ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
Greetings,
WITH more and more atypical Transmissible Spongiform Encephalopathy cases showing up in more and more species here in North America, and the enormous monumental amount of banned mad cow protein in commerce since the infamous partial and voluntary mad cow feed ban inked on paper, with tons and tons crossing back and forth between the USA, Canada, and Mexico, it just does not surprise me of all these "PENDING CLASSIFICATIONS" of human TSE in Canada, and the USA. UK c-BSE transmitted to humans became nvCJD. WE now have atypical strains of BSE in cattle. Mission Texas experiments long ago showed that transmitted USA sheep scrapie to USA bovine, produced a TSE much different than the UK typical c-BSE. SO why would human TSE in the USA look like UK human TSE ? The corruption is mind boggling. The UK saw a suspicious TSE in humans, and science linked it to cattle. North America is awash with human and animal TSE, CJD is rising in young and old, with the same pathology and same symptoms, and none of it is related to the other. isn't that nice. who, what, bestowed such miracles upon North America $
Archive Number 20100405.1091 Published Date 05-APR-2010
Subject PRO/AH/EDR> Prion disease update 1010 (04)
snip...
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
http://whqlibdoc.who.int/publications/2003/9241545887.pdf.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
CANADA CJD UPDATE 2011
CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011
3. Final classification of 49 cases from 2009, 2010, 2011 is pending.
snip...
http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf
USA 2011
USA
National Prion Disease Pathology Surveillance Center
Cases Examined1
(November 1, 2010)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 87 51 43 7 1 0
1999 121 73 65 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 13
2005 344 194 157 36 1 0
2006 383 197 166 29 0 24
2007 377 214 187 27 0 0
2008 394 231 205 25 0 0
2009 425 258 215 43 0 0
2010 333 213 158 33 0 0
TOTAL 38315 22656 1907 328 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.
I also urge you to again notice these disturbing factors in lines 5 and 6 ;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
========end=====tss=====2011
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS. HOW long can this cover-up continue $$$
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Saturday, March 05, 2011
MAD COW DISEASE BSE PRION MEXICO ???
http://bse-atypical.blogspot.com/2011/03/mad-cow-disease-bse-prion-mexico.html
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
snip...
please see all seven threats listed in the USA, and more...FULL TEXT ;
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. ***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
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
Saturday, March 05, 2011
MAD COW DISEASE BSE PRION MEXICO ???
http://bse-atypical.blogspot.com/2011/03/mad-cow-disease-bse-prion-mexico.html
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Wednesday, February 9, 2011
[Docket No. FSIS-2010-0041] Non-Ambulatory Disabled Veal Calves and Other Non-Ambulatory Disabled Livestock at Slaughter; Petitions for Rulemaking
http://downercattle.blogspot.com/2011/02/docket-no-fsis-2010-0041-non-ambulatory.html
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/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
BANNED MAD COW FEED IN COMMERCE IN ALABAMA (where h-g-BSEalabama mad cow was documented)
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.html
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Monday, January 17, 2011
MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011
January 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/mad-cow-update-on-feed-enforcement.html
Wednesday, March 2, 2011
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011 Posted: 3/2/2011
October 28, 2010
http://tseac.blogspot.com/2011/03/transmissible-spongiform.html
http://www.inspection.gc.ca/english/anima/disemala/bseesb/comenqe.shtml
http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml
http://www.fda.gov/AnimalVeterinary/GuidanceComplianceEnforcement/ComplianceEnforcement/BovineSpongiformEncephalopathy/default.htm
http://www.fsis.usda.gov/Fact_Sheets/Bovine_Spongiform_Encephalopathy_BSE/
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Saturday, March 5, 2011
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
Alberta dairy cow found with mad cow disease
Fri Mar 4, 2011 10:05am EST
WINNIPEG, Manitoba (Reuters) - Canadian government officials have found a dairy cow in Alberta with mad cow disease, but the finding is not surprising and shouldn't affect beef exports, a spokesman for the Canadian Food Inspection Agency said on Friday. The agency confirmed the case of bovine spongiform encephalopathy, or BSE as the disease is also known, on February 18 in a 77-month-old dairy cow, spokesman Guy Gravelle said.
In 2003, the first discovery of a cow in Canada with the disease led to closures of numerous export markets to Canadian beef. Most have reopened, other than South Korea and China, and importers are no longer as sensitive to new cases as countries such as Canada now have monitoring systems in place.
Canada continues to be rated a "controlled risk" for the disease by the World Organization for Animal Health, Gravelle said. The newest case may delay any upgrade to Canada's international risk status as a country cannot apply for negligible status sooner than 11 years after the latest-born case.
The cow has been destroyed and no part of its carcass entered the human food or animal feed systems, Gravelle said.
The case, which is believed to be Canada's 18th, should not affect exports of Canadian cattle or beef, he said, as a small number of BSE cases are expected as Canada monitors for the disease.
(Reporting by Rod Nickel; Editing by Walter Bagley)
http://ca.reuters.com/article/domesticNews/idCATRE7233JT20110304
http://www.inspection.gc.ca/english/anima/disemala/bseesb/comenqe.shtml
http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml
Bovine spongiform encephalopathy (BSE) cases confirmed in Canada in 2011
BSE is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.
The following table lists individual animals confirmed to be infected with BSE in Canada in 2011.
Current as of: 2011-02-28
Date confirmed Location Animal type infected Age of animal February 18 Alberta Dairy cow 77 months
http://inspection.gc.ca/english/anima/disemala/rep/2011bseesbe.shtml
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Saturday, March 12, 2011
Variant Creutzfeldt-Jakob Disease in a Canadian resident Infectious Diseases News Brief - March 11, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/variant-creutzfeldt-jakob-disease-in.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
TSS
Fri Mar 4, 2011 10:05am EST
WINNIPEG, Manitoba (Reuters) - Canadian government officials have found a dairy cow in Alberta with mad cow disease, but the finding is not surprising and shouldn't affect beef exports, a spokesman for the Canadian Food Inspection Agency said on Friday. The agency confirmed the case of bovine spongiform encephalopathy, or BSE as the disease is also known, on February 18 in a 77-month-old dairy cow, spokesman Guy Gravelle said.
In 2003, the first discovery of a cow in Canada with the disease led to closures of numerous export markets to Canadian beef. Most have reopened, other than South Korea and China, and importers are no longer as sensitive to new cases as countries such as Canada now have monitoring systems in place.
Canada continues to be rated a "controlled risk" for the disease by the World Organization for Animal Health, Gravelle said. The newest case may delay any upgrade to Canada's international risk status as a country cannot apply for negligible status sooner than 11 years after the latest-born case.
The cow has been destroyed and no part of its carcass entered the human food or animal feed systems, Gravelle said.
The case, which is believed to be Canada's 18th, should not affect exports of Canadian cattle or beef, he said, as a small number of BSE cases are expected as Canada monitors for the disease.
(Reporting by Rod Nickel; Editing by Walter Bagley)
http://ca.reuters.com/article/domesticNews/idCATRE7233JT20110304
http://www.inspection.gc.ca/english/anima/disemala/bseesb/comenqe.shtml
http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml
Bovine spongiform encephalopathy (BSE) cases confirmed in Canada in 2011
BSE is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.
The following table lists individual animals confirmed to be infected with BSE in Canada in 2011.
Current as of: 2011-02-28
Date confirmed Location Animal type infected Age of animal February 18 Alberta Dairy cow 77 months
http://inspection.gc.ca/english/anima/disemala/rep/2011bseesbe.shtml
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Saturday, March 12, 2011
Variant Creutzfeldt-Jakob Disease in a Canadian resident Infectious Diseases News Brief - March 11, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/variant-creutzfeldt-jakob-disease-in.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
TSS
Wednesday, February 2, 2011
Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay
Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay
Julie Ann Edgeworth, Michael Farmer, Anita Sicilia, Paul Tavares, Jonathan Beck, Tracy Campbell, Jessica Lowe, Simon Mead, Peter Rudge, John Collinge, Graham S Jackson
Summary
Background
Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disorder originating from exposure to bovine-spongiform-encephalopathy-like prions. Prion infections are associated with long and clinically silent incubations. The number of asymptomatic individuals with vCJD prion infection is unknown, posing risk to others via blood transfusion, blood products, organ or tissue grafts, and contaminated medical instruments. We aimed to establish the sensitivity and specifi city of a blood-based assay for detection of vCJD prion infection.
Methods
We developed a solid-state binding matrix to capture and concentrate disease-associated prion proteins and coupled this method to direct immunodetection of surface-bound material. Quantitative assay sensitivity was assessed with a serial dilution series of 10.. to 10.1. of vCJD prion-infected brain homogenate into whole human blood, with a baseline control of normal human brain homogenate in whole blood (10..). To establish the sensitivity and specifi city of the assay for detection of endogenous vCJD, we analysed a masked panel of 190 whole blood samples from 21 patients with vCJD, 27 with sporadic CJD, 42 with other neurological diseases, and 100 normal controls. Samples were masked and numbered by individuals independent of the assay and analysis. Each sample was tested twice in independent assay runs; only samples that were reactive in both runs were scored as positive overall.
Findings
We were able to distinguish a 10.1. dilution of exogenous vCJD prion-infected brain from a 10.. dilution of normal brain (mean chemiluminescent signal, 1E3~10. [SD 1E1~10.] for vCJD vs 9E9~10. [4E5~103] for normal brain; p<0E0001).an assay sensitivity that was orders of magnitude higher than any previously reported. 15 samples in the masked panel were scored as positive. All 15 samples were from patients with vCJD, showing an assay sensitivity for vCJD of 71E4% (95% CI 47E8.88E7) and a specifi city of 100% (95% CIs between 97E8% and 100%). Interpretation These initial studies provide a prototype blood test for diagnosis of vCJD in symptomatic individuals, which could allow development of large-scale screening tests for asymptomatic vCJD prion infection. Funding UK Medical Research Council.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)62308-2/abstract
see full text ;
http://download.thelancet.com/pdfs/journals/lancet/PIIS0140673610623082.pdf?id=3d35b1b5aa0ec416:-4a4ca7b:12de9223051:-1b401296700700892
World’s first blood test for vCJD developed in MRC lab
Thursday 3 February 2011
The world’s first accurate blood test for variant Creutzfeldt-Jakob disease (vCJD) has been developed by Medical Research Council (MRC) scientists. The prototype, which is 100,000 times more sensitive than any previous attempt, could transform the diagnosis and screening of the brain disease.
Variant CJD, the human form of BSE (or mad cow disease) first emerged in 1995. The disease, which affects the brain, is believed to have passed from cattle to humans through infected food. It causes personality change, loss of body function, and eventually death.
The research team from the MRC Prion Unit, based at University College London, working with the National Prion Clinic at the National Hospital for Neurology and Neurosurgery (NHNN) tested 190 blood samples, including 21 from individuals known to have vCJD. The blood test was able to detect blood spiked with a dilution of vCJD to within one part per ten billion - 100,000 times more sensitive than any other method developed so far.
Prions, the infectious proteins which cause vCJD and other fatal prion diseases, can inhabit a person’s body for up to 50 years before presenting symptoms. During this time there is a chance a carrier of vCJD infection could pass on the infection to others, for example through blood transfusion or even through surgical and medical instruments as prions can easily attach onto metal surfaces.
A widely available, accurate blood test would enable people to be diagnosed earlier and could also help identify carriers of the disease. This would help measure how widespread the prion infection is in the general population and identify those who are at risk of passing on the infection to others.
Lead author Dr Graham Jackson, Programme Leader at the MRC Prion Unit, said:
“This test comes at the end of many years of meticulous, painstaking research in our Unit and the NHS National Prion Clinic. Although further larger studies are needed to confirm its effectiveness, it’s the best hope yet of a successful early diagnostic test for the disease. This test could potentially go on to allow blood services to screen the population for vCJD infection, assess how many people in the UK are silent carriers and prevent onward transmission of the disease.”
Professor John Collinge, Director of the MRC Prion Unit, said:
“One of the reasons that vCJD is such a dreaded disease and has caused such disruption and expense to health services is the lack of knowledge of who is and who is not a carrier of this infection. The next step will be to test anonymously several thousand blood donors from a country unaffected by BSE in order to gain a better idea of how the test fares in practice. Longer term studies will also be needed to assess what proportion of individuals who test positive for prion infection will then go on to develop the disease later in life.
“The MRC Prion Unit’s research with the NHS National Prion Clinic to improve early diagnosis is an essential part of the wider MRC strategy to develop better treatments for patients. For this to develop, it will be crucial for clinicians to be able to offer treatment before extensive irreversible damage to the brain has occurred. At the moment, a firm diagnosis of vCJD can usually be made only once serious symptoms of the disease have developed which indicate extensive damage to the brain.”
The study ’A blood-based assay for the detection of vCJD prion infection’ is published today in the journal The Lancet.
Ends
Notes to editors:
To arrange an interview with the researchers of this paper, please call the MRC Press Office on 0207 395 2345.
For almost 100 years the Medical Research Council has improved the health of people in the UK and around the world by supporting the highest quality science. The MRC invests in world-class scientists. It has produced 29 Nobel Prize winners and sustains a flourishing environment for internationally recognised research. The MRC focuses on making an impact and provides the financial muscle and scientific expertise behind medical breakthroughs, including one of the first antibiotics penicillin, the structure of DNA and the lethal link between smoking and cancer. Today MRC funded scientists tackle research into the major health challenges of the 21st century. www.mrc.ac.uk
While the number of vCJD samples available for analysis was inherently small, and to date only a small number of healthy donors has been studied, analysis of this blinded panel indicated an assay sensitivity for vCJD of over 71% (15/21, CI 48-89%) and a specificity of 100% (0/169, CI 98-100%).
The NHNN forms part of University College London Hospitals NHS Foundation Trust, one of the largest NHS trusts in the United Kingdom providing first-class acute and specialist services. The Trust is committed to research and development and forms part of UCL Partners which in March 2009 was officially designated as one of the UK's first academic health science centres by the Department of Health. UCLH works closely with UCL, translating research into treatments for patients. www.uclh.nhs.uk
http://www.mrc.ac.uk/Newspublications/News/MRC007683
Annals of Neurology Volume 67, Issue 6, pages 761–770, June 2010
Validation of diagnostic criteria for variant Creutzfeldt–Jakob disease†
Craig A. Heath MD1,*, Sarah A. Cooper MD2, Katy Murray MD1, Andrea Lowman MB ChB (Hons), MRCP3, Colm Henry MB MRCPI MRCGP4, Margaret A. MacLeod MD, MRCP5, Gillian E. Stewart MB ChB1, Martin Zeidler FRCP6, Jan M. MacKenzie7, James W. Ironside FRCPath7, David M. Summers MD1, Richard S. G. Knight FRCP7, Robert G. Will FRCP7Article first published online: 27 JAN 2010
DOI: 10.1002/ana.21987
http://onlinelibrary.wiley.com/doi/10.1002/ana.21987/abstract
Annals of Neurology Volume 69, Issue 1, page 212, January 2011
Letter to the Editor Comment on validation of diagnostic criteria for variant Creutzfeldt-Jakob disease
Ana Lukic MRCP1,2, Simon Mead MRCP, PhD1,2,3, Peter Rudge FRCP1,2, John Collinge FRCP, PhD, FRS1,2,3
Article first published online: 28 JAN 2011
DOI: 10.1002/ana.22273
Copyright © 2010 American Neurological Association
There is no doubt that the development of diagnostic criteria has contributed greatly to epidemiological research in prion diseases, and Heath and colleagues1 emphasize this in surveillance studies of variant Creutzfeldt-Jakob disease (vCJD). We caution, however, against a more broad application in clinical practice, particularly in governing decisions about clinical diagnosis, communication with patients/caregivers, and access to experimental therapies. The physician looking after a young patient with an unexplained rapidly progressive neuropsychiatric syndrome, dementia, or ataxia needs to make prompt clinical decisions. There are treatable alternative diagnoses, and an early firm diagnosis is essential. The pulvinar sign on magnetic resonance imaging is often not identified when patients are first imaged, and a requirement for a clinical duration of 6 months or greater makes a probable diagnosis impossible in the early stages of disease. Physicians who have cared for families affected by vCJD are aware of the complicated psychological issues generated by the perceived mismanagement of the bovine spongiform encephalopathy epidemic, which are often exacerbated by a delay or equivocation about diagnosis. Several families also choose experimental intracerebroventricular pentosan polysulfate therapy, which requires neurosurgery.
In the context of these issues, the role of tonsillar biopsy is underemphasized by Heath et al and the criteria. In our experience of 60 biopsies, by far the largest series worldwide, tonsillar biopsy has 100% sensitivity and specificity, at any stage of the disease. Prion protein deposition in the tonsil can be patchy, and at least 20 germinal centers need to be examined.2The number examined in 1 French case3 reported by Heath et al may not have been adequate to avoid a false-negative result. It is notable that of the 6 most recent patients suspected clinically of having vCJD in the United Kingdom, 3 did not meet epidemiological criteria for probable vCJD while alive. Two of these patients would have been misdiagnosed as sporadic CJD according to the updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob Disease4 criteria; typical vCJD was diagnosed at autopsy in both. In a third patient, with a heterozygous codon 129 genotype reported by Kaski et al,5 the pulvinar sign was not thought to be present by all neuroradiologists, and no tissue was examined. It is reasonable to expect that tonsillar biopsy may have made the correct diagnosis in each of these cases.
Given experience with transfusion-associated secondary vCJD, vCJD prions are likely to be present in significant titer in human blood, a diagnostic blood test based on detection of the infectious agent is clearly possible in principle, and if technologically achieved, will necessitate a complete revision of how we approach diagnosis in this disease.
Potential Conflicts of Interest Nothing to report.
References 1 Heath CA, Cooper SA, Murray K, etal. Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Ann Neurol 2010; 67: 761–770. PubMed,Web of Science® Times Cited: 3 2 Ironside JW, Hilton DA, Ghani A, etal. Retrospective study of prion-protein accumulation in tonsil and appendix tissues. Lancet 2000; 355: 1693–1694. CrossRef,PubMed,ChemPort,Web of Science® Times Cited: 65 3 Brandel JP, Heath CA, Head MW, etal. Variant CJD in France and the United Kingdom: evidence for the same agent strain. Ann Neurol 2009; 65: 249–256. Direct Link: AbstractFull Article (HTML)PDF(255K)References 4 Zerr I, Kallenberg K, Summers DM, et al. Updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob disease. Brain 2009; 132: 2659–2668. CrossRef,PubMed,ChemPort,Web of Science® Times Cited: 15 5 Kaski D, Mead S, Hyare H, etal. Variant CJD in a PRNP codon 129 heterozygous individual. Lancet 2009; 374: 2128. CrossRef,PubMed,Web of Science® Times Cited: 10
http://onlinelibrary.wiley.com/doi/10.1002/ana.22273/abstract
Tuesday, January 25, 2011
Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions
http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Thursday, October 07, 2010
Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice
http://bse-atypical.blogspot.com/2010/10/experimental-transmission-of-h-type.html
Monday, November 22, 2010
Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control
REVIEW ARTICLES
http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html
Tuesday, January 18, 2011
Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
Thursday, July 08, 2010
Nosocomial transmission of sporadic Creutzfeldt-Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/07/nosocomial-transmission-of-sporadic.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
Friday, September 24, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were distributed SEPTEMBER 2010
http://vcjdtransfusion.blogspot.com/2010/09/usa-blood-products-collected-from-donor.html
Wednesday, September 08, 2010
Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010
http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html
Saturday, July 17, 2010
Variant Creutzfeldt-Jakob disease Ironside JW., Haemophilia.
2010 Jul;16 Suppl 5:175-80 REVIEW ARTICLE
http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.html
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
----- Original Message -----
From: Terry S. Singeltary Sr.
To: william.freas@fda.hhs.gov
Cc: rosanna.harvey@fda.hhs.gov ; Emery, Bryan (CBER)
SEE FULL TEXT ;
http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
USA
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
2010
PLEASE NOTE REFERENCE LINES 5. AND 6.
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 120 72 64 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 1(3)
2005 344 194 157 36 1 0
2006 383 197 166 29 0 2(4)
2007 377 214 187 27 0 0
2008 394 231 204 25 0 0
2009 425 259 216 43 0 0
2010 204 124 85 20 0 0
TOTAL 3702(5) 2177(6) 1834 315 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.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
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
HOW many of you recieved a written CJD Questionnaire asking real questions pertaining to route and source (and there are many here in North America) ?
IS every case getting a cjd questionnaire asking real questions ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION USA PRION UNIT
http://cjdquestionnaire.blogspot.com/
TSS
Julie Ann Edgeworth, Michael Farmer, Anita Sicilia, Paul Tavares, Jonathan Beck, Tracy Campbell, Jessica Lowe, Simon Mead, Peter Rudge, John Collinge, Graham S Jackson
Summary
Background
Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disorder originating from exposure to bovine-spongiform-encephalopathy-like prions. Prion infections are associated with long and clinically silent incubations. The number of asymptomatic individuals with vCJD prion infection is unknown, posing risk to others via blood transfusion, blood products, organ or tissue grafts, and contaminated medical instruments. We aimed to establish the sensitivity and specifi city of a blood-based assay for detection of vCJD prion infection.
Methods
We developed a solid-state binding matrix to capture and concentrate disease-associated prion proteins and coupled this method to direct immunodetection of surface-bound material. Quantitative assay sensitivity was assessed with a serial dilution series of 10.. to 10.1. of vCJD prion-infected brain homogenate into whole human blood, with a baseline control of normal human brain homogenate in whole blood (10..). To establish the sensitivity and specifi city of the assay for detection of endogenous vCJD, we analysed a masked panel of 190 whole blood samples from 21 patients with vCJD, 27 with sporadic CJD, 42 with other neurological diseases, and 100 normal controls. Samples were masked and numbered by individuals independent of the assay and analysis. Each sample was tested twice in independent assay runs; only samples that were reactive in both runs were scored as positive overall.
Findings
We were able to distinguish a 10.1. dilution of exogenous vCJD prion-infected brain from a 10.. dilution of normal brain (mean chemiluminescent signal, 1E3~10. [SD 1E1~10.] for vCJD vs 9E9~10. [4E5~103] for normal brain; p<0E0001).an assay sensitivity that was orders of magnitude higher than any previously reported. 15 samples in the masked panel were scored as positive. All 15 samples were from patients with vCJD, showing an assay sensitivity for vCJD of 71E4% (95% CI 47E8.88E7) and a specifi city of 100% (95% CIs between 97E8% and 100%). Interpretation These initial studies provide a prototype blood test for diagnosis of vCJD in symptomatic individuals, which could allow development of large-scale screening tests for asymptomatic vCJD prion infection. Funding UK Medical Research Council.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)62308-2/abstract
see full text ;
http://download.thelancet.com/pdfs/journals/lancet/PIIS0140673610623082.pdf?id=3d35b1b5aa0ec416:-4a4ca7b:12de9223051:-1b401296700700892
World’s first blood test for vCJD developed in MRC lab
Thursday 3 February 2011
The world’s first accurate blood test for variant Creutzfeldt-Jakob disease (vCJD) has been developed by Medical Research Council (MRC) scientists. The prototype, which is 100,000 times more sensitive than any previous attempt, could transform the diagnosis and screening of the brain disease.
Variant CJD, the human form of BSE (or mad cow disease) first emerged in 1995. The disease, which affects the brain, is believed to have passed from cattle to humans through infected food. It causes personality change, loss of body function, and eventually death.
The research team from the MRC Prion Unit, based at University College London, working with the National Prion Clinic at the National Hospital for Neurology and Neurosurgery (NHNN) tested 190 blood samples, including 21 from individuals known to have vCJD. The blood test was able to detect blood spiked with a dilution of vCJD to within one part per ten billion - 100,000 times more sensitive than any other method developed so far.
Prions, the infectious proteins which cause vCJD and other fatal prion diseases, can inhabit a person’s body for up to 50 years before presenting symptoms. During this time there is a chance a carrier of vCJD infection could pass on the infection to others, for example through blood transfusion or even through surgical and medical instruments as prions can easily attach onto metal surfaces.
A widely available, accurate blood test would enable people to be diagnosed earlier and could also help identify carriers of the disease. This would help measure how widespread the prion infection is in the general population and identify those who are at risk of passing on the infection to others.
Lead author Dr Graham Jackson, Programme Leader at the MRC Prion Unit, said:
“This test comes at the end of many years of meticulous, painstaking research in our Unit and the NHS National Prion Clinic. Although further larger studies are needed to confirm its effectiveness, it’s the best hope yet of a successful early diagnostic test for the disease. This test could potentially go on to allow blood services to screen the population for vCJD infection, assess how many people in the UK are silent carriers and prevent onward transmission of the disease.”
Professor John Collinge, Director of the MRC Prion Unit, said:
“One of the reasons that vCJD is such a dreaded disease and has caused such disruption and expense to health services is the lack of knowledge of who is and who is not a carrier of this infection. The next step will be to test anonymously several thousand blood donors from a country unaffected by BSE in order to gain a better idea of how the test fares in practice. Longer term studies will also be needed to assess what proportion of individuals who test positive for prion infection will then go on to develop the disease later in life.
“The MRC Prion Unit’s research with the NHS National Prion Clinic to improve early diagnosis is an essential part of the wider MRC strategy to develop better treatments for patients. For this to develop, it will be crucial for clinicians to be able to offer treatment before extensive irreversible damage to the brain has occurred. At the moment, a firm diagnosis of vCJD can usually be made only once serious symptoms of the disease have developed which indicate extensive damage to the brain.”
The study ’A blood-based assay for the detection of vCJD prion infection’ is published today in the journal The Lancet.
Ends
Notes to editors:
To arrange an interview with the researchers of this paper, please call the MRC Press Office on 0207 395 2345.
For almost 100 years the Medical Research Council has improved the health of people in the UK and around the world by supporting the highest quality science. The MRC invests in world-class scientists. It has produced 29 Nobel Prize winners and sustains a flourishing environment for internationally recognised research. The MRC focuses on making an impact and provides the financial muscle and scientific expertise behind medical breakthroughs, including one of the first antibiotics penicillin, the structure of DNA and the lethal link between smoking and cancer. Today MRC funded scientists tackle research into the major health challenges of the 21st century. www.mrc.ac.uk
While the number of vCJD samples available for analysis was inherently small, and to date only a small number of healthy donors has been studied, analysis of this blinded panel indicated an assay sensitivity for vCJD of over 71% (15/21, CI 48-89%) and a specificity of 100% (0/169, CI 98-100%).
The NHNN forms part of University College London Hospitals NHS Foundation Trust, one of the largest NHS trusts in the United Kingdom providing first-class acute and specialist services. The Trust is committed to research and development and forms part of UCL Partners which in March 2009 was officially designated as one of the UK's first academic health science centres by the Department of Health. UCLH works closely with UCL, translating research into treatments for patients. www.uclh.nhs.uk
http://www.mrc.ac.uk/Newspublications/News/MRC007683
Annals of Neurology Volume 67, Issue 6, pages 761–770, June 2010
Validation of diagnostic criteria for variant Creutzfeldt–Jakob disease†
Craig A. Heath MD1,*, Sarah A. Cooper MD2, Katy Murray MD1, Andrea Lowman MB ChB (Hons), MRCP3, Colm Henry MB MRCPI MRCGP4, Margaret A. MacLeod MD, MRCP5, Gillian E. Stewart MB ChB1, Martin Zeidler FRCP6, Jan M. MacKenzie7, James W. Ironside FRCPath7, David M. Summers MD1, Richard S. G. Knight FRCP7, Robert G. Will FRCP7Article first published online: 27 JAN 2010
DOI: 10.1002/ana.21987
http://onlinelibrary.wiley.com/doi/10.1002/ana.21987/abstract
Annals of Neurology Volume 69, Issue 1, page 212, January 2011
Letter to the Editor Comment on validation of diagnostic criteria for variant Creutzfeldt-Jakob disease
Ana Lukic MRCP1,2, Simon Mead MRCP, PhD1,2,3, Peter Rudge FRCP1,2, John Collinge FRCP, PhD, FRS1,2,3
Article first published online: 28 JAN 2011
DOI: 10.1002/ana.22273
Copyright © 2010 American Neurological Association
There is no doubt that the development of diagnostic criteria has contributed greatly to epidemiological research in prion diseases, and Heath and colleagues1 emphasize this in surveillance studies of variant Creutzfeldt-Jakob disease (vCJD). We caution, however, against a more broad application in clinical practice, particularly in governing decisions about clinical diagnosis, communication with patients/caregivers, and access to experimental therapies. The physician looking after a young patient with an unexplained rapidly progressive neuropsychiatric syndrome, dementia, or ataxia needs to make prompt clinical decisions. There are treatable alternative diagnoses, and an early firm diagnosis is essential. The pulvinar sign on magnetic resonance imaging is often not identified when patients are first imaged, and a requirement for a clinical duration of 6 months or greater makes a probable diagnosis impossible in the early stages of disease. Physicians who have cared for families affected by vCJD are aware of the complicated psychological issues generated by the perceived mismanagement of the bovine spongiform encephalopathy epidemic, which are often exacerbated by a delay or equivocation about diagnosis. Several families also choose experimental intracerebroventricular pentosan polysulfate therapy, which requires neurosurgery.
In the context of these issues, the role of tonsillar biopsy is underemphasized by Heath et al and the criteria. In our experience of 60 biopsies, by far the largest series worldwide, tonsillar biopsy has 100% sensitivity and specificity, at any stage of the disease. Prion protein deposition in the tonsil can be patchy, and at least 20 germinal centers need to be examined.2The number examined in 1 French case3 reported by Heath et al may not have been adequate to avoid a false-negative result. It is notable that of the 6 most recent patients suspected clinically of having vCJD in the United Kingdom, 3 did not meet epidemiological criteria for probable vCJD while alive. Two of these patients would have been misdiagnosed as sporadic CJD according to the updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob Disease4 criteria; typical vCJD was diagnosed at autopsy in both. In a third patient, with a heterozygous codon 129 genotype reported by Kaski et al,5 the pulvinar sign was not thought to be present by all neuroradiologists, and no tissue was examined. It is reasonable to expect that tonsillar biopsy may have made the correct diagnosis in each of these cases.
Given experience with transfusion-associated secondary vCJD, vCJD prions are likely to be present in significant titer in human blood, a diagnostic blood test based on detection of the infectious agent is clearly possible in principle, and if technologically achieved, will necessitate a complete revision of how we approach diagnosis in this disease.
Potential Conflicts of Interest Nothing to report.
References 1 Heath CA, Cooper SA, Murray K, etal. Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Ann Neurol 2010; 67: 761–770. PubMed,Web of Science® Times Cited: 3 2 Ironside JW, Hilton DA, Ghani A, etal. Retrospective study of prion-protein accumulation in tonsil and appendix tissues. Lancet 2000; 355: 1693–1694. CrossRef,PubMed,ChemPort,Web of Science® Times Cited: 65 3 Brandel JP, Heath CA, Head MW, etal. Variant CJD in France and the United Kingdom: evidence for the same agent strain. Ann Neurol 2009; 65: 249–256. Direct Link: AbstractFull Article (HTML)PDF(255K)References 4 Zerr I, Kallenberg K, Summers DM, et al. Updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob disease. Brain 2009; 132: 2659–2668. CrossRef,PubMed,ChemPort,Web of Science® Times Cited: 15 5 Kaski D, Mead S, Hyare H, etal. Variant CJD in a PRNP codon 129 heterozygous individual. Lancet 2009; 374: 2128. CrossRef,PubMed,Web of Science® Times Cited: 10
http://onlinelibrary.wiley.com/doi/10.1002/ana.22273/abstract
Tuesday, January 25, 2011
Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions
http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Thursday, October 07, 2010
Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice
http://bse-atypical.blogspot.com/2010/10/experimental-transmission-of-h-type.html
Monday, November 22, 2010
Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control
REVIEW ARTICLES
http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html
Tuesday, January 18, 2011
Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
Thursday, July 08, 2010
Nosocomial transmission of sporadic Creutzfeldt-Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/07/nosocomial-transmission-of-sporadic.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
Friday, September 24, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were distributed SEPTEMBER 2010
http://vcjdtransfusion.blogspot.com/2010/09/usa-blood-products-collected-from-donor.html
Wednesday, September 08, 2010
Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010
http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html
Saturday, July 17, 2010
Variant Creutzfeldt-Jakob disease Ironside JW., Haemophilia.
2010 Jul;16 Suppl 5:175-80 REVIEW ARTICLE
http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.html
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
----- Original Message -----
From: Terry S. Singeltary Sr.
To: william.freas@fda.hhs.gov
Cc: rosanna.harvey@fda.hhs.gov ; Emery, Bryan (CBER)
SEE FULL TEXT ;
http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
USA
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
2010
PLEASE NOTE REFERENCE LINES 5. AND 6.
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 120 72 64 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 1(3)
2005 344 194 157 36 1 0
2006 383 197 166 29 0 2(4)
2007 377 214 187 27 0 0
2008 394 231 204 25 0 0
2009 425 259 216 43 0 0
2010 204 124 85 20 0 0
TOTAL 3702(5) 2177(6) 1834 315 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.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
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
HOW many of you recieved a written CJD Questionnaire asking real questions pertaining to route and source (and there are many here in North America) ?
IS every case getting a cjd questionnaire asking real questions ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION USA PRION UNIT
http://cjdquestionnaire.blogspot.com/
TSS
Sunday, January 30, 2011
Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?
Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?
COMMERCIAL IN CONFIDENCE
3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy
It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC.
and then another 3 + pages of blank space. ...TSS
http://collections.europarchive.org/tna/20080102164813/http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf
COMMERCIAL IN CONFIDENCE
BSE - CURRENT POSITION WITH VETERINARY LICENCED PRODUCTS (MA.1968)
There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).
1) Vaccines
http://collections.europarchive.org/tna/20080103033809/http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf
NOT FOR PUBLICATION
another 6 pages of blank space. ...TSS
http://collections.europarchive.org/tna/20080103032658/http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf
http://collections.europarchive.org/tna/20080103032631/http://www.bseinquiry.gov.uk/files/yb/1988/11/04003001.pdf
http://collections.europarchive.org/tna/20080103033926/http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf
COMMERCIAL IN CONFIDENCE
http://collections.europarchive.org/tna/20080103034137/http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf
COMMERCIAL IN CONFIDENCE
Medicines Act - Veterinary Products Committee
http://collections.europarchive.org/tna/20080103034140/http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf
COMMERCIAL IN CONFIDENCE
NOT FOR PUBLICATION
COMMITTEE ON SAFETY OF MEDICINES
another 6 pages or so that are blank. ...TSS
http://collections.europarchive.org/tna/20080102185137/http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf
http://collections.europarchive.org/tna/20080102184613/http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf
COMMERCIAL IN CONFIDENCE
NOT FOR PUBLICATION
COMMITTEE ON SAFETY OF MEDICINES
WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY
7.2.1. Products with bovine brain/lymphoid tissue as ingredients and administered by injection...[111]
7.2.2 Products with bovine ingredients (other than brain/lymphoid tissue) and administered by injection...[135]
7.2.3 Tissue implants, open wound dressings, surgical materials, dental and opthalmic products with bovine ingredients...[27]
7.2.4. Products with bovine ingredients and administered topically...[5]
7.2.5 Products with bovine ingredients and administered orally...[9]
7.2.6 Products with other animal/insect/bird ingredients and administered:
a. by injection a: 117
b. by topically b: 6
c. orally c: 8
7.2.7 Products with materials produced from animal material by chemical processes, eg stearic acid, gelatin and lanolin...[156]
With two exceptions, the replies to date have not given any immediate cause for concern, although 176 products do not conform to the CSM/VPC guidelines.
8. The first exception was from which gave very limited information about a very large number of homoepathic medicines with material obtained from cattle and a number with material from the brain. Of these, 53 were injectable products of which 20 were derived from cattle brain. A list of these products is attached as Appendix 1 to Annex D. The second exception relates to the product, 'Surgical Catgut', which is sourced from UK bovine intestines and will contain lymphoid material...
see full text ;
http://collections.europarchive.org/tna/20080102164420/http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf
COMMERCIAL IN CONFIDENCE
http://collections.europarchive.org/tna/20080102164744/http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf
MANAGEMENT IN CONFIDENCE
CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS
http://collections.europarchive.org/tna/20080102184729/http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;
[unknown woman] what group are you with?
[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?
at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.
snip...full text ;
http://bse-atypical.blogspot.com/2010/01/14th-international-congress-on.html
The documents below were provided by Terry S. Singeltary Sr on 8 May 2000.
They are optically character read (scanned into computer) and so may contain typos and unreadable parts.
TIP740203/l 0424 CONFIDENTIAL
snip...
The responses by the companies were presented by Ms Turner and were categorised by MCA standards, the products that were discussed were all low volume usage products eg sutures, heart valves.
8. As the responses included some materials of human origin it was decided that more information should be sought about CJD. There had been 2 recent deaths reported associated with human growth hormone. These were being investigated.
snip...
http://www.mad-cow.org/00/may00_news.html#aaa
5.3.3 The greatest risk, in theory, would be from parenteral injection of material derived from bovine brain or lymphoid tissue. Medicinal products for injection or surgical implantation which are prepared from bovine tissues, or which utilise bovine serum albumin or similar agents in their manufacture, might also be capable of transmitting infectious agents. All medicinal products are licensed under the Medicines Act by the Licensing Authority following guidance, for example from the Committee on Safety of Medicines (CSM), the Committee on Dental and Surgical Materials (CDSM) and their subcommittees. The Licensing Authority have been alerted to potential concern about BSE in medicinal products and will ensure that scrutiny of source materials and manufacturing processes now takes account of BSE agent.
see all 76 pages ;
http://collections.europarchive.org/tna/20080102132706/http://www.bseinquiry.gov.uk/files/ib/ibd1/tab02.pdf
EXPORT OF BRITISH BIOLOGICAL PHARMACEUTICALS
1. Please see the attached note of a recent meeting in Brussels. For Dr. Purford should read Dr. Purves (I think). If the Germans get their way, and it looks as if they might, because of worries about BSE we could end up with a ban on certain bovine materials being exported from the UK for pharmaceutical manufacture. Thse materials include cell cultures of bovine origin (? and also any cultures which have been fed bovine nutrient material), bovine serum, and fetal calf serum.
2. Whilst export of these raw materials may be very limited, it is only a small step to include in this export ban any finished product made from such materials. This would include virtually all biologicals and vaccines. This could have very serious effects on the export trade of British Manufacturers of biologicals because even where they source their bovine ingredients outside the UK it might be impossible or at least very difficult to bypass any export ban.
3. Our own line is that we have not used regulations to restrict the use of British bovine material for non-food use, although certain offals cannot be used for human consumption. ...
http://collections.europarchive.org/tna/20080102220244/http://www.bseinquiry.gov.uk/files/yb/1990/03/13002001.pdf
Export of British 'Biological' Pharmaceuticals
http://collections.europarchive.org/tna/20080102220202/http://www.bseinquiry.gov.uk/files/yb/1990/03/13008001.pdf
http://collections.europarchive.org/tna/20080102215829/http://www.bseinquiry.gov.uk/files/yb/1990/03/13009001.pdf
No papers were presented by our American guests and none covered the subject of pharmaceuticals. ...
http://collections.europarchive.org/tna/20080102220453/http://www.bseinquiry.gov.uk/files/yb/1990/04/02002001.pdf
STANDING COMMITTEE MEETING ON BSE
Thanks for your note. I am disappointed not to have been informed about this meeting in advance and am surprised that Dr. Tyrrell was not involved either. I find it insulting to be told the proceedings were in confidence and find your excuse about only hosting the meeting unconvincing.
http://collections.europarchive.org/tna/20080102220555/http://www.bseinquiry.gov.uk/files/yb/1990/04/06002001.pdf
The documents below were provided by Terry S. Singeltary Sr on 8 May 2000.
They are optically character read (scanned into computer) and so may contain typos and unreadable parts.
TIP740203/l 0424 CONFIDENTIAL
Mr Cunningham CMP3 From: D O Hagger MBI Dr Salisbury MED/IMCD3 Mr Burton PD/STB/PG1B B/17/2 Date: 15.02.1989 Mr Dudley PD/AD4
snip...
89/06.19/8.1 BSE3/1 0191 Hr J Maslin (MAFF) Ref: Maslin3g
From: Dr H Pickles Med SEB/B Date: 3 July 1989
CATTLE BY-PRODUCTS AND BSE
I was interested to see the list of by-products sent to the HSE. Those of particular concern included:
* small intestines: sutures (I thought the source was ovine but you are checking this)
* spinal cord: pharmaceuticals
* thymus: pharmaceuticals
Are you able to give me more information on which UK manufacturers use these materials? Our proposed ban on bovine offal for human consumption would not affect these uses, I assume.
snip...see full text ;
http://www.mad-cow.org/00/may00_news.html
http://www.javno.com/en/world/clanak.php?id=32047
http://creutzfeldt-jakob-disease.blogspot.com/2007/12/risk-factors-for-sporadic-creutzfeldt.html
40,000 human heart valves a year from BSE herds Sun, 3 Sep 2000.
Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas
http://www.mad-cow.org/00/sep00_news.html#hhh
USDA allows diseased animals into human food supply
Mon, 14 Aug 2000. Information provided by Terry S. Singeltary Sr.
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - Report of a visit to the USA - April-May 1989 - G A H Wells [head of England's main veterinary lab -- webmaster]
2. Meeting with USDA, BSE Task Force
http://www.mad-cow.org/00/aug00_late_news.html#hhh
http://www.mad-cow.org/00/may00_news.html#aaa
http://www.mad-cow.org/00/01jan_news.html#aaa
Subject: Louping-ill vaccine documents from November 23rd, 1946
Date: Sat, 9 Sep 2000 17:44:57 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946
NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND
ANNUAL CONGRESS, 1946
snip...
As a result of this experience a large-scale transmision experiment involving the ue of 788 sheep was commenced in 1938 on a farm specially taken for the purpose by the Animal Diseases Research Association with funds provided by the Agricultural Research Council. The experiment was designed to determine the nature of the infective agent and the pathogenesis of the disease. It is only possible here to give a summary of the result which showed that (1) saline suspensions of brain and spinal cord tissue of sheep affected with scrapie were infective to normal sheep when inoculatted intracerebrally or subcutaneously; (2) the incubation period after intracerebral inoculation was seven months and upwards and only 60 percent of the inoculated sheep developed scrapie during a period of four and a half years; (3) the incubation period after subcutaneous inoculation was 15 months and upwards and only about 30 percent of the inoculated sheep developed the disease during the four and a half years: (4) the infective agent was of small size and probably a filtrable virus.
The prolonged incubative period of the disease and the remarkable resistance of the causal agent to formalin are features of distinct interest. It still remains to determine if a biological test can be devised to detect infected animals so that they can be killed for food before they develop clinical symptoms and to explore the possibilities of producing an immunity to the disease.
==================================================================
Greetings List Members,
pretty disturbing document. now, what would stop this from happening with the vaccineCJD in children???
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
http://www.whale.to/v/singeltary.html
MAD COW DISEASE BSE CJD CHILDREN VACCINES
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN VACCINES
TIP740203/l 0424 CONFIDENTIAL
http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html
Research Lead: Dr. David Westaway, University of Alberta
Project: "Extending the spectrum of Prionopathies to Amyotrophic Lateral Sclerosis and Autism"
This project proposes to link the chemistry of the prion protein to the new territory of other nervous system diseases, such as ALS (Lou Gehrig's disease) and the socialization disorder autism -diseases which are at least one thousand times more common than prion diseases. It is believed that a different type or prion protein may operate in other types of brain diseases, which could lead to new ways of thinking about incurable disorders. The project will create changes in the amounts of the various forms of the new membrane protein, and then perform an array of analyses on the behavior and nervous system transmission of laboratory mice. Nervous transmission by electrical impulse can be measured in isolated brain cells, a system that is also convenient to study the effect of stress by adding small amounts of toxins to the fluids bathing the cultures. By these means, the project aims to extend the boundaries of what is considered "prion disease."
Funding: $520,500
http://www.prioninstitute.ca/index.php?page=webpages&menucat=42&id=26&action=displaypage&side=1
Unfolding the Prion Mystery Building and Growing Research Expertise in Alberta Year 4 2008-2009 Annual Report
Dr. David Westaway, University of Alberta Extending the spectrum of prionopathies to amyotrophic lateral sclerosis (ALS) and autism Dr. Westaway’s study aims to extend the boundaries of what is considered prion disease. His project takes the chemistry of the prion protein into the territory of nervous system diseases such as ALS (Lou Gehrig’s disease) and socialization disorder diseases such as autism. These brain diseases are at least 1,000 times more common than diseases currently accepted as prion related. Dr. Westaway hypothesizes that a different type of protein misfolding may operate in brain diseases such as Lou Gehrig’s and autism. This type of protein misfolding may occur in response to stresses in the brain. Unlike misfolded prions, other misfolded proteins may be noninfectious and not viable outside of the affected animal. Dr. Westaway’s research team will investigate these hypotheses by inducing changes in the brain cells of laboratory mice, measuring the resulting electrical impulses in the animals’ nervous systems and analyzing the effect on behaviour. Because nervous transmission by electrical impulse can be measured in isolated brain cells, adding small amounts of toxins to the fluids bathing the cell cultures will make it possible to study the effect of stress. The results could lead to new ways of thinking about nervous system disorders.
http://www.prioninstitute.ca/forms/WEBSITE%20AR.pdf
102
Causes of Death and Neuropathology in Autism Spectrum Disorder: A Medical Examiner Perspective
Kenneth Hutchins1, Mariana Nunez2, Carol Petito2. 1Miami Dade County Medical Examiner Department; 2University of Miami Miller School of Medicine, Department of Pathology
Autism Spectrum Disorder (ASD) is characterized by abnormalities in how patients relate to and communicate with others and their environment . It develops in as many as 1 in 150 children and may be associated with co-morbid disorders including seizures and mental retardation. Because ASD reduces life expectancies, we reviewed autopsy records of 22 consecutive cases from two south Florida Medical Examiner Departments over a 10 year period and correlated cause of death (COD) with clinical history and neuropathology. Patient ages averaged 18±11 yrs and ranged from 3-51 years; 16 were male and 11 were children
http://journals.lww.com/
53
Acute Disseminated Encephalomyelitis in a 16-Year Old Patient After Receiving HPV-Vaccination: A Case Report Xianyuan Song, Francis DiMario Jr., Thomas Ciesielski, Dean Uphoff. Hartford Hospital
Acute acquired demyelination of the central nervous system (CNS) in pediatric patients may lead to a variety of clinical phenotypes depending on the site of demyelination, including optic neuritis, transverse myelitis, neuromyelitis optica, acute disseminated encephalomyelitis (ADEM), and acute multiple sclerosis. Broader definition of ADEM is applied to patients with multiple foci of white matter demyelination. About 50% of cases of ADEM follow viral exanthemata, respiratory and other infections or vaccinations. The clinical course is variable, ranging from a slow progression over weeks to a fulminant course over hours to days. HPV vaccine is only recently developed (approved in 2006), and we have not found any reports documenting the association of administration of HPV vaccine and CNS demyelinating disease (ADEM). We now report a 16-year-old female who presented with acute asymmetric, right greater than left, vision loss. MRI scan and CT showed edema with white matter changes in the right parieto-occipital, parietal junction, and an intrinsic lesion in the optic chiasm and the left optic nerve. No lesions were seen in the spinal cord. She was afebrile and alert. Right parietal biopsy showed acute inflammatory demyelination in the white matter. CSF was negative for oligoclonal bands and anti-NMO antibody, a specific marker for neuromyelitis optica. Other laboratory studies including antinuclear antibody, CMV titer, toxoplasmosis titer, double-stranded DNA, Sjogren antibody, angiotensin-converting enzyme, and antiphospholipid antibody were all normal. The patient's history included 2 injections of HPV vaccine, 2 month and 10 days before her neurological presentation. The clinical, MRI and pathological findings suggest a diagnosis of ADEM. The patient was treated with high dose steroid and IVIG. On discharge, she had some improvement in the right visual fields. ADEM after HPV vaccination is a new occurrence. Here, we report that HPV vaccine may be correlated with the occurrence of ADEM.
http://journals.lww.com/jneuropath/Fulltext/2010/05000/American_Association_of_Neuropathologists,_Inc__.9.aspx
see full text ;
http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html
Terry S. Singeltary Sr. [flounder@wt.net ]
Monday, January 08,200l 3:03 PM
freas@CBS5055530.CBER.FDA.GOV
CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission
To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
BELOW, PAGE 1 ACTUALLY STARTS ON PAGE 13, then when you get to the bottom, part 3 starts at the top.........TSS
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOV
Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Friday, December 01, 2006 2:59 PM
Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION
snip...
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
snip... 48 pages...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Tuesday, January 25, 2011
Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions
http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html
Friday, January 21, 2011
Strain-Specific Barriers against Bovine Prions in Hamsters
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/strain-specific-barriers-against-bovine.html
Wednesday, January 19, 2011
EFSA BIOHAZ Scientific Opinion on the revision of the quantitative risk assessment (QRA) of the BSE risk posed by processed animal proteins (PAPs)
EFSA Journal 2011;9(1):1947
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-biohaz-scientific-opinion-on.html
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html
Tuesday, January 18, 2011
Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
strictly NOT private and confidential $$$
Saturday, January 22, 2011
Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
*** Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html
http://betaamyloidcjd.blogspot.com/
DID EVERYONE THAT LOST A LOVED ONE FILL OUT THEIR CJD QUESTIONNAIRE FROM THE CDC AND OR THE CJD FOUNDATION ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
COMMERCIAL IN CONFIDENCE
3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy
It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC.
and then another 3 + pages of blank space. ...TSS
http://collections.europarchive.org/tna/20080102164813/http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf
COMMERCIAL IN CONFIDENCE
BSE - CURRENT POSITION WITH VETERINARY LICENCED PRODUCTS (MA.1968)
There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).
1) Vaccines
http://collections.europarchive.org/tna/20080103033809/http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf
NOT FOR PUBLICATION
another 6 pages of blank space. ...TSS
http://collections.europarchive.org/tna/20080103032658/http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf
http://collections.europarchive.org/tna/20080103032631/http://www.bseinquiry.gov.uk/files/yb/1988/11/04003001.pdf
http://collections.europarchive.org/tna/20080103033926/http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf
COMMERCIAL IN CONFIDENCE
http://collections.europarchive.org/tna/20080103034137/http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf
COMMERCIAL IN CONFIDENCE
Medicines Act - Veterinary Products Committee
http://collections.europarchive.org/tna/20080103034140/http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf
COMMERCIAL IN CONFIDENCE
NOT FOR PUBLICATION
COMMITTEE ON SAFETY OF MEDICINES
another 6 pages or so that are blank. ...TSS
http://collections.europarchive.org/tna/20080102185137/http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf
http://collections.europarchive.org/tna/20080102184613/http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf
COMMERCIAL IN CONFIDENCE
NOT FOR PUBLICATION
COMMITTEE ON SAFETY OF MEDICINES
WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY
7.2.1. Products with bovine brain/lymphoid tissue as ingredients and administered by injection...[111]
7.2.2 Products with bovine ingredients (other than brain/lymphoid tissue) and administered by injection...[135]
7.2.3 Tissue implants, open wound dressings, surgical materials, dental and opthalmic products with bovine ingredients...[27]
7.2.4. Products with bovine ingredients and administered topically...[5]
7.2.5 Products with bovine ingredients and administered orally...[9]
7.2.6 Products with other animal/insect/bird ingredients and administered:
a. by injection a: 117
b. by topically b: 6
c. orally c: 8
7.2.7 Products with materials produced from animal material by chemical processes, eg stearic acid, gelatin and lanolin...[156]
With two exceptions, the replies to date have not given any immediate cause for concern, although 176 products do not conform to the CSM/VPC guidelines.
8. The first exception was from which gave very limited information about a very large number of homoepathic medicines with material obtained from cattle and a number with material from the brain. Of these, 53 were injectable products of which 20 were derived from cattle brain. A list of these products is attached as Appendix 1 to Annex D. The second exception relates to the product, 'Surgical Catgut', which is sourced from UK bovine intestines and will contain lymphoid material...
see full text ;
http://collections.europarchive.org/tna/20080102164420/http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf
COMMERCIAL IN CONFIDENCE
http://collections.europarchive.org/tna/20080102164744/http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf
MANAGEMENT IN CONFIDENCE
CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS
http://collections.europarchive.org/tna/20080102184729/http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;
[unknown woman] what group are you with?
[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?
at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.
snip...full text ;
http://bse-atypical.blogspot.com/2010/01/14th-international-congress-on.html
The documents below were provided by Terry S. Singeltary Sr on 8 May 2000.
They are optically character read (scanned into computer) and so may contain typos and unreadable parts.
TIP740203/l 0424 CONFIDENTIAL
snip...
The responses by the companies were presented by Ms Turner and were categorised by MCA standards, the products that were discussed were all low volume usage products eg sutures, heart valves.
8. As the responses included some materials of human origin it was decided that more information should be sought about CJD. There had been 2 recent deaths reported associated with human growth hormone. These were being investigated.
snip...
http://www.mad-cow.org/00/may00_news.html#aaa
5.3.3 The greatest risk, in theory, would be from parenteral injection of material derived from bovine brain or lymphoid tissue. Medicinal products for injection or surgical implantation which are prepared from bovine tissues, or which utilise bovine serum albumin or similar agents in their manufacture, might also be capable of transmitting infectious agents. All medicinal products are licensed under the Medicines Act by the Licensing Authority following guidance, for example from the Committee on Safety of Medicines (CSM), the Committee on Dental and Surgical Materials (CDSM) and their subcommittees. The Licensing Authority have been alerted to potential concern about BSE in medicinal products and will ensure that scrutiny of source materials and manufacturing processes now takes account of BSE agent.
see all 76 pages ;
http://collections.europarchive.org/tna/20080102132706/http://www.bseinquiry.gov.uk/files/ib/ibd1/tab02.pdf
EXPORT OF BRITISH BIOLOGICAL PHARMACEUTICALS
1. Please see the attached note of a recent meeting in Brussels. For Dr. Purford should read Dr. Purves (I think). If the Germans get their way, and it looks as if they might, because of worries about BSE we could end up with a ban on certain bovine materials being exported from the UK for pharmaceutical manufacture. Thse materials include cell cultures of bovine origin (? and also any cultures which have been fed bovine nutrient material), bovine serum, and fetal calf serum.
2. Whilst export of these raw materials may be very limited, it is only a small step to include in this export ban any finished product made from such materials. This would include virtually all biologicals and vaccines. This could have very serious effects on the export trade of British Manufacturers of biologicals because even where they source their bovine ingredients outside the UK it might be impossible or at least very difficult to bypass any export ban.
3. Our own line is that we have not used regulations to restrict the use of British bovine material for non-food use, although certain offals cannot be used for human consumption. ...
http://collections.europarchive.org/tna/20080102220244/http://www.bseinquiry.gov.uk/files/yb/1990/03/13002001.pdf
Export of British 'Biological' Pharmaceuticals
http://collections.europarchive.org/tna/20080102220202/http://www.bseinquiry.gov.uk/files/yb/1990/03/13008001.pdf
http://collections.europarchive.org/tna/20080102215829/http://www.bseinquiry.gov.uk/files/yb/1990/03/13009001.pdf
No papers were presented by our American guests and none covered the subject of pharmaceuticals. ...
http://collections.europarchive.org/tna/20080102220453/http://www.bseinquiry.gov.uk/files/yb/1990/04/02002001.pdf
STANDING COMMITTEE MEETING ON BSE
Thanks for your note. I am disappointed not to have been informed about this meeting in advance and am surprised that Dr. Tyrrell was not involved either. I find it insulting to be told the proceedings were in confidence and find your excuse about only hosting the meeting unconvincing.
http://collections.europarchive.org/tna/20080102220555/http://www.bseinquiry.gov.uk/files/yb/1990/04/06002001.pdf
The documents below were provided by Terry S. Singeltary Sr on 8 May 2000.
They are optically character read (scanned into computer) and so may contain typos and unreadable parts.
TIP740203/l 0424 CONFIDENTIAL
Mr Cunningham CMP3 From: D O Hagger MBI Dr Salisbury MED/IMCD3 Mr Burton PD/STB/PG1B B/17/2 Date: 15.02.1989 Mr Dudley PD/AD4
snip...
89/06.19/8.1 BSE3/1 0191 Hr J Maslin (MAFF) Ref: Maslin3g
From: Dr H Pickles Med SEB/B Date: 3 July 1989
CATTLE BY-PRODUCTS AND BSE
I was interested to see the list of by-products sent to the HSE. Those of particular concern included:
* small intestines: sutures (I thought the source was ovine but you are checking this)
* spinal cord: pharmaceuticals
* thymus: pharmaceuticals
Are you able to give me more information on which UK manufacturers use these materials? Our proposed ban on bovine offal for human consumption would not affect these uses, I assume.
snip...see full text ;
http://www.mad-cow.org/00/may00_news.html
http://www.javno.com/en/world/clanak.php?id=32047
http://creutzfeldt-jakob-disease.blogspot.com/2007/12/risk-factors-for-sporadic-creutzfeldt.html
40,000 human heart valves a year from BSE herds Sun, 3 Sep 2000.
Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas
http://www.mad-cow.org/00/sep00_news.html#hhh
USDA allows diseased animals into human food supply
Mon, 14 Aug 2000. Information provided by Terry S. Singeltary Sr.
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - Report of a visit to the USA - April-May 1989 - G A H Wells [head of England's main veterinary lab -- webmaster]
2. Meeting with USDA, BSE Task Force
http://www.mad-cow.org/00/aug00_late_news.html#hhh
http://www.mad-cow.org/00/may00_news.html#aaa
http://www.mad-cow.org/00/01jan_news.html#aaa
Subject: Louping-ill vaccine documents from November 23rd, 1946
Date: Sat, 9 Sep 2000 17:44:57 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946
NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND
ANNUAL CONGRESS, 1946
snip...
As a result of this experience a large-scale transmision experiment involving the ue of 788 sheep was commenced in 1938 on a farm specially taken for the purpose by the Animal Diseases Research Association with funds provided by the Agricultural Research Council. The experiment was designed to determine the nature of the infective agent and the pathogenesis of the disease. It is only possible here to give a summary of the result which showed that (1) saline suspensions of brain and spinal cord tissue of sheep affected with scrapie were infective to normal sheep when inoculatted intracerebrally or subcutaneously; (2) the incubation period after intracerebral inoculation was seven months and upwards and only 60 percent of the inoculated sheep developed scrapie during a period of four and a half years; (3) the incubation period after subcutaneous inoculation was 15 months and upwards and only about 30 percent of the inoculated sheep developed the disease during the four and a half years: (4) the infective agent was of small size and probably a filtrable virus.
The prolonged incubative period of the disease and the remarkable resistance of the causal agent to formalin are features of distinct interest. It still remains to determine if a biological test can be devised to detect infected animals so that they can be killed for food before they develop clinical symptoms and to explore the possibilities of producing an immunity to the disease.
==================================================================
Greetings List Members,
pretty disturbing document. now, what would stop this from happening with the vaccineCJD in children???
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
http://www.whale.to/v/singeltary.html
MAD COW DISEASE BSE CJD CHILDREN VACCINES
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN VACCINES
TIP740203/l 0424 CONFIDENTIAL
http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html
Research Lead: Dr. David Westaway, University of Alberta
Project: "Extending the spectrum of Prionopathies to Amyotrophic Lateral Sclerosis and Autism"
This project proposes to link the chemistry of the prion protein to the new territory of other nervous system diseases, such as ALS (Lou Gehrig's disease) and the socialization disorder autism -diseases which are at least one thousand times more common than prion diseases. It is believed that a different type or prion protein may operate in other types of brain diseases, which could lead to new ways of thinking about incurable disorders. The project will create changes in the amounts of the various forms of the new membrane protein, and then perform an array of analyses on the behavior and nervous system transmission of laboratory mice. Nervous transmission by electrical impulse can be measured in isolated brain cells, a system that is also convenient to study the effect of stress by adding small amounts of toxins to the fluids bathing the cultures. By these means, the project aims to extend the boundaries of what is considered "prion disease."
Funding: $520,500
http://www.prioninstitute.ca/index.php?page=webpages&menucat=42&id=26&action=displaypage&side=1
Unfolding the Prion Mystery Building and Growing Research Expertise in Alberta Year 4 2008-2009 Annual Report
Dr. David Westaway, University of Alberta Extending the spectrum of prionopathies to amyotrophic lateral sclerosis (ALS) and autism Dr. Westaway’s study aims to extend the boundaries of what is considered prion disease. His project takes the chemistry of the prion protein into the territory of nervous system diseases such as ALS (Lou Gehrig’s disease) and socialization disorder diseases such as autism. These brain diseases are at least 1,000 times more common than diseases currently accepted as prion related. Dr. Westaway hypothesizes that a different type of protein misfolding may operate in brain diseases such as Lou Gehrig’s and autism. This type of protein misfolding may occur in response to stresses in the brain. Unlike misfolded prions, other misfolded proteins may be noninfectious and not viable outside of the affected animal. Dr. Westaway’s research team will investigate these hypotheses by inducing changes in the brain cells of laboratory mice, measuring the resulting electrical impulses in the animals’ nervous systems and analyzing the effect on behaviour. Because nervous transmission by electrical impulse can be measured in isolated brain cells, adding small amounts of toxins to the fluids bathing the cell cultures will make it possible to study the effect of stress. The results could lead to new ways of thinking about nervous system disorders.
http://www.prioninstitute.ca/forms/WEBSITE%20AR.pdf
102
Causes of Death and Neuropathology in Autism Spectrum Disorder: A Medical Examiner Perspective
Kenneth Hutchins1, Mariana Nunez2, Carol Petito2. 1Miami Dade County Medical Examiner Department; 2University of Miami Miller School of Medicine, Department of Pathology
Autism Spectrum Disorder (ASD) is characterized by abnormalities in how patients relate to and communicate with others and their environment . It develops in as many as 1 in 150 children and may be associated with co-morbid disorders including seizures and mental retardation. Because ASD reduces life expectancies, we reviewed autopsy records of 22 consecutive cases from two south Florida Medical Examiner Departments over a 10 year period and correlated cause of death (COD) with clinical history and neuropathology. Patient ages averaged 18±11 yrs and ranged from 3-51 years; 16 were male and 11 were children
http://journals.lww.com/
53
Acute Disseminated Encephalomyelitis in a 16-Year Old Patient After Receiving HPV-Vaccination: A Case Report Xianyuan Song, Francis DiMario Jr., Thomas Ciesielski, Dean Uphoff. Hartford Hospital
Acute acquired demyelination of the central nervous system (CNS) in pediatric patients may lead to a variety of clinical phenotypes depending on the site of demyelination, including optic neuritis, transverse myelitis, neuromyelitis optica, acute disseminated encephalomyelitis (ADEM), and acute multiple sclerosis. Broader definition of ADEM is applied to patients with multiple foci of white matter demyelination. About 50% of cases of ADEM follow viral exanthemata, respiratory and other infections or vaccinations. The clinical course is variable, ranging from a slow progression over weeks to a fulminant course over hours to days. HPV vaccine is only recently developed (approved in 2006), and we have not found any reports documenting the association of administration of HPV vaccine and CNS demyelinating disease (ADEM). We now report a 16-year-old female who presented with acute asymmetric, right greater than left, vision loss. MRI scan and CT showed edema with white matter changes in the right parieto-occipital, parietal junction, and an intrinsic lesion in the optic chiasm and the left optic nerve. No lesions were seen in the spinal cord. She was afebrile and alert. Right parietal biopsy showed acute inflammatory demyelination in the white matter. CSF was negative for oligoclonal bands and anti-NMO antibody, a specific marker for neuromyelitis optica. Other laboratory studies including antinuclear antibody, CMV titer, toxoplasmosis titer, double-stranded DNA, Sjogren antibody, angiotensin-converting enzyme, and antiphospholipid antibody were all normal. The patient's history included 2 injections of HPV vaccine, 2 month and 10 days before her neurological presentation. The clinical, MRI and pathological findings suggest a diagnosis of ADEM. The patient was treated with high dose steroid and IVIG. On discharge, she had some improvement in the right visual fields. ADEM after HPV vaccination is a new occurrence. Here, we report that HPV vaccine may be correlated with the occurrence of ADEM.
http://journals.lww.com/jneuropath/Fulltext/2010/05000/American_Association_of_Neuropathologists,_Inc__.9.aspx
see full text ;
http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html
Terry S. Singeltary Sr. [flounder@wt.net ]
Monday, January 08,200l 3:03 PM
freas@CBS5055530.CBER.FDA.GOV
CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission
To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
BELOW, PAGE 1 ACTUALLY STARTS ON PAGE 13, then when you get to the bottom, part 3 starts at the top.........TSS
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOV
Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Friday, December 01, 2006 2:59 PM
Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION
snip...
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
snip... 48 pages...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
Saturday, January 29, 2011
Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate
Jpn. J. Infect. Dis., 64 (1), 81-84, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Tuesday, January 25, 2011
Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions
http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html
Friday, January 21, 2011
Strain-Specific Barriers against Bovine Prions in Hamsters
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/strain-specific-barriers-against-bovine.html
Wednesday, January 19, 2011
EFSA BIOHAZ Scientific Opinion on the revision of the quantitative risk assessment (QRA) of the BSE risk posed by processed animal proteins (PAPs)
EFSA Journal 2011;9(1):1947
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-biohaz-scientific-opinion-on.html
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html
Tuesday, January 18, 2011
Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
strictly NOT private and confidential $$$
Saturday, January 22, 2011
Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
*** Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html
http://betaamyloidcjd.blogspot.com/
DID EVERYONE THAT LOST A LOVED ONE FILL OUT THEIR CJD QUESTIONNAIRE FROM THE CDC AND OR THE CJD FOUNDATION ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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