The 2008 review (PDF 100KB)
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE
Light-touch review Summary and recommendations
1. The Spongiform Encephalopathy Advisory Committee (SEAC) has played an outstanding role in evaluating the scientific evidence relating to Transmissible Spongiform Encephalopathies (TSEs), assessing the risk they represent for human health and responding to the concerns of the public.
2. The Committee works well and is well supported by a highly efficient and effective secretariat. While there are several changes of detail that could be made to improve current arrangements, there is a clear consensus that they are broadly about right.
3. As required in any Cabinet Office review, the options of winding up the Committee and of providing its functions in a different way have been investigated. No sensible alternative arrangements have been identified.
4. That said, it is now clear that the risks from TSEs are low, although further work is needed in some areas. Most who gave evidence to this review could see a time in the not far distant future when SEAC would no longer be needed.
5. Better relations with European institutions are needed, especially with the European Food Safety Authority (EFSA); and greater clarity about the roles and accountabilities of the different bodies is needed.
6. It is heartening to see that virtually all the recommendations from the previous review have been implemented. The Committee has made a strong commitment to openness and has followed it through with rigour. It is essential
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The response to the 2008 review (PDF 21KB)
The “wiring diagram” described in the 2008 response (PDF 100KB)
> 4. That said, it is now clear that the risks from TSEs are low, although further work is needed in some areas. Most
> who gave evidence to this review could see a time in the not far distant future when SEAC would no longer be
I strongly disagree !
I would like to know by each scientist and or politician that made such a crude decision, what scientific rational they based this crude decision on ???
to me, it's like your in a 9 inning baseball game, in the 3rd inning tied up, and someone calls the game.
TWO plus decades into the BSE crisis, and we are still in the prehistoric realms of science in terms of Transmissible Spongiform Encephalopathies, if you look at the overall picture i.e. all species and the different TSEs, sources, routes, environmental risk factors, AND YES, I still believe the United States of America is covering up cases of Transmissible Spongiform Encephalopathy in the USA bovine, i.e. FOR PROFIT $$$
With the ever so emerging infectious TSE, in many species of the wild, game, and livestock, to humans, and espeically international trading of the TSE's due to the OIE and the USDA don't look, don't speak, don't tell policy, I strongly urge SEAC reconsider. It is of my opinion that SEAC's work has just begun, you cannot quit in the 3rd inning of a 9 inning game, one of which may have extra innings. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 7751
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
Wednesday, February 11, 2009 Atypical BSE North America Update February 2009
Saturday, January 24, 2009 Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report
TAFS1 Position Paper on Testing of Cattle for BSE (Revision January 2009)
Wednesday, January 28, 2009
TAFS1 Position Paper on Specified Risk Materials (January, 2009)
TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
TAFS1 Position Paper on Specified Risk Materials
November 25, 2008
Update On Feed Enforcement Activities To Limit The Spread Of BSE
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II ___________________________________
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007
Cattle feed delivered between 01/12/2007 and 01/26/2007
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
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
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
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
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
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV
Date: September 6, 2006 at 7:58 am PST
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Thursday, February 26, 2009
'Harmless' prion protein linked to Alzheimer's disease Non-infectious form of prion protein could cause brain degeneration
Sunday, February 15, 2009
Scientists warn of first ever case of human mad cow disease from blood plasma
Monday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
Saturday, January 24, 2009
Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report
When Atypical Scrapie cross species barriers
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
INFECTED AND SOURCE FLOCKS
There were 20 scrapie infected and source flocks with open statuses (Figure 3) as of April, 30, 2008. Twenty eight new infected and source flocks have been designated in FY 2008 (Figure 4); three source flocks were reported in April. ...snip
POSITIVE SCRAPIE CASES
As of April 30, 2008, 122 new scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2008 (Figure 6). Of these, 103 were field cases and 19* were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected in FY 2008 and reported by May 20, 2008). Positive cases reported for April 2008 are depicted in Figure 7. Eighteen cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 8). The most recent positive goat case was confirmed in February 2008 and originated from the same herd in Michigan as the other FY 2008 goat cases. ...snip
CAPRINE SCRAPIE PREVALENCE STUDY (CSPS)
However, four positive goats have been identified this fiscal year through field investigations. One was a clinical suspect submitted for testing and the other three originated from the birth herd of the clinical case.
ANIMALS SAMPLED FOR SCRAPIE TESTING
As of April 30, 2008, 26,703 animals have been sampled for scrapie testing: 23,378 RSSS, 1,517 goats for the CSPS study, 1,466 regulatory field cases, 270 regulatory third eyelid biopsies, and 72 regulatory rectal biopsies (chart 8).
TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...
PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007
Tuesday, June 3, 2008 SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
Monday, December 1, 2008 When Atypical Scrapie cross species barriers
Wednesday, January 28, 2009 TAFS1 Position Paper on BSE in small ruminants (January 2009)
Monday, September 1, 2008 RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [No. 00-072-1] September 1, 2008
OIE amending the Annex to Decision 2007/453/EC establishing the BSE status of Member States or third countries or regions thereof according to their BSE risk
Thursday, January 31, 2008
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 99th meeting held on 14th December 2007
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION
40. The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base
13 © SEAC 2007
cases in Texas and Alabama, with both scrapie and chronic wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?”
41. A member considered that this question appeared to be primarily related to possible links between animal and human TSEs in the USA. There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA. Current evidence does not suggest that CWD is a significant risk to human health. There are unpublished data from a case of human TSE in the USA that are suggestive of an apparently novel form of prion disease with distinct molecular characteristics. However, it is unclear whether the case had been further characterised, if it could be linked to animal TSEs or if other similar cases had been found in the USA or elsewhere. In relation to the possible public health implications of atypical scrapie, H-type BSE and CWD, research was being conducted to investigate possible links and surveillance was in place to detect any changes in human prion diseases. Although possible links between these diseases and human TSEs are of concern and require research, there is no evidence to suggest immediate public health action is warranted. The possible human health risks from classical scrapie had been discussed earlier in the meeting. Members noted that there are effective channels of discussion and collaboration on research between USA and European groups. Members agreed it is important that to keep a watching brief on new developments on TSEs.
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SEAC stated ;
There is no evidence that sCJD is increasing in the USA
i respectfully beg to differ. from 26 documented sCJD cases in 1996 rising to 157 documented sCJD cases in 2004, with 152 cases in 2005, to 143 in 2006, this would seem to be a rise in documented sporadic CJD cases from 1996 to me. ...TSS
CJD Cases examined ---------------------- Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD
1996 / 42 / 32 / 26 / 4 / 0 / 0 1997 / 115 / 68 / 57 / 9 / 0 / 0 1998 / 93 / 53 / 45 / 7 / 1 / 0 1999 / 114 / 69 / 61 / 8 / 0 / 0 2000 / 151 / 103 / 89 / 14 / 0 / 0 2001 / 208 / 116 / 106 / 9 / 0 / 0 2002 / 255 / 143 / 118 / 23 / 2 / 0 2003 / 272 / 174 / 132 / 41 / 0 / 0 2004 / 334 / 183 / 157 / 21 / 0 / 1* 2005 / 352 / 195 / 152 / 37 / 1 / 0 2006 / 372 / 186 / 143 / 30 / 0 / 1** 2007 / 120 / 68 / 35 / 7 / 0 / 0
A ProMED-mail post
 USA: National Prion Disease Pathology Surveillance Center Date: June 2007 Source: National Prion Disease Pathology Surveillance Center (USA) [edited]
CJD Cases examined ---------------------- Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD
1996 / 42 / 32 / 26 / 4 / 0 / 0 1997 / 115 / 68 / 57 / 9 / 0 / 0 1998 / 93 / 53 / 45 / 7 / 1 / 0 1999 / 114 / 69 / 61 / 8 / 0 / 0 2000 / 151 / 103 / 89 / 14 / 0 / 0 2001 / 208 / 116 / 106 / 9 / 0 / 0 2002 / 255 / 143 / 118 / 23 / 2 / 0 2003 / 272 / 174 / 132 / 41 / 0 / 0 2004 / 334 / 183 / 157 / 21 / 0 / 1* 2005 / 352 / 195 / 152 / 37 / 1 / 0 2006 / 372 / 186 / 143 / 30 / 0 / 1** 2007 / 120 / 68 / 35 / 7 / 0 / 0 TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2
*Acquired in UK ** Acquired in Saudi Arabia *** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007. **** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, 26 from 2007).
-- Cases are listed based on the year of death when available. If the year of death is not available, the year of sample receipt is used.
-- Referrals: Cases with possible or probable prion disease from which brain tissue or blood in the case of familial disease were submitted.
-- Inconclusive: Cases in which the samples were not sufficient to make a diagnosis.
-- Non-vCJD type unknown are cases in which the tissue submitted was adequate to establish the presence but not the type; in all cases, vCJD could be excluded.
-- Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
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Saturday, February 14, 2009 10:18 AM
A case-control study of sporadic Creutzfeldt-Jakob disease in Switzerland: analysis of potential risk factors with regard to an increased CJD incidence in the years 2001-2004
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518