Veterinary Record2011;169:352-353 doi:10.1136/vr.d6007
News ; Reports TSEs
BSE: where are we now?
Control measures for BSE have been effective in significantly reducing the number of cases since the disease was recognised 25 years ago. In a workshop at this year's AHVLA conference, held in Surrey from September 13 to 15, speakers considered the advances and knowledge gaps in the understanding of the disease and ways in which policies across Europe could be adapted to reflect changing circumstances. Arianwen Morris reports
BOVINE spongiform encephalopathy (BSE), a progressive degenerative neurological disease of cattle, was first detected in the UK in 1986 as a result of passive surveillance of farm animal diseases by the Veterinary Investigation Service of the Ministry of Agriculture, Fisheries and Food (MAFF) and submission of material to veterinary pathologists at the Central Veterinary Laboratory in Weybridge.
Discussing the history of the disease, Gerald Wells, the retired head of neuropathology at the Animal Health and Veterinary Laboratories Agency (AHVLA), noted that, in 1987, a paper had been published in Veterinary Record drawing attention to strong resemblances between BSE and the encephalopathies recorded in several other species, such as scrapie in sheep.
Early epidemiological investigations produced evidence that the BSE epidemic had resulted from the use of infectious meat and bone meal in cattle feed and a feed ban was introduced in the UK in 1988 preventing the inclusion of ruminant proteins in ruminant rations. Initially, the hypothesis that BSE was caused by prions had not been widely accepted.
In 1996, a novel form of the human TSE Creutzfeldt–Jakob disease (CJD), termed variant CJD (vCJD), was identified in human beings, giving rise to concerns that BSE had zoonotic potential. Control measures for BSE were tightened as a result and, later the same year, a total ban on feeding any mammalian proteins to farmed animals was enforced.
‘The UK epidemic peaked in 1991 to …
http://veterinaryrecord.bmj.com/content/169/14/352.extract?sid=ab9b5144-1525-4a0f-ab61-74d6a1faaa00
NOW, for the rest of the BSE mad cow saga, what the BVA, OIE, or the USDA fail to tell you ;
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
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"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Thursday, July 21, 2011
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:
August 2011 - Volume 70 - Issue 8 - pp 698-702
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html
Sunday, September 25, 2011
Clinical Heidenhain Variant Of Sporadic Creutzfeldt-Jakob Disease (CJD) With Co-occurrence Of Prion Protein Types 1 and 2
http://creutzfeldt-jakob-disease.blogspot.com/2011/09/clinical-heidenhain-variant-of-sporadic.html
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
MAD COW DISEASE, TEXAS STYLE
http://www.organicconsumers.org/articles/article_23850.cfm
Sunday, May 01, 2011
STUDY OF ATYPICAL BSE 2010 Annual Report May 2011
http://bse-atypical.blogspot.com/2011/05/study-of-atypical-bse-2010-annual.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Canada
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf
Monday, June 20, 2011
2011 Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA
http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html
Thursday, July 14, 2011
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html
I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California
http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html
Monday, June 27, 2011
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease
http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html
Friday, May 13, 2011
EFSA Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/efsa-joint-scientific-opinion-on-any.html
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html
Tuesday, January 18, 2011
Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009 Volume 17, Number 1 January 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html
BSE: TIME TO TAKE H.B. PARRY SERIOUSLY
If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf
Monday, June 27, 2011
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html
Wednesday, September 21, 2011
Evidence for distinct CWD strains in experimental CWD in ferrets
http://chronic-wasting-disease.blogspot.com/2011/09/evidence-for-distinct-cwd-strains-in.html
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip...
full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
1989
IN CONFIDENCE
Perceptions of unconventional slow virus diseases of animals in the USA
Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or about that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. Whether they were scrapie infected sheep or not is unclear.
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Sunday, July 03, 2011
Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD Deer
http://chronic-wasting-disease.blogspot.com/2011/07/prion-disease-detection-pmca-kinetics.html
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html
Sunday, July 27, 2008
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same mistakes...
REFERENCES
snip...see full text ;
http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
COMERCIAL IN CONFIDENCE
SPREADING OF UNPROCESSED BLOOD ON LAND
http://web.archive.org/web/20040315202749/www.bseinquiry.gov.uk/files/yb/1991/02/15003001.pdf
Wednesday, June 29, 2011
TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products
http://tseac.blogspot.com/2011/06/tseac-meeting-august-1-2011-donor.html
Tuesday, May 3, 2011
PRION, TSE, typical, atypical BSE, aka mad cow disease, spray dried blood, feed, and a recipe for disaster
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/prion-tse-typical-atypical-bse-aka-mad.html
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Monday, September 12, 2011
BSE PRION Agriculture Animal Feed Question House of Lords Thursday, 8 September 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/bse-prion-agriculture-animal-feed.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
Friday, August 20, 2010
USDA: Animal Disease Traceability August 2010
http://naiscoolyes.blogspot.com/2010/08/usda-animal-disease-traceability-august.html
Saturday, December 18, 2010
OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
Monday, May 23, 2011
Atypical Prion Diseases in Humans and Animals 2011
Top Curr Chem (2011)
DOI: 10.1007/128_2011_161
# Springer-Verlag Berlin Heidelberg 2011
Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar
Abstract
Although prion diseases, such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep, have long been recognized, our understanding of their epidemiology and pathogenesis is still in its early stages. Progress is hampered by the lengthy incubation periods and the lack of effective ways of monitoring and characterizing these agents. Protease-resistant conformers of the prion protein (PrP), known as the "scrapie form" (PrPSc), are used as disease markers, and for taxonomic purposes, in correlation with clinical, pathological, and genetic data. In humans, prion diseases can arise sporadically (sCJD) or genetically (gCJD and others), caused by mutations in the PrP-gene (PRNP), or as a foodborne infection, with the agent of bovine spongiform encephalopathy (BSE) causing variant CJD (vCJD). Person-to-person spread of human prion disease has only been known to occur following cannibalism (kuru disease in Papua New Guinea) or through medical or surgical treatment (iatrogenic CJD, iCJD). In contrast, scrapie in small ruminants and chronic wasting disease (CWD) in cervids behave as infectious diseases within these species. Recently, however, so-called atypical forms of prion diseases have been discovered in sheep (atypical/Nor98 scrapie) and in cattle, BSE-H and BSE-L. These maladies resemble sporadic or genetic human prion diseases and might be their animal equivalents. This hypothesis also raises the significant public health question of possible epidemiological links between these diseases and their counterparts in humans.
M.A. Tranulis (*)
Norwegian School of Veterinary Science, Oslo, Norway
e-mail: Michael.Tranulis@nvh.no
S.L. Benestad
Norwegian Veterinary Institute, Oslo, Norway
T. Baron
Agence Nationale de Se´curite´ Sanitaire, ANSES, Lyon, France
H. Kretzschmar
Ludwig-Maximilians University of Munich, Munich, Germany
Keywords Animal Atypical Atypical/Nor98 scrapie BSE-H BSE-L Human Prion disease Prion strain Prion type
http://resources.metapress.com/pdf-preview.axd?code=f433r34h34ugg617&size=largest
snip...SEE MORE HERE ;
http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html
Sunday, June 07, 2009
L-TYPE-BSE, H-TYPE-BSE, C-TYPE-BSE, IBNC-TYPE-BSE, TME, CWD, SCRAPIE, CJD, NORTH AMERICA
http://bse-atypical.blogspot.com/2009/06/l-type-bse-h-type-bse-c-type-bse-ibnc.html
Sunday, May 10, 2009
Identification and characterization of bovine spongiform encephalopathy cases diagnosed and NOT diagnosed in the United States
http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html
Sunday, December 28, 2008
MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html
AND THE USDA ET AL KNEW IT TOO ;
""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS
USDA 2003
We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
END...TSS
Suppressed peer review of Harvard study October 31, 2002.
October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html
PLEASE SEE FULL TEXT 98 PAGES HERE ;
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
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:
http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).
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:
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
another question, just how long have these atypical BSE TSEs been around in the bovine ???
Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years Date: April 26, 2007 at 1:08 pm PST 1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN THE HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS NOT BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. .......
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf
2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.
3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/29005001.pdf
IN CONFIDENCE
This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/10/26002001.pdf
COLLINGE THREATENS TO GO TO MEDIA
http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP"
2009 SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
Sunday, September 6, 2009
MAD COW USA 1997 (SEE SECRET VIDEO)
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? (see video at bottom)
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
(SEE VIDEO)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
WHO WILL FOLLOW THE CHILDREN FOR CJD SYMPTOMS ???
Saturday, May 2, 2009
U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM
http://downercattle.blogspot.com/2009/05/us-government-sues-westlandhallmark.html
http://downercattle.blogspot.com/
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/prionet-canada-researchers-in-vancouver.html
Mad Cow Scaremongers
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.
The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.
The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.
The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.
Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.
The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.
The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.
It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.
The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.
There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.
Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.
The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.
Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.
-- Communicated by: Terry S Singeltary Sr
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.
It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
******
http://www.promedmail.org/pls/apex/f?p=2400:1202:888892554804923::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,88784
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
POLITICAL BSe and CJD and THE WOW FACTOR $$$
Monday, September 26, 2011
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011
http://prionopathy.blogspot.com/2011/09/variably-protease-sensitive-prionopathy.html
layperson
TSS
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
a group of progressive and fatal conditions that are associated with prions and affect the brain and nervous system of many animals and humans.
Friday, September 30, 2011
Sunday, September 25, 2011
Mad Cow Scaremongers
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011
Posted On December 20, 2003
--------------------------------------------------------------------------------
Mad Cow Scaremongers
Secretary of Agriculture Ann Veneman says that "beef is absolutely safe to eat." Harvard University experts note that the risk of Americans contracting mad cow disease is "as close to zero as you can get." Every reputable expert tells us that the American meat supply is still safe. And yet a cabal of animal-rights activists and radical opponents of modern farming are already hitting the airwaves for one purpose: to spread fear and needless alarm. These people are activists, not knowledgeable scientists. Their expertise is in scare mongering, not livestock agriculture. Their goal is to promote animal rights and organic-only, 1800s-style agriculture. And their track record is full of doom-and-gloom predictions that never came true.
Who are these masters of disaster? A rogues gallery follows:
John Stauber -- director of the anti-corporate Center for Media & Democracy, and co-author of the 1997 book Mad Cow USA, which was supported financially by the eco-religious Foundation for Deep Ecology. Stauber sits on the national advisory board of the Organic Consumers Association, as reliable a scaremonger as any about the American food supply. Stauber has become a near-ubiquitous media presence in mad-cow-related stories. Just minutes after Secretary Veneman finished her press conference announcing the discovery of a single sick cow, Stauber told CNN -- without any evidence whatsoever -- that it was just "the tip of an invisible iceberg" and that "mad cow disease is spread throughout North America."
Ronnie Cummins -- head of the Organic Consumers Association, a group founded by radical anti-technology guru Jeremy Rifkin. Cummins has openly expressed his hope that a U.S. mad-cow epidemic would fuel a "crisis of confidence" in American food, similar to the one that he claims drove British consumers to "organic" and other high-priced options. In 1998 Cummins told the Minneapolis City Pages that "consumers and farmers would both be better off if people paid twice as much for their meat and ate half as much." This June he confidently told a Canadian Press reporter that "no case of mad cow has ever been found in a cow raised on an organic farm." This, actually, is not true. The British Central Veterinary Laboratory reports that in 1995 (at the height of the UK outbreak), there were 215 confirmed cases of mad cow disease from 36 different organic farms. And Germany's very first case of mad cow disease was diagnosed in a slaughterhouse that only processed organically-raised cattle.
Michael Greger -- a vegetarian activist doctor who maintains a brisk animal-rights speaking schedule and edits the mad-cow-scare web page of the Organic Consumers Association. He recently provided PETA with a laughable treatise suggesting that the SARS outbreak came from livestock farming. Greger titled his mad-cow stump speech "Mad Cow Disease: Plague of the 21st Century?." He argues: "although no pigs or chickens have been found with the disease ... any animal with a brain has the potential to become infected." Greger has yet to produce any evidence to support this claim, largely because there isn't any. Neither hogs nor hens (nor fish, for that matter) suffer from mad-cow-like illnesses. Greger is planning to hit the lecture circuit in an effort to "keep hammering" the meat industry and " keep this momentum going."
Michael Hansen -- the Consumers Union of the United States' self-proclaimed "expert" on genetically enhanced food, bovine growth hormone, mad cow disease, and any other food issue he deems ripe for scaremongering. When the Canadian mad-cow story broke earlier this year, Hansen blithely suggested that American consumers should eat only grass-fed, "organic," and other specialty beef. Hansen's statements on mad cow have appeared in hundreds of media outlets, and his boss, Jean Halloran, has weighed in as well.
Howard Lyman -- one part animal-rights scold, one part revival tent preacher [click here for video]. Lyman trades on the fact that he was brought up in a cattle-ranching family to imply that his strict vegetarianism is somehow more informed than everyone else's dietary choices. Lyman famously (and incorrectly) predicted on the "Oprah" show that mad cow disease among Americans would "make AIDS look like the common cold." Just 14 hours after the U.S. mad-cow announcement, animal-rights terroristand Sierra Club board member Paul Watson published an op-ed asserting that "Howard Lyman predicted this outbreak years ago. Perhaps now the public might pay more attention to this Montana rancher turned vegan. He knows that of which he speaks." It's no coincidence that Lyman is on the advisory board of Watson's violent Sea Shepard Conservation Society. The front page of The Washington Post's "Style" section seconded Watson's misleading praise of Lyman with an article titled "Ex-Cattleman's Warning Was No Bum Steer."
Dave Louthan -- a disgruntled former employee of the Washington state meat processing plant where the first U.S. mad-cow case was detected. After losing the job he loved (slaughtering cows), Louthan launched a crusade against beef producers and the U.S. Department of Agriculture, a personal jihad supported by animal rights activists who must otherwise recoil at his admitted passion for bloodying beef cattle. This is a man who clearly enjoyed his work -- using a bolt gun to kill cows, buffalo, ostrich, emu and alpaca for Vern’s Moses Lake Meats. He told the New York Times that killing is “really fun,” and beats deboning, which he calls “girls’ work.” In the Seattle Times, Louthan added: “I liked to kill cows. I don’t care if I’m hauling them, feeding them or killing them.”
Like many in the meat business, Louthan lost his source of income because of the mad cow scare recklessly promoted by activist groups. But he’s mad, and he’s fighting back. Despite copious evidence to the contrary, he continues to claim that the famous cow he killed (the one that later tested positive) and many others like it were ground into hamburger and entered the human food chain. “The hamburger surprise in your kids’ school lunch,” Dave claims, “has come from mad cows … Your kids will get mad cow from it.” A man of many contradictions, Louthan warns that the U.S. government “is trying to kill you.” He’s calling on anti-beef and animal-rights groups to send him money so he can “keep up the fight.” Yet he admits continuing to eat beef on a daily basis. The verdict is still out on whether or not this former trucker from Texas can successfully change careers from killing cows to assassinating the character of cattlemen.
Terry Singletary -- A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.
As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176
Marion Nestle -- New York University's food scold extraordinaire. Although Nestle concedes that the risk of getting mad cow disease is extremely low, she has nonetheless exploited mad cow fears to promote an anti-corporate, pro-organic creed. She has complained: "Until we have a little consumer protection going on in government, consumers have to take care of themselves." How do consumers do that? By purchasing organic food, of course. Nestle told Fox News: "This is a very good time to buy organic."
Bruce Friedrich -- PETA's director of vegan outreach. Friedrich revealed his true agenda when he argued: "I think it would be a great thing if all of these fast-food outlets, and these slaughterhouses, and these laboratories, and the banks that fund them exploded tomorrow. I think it's perfectly appropriate for people to take bricks and toss them through the windows, and everything else along the line. Hallelujah to the people who are willing to do it" [click here for audio]. There is seemingly nothing Bruce won't do to scare people away from meat, including raising fears about mad cow disease. Under Friedrich's leadership, PETA representatives have been handing out "emergency vegetarian starter kits," and holding anti-meat posters outside restaurants and grocery stores all over the country. PETA has also started an aggressive and misleading (what's new?) advertising campaign to frighten the public into vegetarianism.
Neal Barnard -- the animal-rights movement's not-so-secret weapon against meat. Sure he's a doctor (a non-practicing psychiatrist, actually), but his tirades against dairy foods, beef, chicken, and Atkins-style diets are all informed by his connections to PETA. Barnard sits on the board of The PETA Foundation along with PETA co-founder Ingrid Newkirk. And PETA has funneled nearly $1 million to Barnard's misnamed "Physicians Committee for Responsible Medicine." His virulent opposition to animal-based foods was clear in a recent speech at a Food and Drug Administration hearing, where he referred to cheese as "morphine on a cracker" and "dairy crack." PCRM wasted no time after the mad cow news broke, sending out a press release attacking meat and offering a "vegetarian starter kit" for suddenly fearful carnivores.
Caroline Smith DeWaal -- director of the food safety program at the quintessential food cop, the Center for Science in the Public Interest. Smith DeWaal, who has been advising consumers to grind their own beef, told The Washington Post: "Taco filling, pizza toppings, hot dogs, processed meats, these are all likely products that can expose consumers to mad cow disease."
Wayne Pacelle -- senior vice president of the Humane Society of the United States, a radical animal rights group masquerading as an animal-welfare organization. Pacelle immediately began to lobby the federal government on mad cow, petitioning the U.S. Department of Agriculture the morning after Veneman's announcement. Pacelle's goal is to create "a National Rifle Association of the animal rights movement." His opposition to eating meat is so strong that he has "no problems with the extinction of domestic animals."
Gene Bauston -- co-founder of the animal rights group Farm Sanctuary. This group was recently convicted of 210 counts of election fraud, in connection with the $465,000 it illegally trucked into a Florida ballot initiative that gave constitutional rights to pigs. Farm Sanctuary even paid a $50,000 fine. The group issued an e-mail alert to its approximately 18,000 members, requesting that they write to the USDA about mad cow. It also e-mailed a boilerplate "letter to the editor" to over 1,900 activists, asking them to send it to their local newspapers under their own individual signatures. In a gushing article, The New York Times praised the group for its crusade against the processing of "downer" cows. But the paper of record manages to overlook Farm Sanctuary's early association with the domestic-terrorist Animal Liberation Front, as well as its electioneering mischief.
Mark Ritchie -- scaremonger-in-chief at the anti-corporate, anti-modern-agriculture, anti-free-trade Institute for Agriculture and Trade Policy (IATP). He blames "industrialized beef production and liberalized trade" for mad cow disease. IATP has started distributing sound-bites for radio broadcast via a 1-800 number.
Eric Schlosser -- anti-fast food activist and author of Fast Food Nation, which was essentially a screed against the consumption of hamburgers. It's no surprise that Schlosser is using mad-cow fears to buttress his case. He flatly told CNN: "I don't think anyone should eat ground beef." Schlosser's op-ed in The New York Times was similarly full of doom and gloom.
Andrew Knight -- a Seattle veterinarian who recently took over the day-to-day operations of the radical Northwest Animal Rights Network. Knight is raising mad-cow panic levels without disclosing his animal-rights agenda. His letter in The Washington Times (Excerpt: "I, for one, will be stocking up on veggie burgers") identified him only as "Dr. Andrew Knight, Seattle." The San Diego Union-Tribune printed an expanded version of his Times letter as an op-ed. There he wrote: "it is not improbable that for the one mad cow detected thus far, some 1,700 have passed undetected into the food chain, and that the human form of this lethal disease is silently incubating in numerous unsuspecting beef eaters at present." A subsequent op-ed in the Toronto Star used the exact same line.
Karen Hudson -- a consultant for GRACE Factory Farm Project, which can't stand the idea of efficient, large-scale agriculture. The group even compares animal husbandry to the post-apocalyptic movie, The Matrix. Hudson insists -- without providing any evidence -- that "mad cow disease is the product of an increasingly industrialized food system."
Katherine DiMatteo -- executive director of the Organic Trade Association, which represents the $11 billion organic industry in North America. The group issued a media release arguing: "while the retail price of organic meat is generally greater than conventional, to many consumers, the greater peace of mind is priceless."
Larry Bohlen and Brent Blackwelder -- from the radical green group Friends of the Earth. The organization issued a "fact sheet" on mad cow that includes such topics as "mad cow on the rampage." Blackwelder peddles the familiar and false story that the "best way for people to avoid the risk of mad cow disease is to eat organic, grass fed beef or beef alternatives." Bohlen's mad cow comments have found their way into the Los Angeles Times, The Chicago Tribune, and The Seattle Times.
Peter Lurie and Wenonah Hauter -- food safety "experts" at Ralph Nader's Public Citizen. Their public comments are designed to raise unfounded fears about eating conventionally-raised beef.
Felicia Nestor -- chief food-safety worrier at the "whistleblowers' rights" Government Accountability Project. Nestor worked with Public Citizen to author reports called "The Jungle 2000: Is America's Meat Fit to Eat?" and "Hamburger Hell: The Flip Side of USDA's Salmonella Testing Program." She co-founded the Global Safe Food Alliance, which includes mad cow scaremongers like Public Citizen, the Institute for Agriculture and Trade Policy, and the Organic Consumers Association, along with animal-rights groups like Farm Sanctuary, the Physicians Committee for Responsible Medicine, United Poultry Concerns, and the Humane Society of the United States. Nestor's hysterical complaints about mad cow have turned up in The New York Times.
Andrew Kimbrell and Joseph Mendelson -- executive director and legal director of the Center for Food Safety. The Center for Food Safety (not to be confused with the Food and Drug Administration's Center for Food Safety and Applied Nutrition) gets most of its money from the organic food industry and the lunatic Foundation for Deep Ecology.
Robert Cohen -- an animal-rights radical who is convinced that cow's milk is the root of all evil. Cohen warned cattlemen and dairy farmers that mad cow disease would be "a sign" that Americans should "reject your poisons."
http://www.consumerfreedom.com/article_detail.cfm/a/138-mad-cow-scaremongers
Posted On December 20, 2003
AFTER THE FIRST CASE OF MAD COW DISEASE IN THE USA WAS DOCUMENTED
" Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. "
http://www.consumerfreedom.com/article_detail.cfm/a/138-mad-cow-scaremongers
SO, just who are The Center for Consumer Freedom ;
http://www.consumerfreedom.com/index.cfm
let's take a closer look shall we ;
The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"
CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.
http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom
http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom
snip...SEE FULL TEXT HERE ;
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
UPDATE UPDATE UPDATE
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*** TSE PRION PRION CONFERENCES UPDATES 2015, 2016, AND 2016 ***
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Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/prionet-canada-researchers-in-vancouver.html
PP1:
Does A “Prion-Like” Mechanism Contribute to the Spreading of Neuropathology in Parkinson’s Disease?
Patrik Brundin Neuronal Survival Unit; Wallenberg Neuroscience Center; Dept of Experimental Medical Science; Lund University; Lund, Sweden
Key words: Parkinson’s disease, prion mechanism, alpha-synuclein
Neuropathological aggregates of alpha-synuclein in neuronal cytoplasm and neurites are typical features of Parkinson’s disease (PD). These Lewy neurites and Lewy bodies are prominent in substantia nigra, where dopaminergic neurons degenerate. With advancing disease they are also found in several other widespread brain areas, and it has been suggested that they appear in anterior olfactory structures and the dorsal motor nucleus of the vagal nerve even before the substantia nigra is affected. Recent studies demonstrated that Lewy bodies and neurites appear in grafted embryonic neurons.1-3 They stain for Thioflavin S, are immunoreactive for alpha-synuclein phosphorylated at serine residue 129 and exhibit a fibrillar structure in the electron microscope.4 From 2 to 5% (frequency increases over time) of the grafted dopaminergic neurons display Lewy bodies, starting around one decade after surgery. Despite these changes, some of the PD grafted patients still exhibit signs of functional recovery beyond a decade after surgery. We, and others, are currently exploring possible mechanisms underlying the transfer of alpha-synuclein between cells and their relevance to how neuropathology normally spreads in the PD brain.5,6 We have observed that alpha-synuclein indeed can transfer between cells in culture. The process is clearly time-dependent and once inside the new cell the imported alpha-synuclein can seed aggregation of endogenous alpha-synuclein. Furthermore, we have observed transfer of host-derived alpha-synuclein into embryonic dopamine neurons grafted into the striatum of transgenic mice expressing human alpha-synuclein. We propose that a “prion-like” disease mechanism might contribute to the pathogenesis of PD and other chronic neurodegenerative disorders.6
References
1. Li, et al. Nat Med 2008; 14:501-3. 2. Kordower, et al. Nat Med 2008; 14:504-6. 3. Kordower, et al. Mov Disord 2008; 23:2303-6. 4. Li, et al. Mov Disord 2010; [Epub ahead of print]. 5. Brundin, et al. Nat Rev Neurosci 2008; 9:741-5. 6. Brundin, et al. Nat Rev Mol Cell Biol 2010; 11:301-7. PP: Plenary Lectures Previously published online: www.landesbioscience.com/journals/prion/article/12765
DOI: 10.4161/pri.4.3.12765
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WP8-4: Prion-like Induction of Alzheimer-type Proteopathy in Transgenic Mice
Lary C. Walker
Yerkes Center; Emory University; Atlanta, GA USA
Key words: abeta, Alzheimer, amyloid, prion, seeding, strains, transgenic, transmission
Alzheimer’s disease and prion disease both involve the accumulation of disease-specific proteins in the brain, suggesting pathogenic commonalities. In Alzheimer’s disease, the aggregation of the protein fragment Aßis a seminal event. Similar to the templated corruption of prion protein, cerebral Aßdeposition can be induced in ß-amyloid precursor protein (APP)-transgenic mice and rats by the intracerebral injection of Aß-rich brain extracts from patients with Alzheimer’s disease or APP-transgenic mice. Our studies indicate that the characteristics of the seeded deposits depend on the source of the seeding extract, the type of host, and the seeded brain region. We are using the amyloid-binding agent Pittsburgh Compound B (PIB) as a marker of a potential AD-specific form of multimeric Aß, and are attempting to induce alternative conformations in the transgenic mouse Aß-seeding model. In addition, we are investigating non-intracerebral routes of administration and the ability of heterologous agents to induce Aßdeposition. Analysis of Aß-seeding in vivo could yield fresh insights into the origins of idiopathic Alzheimer’s disease.
Acknowledgements
Key collaborators on these studies are Mathias Jucker (U. Tübingen), Rebecca Rosen (Emory U.) and Harry LeVine III (U. Kentucky). Supported by NIH RR-00165 and the CART Foundation.
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PPo9-1: Prion-like Propagation of SOD1 Misfolding in Amyotrophic Lateral Sclerosis
Neil R. Cashman
University of British Columbia; Vancouver, British Columbia Canada
Key words: protein misfolding, mechanisms of neurodegeneration, transmission
Prion-like propagation of protein misfolding has been implicated in Alzheimer’s, Parkinson’s and Huntington’s diseases, and the tauopathies. Amyotrophic lateral sclerosis (ALS) is a common and incurable adult motor neuron disease, in which mutation of the free-radical defense enzyme superoxide dismutase 1 (SOD1) is responsible for a subtype of familial ALS (fALS). We demonstrate that transfection of fALS SOD1 mutants G127X and G85R, as well as overexpression of non-mutant wild-type (wt) SOD1, can induce misfolding of natively-structured wild-type SOD1 in human mesenchymal and neural cell lines, as determined by molecular surface immunoreactivity with misfolding-specific monoclonal antibodies (mAbs), acquisition of protease sensitivity (suggesting structural loosening), generation of reactive oxygen species (ROS) and formation of non-native intermolecular disulfide bonds. Serial transmission of SOD1 misfolding was established by incubation in conditioned media from mtSOD1- or wtSOD1-transfected HEK cells, and knockdown of endogenous SOD1 expression in HEK cells by siRNA abrogated the transmission of SOD1 misfolding, consistent with endogenously expressed SOD1 being the substrate for conformational conversion. Pre-incubation of SOD1-transfected conditioned media with poly-specific SOD1 antibodies or misfolding-specific mAbs also blocked intercellular transducing activity, and passive administration of misfolding-specific mAbs extends survival in the G37R transgenic mouse model of ALS. We conclude that misfolded SOD1 participates in a template-directed misfolding cascade which provides a plausable molecular mechanism for progression of familial and sporadic ALS. Antibody-mediated neutralization of SOD1 misfolding propagation could prove beneficial in human ALS.
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http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Alimentary prion infections: Touch-down in the intestine
Volume 5, Issue 1 January/February/March 2011 Bianca Da Costa Dias, Katarina Jovanovic and Stefan F.T. Weiss View affiliations Hide affiliations Bianca Da Costa DiasSchool of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa Katarina JovanovicSchool of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa Stefan F.T. WeissCorresponding author: stefan.weiss@wits.ac.za School of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa
Neurodegenerative diseases are caused by proteinaceous aggregates, usually consisting of misfolded proteins which are often typified by a high proportion of ß-sheets, which accumulate in the Central Nervous System. These diseases, including Morbus Alzheimer, Parkinson disease and Transmissible Spongiform Encephalopathies (TSEs) also termed prion disorders, afflict a substantial proportion of the human population and as such the etiology and pathogenesis of these diseases has been the focus of mounting research. Although many of these diseases arise from genetic mutations or are sporadic in nature, the possible horizontal transmissibility of neurodegenerative diseases poses a great threat to population health. In this article we discuss recent studies which suggest that the “non-transmissible” status bestowed upon Alzheimer and Parkinson diseases may need to be revised as these diseases have been successfully induced through tissue transplants. Furthermore, we highlight the importance of investigating the “natural” mechanism of prion transmission including peroral and perenteral transmission, proposed routes of gastrointestinal uptake and neuroinvasion of ingested infectious prion proteins. We examine the multitude of factors which may influence oral transmissibility and discuss the zoonotic threats which Chronic Wasting Disease (CWD), Bovine Spongiform Encephalopathy (BSE) and Scrapie may pose resulting in vCJD or related disorders. In addition, we suggest that the 37 kDa/67 kDa laminin receptor on the cell surface of enterocytes, a major cell population in the intestine, may play an important role in the intestinal pathophysiology of alimentary prion infections.
http://www.landesbioscience.com/journals/prion/article/14283
Commentary ß-amyloid oligomers and prion protein: Fatal attraction?
Volume 5, Issue 1 January/February/March 2011 Gianluigi Forloni and Claudia Balducci
Gianluigi Forloni Corresponding author: forloni@marionegri.it
Claudia Balducci Biology of Neurodegenerative Diseases Lab; Department of Neuroscience; “Mario Negri” Institute for Pharmacological Research; Milano, Italy
The relationship between Alzheimer disease (AD) and prion-related encephalopathies (TSE) has been proposed by different points of view. Recently, the scientific attention has been attracted by the results proposing the possibility that PrPc, the protein whose pathologic form is responsible of TSE, can mediated the toxic effect of ß amyloid (Aß) oligomers. The oligomers are considered the culprit of the neurodegenerative process associated to AD, although the pathogenic mechanism activated by these small aggregates remain to be elucidated. In the initial study based on the binding screening PrPc was identified as ligand /receptor of Aß oligomers, while long term potentiation (LTP) analysis in vitro and behavioural studies in vivo, demonstrated that the absence of PrPc abolished the damage induced by Aß oligomers. The high affinity binding Aß oligomers-PrPc has been confirmed, whereas a functional role of this association has been excluded by three different studies. We approached this issue by the direct application of Aß oligomers in the brain followed by the behavioural examination of memory deficits. Our data using PrP knock-out mice suggest that Aß 1-42 oligomers are responsible for cognitive impairment in AD but PrPc is not required for their effect. Similarly, in two other studies the LTP alterations induced by Aß 1-42 oligomers was not influenced by the absence of PrP. Possible explanations of these contradictory results are discussed.
http://www.landesbioscience.com/journals/prion/article/14367/
http://www.landesbioscience.com/journals/prion/toc/volume/5/issue/1/
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE.
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/prionet-canada-researchers-in-vancouver.html
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
Monday, May 23, 2011
Atypical Prion Diseases in Humans and Animals 2011
Top Curr Chem (2011)
DOI: 10.1007/128_2011_161
# Springer-Verlag Berlin Heidelberg 2011
Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar
Abstract
Although prion diseases, such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep, have long been recognized, our understanding of their epidemiology and pathogenesis is still in its early stages. Progress is hampered by the lengthy incubation periods and the lack of effective ways of monitoring and characterizing these agents. Protease-resistant conformers of the prion protein (PrP), known as the "scrapie form" (PrPSc), are used as disease markers, and for taxonomic purposes, in correlation with clinical, pathological, and genetic data. In humans, prion diseases can arise sporadically (sCJD) or genetically (gCJD and others), caused by mutations in the PrP-gene (PRNP), or as a foodborne infection, with the agent of bovine spongiform encephalopathy (BSE) causing variant CJD (vCJD). Person-to-person spread of human prion disease has only been known to occur following cannibalism (kuru disease in Papua New Guinea) or through medical or surgical treatment (iatrogenic CJD, iCJD). In contrast, scrapie in small ruminants and chronic wasting disease (CWD) in cervids behave as infectious diseases within these species. Recently, however, so-called atypical forms of prion diseases have been discovered in sheep (atypical/Nor98 scrapie) and in cattle, BSE-H and BSE-L. These maladies resemble sporadic or genetic human prion diseases and might be their animal equivalents. This hypothesis also raises the significant public health question of possible epidemiological links between these diseases and their counterparts in humans.
M.A. Tranulis (*)
Norwegian School of Veterinary Science, Oslo, Norway
e-mail: Michael.Tranulis@nvh.no
S.L. Benestad
Norwegian Veterinary Institute, Oslo, Norway
T. Baron
Agence Nationale de Se´curite´ Sanitaire, ANSES, Lyon, France
H. Kretzschmar
Ludwig-Maximilians University of Munich, Munich, Germany
Keywords Animal Atypical Atypical/Nor98 scrapie BSE-H BSE-L Human Prion disease Prion strain Prion type
http://resources.metapress.com/pdf-preview.axd?code=f433r34h34ugg617&size=largest
snip...SEE MORE HERE ;
http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html
Friday, October 22, 2010
Peripherally Applied Aß-Containing Inoculates Induce Cerebral ß-Amyloidosis
http://betaamyloidcjd.blogspot.com/2010/10/peripherally-applied-containing.html
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight
Date: 5 January 1993
Copies:
Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
http://betaamyloidcjd.blogspot.com/
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"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Thursday, July 21, 2011
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:
August 2011 - Volume 70 - Issue 8 - pp 698-702
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
MAD COW DISEASE, TEXAS STYLE
http://www.organicconsumers.org/articles/article_23850.cfm
Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html
Tuesday, January 18, 2011
Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........
http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf
RISK OF BSE TO SHEEP VIA FEED
http://collections.europarchive.org/tna/20090114022605/http://www.bseinquiry.gov.uk/files/sc/seac31/tab01.pdf
Marion Simmons communicated surprising evidence for oral transmissibility of Nor98/atypical scrapie in neonatal sheep and although bioassay is ongoing, infectivity of the distal ileum of 12 and 24 month infected sheep is positive in Tg338 mice.
http://www.goatbse.eu/site/index.php?option=com_content&view=article&id=94:minutes-workshop-2010&catid=9:popular&Itemid=22
SUMMARY REPORTS OF MAFF BSE TRANSMISSION STUDIES AT THE CVL ;
http://collections.europarchive.org/tna/20090114023010/http://www.bseinquiry.gov.uk/files/sc/seac18/tab02b.pdf
THE RISK TO HUMANS FROM SHEEP;
http://collections.europarchive.org/tna/20090114022915/http://www.bseinquiry.gov.uk/files/sc/seac24/tab03.pdf
EXPERIMENTAL TRANSMISSION OF BSE TO SHEEP
http://collections.europarchive.org/tna/20090114023211/http://www.bseinquiry.gov.uk/files/sc/seac25/tab05.pdf
SHEEP AND BSE
PERSONAL AND CONFIDENTIAL
SHEEP AND BSE
A. The experimental transmission of BSE to sheep.
Studies have shown that the ''negative'' line NPU flock of Cheviots can be experimentally infected with BSE by intracerebral (ic) or oral challenge (the latter being equivalent to 0.5 gram of a pool of four cow brains from animals confirmed to have BSE).
http://collections.europarchive.org/tna/20090506010048/http://www.bseinquiry.gov.uk/files/sc/seac33/tab02.pdf
RB264
BSE - TRANSMISSION STUDIES
http://collections.europarchive.org/tna/20090113230127/http://www.bseinquiry.gov.uk/files/sc/Seac06/tab06.pdf
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY
snip...
A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates.
One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html
Epidemiology of Scrapie in the United States 1977
http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
Thursday, July 14, 2011
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html
UPDATE TSE PRION DISEASE NORTH AMERICA...FOR YOU INFORMATION, things you might not be aware of...TSS
Monday, June 27, 2011
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip...
full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
1989
IN CONFIDENCE
Perceptions of unconventional slow virus diseases of animals in the USA
Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or about that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. Whether they were scrapie infected sheep or not is unclear.
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html
CENTAUR GLOBAL NETWORK INFORMATION
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals. It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
http://centaur.vri.cz.web.atin.cz/docs/cnfi/2011-06-16-110.pdf
CANADA CJD UPDATE 2011
CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011
3. Final classification of 49 cases from 2009, 2010, 2011 is pending.
snip...
http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf
USA 2011
USA
National Prion Disease Pathology Surveillance Center
Cases Examined1
(November 1, 2010)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 ; earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 87 51 43 7 1 0
1999 121 73 65 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 13
2005 344 194 157 36 1 0
2006 383 197 166 29 0 24
2007 377 214 187 27 0 0
2008 394 231 205 25 0 0
2009 425 258 215 43 0 0
2010 333 213 158 33 0 0
TOTAL 38315 22656 1907 328 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.
I also urge you to again notice these disturbing factors in lines 5 and 6 ;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
========end=====tss=====2011
UPDATE JULY 2011 MORE OF THE "PENDING CLASSIFICATION CREUTZFELDT JAKOB DISEASE'' STEADY INCREASING...TSS
case; 5 Includes 13 cases in which the diagnosis is pending, and 18 inconclusive cases; 6 Includes 18 (15 from 2011) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
see video here ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
Friday, February 11, 2011
Creutzfeldt-Jakob disease (CJD) biannual update (2010/1) Emerging infections/CJD
http://creutzfeldt-jakob-disease.blogspot.com/2011/02/creutzfeldt-jakob-disease-cjd-biannual.html
Friday, April 15, 2011
PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PROJECTS, RESEARCH FUNDING, BSE VOLUNTARY TESTING UPDATE IN NORTH AMERICA 2011
http://prionunitusaupdate2008.blogspot.com/2011/04/prion-transmissible-spongiform.html
PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY RESEARCH FUNDING U.S.A.
COMPARE TO USA PRION FUNDING 2011
"which includes the ___elimination___ of Prion activities ($5,473,000),"
All Other Emerging and Zoonotic Infectious Diseases CDC‘s FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
THE PATHOLOGICAL PROTEIN
BY Philip Yam
Yam Philip Yam News Editor Scientific American www.sciam.com
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.
CHAPTER 14
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. ...
snip...
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
http://books.google.com/books?id=ePbrQNFrHtoC&pg=PA223&lpg=PA223&dq=the+pathological+protein+laying+odds+It%E2%80%99s+not+hard+to+get+Terry+Singeltary+going&source=bl&ots=um0PFAZSZD&sig=JWaGR7M7-1WeAr2qAXq8D6J_jak&hl=en&ei=MhtjS8jMJM2ztgeFoa2iBg&sa=X&oi=book_result&ct=result&resnum=1&ved=0CAcQ6AEwAA#v=onepage&q=&f=false
http://www.springerlink.com/content/r2k2622661473336/fulltext.pdf?page=1
http://www.thepathologicalprotein.com/
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
Newsdesk
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 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.
http://linkinghub.elsevier.com/retrieve/pii/S1473309903007151
http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(03)00715-1/fulltext
http://www.mdconsult.com/das/article/body/180784492-2/jorg=journal&source=&sp=13979213&sid=0/N/368742/1.html?issn=14733099
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176
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:
http://service.spiegel.de/digas/find?DID=18578755
"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. ...
http://www.spiegel.de/spiegel/print/d-18578755.html
http://wissen.spiegel.de/wissen/image/show.html?did=18578755&aref=image024/E0108/SCSP200100901440145.pdf&thumb=false
http://service.spiegel.de/digas/servlet/find/DID=18578755
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.
http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
layperson
Terry S. Singeltary Sr.
UPDATE OCTOBER 4, 2011
04/10/2011
New research shows Alzheimer's disease may originate from the infectious prion disease.
Alzheimer's disease may originate in a similar form to the infectious prion disease, according to new research.
The University of Texas Health Science Centre has published a study showing a potentially infectious spreading of Alzheimer's in animal models.
"Our findings open the possibility that some of the sporadic Alzheimer's cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease," stated Claudio Soto, Ph.D., professor of neurology at the University of Texas....
http://www.barchester.com/Healthcare-News/Alzheimer's-disease-may-be-transmissible/376/4827
Tuesday, October 4, 2011
De novo induction of amyloid-β deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
De novo induction of amyloid-ß deposition in vivo
R Morales1,2, C Duran-Aniotz1,3, J Castilla2,4, L D Estrada2,5 and C Soto1,2
1Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, Houston, TX, USA 2University of Texas Medical Branch at Galveston, Galveston, TX, USA 3Universidad de Los Andes, Facultad de Medicina. Av. San Carlos de Apoquindo 2200, Las Condes, Santiago, Chile 4CIC bioGUNE, Parque Tecnologico de Biskaia, Ed 800, 48160 Derio and IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain
Correspondence: Dr C Soto, Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030, USA. E-mail: Claudio.Soto@uth.tmc.edu
5Current address: Laboratorio de Señalización Celular, Centro de Envejecimiento y Regeneración. P. Universidad Catolica de Chile, Santiago, Chile.
Received 8 March 2011; Revised 15 August 2011; Accepted 25 August 2011; Published online 4 October 2011.
Abstract
Alzheimer's disease (AD), the most common type of senile dementia, is associated to the build-up of misfolded amyloid-ß (Aß) in the brain. Although compelling evidences indicate that the misfolding and oligomerization of Aß is the triggering event in AD, the mechanisms responsible for the initiation of Aß accumulation are unknown. In this study, we show that Aß deposition can be induced by injection of AD brain extracts into animals, which, without exposure to this material, will never develop these alterations. The accumulation of Aß deposits increased progressively with the time after inoculation, and the Aß lesions were observed in brain areas far from the injection site. Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention.
Keywords:
amyloid; prion; protein misfolding; disease transmission
http://www.nature.com/mp/journal/vaop/ncurrent/abs/mp2011120a.html
see more here ;
http://betaamyloidcjd.blogspot.com/2011/10/de-novo-induction-of-amyloid-deposition.html
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/alzheimers-disease-is-transmissible.html
TSS
Posted On December 20, 2003
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Mad Cow Scaremongers
Secretary of Agriculture Ann Veneman says that "beef is absolutely safe to eat." Harvard University experts note that the risk of Americans contracting mad cow disease is "as close to zero as you can get." Every reputable expert tells us that the American meat supply is still safe. And yet a cabal of animal-rights activists and radical opponents of modern farming are already hitting the airwaves for one purpose: to spread fear and needless alarm. These people are activists, not knowledgeable scientists. Their expertise is in scare mongering, not livestock agriculture. Their goal is to promote animal rights and organic-only, 1800s-style agriculture. And their track record is full of doom-and-gloom predictions that never came true.
Who are these masters of disaster? A rogues gallery follows:
John Stauber -- director of the anti-corporate Center for Media & Democracy, and co-author of the 1997 book Mad Cow USA, which was supported financially by the eco-religious Foundation for Deep Ecology. Stauber sits on the national advisory board of the Organic Consumers Association, as reliable a scaremonger as any about the American food supply. Stauber has become a near-ubiquitous media presence in mad-cow-related stories. Just minutes after Secretary Veneman finished her press conference announcing the discovery of a single sick cow, Stauber told CNN -- without any evidence whatsoever -- that it was just "the tip of an invisible iceberg" and that "mad cow disease is spread throughout North America."
Ronnie Cummins -- head of the Organic Consumers Association, a group founded by radical anti-technology guru Jeremy Rifkin. Cummins has openly expressed his hope that a U.S. mad-cow epidemic would fuel a "crisis of confidence" in American food, similar to the one that he claims drove British consumers to "organic" and other high-priced options. In 1998 Cummins told the Minneapolis City Pages that "consumers and farmers would both be better off if people paid twice as much for their meat and ate half as much." This June he confidently told a Canadian Press reporter that "no case of mad cow has ever been found in a cow raised on an organic farm." This, actually, is not true. The British Central Veterinary Laboratory reports that in 1995 (at the height of the UK outbreak), there were 215 confirmed cases of mad cow disease from 36 different organic farms. And Germany's very first case of mad cow disease was diagnosed in a slaughterhouse that only processed organically-raised cattle.
Michael Greger -- a vegetarian activist doctor who maintains a brisk animal-rights speaking schedule and edits the mad-cow-scare web page of the Organic Consumers Association. He recently provided PETA with a laughable treatise suggesting that the SARS outbreak came from livestock farming. Greger titled his mad-cow stump speech "Mad Cow Disease: Plague of the 21st Century?." He argues: "although no pigs or chickens have been found with the disease ... any animal with a brain has the potential to become infected." Greger has yet to produce any evidence to support this claim, largely because there isn't any. Neither hogs nor hens (nor fish, for that matter) suffer from mad-cow-like illnesses. Greger is planning to hit the lecture circuit in an effort to "keep hammering" the meat industry and " keep this momentum going."
Michael Hansen -- the Consumers Union of the United States' self-proclaimed "expert" on genetically enhanced food, bovine growth hormone, mad cow disease, and any other food issue he deems ripe for scaremongering. When the Canadian mad-cow story broke earlier this year, Hansen blithely suggested that American consumers should eat only grass-fed, "organic," and other specialty beef. Hansen's statements on mad cow have appeared in hundreds of media outlets, and his boss, Jean Halloran, has weighed in as well.
Howard Lyman -- one part animal-rights scold, one part revival tent preacher [click here for video]. Lyman trades on the fact that he was brought up in a cattle-ranching family to imply that his strict vegetarianism is somehow more informed than everyone else's dietary choices. Lyman famously (and incorrectly) predicted on the "Oprah" show that mad cow disease among Americans would "make AIDS look like the common cold." Just 14 hours after the U.S. mad-cow announcement, animal-rights terroristand Sierra Club board member Paul Watson published an op-ed asserting that "Howard Lyman predicted this outbreak years ago. Perhaps now the public might pay more attention to this Montana rancher turned vegan. He knows that of which he speaks." It's no coincidence that Lyman is on the advisory board of Watson's violent Sea Shepard Conservation Society. The front page of The Washington Post's "Style" section seconded Watson's misleading praise of Lyman with an article titled "Ex-Cattleman's Warning Was No Bum Steer."
Dave Louthan -- a disgruntled former employee of the Washington state meat processing plant where the first U.S. mad-cow case was detected. After losing the job he loved (slaughtering cows), Louthan launched a crusade against beef producers and the U.S. Department of Agriculture, a personal jihad supported by animal rights activists who must otherwise recoil at his admitted passion for bloodying beef cattle. This is a man who clearly enjoyed his work -- using a bolt gun to kill cows, buffalo, ostrich, emu and alpaca for Vern’s Moses Lake Meats. He told the New York Times that killing is “really fun,” and beats deboning, which he calls “girls’ work.” In the Seattle Times, Louthan added: “I liked to kill cows. I don’t care if I’m hauling them, feeding them or killing them.”
Like many in the meat business, Louthan lost his source of income because of the mad cow scare recklessly promoted by activist groups. But he’s mad, and he’s fighting back. Despite copious evidence to the contrary, he continues to claim that the famous cow he killed (the one that later tested positive) and many others like it were ground into hamburger and entered the human food chain. “The hamburger surprise in your kids’ school lunch,” Dave claims, “has come from mad cows … Your kids will get mad cow from it.” A man of many contradictions, Louthan warns that the U.S. government “is trying to kill you.” He’s calling on anti-beef and animal-rights groups to send him money so he can “keep up the fight.” Yet he admits continuing to eat beef on a daily basis. The verdict is still out on whether or not this former trucker from Texas can successfully change careers from killing cows to assassinating the character of cattlemen.
Terry Singletary -- A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.
As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176
Marion Nestle -- New York University's food scold extraordinaire. Although Nestle concedes that the risk of getting mad cow disease is extremely low, she has nonetheless exploited mad cow fears to promote an anti-corporate, pro-organic creed. She has complained: "Until we have a little consumer protection going on in government, consumers have to take care of themselves." How do consumers do that? By purchasing organic food, of course. Nestle told Fox News: "This is a very good time to buy organic."
Bruce Friedrich -- PETA's director of vegan outreach. Friedrich revealed his true agenda when he argued: "I think it would be a great thing if all of these fast-food outlets, and these slaughterhouses, and these laboratories, and the banks that fund them exploded tomorrow. I think it's perfectly appropriate for people to take bricks and toss them through the windows, and everything else along the line. Hallelujah to the people who are willing to do it" [click here for audio]. There is seemingly nothing Bruce won't do to scare people away from meat, including raising fears about mad cow disease. Under Friedrich's leadership, PETA representatives have been handing out "emergency vegetarian starter kits," and holding anti-meat posters outside restaurants and grocery stores all over the country. PETA has also started an aggressive and misleading (what's new?) advertising campaign to frighten the public into vegetarianism.
Neal Barnard -- the animal-rights movement's not-so-secret weapon against meat. Sure he's a doctor (a non-practicing psychiatrist, actually), but his tirades against dairy foods, beef, chicken, and Atkins-style diets are all informed by his connections to PETA. Barnard sits on the board of The PETA Foundation along with PETA co-founder Ingrid Newkirk. And PETA has funneled nearly $1 million to Barnard's misnamed "Physicians Committee for Responsible Medicine." His virulent opposition to animal-based foods was clear in a recent speech at a Food and Drug Administration hearing, where he referred to cheese as "morphine on a cracker" and "dairy crack." PCRM wasted no time after the mad cow news broke, sending out a press release attacking meat and offering a "vegetarian starter kit" for suddenly fearful carnivores.
Caroline Smith DeWaal -- director of the food safety program at the quintessential food cop, the Center for Science in the Public Interest. Smith DeWaal, who has been advising consumers to grind their own beef, told The Washington Post: "Taco filling, pizza toppings, hot dogs, processed meats, these are all likely products that can expose consumers to mad cow disease."
Wayne Pacelle -- senior vice president of the Humane Society of the United States, a radical animal rights group masquerading as an animal-welfare organization. Pacelle immediately began to lobby the federal government on mad cow, petitioning the U.S. Department of Agriculture the morning after Veneman's announcement. Pacelle's goal is to create "a National Rifle Association of the animal rights movement." His opposition to eating meat is so strong that he has "no problems with the extinction of domestic animals."
Gene Bauston -- co-founder of the animal rights group Farm Sanctuary. This group was recently convicted of 210 counts of election fraud, in connection with the $465,000 it illegally trucked into a Florida ballot initiative that gave constitutional rights to pigs. Farm Sanctuary even paid a $50,000 fine. The group issued an e-mail alert to its approximately 18,000 members, requesting that they write to the USDA about mad cow. It also e-mailed a boilerplate "letter to the editor" to over 1,900 activists, asking them to send it to their local newspapers under their own individual signatures. In a gushing article, The New York Times praised the group for its crusade against the processing of "downer" cows. But the paper of record manages to overlook Farm Sanctuary's early association with the domestic-terrorist Animal Liberation Front, as well as its electioneering mischief.
Mark Ritchie -- scaremonger-in-chief at the anti-corporate, anti-modern-agriculture, anti-free-trade Institute for Agriculture and Trade Policy (IATP). He blames "industrialized beef production and liberalized trade" for mad cow disease. IATP has started distributing sound-bites for radio broadcast via a 1-800 number.
Eric Schlosser -- anti-fast food activist and author of Fast Food Nation, which was essentially a screed against the consumption of hamburgers. It's no surprise that Schlosser is using mad-cow fears to buttress his case. He flatly told CNN: "I don't think anyone should eat ground beef." Schlosser's op-ed in The New York Times was similarly full of doom and gloom.
Andrew Knight -- a Seattle veterinarian who recently took over the day-to-day operations of the radical Northwest Animal Rights Network. Knight is raising mad-cow panic levels without disclosing his animal-rights agenda. His letter in The Washington Times (Excerpt: "I, for one, will be stocking up on veggie burgers") identified him only as "Dr. Andrew Knight, Seattle." The San Diego Union-Tribune printed an expanded version of his Times letter as an op-ed. There he wrote: "it is not improbable that for the one mad cow detected thus far, some 1,700 have passed undetected into the food chain, and that the human form of this lethal disease is silently incubating in numerous unsuspecting beef eaters at present." A subsequent op-ed in the Toronto Star used the exact same line.
Karen Hudson -- a consultant for GRACE Factory Farm Project, which can't stand the idea of efficient, large-scale agriculture. The group even compares animal husbandry to the post-apocalyptic movie, The Matrix. Hudson insists -- without providing any evidence -- that "mad cow disease is the product of an increasingly industrialized food system."
Katherine DiMatteo -- executive director of the Organic Trade Association, which represents the $11 billion organic industry in North America. The group issued a media release arguing: "while the retail price of organic meat is generally greater than conventional, to many consumers, the greater peace of mind is priceless."
Larry Bohlen and Brent Blackwelder -- from the radical green group Friends of the Earth. The organization issued a "fact sheet" on mad cow that includes such topics as "mad cow on the rampage." Blackwelder peddles the familiar and false story that the "best way for people to avoid the risk of mad cow disease is to eat organic, grass fed beef or beef alternatives." Bohlen's mad cow comments have found their way into the Los Angeles Times, The Chicago Tribune, and The Seattle Times.
Peter Lurie and Wenonah Hauter -- food safety "experts" at Ralph Nader's Public Citizen. Their public comments are designed to raise unfounded fears about eating conventionally-raised beef.
Felicia Nestor -- chief food-safety worrier at the "whistleblowers' rights" Government Accountability Project. Nestor worked with Public Citizen to author reports called "The Jungle 2000: Is America's Meat Fit to Eat?" and "Hamburger Hell: The Flip Side of USDA's Salmonella Testing Program." She co-founded the Global Safe Food Alliance, which includes mad cow scaremongers like Public Citizen, the Institute for Agriculture and Trade Policy, and the Organic Consumers Association, along with animal-rights groups like Farm Sanctuary, the Physicians Committee for Responsible Medicine, United Poultry Concerns, and the Humane Society of the United States. Nestor's hysterical complaints about mad cow have turned up in The New York Times.
Andrew Kimbrell and Joseph Mendelson -- executive director and legal director of the Center for Food Safety. The Center for Food Safety (not to be confused with the Food and Drug Administration's Center for Food Safety and Applied Nutrition) gets most of its money from the organic food industry and the lunatic Foundation for Deep Ecology.
Robert Cohen -- an animal-rights radical who is convinced that cow's milk is the root of all evil. Cohen warned cattlemen and dairy farmers that mad cow disease would be "a sign" that Americans should "reject your poisons."
http://www.consumerfreedom.com/article_detail.cfm/a/138-mad-cow-scaremongers
Posted On December 20, 2003
AFTER THE FIRST CASE OF MAD COW DISEASE IN THE USA WAS DOCUMENTED
" Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. "
http://www.consumerfreedom.com/article_detail.cfm/a/138-mad-cow-scaremongers
SO, just who are The Center for Consumer Freedom ;
http://www.consumerfreedom.com/index.cfm
let's take a closer look shall we ;
The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"
CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.
http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom
http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom
snip...SEE FULL TEXT HERE ;
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
UPDATE UPDATE UPDATE
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*** TSE PRION PRION CONFERENCES UPDATES 2015, 2016, AND 2016 ***
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TSE PRION ZOONOSIS 2018
CDC STRONGLY SUGGEST IN 2017;
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal.
SEE FULL REPORT BELOW!
SUNDAY, DECEMBER 10, 2017
Detection of Prions in Blood of Cervids at the Asymptomatic Stage of Chronic Wasting Disease
The results showed a sensitivity of 100% in animals with very poor body condition that were IHC-positive in both brain and lymph nodes, 96% in asymptomatic deer IHC-positive in brain and lymph nodes and 53% in animals at early stages of infection that were IHC-positive only in lymph nodes. The overall mean diagnostic sensitivity was 79.3% with 100% specificity. These findings show that PMCA might be useful as a blood test for routine, live animal diagnosis of CWD.
CHRONIC WASTING DISEASE CWD TSE PRION ZOONOTIC ZOONOSIS
PRICE OF TSE PRION POKER GOES UP!
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.
Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.
Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.
To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.
Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
Thursday, November 16, 2017
Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination
MONDAY, NOVEMBER 06, 2017
Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque
''On secondary and tertiary transmissions, however, the proportion of PrPres positive animals gradually increased to almost 100%.
''Recent communications suggest that a similar situation might exist in other models of experimental exposure to prions involving swine32 and cattle33.''
''Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque''
i am thinking of that 10,000,000 POUNDS OF BLOOD LACED MEAT AND BONE MEAL IN COMMERCE WARNING LETTER back in 2007, see;
SATURDAY, NOVEMBER 4, 2017
FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006
FRIDAY, NOVEMBER 3, 2017
BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW
''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''
IN CONFIDENCE
TUESDAY, JULY 18, 2017
USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
SUNDAY, JULY 30, 2017
Do we need to explain the occurrence of atypical scrapie?
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
snip...see full Singeltary Nature comment here;
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO 4
November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk.
However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1
92/11.4/1.1
BSE101/1 0137 4.
The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion.
The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis
Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00
WEDNESDAY, NOVEMBER 1, 2017
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
END OF UPDATE...TSS
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/prionet-canada-researchers-in-vancouver.html
PP1:
Does A “Prion-Like” Mechanism Contribute to the Spreading of Neuropathology in Parkinson’s Disease?
Patrik Brundin Neuronal Survival Unit; Wallenberg Neuroscience Center; Dept of Experimental Medical Science; Lund University; Lund, Sweden
Key words: Parkinson’s disease, prion mechanism, alpha-synuclein
Neuropathological aggregates of alpha-synuclein in neuronal cytoplasm and neurites are typical features of Parkinson’s disease (PD). These Lewy neurites and Lewy bodies are prominent in substantia nigra, where dopaminergic neurons degenerate. With advancing disease they are also found in several other widespread brain areas, and it has been suggested that they appear in anterior olfactory structures and the dorsal motor nucleus of the vagal nerve even before the substantia nigra is affected. Recent studies demonstrated that Lewy bodies and neurites appear in grafted embryonic neurons.1-3 They stain for Thioflavin S, are immunoreactive for alpha-synuclein phosphorylated at serine residue 129 and exhibit a fibrillar structure in the electron microscope.4 From 2 to 5% (frequency increases over time) of the grafted dopaminergic neurons display Lewy bodies, starting around one decade after surgery. Despite these changes, some of the PD grafted patients still exhibit signs of functional recovery beyond a decade after surgery. We, and others, are currently exploring possible mechanisms underlying the transfer of alpha-synuclein between cells and their relevance to how neuropathology normally spreads in the PD brain.5,6 We have observed that alpha-synuclein indeed can transfer between cells in culture. The process is clearly time-dependent and once inside the new cell the imported alpha-synuclein can seed aggregation of endogenous alpha-synuclein. Furthermore, we have observed transfer of host-derived alpha-synuclein into embryonic dopamine neurons grafted into the striatum of transgenic mice expressing human alpha-synuclein. We propose that a “prion-like” disease mechanism might contribute to the pathogenesis of PD and other chronic neurodegenerative disorders.6
References
1. Li, et al. Nat Med 2008; 14:501-3. 2. Kordower, et al. Nat Med 2008; 14:504-6. 3. Kordower, et al. Mov Disord 2008; 23:2303-6. 4. Li, et al. Mov Disord 2010; [Epub ahead of print]. 5. Brundin, et al. Nat Rev Neurosci 2008; 9:741-5. 6. Brundin, et al. Nat Rev Mol Cell Biol 2010; 11:301-7. PP: Plenary Lectures Previously published online: www.landesbioscience.com/journals/prion/article/12765
DOI: 10.4161/pri.4.3.12765
===========================
WP8-4: Prion-like Induction of Alzheimer-type Proteopathy in Transgenic Mice
Lary C. Walker
Yerkes Center; Emory University; Atlanta, GA USA
Key words: abeta, Alzheimer, amyloid, prion, seeding, strains, transgenic, transmission
Alzheimer’s disease and prion disease both involve the accumulation of disease-specific proteins in the brain, suggesting pathogenic commonalities. In Alzheimer’s disease, the aggregation of the protein fragment Aßis a seminal event. Similar to the templated corruption of prion protein, cerebral Aßdeposition can be induced in ß-amyloid precursor protein (APP)-transgenic mice and rats by the intracerebral injection of Aß-rich brain extracts from patients with Alzheimer’s disease or APP-transgenic mice. Our studies indicate that the characteristics of the seeded deposits depend on the source of the seeding extract, the type of host, and the seeded brain region. We are using the amyloid-binding agent Pittsburgh Compound B (PIB) as a marker of a potential AD-specific form of multimeric Aß, and are attempting to induce alternative conformations in the transgenic mouse Aß-seeding model. In addition, we are investigating non-intracerebral routes of administration and the ability of heterologous agents to induce Aßdeposition. Analysis of Aß-seeding in vivo could yield fresh insights into the origins of idiopathic Alzheimer’s disease.
Acknowledgements
Key collaborators on these studies are Mathias Jucker (U. Tübingen), Rebecca Rosen (Emory U.) and Harry LeVine III (U. Kentucky). Supported by NIH RR-00165 and the CART Foundation.
===========================
PPo9-1: Prion-like Propagation of SOD1 Misfolding in Amyotrophic Lateral Sclerosis
Neil R. Cashman
University of British Columbia; Vancouver, British Columbia Canada
Key words: protein misfolding, mechanisms of neurodegeneration, transmission
Prion-like propagation of protein misfolding has been implicated in Alzheimer’s, Parkinson’s and Huntington’s diseases, and the tauopathies. Amyotrophic lateral sclerosis (ALS) is a common and incurable adult motor neuron disease, in which mutation of the free-radical defense enzyme superoxide dismutase 1 (SOD1) is responsible for a subtype of familial ALS (fALS). We demonstrate that transfection of fALS SOD1 mutants G127X and G85R, as well as overexpression of non-mutant wild-type (wt) SOD1, can induce misfolding of natively-structured wild-type SOD1 in human mesenchymal and neural cell lines, as determined by molecular surface immunoreactivity with misfolding-specific monoclonal antibodies (mAbs), acquisition of protease sensitivity (suggesting structural loosening), generation of reactive oxygen species (ROS) and formation of non-native intermolecular disulfide bonds. Serial transmission of SOD1 misfolding was established by incubation in conditioned media from mtSOD1- or wtSOD1-transfected HEK cells, and knockdown of endogenous SOD1 expression in HEK cells by siRNA abrogated the transmission of SOD1 misfolding, consistent with endogenously expressed SOD1 being the substrate for conformational conversion. Pre-incubation of SOD1-transfected conditioned media with poly-specific SOD1 antibodies or misfolding-specific mAbs also blocked intercellular transducing activity, and passive administration of misfolding-specific mAbs extends survival in the G37R transgenic mouse model of ALS. We conclude that misfolded SOD1 participates in a template-directed misfolding cascade which provides a plausable molecular mechanism for progression of familial and sporadic ALS. Antibody-mediated neutralization of SOD1 misfolding propagation could prove beneficial in human ALS.
================
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Alimentary prion infections: Touch-down in the intestine
Volume 5, Issue 1 January/February/March 2011 Bianca Da Costa Dias, Katarina Jovanovic and Stefan F.T. Weiss View affiliations Hide affiliations Bianca Da Costa DiasSchool of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa Katarina JovanovicSchool of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa Stefan F.T. WeissCorresponding author: stefan.weiss@wits.ac.za School of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa
Neurodegenerative diseases are caused by proteinaceous aggregates, usually consisting of misfolded proteins which are often typified by a high proportion of ß-sheets, which accumulate in the Central Nervous System. These diseases, including Morbus Alzheimer, Parkinson disease and Transmissible Spongiform Encephalopathies (TSEs) also termed prion disorders, afflict a substantial proportion of the human population and as such the etiology and pathogenesis of these diseases has been the focus of mounting research. Although many of these diseases arise from genetic mutations or are sporadic in nature, the possible horizontal transmissibility of neurodegenerative diseases poses a great threat to population health. In this article we discuss recent studies which suggest that the “non-transmissible” status bestowed upon Alzheimer and Parkinson diseases may need to be revised as these diseases have been successfully induced through tissue transplants. Furthermore, we highlight the importance of investigating the “natural” mechanism of prion transmission including peroral and perenteral transmission, proposed routes of gastrointestinal uptake and neuroinvasion of ingested infectious prion proteins. We examine the multitude of factors which may influence oral transmissibility and discuss the zoonotic threats which Chronic Wasting Disease (CWD), Bovine Spongiform Encephalopathy (BSE) and Scrapie may pose resulting in vCJD or related disorders. In addition, we suggest that the 37 kDa/67 kDa laminin receptor on the cell surface of enterocytes, a major cell population in the intestine, may play an important role in the intestinal pathophysiology of alimentary prion infections.
http://www.landesbioscience.com/journals/prion/article/14283
Commentary ß-amyloid oligomers and prion protein: Fatal attraction?
Volume 5, Issue 1 January/February/March 2011 Gianluigi Forloni and Claudia Balducci
Gianluigi Forloni Corresponding author: forloni@marionegri.it
Claudia Balducci Biology of Neurodegenerative Diseases Lab; Department of Neuroscience; “Mario Negri” Institute for Pharmacological Research; Milano, Italy
The relationship between Alzheimer disease (AD) and prion-related encephalopathies (TSE) has been proposed by different points of view. Recently, the scientific attention has been attracted by the results proposing the possibility that PrPc, the protein whose pathologic form is responsible of TSE, can mediated the toxic effect of ß amyloid (Aß) oligomers. The oligomers are considered the culprit of the neurodegenerative process associated to AD, although the pathogenic mechanism activated by these small aggregates remain to be elucidated. In the initial study based on the binding screening PrPc was identified as ligand /receptor of Aß oligomers, while long term potentiation (LTP) analysis in vitro and behavioural studies in vivo, demonstrated that the absence of PrPc abolished the damage induced by Aß oligomers. The high affinity binding Aß oligomers-PrPc has been confirmed, whereas a functional role of this association has been excluded by three different studies. We approached this issue by the direct application of Aß oligomers in the brain followed by the behavioural examination of memory deficits. Our data using PrP knock-out mice suggest that Aß 1-42 oligomers are responsible for cognitive impairment in AD but PrPc is not required for their effect. Similarly, in two other studies the LTP alterations induced by Aß 1-42 oligomers was not influenced by the absence of PrP. Possible explanations of these contradictory results are discussed.
http://www.landesbioscience.com/journals/prion/article/14367/
http://www.landesbioscience.com/journals/prion/toc/volume/5/issue/1/
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE.
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/prionet-canada-researchers-in-vancouver.html
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
Monday, May 23, 2011
Atypical Prion Diseases in Humans and Animals 2011
Top Curr Chem (2011)
DOI: 10.1007/128_2011_161
# Springer-Verlag Berlin Heidelberg 2011
Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar
Abstract
Although prion diseases, such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie in sheep, have long been recognized, our understanding of their epidemiology and pathogenesis is still in its early stages. Progress is hampered by the lengthy incubation periods and the lack of effective ways of monitoring and characterizing these agents. Protease-resistant conformers of the prion protein (PrP), known as the "scrapie form" (PrPSc), are used as disease markers, and for taxonomic purposes, in correlation with clinical, pathological, and genetic data. In humans, prion diseases can arise sporadically (sCJD) or genetically (gCJD and others), caused by mutations in the PrP-gene (PRNP), or as a foodborne infection, with the agent of bovine spongiform encephalopathy (BSE) causing variant CJD (vCJD). Person-to-person spread of human prion disease has only been known to occur following cannibalism (kuru disease in Papua New Guinea) or through medical or surgical treatment (iatrogenic CJD, iCJD). In contrast, scrapie in small ruminants and chronic wasting disease (CWD) in cervids behave as infectious diseases within these species. Recently, however, so-called atypical forms of prion diseases have been discovered in sheep (atypical/Nor98 scrapie) and in cattle, BSE-H and BSE-L. These maladies resemble sporadic or genetic human prion diseases and might be their animal equivalents. This hypothesis also raises the significant public health question of possible epidemiological links between these diseases and their counterparts in humans.
M.A. Tranulis (*)
Norwegian School of Veterinary Science, Oslo, Norway
e-mail: Michael.Tranulis@nvh.no
S.L. Benestad
Norwegian Veterinary Institute, Oslo, Norway
T. Baron
Agence Nationale de Se´curite´ Sanitaire, ANSES, Lyon, France
H. Kretzschmar
Ludwig-Maximilians University of Munich, Munich, Germany
Keywords Animal Atypical Atypical/Nor98 scrapie BSE-H BSE-L Human Prion disease Prion strain Prion type
http://resources.metapress.com/pdf-preview.axd?code=f433r34h34ugg617&size=largest
snip...SEE MORE HERE ;
http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html
Friday, October 22, 2010
Peripherally Applied Aß-Containing Inoculates Induce Cerebral ß-Amyloidosis
http://betaamyloidcjd.blogspot.com/2010/10/peripherally-applied-containing.html
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight
Date: 5 January 1993
Copies:
Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
http://betaamyloidcjd.blogspot.com/
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"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Thursday, July 21, 2011
A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:
August 2011 - Volume 70 - Issue 8 - pp 698-702
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
Wednesday, June 15, 2011
Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html
MAD COW DISEASE, TEXAS STYLE
http://www.organicconsumers.org/articles/article_23850.cfm
Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html
Wednesday, January 19, 2011
EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html
Tuesday, January 18, 2011
Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........
http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf
RISK OF BSE TO SHEEP VIA FEED
http://collections.europarchive.org/tna/20090114022605/http://www.bseinquiry.gov.uk/files/sc/seac31/tab01.pdf
Marion Simmons communicated surprising evidence for oral transmissibility of Nor98/atypical scrapie in neonatal sheep and although bioassay is ongoing, infectivity of the distal ileum of 12 and 24 month infected sheep is positive in Tg338 mice.
http://www.goatbse.eu/site/index.php?option=com_content&view=article&id=94:minutes-workshop-2010&catid=9:popular&Itemid=22
SUMMARY REPORTS OF MAFF BSE TRANSMISSION STUDIES AT THE CVL ;
http://collections.europarchive.org/tna/20090114023010/http://www.bseinquiry.gov.uk/files/sc/seac18/tab02b.pdf
THE RISK TO HUMANS FROM SHEEP;
http://collections.europarchive.org/tna/20090114022915/http://www.bseinquiry.gov.uk/files/sc/seac24/tab03.pdf
EXPERIMENTAL TRANSMISSION OF BSE TO SHEEP
http://collections.europarchive.org/tna/20090114023211/http://www.bseinquiry.gov.uk/files/sc/seac25/tab05.pdf
SHEEP AND BSE
PERSONAL AND CONFIDENTIAL
SHEEP AND BSE
A. The experimental transmission of BSE to sheep.
Studies have shown that the ''negative'' line NPU flock of Cheviots can be experimentally infected with BSE by intracerebral (ic) or oral challenge (the latter being equivalent to 0.5 gram of a pool of four cow brains from animals confirmed to have BSE).
http://collections.europarchive.org/tna/20090506010048/http://www.bseinquiry.gov.uk/files/sc/seac33/tab02.pdf
RB264
BSE - TRANSMISSION STUDIES
http://collections.europarchive.org/tna/20090113230127/http://www.bseinquiry.gov.uk/files/sc/Seac06/tab06.pdf
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY
snip...
A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates.
One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html
Epidemiology of Scrapie in the United States 1977
http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
Thursday, July 14, 2011
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html
UPDATE TSE PRION DISEASE NORTH AMERICA...FOR YOU INFORMATION, things you might not be aware of...TSS
Monday, June 27, 2011
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip...
full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
1989
IN CONFIDENCE
Perceptions of unconventional slow virus diseases of animals in the USA
Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or about that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. Whether they were scrapie infected sheep or not is unclear.
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html
CENTAUR GLOBAL NETWORK INFORMATION
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals. It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
http://centaur.vri.cz.web.atin.cz/docs/cnfi/2011-06-16-110.pdf
CANADA CJD UPDATE 2011
CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011
3. Final classification of 49 cases from 2009, 2010, 2011 is pending.
snip...
http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf
USA 2011
USA
National Prion Disease Pathology Surveillance Center
Cases Examined1
(November 1, 2010)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 ; earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 87 51 43 7 1 0
1999 121 73 65 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 13
2005 344 194 157 36 1 0
2006 383 197 166 29 0 24
2007 377 214 187 27 0 0
2008 394 231 205 25 0 0
2009 425 258 215 43 0 0
2010 333 213 158 33 0 0
TOTAL 38315 22656 1907 328 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.
I also urge you to again notice these disturbing factors in lines 5 and 6 ;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
========end=====tss=====2011
UPDATE JULY 2011 MORE OF THE "PENDING CLASSIFICATION CREUTZFELDT JAKOB DISEASE'' STEADY INCREASING...TSS
case; 5 Includes 13 cases in which the diagnosis is pending, and 18 inconclusive cases; 6 Includes 18 (15 from 2011) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
see video here ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
Friday, February 11, 2011
Creutzfeldt-Jakob disease (CJD) biannual update (2010/1) Emerging infections/CJD
http://creutzfeldt-jakob-disease.blogspot.com/2011/02/creutzfeldt-jakob-disease-cjd-biannual.html
Friday, April 15, 2011
PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PROJECTS, RESEARCH FUNDING, BSE VOLUNTARY TESTING UPDATE IN NORTH AMERICA 2011
http://prionunitusaupdate2008.blogspot.com/2011/04/prion-transmissible-spongiform.html
PRION TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY RESEARCH FUNDING U.S.A.
COMPARE TO USA PRION FUNDING 2011
"which includes the ___elimination___ of Prion activities ($5,473,000),"
All Other Emerging and Zoonotic Infectious Diseases CDC‘s FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
THE PATHOLOGICAL PROTEIN
BY Philip Yam
Yam Philip Yam News Editor Scientific American www.sciam.com
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.
CHAPTER 14
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. ...
snip...
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
http://books.google.com/books?id=ePbrQNFrHtoC&pg=PA223&lpg=PA223&dq=the+pathological+protein+laying+odds+It%E2%80%99s+not+hard+to+get+Terry+Singeltary+going&source=bl&ots=um0PFAZSZD&sig=JWaGR7M7-1WeAr2qAXq8D6J_jak&hl=en&ei=MhtjS8jMJM2ztgeFoa2iBg&sa=X&oi=book_result&ct=result&resnum=1&ved=0CAcQ6AEwAA#v=onepage&q=&f=false
http://www.springerlink.com/content/r2k2622661473336/fulltext.pdf?page=1
http://www.thepathologicalprotein.com/
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
Newsdesk
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 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.
http://linkinghub.elsevier.com/retrieve/pii/S1473309903007151
http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(03)00715-1/fulltext
http://www.mdconsult.com/das/article/body/180784492-2/jorg=journal&source=&sp=13979213&sid=0/N/368742/1.html?issn=14733099
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176
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:
http://service.spiegel.de/digas/find?DID=18578755
"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. ...
http://www.spiegel.de/spiegel/print/d-18578755.html
http://wissen.spiegel.de/wissen/image/show.html?did=18578755&aref=image024/E0108/SCSP200100901440145.pdf&thumb=false
http://service.spiegel.de/digas/servlet/find/DID=18578755
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.
http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
layperson
Terry S. Singeltary Sr.
UPDATE OCTOBER 4, 2011
04/10/2011
New research shows Alzheimer's disease may originate from the infectious prion disease.
Alzheimer's disease may originate in a similar form to the infectious prion disease, according to new research.
The University of Texas Health Science Centre has published a study showing a potentially infectious spreading of Alzheimer's in animal models.
"Our findings open the possibility that some of the sporadic Alzheimer's cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease," stated Claudio Soto, Ph.D., professor of neurology at the University of Texas....
http://www.barchester.com/Healthcare-News/Alzheimer's-disease-may-be-transmissible/376/4827
Tuesday, October 4, 2011
De novo induction of amyloid-β deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
De novo induction of amyloid-ß deposition in vivo
R Morales1,2, C Duran-Aniotz1,3, J Castilla2,4, L D Estrada2,5 and C Soto1,2
1Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, Houston, TX, USA 2University of Texas Medical Branch at Galveston, Galveston, TX, USA 3Universidad de Los Andes, Facultad de Medicina. Av. San Carlos de Apoquindo 2200, Las Condes, Santiago, Chile 4CIC bioGUNE, Parque Tecnologico de Biskaia, Ed 800, 48160 Derio and IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain
Correspondence: Dr C Soto, Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030, USA. E-mail: Claudio.Soto@uth.tmc.edu
5Current address: Laboratorio de Señalización Celular, Centro de Envejecimiento y Regeneración. P. Universidad Catolica de Chile, Santiago, Chile.
Received 8 March 2011; Revised 15 August 2011; Accepted 25 August 2011; Published online 4 October 2011.
Abstract
Alzheimer's disease (AD), the most common type of senile dementia, is associated to the build-up of misfolded amyloid-ß (Aß) in the brain. Although compelling evidences indicate that the misfolding and oligomerization of Aß is the triggering event in AD, the mechanisms responsible for the initiation of Aß accumulation are unknown. In this study, we show that Aß deposition can be induced by injection of AD brain extracts into animals, which, without exposure to this material, will never develop these alterations. The accumulation of Aß deposits increased progressively with the time after inoculation, and the Aß lesions were observed in brain areas far from the injection site. Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention.
Keywords:
amyloid; prion; protein misfolding; disease transmission
http://www.nature.com/mp/journal/vaop/ncurrent/abs/mp2011120a.html
see more here ;
http://betaamyloidcjd.blogspot.com/2011/10/de-novo-induction-of-amyloid-deposition.html
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/alzheimers-disease-is-transmissible.html
TSS