Sunday, August 11, 2013

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

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



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



please see ;



HD.18: Creutzfeldt-Jakob disease reporting in Canada


Zheng Wang,1 Gerard H. Jansen,1,2 Elina Olsen,1 Rolande D'Amour,1 Stacy Sabourin,1 Tim Connolly,1 Jennifer Kruse,1 Neil Cashman,3 and Michael Coulthart1


1Public Health Agency of Canada; Ottawa, ON CA; 2Department of Pathology; Ottawa Hospital; Ottawa, ON CA; 3Brain Research Centre; University of British Columbia; Vancouver, BC CA


Background. To deal with risks of infectious transmission of Creutzfeldt-Jakob disease (CJD), in 1998 the Government of Canada launched a prospective national CJD surveillance system (CJDSS). In 2000, CJD became nationally notifiable in Canada, and since then all Canadian Provinces and Territories (P/Ts) have made CJD reportable. It has been recognized that the CJDSS registers more cases of CJD than are reported to P/T Ministries of Health (PTMH). Because the CJDSS may not legally share personal information with PTMH, in 2008 the CJDSS began to systematically discuss the issue of CJD reporting with referring health care professionals (HCP). The present study was undertaken to estimate any changes in P/T CJD reporting from 2008, and to identify possible areas for further improvement.


Materials and Methods. P/T CJD data were retrieved from the Public Health Agency of Canada's National Notifiable Disease System (NNDS) database, and compared with CJDSS data. CJDSS intake sheets were examined, to determine if the case had been reported to the PTMH at the time of notification.


Results. From 2005 to 2010, NNDS received complete data on CJD from 5 P/Ts. During the same period, 134 cases of CJD (probable or neuropathologically confirmed) were reported by the 5 P/Ts while 210 CJD deaths (probable or definite) were recorded in the CJDSS from the same 5 P/Ts. Between 2008 and 2010 there was an increase of ~48% in P/T CJD reports compared with the period 2005-2007. In contrast, the CJDSS registered only ~12% more CJD deaths between 2008 and 2010 compared with 2005-2007, supporting an interpretation of improved P/T reporting. Examination of intake sheets from 172 notifications that were made to the CJDSS from the same 5 P/Ts between 2008 and 2010 revealed that 30 were known to have been reported to PTMH at the time of referring (24 were CJD, 5 were non-CJD, and 1 was unclassifiable). 142 were not reported or had unknown reporting status. Reasons cited by HCPs for not reporting included (1) uncertainty of the CJD diagnosis; (2) uncertainty regarding responsibility for reporting; (3) lack of awareness that CJD is reportable; and (4) uncertainty regarding when or how to report.


Conclusion. The considerable increase of CJD reports in P/Ts since 2008 occurred concurrently with efforts of the CJDSS to engage HCPs on the issue of CJD reporting requirements. P/T CJD reports may include non-CJD cases. Inter-jurisdiction collaboration is underway to further improve CJD reporting.




 HD.15: Prion disease among Asians and Pacific Islanders in the United States, 2003-2009


Ryan A.Maddox,1 Robert C. Holman,1 Arialdi M. Minino,2 Janis E. Blevins,3 Lawrence B. Schonberqer1 and Ermias D. Belay1


1National Center for Emerging and Zoonotic Infectious Diseases; Centers for Disease Control and Prevention; Atlanta, GA USA; 2National Center for Health Statistics; Centers for Disease Control and Prevention; Hyattsville, MD USA; 3National Prion Disease Pathology Surveillance Center (NPDPSC); Case Western Reserve University; Cleveland, OH USA


Introduction. Asians and Pacific Islanders (APIs) comprise approximately 5% of the United Stares population. The occurrence of Creurzfeldt-Jakob disease (CJD) and other prion diseases among APIs in the United Stares has not been widely investigated.


Materials and Methods. API prion disease decedents were identified from the United Stares national multiple cause-of-death data and the National Prion Disease Pathology Surveillance Center database for 2003-2009. Relevant portions of medical records and results from neuropathologic and generic resting for API prion disease decedents were obtained and reviewed, as available.


Results. During 2003-2009, 60 API prion disease decedents were identified. 34 of these decedents had additional race information available, with 15 API decedents classified as Filipino (44%), 13 as Japanese (38%), 5 as Chinese (15%) and 1 as Hawaiian (3%). The average annual age-adjusted incidence was 0.7 per million population, significantly lower than that for whites (p < 0.001). Over half (55%) of the API deaths occurred in California or Hawaii, the states with the highest API populations. The median age at death was 66.5 y (range 40-87 y), similar to that for whites (68 y). Neuropathology reports and/ or medical records were available for 24 of the decedents, for 20 cases with a reported disease onset date, the median duration of illness was 4.5 mo (range 1-66 mo). Twenty of 22 decedents (91 %) had sporadic CJD, while the remaining 2 decedents (9%) had familial CJD. All 20 decedents with generic testing results available were methionine homozygous at codon 129.


Conclusion. For 2003-2009, the reported prion disease incidence among APIs in the United States was significantly lower than that for whites. Underreporting of API race may contribute at least partly to this lower incidence, but generic factors may influence prion disease susceptibility as well. Because the API race is heterogeneous, further study of prion diseases among specific API ethnic groups is warranted.




HD.23: Creutzfeldt-Jakob disease among American Indians and Alaska natives in the United States, 1983-2009


Robert C. Holman, Ryan A. Maddox, Arianne M. Folkema, Arialdi M. Minino, Ermias D. Belay and Lawrence B. Schonberger


CDC; Atlanta, GA, USA


Background and Introduction. Creutzfeldt-jakob disease (CJD) occurrence among American Indians and Alaska Natives (AI/ ANs) is of special interest, in part because of the high prevalence of hunting and venison consumption in this population. Such behaviors could place AI/ANs at increased risk of prion disease if chronic wasting disease (CWO) were found to transmit to humans.


Materials and Methods. Death records with CJD as any listed cause of death for US residents identified from the national multiple cause-of-death data and other surveillance mechanisms for 1983 through 2009 were analyzed, and incidence was calculated by race. Available death certificates and medical records were collected and examined for AI/AN decedents.


Results. During 1983 through 2009, 15 decedents with CJD as a cause of death were reported as AI/AN race. The average annual age-adjusted CJD incidence for AI/ANs was 0.39 per 1,000,000 persons. The rate for whites (1.07) was higher compared with that for AI/ANs (RR = 2.9, 95% CI = 1.8-4.9) and blacks were similar (0.41; RR = 1.1, 95% CI = 0.7-1.9). The median age at death was 65 y (range 39-85 y), similar to those for whites and blacks (68 and 66 y, respectively); four (27%) AI/AN decedents were younger than 55 y of age. Most of the AI/AN decedents were males (60%). Decedents were reported from 13 states; none resided in the states with the longest known presence of CWD, Colorado, Wyoming, and Nebraska.


Conclusion. The reported CJD incidence for AI/ANs appears lower than that for whites and similar to that for blacks, although the CJD incidence for AI/ANs is likely underestimated due to racial misclassification of AI/ANs. Continued monitoring of CJD occurrence in this population is important as CWD spreads into new areas.




 HD.11: Developing new epidemiological prion disease databases (epiCJD)


Jose E.Cunha,1 Aline E. Vasconcelos,2 Joao R. Oliveira,3 and Rosalie B. Belian4,5


1LIKA/UFPE; Recife, PE Brazil; 2Keizo Asami Laboratory; Federal University of Pernambuco; Recife; Brazil; Recife, PE Brazil; 3Neuropsichiatry Department; Federal University of Pernambuco; Recife; Brazil; Recife, PE Brazil; 4Medicine Department; Federal University of Pernambuco; Recife, PE Brazil; 5Medicine Department; Federal University of Pernambuco; Recife; Brazil; Recife, PE Brazil


Background. Prion disease (PrD) or Transmissible Spongiform Encephalopathy (TSE) is a group of rare diseases which affecting several mammals, including man. According to molecular profiles, such as the presentation of codon 129, those diseases show a broad of histopathological, clinical and molecular characteristics, resulting in a challenging diagnosis. Recently, an unusual association of CJD with catatonia was reported and others reports are also showing that psychiatric symptoms, such as depression, are more common that previously assumed. Recognize clinical trait are an important step to include PrD in differential diagnosis and give the most informative scenario as possible to patients relatives in order to precede future therapies. However, illness with great heterogeneity requires standard protocols and active surveillance able to identify new features. Databases are an extraordinary approach that provides to us the possibility to catalog and monitoring a number of biological information such as genetic variation and epidemiological traits. In order to improve knowledge and better recognition of symptoms and characteristics of PrD, we are implementing the epiCJD database and an information system to collect information about these illnesses from scientific publication around the world allowing to anyone visualize reported cases through a unique website (which will be released next April).


Materials and Methods. To feed our database, we performed an active search in Pubmed bank and looked for reported cases only. Reviews and metanalysis were not considered in this search in order to avoid the occurrence of redundancies. We have cataloged epidemiological, genetic and socio-demographic data related to each reported case. A link for the original case is presented to provide a depth understanding of the cases. Users can perform searches with any data available in the database, such as the number of cases reported at a specific country or city, by clinical symptoms or a combination of different kind of information. Besides, graphics and metaanalysis will be allowed. epiCJD can be accessed through the dcjBRASIL platform in English or Portuguese. This website contains information about PrD oriented to general public and health professionals aiming to diminish the lack of information, mainly in Brazil.


Conclusion. epiCJD can be accessed by researchers, students and general public allowing them to recognize symptoms related to PrD. This approach can also contribute to surveillance of these illnesses providing to public health agencies a new way to monitor PrD around the world.




 please note, there was not updated data from the Prion unit for all CJD over all for the USA, so here is the latest from Dr. Gambetti’s Prion Unit site, June 30, 2013, so I submit the following from the USA Prion Unit ;


National Prion Disease Pathology Surveillance Center Cases Examined1 (June 30, 2013)


Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD


1996 & earlier 52 34 29 4 0 0


1997 114 68 59 9 0 0


1998 88 52 44 7 1 0


1999 123 74 65 8 1 0


2000 145 103 89 14 0 0


2001 212 120 110 10 0 0


2002 248 149 125 22 2 0


2003 266 168 137 31 0 0


2004 326 187 164 22 0 13


2005 344 194 157 36 1 0


2006 381 195 165 28 0 24


2007 378 214 186 28 0 0


2008 396 232 207 25 0 0


2009 422 256 213 42 1 0


2010 414 258 217 41 0 0


2011 411 257 215 42 0 0


2012 421 253 217 36 0 0


2013 181 112 73 28 0 0


TOTAL 49225 29266 2472 433 6 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 7 cases in which the diagnosis is pending, and 19 inconclusive cases;


6 Includes 12 (11 from 2013) cases with type determination pending in which the diagnosis of vCJD has been excluded. The sporadic cases include 2407 cases of sporadic Creutzfeldt-Jakob disease (sCJD), 48 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 17 cases of sporadic Fatal Insomnia (sFI).







PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.



please see ;



> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.



CJD Deaths Reported by CJDSS1, 1994-20122


As of May 31, 2012


Deaths of Definite and Probable CJD


Year Sporadic Iatrogenic Familial GSS FFI vCJD Total


1994 2 0 0 1 0 0 3


1995 3 0 0 0 0 0 3


1996 13 0 0 0 0 0 13


1997 16 0 1 1 0 0 18


1998 22 1 0 1 0 0 24


1999 26 2 2 1 0 0 31


2000 32 0 0 3 0 0 35


2001 27 0 2 1 0 0 30


2002 31 0 2 2 0 1 36


2003 27 1 1 0 0 0 29


2004 42 0 1 0 0 0 43


2005 42 0 0 2 0 0 44


2006 39 0 1 3 1 0 44


2007 35 0 0 4 0 0 39


2008 48 0 1 0 0 0 49


2009 48 0 3 2 0 0 53


2010 34 0 3 0 0 0 37


2011 37 0 2 1 0 1 41


2012 1 0 0 0 0 0 1


Total 525 4 19 22 1 2 573


1. CJDSS began in 1998


2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional


3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.


CJD Deaths Reported by CJDSS1, 1994-20122


As of May 31, 2012














National Prion Disease Pathology Surveillance Center


Cases Examined1


(May 18, 2012)


Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD


1996 & earlier 50 32 28 4 0 0


1997 114 68 59 9 0 0


1998 88 52 44 7 1 0


1999 123 74 65 8 1 0


2000 145 103 89 14 0 0


2001 210 120 110 10 0 0


2002 248 149 125 22 2 0


2003 266 168 137 31 0 0


2004 326 187 164 22 0 13


2005 344 194 157 36 1 0


2006 382 196 166 28 0 24


2007 377 213 185 28 0 0


2008 396 232 206 26 0 0


2009 423 256 212 43 1 0


2010 413 257 216 41 0 0


2011 410 257 213 43 0 0


2012 153 82 51 15 0 0


TOTAL 44685 26406 2227 387 6 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 14 cases in which the diagnosis is pending, and 18 inconclusive cases;


6 Includes 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).


Rev 5/18/2012




> 6 Includes


> 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded.


> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).



WELL, it seems the USA mad cow strains in humans classified as type determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased over the years, and the same old song and dance continues with sporadic CJD cases $$$







CJD surveillance in the Canada and the USA has been in place well long enough, for this same excuse (improved P/T reporting) year after year of reporting increases to be a valid excuse anymore, in my opinion.


I don’t buy this same old song and dance anymore.


it’s the same recording we hear year after year, decade after decade, happenstance of bad luck, increase is due to better surveillance, yada, yada, yada $$$


North America is awash in animal Transmissible Spongiform Encephalopathy TSE prion disease in many, many species. All of which are consumed/exposed in many different ways, by humans and animals.


This excuse ‘’improved P/T reporting’’ is old, and it is what it is, an excuse, to protect the industries that are involved. nothing has changed in almost 3 decades, except the people. it’s the same old BSe.


I will report on disturbing iatrogenic risk factors, cjd in the UK, and more data on the TSE prion disease in different species, and more from prion2013 as I can get it put together.


I want to thank Prion2013, and all the scientist and doctors and such that are working so hard to solve the many riddles of the TSE prion disease. ...TSS




Thursday, April 4, 2013


Variably protease-sensitive prionopathy in the UK: a retrospective review 1991–2008


Brain (2013) 136 (4): 1102-1115. doi: 10.1093/brain/aws366




*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.






OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles


Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA


Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.


Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.


Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.


In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.


Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.


The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.




Saturday, July 6, 2013


Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy


Research Article




Monday, January 14, 2013


Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe




Monday, December 31, 2012


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




Saturday, December 29, 2012






Sunday, February 12, 2012


National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas




Monday, August 9, 2010


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




Wednesday, March 28, 2012









*** please remember this word for later reference of a new prion disease, or rather, another new prion disease, or maybe just the same one.. ..TSS







Sunday, August 09, 2009


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





Tuesday, August 18, 2009


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





Monday, October 10, 2011


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




EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.







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




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






Saturday, June 25, 2011


Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque


"BSE-L in North America may have existed for decades"




Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.




The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...




Monday, September 26, 2011


L-BSE BASE prion and atypical sporadic CJD




Tuesday, November 02, 2010




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


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













2012 atypical L-type BSE BASE California reports



Saturday, August 4, 2012


Final Feed Investigation Summary - California BSE Case - July 2012






Summary Report BSE 2012


Executive Summary




Saturday, August 4, 2012


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







Canada has had a COVER-UP policy of mad cow disease since about the 17th case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored $$$



THIS proves there is indeed an epidemic of mad cow disease in North America, and it has been covered up for years and years, if not for decades, and it’s getting worse $$$



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





Wednesday, August 11, 2010






Thursday, August 19, 2010






Friday, March 4, 2011


Alberta dairy cow found with mad cow disease




Reasons for the New Regulation Order No. 23 (as well as amending Order No. 149) of the State Committee for Veterinary Medicine name BSE as the reason for new import requirement. The legal title for Order No. 23 is "On Urgent Measures Aimed at Prevention and Elimination of BSE and Other Prion Infections in Cattle”. Neither Order explains how the threat of introduction of BSE can be addressed through the inspection of producers of all products of animal origin including fish, dairy products, poultry and pork. It is not clear what other concerns are addressed through the proposed inspections. Formal Notification of Trading Partners On August 3rd, Ukraine's Notification and Enquiry Point issued a legal Notification G/SPS/N/UKR/3/Rev.1 found on the Official WTO Website (Committee on Sanitary and Phytosanitary Measures)





Tuesday, June 26, 2012


Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012


type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA





Wednesday, June 13, 2012






Wednesday, April 4, 2012


Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68




Thursday, February 16, 2012


Bovine Spongiform Encephalopathy BSE






Wednesday, February 16, 2011










Sunday, April 18, 2010






Thursday, March 29, 2012


atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012


NIAA Annual Conference April 11-14, 2011San Antonio, Texas




Thursday, February 23, 2012


Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012




Wednesday, April 4, 2012


20120402 - Breach of quarantine/Violation de la mise en quarantaine of an ongoing Scrapie investigation




Monday, June 11, 2012


another atypical Nor-98 Scrapie case documented in Canada for 2012




Monday, April 25, 2011


Experimental Oral Transmission of Atypical Scrapie to Sheep


Volume 17, Number 5-May 2011 However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40).




***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.




*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.




*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.




Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.


Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.


(i) the unsuspected potential abilities of atypical scrapie to cross species barriers


(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier


These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.





Friday, February 11, 2011


Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues





Friday, July 26, 2013


Voluntary Scrapie Program USA UPDATE July 26, 2013 increase in FY 2013 is not statistically meaningful due to the sample size




Sunday, July 21, 2013


As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?




Tuesday, July 2, 2013


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





 Sunday, August 21, 2011


The British disease, or a disease gone global, The TSE Prion Disease


(see video here)







(see video at bottom)





Sunday, September 6, 2009









Creutzfeldt-Jakob Disease Public Health Crisis














JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733


Diagnosis and Reporting of Creutzfeldt-Jakob Disease


Terry S. Singeltary, Sr Bacliff, Tex


Since this article does not have an abstract, we have provided the first 150 words of the full text.


KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.


References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.





Published March 26, 2003


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States


Terry S. Singeltary, retired (medically)


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?


Published March 26, 2003







BY Philip Yam


Yam Philip Yam News Editor Scientific American


Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.




Laying Odds


Are prion diseases more prevalent than we thought?


Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?


Revisiting Sporadic CJD


It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.


Singeltary has similar inclinations. ...






Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9


June 2003


BY Philip Yam




Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.









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




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.




12 years independent research of available data




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.




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.





CJD Singeltary submission to PLOS ;


No competing interests declared.


see full text ;







The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI


Tracking spongiform encephalopathies in North America




Xavier Bosch


“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...










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


Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003


Date: Tue, 29 Jul 2003 17:35:30 –0500


From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy




Volume 3, Number 8 01 August 2003




Tracking spongiform encephalopathies in North America


Xavier Bosch


My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.







> > > he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. < < <


actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article.




Full Text


Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.




Re: vCJD in the USA * BSE in U.S.


15 November 1999 Terry S Singeltary, NA


In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease.


Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know.


My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following;


vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD.


The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?


CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997.


So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.


No BSE in the U.S.A.? I would not be so sure of that considering that since 1990;


Since 1990 the U.S. has raised 1,250,880,700 cattle;


Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;


There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;


Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;


Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.


I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.


Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.


It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........


The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.


Terry S. Singeltary Sr.


P.O. Box 42, Bacliff, Texas 77518 USA


Competing interests:None declared






U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...



2 January 2000


Terry S Singeltary


In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.


The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;


"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."


Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.


Something else I find odd, page 16;


"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."


A few more factors to consider, page 15;


"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."


"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."


"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."


Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow.


Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.


To be continued...


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


Competing interests:None declared





DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link auf diesen Artikel im Archiv:






"Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.


Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich verpflichteten sich fünf Unternehmen, darunter Branchenführer wie GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus unverdächtigem Material herzustellen.



"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...











Thursday, June 6, 2013






since our fine federal friends have decided not to give out any more reports on the USA breaches of the feed ban and surveillance etc. for the BSE TSE prion mad cow type disease in the USDA livestock, I thought I might attempt it. I swear, I just don’t understand the logic of the SSS policy, and that includes all of it. I assure you, it would be much easier, and probably better for the FDA and the USDA INC., if they would simply put some kind of report out for Pete’s sake, instead of me doing it after I get mad, because I am going to put it all out there. the truth.


PLEASE BE ADVISED, any breach of any of the above classifications OAI, VAI, RTS, CAN lead to breaches into the feed BSE TSE prion protocols, and CAN lead to the eventual suspect tainted feed reaching livestock. please, if any USDA official out there disputes this, please explain then how they could not. paperwork errors can eventually lead to breaches of the BSE TSE prion mad cow feed ban reaching livestock, or contamination and exposure there from, as well.


I would sure like to see the full reports of just these ;


4018 CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y


9367 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N


9446 DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N


9447 DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods 13553 County Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N


see full list of the fda mad cow bse feed follies, toward the bottom, after a short brief update on the mad cow bse follies, and our good friend Lester Crawford that was at the FDA.


ALSO, I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$










Inspections conducted by State and FDA investigators are classified to reflect the compliance status at the time of the inspection, based upon whether objectionable conditions were documented. Based on the conditions found, inspection results are recorded in one of three classifications:


OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.


VAI (Voluntary Action Indicated) when inspectors find objectionable conditions or practices that do not meet the threshold of regulatory significance, but warrant an advisory to inform the establishment that inspectors found conditions or practices that should be voluntarily corrected. VAI violations are typically technical violations of the 1997 BSE Feed Rule. These violations include minor recordkeeping lapses or conditions involving non-ruminant feeds.


NAI (No Action Indicated) when inspectors find no objectionable conditions or practices or, if they find objectionable conditions, those conditions are of a minor nature and do not justify further actions.





when sound science was bought off by junk science, in regards to the BSE TSE prion mad cow type disease, by the USDA, CFIA, WHO, OIE, et al. $$$


when the infamous, and fraudulently USDA, FSIS, APHIS, FDA, gold card was taken away that infamous day in December of 2003, all cards were off the table, it was time to change the science, and change they did. ...tss


 snip. ...please see full text ;




Thursday, June 6, 2013







Suspect symptoms


What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?


28 Mar 01


Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.


Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.


Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.


"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.


Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.


Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.


As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.


"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.


But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.


People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.


But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."


There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.


Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.













January 28, 2007



Greetings APHIS,



I would kindly like to submit the following to ;














Owens, Julie


From: Terry S. Singeltary Sr. []


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


To: FSIS Regulations Comments


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


Page 1 of 98 8/3/2006



Greetings FSIS, I would kindly like to comment on the following ;






Response to Public Comments on the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005



INTRODUCTION The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website:


Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler,

and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment.


Please bear the following points in mind:






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


From: Terry S. Singeltary Sr. []


Sent: Tuesday, February 18, 2003 12:45 PM


To: Freas, William


Cc: Langford, Sheila


Subject: Re: re-vCJD/blood and meeting of Feb. 20, 2003


Greetings FDA,


Variant Creutzfeldt-Jakob Disease Guidance Topic of Feb. 20 TSE Cmte.


[Committee Meeting on February 20, 2003]


FDA’s Transmissible Spongiform Encephalopathies Advisory Committee will meet Feb. 20 to hear updates on the implementation of the agency’s variant Creutzfeldt-Jakob Disease guidance and its effect on blood supply. FULL STORY>>



my name is Terry S. Singeltary Sr., and i lost my mother to hvCJD, one of six known phenotypes of sporadic CJD. i would like to observe this meeting or participate, but have no financial means to do so with. i am disabled from neck injury. anyway, i am not sure if a waiver of fees is possible? i belong to several groups trying to track the true extent of CJDs and trying to find the truth. with CJDs not being reportable but only in a handful of states, and the fact there is no CJD Questionnaire being issued to victims and their families that asks any questions pertaining to route and source, i think to track tainted blood will be futile. i had a major neck surgery in 2001 (3rd), and not _one_ question pertaining to CJD/TSE on any paperwork (and damn near died from MRSA after refusing blood and cadaver bone for fear of risk of CJD/TSEs, go figure, 7 weeks vancomycin via PIC long-line straight to heart). luckily i had informed my neurosurgeon and he did use some disposable instruments and a bone grinder that would not be used again. i would like to submit my concerns on the vCJD _only_ theory as being a total mistake, and that no one knows just how many strains are actually linked to tainted meat and the oral route (one of many potential routes). Asante/Collinge et al have major findings on sporadic CJD, why in the hell is this not making big news in the USA? ($$$) the fact that with the new findings from Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc, the commonest sporadic CJD, i only ponder how many of the sporadic CJDs in the USA are tied to this alternate phenotype? these new findings are very serious, and should have a major impact on the way sporadic CJDs are now treated as opposed to the vCJD that was thought to be the only TSE tied to ingesting beef, in the medical/surgical arena. these new findings should have a major impact on the way sporadic CJD is ignored, and should now be moved to the forefront of research as with vCJD/nvCJD. the USA has many TSEs, the USA lacks sufficient testing for TSEs in cattle, and the USA still refuses to rapid TSE test USA cattle in sufficient numbers to find, when the late Dr. Richard Marsh had proven that mink had gone down with a TSE (TME), from being fed on 95%+ downer cattle. the GAO has also warned the industry and the FDA that the ruminant-to-ruminant feed ban has to significantly improved if they expect to keep BSE/TSEs out of USA cattle. Scrapie has increased significantly, and CWD is spreading. with the titre of infectivity for lethal dose getting smaller (.1 gram lethal), seems the risk of transmission through various potential routes and sources are rising. all this should warrant CJD/TSEs in humans in the USA to be made reportable on a National bases immediately, and a CJD questionnaire to all CJD/TSE victims and their families. to flounder on these two very important issues, will only allow the agent to spread further...




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



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


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


From: "Asante, Emmanuel A"


To: "''"


Dear Terry,


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


Thank you for your interest in the paper.


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


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


Emmanuel Asante






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









Freas, William



From: Terry S. Singeltary Sr. []


Sent: Monday, January 08,2001 3:03 PM


To: freas@CBS5055530.CBER.FDA.GOV


Subject: 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,


I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version).


I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below).


So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here:


remember AIDS/HIV, 'no problem to heterosexuals in the U.S.?


no need to go into that, you know of this blunder:


DO NOT make these same stupid mistakes again with human/animal TSE's aka MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother to sCJD as well (both cases confirmed). I have seen many deaths, from many diseases. I have never seen anything as CJD, I still see my Mom laying helpless, jerking tremendously, and screaming "God, what's wrong with me, why can't I stop this". I still see this, and will never forget. Approximately 10 weeks from 1st of symptoms to death. This is what drives me. I have learned more in 3 years about not only human/animal TSE's but the cattle/rendering/feeding industry/government than i ever wished to.


I think you are all aware of CJD vs vCJD, but i don't think you all know the facts of human/animal TSE's as a whole, they are all very very similar, and are all tied to the same thing, GREED and MAN.


I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, eyelid test, anything at whatever cost, we need a test FAST.


DO NOT let the incubation time period of these TSEs fool you.


To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. from the BVA and the URL is posted in my (long version).


U.S.A. should make all human/animal TSE's notifiable at all ages, with requirements for a thorough surveillance and post-mortem examinations free of charge, if you are serious about eradicating this horrible disease in man and animal.


There is histopathology reports describing “_florid_ plaques" in CJD victims in the USA and some of these victims are getting younger. I have copies of such autopsies, there has to be more. PLUS, sub-clinical human TSE's will most definitely be a problem.


THEN think of vaccineCJD in children and the bovine tissues used in the manufacturing process, think of the FACT that this agent surviving 6OO*C. PNAS -- Brown et al. 97 (7): 3418 scrapie agent live at 600*C


Then think of the CONFIDENTIAL documents of what was known of human/animal TSE and vaccines in the mid to late 80s, it was all about depletion of stock, to hell with the kids, BUT yet they knew. To think of the recall and worry of TSE's from the polio vaccine, (one taken orally i think?), but yet neglect to act on the other potential TSE vaccines (inoculations, the most effective mode to transmit TSEs) of which thousands of doses were kept and used, to deplete stockpile, again would be foolish.


--Oral polio; up to 1988, foetal calf serum was used from UK and New Zealand (pooled); since 1988 foetal calf serum only from New Zealand. Large stocks are held.


--Rubella; bulk was made before 1979 from foetal calf serum from UK and New Zealand. None has been made as there are some 15 years stock.


--Diphtheria; UK bovine beef muscle and ox heart is used but since the end of 1988 this has been sourced from Eire. There are 1,250 litres of stock.


--Tetanus; this involves bovine material from the UK mainly Scottish. There are 21,000 litres of stock.


--Pertussis; uses bovine material from the UK. There are 63,000 litres of stock.


--They consider that to switch to a non-UK source will take a minimum of 6-18 months and to switch to a non-bovine source will take a minimum of five years.


3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are sourced from the USA and the company believes that US material only is used.






BSE3/1 0251


4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK. there are 440,000 units of stock. They have also got MMR using bovine serum from the UK.


5. XXXXXXXXXXX have influenza, rubella, measles, MMR vaccines likely to be used in children. Of those they think that only MMR contains bovine material which is probably a French origin.


6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial. These use veal material, some of which has come from the UK and has been made by XXXXXXXXXXX (see above).


I have documents of imports from known BSE Countries, of ferments, whole blood, antiallergenic preparations,




human blood plasma, normal human blood sera, human immune blood sera, fetal bovine serum, and other blood fractions not elsewhere specified or included, imported glands, catgut, vaccines for both human/animal, as late as 1998. Let us not forget about PITUITARY EXTRACT. This was used to help COWS super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease.






How much of this was used in the U.S.?


Please do not keep making the same mistakes;


'Absence of evidence is not evidence of absence'. What are the U.S. rules for importing and manufacturing vaccines, medicines and medical devices?


Does the U.S.A. allow sourcing of raw material of ruminants from the U.S.A.?


U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds.?


The U.S. rendering system would easily amplify T.S.E.'s: Have we increased the stability of the system (improved heat treatments) since the EU SSC report on the U.S.A. was published in july 2000?


What is done to avoid cross-contaminations in the U.S.A.?


How can the U.S. control absence of cross-contaminations of animal TSE's when pig and horse MBM and even deer and elk are allowed in ruminant feed, as well as bovine blood?


I sadly think of the rendering and feeding policy before the Aug. 4, 1997 'partial' feed ban, where anything went, from the city police horse, to the circus elephant, i will not mention all the scrapie infected sheep. I am surprised that we have not included man 'aka soyent green'. It is a disgusting industry and nothing more than greed fuels it.


When will the U.S.. start real surveillance of the U.S. bovine population (not passive, this will not work)?


When will U.S. start removing SRMs?


Have they stopped the use of pneumatic stunners in the U.S.?


If so, will we stop it in all U.S. abattoirs or only in those abattoirs exporting to Europe?


If not, WHY NOT?


same questions for removal of SRM in the U.S.A., or just for export?


If not, WHY NOT?


How do we now sterilize surgical/dental instruments in the U.S.A.?


Where have we been sourcing surgical catgut?


(i have copies of imports to U.S., and it would floor you) hen will re-usable surgical instruments be banned?


Unregulated "foods" such as 'nutritional supplements' containing various extracts from ruminants, whether imported or derived from




US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or at least very seriously regulated. (neighbors Mom, whom also died from CJD, had been taking bovine based supplement, which contained brain, eye, and many other bovine/ovine tissues for years, 'IPLEX').


What is the use of banning blood or tissue donors from Germany, France, etc... when the U.S.A. continues exposing cattle, sheep and people to SRM, refuses to have a serious feed ban, refuses to do systematic BSE-surveillance?


The FDA should feel responsible for the safety of what people eat, prohibit the most dangerous foods, not only prohibit a few more donors - the FDA should be responsible for the safe sourcing of medical devices, not only rely on banning donors "from Europe" The 'real' risks are here in the U.S. as well, and nave been for some time.


We must not forget the studies that have proven infectivity in blood from TSE's.


The Lancet, November 9, 1985


Sir, --Professor Manuelidis and his colleagues (Oct 19, p896) report " transmission to animals of Creutzfeldt-Jakob disease (CJD) from the buffy coat from two patients. We also transmitted the disease from whole blood samples of a patient (and of mice) infected with CJD.1 Brain, Cornea, and urine from this patient were also infectious, and the clinicopathological findings2 are summarised as follows.




Samples,were taken aseptically at necropsy. 10% crude homogenates of brain and cornea in saline, whole blood (after crushing a clot), and untreated CSF and urine were innoculated intracerebrally into CF1 strain mice (20 ul per animal). Some mice showed emaciation, bradykinesia, rigidity of the body and tail, and sometimes tremor after long incubation periods. Tissues obtained after the animal died (or was killed) were studied histologically (table). Animals infected by various inocula showed common pathological changes, consisting of severe spongiform changes, glial proliferation, and a moderate loss of nerve cells. A few mice inoculated with brain tissue or urine had the same amyloid plaque found in patients and animals with CJD.3




Department of Neuropathology,

Neurological Institute,

Faculty of Medicine,

Kyushu University, Fukuoka812, Japan


JUN TATEISHI (full text-long version)




CWD and transmission to man will be no different than other TSE's.


"Clearly, it is premature to draw firm conclusions about CWD assing naturally into humans, cattle and sheep, but the present esults suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has




caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs,"


G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O'Rourke3, L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M. Smits2 and B. Caughey1,7


or more recently transmission of BSE to sheep via whole blood Research letters Volume 356, Number 9234 16 September 2000


Transmission of BSE by blood transfusion in sheep Lancet 2000; 356: 999 – 1000


F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock


See Commentary


"We have shown that it is possible to transmit bovine spongiform encephalopathy (BSE) to a sheep by transfusion with whole blood taken from another sheep during the symptom-free phase of an experimental BSE infection. BSE and variant Creutzfeldt-Jakob disease (vCJD) in human beings are caused by the same infectious agent, and the sheep-BSE experimental model has a similar pathogenesis to that of human vCJD. Although UK blood transfusions are leucodepleted--a possible protective measure against any risk from blood transmission-- this report suggests that blood donated by symptom-free vCJD-infected human beings may represent a risk of spread of vCJD infection among the human population of the UK."


"The demonstration that the new variant of Creutzfeldt-Jakob disease (vCJD) is caused by the same agent that causes bovine spongiform encephalopathy (BSE) in cattle1 has raised concerns that blood from human beings in the symptom-free stages of vCJD could transmit infection to recipients of blood transfusions (full text long version)" and...


"The large number of cases (1040), temporal clustering of the outbreaks (15 in the first 6 months of 1997), the high in-flock incidence, and the exceptional involvement of goats (390 cases), suggested an accidental infection. The source of the epidemic might have been TSE-contaminated meat and bonemeal, but eight flocks had never been fed any commercial feedstuff. Infection might have risen from the use of a formol-inactivated vaccine against contagious agalactia prepared by a single laboratory with brain and mammary gland homogenates of sheep infected with Mycoplasma agalactiae. Although clinical signs of TSE in the donor sheep have not been found, it is possible that one or more of them were harbouring the infectious agent. Between 1995 and 1996, this vaccine was given subcutaneously to 15 of the affected flocks (to one flock in 1994) ; in these animals the disease appeared between 23 and 35 months after vaccination. No information is available for herd 13 because it was made up of stolen animals. Sheep from the remaining three flocks (1-3, figure) did not receive the vaccine, thus suggesting a naturally occurring disease.” (again, full text long version).


IN SHORT, please do under estimate this data and or human/animal TSE's including CWD in the U.S.A.


A few last words, please.


The cattle industry would love to have us turn our focus to CWD and forget about our own home grown TSE in Bovines. This would be easy to do. Marsh's work was from downer cattle feed, NOT downer deer/elk feed. This has been proven.




There should be NO LESS THAN 1,000,000 tests for BSE/TSE in 2001 for U.S.A. French are testing 20,000 a week. The tests are available. Why wait until we stumble across a case from passive surveillance, by then it is to late. IF we want the truth, this is a must???


United States Total ,Bovine Brain Submissions by State,


May 10, 1990 thru October 31, 2000


Total 11,700


FROM 1.5 BILLION HEAD OF CATTLE since 1990 ???


with same feeding and rendering practices as that of U.K. for years and years, same scrapie infected sheep used in feed, for years and years, 950 scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known to date. (hmmm, i am thinking why there is not a variant scrapid, that is totally different than all the rest)? just being sarcastic.


with only PARTIAL FEED BAN implemented on Aug. 4, 1997???

(you really need to reconsider that blood meal etc. 'TOTAL BAN')




AND PLEASE FOR GODS SAKE, STOP saying vCJD victims are the only ones tied to this environmental death sentence. "PROVE IT". It's just not true. The 'CHOSEN ONES' are not the only ones dying because of this man-made death sentence. When making regulations for human health from human/animal TSEs, you had better include ALL human TSE's, not just vCJD. Do NOT underestimate sporadic CJD with the 'prehistoric' testing available to date. This could be a deadly mistake. Remember, sCJD kills much faster from 1st onset of symptoms to death, and hvCJD is the fastest. Could it just be a higher titre of infectivity, or route or source, or all three?


Last, but not least. The illegal/legal harvesting of body parts and tissues will come back to haunt you. Maybe not morally, but due to NO background checks and human TSEs, again it i will continue to spread.


Stupidity, Ignorance and Greed is what fuels this disease.

You must stop all of this, and ACT AT ONCE...











"different strains (of same disease), different routes of infection (of same disease), different infectivity levels (dose rate) of the (same disease) = different symptoms, different lengths of illness from 1st onset of illness to death, (of the same disease) + different cultures = different geographical locations = different strains (of same disease)...TSS"




DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)


The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why???? than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!!


Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a is a big fat sponge...the agent continues to eat the brain can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....


Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any is ALL gonna be sporadic!!!


And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...


Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and aggressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"


again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.


You need to watch your back........but keep picking at a buzzard to the just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)