Grassfarmer said:
bse-tester said:
Let us not forget how many millions of tons of TSE contaminated meat was consumed within the UK prior to the fire pits being filled with the carcasses of those that were diagnosed. Perhaps that meat may have had something to do with it????
Talk about ignorance of the subject bse-tester - what fire pits would those be? perhaps the ones that were used to deal with the 2001 outbreak of foot and mouth disease in the UK? 15 to 20 years after the large numbers of BSE cases occurred. No animal in the UK either proven or suspected of having BSE was ever burnt in an open pit. Talk about damaging your credibility :roll: :roll: :roll:
As Kathy says I hope the accuracy of your BSE test is better.
BSE: OPEN CREMATION OF CARCASSES
1. THIS NOTE IS TO INFORM THE PARLIAMENTARY SECRETARY (MR MACLEAN) OF THE NEED TO CARRY OUT AN OPEN CREMATION IN THE SOUTH WEST REGION.
Background
2. In disposing of BSE carcasses, either by incineration or burial, it has been our policy to avoid open cremations if at all possible. This is because of the adverse public reaction to THOSE WHICH TOOK PLACE IN THE SOUTH WEST in the early months of the slaughter policy.
snip...
Conclusion
4. In view of this an open cremation in the area is not UNAVOIDABLE. ...
http://www.bseinquiry.gov.uk/files/yb/1990/03/07007001.pdf
DISPOSAL OF BSE CARCASES: OPEN CREMATION
1. The Parliamentary Secretary will wish to be aware that an open cremation of BSE CARCASES took place yesterday evening in Devon. ...
http://www.bseinquiry.gov.uk/files/yb/1990/12/19001001.pdf
FURY AS COWS ARE BURNED
A SECRET operation to dispose of more than 100 BSE INFECTED CATTLE...
http://www.bseinquiry.gov.uk/files/yb/1990/12/19005001.pdf
July 2009
Greetings,
Finally, let us postulate shall we. Let us just postulate that for just this one time, that mad cow disease and all other Transmissible Spongiform Encephalopathies in all other species, that have been feeding on these species, and in the laboratory studies that proves oral transmission in many different species of these TSE, and in some the lateral and vertical transmission, let us all ignore this as well, just this one time. let's just for this one second play like the spontaneous mad cow disease is for real (which i don't believe for one second), and that mad cow disease just pops up from now and then, i believe it was guesstimated to be around to be like sporadic CJD i.e. 1-2 humans per million. but some studies suggested 3 to 8 cases of spontaneous BSE per million head of cattle, but lets just say for grins, 1-2 per million as with sporadic CJD. Therefore, if we have about 100 million cattle in the U.S., we should have 100-200 cases of BSE each year, if you consider 100 million head of cattle per year in the USA.
so, my question, WHERE ARE THESE MAD COWS AT, AND OR WHERE ARE THEY BURIED AT since that last case of mad cow disease in the USA was made public around March of 2006 ???
by what miracle and how has the USA bovine been protected from mad cow disease for so many years, decades $$$
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Disposal of meat and bone meal (MBM) derived from specified risk material (SRM) and over thirty month scheme carcasses by landfill The Committee was asked to consider a quantitative risk assessment of the disposal of meat and bone meal derived from specified risk material and over thirty month scheme carcasses by landfill, prepared in response to a request from the Committee at its June 1999 meeting.
The Committee was asked whether, in the light of the results of the risk assessment, it held to its earlier published (June 1999) view that landfill was an acceptable outlet for MBM of any origin, although it retained a preference for incineration. The Committee reiterated that it had a strong preference for incineration as the favoured route for the disposal of MBM and were uneasy about the use of landfill for the disposal of this material. If there were cases where incineration was not practical the Committee felt it would be preferable for any material going to landfill to be pressure-cooked first or possibly stored above ground prior to incineration.
http://www.seac.gov.uk/summaries/summ_0700.htm
Disposal of BSE suspect carcases It is the Department's policy to dispose of BSE suspects by incineration wherever feasible. No BSE suspect carcases have been landfilled since 1991.
http://www.defra.gov.uk/animalh/bse/publichealth/notification.html#disp
OPINION ON
THE USE OF BURIAL FOR DEALING WITH ANIMAL
CARCASSES AND OTHER ANIMAL MATERIALS THAT
MIGHT CONTAIN BSE/TSE
ADOPTED BY THE
SCIENTIFIC STEERING COMMITTEE
MEETING OF 16-17 JANUARY 2003
The details of the SSC's evaluation are provided in the attached report. The SSC
concludes as follows:
(1) The term "burial" includes a diversity of disposal conditions. Although burial is
widely used for disposal of waste the degradation process essential for BSE/TSE
infectivity reduction is very difficult to control. The extent to which such an
infectivity reduction can occur as a consequence of burial is poorly characterised.
It would appear to be a slow process in various circumstances.
(2) A number of concerns have been identified including potential for groundwater
contamination, dispersal/transmission by birds/animals/insects, accidental
uncovering by man.
(3) In the absence of any new data the SSC confirms its previous opinion that animal
material which could possibly be contaminated with BSE/TSEs, burial poses a
risk except under highly controlled conditions (e.g., controlled landfill).
SNIP...
4. CONCLUSION
In the absence of new evidence the opinion of the SSC "Opinion on Fallen Stock"
(SSC 25th June 1999) must be endorsed strongly that land burial of all animals and
material derived from them for which there is a possibility that they could
incorporate BSE/TSEs poses a significant risk. Only in exceptional circumstances
where there could be a considerable delay in implementing a safe means of disposal
should burial of such materials be considered. Guidelines should be made available
to aid on burial site selection.
4 PAGES;
http://europa.eu.int/comm/food/fs/sc/ssc/out309_en.pdf
HERE in the USA, we use the S.S.S. policy, shoot, shovel, and shut the hell up. ...
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.
http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
BSE CARCASE INCINERATION : UPDATE
1. In the first 9 months of 1989, 69% of suspect carcases were incinerated and 31% were buried. ...
http://www.bseinquiry.gov.uk/files/yb/1989/12/12009001.pdf
http://www.bseinquiry.gov.uk/files/yb/1990/12/10003001.pdf
Neither did Mr Hogg specify the date of burials, but he did tell Dr Strang that three BSE-suspect carcasses had been buried last year.
Asked by Dr Strang to list the methods of disposal that are permitted, compared with the methods at present in operation, Mr Hogg did not provide an answer to the question.
Mr Hogg did not say that no material from BSE suspects was allowed to be buried in landfill sites. However, a British government paper submitted to the EU before last year's Florence summit said that 57 legal instruments had been passed between June 1988 and May 1996, including "a requirement that all cattle which are suspected of having BSE are slaughtered and destroyed".
Early this morning, in a further twist to the story, a MAFF spokesman said that Mr Hogg had given wrong information in his answers. "There has been a mistake and a new reply will be published tomorrow," he said.
Last month, in a written Commons reply, Ms Jackson was told by the Agriculture minister Tony Baldry: "Cattle suspected of showing clinical signs of the disease are disposed of by direct incineration in plants contracted to MAFF."
Mr Baldry said that BSE suspects were not slaughtered under the over- 30-month scheme - the precautionary measure demanded by the EU as a prerequisite for lifting the ban on beef exports.
Ms Jackson subsequently raised the question of BSE burial in a Commons debate on 17 February. She was told by Roger Freeman, the Cabinet minister in charge of the cattle cull: "There are no mass graves in our countryside and there is no fear of disease."
http://www.independent.co.uk/news/buried-bse-cattle-pose-health-risk-1272065.html
The most pressing recommendation is however that carcases of affected animals should be condemned and destroyed...
http://www.bseinquiry.gov.uk/files/yb/1988/06/23002001.pdf
The need to revert to mass incineration in exceptional circumstances cannot, however, be entirely precluded.
http://www.bseinquiry.gov.uk/files/yb/1988/12/02006001.pdf
is burial wise ?
http://www.bseinquiry.gov.uk/files/yb/1988/12/13003001.pdf
http://www.bseinquiry.gov.uk/files/yb/1988/12/19002001.pdf
BSE: CARCASE DISPOSAL: PROBLEMS
1. AN AVERAGE OF 130 CARCASES PER WEEK were currently being disposed of by burial OR BURNING.
http://www.bseinquiry.gov.uk/files/yb/1989/04/00005001.pdf
Carcase Disposal - Current Arrangements
2. BSE carcases are disposed of by burial or cremation on or off farm.
snip...
Cremation
(a) On Farm 1733
http://www.bseinquiry.gov.uk/files/yb/1989/04/00009001.pdf
see bovine incinerator
http://www.bseinquiry.gov.uk/files/yb/1989/04/03006001.pdf
PROVISION ON INCINERATION
http://www.bseinquiry.gov.uk/files/yb/1989/05/02007001.pdf
Commercial incineration
http://www.bseinquiry.gov.uk/files/yb/1989/06/20017001.pdf
http://www.bseinquiry.gov.uk/files/yb/1990/12/18003001.pdf
Epidemiology Update March 23, 2006
As of today, 13 locations and 32 movements of cattle have been examined with
27 of those being substantially completed. Additional investigations of
locations and herds will continue. In addition, state and federal officials
have confirmed that a black bull calf was born in 2005 to the index animal
(the red cow). The calf was taken by the owner to a local stockyard in July
2005 where the calf died. The calf was appropriately disposed of in a local
landfill and did not enter the human or animal food chain.
http://www.aphis.usda.gov/newsroom/hot_issues/bse/bse_al_epi-update.shtml
> The calf was appropriately disposed of in a local
> landfill and did not enter the human or animal food chain.
well, back at the ranch with larry, curly and mo heading up the USDA et al,
what would you expect, nothing less than shoot, shovel and shut the hell up.
no mad cow in USA, feed ban working, no civil war in Iraq either.
but what has past history shown us, evidently it has shown the USDA et al
nothing ;
http://www.prwatch.org/node/4624
Sunday, April 12, 2009
BSE MAD COW TESTING USA 2009 FIGURES
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.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/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
Saturday, June 13, 2009
BSE FEED VIOLATIONS USA UPDATE From 01/01/2009 To 06/10/2009
http://madcowfeed.blogspot.com/2009/06/bse-feed-violations-usa-update-from.html
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Rare BSE mutation raises concerns over risks to public health
SIR - Atypical forms (known as H- and L-type) of bovine spongiform encephalopathy (BSE) have recently appeared in several European countries as well as in Japan, Canada and the United States. This raises the unwelcome possibility that variant Creutzfeldt-Jakob disease (vCJD) could increase in the human population. Of the atypical BSE cases tested so far, a mutation in the prion protein gene (PRNP) has been detected in just one, a cow in Alabama with BSE; her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008). This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail:
[email protected] Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA
NATURE|Vol 457|26 February 2009
http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html
see full text ;
Monday, May 11, 2009
Rare BSE mutation raises concerns over risks to public health
http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html
Monday, June 01, 2009
Biochemical typing of pathological prion protein in aging cattle with BSE
snip...
Greetings,
O.K., let me get this straight, we have typical, U.K. c-BSE, we have now a spontaneous atypical h-BSE and l-BSE, of which they are now just calling an 'old cow disease', which happens spontaneously without any route or source, just happens.
OH, and then we have the new/old ibncBSE, of which is just another 'old cow prion disease', another one of those spontaneous events $$$
IT SEEMS there is a pattern here to make all Transmissible Spongiform Encephalopathies a spontaneous event, even though there is no such evidence what so ever.
WITH all the sub-types of TSE showing up now in the Scrapie, BSE, CWD, (all of which has been rendered and fed back to livestock producing animals for human and animal feed), and even in humans i.e. CJD, there is no way, they know for a fact that all are of a spontaneous, sporadic event, that just happened due to a twisted up protein that folded the wrong way by itself, from no route and no source. they do NOT know if any of these atypical TSE are of a spontaneous old cows prion disease or not, but yet they preach it like it's the gospel $$$
I don't believe them today, and i will never believe that 85%+ of all human sporadic CJD, just happens without any route and source from anything. ...
kind regards, terry
Absence of spontaneous disease and comparative prion susceptibility of transgenic mice expressing mutant human prion proteins
snip... see full text ;
http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.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
DOI: 10.3201/eid1508.081218
Suggested citation for this article: Espinosa J-C, Herva M-E, Andréoletti O, Padilla D, Lacroux C, Cassard H, et al.
Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie.
Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
Transgenic Mice Expressing Porcine Prion Protein Resistant to Classical Scrapie but Susceptible to Sheep Bovine Spongiform Encephalopathy and Atypical Scrapie
Juan-Carlos Espinosa,1 María-Eugenia Herva,1 Olivier Andréoletti, Danielle Padilla, Caroline Lacroux, Hervé Cassard, Isabelle Lantier, Joaquin Castilla, and Juan-María Torres
Author affiliations: Centro de Investigación en Sanidad Animal, Madrid, Spain (J.-C. Espinosa, M.-E. Herva, D. Padilla, J. Castilla, J.-M. Torres); École Nationale Vétérinaire de Toulouse, Toulouse, France (O. Andréoletti, C. Lacroux, H. Cassard); and Centre Institut National de la Recherche Agronomique de Tours, Nouzilly, France (I. Lantier)
1These authors contributed equally to this article.
How susceptible pigs are to infection with sheep prions is unknown. We show, through transmission experiments in transgenic mice expressing porcine prion protein (PrP), that the susceptibility of this mouse model to bovine spongiform encephalopathy (BSE) can be enhanced after its passage in ARQ sheep, indicating that the pathogenicity of the BSE agent is modified after passage in sheep. Transgenic mice expressing porcine PrP were, nevertheless, completely resistant to infection with a broad panel of classical scrapie isolates from different sheep PrP genotypes and with different biochemical characteristics. The atypical (Nor98 like) isolate (SC-PS152) was the only scrapie isolate capable of transmission in these mice, although with a marked transmission barrier. Unexpectedly, the atypical scrapie agent appeared to undergo a strain phenotype shift upon transmission to porcine-PrP transgenic mice and acquired new strain properties, suggesting that atypical scrapie agent may exhibit different phenotypes depending on the host cellular PrP or other genetic factors.
snip...
Discussion
In this study, transgenic mice expressing porcine PrP (8) were used to assess the transmission capacity of a wide range of TSE agents from sheep. Our results indicated that none of the classical scrapie isolates tested was transmitted to our porcine PrP mouse model after intracerebral inoculation (Table), suggesting a highly (if not completely) resistance to the classical scrapie strains tested independently of their origin and biochemical signature. The absence of successful transmission of the SC-PS48 isolates with an unglycosylated bands of 19 kDa-like BSE suggests a BSE-unrelated origin for these BSE-like scrapie strains.
The atypical isolate SC-PS152 was the only scrapie isolate able to infect the Po-PrP mouse model after intracerebral inoculation (Table), albeit with a low efficiency of infection in the first passage (attack rate 16%). These results suggest the potential ability of atypical scrapie prions to infect pigs, although with a strong transmission barrier. Given the increasing number of atypical scrapie cases found in Europe and in North America, the potential ability of atypical scrapie to adapt to the pig becoming more easily transmitted could raise concerns about the potential danger of feeding ruminant meat and bone meal to swine.
In our transmission experiments, an obviously shorter survival period (458 ± 11 dpi) and an increased attack rate (100%) were observed in PoPrP-Tg001 mice inoculated with sheep BSE (Table) compared with those inoculated with the original cattle BSE (>650 dpi, 19%). These last figures correlate well with those reported for other cattle BSE isolates (Table). Differences in survival times were maintained after subsequent passages in this mouse model (Table), suggesting that the increased infectivity of sheep BSE cannot be linked to a higher infectious titer in the initial inoculum but must be the outcome of a modification in the pathogenicity of the agent. We can also rule out that the primary amino acid sequence of the ovine PrPSC leads to more efficient conversion of porcine PrPC because scrapie isolates from sheep with the same ARQ-PrP genotype were not able to infect these mice (Table). Taken together, the increased infectivity of sheep BSE in the porcine PrP mouse model must be considered as increased pathogenicity of the agent attributable to its passage in sheep. These features support previous results indicating that the BSE agent modifies its biological properties after passage in sheep, with the result that its pathogenicity increases in transgenic mice expressing bovine PrP (24). An increased pathogenicity of ovine BSE was also reported in conventional RIII mice when compared with retrospective cattle BSE experiments (36). In other prion strains, passage through an intermediate species has also been noted to alter host susceptibility (37).
The enhanced infectivity of the BSE agent after its passage in ARQ sheep raises concern about its potential danger for other species, including humans. This question, as well as others related to the infectivity of the new porcine prion generated in this study, is currently being addressed in transmission experiments using transgenic mice expressing human PrP.
Upon passages in porcine PrP transgenic mice, the BSE agent retained most of its biochemical properties, except for its PrPres glycoprofile in which some differences were appreciable. Our comparative analysis of cattle BSE and sheep BSE upon transmission in porcine PrP transgenic mice showed that both agents exhibit similar molecular (Figure 2) and neuropathologic properties (Figure 4). These features were preserved after subsequent passages. These results suggest that, despite their modified pathogenicity, the 2 porcine prions generated share the same biochemical and neuropathologic properties, regardless of whether the BSE agent used to inoculate the mice was obtained from ARQ sheep or cows. In agreement with these results, the increased infectivity of sheep BSE previously observed upon transmission in bovine PrP transgenic mice was not reflected in its molecular or neuropathologic properties (24).
The atypical scrapie (SC-PS152) agent appeared to undergo a strain phenotype shift upon transmission to porcine PrP transgenic mice. Surprisingly, this novel strain phenotype was similar to that of sheep BSE propagated in the same mice in terms of several features: 1) survival times observed after stabilization in PoPrP-Tg001 mice (second passages) were similar (Table); 2) PrPres molecular profiles of the 2 agents in porcine PrP mice were indistinguishable (Figure 3); and 3) vacuolation profiles observed in second passages largely overlapped (Figure 4).
These findings could reflect the evolutionary potential of prion agents upon transmission to a foreign host able to promote strain shift and emergence of new properties (38,39). The converging molecular, neuropathologic, and biological properties of atypical scrapie and sheep BSE upon propagation in porcine transgenic mice could be the consequence of a restriction imposed by the porcine PrPC, which might only admit a few options as it changes its conformation to PrPSC.
Our results could also suggest a common origin for sheep BSE and atypical scrapie agents, which may exhibit different phenotypes depending on the host PrPC or other host factors.
Although this last explanation seems to be less likely, so far we cannot draw any definitive conclusion on this issue. Whichever the case, the ability of an atypical scrapie to infect other species and its potential capacity to undergo a strain phenotype shift in the new host prompts new concerns about the possible spread of this uncommon TSE in other species as a masked prion undistinguishable from other strains.
snip... see full text ;
http://www.cdc.gov/eid/content/15/8/pdfs/08-1218.pdf
Saturday, May 2, 2009
APHIS AND WHO PLAN TO EXEMPT THE ATYPICAL SCRAPIE NOR-98 FROM REGULATIONS AT MEETING THIS MONTH
http://nor-98.blogspot.com/2009/05/aphis-and-who-plan-to-exempt-atypical.html
SEE HISTORY OF THE NOR-98 CASES DOCUMENTED IN THE USA, to date ;
Wednesday, July 1, 2009
Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)
http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html
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
http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html
IN CONFIDENCE
TRANSMISSION TO CHIMPANZEE'S
1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not. 2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of filed isolates subsequently strain typed in mice be inoculated by the appropriate routes (i/c, i/p and i/v).
3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
4. In view of Dr. Gibbs' probable use of chimpanzees Mr. Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
5. A positive result from a chimpanzee challenged severely 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.
A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding man's susceptibility. In the meantime no doubt the negativity would be used defensively. IT WOULD HOWEVER BE COUNTERPRODUCTIVE IF THE EXPERIMENT BECAME POSITIVE. We may learn more about public reactions following next Monday's meeting.
R. Bradley
23 September 1990
CVO (+ Mr Wells' comments)
Dr T W A Little
Dr B J Shreeve
90/9.23/1.1
http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
IN CONFIDENCE
CHIMPANZEES
http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf
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://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.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.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle,
*** did not produce the same clinical signs of brain lesions characteristic of BSE. ***
3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result 337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells, G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice, Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I., Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier, Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I., Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate that 'New Variant' CJD is Caused by the BSE Agent, Nature, 389, 498–501 339 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R., Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994) Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases, 169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4 SCIENCE 84 would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345 3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility.
http://www.bseinquiry.gov.uk/pdf/volume2/chapter3.pdf
http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf
Visit to USA ... info on BSE and Scrapie
http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Friday, May 29, 2009
Characterization of a U.S. Sheep Scrapie Isolate with Short Incubation Time
http://scrapie-usa.blogspot.com/2009/05/characterization-of-us-sheep-scrapie.html
Sunday, May 17, 2009
WHO WILL WATCH THE CHILDREN ?
USDA CERTIFIED DEAD STOCK DOWNER COW SCHOOL LUNCH PROGRAM
IF you think for one minute the largest beef recall in USA history was due to a few bovines being mistreated, think again. These dead stock downer cattle are the most high risk cattle for mad cow diseases, and other disease, and we have been feeding them to children all across the USA via the school lunch program for years. who will watch the children in the years, decades to come for CJD ??? or will any cases there from just be another spontaneous and or sporadic event i.e. happenstance of bad luck $$$
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
SPORADIC CJD CASES RISING IN U.S.A 2009 UPDATE
Monday, April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
National Prion Disease Pathology Surveillance Center Cases Examined1
(December 31, 2008)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 42 32 28 4 0 0
1997 115 68 59 9 0 0
1998 93 53 45 7 1 0
1999 115 69 61 8 0 0
2000 151 103 89 14 0 0
2001 210 118 108 9 0 0
2002 258 147 123 22 2 0
2003 273 176 135 41 0 0
2004 335 184 162 21 0 13
2005 346 193 154 38 1 0
2006 380 192 159 32 0 14
2007 370 212 185 26 0 0
2008 383 228 182 23 0 0
TOTAL 30715 17756 1490 254 4 2
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 acquired in Saudi Arabia; 5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Rev 2/13/09 National
http://www.cjdsurveillance.com/pdf/case-table.pdf
http://www.cjdsurveillance.com/resources-casereport.html
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
*5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; *6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Greetings,
it would be interesting to know what year these atypical cases occurred, as opposed to lumping them in with the totals only.
are they accumulating ?
did they occur in one year, two years, same state, same city ?
location would be very interesting ?
age group ?
sex ?
how was it determined that nvCJD was ruled out ?
from 1997, the year i started dealing with this nightmare, there were 28 cases (per this report), up until 2007 where the total was 185 cases (per this report), and to date 2008 is at 182. a staggering increase in my opinion, for something that just happens spontaneously as some would have us believe. i don't believe it, not in 85%+ of all sporadic CJD cases. actually, i do not believe yet that anyone has proven that any of the sporadic CJD cases have been proven to be a spontaneous misfolding of a protein. there are many potential routes and sources for the sporadic CJD's. ...TSS
please see full text here ;
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
Saturday, April 04, 2009
An unusually presenting case of sCJD-The VV1 subtype Volume 111, Issue 3, Pages 282-291 (April 2009)
http://creutzfeldt-jakob-disease.blogspot.com/2009/04/unusually-presenting-case-of-scjdthe.html
IT seems we have come full circle from the 'ORIGINAL 10' i.e. the 1st 10 adolescents in the UKBSEnvCJD only theory. and now we find us at the 1st 10 in USA, or is it the first 10, or the tip of the iceburg, many that went undocumented ???
PLEASE tell me how two events can be so different ??? from the U.K. first 10, to some 13 years later, the U.S. first ten $$$
lets look at the full circle, to date ;
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
VS
Sunday, August 10, 2008
A New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html
Monday, June 22, 2009
PrPTSE in muscle-associated lymphatic tissue during the preclinical stage of mice orally-infected with BSE
http://bse-atypical.blogspot.com/2009/06/prptse-in-muscle-associated-lymphatic.html
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
please see sources here ;
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
Elsevier Editorial System(tm) for The Lancet Infectious Diseases 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. snip...
see full text 31 pages ;
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
see also BMJ year 2000 and 1999 ;
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... Terry S Singeltary (2 January 2000)
--------------------------------------------------------------------------------
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... 2 January 2000
Terry S Singeltary retired Send response to journal: Re: U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.
To be continued...
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
Re: vCJD in the USA * BSE in U.S. Terry S Singeltary (15 November 1999)
In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease. Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know. My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD. The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?
CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.
No BSE in the U.S.A.? I would not be so sure of that considering that since 1990;
Since 1990 the U.S. has raised 1,250,880,700 cattle;
Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;
There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;
Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;
Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.
I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.
Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.
It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........
The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.
Terry S. Singeltary Sr. P.O. Box 42, Bacliff, Texas 77518 USA
[email protected]
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
TSS