techniques. As the area in the brain where the PrPres is deposited can differ drastically between the types, it is essential to ascertain that the sampling techniques and analyses are adapted to these new types. As these new strains seem more virulent than classic types, they represent one of the next challenges in the field of prions.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
http://www.prion2008.com/
Tuesday, November 11, 2008
Transmission of atypical bovine prions to mice transgenic for human prion protein
DOI: 10.3201/eid1412.080941
http://bse-atypical.blogspot.com/2008/11/transmission-of-atypical-bovine-prions.html
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Tuesday, June 3, 2008
SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html
SCRAPIE USA
http://scrapie-usa.blogspot.com/
Sunday, September 07, 2008
CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA
http://chronic-wasting-disease.blogspot.com/2008/09/cwd-live-test-and-political-aspects-or.html
Saturday, October 18, 2008
WYOMING STAR VALLEY MOOSE TESTS POSITIVE FOR CWD
http://chronic-wasting-disease.blogspot.com/2008/10/wyoming-star-valley-moose-tests.html
http://chronic-wasting-disease.blogspot.com/
Friday, December 12, 2008
The prion strain phenomenon: Molecular basis and unprecedented features
http://bse-atypical.blogspot.com/2008/12/prion-strain-phenomenon-molecular-basis.html
Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC -254 Accepted - Volume 11
http://www.fda.gov/OHRMS/DOCKETS/DOCKETS/02n0276/02N-0276-EC-254.htm
http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
PART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
Monday, December 08, 2008
vCJD & dental treatment
http://creutzfeldt-jakob-disease.blogspot.com/2008/12/vcjd-dental-treatment.html
Friday, December 12, 2008
Prions in Milk from Ewes Incubating Natural Scrapie
http://scrapie-usa.blogspot.com/2008/12/prions-in-milk-from-ewes-incubating.html
Friday, December 05, 2008
Detection of Prion Infectivity in Fat Tissues of Scrapie-Infected Mice
http://scrapie-usa.blogspot.com/2008/12/detection-of-prion-infectivity-in-fat.html
REPORT ON CURRENT & FUTURE SURVEILLANCE FOR BOVINE SPONGIFORM ENCEPHALOPATHY
http://madcowtesting.blogspot.com/2008/11/report-on-current-future-surveillance.html
November 25, 2008
Update On Feed Enforcement Activities To Limit The Spread Of BSE
http://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.html
Plasma & Serum Proteins Receive Continued FDA Approval
4/25/2008 APC, Inc. is pleased to advise our customers and industry partners that as anticipated, the Food and Drug Administration (FDA) will continue to allow the use of bovine blood, plasma and serum proteins in ruminant feeds.
In April 2008 FDA announced the publication of its Final Rule for 21 CFR Part 589.2001 - Substances Prohibited From Use in Animal Food or Feed. FDA specifically stated in their opinion that, "FDA is not prohibiting the use of blood and blood products in animal feed because we believe such a prohibition would do very little to reduce the risk of BSE transmission."
Known as a leader in developing nutritional products for the swine industry, where 95% of pig starter diets in the United States contain functional proteins, APC has more recently developed their line of colostrum replacers, supplements, feed additives and milk replacer ingredients for calves. Products include plasma, serum and immunoglobulin concentrate based Acquire®, Lifeline®, Gammulin® and Nutrapro® used to optimize the health and performance of calves.
To view the full report for Final Rule 21 CFR Part 589.2001 visit:
http://www.fda.gov/OHRMS/DOCKETS/98fr/FDA-2002-N-0031-nfr.pdf
To view the complete Feed Rule 21 CFR Part 589 visit:
http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=589&showFR=1
Friday, November 21, 2008
Plasma & Serum Proteins Receive Continued FDA Approval
http://madcowfeed.blogspot.com/2008/11/plasma-serum-proteins-receive-continued.html
http://madcowfeed.blogspot.com/
Thursday, November 27, 2008
Prion diseases are efficiently transmitted by blood transfusion in sheep
http://vcjdblood.blogspot.com/2008/11/prion-diseases-are-efficiently.html
stupid is, as stupid does. (forest gump)
Thank You,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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