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Incidence of CJD Deaths Reported by CJD-SS in Canada as of July 31, 2010

Posted Aug 18 2010 12:21pm
PLEASE NOTE before going any further ;

> 4. Final classification of 64 cases from 2008/09/10 is pending

WHAT could these unusual cases of CJD be ?

WHAT are the ages, clinical symptoms, time frame from onset of clinical symptoms to death, pathology, many unanswered questions here ?

COULD these 64 cases be from mad cow disease ?

c-BSE, h-BSE, and l-BSE, have all three been documented in Canada, and none is related to human CJD there from ?

This same statement ;

> 4. Final classification of 64 cases from 2008/09/10 is pending

resembles what the USA Prion Unit states about USA cases, but omits one thing ''vCJD has been excluded'' ;

> 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.

ARE any of these cases in Canada the same as the cases in the USA i.e. some being the PRIONPATHY, the genetic CJD that's not genetic, but sporadic ?

MANY unanswered questions here, for a country with mad cow disease of 3 strains documented, but none related to human TSE ?

MANY unanswered questions, what about blood there from ?

Terry S. Singeltary Sr.


Incidence of CJD Deaths Reported by CJD-SS in Canada as of July 31, 2010

Year of Death Total CJD Cases Population of Canada Incidence Rate

1999 31 30,401,286 1.02

2000 35 30,685,730 1.14

2001 30 31,019,020 0.97

2002¹ 36 31,353,656 1.15

2003 29 31,639,670 0.92

2004 43 31,940,676 1.35

2005 44 32,245,209 1.36

2006 44 32,576,074 1.35

2007 36 32,931,956 1.09

2008 43 33,327,337 1.29

2009² 45 33,739,814 1.33

2010² 5 33,841,500 0.15

1. As of September 2002, CJD cases include both definite and probable cases of CJD

2. Data from 1999 to 2008 are complete, and data for 2009 and 2010 are provisional

3. 2009 Population Source: Statistics Canada, Demography Division

4. Final classification of 64 cases from 2008/09/10 is pending.

World Wide average occurrence of CJD is approximately 1-2 per million population


CJD Deaths Reported by CJDSS1, 1994-20102 As of July 31, 2010

Deaths of Definite and Probable CJD Year Sporadic Iatrogenic Familial GSS FFI vCJD Total

1994 2 0 1 0 3

1995 3 0 3

1996 13 0 13

1997 16 0 1 0 18

1998 22 1 0 1 0 24

1999 26 2 1 0 31

2000 32 0 3 0 35

2001 27 0 2 1 0 30

2002 31 0 2 0 1 36

2003 27 1 0 29

2004 42 0 1 0 43

2005 42 0 2 0 44

2006 39 0 1 3 1 0 44

2007 32 0 4 0 36

2008 42 0 1 0 43

2009 44 0 1 0 45

2010 4 1 5

Total 444 4 13 19 1 482

1. CJDSS began in April 1998

2. Data before April 1998 are retrospective and partial, data from 1999 to 2008 are complete, and data for 2009 and 2010 are provisional

3. Final classification of 64 cases from 2007/08/09 is pending.


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.

Wednesday, August 11, 2010


REMEMBER, bse aka mad cow disease has mutated into several different strains. atypical BSE is more virulent that typical c-BSE. cjd there from ? anyone's guess, but look at the science to date. it is very very disturbing...TSS

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

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)

Tuesday, August 03, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein

Monday, August 9, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?


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

Saturday, August 14, 2010

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

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

Wednesday, July 28, 2010

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

Tuesday, March 16, 2010



Proof Committee Hansard

RRA&T 2 Senate Friday, 5 February 2010


[9.03 am]

BELLINGER, Mr Brad, Chairman, Australian Beef Association

CARTER, Mr John Edward, Director, Australian Beef Association

CHAIR—Welcome. Would you like to make an opening statement?

Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so
You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heidenhain variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state
The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.

Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states
The BSC policy was set up for one purpose only, trade—the illegal trading of all strains of TSE globally throughout North America, which is home to CBSC, IBSC and HBSC, many scrapie strains and two strains of CJD to date. (please note typo error, those should have read cBSE, lBSE, and hBSE...tss)

I would also like, while I have the opportunity, to explain the beef-off-the-shelves myth. At the first Senate hearing on 14 December, it was explained that the reason why they allowed BSC beef into Australia was the beef-off-the-shelves policy, whereby if we found a case of BSC in Australia they would have to recall all—

Friday, 5 February 2010 Senate RRA&T 3


Senator HEFFERNAN—Which of course is total BS.

Mr Bellinger—Correct. This is written in the FSANZ document—Food Standards Australia New Zealand. Why isn’t this same policy in New Zealand? It is not—it is only in Australia. We are the only country in the world to have this idiotic policy. So we again call for the tabling of the WTO obligations paperwork. We do not believe that exists.

snip...see full text 110 pages ;

for those interested, please see much more here ;

Tuesday, July 13, 2010

AUSTRALIAN QUESTIONNAIRE TO ASSESS BSE RISK (OIE) Terrestrial Animal Health Code, 2009 and USA export risk factor for BSE to Australia

Saturday, August 14, 2010


US denies it's illegally sending beef to Australia ?

Friday, 13/08/2010

Saturday, June 19, 2010


Sunday, August 15, 2010


Tuesday, July 27, 2010

Spontaneous generation of mammalian prions


Thursday, August 12, 2010

USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010

Friday, August 13, 2010

Creutzfeldt-Jakob disease (CJD) biannual update 13 August 2010 UK Iatrogenic CJD Incidents Report

Thursday, August 12, 2010

Seven main threats for the future linked to prions

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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