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In a [http://www.prweek.com/uk/news/article/564125/Primed+pump/ follow up story] (sub req'd), PR Week reports:
Check out this introduction article on Geothermal power:
http://www.articleworld.org/Geothermal_power
The Pew Charitable Trusts were established by the heirs of the Sun Oil (Sunoco) fortune. J. Howard Pew and it's current board is mostly made up of Pew family members. It's purpose is tax avoidance and increased personal profits for Pew family members and friends through manipulation of public opinion.
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Credibility is the cornerstone of PR. The Pew foundation has been a master of this art. It's frequently branded as "liberal" and "environmental" but when the bottom line detail is programs are studied the truth is seen.
A duck in a rain coat is still a duck.
##################### Bovine Spongiform Encephalopathy #####################
Subject: PrP(d) accumulation in organs of ARQ/ARQ sheep experimentally infected with BSE by peripheral routes
Date: June 19, 2006 at 8:11 am PST
PrP(d) accumulation in organs of ARQ/ARQ sheep experimentally infected with BSE by peripheral routes.
Lezmi S, Ronzon F, Bencsik A, Bedin A, Calavas D, Richard Y, Simon S, Grassi J, Baron T.
Agence Francaise de Securite Sanitaire des Aliments (AFSSA), Lyon cedex 07, France.
To study the pathogenesis of bovine spongiform encephalopathy infection in small ruminants, two Lacaune sheep with the AA136RR154QQ171 and one with the AA136RR154RR171 genotype for the prion protein, were inoculated with a brain homogenate from a French cattle BSE case by peripheral routes. Sheep with the ARQ/ARQ genotype are considered as susceptible to prion diseases contrary to those with the ARR/ARR genotype. The accumulation of disease-associated prion protein (PrP(d)) was analysed by biochemical and immunohistochemical methods. No PrP(d) accumulation was detected in samples from the ARR/ARR sheep 2 years post inoculation. In the two ARQ/ARQ sheep that had scrapie-like clinical symptoms, PrP(d) was found in the central, sympathetic and enteric nervous systems and in lymphoid organs. Remarkably, PrP(d) was also detected in some muscle types as well as in all peripheral nerves that had not been reported previously thus revealing a widespread distribution of BSE-associated PrP(d) in sheep tissues.
snip...
Results and Discussion
For all samples analysed from the ARR/ARR sheep, no PrPd was detected by any of the three
PrPd detection methods used (table 1). This result correlates with the higher genetic resistance
to TSE associated with this genotype naturally affected with scrapie (Elsen et al., 1999) or
orally infected with the BSE agent (Jeffrey et al., 2001). However, resistance of the
ARR/ARR sheep challenged with TSE infection is not considered complete since natural
scrapie cases have been reported in sheep with this genotype (Buschmann et al., 2004); (Ikeda
et al., 1995) (French surveillance program; unpublished data). Furthermore, BSE has been
transmitted to ARR/ARR sheep by the intra-cerebral route (Houston et al., 2003b).
In both ARQ/ARQ sheep, the CNS (including retina), the lymphoid system and the
autonomous nervous system were identified by each method as major sites of PrPd
accumulation (table 1 ; figure 1) and were also described earlier by other groups in
experimentally BSE affected sheep (Foster et al., 2001; Jeffrey et al., 2001) as well as in
naturally scrapie-affected sheep (Jeffrey et al., 2001; van Keulen et al., 1999). In the CNS, the
quantities of abnormal PrP, expressed as equivalent in recPrP, were estimated by ELISA at up
to 13000 ng/g of brainstem tissue. Comparatively, the levels found in 13 ARQ/ARQ or
ARQ/VRQ sheep clinically affected with natural scrapie averaged 40 000 ± 20 000 ng of
PrPd/g of CNS tissues. Lymphoid organs accumulated lower levels of PrPd and large
quantities of material were required to detect a signal by WB in the mandibular or iliac medial
Copyright @ Acta Biochimica Polonica, Paper in Press, No. 1273
- 5 -
lymph nodes (LN) of SB3 (Figure 1). In the spleen of SB1 and SB3, 46 and 2 ng equivalent of
PrPd/g of tissue were detected, respectively. In the ileum, 232 ng equivalent of PrPd /g of
tissue was detected and correlated with a higher number and size of germinal centres when
compared to spleen or iliac LN. The mean quantity of PrPd in the CNS was 187 and 36 fold
greater than the quantities determined respectively in spleen and in the intestine.
Qualitatively, different types of PrPd deposits in the brain were identified from the frontal
cortex to the lumbar spinal cord. These PrPd deposits were mainly identical to those
previously identified in scrapie- or BSE-affected sheep (Gonzalez et al., 2002; Ryder et al.,
2001). In the retina, PrPd accumulation was mainly detected in the ganglionar layer (1), intern
(2) and extern (4) plexiform layers (numbers corresponding to the different layers in the
retina, figure 2a). Interestingly, in the enteric nervous system of ARQ/ARQ sheep, PrPd was
detected associated with neurons (figure 2g) as well as in the coeliac ganglia in which intraand
peri-neuronal PrPd deposits were visualized (figure 2h). In the adrenal gland, two types of
PrPd accumulation were observed as dense intracellular or synaptic-like deposits (figure 2i).
In lymphoid organs, PrPd was detected in germinal centres of secondary lymphoid follicles,
in follicular dendritic cells and in tingible body macrophages (figure 2j). PrPd was also
detected in cells with a morphology consistent with macrophages in the subcapsular sinus of
some lymph nodes (figure 2j, arrowhead, table 1*). These observations are in agreement with
previous results obtained both in sheep naturally affected with scrapie (Ersdal et al., 2005);
(Jeffrey et al., 2000); (Lezmi et al., 2001) and in experimentally BSE-infected sheep (Lezmi
et al., 2001); (Jeffrey et al., 2001). Interestingly, not all germinal centres were labelled for
PrPd; this partial absence of labelling in germinal centres (as in tonsils) was not observed in
samples from 13 natural scrapie-infected sheep in which all lymphoid germinal centres were
positively labelled for PrPd. This agreed with data describing an early and systematic immune
system involvement in lambs affected with scrapie (Andreoletti et al., 2000) which was not a
Copyright @ Acta Biochimica Polonica, Paper in Press, No. 1273
- 6 -
feature of BSE agent infection in sheep during the first passage (Jeffrey et al., 2001; Martin et
al., 2005).
In our study, as opposed to previous published results, in both ARQ/ARQ sheep, PrPd was
detected by IHC in all motor nerves and associated with Schwann’s cells (figure 2d, e). PrPd
deposits were similarly detected in all other tissue samples containing peripheral nerves, most
notably in nerves in muscle samples. This observation was not reported in other studies with
sheep BSE (Foster et al., 2001; Jeffrey et al., 2001). However, we observed the same type of
deposits in two other sheep (ARQ/VRQ) naturally affected with scrapie (data not shown) and
two previous articles report similar data in sheep with natural scrapie (Archer et al., 2004);
(Groschup et al., 1999).
PrPd presence was also identified in striated muscles for both ARQ/ARQ sheep. These
deposits were associated with neuromuscular spindles that are highly innervated structures
made of groups of myocytes surrounded by a thin fibrous capsule (figure 2k, l) and are a
specialized subset of myocytes implicated in proprioception. In the tongue of sheep, the
accumulation of PrPd in these structures was less evident. Only one study reported the PrPd
presence in the muscle of sheep affected with scrapie using IHC and ELISA (Andreoletti et
al., 2004). Here, sampling and analysis of different muscles were not systematic and thus the
ELISA/IHC results were not correlated. However, the accumulation in muscle tissue of PrPd
in sheep affected with scrapie is not systematic (Andreoletti et al., 2004). Recently,
pathological prion protein was detected in muscles of hamsters and mice infected with rodentadapted
BSE or vCJD (Thomzig et al., 2006). Previously, other studies failed to detect prion
in nerves and muscles of BSE- or scrapie-infected sheep (Foster et al., 2001); (Hamir et al.,
2004) possibly relying on the use of different pre-treatments and antibodies.
In conclusion, we have shown that the inoculation of the BSE agent of French origin by
peripheral routes to Lacaune sheep lead to the development of the clinical disease only in
Copyright @ Acta Biochimica Polonica, Paper in Press, No. 1273
- 7 -
ARQ/ARQ sheep. The distribution of PrPd in ARQ/ARQ sheep infected with BSE was very
similar to that described in natural scrapie. Overall, we demonstrated for the first time the
presence of PrPd in muscles and nerves of sheep infected experimentally with BSE agent,
which stresses the potential risk for humans related to consumption of sheep products from
sheep naturally infected with BSE. ...
snip...end...TSS
http://www.actabp.pl/pdf/Preprint/20061273.pdf
TSS
#################### https://lists.aegee.org/bse-l.html ####################
archives of http://mp3.rbnlive.com/Karen06.html the first of this radio show for MAY14 With Doug Herman she says its the policy of gov. to control us with disasters and crisis management
MilitaryWeek.com
Without Reservation
by Karen Kwiatkowski, Ph.D., Lt. Col. USAF (ret.)
posted 12 Jun 06
The Rise and Fall of a Great Leader
A freakishly successful character – a man no one, not family, or friend, or peer, or supervisor, ever expected to make much of himself – is again in the news.
He appears boyish in his photographs, and in many ways seems younger than he is. In spite of his apparent success as a powerful leader of men, he is plagued by stories of a misspent youth and early adult years. His success has been marred by repeated anecdotes, many of them ugly, some less than honorable, often insulting.
He purports to be a religious man, yet has lives and acts in such a way that gentle clergy, preaching to thousands of their religious faithful demure, and turn their heads away. Many of the faithful weep at his public piety, asking God, "Why?"
An icon of a grand and glorious human battlefield, he believes deeply in the righteousness of his cause.
No, I am not speaking of the American President. Instead, lying peacefully deceased for the final time, we hope, is Jordanian-born Abu Mus'ab al-Zarqawi
Much has been written about the forsaken Zarqawi. While the 500-pound bombs found their target on June 7th, the jig was up a few months ago, when the mainstream American press began seriously questioning the Zarqawi myth. It was a good myth, and it died a suitable death, just before being completely politically discredited back home in America.
George W. Bush is happy that this tattooed Muslim miscreant has been delivered head-on-a-platter-style, as are we all. Bush said this means, "the ideology of terror has lost one of its most visible and aggressive leaders."
This interesting statement comes on the heels of another, even larger, explosion – that of American interest in what Marines and Army troops are doing in places like Haditha Indeed, one might logically ask what is an "ideology of terror" and who best demonstrates it?
Of course, President Bush and his administration, and the genuflecting American Congress will not ask this question. The problem of culpability will be left to local, military and international courtrooms years from now, and only after the leaders of the Bush administration have been pardoned in advance and cozily ensconced within new compounds in St Michaels, Maryland and old ranches in Wyoming, New Mexico, and Texas.
Are there lessons in the Zarqawi case? As Bush himself has said, no decrease in violence in Iraq is expected. As the 24-hour curfew in Iraq cities on Friday after Zarqawi’s death illustrated, even more violence was, and is, expected. Now that Al Qaeda’s numero uno in Iraq is dead, will American troops come home, and cease the occupation of Iraq? Actually, more American troops are on their way to Iraq, as Iraq soldiers desert in droves,. and the coalition of the willing evaporates completely. Analyses of the impact of Zarqawi’s death on the future of Iraq are generally pessimistic
But there is something to be learned from the violent end of Zarqawi. This man, both in truth and in myth, had become a distinct liability for his many fathers. He was increasingly at odds with al Qaeda for his lack of strict Islamic creed and his ineffectiveness. He had been steadily losing support of average Iraqis as they try to determine how best to retake their country from American military and economic domination. Lastly, he was a growing political liability for the American and British media campaign promoting the idea that failures of occupation were just because of Iraqi dead-enders and foreign agents, like those Zarqawi supposedly led.
In practical terms, the death of Zarqawi means little to the Iraqis, or to Iraq. It does not seriously alter the path that country is on, whether towards more tyranny and chaos, or towards some distant peace and prosperity. However, the lessons that American politicians and leaders may take from the death of Zarqawi could be far more significant.
What are these lessons for political leaders? I can think of three. First, political propaganda is designed for a purpose, and when it no longer works efficiently towards that purpose, it is adapted, altered and modified. Emotional attachment to outdated, counterproductive propaganda has no place in the cold rational world of political power.
Second, myths may be created, and they may be destroyed. Along these lines, there has been some debate over who will receive the $25 million bounty for the head of Zarqawi. Would it be seemly to award this bounty to our own people, whether American intelligence or Iraqi puppets? What would the published identity of the "finder" of Zarqawi say about our long-term use of this Jordanian thug in the past several years? Myths, unlike diamonds, are not forever.
A final lesson from the life and death of Zarqawi is that decisions will, at some point, be made. Like 500-pound laser-guided bombs, these decisions can rain down on their unsuspecting targets with deadly and destructive results.
George W. Bush is today, by his own characterization, the leader of the "free" world, and the "decider." The American Congress, by its own characterization, is a constitutionally constrained legislative and deliberative body, owning the sole authority in America to declare war, and honorably bound to the service and interests of average Americans – some 65% of whom believe invading Iraq was the wrong thing to do, and oppose the continued occupation.
These fanciful tales – Bush as Freedom Fighter and the republican nobility of the American Congress – like all political myths, have a limited useful lifespan. Like the Zarqari fairy tale, they become vulnerable and unprotected when Americans themselves begin to look at the evidence.
© 2006 Karen Kwiatkowski
##################### Bovine Spongiform Encephalopathy #####################
CJD WATCH MESSAGE BOARD
TSS
EXPORT of potential USDA CERTIFIED ATYPICAL AND TYPICAL TSE
Sat Jun 17, 2006 13:19
71.248.130.63
Greetings,
Thought some of you might be interested in the USDA exports of potential USDA CERTIFIED ATYPICAL AND TYPICAL MAD COW BRAINS, SWEETBREADS, BOVINE FROZEN OFFAL, AND LIVE CATTLE. Interestingly, the USA may be the one to blame from there consistent lies and deceit and what they have exported globally for decades, to blame for spreading sporadic CJD around the globe.
Looking from stats at ;
http://www.fas.usda.gov/ustrade/ustlists/ExCmdty.asp?QI=370619655344&type=1&code=02
then searching here ;
http://www.fas.usda.gov/ustrade/USTEXHS10.asp?QI=370619655344
SEEMS that Mexico received from the USA a boat load of potential mad cow brains 0206290030 between 2001 to 2005, Mexico received the most compared to COTE D'IVOIRE which was next in line, followed by ROMANIA, GREECE, SINGAPORE, GERMANY AND SWEDEN. ...
NEXT, looking at SWEETBREADS 0206290040 the USA exported, and whatever phenotype of TSE that went along, we have as follows;
MEXICO AGAIN receiving a boat load of sweetbreads, followed by ARGENTINA, JAPAN, URUGUAY, COLOMBIA, ISRAEL, BULGARIA, HONG KONG, VENEZUELA, United Arab Emirates, Switzerland, Singapore, Netherlands, The Bahamas, and the Dominican Republic. ...
THE LIST for BOVINE OFFAL FROZEN 020629 EXPORTED FROM THE USA ACROSS THE GLOBE IS PHENOMENAL WITH JAPAN RECEIVING THE MOST FROM 1998 TO 2003, FOLLOWED BY MEXICO, and from here the list is staggering along with the amount of potential TSE tainted materials. ...
FINALLY, LIVE CATTLE WITH CANADA RECEIVING THE MOST, FOLLOWED BY MEXICO, KOREA REPUBLIC OF, followed by many more countries with smaller amounts. ...
WHEN the OIE did away with the BSE GBR risk assessments to ride saddle with GW and his legal tool to trade TSE globally i.e. the BSE MRR policy, 20 years of fighting this disease went down the drain, just so he could trade his precious commodities and futures. THIS BSe about how now the USA having an epidemic of a spontaneous TSE in cattle and humans, as sporadic CJD triples in 3 years in the USA, is simply absurd. nothing is spontaneous about it, there is absolutely no science to back these 'spontaneous' statements up. ...
US "Atypical" Mad Cow Threat Was Predicted
http://www.prwatch.org/node/4883
TSS
#################### https://lists.aegee.org/bse-l.html ####################
##################### Bovine Spongiform Encephalopathy #####################
Subject: DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES
Date: June 17, 2006 at 6:56 pm PST
Greetings list members,
here i go again. i must bring those mad sheep of mad river valley up again.
what about those mouse bio-assays? can one of the aphis/usda lurkers on this list, can one of them please comment please?
a declaration of emergency was announced ;
>> Imported
>> Belgium/Netherlands
>> Sheep Test Results
>> Background
>> Factsheet
>> Veterinary Services April 2002
>> APHIS
>
>
>
> snip...
>
>> Additional tests will be conducted to determine
>> exactly what TSE the animals haveBSE or scrapie.
>> These tests involve the use of bioassays that consist
>> of injecting mice with tissue from the infected animals
>> and waiting for them to develop disease. This testing
>> may take at least 2 to 3 years to complete.
>
>
>
> http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahvtsheeptr.pdf
>
> DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E.
> (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES
>
> http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2000_register&docid=fr20jy00-31
>
>
> DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E
> (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [2]
>
> http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2000_register&docid=fr20jy00-32
>
>
> or if those old urls dont work, go here;
>
> DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E
> (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES
> - Terry S.
> Singeltary Sr. 7/20/00 (0)
>
> [Federal Register: July 20, 2000 (Volume 65, Number 140)] [Notices]
> [Page 45018] >From the Federal Register Online via GPO Access
> [wais.access.gpo.gov] [DOCID:fr20jy00-32]
>
> -----------------------------------------------------------------------
>
> DEPARTMENT OF AGRICULTURE
>
> Office of the Secretary
>
> [Docket No. 00-072-1]
>
> Declaration of Extraordinary Emergency Because of an Atypical
> Transmissible Spongiform Encephalopathy (Prion Disease) of Foreign Origin
>
> A transmissible spongiform encephalopathy (TSE) (prion disease) of
> foreign origin has been detected in the United States. It is different
> from TSE's previously diagnosed in the United States. The TSE was
> detected in the progeny of imported sheep. The imported sheep and
> their progeny are under quarantine in Vermont. Transmissible
> spongiform encephalopathies are degenerative fatal diseases that can
> affect livestock. TSE's are caused by similar, as yet uncharacterized,
> agents that usually produce spongiform changes in the brain.
> Post-mortem analysis has indicated positive results for an atypical
> TSE of foreign origin in four sheep in Vermont. Because of the
> potentially serious consequences of allowing the disease to spread to
> other livestock in the United States, it is necessary to seize and
> dispose of those flocks of sheep in Vermont that are affected with or
> exposed to the disease, and their germ plasm. The existence of the
> atypical TSE of foreign origin represents a threat to U.S. livestock.
> It constitutes a real danger to the national economy and a potential
> serious burden on interstate and foreign commerce. The Department has
> reviewed the measures being taken by Vermont to quarantine and
> regulate the flocks in question and has consulted with appropriate
> officials in the State of Vermont. Based on such review and
> consultation, the Department has determined that Vermont does not have
> the funds to compensate flock owners for the seizure and disposal of
> flocks affected with or exposed to the disease, and their germ plasm.
> Without such funds, it will be unlikely to achieve expeditious
> disposal of the flocks and germ plasm. Therefore, the Department has
> determined that an extraordinary emergency exists because of the
> existence of the atypical TSE in Vermont. This declaration of
> extraordinary emergency authorizes the Secretary to seize, quarantine,
> and dispose of, in such manner as he deems necessary, any animals that
> he finds are affected with or exposed to the disease in question, and
> their germ plasm, and otherwise to carry out the provisions and
> purposes of the Act of July 2, 1962 (21 U.S.C. 134-134h). The State of
> Vermont has been informed of these facts.
>
> Dated: This declaration of extraordinary emergency shall become
> effective July 14, 2000. Dan Glickman, Secretary of Agriculture. [FR
> Doc. 00-18367 Filed 7-19-00; 8:45 am] BILLING CODE 3410-34-P
>
> http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2000_register&docid=fr20jy00-32
================================
> [Federal Register: July 20, 2000 (Volume 65, Number 140)] [Notices]
> [Page 45018] >From the Federal Register Online via GPO Access
> [wais.access.gpo.gov] [DOCID:fr20jy00-31]
>
> ========================================================================
> Notices Federal Register
> ________________________________________________________________________
>
> This section of the FEDERAL REGISTER contains documents other than
> rules or proposed rules that are applicable to the public. Notices of
> hearings and investigations, committee meetings, agency decisions and
> rulings, delegations of authority, filing of petitions and
> applications and agency statements of organization and functions are
> examples of documents appearing in this section.
>
> ========================================================================
>
> [[Page 45018]]
>
> -----------------------------------------------------------------------
>
> DEPARTMENT OF AGRICULTURE
>
> Office of the Secretary
>
> [Docket No. 00-072-2]
>
> Declaration of Emergency Because of an Atypical Transmissible
> Spongiform Encephalopathy (Prion Disease) of Foreign Origin
>
> A transmissible spongiform encephalopathy (TSE) (prion disease) of
> foreign origin has been detected in the United States. It is different
> from TSE's previously diagnosed in the United States. The TSE was
> detected in the progeny of imported sheep. The imported sheep and
> their progeny are under quarantine in Vermont. Transmissible
> spongiform encephalopathies are degenerative fatal diseases that can
> affect livestock. TSE's are caused by similar, as yet uncharacterized,
> agents that usually produce spongiform changes in the brain.
> Post-mortem analysis has indicated positive results for an atypical
> TSE of foreign origin in four sheep in Vermont. Because of the
> potentially serious consequences of allowing the disease to spread to
> other livestock in the United States, it is necessary to seize and
> dispose of those flocks of sheep in Vermont that are affected with or
> exposed to the disease, and their germ plasm. The existence of the
> atypical TSE of foreign origin represents a threat to U.S. livestock.
> It constitutes a real danger to the national economy and a potential
> serious burden on interstate and foreign commerce. APHIS has
> insufficient funds to carry out the seizure and disposal of animals
> and germ plasm necessary to eliminate this disease risk. These funds
> would be used to compensate the owners of the animals and germ plasm
> for their seizure and disposal in accordance with 21 U.S.C. 134a.
> Therefore, in accordance with the provisions of the Act of September
> 25, 1981, as amended (7 U.S.C. 147b), I declare that there is an
> emergency that threatens the livestock industry of this country and
> hereby authorize the transfer and use of such funds as may be
> necessary from appropriations or other funds available to agencies or
> corporations of the United States Department of Agriculture to seize
> and dispose of animals that are affected with or exposed to this TSE,
> and their germplasm, in accordance with 21 U.S.C. 134a.
>
> Dated: This declaration of emergency shall become effective July 14,
> 2000. Dan Glickman, Secretary of Agriculture. [FR Doc. 00-18368 Filed
> 7-19-00; 8:45 am] BILLING CODE 3410-34-P
>
> I was told that ;
>
>
> -------- Original Message --------
> Subject: Re: hello Dr. Sutton...question please...scrapie...TSS
> Date: Thu, 20 May 2004 14:36:09 -0400
> From: Jim.D.Rogers@aphis.usda.gov
> To: flounder@wt.net
snip...
FULL TEXT AND THREAD BETWEEN TSS, MAFF, USDA AND DR. DETWILER HERE ;
https://web01.aphis.usda.gov/regpublic.nsf/168556f5aa7a82ba85256ed00044eb1f/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument
Greetings again BSE-L members,
NOW, i cannot for the life of me figure out why we have not heard anything about those mouse bio-assays of those mad sheep of mad river valley, and atypical TSE ? i mean hell, there was a DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES and we never hear of final results, is this not another case of the TEXAS BSE PROTOCOLS of just never confirming anything unless the GAO gets involved? maybe USDA could comment on this now? or is this too like those WMD, just something that never existed? i know Dr. Detwiler is out of the loop on this now, but there are others here that could answer this question if they wanted too and or could???
QUOTE ;
1998
Dr. Detwiler replied. "There is new research which shows that sheep can contract BSE" ......"information I can't divulge".....end
WHY, after some 7 years, do we still not have any answers ???
WHERE are those mouse bio-assays ???
PLEASE look on every shelf, maybe same one that those TEXAS MAD COW tissue samples were left on for 7+ months before finally confirming after a Congressional order and or end around, they could be there. ...
still disgusted in sunny Bacliff, Texas
Terry S. Singeltary Sr.
FSA 06/06/03 AGENDA 3.1, 15 JUNE 2006
ATYPICAL SCRAPIE IN SMALL RUMINANTS: CONSIDERATION OF THE
CURRENT PRECAUTIONARY RISK MANAGEMENT MEASURES
Executive Summary
1. This paper provides information on atypical scrapie (a transmissible spongiform
encephalopathy (TSE)) in sheep and goats and the precautionary measures
currently in place to protect consumers from the possible risks from TSEs in
these species. There are a great many unknowns about atypical scrapie,
including the potential implications, if any, for human health.
2. It also reports on the views of stakeholders and consumer focus groups who
were asked whether, in the light of this uncertainty, additional precautionary
measures were needed and for their views on the Agency’s advice on this
subject.
3. The Board is asked to:
• note that the Agency’s advice has been reworded to take account of the views
of stakeholders and the consumer focus groups and will be tested further
• note that the background information on sheep TSEs on the Agency’s website
will be reviewed
• note that the agricultural departments are planning to review the Ram
Genotyping Scheme
• note that surveillance for atypical scrapie will be maintained in order to detect
any changes in prevalence.
• agree that the Agency’s advice and recommendations on precautionary
measures should be kept under review and be brought back to the Board if
there are significant changes in the understanding of the risk.
• agree that developments on atypical scrapie be kept under review to enable
contingency policy to be refined as new information emerges.
• agree that the Agency should open discussions with the European
Commission on the issue of the identification of meat from older sheep or
goats and natural sausage casings made from sheep intestines to enable
consumer choice.
2
TSE DIVISION
Contacts:
Alison Gleadle Tel: 020 7276 8303
Email: alison.gleadle@foodstandards.gsi.gov.uk
Irene Hill Tel: 020 7276 8324
Email: irene.hill@foodstandards.gsi.gov.uk
3
FSA 06/06/03 AGENDA ITEM 3.1, 15 JUNE 2006
ATYPICAL SCRAPIE IN SHEEP AND GOATS: CONSIDERATION OF THE
CURRENT PRECAUTIONARY RISK MANAGEMENT MEASURES
Issue
1. To consider whether the Agency should recommend, on the basis of current
evidence, that additional precautionary measures are needed to reduce the
possible risk to consumers from atypical scrapie.......
snip...
Conclusions
27. Atypical scrapie is definitely present in the UK flock, and in the flocks of other
Member States (MS), and animals with atypical scrapie have, and will be,
entering the food supply. However it is not known if this constitutes any risk to
human health. Unlike the situation when BSE was first discovered in cattle,
precautionary measures are already in place. Based on the limited knowledge of
the distribution of infectivity in atypical scrapie, the SEAC Subgroup concluded
that the SRM requirements that were put in place on a precautionary basis for
BSE in sheep may provide at least a similar level of protection against the
possible risk from atypical scrapie.
28. The consideration of the proportionality of any additional precautionary measures
is very difficult when the human health risk is unknown, and, as reported by
SEAC, there is insufficient data to carry out a risk assessment.
29. Any additional precautionary measures that could be put in place have a high
economic cost, are currently highly impractical (see Annex 1 for details) and
would impose a cost on industry that would, according to industry stakeholders,
be likely to bring into question the economic viability of sheep farming. ...
snip...
full text ;
http://www.food.gov.uk/multimedia/pdfs/fsa060603.pdf
FSA 06/06/04 AGENDA ITEM 3.2, 15 JUNE 2006
BSE AND SHEEP CONTINGENCY POLICY
Executive Summary
1. This paper asks the Board to agree, for purposes of contingency planning, a
possible approach to a graduated strengthening of measures to protect
consumers in response to one or more findings of BSE in the current UK sheep
flock.
2. The paper also notes the high level of uncertainty around estimates of the
possible risk from BSE in sheep and that, if BSE were ever found in a UK sheep,
the estimate of the risk to consumers would depend on the accumulated results
of surveillance for BSE in sheep up to that time. It therefore recommends that the
policy be kept under review and that any policy agreed now on a contingency
basis should urgently be reconfirmed taking into account the circumstances at the
time of any finding of BSE in a UK sheep.
3. The Board is invited to:
• note that, in the event of confirmation of BSE in a sheep, targeted testing of
animals in the affected flock or flocks would be carried out to assist in
determining the potential spread of the disease and whether it may have
entered the food supply (paragraph 9).
• agree that an expert group be set up to advise on what additional surveillance
should be put in place, if BSE were to be found in a UK sheep, to improve
estimates of prevalence of BSE in UK sheep (paragraph 13).
• agree that, on current knowledge, it would advise the following graduated
response to one or more findings of BSE in the current UK sheep flock:
• one finding of BSE in sheep - remove additional SRM;
• two findings of BSE in unrelated flocks - exclude sheep aged over 12
months from the food supply and remove the additional SRM from the
remaining sheep;
• three findings of BSE in unrelated flocks - allow into the food supply only
sheep that were either genetically resistant to BSE or semi-resistant and
aged under 12 months and remove the additional SRM from those sheep
(paragraph 20).
2
• agree that its contingency policy for a finding of BSE in sheep should be kept
under review and be urgently reconfirmed should BSE actually be found in a
UK sheep (paragraph 22).
• comment on the outline handling plan at Annex F and the strategy for the
external communication that would be needed (paragraph 30).
TSE Division
Contacts:
Alison Gleadle Tel: 020 7276 8303 (GTN 7276 8303)
Email: alison.gleadle@foodstandards.gsi.gov.uk
David Carruthers Tel: 020 7276 8305 (GTN 7276 8305)
Email: david.carruthers@foodstandards.gsi.gov.uk
snip...
http://www.food.gov.uk/multimedia/pdfs/fsa060604.pdf
Subject: REPORT OF THE COMMITTEE ON SCRAPIE November 9, 2005 USAHA
Date: February 12, 2006 at 1:03 pm PST
REPORT OF THE COMMITTEE ON SCRAPIE
Chair: Dr. Jim Logan, Cheyenne, WY
Vice Chair: Dr. Joe D. Ross, Sonora, TX
Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN.
The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance.
The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings.
Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories.
For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS.
To reduce/eliminate these problems, the Program has placed additional quality requirements on the testing laboratories: additional review of final reports, additional coding systems for testing operations, strict follow-up and reports to NVSL on corrective actions, dual data entry systems, and more frequent inspections.
The Agricultural Research Services (ARS) Scrapie Research Update was given by Janet Alverson, USDA- ARS. Dr. Alverson reported on the effect of multiple births and fetal position within the uterus on PrP-Sc accumulation in fetal cotyledons. Fetal cotyledons of fetuses with
resistant genotypes can accumulate PrP-Sc when positioned next to a fetus of susceptible genotype with cotyledons positive for PrP-Sc accumulation.
Scrapie Surveillance Evaluation Working Group Update was presented by Tracey Lynn, Epidemiologist with the National Surveillance Unit, Center for Epidemiology and Animal Health (CEAH). The presentation provided a background on evaluation, a quick review of analyses completed to date by the scrapie surveillance evaluation working group, and some of the preliminary findings. The process of surveillance system evaluation is undertaken to assist a disease control program with identifying possible improvements to their surveillance system, and includes an assessment of the overall utility of the system, identification of potential gaps in coverage, and an evaluation of the overall performance of the system. The scrapie surveillance evaluation working group reviewed the structure and processes of the scrapie surveillance program, as well as various quality and effectiveness measures.
Overall, 98-99% of surveillance samples come from the Regulatory Scrapie Surveillance System (RSSS), so the RSSS system has been the primary focus of the evaluation process. The working group developed a flow chart indicating the flow of sheep through RSSS, which identified potential gaps in surveillance coverage, including custom kill plants and sheep being exported to Mexico. Spatial analyses can assist in identifying areas with high density sheep populations with lower levels of RSSS sampling. Identification compliance is being evaluated by reviewing reports from slaughter plants on the proportion of animals with appropriate identification. Additional analyses remain, including defining the most appropriate economic analyses, and comparing the surveillance system with developing surveillance standards. The working group hopes to have a draft written report for review by the end of the year.
Giving the Update on Scrapie Diagnostics and Susceptibility was Katherine O’Roarke, Research Microbiologist, USDA-ARS. "What’s New in Scrapie" -- Biopsy sampling of the third eyelid or tonsillar lymphoid tissue is a useful live animal test for scrapie. The biopsy sample is examined for accumulation of the abnormal prion protein using immunohistochemistry. A joint project conducted by the Veterinary Laboratory Agencies and the Moredun Institute in the United Kingdom has developed an alternative technique in which tissue is collected from the narrow band of lymphoid tissue near the rectal-anal junction. The morphology of the lymphoid follicles is similar in the tonsil, retropharyngeal lymph nodes, third eyelid, and rectal-anal mucosal tissue. A report on more than 300 sheep in the United Kingdom (UK), prepared by Drs. Lorenzo Gonzalez and Jeffrey Martin, will describe the sensitivity, specificity, and optimal collection interval for this technique in a variety of breeds of British sheep. ARS has done a preliminary evaluation of the technique in US sheep. Samples of third eyelid and rectal-mucosal tissue were collected from 56 sheep. Forty-two (42) sheep had negative biopsies at both sites; most of these sheep have been necropsied and no PrP-d was found in retropharyngeal lymph node or tonsil, showing good agreement with the antemortem biopsies. Fourteen (14) sheep had positive rectal biopsy samples; of those, only 12 had positive eyelid biopsies. These sheep will be monitored for disease development. However, the protocol is identical for all samples and it is probable that these sheep represent false negative third eyelid results. Abstracts of reports on the UK studies indicate that sensitivity of the test was 70% in the UK; similar large scale testing on US sheep is necessary. The biopsy tissue is somewhat difficult to handle in the tissue processing laboratory and adaptation to an ELISA format may improve test performance.
Alexia McKnight, Assistant Professor of Radiology, University of Pennsylvania, reviewed magnetic resonance imaging (MRI) diagnostics before the committee. A synopsis containing references is attached at the end of this report. Dr. McKnight asked the question, "could MRI be a cost-effective screening test, estimated at $25-30 each with results immediately available." The committee feels that it is not practical as compared to other alternatives currently available. However, the committee expressed interest in future reference to this technology.
Dr. Diane Sutton lead the Uniform Methods and Rules (UM&R) and Regulatory Issues Discussion. Several modifications to the UM&R were discussed. Eight issues were identified and communicated to the APHIS scrapie program coordinator. The committee acknowledged that APHIS and the industry is adequately addressing the year-to-year industry concerns.
Dr. Kris Petrini representing the North Central United States Animal Health Association District presented five recommendations to the Committee. During the discussions regarding these recommendations it was evident that all five issues had been addressed during the year at this Committee meeting.
The Committee approved a recommendation that USDA-APHIS-VS continue to provide indemnity funds for animals that have been designated for testing in Flocks Under Investigation as an alternative to third eyelid testing after consultation with the designated Scrapie Epidemiologist (DSE) and the Regional Area Epidemiologist (RAE).
The 2004 Resolutions along with their responses were reviewed by the Committee.
A Resolution concerning premises registration and identification was approved by the Committee and forwarded to the Committee on Nominations and Resolutions.
Committee on Scrapie
Status Report-Fiscal Year 2005: Cooperative State-Federal Scrapie Eradication Program
Submitted by Diane Sutton, DVM and Gary Ross, DVM
National Center for Animal Health Programs, APHIS, USDA
In Fiscal Year 2005 the Scrapie Eradication Program focused on: (1) utilization of a genetic based approach to flock clean-up plans; (2) cleaning up infected and source flocks; (3) tracing and testing exposed animals and flocks; (4) expansion of regulatory slaughter surveillance (RSSS); (5) conducting considtent state reviews, (6) producer education; (7) upgrading of the Scrapie National Generic Database and (8) publishing the updated Scrapie Eradication Uniform Methods and Rules (UM&R). The current Scrapie Eradication UM&R is posted at http://www.aphis.usda.gov/vs/nahps/scrapie/umr-scrapie-erad.pdf.
Consistent State Reviews
States must meet the requirements in 9 CFR 79.6 in order to move sheep and goats in interstate commerce with minimal restrictions. Twenty seven states have enacted the required identification rules, the remaining states have submitted a work plan that describes the steps that will be taken to comply and provided a timeline for completing significant milestones. USDA is conducting onsite scrapie program consistent state reviews and has completed reviews in 12 states. States must be in full compliance by the end of their current rule making cycle. States not in full compliance at that time will be removed from the consistent state list. Removal from the list would create a significant impact on the interstate movement of sheep and goats from those States.
Scrapie Flock Certification Program
As of September 30, 2005, there were 1,961 flocks participating in the Scrapie Flock Certification Program (SFCP). Of these flocks 188 were certified flocks, 1,770 were complete monitored flocks, and 3 were selective monitored flocks (figure 2). There were 209 flocks newly enrolled and 53 newly certified (13 with status dates in FY 2005 and 40 with status dates in previous years) in FY 2005 (figure 3).
Infected and Source Flocks
As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats.
Regulatory Scrapie Slaughter Surveillance (RSSS)
RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm . RSSS started April 1,
2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below.
Scrapie Testing
In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9).
Animal ID
As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises.
*This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans.
http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf
Subject: SCRAPIE USA UPDATE AS of March 31, 2006 2 NEW CASES IN GOAT, 82
INFECTED SOURCE FLOCKS, 19 INFECTED RSSS
Date: April 30, 2006 at 4:49 pm PST
SCRAPIE USA UPDATE AS of March 31, 2006
2 NEW CASES IN GOAT, 82 INFECTED SOURCE FLOCKS, WITH 4 NEW INFECTED SOURCE
FLOCKS IN MARCH, WITH 19 SCRAPIE INFECTED RSSS REPORTED BY NVSL
http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html
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
Published online before print October 20, 2005
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102
Medical Sciences
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes
( sheep prion | transgenic mice )
Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||, Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude *
*Virologie Immunologie Moléculaires and ||Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. 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.
--------------------------------------------------------------------------------
Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper.
A.L.D. and V.B. contributed equally to this work.
To whom correspondence should be addressed.
Hubert Laude, E-mail: laude@jouy.inra.fr
www.pnas.org/cgi/doi/10.1073/pnas.0502296102
http://www.pnas.org/cgi/content/abstract/0502296102v1
Of greatest interest today is the BSE agent because it is the presumptive cause of new variant CJD and must be considered a demonstrated risk to human health. The scrapie agent poses a theoretical risk to human health.
Today we ask you to consider the implications of two theoretical possibilities: the first, that sheep and goats in BSE countries theoretically might be infected with the BSE agent, and Professor Almond, who headed a subcommittee of the United Kingdom's Spongiform Encephalopathy Advisory Committee, has agreed to review that topic for us today.
Then scrapie, which theoretically might be a human pathogen, though there's no hard evidence for that, and of course, some number of sheep and goats in many countries, including the United States, are infected with the scrapie agent.
Now, let me say now that no U.S. government regulatory authority would ever knowingly permit humans or animals to be exposed to a product containing the scrapie agent, but considering the nature of the scrapie agent and the disease, we are not so naive as to think that such exposures have not already occurred. ...
FULL TEXT ;
http://www.fda.gov/ohrms/dockets/ac/99/transcpt/3518t2.rtf
http://72.14.209.104/searchq=cache:pKJPlLI2R44J:www.fda.gov/ohrms/dockets/ac/99/transcpt/3518t2.rtf+scrapie+strains+breed+east+friesian&hl=en&gl=us&ct=clnk&cd=23
TSS
#################### https://lists.aegee.org/bse-l.html ####################
Having a social science background, my opinion of Ms. Coulton is that
she is a modern day Horatio Alger. Average is all respects, she
has found her way to stardom using the only means available to the
very mediocre. How do you get people to pay attention to you when
you only have a modest intellect? Dare to say the unthinkable! It
will get you noticed. That is why she is in the conservative camp.
It simply gets her more noticed. What if people hate you and dismiss
you as a look? Surround yourself with the highest amount of moral
credibility a woman can have in modern Western society - be very, very thin. (Lets face it, if she were a fat or even average sized
WOMAN, she could not get away with what she does.) And being that
thin brings her even more attention. I have often wondered why women
buy into weight obsession (if they didn't, it would go away.) Why will an Oprah audience clap harder for a woman who dropped 50lbs than
a Noble Prize winner? Because most of them can never be a Noble Prize winner, so losing weight is their way to Cinderella hood. I think part of Coulton's appeal is that deep down the public understands she is below mediocre in all respects, but she is a queen just by virtue of wanting it badly enough. Even if they don't choose
to take it, I think she reminds them they too can have their 15 minutes of fame if they so desire. To me, it is very sad any human
needs attention that badly. On the other hand, I came across a bumper sticker I had never seen before. "Would someone PLEASE give
Bush a ****job so we can impeach him too?" After I stopped retching at the thought of it, I wondered WHO could possible love their county
THAT much???? Only Ms. Coulton came to mind!
Subject: SEAC Position statement vCJD and Endodontic dentistry and atypical TSE ???
Date: June 14, 2006 at 12:56 pm PST
SEAC
Position Statement
--------------------------------------------------------------------------------
Position statement vCJD and Endodontic dentistry
Issue
1. The Department of Health (DH) asked SEAC to advise on the findings and implications of a preliminary risk assessment of potential vCJD transmission via endodontic procedures (dental procedures involved in the maintenance of dental pulp and the treatment of the pulp cavity) 1. This is particularly pertinent because of the large number of endodontic procedures undertaken in the UK.
Background
2. There are no reported definite or suspected cases of vCJD transmission arising from dental procedures. However, prions are more resistant than other types of infectious agent to the conventional cleaning and sterilisation practices used to decontaminate dental instruments 2. Therefore, should dental instruments become contaminated from tissues in the oral cavity of infected individuals, there is a risk of transmission to subsequent patients.
3. A quantitative DH risk assessment 3, accepted by SEAC in 2003, considered two possible mechanisms for the transfer of vCJD infectivity via dental instruments: (i) accidental abrasion of the lingual tonsil, known to carry infectivity in vCJD cases; and (ii) contact with dental pulp that evidence from animal studies suggested may be infective. On the basis of the information available, the DH analysis suggested that the risk of transmission to individual patients via accidental abrasion of the lingual tonsil is very low. Furthermore, should dental pulp be infective, the risk of transmission via endodontic procedures, although higher, is also low. Although a very large number of dental procedures are conducted, the relative risk to public health from potential transmission via dental, compared with hospital, surgery was considered to be relatively low.
4. In 2006, SEAC considered a new preliminary risk assessment by DH of the risks of vCJD transmission via endodontic procedures, taking into account new information on decontamination of dental instruments, the potential infectivity of dental pulp, and the possible existence of subclinical vCJD carrier cases.
Endodontic instruments
5. Evidence suggests that the files and reamers used in endodontic procedures are reused and are difficult to reliably decontaminate 4. Appreciable quantities of residual material remain adherent to the surface after normal cleaning and sterilisation 5. Thus, there is potential for transfer of dental pulp between patients undergoing endodontic procedures.
vCJD infectivity in dental tissues
6. There are no data on vCJD infectivity in dental pulp. Although no abnormal prions were found in a study of dental tissues, including dental pulp, from vCJD cases 6, dental pulp includes blood and peripheral nerve tissue known to carry vCJD infectivity 7,8. In addition, appreciable infectivity has been found in the dental pulp of hamsters with hamster scrapie 9. Although it is possible that the peripheral nerve may only become infective close to, or after, the onset of clinical vCJD, inflammation may promote the propagation of prions 10. Thus, although the data are limited and indirect, it is reasonable to assume that the dental pulp of individuals subclinically-infected with vCJD may be infectious although the level of infectivity is unknown. Studies underway will provide direct data on the infectivity in dental tissues from vCJD cases.
Subclinical carrier state
7. A study of humanised mice showed that vCJD infections may not always progress to clinical disease within the normal lifespan of the animals 11. Another study suggested that prion infections in mice that remain at a subclinical level can be transmitted to other mice, resulting in clinical disease 12. Thus, there is evidence to suggest that individuals infected with the BSE / vCJD agent may remain in a subclinical infection carrier state instead of developing vCJD. A discrepancy between prevalence estimates based on a survey of abnormal prion protein in appendix and tonsil tissue and data on vCJD cases supports this hypothesis 13. As no diagnostic test exists to identify such individuals, they could over the course of their lives be potential sources of numerous secondary infections arising from invasive medical or dental procedures.
8. The prevalence of subclinical infection in the UK population is uncertain. A recent estimate suggests the number of subclinical carriers may be of the order of several thousand 14. SEAC has strongly recommended that further studies to ascertain better the prevalence of vCJD infection be urgently considered 15.
Transmission risks
9. The new DH analysis suggests that, on the basis that residual dental pulp on endodontic files and reamers is transferred relatively efficiently to patients on reuse, dental pulp is as infective as peripheral nerve tissue and a subclinical carrier population for vCJD exists, a self-sustaining vCJD epidemic arising from endodontic surgery is plausible. There are uncertainties about the efficiency of vCJD transmission via endodontic procedures, the vCJD infectivity of dental pulp and the existence of a subclinical infection carrier state. However, even if a self-sustaining epidemic were not possible, clusters of vCJD infections could arise from the use of instruments contaminated with the vCJD agent from endodontic procedures on infected patients. Interactions between this and other routes of secondary transmission, such as blood transfusion and hospital surgery, would make a self-sustaining epidemic more likely.
Potential risk reduction measures
10. Endodontic files and reamers have a limited lifespan, restricting the number of possible secondary transmissions. Improving the effectiveness of procedures used to decontaminate dental instruments would reduce the risk of transmission. Restricting endodontic files and reamers to single use would prevent potential secondary transmission via these instruments.
Conclusions
11. A preliminary risk assessment produced by DH suggests that vCJD transmission via endodontic dentistry may, under certain hypothetical but plausible scenarios, be sufficient to sustain a secondary vCJD epidemic. However, there are uncertainties around the data and assumptions underpinning the assessment. Research underway will address some of these uncertainties and allow the risk assessment to be refined. Once the research is complete and / or other data become available, the risks should be reassessed. A watching brief should be maintained.
12. It is unclear whether or not vCJD infectivity can be transmitted via endodontic files and reamers. However, given the plausibility of such a scenario and the large number of procedures undertaken annually, it would be prudent to consider restricting these instruments to single use as a precautionary measure. Since sufficiently rigorous decontamination of these instruments is difficult, single use of these instruments would eliminate this risk, should it exist.
SEAC
May 2006
--------------------------------------------------------------------------------
1. Department of Health. Dentistry and vCJD: the implications of a “carrier state” for a self-sustaining epidemic due to endodontic dentistry. A Preliminary Risk Assessment. Unpublished.
2. Smith et al. (2003) Prions and the oral cavity. J. Dent. Res. 82, 769-775.
3. Department of Health. (2003) Risk assessment for vCJD and dentistry.
4. Letters et al. (2005) A study of visual and blood contamination on reprocessed endodontic files from general dental practice. Br. Dent. J. 199, 522-525.
5. Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241.
6. Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343.
7. SEAC 91 minutes paragraph 9. www.seac.gov.uk/papers/papers.htm
8. Department of Health (2005) Assessing the risk of vCJD transmission via surgery: an interim view. Unpublished.
9. Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047.
10. Heikenwalder et al. (2005) Chronic lymphocytic inflammation specifies the organ tropism of prions. Science. 307, 1107-1110.
11. Bishop et al. (2006) Predicting susceptibility and incubation time of human-to-human transmission of vCJD. Lancet Neurology.
12. Hill et al. (2000) Species-barrier-independent prion replication in apparently resistant species. Proc. Natl. Acad. Sci. USA. 97, 10248-10253.
13. SEAC Epidemiology Subgroup (2005) Position statement on the vCJD epidemic. www.seac.gov.uk/statements/state260106subgroup.htm
14. Clarke & Ghani. (2005) Projections of future course of the primary vCJD epidemic in the UK: inclusion of subclinical infection and the possibility of wider genetic susceptibility. R. J. Soc. Interface.
15. SEAC (2005) SEAC response to the SEAC Epidemiology Subgroup statement on the vCJD epidemic. www.seac.gov.uk/statements/state260106.htm
Page updated: 8th May 2006
http://www.seac.gov.uk/statements/statement0506.htm
Greetings,
WITH the new atypical TSE in cattle in the USA, new atypical TSE in sheep and goat (USA imported from UK?), real definitions of SRMs now???, this brings into question once again of the ukbsenvcjd only theory, especially in terms of iCJD i.e. 'friendly fire'. what about those 'unknown' strains of sporadic CJD popping up now???
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is
with a human TSE surveillance system that is terrible
flawed. in 1997 cases of the _reported_ cases of cjd
were at 54, to 163 _reported_ cases in 2004. see stats
here;
p.s. please note the 47 PENDING CASES to Sept. 2005
p.s. please note the 2005 Prion D. total 120(8)
8=includes 51 type pending, 1 TYPE UNKNOWN ???
p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???
p.s. please note 2004 prion disease (6) 6=7 TYPE
UNKNOWN???
http://www.cjdsurveillance.com/resources-casereport.html
TSS
Subject: ENDOSCOPY EQUIPMENT (Terminal ileal biopsies should not be used) and CJD (ALL PHENOTYPES)
Date: March 8, 2005 at 1:09 pm PST
-------- Original Message --------
Subject: Terminal ileal biopsies should not be used to document extent of colonoscopic examination
Date: Tue, 8 Mar 2005 09:17:50 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy #####################
Greetings again,
seems Bramble et al have failed to take heed to the latest data on
atypical TSEs. UNTIL the BSE/nvCJD 'ONLY THEORY' is put to rest
once and for all, this agent will continue to spread. with the findings
of the testing with CDI from Prusiner et al and Aguzzi continued
warnings of muscle tissue and Collinge warnings about sporadic CJD,
to continue with this BSE/nvCJD 'ONLY THEORY' should be regarded
with great suspicion. WITH many atypical TSEs showing up in cattle,
sheep and goats in many different parts of the Globe, with the findings
of BASE in cattle in Italy of Identification of a second bovine
amyloidotic spongiform encephalopathy: Molecular similarities
with sporadic Creutzfeldt-Jakob disease
http://www.pnas.org/cgi/content/abstract/0305777101v1
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human
health THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy
Fournier*, Virginie Nouvel*, Hermann Boe*, DomÃnÃque Marcé*, François
Lamoury*, Nicolas Kopp [Dagger ] , Jean-Jacques Hauw§, James Ironside¶,
Moira Bruce [||] , Dominique Dormont*, and Jean-Philippe Deslys* et al,
that The agent responsible for French iatrogenic growth hormone-linked
CJD taken as a control is very different from vCJD but is similar to
that found in one case of sporadic CJD and one sheep scrapie isolate;
http://www.pnas.org/cgi/content/full/041490898v1
Characterization of two distinct prion strains derived from bovine
spongiform encephalopathy transmissions to inbred mice
http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471
WITH ALL THIS DATA, TO CONTINUE TO WARN ONLY OF THE nvCJD
threat will only allow this agent to continue to spread...TSS
Gut 2005;54:566
© 2005 by BMJ Publishing Group Ltd & British Society of Gastroenterology
------------------------------------------------------------------------
LETTER
Terminal ileal biopsies should not be used to document extent of
colonoscopic examination
M D Rutter1 and M G Bramble2
1 University Hospital of North Tees, Stockton-on-Tees, Cleveland, UK
2 James Cook University Hospital, Middlesbrough, Cleveland, UK
Correspondence to:
Dr M D Rutter
University Hospital of North Tees, Stockton-on-Tees, Cleveland, TS19
8PE, UK; matt.rutter@nth.nhs.uk
Keywords: ileal biopsies; colonoscopy; guidelines
The first 150 words of the full text
of this article
appear below.
We commend the British Society of Gastroenterology and the authors for
the excellent publication of guidelines for the management of
inflammatory bowel disease in adults (Gut 2004;53(suppl V):v1v16).
However, we feel that their recommendation for routine terminal ileal
biopsying is inappropriate. Although it is important to biopsy the
terminal ileum if there is macroscopic evidence of an abnormality, their
statement that "a terminal ileal biopsy performed at colonoscopy
documents the extent of examination" is not recommended practice, due to
the potential risk of variant Creutzfeld-Jacob disease transmission from
prion proteins which are prevalent in the lymphoid tissue of Peyers
patches in the ileum. Although the use of disposable forceps may reduce
the risk of transmission, there could still be contamination of the
intubation channel of the colonoscope and prion protein is resistant to
the standard endoscopic cleaning process.1 If the extent of examination
needs to . . . [Full text of this article
]
http://gut.bmjjournals.com/cgi/content/extract/54/4/566-a
-------- Original Message --------
Subject: Re: gutjnl_el;110 Terry S. Singeltary Sr. (22 Aug 2003) ""CJDs
(all human TSEs) and Endoscopy Equipment
Date: Tue, 26 Aug 2003 15:10:51 -0500
From: "Terry S. Singeltary Sr."
To: Robin.Spiller@nottingham.ac.uk
hello Professor Spiller and GUT, this has become a real challenge trying
to raise my concerns to GUT about sporadic CJD. but i will not give up.
you only have to see it once. i hope you take the time to read over all
data below...thank you > unsubstantiated opinion and emotion these are
not my unsubstantiated opinions, they are backed up by science
(transmission studies and or lack of transmissions studies), and i will
try and leave my emotions out. > I feel that we need a proper evidence
based approach to this. > There is too much unsubstantiated opinion i
agree... to categorically state that nv/v CJD is the only risk to
endoscopy equipment, while ignoring all other TSEs, is very
unsubstantiated. i will try and give more evidence for my concerns
below. 1st, there has never been to date any _documented_ transmission
of nv/v CJD via the medical surgical arena. this has only been
hypothesized... 2nd, However, there has been _documented_ evidence of
transmission of sporadic CJD via the medical and surgical arena. TO
continue to hide behind the nv/v CJD only theory, when there are over 20
strains of scrapie, most of which transmits to all mammalian species
that has been tried upon, CWD which no one knows if or if not it can
transmit to humans (to date no transmission studies of any TSEs done on
man), but studies have shown transmission to humans as easy as BSE, and
does transmit to primate. there are now 6 _documented_ phenotypes of
sporadic CJD. with CWD and Scrapie running rampant in the USA, no real
active surveillance in cattle for TSEs and no rapid testing done to find
BSE agent (48,000+ BSE/TSE test in 14 years TOTAL USA), who knows how
these strains of CJD will act and how they will transmit. also, in vitro
experiments have demonstrated that scrapie/cwd prions are as efficient
as BSE prions in transforming normal human prion protein to PrPSc. this
data strongly supports that scrapie/cwd is as infectious as BSE. IN
fact, scrapie seems to be more infectious than BSE due to higher
concentration of TSE infectious agents in ovine muscle meat and other
parts of the sheep, when compared to cattle, and CWD could even be more
infectious than all of them, if you consider how it has rapidly spread
across the USA. but to categorically state that only nv/v CJD to be of
risk to endoscopy equipment when no such documented transmission has
ever been documented, while ignoring such similar medical _documented_
transmissions in sporadic CJD, this is very disturbing and most
unsubstantiated, and potentially risking TSE exposure to millions and
millions due to nothing more than denial and wishful thinking. if i
could deny this and wish it away, i would have done this six years ago.
but we cant, all we can do is warn the public and the medical community
of what we know to date. i am surprised GUT has chosen not to do this,
and only to go with the BSE/nv/v/CJD only theory. 85%+ of all CJDs don't
just happen without route and source. my fear is a great deal are being
mis-diagnosed and un-reported, but being acquired via the medical
surgical arena. but one will never know without making all human TSEs
reportable in every State, and issuing a CJD Questionnaire to all
families of victims of CJD/TSE and asking the _real_ questions that
pertain to route and source of agent...TSS REFERENCES
snip...end
http://neuro-mancer.mgh.harvard.edu/ubb/Forum24/HTML/000145.html
FULL TEXT ;
http://www.vegsource.com/talk/madcow/messages/93658.html
TSS
HISTORY OF GUT, ENDOSCOPY, CJD AND TSS
http://www.vegsource.com/talk/madcow/messages/93658.html
http://www.google.com/search?num=30&hl=en&lr=&edition=us&ie=UTF-8&search=search&tab=wn&scoring=d&q=CJD+ENDOSCOPY+TSS&btnmeta%3Dsearch%3Dsearch=Search+the+Web
MAD COW i.e. all TSE 'FRIENDLY FIRE' GETTING SERIOUS (iCJD)
##################### Bovine Spongiform Encephalopathy #####################
CJD WATCH MESSAGE BOARD
TSS
Detection and Localization of PrPSc in the Skeletal Muscle
Thu Mar 2, 2006 10:40
70.110.86.250
© 2006 American Society for Investigative Pathology
Detection and Localization of PrPSc in the Skeletal Muscle of Patients with Variant, Iatrogenic, and Sporadic Forms of Creutzfeldt-Jakob Disease
Alexander H. Peden, Diane L. Ritchie, Mark W. Head and James W. Ironside
From the National Creutzfeldt-Jakob Disease Surveillance Unit and Division of Pathology, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom
Variant Creutzfeldt-Jakob disease (vCJD) differs from other human prion diseases in that the pathogenic prion protein PrPSc can be detected to a greater extent at extraneuronal sites throughout the body, principally within lymphoid tissues. However, a recent study using a high-sensitivity Western blotting technique revealed low levels of PrPSc in skeletal muscle from a quarter of Swiss patients with sporadic CJD (sCJD). This posed the question of whether PrPSc in muscle could also be detected in vCJD, sCJD, and iatrogenic (iCJD) patients from other populations. Therefore, we have used the same high-sensitivity Western blotting technique, in combination with paraffin-embedded tissue blotting, to screen for PrPSc in muscle tissue specimens taken at autopsy from 49 CJD patients in the United Kingdom. These techniques identified muscle PrPSc in 8 of 17 vCJD, 7 of 26 sCJD, and 2 of 5 iCJD patients. Paraffin-embedded tissue blotting analysis showed PrPSc in skeletal muscle in localized anatomical structures that had the morphological and immunohistochemical characteristics of nerve fibers. The detection of PrPSc in muscle tissue from all forms of CJD indicates the possible presence of infectivity in these tissues, suggesting important implications for assessing the potential risk of iatrogenic spread via contaminated surgical instruments.
http://ajp.amjpathol.org/cgi/content/abstract/168/3/927
TSS
#################### https://lists.aegee.org/bse-l.html ####################
BSE ALSO;
PrPSc distribution of a natural case of bovine spongiform encephalopathy
Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Kannondai, Tsukuba 305-0856 Japan gan@affrc.go.jp
Abstract
Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes progressive neurodegeneration of the central nervous system. Infectivity of BSE agent is accompanied with an abnormal isoform of prion protein (PrPSc). The specified risk materials (SRM) are tissues potentially carrying BSE infectivity. The following tissues are designated as SRM in Japan: the skull including the brain and eyes but excluding the glossa and the masse- ter muscle, the vertebral column excluding the vertebrae of the tail, spinal cord, distal illeum. For a risk management step, the use of SRM in both animal feed or human food has been prohibited. However, detailed PrPSc distribution remains obscure in BSE cattle and it has caused controversies
about definitions of SRM. Therefore we have examined PrPSc distribution in a BSE cattle by Western blotting to reassess definitions of SRM. The 11th BSE case in Japan was detected in fallen stock surveillance. The carcass was stocked in the refrigerator. For the detection of PrPSc, 200 mg of tissue samples were homogenized. Following collagenase treatment, samples were digested with proteinase K. After digestion, PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets were subjected to Western blotting using the standard procedure. Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish peroxidase was used for the detection of PrPSc. PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve). Our results suggest that the currently accepted definitions of SRM in 9/13/2005
179
Page 10 of 17
BSE cattle may need to be reexamined.
T. Kitamoto (Ed.)
PRIONS
Food and Drug Safety
================
ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004; Bovine spongiform encephalopathy (BSE) in Japan
snip...
"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion" NO. Date conf. Farm Birth place and Date Age at diagnosis 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21 Test results # 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative b = atypical BSE case c = case of BSE in a young animal b,c, No PrPSc on IHC, and no spongiform change on histology International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004. Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; kitamoto@mail.tains.tohoku.ac.jp Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: kvomi-sasaki@mail.tains.tohoku.ac.ip ================================= 9/13/2005
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
Page 11 of 17 From: TSS () Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Date: August 26, 2005 at 10:24 am PST Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Jpn. J. Infect. Dis., 56, 221-222, 2003 Laboratory and Epidemiology Communications Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2 Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata (Accepted December 2, 2003) *Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640,
Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail: yamakawa@nih.go.jp
Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC, all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus. An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane 2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-monthold
Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect positive signals of PrPSc (data not shown). Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype, have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal (MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF report, the previous seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed. However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present cases remains to be investigated.
REFERENCES Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383, 685690.
Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J.
(1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389, 498-501.
Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389, 448-450.
Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK.
Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel
molecular and neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen,
October 8-10.
Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie. International Conference on Prion Disease: from
basic research to intervention concepts. Gasreig, Munhen, October 8-10.
Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE
prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366.
9/13/2005
Page 12 of 17 SEE SLIDES IN PDF FILE; http://www.nih.go.jp/JJID/56/221.pdf
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
AND CWD;
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§ 1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA. *These authors contributed equally to this work. †Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA. ‡Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. §To whom correspondence should be addressed: E-mail: gtell2@uky.edu Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD. To test whether skeletal muscle of diseased cervids.........SNIP....END
TSS
A female Rush Limbaugh who appeals to the morons that now seem to make up most of American society. The wealthy elite have done their dumbing-down of what used to be admirable human beings very well, as evidenced by scum like Coulter being popular. Whether America was ever truly "a great country" I don't know. It's definitely the largest collection of psychos in history now. I look forward to its end.
hi john,
indeed, usda et al should have listened to you, sheldon, and everybody else
that have tried to tell them for eons about TSE in the USA. but instead,
USDA et al goes into cover-up mode, which is why this agent has now mutated
and spread to hell and back. in essence, the USA was worse than the UK about
spreading the agent via exports.
now, well, i think it is too late. lets compare ;
IN CONFIDENCE Perceptions of unconventional slow virus disease of animals in
the USA
G A H Wells
REPORT OF A VISIT TO THE USA APRIL-MAY 1989
john, check out pages 13 to 17
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Gerald Wells: Report of the Visit to USA, April-May 1989
snip...
The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...
snip...
It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...
snip...
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_...
snip...
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle
R.F. Marsh* and G.R. Hartsough
.Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin
53092
ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.
INTRODUCTION
Transmissible mink encephalopathy (TME) was first reported in 1965 by
Hartsough
and Burger who demonstrated that the disease was transmissible with a long
incubation
period, and that affected mink had a spongiform encephalopathy similar to
that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough,
1965).
Because of the similarity between TME and scrapie, and the subsequent
finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it
was
concluded that TME most likely resulted from feeding mink scrapie-infecied
sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time
provided
evidence that they may be different. Epidemiologic studies on previous
incidences of
TME indicated that the incubation periods in field cases were between six
months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie
could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular
strain of
scrapie which might be highly pathogenic for mink, 21 different strains of
the scrapie
agent, including their sheep or goat sources, were inoculated into a total
of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation
period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was
either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a
scrapie-like agent
from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville,
Wisconsin
reported that many of his mink were "acting funny", and some had died. At
this time, we
visited the farm and found that approximately 10% of all adult mink were
showing
typical signs of TME: insidious onset characterized by subtle behavioral
changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen
rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and
tails arched over
their _backs like squirrels. These signs were followed by progressive
deterioration of
neurologic function beginning with locomoior incoordination, long periods of
somnolence
in which the affected mink would stand motionless with its head in the
corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks,
approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared
feeding
practices, we obtained a careful history of feed ingredients used over the
past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or
dead dairy
cattle and a few horses. Sheep had never been fed.
Experimental Transmission.
The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after
incubation
periods of four months. To investigate the possible involvement of cattle in
this disease
cycle, two six-week old castrated Holstein bull calves were inoculated
intracerebrally
with a brain suspension from affected mink. Each developed a fatal
spongiform
encephalopathy after incubation periods of 18 and 19 months.
DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle
and
we have alerted bovine practitioners that there may exist an as yet
unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough,
1986). A new
bovine spongiform encephalopathy has recently been reported in England
(Wells et al.,
1987), and investigators are presently studying its transmissibility and
possible
relationship to scrapie. Because this new bovine disease in England is
characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely
it would be
confused with rabies in the United Stales and not be diagnosed. Presently,
brains from
cattle in the United States which are suspected of rabies infection are only
tested with
anti-rabies virus antibody and are not examined histopathologically for
lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the
backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no
agent-
specific proteins or nucleic acids identified for these transmissible
neuropathogens, one
means of distinguishing them is by animal passage and selection of the
biotype which
grows best in a particular host. This procedure has been used to separate
hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The
intracerebral
backpassage of the experimental bovine agent resulted in incubations of only
four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine
passage.
Mink fed infected bovine brain remain normal after six months. It will be
essential to
demonstrate oral transmission fiom bovine to mink it this proposed
epidemiologic
association is to be confirmed.
ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life
Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the
United
States Department of Agriculture. The authors also wish to acknowledge the
help and
encouragement of Robert Hanson who died during the course of these
investigations.
REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II.
Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and
Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I.
Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of
the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow
transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp
451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in
cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal
Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D.,
Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform
encephalopathy
in cattle. Vet. Rec. 121:419-420.
MARSH
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
WORLD ASSOCIATION FOR BUIATRICS
Edinburgh 8 -12 July 1996
http://www.bseinquiry.gov.uk/files/mb/m09/tab04.pdf
Transmission Studies of BSE in Sheep
http://www.bseinquiry.gov.uk/files/mb/m09/tab01.pdf
J. Comp. Path. 2006, Vol. 134, 63-69
Experimental Second Passage of Chronic Wasting
Disease (CWDmule deer) Agent to Cattle
A. N. Hamir, R. A. Kunkle, J. M. Miller, J. J. Greenlee and J. A. Richt
Agricultural Research Service, United States Department of Agriculture,
National Animal Disease Center, 2300 Dayton
Avenue, P.O. Box 70, Ames, IA 50010, USA
Summary
To compare clinicopathological findings in first and second passage chronic
wasting disease (CWDmule deer)
in cattle, six calves were inoculated intracerebrally with brain tissue
derived froma first-passageCWD-affected
calf in an earlier experiment. Two uninoculated calves served as controls.
The inoculated animals began to
lose both appetite and weight 10-12 months later, and five subsequently
developed clinical signs of central
nervous system (CNS) abnormality. By 16.5 months, all cattle had been
subjected to euthanasia because of
poor prognosis. None of the animals showed microscopical lesions of
spongiform encephalopathy (SE) but
PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and
rapid Western blot (WB)
techniques. Thus, intracerebrally inoculated cattle not only amplified CWD
PrPres from mule deer but also
developed clinicalCNSsigns in the absence of SElesions.This situation has
also been shown to occur in cattle
inoculated with the scrapie agent. The study confirmed that the diagnostic
techniques currently used for
diagnosis of bovine spongiformencephalopathy (BSE) in theUS would detect
CWDin cattle, should it occur
naturally. Furthermore, it raised the possibility of distinguishing
CWDfromBSE in cattle, due to the absence
of neuropathological lesions and to a distinctive multifocal distribution of
PrPres, as demonstrated by IHC
which, in this study, appeared to be more sensitive than the WB technique.
snip...
Discussion
CWD, like all other TSEs, is characterized by a long
incubation period, which in deer is seldom less
than 18 months (Williams and Young, 1992). In an
experimental study of cattle inoculated intracerebrally
with CWD from mule deer (first passage),
amplification of PrPres was demonstrated in only
five of 13 (38%) cattle, after incubation periods
that ranged from 23 to 63 months (Hamir et al.,
2001a, 2005a). In contrast, all inoculated cattle in
the present study were positive for PrPres within
16.5 months. This increased attack rate with shorter
incubation periods probably indicates adaptation
of the CWDmule deer agent to a new host. It could
also be argued that the inoculum used for the
primary passage (Hamir et al., 2001a, 2005a) had a
lower infectivity titre than that used for the second
passage. However, the former successfully transmitted
CWD to each of five white tailed deer within
two years of intracerebral inoculation (Kunkle et al.,
Unpublished).
In cervids, clinical CWD is characterized by
emaciation, changes in behaviour, and excessive
salivation (Williams and Young, 1992). Although
the latter was not observed in the CWD inoculated
cattle, all animals showed anorexia and considerable
weight loss. Five cattle also showed intermittent
neurological signs. Although none of these
animals showed histopathological changes in the
brain, all were shown to be positive for PrPres by the
IHC and WB methods. The presence of isolated
vacuoles in the red nucleus is regarded as an
incidental finding in cattle (McGill and Wells,
1993).
The uniform susceptibility, relatively short incubation,
and absence of microscopical lesions in
cattle given CWD brain material passaged once
through cattle resembled findings in cattle inoculated
intracerebrally with the scrapie agent (Cutlip
et al., 1997). In that experiment, 100% of cattle
died 14-18 months after inoculation with material
from the first cattle-passage of a US strain of the
scrapie agent; none showed microscopical lesions
and all were positive for PrPres.
In the present experiment, the possibility that
the PrPres seen in tissue sections represented
residual CWD material from the inoculum was
ruled out because of the multifocal distribution of
PrPres throughout the brain (excluding cerebellar
folia) and cervical spinal cord of most of the
affected animals. Had the PrPres represented
residual inoculum, it would probably have been
confined to the sites of deposition in the midbrain
or cerebrum. Moreover, in studies on sheep
scrapie, Hamir et al. (2002) showed that intracerebrally
inoculated brain material containing PrPres
was present for only a few days in sufficient quantity
to be detectable immunohistochemically.
The present work confirms previous observations
that PrPres IHC labelling in cattle inoculated
with the mule deer CWD agent is multifocal
and glial cell-associated. This unusual pattern was
first reported in descriptions of the primary CWD
transmission to cattle (Hamir et al., 2001a, 2005a),
and the study described here showed that it was
maintained through the second passage in cattle.
Further studies now in progress will determine
whether this feature also characterizes CWD transmission
to cattle fromother cervid species other than
mule deer, namely, white tailed deer and elk.
In this and an earlier study of CWD in cattle
(Hamir et al., 2001a), IHC labelling differed from
that seen in cattle with BSE or experimental
transmissible mink encephalopathy (TME), both
of which are associated with widespread diffuse
labelling of grey matter neuropil, with labelled
particles that are not obviously cell-associated
except occasionally at neuronal cell membranes
(Wells and Willsmith, 1995; Hamir et al., 2005a).
The IHC pattern in bovine CWD also contrasts
markedly with that seen in scrapie-inoculated
cattle, in which intracytoplasmic labelling of
neurons is a prominent feature (Cutlip et al.,
1994, 1997).
When brainstems of CWD-infected cattle were
analysed by WB for the presence of PrPres, only
three of six samples were found to be positive
(Table 1). In contrast, all samples from the
midbrain area were positive by this technique
(Table 1; Fig. 5). It was noteworthy, however, that
both brainstem and midbrain sections of all
animals infected with CWD gave positive IHC
results (Table 1) and a positive WB was associated
with strong IHC labelling. This may indicate that
the IHC procedure is more sensitive than the WB
method for cattle-passaged CWD. However, given
the multifocal nature of PrPres distribution in the
CNS of CWD-infected cattle, this result is not
surprising. WB analysis requires a small sample of
brain tissue (e.g. 0.2 g, as in the present study) to
produce a 10% homogenate; approximately 10 ml
(1 mg brain tissue equivalent) of this homogenate
are loaded on to an SDS-PAGE gel for further
analysis. Bearing in mind the multifocal pattern of
PrPres distribution, the brain tissue used for the
preparation of WB homogenate, unlike the large
amount examined in the IHC procedure, might
well contain few if any foci of PrPres deposition,
whereas the larger piece of tissue section used for
IHC may contain detectable PrPres. In this respect,
therefore, the IHC method would seem preferable
to the WB procedure and to other procedures (e.g.
ELISA-based tests) in which only small amounts of
tissue are used for analysis.
In comparison with experimental TME in cattle
(Hamir et al., 2005b), the experimental bovine
CWD in this study was associated with less extensive
IHC labelling in non-CNS (i.e. other than brain
and spinal cord) neural tissues. Whereas the retina
was positive in all cattle inoculated with TME, none
of the CWD-infected cattle in this experiment had
any retinal labelling. Similarly, in the present study
there was no labelling in the pituitary gland, a
tissue sometimes positive in TME-infected cattle.
Because the incubation time for second passage
CWD transmission (mean of 468 days) was only
slightly longer than for TME (mean of 430 days), it
seems likely that these different tissue affinities
reflect a biological difference between these two
TSE agents.
PrPres IHC labelling was not observed in striated
muscles (heart, tongue, masseter, diaphragm) of
the experimental animals. This observation
accorded with our previous findings (Hamir et al.,
2004a) in which striated muscle tissues from 20
animals (cattle, sheep, elk and raccoons) were
examined for PrPres. In these animals, all of which
had developed a TSE after experimental inoculation,
PrPres was found by IHC examination in the
brains, but not in muscle tissues. However, recent
investigations with an enriched WB technique
(Mulcahy et al., 2004) have enabled us to detect
PrPres in the tongues of some sheep and elk
experimentally inoculated with scrapie and CWD,
respectively. This technique failed, however, to
detect PrPres in cattle inoculated with CWD or
TME (Bessen et al., unpublished). This study is still
in progress, and the tongues of TSE-infected
animals are currently being tested after careful
removal from the carcasses to ensure non-contamination
with infected brain material.
The present study and a previous experiment
(Hamir et al., 2005a) have established the biological
characteristics of the CWDmule deer agent in cattle.
However, isolates of CWD from other cervids (e.g.
CWDwhite-tailed and CWDelk) may differ. Transmission
experiments with different CWD isolates
are therefore needed to examine the possibility of
variation in the CWD agent in wild cervids. Such
experiments have recently been initiated at the
National Animal Disease Center (NADC).............snip...END...TSS
ALSO, I THINK THE DOWNER COW FIGURE IS UNDERESTIMATED;
Released May 5, 2005, by the National Agricultural Statistics Service
(NASS), Agricultural Statistics Board, U.S. Department
of Agriculture. For information on Non-ambulatory Cattle and Calves call
Mike Miller at 720-3040, office hours 7:30 a.m. to
4:30 p.m. ET.
Non-Ambulatory Cattle and Calves
Non-ambulatory cattle and calves in the United States totaled 465,000 head
during 2003 and
450,000 head during 2004. The number of non-ambulatory cattle 500 pounds or
greater totaled
280,000 head in 2003 and 270,000 head in 2004. The number of calves under
500 pounds reported
as non-ambulatory totaled 185,000 head in 2003 and 180,000 head in 2004.
The number of operations that reported non-ambulatory cattle and calves was
103,000 in 2003 and
81,000 in 2004. In 2003, there were 66,800 beef cow operations reporting
non-ambulatory cattle
and calves compared to 49,700 in 2004. There were 22,800 dairy operations
reporting nonambulatory
cattle and calves in 2003 compared to 23,000 in 2004.
This report is released as a cooperative effort between the National
Agricultural Statistics Service
and Animal and Plant Health Inspection Service - Veterinary Services. Data
for this report were
collected on the January 1, 2004 and 2005 Cattle Surveys. .......END....TSS
From: TSS ()
Subject: Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus)
Date: October 19, 2005 at 8:33 am PST
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel
Monkeys (Saimiri sciureus)
Richard F. Marsh,1, Anthony E. Kincaid,2 Richard A. Bessen,3 and Jason C.
Bartz4*
Department of Animal Health and Biomedical Sciences, University of
Wisconsin, Madison 53706,1 Department of Physical Therapy,2 Department of
Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska
68178,4 Department of Veterinary Molecular Biology, Montana State
University, Bozeman, Montana 597183
Received 3 May 2005/ Accepted 10 August 2005
Chronic wasting disease (CWD) is an emerging prion disease of deer and elk.
The risk of CWD transmission to humans following exposure to CWD-infected
tissues is unknown. To assess the susceptibility of nonhuman primates to
CWD, two squirrel monkeys were inoculated with brain tissue from a
CWD-infected mule deer. The CWD-inoculated squirrel monkeys developed a
progressive neurodegenerative disease and were euthanized at 31 and 34
months postinfection. Brain tissue from the CWD-infected squirrel monkeys
contained the abnormal isoform of the prion protein, PrP-res, and displayed
spongiform degeneration. This is the first reported transmission of CWD to
primates.
----------------------------------------------------------------------------
----
* Corresponding author. Mailing address: Department of Medical Microbiology
and Immunology, Creighton University, 2500 California Plaza, Omaha, NE
68178. Phone: (402) 280-1811. Fax: (402) 280-1875. E-mail:
jbartz@creighton.edu .
Deceased.
----------------------------------------------------------------------------
----
Journal of Virology, November 2005, p. 13794-13796, Vol. 79, No. 21
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
http://jvi.asm.org/cgi/content/abstract/79/21/13794?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=cwd&searchid=1129736446553_4280&stored_search=&FIRSTINDEX=0&volume=79&issue=21&journalcode=jvi
===================================
Intra- & Inter-species Transmission of Chronic Wasting Disease (Show All
REXs)
Description: This research is intended to investigate the intra- and
inter-species transmissibility of the causative agent of chronic wasting
disease (CWD), believed to be a structurally modified form of the prion
protein (PrPCWD), of white-tailed deer (Odocoileus virginianus). Our lab has
identified five alleles in the PrP-coding region of white-tailed deer from
the CWD-affected region of southern Wisconsin. Combinations of the alleles
represent variability within the population and may result in differences in
incubation period, levels of susceptibility, variable clinical symptoms
and/or pathology within deer. We will test these ideas by inoculating
white-tailed deer of known genotype with known-genotype PrPCWD and by
conducting cell-free conversion experiments with the possible combinations
of PrPCWD. We believe environment may be a reservoir of CWD, which opens
possibilities of transmission to wildlife that share habitat with
white-tailed deer. We will identify the species that consume deer carrion,
as they are the most likely to encounter PrPCWD, collect 100 of each species
from the CWD-affected region of southern Wisconsin and evaluate them for
lesion profiles indicative of prion disease. We believe the primary carrion
consumers will include coyote (Canis latrans), red fox (Vulpes vulpes), gray
fox (Urocyon cinereoargenteus), raccoon (Procyon lotor), striped skunk
(Mephitis mephitis), Virginia opossum (Didelphis virginiana), and mink
(Mustela vison). Since species barriers are difficult to cross we dont
expect to find a large prevalence of prion disease in this population of
wildlife. To address the possibility of transmission to these species, we
will inoculate raccoons, striped skunks, Virginia opossums and Eastern
cottontails (Sylvilagus floridanus) with PrPCWD. We will test transmission
to other species by cell-free conversion with as many species as possible,
starting with those whose life history are most likely to expose them to
PrPCWD. The species that we are collecting from the CWD-affected region of
southern Wisconsin for prion disease assessment are a significant collection
that we will use to survey a range of other wildlife diseases. This is a
five-year project with publications anticipated in the third through fifth
year. Students that would join me for work could experience lab or field
work. We will be placing dead deer on the landscape, setting
remote-triggered cameras on the deer and checking the cameras every other
day. We will collect raccoons, skunks, opossums, coyotes and foxes from
trappers and conduct necropsies on them at the WVDL. We will be running
Western blots for TSE testing on the brains of the animals we necropsy. We
will do PCR/Sequencing on the prion-coding region of each species, clone it
into an expression vector and conduct cell-free conversions on the resulting
protein.
Date: Feb 20
Week: Week 1 (Week of Feb 20)
Location (where students meet host): Room 237 Animal Health & Biomedical
Sciences Building, 1656 Linden Drive
Meets From: 3:30 pm until 5:30 pm
Pre-REX Reading: None
Laboratory:
Lab Address: 237 Animal Health & Biomedical Sciences Bldg, 1656 Linden Drive
Lab Phone: 262-7362
Lab Website: http://www.ahabs.wisc.edu/Faculty/Aiken-j/index.html
Department or Institute: Animal Health & Biomedical Sciences
College or School: School of Veterinary Medicine
Host: Dr. Judd Aiken
Host Email: jma@ahabs.wisc.edu
Host Phone: 262-7362
Co-Host: Chad Johnson
Co-Host Email: cjjohns3@students.wisc.edu
Co-Host Phone:
Total Number of Students Allowed: 5
Number of Openings: 0
================================
USA EXPORTS
2006
http://www.ers.usda.gov/Briefing/Cattle/Data/AnnualLivestockTable.xls
TOP FIVE COUNTRIES IMPORTING USDA MAD COW PRODUCTS
The Economic Impact of BSE
on the U.S. Beef Industry:
Product Value Losses, Regulatory
Costs, and Consumer Reactions
3.4 U.S. Beef Export Customers
Table 3.4 provides a dollar value ranking,
by country, of beef export shipments during
2003. Five countries, Japan, Mexico, South
Korea, Canada, and Hong Kong, were the
recipients of 90 percent of U.S .beef exports
during 2003, based on value. Japan, historically
the largest U.S. beef export customer,
represented 35 percent of U.S. beef exports
during 2003.
http://www.ksda.gov/Default.aspx?tabid=349&mid=2252&ctl=Download&method=attachment&EntryId=479
WHOS EATING THOSE USDA MAD COW BRAINS OF AN ATYPICAL STRAIN ?
0206.29.0010: HEARTS OF BOVINE ANIMALS, EDIBLE, FROZEN
Skip this table
U.S. Domestic Exports: December 2003 and 2003 Year-to-Date,
not Seasonally Adjusted
(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilograms) December 2003 2003, through December
Quantity Value Quantity Value
WORLD TOTAL 1,180,635 1,038 17,267,397 12,630
Angola 0 0 47,849 31
China 0 0 97,868 41
Colombia 0 0 355,787 379
Costa Rica 0 0 4,816 4
El Salvador 4,545 4 4,545 4
Greece 0 0 15,000 6
Guatemala 0 0 19,051 18
Honduras 0 0 9,780 8
Hong Kong 45,347 110 454,574 862
Indonesia 597,243 459 8,098,035 4,681
Ivory Coast 0 0 27,216 8
Japan 0 0 19,835 20
Korea, South 49,890 50 213,036 213
Lithuania 0 0 55,194 31
Mexico 280,421 234 2,664,118 2,384
Netherlands 0 0 108,698 61
Peru 0 0 452,116 458
Russia 203,189 181 4,528,474 3,280
Saudi Arabia 0 0 3,293 6
Singapore 0 0 44,906 21
Switzerland 0 0 8,010 8
United Arab Emirates 0 0 135 3
United Kingdom 0 0 35,061 105
0206.29.0020: KIDNEYS OF BOVINE ANIMALS, EDIBLE, FROZEN
Skip this table
U.S. Domestic Exports: December 2003 and 2003 Year-to-Date,
not Seasonally Adjusted
(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilograms) December 2003 2003, through December
Quantity Value Quantity Value
WORLD TOTAL 330,004 231 3,566,918 1,818
China 49,424 26 141,576 64
Gabon 0 0 49,437 28
Greece 0 0 966 6
Indonesia 0 0 23,610 15
Ivory Coast 49,891 25 1,699,427 704
Jamaica 115,626 67 875,874 436
Mexico 115,063 113 521,638 465
Russia 0 0 115,377 70
Saudi Arabia 0 0 1,660 3
South Africa 0 0 111,960 18
Thailand 0 0 25,393 10
0206.29.0030: BRAINS OF BOVINE ANIMALS, EDIBLE, FROZEN
Skip this table
U.S. Domestic Exports: December 2003 and 2003 Year-to-Date,
not Seasonally Adjusted
(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilograms) December 2003 2003, through December
Quantity Value Quantity Value
WORLD TOTAL 57,279 56 192,198 225
Ivory Coast 0 0 24,971 8
Mexico 57,279 56 161,158 211
Sweden 0 0 6,069 6
0206.29.0040: SWEATBREADS OF BOVINE ANIMALS, EDIBLE, FROZEN
Skip this table
U.S. Domestic Exports: December 2003 and 2003 Year-to-Date,
not Seasonally Adjusted
(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilograms) December 2003 2003, through December
Quantity Value Quantity Value
WORLD TOTAL 48,735 69 581,306 689
Bahamas 0 0 4,551 5
Hong Kong 0 0 48,988 15
Japan 0 0 18,629 51
Mexico 48,735 69 507,453 611
Switzerland 0 0 1,685 6
0206.29.0050: LIPS OF BOVINE ANIMALS, EDIBLE, FROZEN
Skip this table
U.S. Domestic Exports: December 2003 and 2003 Year-to-Date,
not Seasonally Adjusted
(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilograms) December 2003 2003, through December
Quantity Value Quantity Value
WORLD TOTAL 620,626 1,393 16,539,594 23,262
Hong Kong 0 0 23,587 8
Mexico 620,626 1,393 16,513,038 23,245
Taiwan 0 0 2,969 10
0206.29.0090: OFFAL OF BOVINE ANIMALS, EDIBLE, NESOI, FROZEN
Skip this table
U.S. Domestic Exports: December 2003 and 2003 Year-to-Date,
not Seasonally Adjusted
(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilograms) December 2003 2003, through December
Quantity Value Quantity Value
WORLD TOTAL 8,464,956 16,117 118,262,413 197,532
Argentina 1,497 9 1,497 9
Australia 6,103 6 72,627 71
Bahamas 0 0 25,367 55
Barbados 0 0 1,282 6
Belgium 0 0 718,837 142
Bulgaria 0 0 328,698 261
Burkina 0 0 23,496 21
Canada 304,064 276 8,137,388 6,048
China 734,212 1,750 7,554,286 16,429
Colombia 0 0 109,398 141
Costa Rica 0 0 53,911 37
Denmark 0 0 8,327 33
Dominican Republic 19,578 168 112,192 767
Egypt 0 0 167,000 96
Federal Rep. of Germany 104,016 21 2,266,317 583
Gabon 24,494 16 339,168 177
Greece 23,610 26 47,220 51
Guatemala 0 0 200,509 233
Guyana 0 0 11,555 12
Hong Kong 339,453 704 4,490,896 7,651
Indonesia 104,013 108 1,231,976 666
Israel 0 0 119,230 121
Ivory Coast 0 0 1,429,316 876
Jamaica 79,203 73 780,910 696
Japan 2,614,703 7,006 29,370,030 78,245
Jordan 0 0 72,709 390
Korea, South 1,084,495 2,217 19,825,887 37,280
Macedonia (Skopje) 0 0 143,699 51
Malaysia 0 0 24,776 10
Mexico 2,463,516 2,922 30,710,290 37,936
Netherlands 0 0 38,512 65
Nicaragua 0 0 9,411 11
Panama 0 0 480,391 472
Peru 0 0 47,135 29
Philippines 37,875 15 216,218 116
Poland 47,175 36 954,552 532
Romania 0 0 991,737 765
Russia 368,385 325 3,490,349 2,441
Singapore 0 0 5,307 15
St Lucia 2,442 3 10,896 14
Sweden 0 0 46,200 45
Taiwan 106,122 436 1,601,333 3,327
Turks and Caicos Islands 0 0 8,536 14
United Arab Emirates 0 0 27,439 130
United Kingdom 0 0 1,842,710 369
Uruguay 0 0 112,893 95
Top of page
http://www.ita.doc.gov/td/industry/otea/Trade-Detail/Latest-December/Exports/02/020629.html
0206.21.0000: TONGUES OF BOVINE ANIMALS, EDIBLE, FROZEN
Skip this table
U.S. Domestic Exports: December 2003 and 2003 Year-to-Date,
not Seasonally Adjusted
(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilograms) December 2003 2003, through December
Quantity Value Quantity Value
WORLD TOTAL 1,377,073 7,372 27,349,941 105,661
Canada 0 0 5,159 7
China 66,968 208 675,449 1,382
Costa Rica 0 0 6,567 18
Hong Kong 121,237 431 2,176,415 3,917
Indonesia 24,957 13 39,957 17
Japan 920,049 5,943 17,255,240 83,562
Korea, South 89,412 404 2,435,561 8,129
Malaysia 0 0 23,596 10
Mexico 45,264 126 1,258,740 3,282
Poland 0 0 23,596 14
Russia 51,472 49 3,083,619 3,942
Taiwan 57,714 198 354,691 1,260
Vietnam 0 0 11,351 121
Top of page
Source: Foreign Trade Division
, U.S. Census Bureau.
Presented by: Office of Trade and Economic Analysis (OTEA),
International Trade Administration, U.S. Department of Commerce.
http://www.ita.doc.gov/td/industry/otea/Trade-Detail/Latest-December/Exports/02/020621.html
##################### Bovine Spongiform Encephalopathy #####################
Subject: USDA, SPONTANEOUS MAD COW DISEASE, THE TOOTH FAIRY AND SANTA CLAUS
Date: June 12, 2006 at 5:18 am PST
IF we all believe the BSe that the USDA is trying to put out now about atypical BSE in USA cattle just arising spontaneously,
then we all should believe in the tooth fairy and santa claus as well.
IF USA scrapie transmitted to USA cattle long ago in experiments in a lab in Mission Texas did not produce UK BSE,
but something very different, then why would USA TSE cattle produce the UK human version of mad cow i.e. nvCJD?
IT wouldn't. USA sporadic cjd is increasing, the USA also has atypical human cases of unknown origin as well?
THERE are over 20 strains of scrapie, plus the atypical in sheep, and these strains are increasing in numbers.
SCRAPIE, CWD, AND TSE IN CATTLE i.e. ANIMAL TSE RAMPANT IN USA FOR DECADES, and amplified via rendering and
feeding practices, where USDA triple firewalls against BSE were nothing more than a mere smoke screen.
NO test tube TSE by either Prusiner or Soto, to date, have ever produced a TSE identical to the sporadic CJD. IN fact,
no test tube TSE has ever been produced that resembles _any_ natural field TSE.
IF you feed BSE tainted materials to cattle and primate, you have BSE and nvCJD.
IF you feed USA sheep strain to USA cattle, you get USA TSE.
IF you feed USA tainted cattle to humans, you get USA mad cow disease.
IF you feed sporadic CJD to primate you get a CJD infected primate.
NOTHING spontaneous about it at all.
USA is in a very unique situation. there are more documented TSE in different species than any other country,
all of which have been rendered and fed back to animals for human and animal consumption, for decades. Millions exposed,
and of these Millions, how many surgical and dental procedures have been done on these exposed, to pass on to others,
via the 'friendly fire' mode of transmission?
IF, the spontaneous TSE was true, then this would be Prusiner and everyone else that is trying to cash in on this agent with
there TSE rapid test, this would be there dream come true. IT would require mandatory BSE/TSE testing of all species,
due to the fact you could not ever eradicate it through any intervention. BUT, then again, the spontaneous TSE is like believing
in the tooth fairy or santa clause will be arriving at your house this year.
How long can this sharade continue $
How many more will become exposed and have to die $
Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease
Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli *
*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)
Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.
--------------------------------------------------------------------------------
C.C. and G.Z. contributed equally to this work.
||To whom correspondence should be addressed.
E-mail: salvatore.monaco@mail.univr.it.
www.pnas.org/cgi/doi/10.1073/pnas.0305777101
http://www.pnas.org/cgi/content/abstract/0305777101v1
: 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
Atypical cases of TSE in cases of TSE in
cattle and sheep cattle and sheep
H. De H. De Bosschere Bosschere
CODA/CERVA CODA/CERVA
Nat. Ref. Lab. Vet. Nat. Ref. Lab. Vet. TSEs TSEs
Belgium
http://www.var.fgov.be/pdf/1100_TSEDAY.pdf
USDA 2004 ENHANCED BSE SURVEILLANCE PROGRAM AND HOW NOT TO FIND BSE CASES (OFFICIAL DRAFT OIG REPORT)
snip...
CATTLE With CNS Symptoms Were NOT Always Tested
snip...
Between FYs 2002 and 2004, FSIS condemned 680 cattle of all ages due to CNS symptoms. About 357 of these could be classified as adult. We could validate that ONLY 162 were tested for BSE (per APHIS records. ...
snip...
WE interviewed officials at five laboratories that test for rabies. Those officials CONFIRMED THEY ARE NOT REQUIRED TO SUBMIT RABIES-NEGATIVE SAMPLES TO APHIS FOR BSE TESTING. A South Dakota laboratory official said they were not aware they could submit rabies-negative samples to APHIS for BSE testing. A laboratory official in another State said all rabies-negative cases were not submitted to APHIS because BSE was ''NOT ON THEIR RADAR SCREEN." Officials from New York, Wisconsin, TEXAS, and Iowa advised they would NOT submit samples from animals they consider too young. Four of the five States contacted defined this age as 24 months; Wisconsin defined it as 30 months. TEXAS officials also advised that they do not always have sufficient tissue remaining to submit a BSE sample. ...
snip...
FULL TEXT 54 PAGES OF HOW NOT TO FIND BSE IN USA ;
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_july_13_ig_rep.pdf
HUMAN TSE USA 2005
Animal Prion Diseases Relevant to Humans (unknown types?)
Thu Oct 27, 2005 12:05
71.248.128.109
About Human Prion Diseases /
Animal Prion Diseases Relevant to Humans
Bovine Spongiform Encephalopathy (BSE) is a prion
disease of cattle. Since 1986, when BSE was recognized,
over 180,000 cattle in the UK have developed the
disease, and approximately one to three million are
likely to have been infected with the BSE agent, most
of which were slaughtered for human consumption before
developing signs of the disease. The origin of the
first case of BSE is unknown, but the epidemic was
caused by the recycling of processed waste parts of
cattle, some of which were infected with the BSE agent
and given to other cattle in feed. Control measures
have resulted in the consistent decline of the epidemic
in the UK since 1992. Infected cattle and feed exported
from the UK have resulted in smaller epidemics in other
European countries, where control measures were applied
later.
Compelling evidence indicates that BSE can be
transmitted to humans through the consumption of prion
contaminated meat. BSE-infected individuals eventually
develop vCJD with an incubation time believed to be on
average 10 years. As of November 2004, three cases of
BSE have been reported in North America. One had been
imported to Canada from the UK, one was grown in
Canada, and one discovered in the USA but of Canadian
origin. There has been only one case of vCJD reported
in the USA, but the patient most likely acquired the
disease in the United Kingdom. If current control
measures intended to protect public and animal health
are well enforced, the cattle epidemic should be
largely under control and any remaining risk to humans
through beef consumption should be very small. (For
more details see Smith et al. British Medical Bulletin,
66: 185. 2003.)
Chronic Wasting Disease (CWD) is a prion disease of elk
and deer, both free range and in captivity. CWD is
endemic in areas of Colorado, Wyoming, and Nebraska,
but new foci of this disease have been detected in
Nebraska, South Dakota, New Mexico, Wisconsin,
Mississippi Kansas, Oklahoma, Minnesota, Montana, and
Canada. Since there are an estimated 22 million elk and
deer in the USA and a large number of hunters who
consume elk and deer meat, there is the possibility
that CWD can be transmitted from elk and deer to
humans. As of November 2004, the NPDPSC has examined 26
hunters with a suspected prion disease. However, all of
them appeared to have either typical sporadic or
familial forms of the disease. The NPDPSC coordinates
with the Centers for Disease Control and state health
departments to monitor cases from CWD-endemic areas.
Furthermore, it is doing experimental research on CWD
transmissibility using animal models. (For details see
Sigurdson et al. British Medical Bulletin. 66: 199.
2003 and Belay et al. Emerging Infectious Diseases.
10(6): 977. 2004.)
http://www.cjdsurveillance.com/abouthpd-animal.html
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is
with a human TSE surveillance system that is terrible
flawed. in 1997 cases of the _reported_ cases of cjd
were at 54, to 163 _reported_ cases in 2004. see stats
here;
p.s. please note the 47 PENDING CASES to Sept. 2005
p.s. please note the 2005 Prion D. total 120(8)
8=includes 51 type pending, 1 TYPE UNKNOWN ???
p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???
p.s. please note 2004 prion disease (6) 6=7 TYPE
UNKNOWN???
http://www.cjdsurveillance.com/resources-casereport.html
CWD TO HUMANS = sCJD ???
AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.
snip...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
snip...end
full text ;
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
VERY VERY IMPORTANT THING TO REMEMBER
>> Differences in tissue distribution could require new regulations
>> regarding specific risk material (SRM) removal.
Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
Project Number: 3625-32000-073-07
Project Type: Specific C/A
Start Date: Sep 15, 2004
End Date: Sep 14, 2007
Objective:
The objective of this cooperative research project with Dr. Maria Caramelli
from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct
comparative studies with the U.S. bovine spongiform encephalopathy (BSE)
isolate and the atypical BSE isolates identified in Italy. The studies will
cover the following areas: 1. Evaluation of present diagnostics tools used
in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison
of the U.S. BSE isolate and other typical BSE isolates with atypical BSE
cases. 3. Studies on transmissibility and tissue distribution of atypical
BSE isolates in cattle and other species.
Approach:
This project will be done as a Specific Cooperative Agreement with the
Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del
Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance
program to analyze the effectiveness of the U.S diagnostic tools for
detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE
isolate with atypical BSE isolates will provide further characterization of
the U.S. BSE isolate. Transmission studies are already underway using brain
homogenates from atypical BSE cases into mice, cattle and sheep. It will be
critical to see whether the atypical BSE isolates behave similarly to
typical BSE isolates in terms of transmissibility and disease pathogenesis.
If transmission occurs, tissue distribution comparisons will be made between
cattle infected with the atypical BSE isolate and the U.S. BSE isolate.
Differences in tissue distribution could require new regulations regarding
specific risk material (SRM) removal.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490
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. 32 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. 33 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.
34 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.
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543
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. 33
http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546
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.
34 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, 35
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. 36 It was also felt that the results of such an experiment would be
hard to interpret. While a negative result 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. 37 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. 38
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820550
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm
REPORT OF THE COMMITTEE ON SCRAPIE
Chair: Dr. Jim Logan, Cheyenne, WY
Vice Chair: Dr. Joe D. Ross, Sonora, TX
Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN.
The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance.
The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings.
Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories.
For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS.
snip...
Infected and Source Flocks
As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats.
Regulatory Scrapie Slaughter Surveillance (RSSS)
RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm . RSSS started April 1,
2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below.
Scrapie Testing
In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9).
Animal ID
As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises.
*This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans.
http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf
Date: April 30, 2006 at 4:49 pm PST
SCRAPIE USA UPDATE AS of March 31, 2006
2 NEW CASES IN GOAT, 82 INFECTED SOURCE FLOCKS, WITH 4 NEW INFECTED SOURCE
FLOCKS IN MARCH, WITH 19 SCRAPIE INFECTED RSSS REPORTED BY NVSL
http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html
Published online before print October 20, 2005
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102
Medical Sciences
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes
( sheep prion | transgenic mice )
Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||, Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude *
*Virologie Immunologie Moléculaires and ||Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. 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.
--------------------------------------------------------------------------------
Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper.
A.L.D. and V.B. contributed equally to this work.
To whom correspondence should be addressed.
Hubert Laude, E-mail: laude@jouy.inra.fr
www.pnas.org/cgi/doi/10.1073/pnas.0502296102
http://www.pnas.org/cgi/content/abstract/0502296102v1
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
Like lambs to the slaughter
31 March 2001
Debora MacKenzie
Magazine issue 2284
What if you can catch old-fashioned CJD by eating meat from a sheep infected
with scrapie?
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 ...
The complete article is 889 words long.
full text;
http://www.newscientist.com/article.ns?id=mg16922840.300
Neurobiology
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*,
Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James
Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys*
* Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction
des Sciences du Vivant/Département de Recherche Medicale, Centre de
Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc,
BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre
Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de
Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital,
75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western
General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and
Institute for Animal Health, Neuropathogenesis Unit, West Mains Road,
Edinburgh EH9 3JF, United Kingdom
Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)
Abstract
There is substantial scientific evidence to support the notion that bovine
spongiform encephalopathy (BSE) has contaminated human beings, causing
variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns
about the possibility of an iatrogenic secondary transmission to humans,
because the biological properties of the primate-adapted BSE agent are
unknown. We show that (i) BSE can be transmitted from primate to primate by
intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD
to humans could be readily recognized pathologically, whether it occurs by
the central or peripheral route. Strain typing in mice demonstrates that the
BSE agent adapts to macaques in the same way as it does to humans and
confirms that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. The agent responsible for French iatrogenic
growth hormone-linked CJD taken as a control is very different from vCJD but
is similar to that found in one case of sporadic CJD and one sheep scrapie
isolate. These data will be key in identifying the origin of human cases of
prion disease, including accidental vCJD transmission, and could provide
bases for vCJD risk assessment.
http://www.pnas.org/cgi/content/full/041490898v1
USDA CWD PROGRAM
http://www.aphis.usda.gov/vs/nahps/cwd/
USDA CWD MAP (slow to update)
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html
DRAFT
WYOMING GAME AND FISH DEPARTMENT
CHRONIC WASTING DISEASE MANAGEMENT PLAN
February 17, 2006
snip...
5. Predicted population effects on free-ranging elk based on captive elk chronically exposed to the CWD prion.
Forty-three female elk calves were trapped at the National Elk Refuge and transported to Sybille in February 2002. Elk were housed in pens, assumed to be environmentally contaminated with the CWD prion. Elk will be held throughout their lifetimes. Elk dying will be examined and cause of death determined. From these data, it will should be possible to model free-ranging elk mortality and population dynamics under extreme circumstances of CWD prion exposure and transmission. As of December 2005 (46 months post capture), 11 of 43 elk have died due to CWD. This compares to 100% mortality in less than 25 months in elk orally inoculated with different dosages of the CWD prion.
REVISED DRAFT
http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J.
Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§
1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders
Brown Center on Aging, 3Department of Neurology, University of Kentucky,
Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and
Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado
Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA.
*These authors contributed equally to this work.
†Present address: Department of Infectology, Scripps Research Institute,
5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA.
‡Present address: Institute of Neuropathology, University of Zurich,
Schmelzbergstrasse 12, 8091 Zurich, Switzerland.
§To whom correspondence should be addressed: E-mail: gtell2@uky.edu
Prions are transmissible proteinaceous agents of mammals that cause fatal
neurodegenerative diseases of the central nervous system (CNS). The presence
of infectivity in skeletal muscle of experimentally infected mice raised the
possibility that dietary exposure to prions might occur through meat
consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious
prion disease of North American cervids, is of particular concern. The
emergence of CWD in an increasingly wide geographic area and the
interspecies transmission of bovine spongiform encephalopathy (BSE) to
humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns
about zoonotic transmission of CWD.
To test whether skeletal muscle of diseased cervids contained prion
infectivity, Tg(CerPrP)1536 mice (2) expressing cervid prion protein
(CerPrP), were inoculated intracerebrally with extracts prepared from the
semitendinosus/semimembranosus muscle group of CWD-affected mule deer or
from CWD-negative deer. The availability of CNS materials also afforded
direct comparisons of prion infectivity in skeletal muscle and brain. All
skeletal muscle extracts from CWD-affected deer induced progressive
neurological dysfunction in Tg(CerPrP)1536 mice with mean incubation times
ranging between 360 and ~490 d, whereas the incubation times of prions from
the CNS ranged from ~230 to 280 d (Table 1). For each inoculation group, the
diagnosis of prion disease was confirmed by the presence of PrPSc in the
brains of multiple infected Tg(CerPrP)1536 mice (see supporting online
material for examples). In contrast, skeletal muscle and brain material from
CWD-negative deer failed to induce disease in Tg(CerPrP)1536 mice (Table 1)
and PrPSc was not detected in the brains of sacrificed asymptomatic mice as
late as 523 d after inoculation (supporting online material).
Our results show that skeletal muscle as well as CNS tissue of deer with CWD
contains infectious prions. Similar analyses of skeletal muscle BSE-affected
cattle did not reveal high levels of prion infectivity (3). It will be
important to assess the cellular location of PrPSc in muscle. Notably, while
PrPSc has been detected in muscles of scrapie-affected sheep (4), previous
studies failed to detect PrPSc by immunohistochemical analysis of skeletal
muscle from deer with natural or experimental CWD (5, 6). Since the time of
disease onset is inversely proportional to prion dose (7), the longer
incubation times of prions from skeletal muscle extracts compared to matched
brain samples indicated that prion titers were lower in muscle than in CNS
where infectivity titers are known to reach high levels. Although possible
effects of CWD strains or strain mixtures on these incubation times cannot
be excluded, the variable 360 to ~490 d incubation times suggested a range
of prion titers in skeletal muscles of CWD-affected deer. Muscle prion
titers at the high end of the range produced the fastest incubation times
that were ~30% longer than the incubation times of prions from the CNS of
the same animal. Since all mice in each inoculation group developed disease,
prion titers in muscle samples producing the longest incubation times were
higher than the end point of the bioassay, defined as the infectious dose at
which half the inoculated mice develop disease. Studies are in progress to
accurately assess prion titers.
While the risk of exposure to CWD infectivity following consumption of
prions in muscle is mitigated by relatively inefficient prion transmission
via the oral route (8), these
results show that semitendinosus/semimembranosus muscle, which is likely to
be consumed by humans, is a significant source of prion infectivity. Humans
consuming or handling meat from CWD-infected deer are therefore at risk to
prion exposure.
References and Notes
1. P. J. Bosque et al., Proc. Natl. Acad. Sci. U.S.A. 99, 3812 (2002).
2. S. R. Browning et al., J. Virol. 78, 13345 (2004).
3. A. Buschmann, M. H. Groschup, J. Infect. Dis. 192, 934 (2005).
4. O. Andreoletti et al., Nat. Med. 10, 591 (2004).
5. T. R. Spraker et al., Vet. Pathol. 39, 110 (2002).
6. A. N. Hamir, J. M. Miller, R. C. Cutlip, Vet. Pathol. 41, 78 (2004).
7. S. B. Prusiner et al., Biochemistry 21, 4883 (1980).
8. M. Prinz et al., Am. J. Pathol. 162, 1103 (2003).
9. This work was supported by grants from the U.S. Public Health Service
2RO1 NS040334-04 from the National Institute of Neurological Disorders and
Stroke and N01-AI-25491 from the National Institute of Allergy and
Infectious Diseases.
Supporting Online Material
www.sciencemag.org/
Materials and Methods
Fig. S1
21 November 2005; accepted 13 January 2006 Published online 26 January 2006;
10.1126/science.1122864 Include this information when citing this paper.
Table 1. Incubation times following inoculation of Tg(CerPrP)1536 mice with
prions from skeletal muscle and brain samples of CWD-affected deer.
Inocula Incubation time, mean d ± SEM (n/n0)*
Skeletal muscle Brain
CWD-affected deer
H92 360 ± 2 d (6/6) 283 ± 7 d (6/6)
33968 367 ± 9 d (8/8) 278 ± 11 d (6/6)
5941 427 ± 18 d (7/7)
D10 483 ± 8 d (8/8) 231 ± 17 d (7/7)
D08 492 ± 4 d (7/7)
Averages 426 d 264 d
Non-diseased deer
FPS 6.98 >523 d (0/6)
FPS 9.98 >454 d (0/7) >454 d (0/6)
None >490 d (0/6)
PBS >589 d (0/5)
*The number of mice developing prion disease divided by the original number
of inoculated mice is shown in parentheses. Mice dying of intercurrent
illnesses were excluded.
http://www.sciencemag.org/
www.sciencemag.org/
Supporting Online Material for
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Rachel C. Angers, Shawn R. Browning, Tanya S. Seward, Christina J.
Sigurdson,
Michael W. Miller, Edward A. Hoover, Glenn C. Telling§
§To whom correspondence should be addressed: E-mail: gtell2@uky.edu
Published 26 January 2006 on Science Express
DOI: 10.1126/science.1122864
This PDF file includes:
Materials and Methods
Fig. S1
Supporting Online Materials
Materials and Methods
Homogenates of semitendinosus/semimembranosus muscle (10% w/v in phosphate
buffered saline) were prepared from five emaciated and somnolent mule deer,
naturally
infected with CWD at the Colorado Division of Wildlife, Wildlife Research
Center.
These deer were identified as D10, D08, 33968, H92, and 5941. CWD infection
was
confirmed in all cases by the presence of histologic lesions in the brain
including
spongiform degeneration of the perikaryon, the immunohistochemical detection
of
disease-associated PrP in brain and tonsil, or by immunoblotting of
protease-resistant,
disease associated PrP (CerPrPSc). Semitendinosus/semimembranosus muscle was
also
obtained from two asymptomatic, mock inoculated deer, referred to as FPS
6.68 and 9.98,
that originated from a CWD non-endemic area and which were held indoors at
Colorado
State University from ten days of age. These control deer were confirmed
negative for
CWD by histopathological and immunohistochemical analysis of brain tissue at
autopsy.
The utmost care was taken to avoid inclusion of obvious nervous tissue when
muscle
biopsies were prepared and to ensure that contamination of skeletal muscle
samples with
CNS tissue did not occur. Fresh, single-use instruments were used to collect
each sample
biopsy and a central piece from each sample was prepared with fresh,
disposable
instruments to further isolate muscle tissue for inoculum preparation. Brain
samples for
transmission were prepared separately from muscle as additional insurance
against cross
contamination.
1
Groups of anesthetized Tg(CerPrP)1536 mice were inoculated intracerebrally
with 30 µl
of 1 % skeletal muscle or brain extracts prepared in phosphate buffered
saline (PBS).
Inoculated Tg(CerPrP) mice were diagnosed with prion disease following the
progressive
development of at least three neurologic symptoms including truncal ataxia,
‘plastic’ tail,
loss of extensor reflex, difficultly righting, and slowed movement. The time
from
inoculation to the onset of clinical signs is referred to as the incubation
time.
For PrP analysis in brain extracts of Tg(CerPrP)1536 mice, 10 % homogenates
prepared
in PBS were either untreated (-) or treated (+) with 40 µg/ml proteinase K
(PK) for one
hour at 37oC in the presence of 2% sarkosyl. Proteins were separated by
sodium dodecyl
sulfate polyacrylamide gel electrophoresis, analyzed by immunoblotting using
anti PrP
monoclonal antibody 6H4 (Prionics AG, Switzerland), incubated with
appropriate
secondary antibody, developed using ECL-plus detection (Amersham), and
analyzed
using a FLA-5000 scanner (Fuji).
2
Fig. S1
PrP in brain extracts from representative Tg(CerPrP)1536 mice receiving
muscle or CNS
tissue inocula from CWD-affected or CWD-negative deer. Extracts were either
treated
(+) or untreated (-) with proteinase K (PK) as indicated. The positions of
protein
molecular weight markers at 21.3, 28.7, 33.5 kDa (from bottom to top) are
shown to the
left of the immunoblot.
3
http://www.sciencemag.org/
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W. Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †University of Wyoming, Laramie, Wyoming, USA; ‡Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA
Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
Research
Environmental Sources of Prion Transmission in Mule Deer
Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University of Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort Collins, Colorado, USA
Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm
http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm
ATYPICAL TSEs in USA CATTLE AND SHEEP ?
http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf
UKBSEnvCJD only theory Singeltary et al 2006
(please note, et al in this term means all victims and familes of the sporadic CJD
that are still looking for answers. ...TSS)
http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13
http://www.microbes.info/forums/index.php?showtopic=306
NEW STRAIN OF TSE USA CATTLE OR JUST INCOMPETENCE IN TESTING???
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm
CJD WATCH MESSAGE BOARD
http://disc.server.com/Indices/167318.html
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
#################### https://lists.aegee.org/bse-l.html ####################
She certainly knows her way around an Adam's apple. Please don't include me in your comment ". . .the fact that she is one of the leading political writers of our age says something about the rest of US." I know exactly what she is, and she is no political writer. Spare me.
Good luck with the suit. I had Baycol do the same thing -- all of these meds are bogus!!
Of all the PR firms... I'd rank Ruder Finn one of the most fishy. I cannot imagine them losing the Tuna account.
- Amanda Chapel
Kevin Foley
This is a clear cut First Amendment issue: Ms. Cochran on June 7:
"We also emphasized that RTNDA opposes any attempt to regulate the form of identification and said those decisions are clearly part of the First Amendment."
Here's what the Las Vegas Review-Journal had to say: Thanks to cable TV and the Internet, Americans now have more sources of news than ever before. If viewers believe a news source is slanting its coverage or purposely leaving out part of the story, they can and do flee in droves to other sources. The government has no role here. It's called "the free market.
I took zyprexa which was ineffective for my condition and gave me diabetes.
{Only 9 percent of adult Americans think the pharmaceutical industry can be trusted right around the same rating as big tobacco}
Zyprexa, which is used for the treatment of psychiatric disorders, such as schizophrenia and bipolar disorder, accounted for 32% of Eli Lilly's $14.6 billion revenue last year.
Zyprexa is the product name for Olanzapine,it is Lilly's top selling drug.It was approved by the FDA in 1996 ,an 'atypical' antipsychotic a newer class of drugs without the motor side effects of the older Thorazine.Zyprexa has been linked to causing diabetes and pancreatitis.
Did you know that Lilly made nearly $3 billion last year on diabetic meds, Actos,Humulin and Byetta?
Yes! They sell a drug that can cause diabetes and then turn a profit on the drugs that treat the condition that they may have caused in the first place!
I was prescribed Zyprexa from 1996 until 2000.
In early 2000 i was shocked to have an A1C test result of 13.9 (normal is 4-6) I have no history of diabetes in my family.
----
Daniel Haszard http://www.zyprexa-victims.com
Check out the latest on our SourceWatch article by clicking here on [[Vets for Freedom]]. Kudos to researcher and contributor Artificial Intelligence for documenting this information below, posted on [[Vets for Freedom]] with additional documentation:
An internet search for ''"Vets for Freedom" + fundraising'' arrives at a donation page bearing the same logos and information as other VFF web pages. However, the web address is that for DonationReport.com (plus an extension code for VFF).
The connection for the DonationReport.com [http://www.donationreport.com website] arrives at a Login page requiring both a User ID and Password—which belongs to eDonation.com, a member of [[The Donatelli Group]], a fundraising company that has raised campaign funds for the [[Republican National Committee]], [[Republican National Convention]], [[Bush-Cheney '04 Inc.]], [[John McCain]], the NRA, and an exhaustive list of members of the [[U.S. Senate]] and [[U.S. House of Representatives]] and other political organizations. [http://www.campaignsolutions.com/contents/clients/]
The Donatelli Group is associated with [[Creative Response Concepts]], the [[public relations]] firm that advised [[Swift Boat Veterans for Truth]], the "organization that accused [[John Kerry|Kerry]] of inflating his Vietnam War record" during the 2004 presidential campaign.
propoganda needs to be acknowledged as such. Over the last fifteen years, Fox News has transformed "news" into editorials-- not just for its own station, but also for every other news station. First of all, the recognition that objective reporting is not possible has resulted in opinion pieces replacing that objective reporting. Secondly, stations have learned that preaching to the choir (as this website tends to do) secures a base audience that strengthens that business or organization in an otherwise too competitive market. Whether it's from Rush Limbaugh or Noam Chomsky, Fox News or CNN, politically biased perspective replaces raw (albeit organized) data that acknowledges as many sides as possible (not just Republican, Democrat, Libertarian, Greenie, or Radical, but rather uncategorizable data). Unfortunately, as many people who take Fox News at face value also take Moore at face value. No source of information openly admits that it is biased or explains how it is biased.
We're not thinking for ourselves. We're buying (literally purchasing) polarized identities. These identities disable us from thinking outside these thematic paradigms. The paradigms decide who we vote for, and even whether or not we vote. The paradigms oppose us to people we could otherwise understand. We defend the limits of this thinking: If you cross this line, you are no longer one of us. We inherently repress any acknowledgement of whatever in ourselves does not abide by our polarized definitions for ourselves. We become neurotic about certain "political" subjects. We are trapped in these identities.
This is the true nature of democratized media: freedom of choice means you chose freely and so can be defined by that choice, until you are bound by that choice and no longer free.
--Gray Kane
PR Week has an [http://www.prweek.com/us/sectors/crisiscommunications/article/560023/ interview with John Mann], one of the jurors in the trial, who says reaching the guilty verdict was "not a terribly emotional decision" because "There were concrete facts, and the numbers were just not adding up" (subscription required).
[[John Stodder]], Dowie's assistant at Fleishman-Hillard (who was convicted on 12 counts) has his own weblog, which includes [http://johnstodderinexile.wordpress.com/2006/05/17/after-the-verdict/ his reaction to the verdict]: "I can't write anything specific about the jury's verdict yesterday. The process is not really over. So there's not a lot I can say right now, other than to echo my attorney's disappointment and disagreement with this result. ... It’s not appropriate for me to get into the details, except to say that my plea of 'not guilty' was sincere, and based not only an examination of my own heart, but also on my understanding of the law. I value the relationships I had with my clients thus would never have presented a bill to them for services they didn’t receive. Obviously the jury differed with my position. I don’t expect anyone to lightly dismiss the weight of that verdict. So until I’m at greater liberty to explain myself, I just have to deal with the fact that many will conclude the jury is right."
Stodder's blog post also includes a comment from one of his friends, Suzanne Reed: "Your integrity is impeccable and irrefutable. There is no amount of evidence that anyone, anywhere could present to me that would convince me that you are guilty of the charges that were brought against you."
USDA 2004 ENHANCED BSE SURVEILLANCE PROGRAM AND HOW NOT TO FIND BSE CASES (OFFICIAL DRAFT OIG REPORT)
snip...
CATTLE With CNS Symptoms Were NOT Always Tested
snip...
Between FYs 2002 and 2004, FSIS condemned 680 cattle of all ages due to CNS symptoms. About 357 of these could be classified as adult. We could validate that ONLY 162 were tested for BSE (per APHIS records. ...
snip...
WE interviewed officials at five laboratories that test for rabies. Those officials CONFIRMED THEY ARE NOT REQUIRED TO SUBMIT RABIES-NEGATIVE SAMPLES TO APHIS FOR BSE TESTING. A South Dakota laboratory official said they were not aware they could submit rabies-negative samples to APHIS for BSE testing. A laboratory official in another State said all rabies-negative cases were not submitted to APHIS because BSE was ''NOT ON THEIR RADAR SCREEN." Officials from New York, Wisconsin, TEXAS, and Iowa advised they would NOT submit samples from animals they consider too young. Four of the five States contacted defined this age as 24 months; Wisconsin defined it as 30 months. TEXAS officials also advised that they do not always have sufficient tissue remaining to submit a BSE sample. ...
snip...
FULL TEXT 54 PAGES OF HOW NOT TO FIND BSE IN USA ;
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_july_13_ig_rep.pdf
SEE MORE BSe from APHIS ;
TSE Disease Surveillance
Data from APHIS animal disease surveillance programs can be used to
detect occurrences of disease, provide information for better policy
decisions, and better understand the diseases. Most surveillance
programs are based on data from live-animal tests; however, since such
tests are generally unavailable for TSE's, in this area APHIS generally
relies on observation of animals exhibiting signs of TSE's and tissue
samples from dead animals. Since 1990, animals targeted for BSE
surveillance by APHIS include cattle exhibiting signs of neurological
disease in the field (i.e., prior to being brought to slaughter),
cattle condemned at slaughter for neurologic reasons, rabies-negative
cattle submitted to public health laboratories,\3\ neurologic cases
submitted to veterinary diagnostic laboratories and teaching hospitals,
nonambulatory cattle (``downer cattle'') over 24 months of age at
slaughter, and adult cattle dying from unknown causes on farms. The
primary reason we target downer animals is that surveillance data from
European countries in which BSE has been detected indicate that downer
cattle have a greater incidence of BSE.\4\ If BSE enters the United
States, downer cattle testing programs are likely to first reveal it.
---------------------------------------------------------------------------
SNIP...
Summary of Issues Open for Comment
[sbull] What is the preferred approach and associated costs to
affected parties for controlling risks associated with disposal of
nonambulatory and dead livestock?
[sbull] Are there any cross-cutting issues between safe disposal of
specified risk materials such as brain and spinal cord and safe
disposal options for downer and on-farm dead animals?
[sbull] Are there practical ways to cull higher-risk downer cattle,
e.g. cattle that may have a non-obvious CNS condition, before they are
sent to slaughter? How should risk factors such as age, physical
condition, and the source and type of cattle be considered when sending
downer cattle to slaughter? What would such culling cost affected
parties?
[sbull] Since APHIS currently relies on collecting samples from
downer animals, at slaughter and other locations, as a key part of BSE
surveillance, how could we continue to obtain samples for testing from
downer cattle if they are not sent to slaughter?
[sbull] What carcass disposal methods are safe, fast, complete, and
environmentally acceptable? What combination of regulatory
requirements, incentives, and cooperative relationships with production
and disposal industries would result in sustainable procedures for the
safe disposal of dead stock, and what are the costs associated with
such solutions?
[sbull] Can rendering be an effective means for safely disposing of
dead stock in a manner that minimizes risks of spreading BSE and other
animal diseases? Under what conditions? What are the associated
technical, economic, regional, environmental, and practical business
issues?
[sbull] What are equitable ways to share the costs of dead stock
disposal, to concentrate and increase economic opportunities and social
benefits that can be associated with responsible dead stock disposal?
[sbull] What businesses, levels of government, or other parties
should be involved in dead stock disposal? Should such programs be
organized on the
[[Page 2711]]
county or State level, a regional level, or a national level, and what
role should the Federal Government play?
[sbull] Is there a need to particularly address disposal of sheep
and goats with regard to scrapie, and disposal of captive elk and deer
with regard to CWD? What dead stock disposal issues are common to all
species, and what issues are of particular importance to different
types of producers?
Done in Washington, DC, this 15th day of January 2003.
Bill Hawks,
Under Secretary for Marketing and Regulatory Programs.
[FR Doc. 03-1210 Filed 1-17-03; 8:45 am]
BILLING CODE 3410-34-P
http://a257.g.akamaitech.net/7/257/2422/14mar20010800/edocket.access.gpo.gov/2003/03-1210.htm
TSS
USDA CONFIRMS BSE Tests on U.S. Cows Found Identical to Atypical Cases in France
Date: June 6, 2006 at 7:22 am PST
BSE Tests on U.S. Cows Found Identical to Atypical Cases in France 06/05/06 07:55
OMAHA (DTN) -- A USDA official confirmed the positive BSE tests in two U.S.-born cattle were indeed an "atypical" type of the disease.
A USDA spokesman acknowledged Friday positive BSE tests from two domestic-born cattle were from a rare strain of the disease found in a small number of European cases.
BSE, scientifically known as bovine spongiform encephalopathy and commonly known as mad cow disease, is a degenerative, fatal disease affecting the central nervous system of adult cattle.
USDA officials have declined in the past to provide such details, but released information Friday after a French researcher revealed earlier this week that the cases in Texas last year and Alabama last spring were identical to "atypical" cases of BSE found in France.
Scientists from around the world are trying to quantify the significance of these rare cases. They also want to know if these cases may be sporadic.
In an e-mail, a USDA spokesman said the cases raise "many unanswered questions about these unusual findings, and additional research is needed to help characterize the significance -- or lack of significance -- of any of these findings."
The USDA spokesperson said nothing in the test results of the two cattle justifies any changes in surveillance, disease control or public-health measures already being taken in the U.S.
http://www.news.farmpage.com/index.cfm?show=4&id=16987
Cattle disease might be unknown strain of BSE
05/06/2006 09:00:00
Farmers Weekly
Scientists across Europe and the United States are following the emergence of a new Transmissible Spongiform Encephalopathy (TSE) in cattle that could be a new strain of BSE.
Speaking last weekend at an international conference on prion diseases in domestic livestock (such as BSE in cows and scrapie in sheep and goats) scientists from France and Italy described how the disease had been detected in a small number of cattle ranging from five to 15 years old.
The strain differs from BSE in that it has a longer incubation time and is consequently being found in older cattle.
The new strain also demonstrates different characteristics from BSE in laboratory tests and was originally detected through active surveillance of live animals rather than during inspection of a suspect fallen animal.
Marion Simmons of the Veterinary Laboratory Agency at Weybridge urged caution saying there are not yet sufficient supporting data to suggest that the disease is a new strain of BSE.
http://www.fwi.co.uk/Articles/2006/06/05/95055/Cattle+disease+might+be+unknown+strain+of+BSE.html
BASE in cattle in Italy of Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with
sporadic Creutzfeldt-Jakob disease
http://www.pnas.org/cgi/content/abstract/0305777101v1
Singeltary et al
http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13
##################### Bovine Spongiform Encephalopathy #####################
I thought some might be interested in this ;
Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
Project Number: 3625-32000-073-07
Project Type: Specific C/A
Start Date: Sep 15, 2004
End Date: Sep 14, 2007
Objective:
The objective of this cooperative research project with Dr. Maria Caramelli
from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct
comparative studies with the U.S. bovine spongiform encephalopathy (BSE)
isolate and the atypical BSE isolates identified in Italy. The studies will
cover the following areas: 1. Evaluation of present diagnostics tools used
in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison
of the U.S. BSE isolate and other typical BSE isolates with atypical BSE
cases. 3. Studies on transmissibility and tissue distribution of atypical
BSE isolates in cattle and other species.
Approach:
This project will be done as a Specific Cooperative Agreement with the
Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del
Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance
program to analyze the effectiveness of the U.S diagnostic tools for
detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE
isolate with atypical BSE isolates will provide further characterization of
the U.S. BSE isolate. Transmission studies are already underway using brain
homogenates from atypical BSE cases into mice, cattle and sheep. It will be
critical to see whether the atypical BSE isolates behave similarly to
typical BSE isolates in terms of transmissibility and disease pathogenesis.
If transmission occurs, tissue distribution comparisons will be made between
cattle infected with the atypical BSE isolate and the U.S. BSE isolate.
Differences in tissue distribution could require new regulations regarding
specific risk material (SRM) removal.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490
Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
2005 Annual Report
This report serves to document research conducted under a specific
cooperative agreement between ARS and the Italian Reference Centre for
Animal TSE (CEA) at the Istituto Zooprofilattico Sperimentale, Turin, Italy.
Additional details of research can be found in then report for the parent
project 3625-32000-073-00D, Transmission, Differentiation, and Pathobiology
of Transmissible Spongiform Encephalopathies. The aim of the cooperative
research project conducted by the CEA and ARS is to compare the U.S. bovine
spongiform encephalopathy (BSE) isolate and the bovine amyloidotic
spongiform encephalopathy isolates (BASE) identified in Italy. The first
objective was to determine whether diagnostic methods routinely used by USDA
are able to identify the Italian BASE cases. For this purpose, CEA received
the immunohistochemistry (IHC) protocol developed by APHIS-USDA. The IHC
protocol was reproduced and standardized in the CEA laboratory and will be
applied to the Italian BSE and BASE cases. Furthermore, fixed brainstem
sections and frozen brainstem material from Italian BSE and BASE cases will
be sent to ARS for analysis using USDA IHC and Western blot (WB) methods.
These studies will enable us to determine whether the present diagnostic
tools (IHC and WB) employed at the USDA will be able to detect the Italian
BASE cases and also enable us to compare Italian BSE and BASE with the U.S.
BSE cases.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpa
rs=true&fy=2005
Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock
Title: Where We've Been and Where We're Going with Bse Testing in the United
States
Authors
item Hall, Mark - NVSL-APHIS-USDA
item Richt, Juergen
item Davis, Arthur - NVSL-APHIS-USDA
item Levings, Randall - NVSL-APHIS-USDA
Submitted to: American Association of Veterinary Laboratory Diagnosticians
Publication Type: Abstract
Publication Acceptance Date: September 1, 2005
Publication Date: November 3, 2005
Citation: Hall, M.S., Richt, J.A., Davis, A.J., Levings, R.L. 2005. Where
We've Been and Where We're Going with Bse Testing in the United States
[abstract]. 48th Annual Meeting of the American Association of Veterinary
Laboratory Diagnosticians. P. 20.
Technical Abstract: A review of the laboratory aspects of the United States
Department of Agriculture's (USDA) Bovine Spongiform Encephalopathy (BSE)
Surveillance Program from its beginning to the present day will be provided.
Validated diagnostic tests for BSE require brain tissue. There are no ante
mortem (blood/serum) tests for BSE available at present. From a historical
perspective, diagnostic tests for BSE continue to evolve. The original
diagnostic test method was histopathology in which sections of brain were
examined under a microscope, and the classical vacuoles and spongiform
change in specific areas of the brain would allow a diagnosis to be made.
This method was accurate but only allowed a diagnosis to be made relatively
late in the course of the disease. In the mid-1990s, immunohistochemistry
(IHC) and Western blotting were developed which allow the detection of the
abnormal form of the prion protein (PrPSc) and a diagnosis could be made
prior to the development of spongiform changes and clinical signs. In the
past decade, so-called "rapid tests" have been introduced commercially for
BSE. Five commercial tests are currently licensed/permitted in the United
States for BSE. These licensed tests include the Prionics Western blot,
Prionics ELISA, Enfer/Abbott ELISA, IDEXX ELISA, and the BioRad ELISA. This
presentation will discuss various attributes of the validated test methods
available today. Both IHC and Western blot are considered confirmatory tests
for BSE by the World Organisation of Animal Health (OIE). IHC provides for a
specific immunological detection of PrPSc and enables the specific
anatomical location to be determined. Western blot provides both
immunological detection of PrPSc as well as specific molecular weight
characterizations; certain Western blot procedures can be extremely
sensitive due to various concentration procedures before analysis of the
sample. The OIE recommended Western blot and IHC methods for confirmatory
diagnosis of BSE used by USDA and the Veterinary Laboratories Agency in
Weybridge, England, will be discussed. The overall enhanced testing plan
that has been used for the past 18 months will be described including
changes that have occurred during this time. The USDA's BSE enhanced
surveillance plan has been a very successful national surveillance testing
program that has been a shared effort between state veterinary diagnostic
laboratories as part of the National Animal Health Laboratory Network and
the National Veterinary Services Laboratories.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=18
3829
NEW STRAIN OF TSE USA CATTLE OR JUST INCOMPETENCE IN TESTING???
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
Greetings again,
I was going over the data from the 1st documented BSE/TSE cow
in the USA and find it disturbing USDA thought it important enough
to use WB to verify there immunohistochemistry test then ;
TSEs Touch Off
ARS Research
A year ago this month, a group of ARS
scientists and technicians gave up their Christmas time off and even
delayed family vacations to provide characterization of the first case
of bovine spongiform encephalopathy (BSE)-commonly called mad cow
disease-to be found in the United States.
On December 23, 2003, a Canadian cow shipped to slaughter from a farm in
Mabton, Washington, had come up presumptively positive for BSE in
testing by USDA's Animal and Plant Health Inspection Service (APHIS),
which has diagnostic responsibility and regulatory oversight for BSE
issues. APHIS had already used the "gold standard" diagnostic
immunohistochemistry test, which was originally developed by ARS. But
for the first U.S. case of BSE, APHIS wanted additional scientific
information that could be provided by the Western blot test.
So APHIS put in a high-priority call to veterinary medical officer
Juergen Richt and his colleagues at the Virus and Prion Diseases of
Livestock Laboratory, which is part of ARS's National Animal Disease
Center (NADC) in Ames, Iowa.
"We had experience with the Western blot test and we had all the
reagents on hand," explains Richt. "So we put our holiday plans on hold
and got everything ready so that APHIS would have verification of the
results from the immunohistochemistry test." ........... snip
full text;
http://www.ars.usda.gov/is/AR/archive/dec04/tse1204.htm
http://www.ars.usda.gov/is/AR/archive/dec04/
HOWEVER, on the 2nd suspect Texas mad cow, not the stumbling and staggering
one they refused to test at all here ;
FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over the
weekend FDA was able to track down all the implicated material. That
material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known as
"mad cow disease," can exhibit such symptoms. In this case, there is no way
now to test for BSE. But even if the cow had BSE, FDA's animal feed rule
would prohibit the feeding of its rendered protein to other ruminant animals
(e.g., cows, goats, sheep, bison). ...
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
BUT, i am speaking of the suspect Texas mad cow where tissue samples sat on
the shelf for 7+ months and then it took an act of Congress, thanks to the
Honorable Phyllis Fong of the OIG, and an end around Johanns, Dehaven et al
to get those samples to Weybridge for confirmation, where it was finally
confirmed ;
The animal was selected for testing because, as a non-ambulatory animal, it
was considered to be at higher risk for BSE. An initial screening test on
the animal in November 2004 was inconclusive, triggering USDA to conduct the
internationally accepted confirmatory IHC tests. Those test results were
negative. Earlier this month, USDA's Office of the Inspector General
recommended further testing of the seven-month-old sample using another
internationally recognized confirmatory test, the Western blot. Unlike the
IHC, the Western blot was reactive, prompting USDA to send samples from the
animal to the Weybridge laboratory for further analysis. ...
Last Modified: 06/24/2005
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retriev
econtent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/1/_th/J_2_9D/_s.7_0_A/7_0_1OB?
PC_7_2_5JM_contentid=2005%2F06%2F0232.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_p
arentnav=LATEST_RELEASES&PC_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM
EVEN more disturbing is the fact that Dr. Detwiler, former top TSE expert at
USDA, tried to tell this Administration this in 2003, and they refused to
listen, this just before she left USDA ;
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
====================================================
Taking a Quality Sample
Too Little Tissue Submitted Too Little Tissue Submitted
NOTE: The samples in these photos are suitable for ELISA testing and if
negative by ELISA there would not be a problem, but if the results were
inconclusive then it would be difficult to process for IHC and additional
testing.
August 24, 2004 Taking a Quality Sample: E4
snip...end
http://www.aphis.usda.gov/vs/nvsl/BSE/Manual/appendixe.pdf
Getting a Sample of Sufficient Quality
Unless the sample is of sufficient quality, it will be unusable and
not count towards the survey. Please see Appendix E for
guidance on collecting a quality sample. If the sample is not of
sufficient quality, STOP: DO NOT TAKE THE SAMPLE. This
does NOT apply to samples taken from:
. animals that are highly suspicious for BSE or that
involve an FAD investigation
. animals that were condemned in an antemortem
inspection BSE sampling using a spoon
Step 1
. Place head upright
- On head rack or barrel
- On table edge
- On the ground facing down if no other option
snip...
http://www.aphis.usda.gov/vs/nvsl/BSE/procedure_manual.pdf
NOW, if we go back further, is this really any surprise ;
>> Differences in tissue distribution could require new regulations
>> regarding specific risk material (SRM) removal.
snip...end
full text ;
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
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. 32 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. 33 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.
34 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.
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543
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. 33
http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546
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.
34 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, 35
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. 36 It was also felt that the results of such an experiment would be
hard to interpret. While a negative result 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. 37 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. 38
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820550
http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm
UKBSEnvCJD only theory Singeltary et al 2006
http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13
http://www.microbes.info/forums/index.php?showtopic=306
CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm
CJD WATCH MESSAGE BOARD
http://disc.server.com/Indices/167318.html
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Thursday, June 01, 2006 2:33 PM
Subject: BSE, BOVINE - USA: ATYPICAL STRAIN
##################### Bovine Spongiform Encephalopathy
#####################
BSE, BOVINE - USA: ATYPICAL STRAIN
**********************************
A ProMED-mail post
ProMED-mail, a program of the
International Society for Infectious Diseases
Date: 31 May 2006
From: Terry S. Singletary and Mary Marshall
Source: Rapid City Journal [edited]
The 2 cases of bovine spongiform encephalopathy found in U.S. cattle
over the past year came from a rare strain of BSE found largely in
Europe that scientists are only beginning to identify, according to
research by a French scientist.
Researchers in France and Italy who presented their work at an
international conference in London reported 2 rare strains of bovine
spongiform encephalopathy that are harder to detect and affect mainly
older cattle.
Thierry Baron of the French Food Safety Agency presented research
indicating that a 12-year-old Texas cow testing positive for BSE in
June 2005, and the 10-year-old Alabama cow that tested positive in
March [2006?], showed identical testing patterns to a small number of
BSE cases in France, Sweden and Poland.
Animal scientists are calling such strains "atypical" BSE, which is
different from the "typical" BSE caused by cattle eating feed with
ruminant offal contaminated with a BSE protein.
They don't know whether the atypical strains are caused by something
else or simply appear spontaneously in older, susceptible cattle.
Art Davis, a U.S. Department of Agriculture (USDA) scientist for the
Animal and Plant Health Inspection Service (APHIS) at the National
Veterinary Services Laboratory in Ames, Iowa, said in his
presentation Sunday at the London conference that the Texas and
Alabama test results showed completely different prion patterns than
the Washington state case discovered in December 2003.
"The classical lesions were not there," Davis said of the cases. The
Washington state cow originated in Alberta, Canada, near where
several other BSE cases have been found.
The "typical" BSE strain caused a mad cow disease epidemic in Great
Britain beginning in the mid-1980s that killed 184 000 cattle and
more than 100 people who contracted a human form of the disease
caused by eating contaminated beef products.
The scientific evidence shows that in almost all cattle cases, the
fatal neurological disorder was contracted through contaminated meat
and bone meal fed to the cow, typically at a young age.
However, scientists finding atypical cases of BSE are beginning to
question if there has been a change in the abnormal protein that
causes BSE or if cattle might be susceptible to a sporadic BSE
affecting older cattle.
Danny Matthews, head of transmissible spongiform encephalopathies at
England's Veterinary Laboratories Agency, said recent research on
atypical cases of BSE raises questions over whether older cattle can
sporadically get the disease or if there are more strains of BSE than
previously understood. Scientists might also be facing something new,
such as "son of BSE," he said.
"We don't fully understand what atypical BSE means," Matthews said.
"Is it spontaneous or another source causing it? Time will tell."
Although the test patterns in the U.S. cases and atypical cases in
Europe closely matched, Baron said there were no known links among
any of the positive animals. The French Food Safety Agency sent a
researcher to the United States to study the positive Texas case and
compare its results to known cases in France that did not match the
typical BSE positive tests.
"You could place them side-by-side and not tell the difference," Baron said.
Baron also raised the prospect that the disease could be sporadic in
at least a small number of older cattle. He said, however, such a
conclusion would be hard to determine because of the small number of
cattle with this atypical strain globally.
Dr. Sam Holland, South Dakota's state veterinarian, said there are
many strains of BSE and varying degrees of infectiousness of the
agent.
"What if the scenario is there is an atypical prion out there that is
much less infective, has a longer incubation period and has not been
recognized as part of the Great Britain BSE experience identified in
1985 and '86?" Holland said. "There could be others out there that we
haven't recognized yet."
He said it is possible the atypical strains are not caused by
contaminated feed and that it still makes sense to continue the ban
on ruminant offal in cattle feed to prevent the spread of typical BSE
and eventually to eliminate that disease.
"Based on what we know about BSE, it makes good sense to -- number
one -- keep some surveillance in place; number 2, watch what we
import and restrict shipments and movements from places that have had
those syndromes; and, number 3, with what we know about BSE, it seems
to be very prudent to keep our ruminant offal ban in place," Holland
said.
"At least for typical BSE's, it seems to be very effective. It's
probably reasonable to continue the ruminant offal ban even after the
last typical BSE case has been eliminated."
Editor's note: DTN, a private company based in Omaha, Neb., provides
information to agriculture, energy trading markets and other
weather-sensitive industries. The Rapid City Journal received a copy
of DTN's story and expanded on it.
[Byline: Chris Clayton]
--
Terry S. Singletary
and
Mary Marshall
[An atypical form has been found in sheep with scrapie. Other
countries have indicated an atypical form of BSE. It seems logical
that the US would have an a atypical form as well. The case might
even be made that new variant CJD is an atypical form of CJD. Clearly
there is more to the TSE diseases than we fully comprehend. - Mod.TG]
[see also:
2005
----
Scrapie, atypical, ovine - Falkland Islands 20051120.3371
2004
----
Scrapie, atypical, sheep - UK and Ireland 20041210.3274
Scrapie, atypical, sheep - UK (02) 20040409.0965
Scrapie, atypical, sheep - UK20040408.0952
BSE, atypical - France: OIE 20040201.0391
Scrapie, atypical, sheep - France: OIE 20040201.0390
BSE - France: distinct molecular phenotypes 20040107.0076
2003
----
Scrapie - Norway: new phenotype 20031117.2857
BSE - Japan (08): 9th case, lab findings 20031115.2838
BSE, atypical case - Italy: OIE 20031022.2649
BSE - Italy: atypical, suspected 20031012.2576
BSE - Japan (06): atypical 20031009.2547
BSE - Japan (05): atypical 20031008.2526
BSE - Japan (04): atypical 20031007.2511
2002
----
BSE? Sheep - USA (Vermont) 20020412.3937
2000
----
BSE? sheep - USA (Vermont) (06) 20000724.1223
BSE? sheep - USA (Vermont) 20000717.1184
1996
----
CJD sporadic vs variant differences 19960526.0990]
...............tg/pg/lm
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Yes, he was a republican -- thanks for catching that.
Isn't he a Republican?
Hi Bob - sorry for taking so long to respond. The broken links were caused by my weblog software completely crapping out shortly after I posted here. The original links will now work, but your summary is fine.
My apologies for any confusion.
Regards, Grant
Frankly, Wood doesn't know the history of documentary.
And I'm not sure why he would quote a pr exec who worked for
1-800-GOT-JUNK? and is only 27 (not that there aren't young
people who understand docs).
Too many people (which sadly includes far too many
journalists and critics) don't understand there is more
than one genre of documentary.
Documentaries don't have to be in the tradition
format with a voice of god narrator.
Moore's films are personal essay films which
have a long history and never have had to be "balanced."
Others are are less personal, but are political essays.
The question isn't whether these films are documentaries,
but whether they are good documentaries and whether
they are effective at getting their message across.
And there are bad documentaries which can be good
organizing tools while there are good docs which
may be too complex, too personal, or too indiosyncratic
to be effective politically. People need to look
critically at any kind of media.
I was watching Criterion's new DVD of Harlan Country, USA
which is a great documentary more than decade older
than Roger & Me (as well as very different) which tells
a story, a story which wasn't being told, from the
perspective of the subjects.
http://criterionco.com/asp/release.asp?id=334
http://ari.typepad.com blog
http://flickr.com/photos/ari/ photos
http://del.icio.us/tigerbeat interesting articles & sites