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From: TSS ()
Subject: BSE, BOVINE - CANADA (04): (BRITISH COLUMBIA) ProMED
Date: November 30, 2008 at 2:29 pm PST


----- Original Message -----
From: "TERRY SINGELTARY"
To:
Sent: Wednesday, November 19, 2008 9:14 AM
Subject: [BSE-L] BSE, BOVINE - CANADA (04): (BRITISH COLUMBIA) ProMED


-------------------- BSE-L@LISTS.AEGEE.ORG --------------------

BSE, BOVINE - CANADA (04): (BRITISH COLUMBIA)
*********************************************
A ProMED-mail post

ProMED-mail is a program of the
International Society for Infectious Diseases

Date: Tue 18 Nov 2008
Source: eFluxMedia [edited]


The Canadian Food Inspection Agency [CFIA] confirmed on Monday [17
Nov 2008] a new case of mad cow disease (bovine spongiform
encephalopathy, BSE) in a 7-year-old dairy cow born well after Ottawa
banned feed practices thought to spread the disease. It is the
country's 15th case. The animal was discovered on a farm in the
Pacific province of British Columbia.

The agency said no part of the animal's carcass entered the human
food or animal feed supply. It also added that regulators are also
tracking down other animals in the cow's herd when it was born.

Canada has been deemed a "controlled risk" country for mad cow
disease by the World Organization for Animal Health (OIE) because of
its surveillance and control measures. The CFIA said the new case
should not affect that classification.

Bovine spongiform encephalopathy or mad-cow disease emerged first in
British cattle. It is deadly and has an unusually long incubation
period of around 4 years. It also appears rarely in humans under a
different form, called new variant Creutzfeldt-Jakob disease (vCJD or nvCJD).

The disease has already killed almost 200 people in Britain. It is
unclear if the disease is transmitted to humans through consumption
of infected meat, but this is the most likely path. The cattle in
Britain get it from being fed the remains of other infected cows. The
misfolded protein called a prion, which carries the disease, is much
more resistant to heat than common viruses or bacteria, and it is
generally believed that normal cooking processes do not destroy it.

Even though its human form is the most common human prion disease, it
is still rare and only occurs in about one out of every one million
people (except if you live in Britain). In more than 85 percent of
cases, the duration of the disease between onset of symptoms and
death is less than 1 year (median: 4 months). It is incurable and fatal.

[Byline: Anna Boyd]

--
Communicated by:
ProMED-mail Rapporteur Brent Barrett

[Although feeding of mammalian tissue back to cattle is believed to
be the method inducing BSE, there is evidence that there are several
forms of the disease. One of those forms is a sporadic form, which
does not seem to be related to mammalian tissue in the feed. Banning
the mammalian tissue in feed is frequently referred to as the "feed ban."

This may be one of the sporadic forms. - Mod.TG

The Pacific province of British Columbia can be located on the
HealthMap/ProMED-mail interactive map of Canada at
. - CopyEd.MJ]

[see also:
BSE, bovine - Canada (03): (AB) 20080819.2580
BSE, bovine - Canada (02): (BC) 20080623.1941
BSE update 2008 (02) 20080529.1738
BSE update 2008 (01) 20080229.0831
BSE, bovine - Canada (AB) 20080226.0786
2007
----
BSE - Japan: new case, milk replacers 20071223.4122
BSE, bovine - Canada (AB) (03) 20071218.4076
BSE, bovine - Canada (BC) 20070502.1430
BSE, bovine - Canada (AB) (02) 20070308.0813
BSE, bovine - New Zealand: new import rules 20070302.0734
BSE, bovine - Canada (AB) 20070208.0499]
...................................tg/mj/dk

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ProMED-mail makes every effort to verify the reports that
are posted, but the accuracy and completeness of the
information, and of any statements or opinions based
thereon, are not guaranteed. The reader assumes all risks in
using information posted or archived by ProMED-mail. ISID
and its associated service providers shall not be held
responsible for errors or omissions or held liable for any
damages incurred as a result of use or reliance upon posted
or archived material.
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Become a ProMED-mail Premium Subscriber at

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----- Original Message -----
From: "TERRY SINGELTARY"
To:
Cc:
Sent: Wednesday, November 19, 2008 9:08 AM
Subject: Re: PRO/AH/EDR> BSE, bovine - Canada (04): (BC)

> This may be one of the sporadic forms. - Mod.TG

please note, 'one of the sporadic forms', has _not_ been proven. so to state this in a release, would only be a _hypothetical_. ...please note the following

kind regards, terry

International Journal of Medical Sciences ISSN 1449-1907 www.medsci.org 2008 5(6):347-353 © Ivyspring International Publisher. All rights reserved

Review

Prion propagation in vitro: are we there yet?

Chongsuk Ryou .. and Charles E. Mays Sanders Brown Center on Aging and Department of Microbiology, Immunology & Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY, U.S.A. .. Correspondence to: Dr. Chongsuk Ryou, 800 Rose St. HSRB-326, Lexington, KY 40536. Phone: (859) 257 4016; Fax: (859) 257 8382; E-mail: cryou2@email.uky.edu Received: 2008.11.03; Accepted: 2008.11.10; Published: 2008.11.11

Prion diseases are caused by proteinaceous pathogens termed prions. Although the details of the mechanism of prion propagation are not fully understood, conformational conversion of cellular prion protein (PrPC) to misfolded, disease-associated scrapie prion protein (PrPSc) is considered the essential biochemical event for prion replication. Currently, studying prion replication in vitro is difficult due to the lack of a system which fully recapitulates the in vivo phenomenon. Over the last 15 years, a number of in vitro systems supporting PrPC conversion, PrPSc amplification, or amyloid fibril formation have been established. In this review, we describe the evolving methodology of in vitro prion propagation assays and discuss their ability in reflecting prion propagation in vivo.

snip...

Conclusion Several different in vitro systems have been devised and tested for successful conversion of PrPC or amplification of PrPSc. Using these methods, many previously unknown but fundamental aspects of prion propagation have been studied. However, we are still far away from the complete understading of the mechanistic details of the process despite the efforts reviewed in this article. On the basis of the protein-only hypothesis, prion propagation is believed to faciliated by a biochemical event known as a conformational conversion of PrPC to PrPSc. The ultimate goal of the in vitro systems is to re-create the condition that faithfully recapitulates prion propagation in vivo. In an ideal condition, a test tube containing both PrP isoforms only should be sufficient to reconstitute the replication process. However, the current form of in vitro reconsititution is not the bona fide system respresenting the in vivo phenomenon. One of the major obstacles is involved in unintended inclusion of cellular factors other than PrP isoforms. Furthermore, our limited knowledge on cofactor molecules makes it more difficult to conceive insight into what has occurred in prion propation in vitro. Despite the limitation in the current form of in vitro conversion assays, simplicity of the systems over cell-based and animal systems has been advantageous. Utilization of these tools will slowly unwind the complicated molecular characteristics of prions such as the species barrier and strain properties. They will also be useful in validating the necessary environment for conversion and estimating the transmissibility of disease. By manipulating the systems, the application can be extended to a sensitive diagnosis of prions and a high-throughput screening of potent anti-prion reagents.

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2583336&blobtype=pdf

Perspectives BIOMEDICINE: A Fresh Look at BSE Bruce Chesebro*

Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle form of a family of progressive brain diseases. These diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease (CWD) in deer and elk. They are also known as either "prion diseases" because of the association of a misfolded cellular prion protein in pathogenesis or "transmissible spongiform encephalopathies" (TSEs) because of the spongelike nature of the damaged brain tissue (1).

The recent discovery of two BSE-infected cows, one in Canada and one in the United States, has dramatically increased concern in North America among meat producers and consumers alike over the extent to which BSE poses a threat to humans as well as to domestic and wild animals. The European BSE epidemic of the late-1980s seems to have been initiated a decade earlier in the United Kingdom by changes in the production of meat and bone meal (MBM) from rendered livestock, which led to contamination of MBM with the BSE infectious agent. Furthermore, the fact that UK farmers fed this rendered MBM to younger animals and that this MBM was distributed to many countries may have contributed to the ensuing BSE epidemic in the United Kingdom and internationally (2).

Despite extensive knowledge about the spread of BSE through contaminated MBM, the source of BSE in Europe remains an unsolved mystery (2). It has been proposed that BSE could be derived from a cross-species infection, perhaps through contamination of MBM by scrapie-infected sheep tissues (see the figure). Alternatively, BSE may have been an endemic disease in cattle that went unnoticed because of its low level of horizontal transmission. Lastly, BSE might have originated by "spontaneous" misfolding of the normal cellular prion protein into the disease-associated abnormal isoform (3), which is postulated to be the infectious agent or "prion."

Five possible sources of BSE in North American cattle. Sheep, deer, and elk could spread prion diseases (TSEs) to cattle through direct animal contact or contamination of pastures. Endemic BSE has not been proven to exist anywhere in the world, but it is difficult to exclude this possibility because of the inefficient spread of BSE infectivity between individual animals (2). BSE caused by spontaneous misfolding of the prion protein has not been proven. CREDIT: KATHARINE SUTLIFF/SCIENCE

snip...

Nevertheless, the idea that BSE might originate due to the spontaneous misfolding of prion proteins has received renewed interest in the wake of reports suggesting the occurrence of atypical BSE (9-11). These results imply that new strains of cattle BSE might have originated separately from the main UK outbreak. Where and how might such strains have originated? Although such rare events cannot be studied directly, any number of sources of the original BSE strain could also explain the discovery of additional BSE strains in cattle (see the figure). However, it would be worrisome if spontaneous BSE were really a valid etiology because such a mechanism would be impossible to prevent--unlike other possible scenarios that could be controlled by large-scale eradication of TSE-positive animals.

Another way to look at this problem is to examine evidence for possible spontaneous TSE disease in other animals besides cattle. Spontaneous BSE would be extremely difficult to detect in cattle, where horizontal spread is minimal. However, in the case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at birth as well as between adults, spontaneous disease should be detectable as new foci of clinical infection. In the early 1950s scrapie was eradicated in both Australia and New Zealand, and the mainland of both these countries has remained scrapie-free ever since. This scrapie-free status is not the result of selection of sheep resistant to scrapie because sheep from New Zealand are as susceptible as their UK counterparts to experimental scrapie infection (12). These experiments of man and nature appear to indicate that spontaneous clinical scrapie does not occur in sheep. Similarly, because CWD is known to spread horizontally, the lack of CWD in the deer or elk of eastern North America but its presence in western regions would also argue against a spontaneous disease mechanism. This is particularly noteworthy in New Zealand, where there are large numbers of deer and elk farms and yet no evidence of spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer, this would suggest that spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are unlikely to be found in cattle or humans. The main caveat to this notion is that spontaneous disease may arise in some animal species but not others. In humans, sCJD--which is considered by some researchers to begin by spontaneous misfolding of the prion protein--usually takes more than 50 years to appear. Thus, in animals with a shorter life-span, such as sheep, deer, and cattle, an analogous disease mechanism might not have time to develop.

What can we conclude so far about BSE in North America? Is the BSE detected in two North American cows sporadic or spontaneous or both? "Sporadic" pertains to the rarity of disease occurrence. "Spontaneous" pertains to a possible mechanism of origin of the disease. These are not equivalent terms. The rarity of BSE in North America qualifies it as a sporadic disease, but this low incidence does not provide information about cause. For the two reported North American BSE cases, exposure to contaminated MBM remains the most likely culprit. However, other mechanisms are still possible, including cross-infection by sheep with scrapie or cervids with CWD, horizontal transmission from cattle with endemic BSE, and spontaneous disease in individual cattle. Based on our understanding of other TSEs, the spontaneous mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE of unknown etiology--might be a better term to describe the origin of this malady. ...

snip...full text ;

http://www.sciencemag.org/cgi/content/full/sci;305/5692/1918

Release No. 0106.04

Contact: Office of Communications (202) 720-4623

Transcript of Remarks From Technical Briefing on BSE and Related Issues With Agriculture Secretary Ann M. Veneman and USDA Chief Veterinary Officer Dr. Ron DeHaven Washington D.C. - March 15, 2004

snip...

OPERATOR : "Yes. Our next one is coming from Elizabeth Weiss. Please state your company."

ELIZABETH WEISS: "This is Elizabeth Weiss with USA Today."

"I actually had two questions. First off, when you say you're looking for 1 in 10,000 cases, is USDA doing any work to find out the possibility of whether or not BSE exists in a spontaneous form in the way that it does in humans and elk populations?

"And secondly, how will any of this fit into some of the consternation that's been raised in California and with the Midwest packer that wanted to test all of its cattle?

"Thanks."

DR. DEHAVEN: "All right. I think we've got three different questions in there, and I'll try to touch on each one of them.

"First of all, let me correct just a technical issue, and that is you mentioned 1 in 10,000. And actually our surveillance system currently is designed, the one that we have in place now is designed to detect 1 positive in 1 million cattle, and I gave some numbers between 200,000 and 268,000 that would allow us to detect 1 in 10 million as opposed to 1 in 10,000.

"So we would, if we were able to collect in the ballpark of those numbers of samples then we with increasing numbers of samples have an increasingly statistically valid sample from which to determine, one, whether or not the disease exists and, if so, at what prevalence level.

"So our real emphasis is to test as many of those animals as we can, ensure that we get an appropriate geographical distribution, but not setting a specific number as far as a target. Again, consistent with the recommendation from the International Review Team, their recommendation was to test all of them.

"So that's consistent with where we're going is to test as many as we possibly can.

"As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.

"Again, it's a very difficult situation to prove a negative.

"So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.

snip...

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2004/03/0106.html

UK TESTING FINISHED NEXT WEEK

Matthews confirmed that the brain tissue samples from the US animal had arrived at Weybridge. Test results were likely to be ready by the end of next week, he said.

The suspect animal has already undergone a series of tests. A rapid screening test on Nov. 15 returned inconclusive results. Sophisticated immunohistochemistry (IHC) tests cleared the animal of any infection, but a third round of testing using a Western blot procedure showed a "weak positive".

Weybridge will do an IHC test plus three kinds of Western Blot tests on the samples. They will use "methods of slightly different analytical sensitivity that give us the greatest number of opportunities to interpret what we see," he said.

US beef industry leaders say scientists should not speculate about the unusual case.

"There's no evidence that it's atypical ... and there's absolutely no evidence that it's spontaneous," said Gary Weber, head of regulatory affairs at the National Cattlemen's Beef Association.

Matthews noted scientists are still grappling with what is typical and atypical BSE.

"Far too few people have looked at BSE in depth using all of the tests to be able to define 'this is normal and that one isn't'," he said.

Weber noted Japan used the term to describe two very young infected cattle because BSE is usually found in older animals. Italy labeled a case "atypical" because the misshaped prions were found in unexpected parts of the animal's brain. ...snip...end

http://www.agobservatory.org/headlines.cfm?refID=73207

Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease

http://cdc.gov/ncidod/dvrd/bse/

http://www.defra.gov.uk/animalh/bse/pdf/hillreport.pdf

Spontaneous occurrence 14. Spontaneous cases of classical CJD in humans are found at a rate of about 1/million around the world (Will, 1993), without appreciable racial or geographical variation except in a few specific cases, notably Jews of Libyan origin that have a mutation in the open reading frame of the PRNP gene (Chapman and Korczyn, 1991). Thus it is theoretically possible that spontaneous cases of BSE could occur as a consequence of a germ line mutation, in which case relatives would also have a certain or increased incidence of the disease, or a somatic mutation, which would be unlikely to be detectable unless the appropriate tissue were identified, or after some transformation in the PrP protein in the animal concerned. BSE was unknown prior to its detection in Britain in the mid 1980s, and Index cases found around the world since then can all be explained in terms of export from the UK directly or indirectly of cattle or of feed components. No BSE affected animals have been reported in many developed countries with large cattle populations, including Australia, New Zealand, Norway and Sweden, which have mixed cattle populations; and the only infected animal detected in the US was of Canadian origin. The disease seems to have a highly homogeneous aetiology (e.g. Bruce, 2003). 15. Data from the USA, where the dairy population in particular is highly related to that in GB provide an upper limit to the spontaneous rate. A programme of testing is in place of a target population of adult cattle exhibiting some clinical sign that might be consistent with BSE (animals reported as having CNS or clinical signs of BSE or were non-ambulatory). In the intensive programme from June 2004 over 375000 animals were tested in the following 12 months. No positive results have yet been obtained in these or previous tests (USDA BSE Testing). This implies a putative upper limit of under 10 per million in this target group. Assuming, as analysis has shown, the relative risk in this group is about 30 times higher than in the population as a whole (European Commission, 2002c), then the incidence in the population as a whole is under 3 per 10 million. This figure could possibly be biased downwards if affected animals are diagnosed and disposed of without being tested. Taking account of testing done and the lack of clinical cases seen in many other countries also, it seems highly unlikely that the spontaneous rate can be as much as 3 per 10 million head. Nor can spontaneous occurrence explain incidences of ca. 30 cases of BARBs per year in 2002/4 in the UK adult cattle population of ca. 4 million. [NOTE ADDED 30 JUNE: The recent confirmation of a previously inconclusive case in the USA affects these calculations. If the animal did not have access to infected feed, the calculations have to be revised: they suggest a sporadic incidence in the population of 1/(375000 x 30) or almost 1 per 10 million, with the upper limit under 5 per 10 million.] 16. Calculation of a maximum rate of possible transformation from scrapie to BSE is less feasible. Nevertheless, BSE appears not to have arisen in the UK until around the early 1980s, despite the presence of scrapie in sheep here for at least 200 years. Although a change in the scrapie prion may have been the cause of the initial cases of BSE, the difference between their properties in mice and the uniformity of the BSE brain lesions suggest it is unlikely that more than one such mutation was the source of BSE. It is most unlikely that the same mutation could be occurring often enough to contribute significantly to BARBs cases. Furthermore BARBs cases do not match the geographical distribution of the sheep population. The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very

http://www.defra.gov.uk/animalh/bse/pdf/hillreport.pdf

242 Atypical and classical BSE are different strains based upon Western blot profiles 243 (Hill, 2004; Normile, 2004; Baron et al., 2006), and this study indicates that disease Page 11 of 23 Journal of Animal Science Downloaded from jas.fass.org by on November 12, 2008. 12 progresses via different routes for these strains. The disparate 244 routes of pathogenesis in 245 atypical BSE can occur by 1 of 2 means. One possibility is that the source of infectivity 246 in atypical BSE is exposure to contaminated feedstuffs, as is the case for classical BSE, 247 but progression occurs in a disparate manner that bypasses the influence of the indel 248 polymorphisms. The other possibility is that atypical BSE is occurring spontaneously in 249 the host. Support for atypical BSE occurring spontaneously are the parallels to sporadic 250 TSE in humans, specifically, occurrence in older hosts and a comparable low incidence 251 rate (Baron and Biacabe, 2006). Furthermore, atypical BSE occurs as isolated, sporadic 252 cases in contrast to the clustering of cases observed for feed borne classical BSE 253 (Donnelly et al., 1997). Interestingly, the only native born cases of BSE in the United 254 States identified to date have been classified as atypical BSE.

255 No experiment can conclusively confirm a spontaneous nature for atypical BSE.

snip...end

http://jas.fass.org/cgi/reprint/jas.2007-0208v1.pdf

2:00 Sporadic CJD and Atypical BSE: Two Children of One Protein Maurizio Pocchiari, Ph.D., Director of Research, Virology, Istituto Superiore Di Sanita The identification of forms of TSE diseases in cattle caused by prion strains different from BSE has raised new concerns on the possibility that these novel agents might induce disease in humans with a phenotype resembling sporadic CJD. The analysis of the distribution of the different molecular subtypes of sporadic CJD might give some answers.

http://www.healthtech.com/Conferences_Overview.aspx?c=518&id=59662&c=518

Sunday, November 16, 2008 Resistance of Bovine Spongiform Encephalopathy (BSE) Prions to Inactivation

http://bse-atypical.blogspot.com/2008/11/resistance-of-bovine-spongiform.html

USA PRION UNIT BLOG

http://prionunitusaupdate2008.blogspot.com/

Sunday, April 20, 2008 Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

see full text ;

http://prionunitusaupdate2008.blogspot.com/2008/04/progress-report-from-national-prion.html

CJD TEXAS (cjd clusters)

http://cjdtexas.blogspot.com/

USA WRITTEN CJD QUESTIONNAIRE ???

http://cjdquestionnaire.blogspot.com/

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

http://www.cjdfoundation.org/fact.html

TSS

Tuesday, November 11, 2008 Transmission of atypical bovine prions to mice transgenic for human prion protein DOI: 10.3201/eid1412.080941

http://bse-atypical.blogspot.com/2008/11/transmission-of-atypical-bovine-prions.html

Tuesday, November 11, 2008 SaBTO Summary of 1st Public Meeting - variant CJD and blood Tuesday 21st October 2008, 2pm-4pm

http://vcjdblood.blogspot.com/2008/11/sabto-summary-of-1st-public-meeting.html

Friday, August 29, 2008

CREEKSTONE VS USDA COURT OF APPEALS, BUSH SAYS, NO WAY, NO HOW

http://madcowtesting.blogspot.com/2008/08/creekstone-vs-usda-court-of-appeals.html

TSS

----- Original Message ----- From: "ProMED-mail" To: Sent: Wednesday, November 19, 2008 7:41 AM Subject: PRO/AH/EDR> BSE, bovine - Canada (04): (BC)

BSE, BOVINE - CANADA (04): (BRITISH COLUMBIA) ********************************************* A ProMED-mail post ProMED-mail is a program of the International Society for Infectious Diseases

Date: Tue 18 Nov 2008 Source: eFluxMedia [edited]

The Canadian Food Inspection Agency [CFIA] confirmed on Monday [17 Nov 2008] a new case of mad cow disease (bovine spongiform encephalopathy, BSE) in a 7-year-old dairy cow born well after Ottawa banned feed practices thought to spread the disease. It is the country's 15th case. The animal was discovered on a farm in the Pacific province of British Columbia.

The agency said no part of the animal's carcass entered the human food or animal feed supply. It also added that regulators are also tracking down other animals in the cow's herd when it was born.

Canada has been deemed a "controlled risk" country for mad cow disease by the World Organization for Animal Health (OIE) because of its surveillance and control measures. The CFIA said the new case should not affect that classification.

Bovine spongiform encephalopathy or mad-cow disease emerged first in British cattle. It is deadly and has an unusually long incubation period of around 4 years. It also appears rarely in humans under a different form, called new variant Creutzfeldt-Jakob disease (vCJD or nvCJD).

The disease has already killed almost 200 people in Britain. It is unclear if the disease is transmitted to humans through consumption of infected meat, but this is the most likely path. The cattle in Britain get it from being fed the remains of other infected cows. The misfolded protein called a prion, which carries the disease, is much more resistant to heat than common viruses or bacteria, and it is generally believed that normal cooking processes do not destroy it.

Even though its human form is the most common human prion disease, it is still rare and only occurs in about one out of every one million people (except if you live in Britain). In more than 85 percent of cases, the duration of the disease between onset of symptoms and death is less than 1 year (median: 4 months). It is incurable and fatal.

[Byline: Anna Boyd]

-- Communicated by: ProMED-mail Rapporteur Brent Barrett

[Although feeding of mammalian tissue back to cattle is believed to be the method inducing BSE, there is evidence that there are several forms of the disease. One of those forms is a sporadic form, which does not seem to be related to mammalian tissue in the feed. Banning the mammalian tissue in feed is frequently referred to as the "feed ban."

This may be one of the sporadic forms. - Mod.TG

The Pacific province of British Columbia can be located on the HealthMap/ProMED-mail interactive map of Canada at . - CopyEd.MJ]

[see also: BSE, bovine - Canada (03): (AB) 20080819.2580 BSE, bovine - Canada (02): (BC) 20080623.1941 BSE update 2008 (02) 20080529.1738 BSE update 2008 (01) 20080229.0831 BSE, bovine - Canada (AB) 20080226.0786 2007 ---- BSE - Japan: new case, milk replacers 20071223.4122 BSE, bovine - Canada (AB) (03) 20071218.4076 BSE, bovine - Canada (BC) 20070502.1430 BSE, bovine - Canada (AB) (02) 20070308.0813 BSE, bovine - New Zealand: new import rules 20070302.0734 BSE, bovine - Canada (AB) 20070208.0499] ...................................tg/mj/dk

*##########################################################* ************************************************************ ProMED-mail makes every effort to verify the reports that are posted, but the accuracy and completeness of the information, and of any statements or opinions based thereon, are not guaranteed. The reader assumes all risks in using information posted or archived by ProMED-mail. ISID and its associated service providers shall not be held responsible for errors or omissions or held liable for any damages incurred as a result of use or reliance upon posted or archived material. ************************************************************ Become a ProMED-mail Premium Subscriber at ************************************************************ Visit ProMED-mail's web site at . Send all items for posting to: promed@promedmail.org (NOT to an individual moderator). If you do not give your full name and affiliation, it may not be posted. Send commands to subscribe/unsubscribe, get archives, help, etc. to: majordomo@promedmail.org. For assistance from a human being send mail to: owner-promed@promedmail.org. ############################################################

REPORT ON THE INVESTIGATION OF THE THIRTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA BACKGROUND


On June 2, 2008 a cow on a dairy operation in the Fraser Valley area of British Columbia was destroyed following a brief illness. The carcass was collected from the farm by a disposal company on June 3, 2008, and subsequently selected for sampling by the Canadian Food Inspection Agency (CFIA) under Canada's National BSE Surveillance Program. Diagnostic specimens were submitted to the British Columbia Ministry of Agriculture and Lands (BCMAL) Laboratory, where they were screened for BSE using a Prionics Check PrioSTRIP rapid test (June 3, 2008). The result of this preliminary test did not rule out BSE. In accordance with the prescribed testing protocol, the test was repeated and produced a second reaction. Samples were then forwarded to the National BSE Reference Laboratory in Lethbridge, Alberta, where rapid screening tests to validate these results were also positive (Prionics Check Prio-strip - June 5, 2008; Prionics Check Western Blot - June 6, 2008; Hybrid Western Blot - June 6, 2008; BioRad TeSeE Elisa - June 6, 2008). On June 12, 2008, these results were confirmed by the Scrapie Associated Fibril Immunoblot. As the positive sample was submitted from a third party premise, the CFIA conducted an investigation to confirm the sample's identity using DNA analysis. No part of the carcass of the affected animal entered the human food supply and no specified risk materials (SRM) entered the animal feed chain.

The CFIA immediately initiated an epidemiological investigation based on the recommended BSE guidelines of the World Organisation for Animal Health (OIE). Specifically, the CFIA investigated:

the birth cohort (all cattle born in the same herd as, and within 12 months of the birth of the BSE-positive animal); the feed cohort (all cattle which during their first year of life, were reared with the BSE positive animal and which investigation showed consumed the same potentially contaminated feed during that period); and feed to which the animal may have been exposed early in its life. ANIMAL INVESTIGATION The positive animal was a Holstein cow born on April 22, 2003, and was 61 months of age at the time of death. The animal was born, raised and spent its entire life on the same farm. The cow had been non-ambulatory (downer) and receiving medical care for two weeks. However, when the animal's condition failed to improve the producer elected to humanely destroy it, and because it met the inclusion criteria of Canada's National BSE Surveillance Program, arrangements were made to forward appropriate samples for laboratory evaluation.

The birth farm is a dedicated dairy operation. The feed cohort was determined to comprise 207 animals, which along with the case animal, were raised on the birth farm. This cohort consisted entirely of Holstein females. No males were retained or raised on the farm and therefore males were excluded from the investigation because they were not exposed to the same potentially contaminated feed as the case animal. The trace-out investigation of the feed cohort located 79 live animals on the premises. These animals are currently under quarantine pending humane destruction and disposal. The following is the disposition of the remaining 128 feed cohort animals:

102 animals were traced and confirmed to have died or been slaughtered; 13 animals were traced and presumed to have died or been slaughtered; and 13 animals were determined to be untraceable because of records limitations. FEED INVESTIGATION The feed investigation focused on feeds to which the case animal may have had access during its first year of life and on the manufacturing practices used to produce each of these feeds.

All feed products to which the BSE case animal had access were intended for feeding to ruminants. These consisted of farm-grown and purchased forages and feed products from four different commercial suppliers. On-farm mixing equipment consisted of a mixer wagon used to combine forages with commercial products for lactating and dry cows and heifers. A dog on the farm was fed in the house, away from the dairy operation, thereby eliminating pet food as a potential source of prohibited material.

For the first two months of its life, the BSE case animal was housed individually in a calf hutch and fed milk and commercially prepared heifer ration. From two to twelve months of age, the animal was housed in a series of indoor group pens with animals of similar age and continued to be fed heifer ration as well as distiller's grains and trace mineralized salt.

Other commercial products used on the farm included complete rations for the lactating and dry cows as well as a dry cow mineral. These products were not fed to the BSE case animal prior to twelve months of age, however, the same on-farm mixer wagon was used to mix rations for both the BSE case animal and the older animals.

The trace mineralized salt blocks, dry cow mineral and distiller's grains used on-farm were obtained from specialized facilities not handling prohibited material and delivered in dedicated trucks. These products were ruled out as possible sources of contamination.

Following the recommendations of the World Health Organization, Canada implemented a ruminant feed ban in 1997 prohibiting the use of certain animal protein products, known as prohibited material, in the manufacture of feed intended for ruminants. However, these materials could be utilized in the manufacture of feeds for non-ruminant species provided that appropriate measures were taken to avoid contamination of ruminant feed.

Investigation at the commercial feed manufacturer which was the sole supplier of heifer ration and some dry cow ration, identified that this facility utilized prohibited material in the preparation of rations for non-ruminant species. Components of this facility were dedicated to the manufacture of feeds not containing prohibited material in the formula. However, bulk ingredient receiving and finished feed conveyances were cross-utilized. Written procedures and production records were insufficient to rule out possible contamination with prohibited material at these points affecting both ration types delivered to the case farm.

Investigation at a second commercial feed manufacturer that supplied the farm with the majority of both lactation and dry cow rations showed the facility handled prohibited material for a short period of time during the timeframe of interest. Review of production records for the feeds of interest did not identify avenues of contamination with prohibited material.

Investigation at the third commercial feed manufacturer that supplied the farm with some dry cow ration revealed this facility was not handling prohibited material during the time frame of interest. Feeds from this facility were delivered in company owned trucks and were ruled out.

The fourth commercial feed manufacturer supplied the farm with one delivery of each of lactation ration and dry cow ration when the case animal was eleven months old. Investigation revealed that the facility was using prohibited material at this time. Written procedures to prevent contamination with prohibited material were in place, however, review of the production records identified the lactation feed was stored in a load out bin that previously contained a prohibited material feed without documented cleanout in between.

Considering the farm's feeding regime and specific production records reviewed, a likely source of exposure to BSE infectivity was the heifer ration. However, potential ingestion of dry cow ration from the first manufacturer or the single delivery of lactation ration from the fourth manufacturer exists and potential contamination of these products cannot be ruled out.

INVESTIGATION OVERVIEW The detection of this case does not change any of Canada's BSE risk parameters. The location and age of the animal are consistent with previous cases. Surveillance results to date, including this case, reflect an extremely low level of BSE in Canada.

Since the confirmation of BSE in a native-born animal in May 2003, Canada has significantly increased its targeted testing of cattle in high-risk categories advocated by the OIE (including non-ambulatory animals). This effort is directed at determining the level of BSE in Canada, while monitoring the effectiveness of the risk-mitigating measures in place. Canada's National BSE Surveillance Program continues to demonstrate an extremely low level of BSE in Canada, with 13 positive animals detected.

With respect to BSE, the safety of beef produced in Canada is assured by public health measures enacted in 2003. The removal of specific risk material (SRM) - the tissues that have been demonstrated to have the potential to harbour BSE infectivity - from all animals slaughtered for human consumption is the most effective single measure to protect consumers in Canada and importing countries from exposure to BSE infectivity in meat products.

As demonstrated by the surveillance system, the feed ban implemented in 1997 is effectively preventing the amplification of BSE in Canada's feed system. Additional regulations to enhance Canada's feed ban were enacted in 2007. The most important change is the removal of SRM from all animal feeds, pet food and fertilizer. The enhancement will accelerate progress toward eradicating BSE from the national cattle herd by preventing more than 99 per cent of potential BSE infectivity from entering the Canadian feed system. These measures are effectively minimizing the risk of BSE transmission.

Canada is officially categorized under the OIE's science-based system as a controlled BSE risk country. This status clearly recognizes the effectiveness of Canada's surveillance, mitigation and eradication measures, and acknowledges the work done by all levels of government, the cattle industry, veterinarians and ranchers to effectively manage and eventually eradicate BSE in Canada.


Date modified: 2008-11-06


http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/bccb2008/13investe.shtml

ONE HUNDRED AND FIRST MEETING OF THE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE

Oct 23, 2008 at 9:00 AM


http://seac992007.blogspot.com/2008/10/one-hundred-and-first-meeting-of_23.html

http://flounder068.vox.com/library/post/one-hundred-and-first-meeting-of-the-spongiform-encephalopathy-advisory-committee.html

Wednesday, June 11, 2008

OIE Recognition of the BSE Status of Members RESOLUTION No. XXI (Adopted by
the International Committee of the OIE on 27 May 2008)


snip...SEE FULL TEXT with facts and sources @ ;


http://usdavskorea.blogspot.com/2008/06/oie-recognition-of-bse-status-of.html

http://organicconsumers.org/forum/index.php?showtopic=1566


Friday, April 25, 2008

Substances Prohibited From Use in Animal Food or Feed [Docket No.
2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46

http://madcowfeed.blogspot.com/2008/04/substances-prohibited-from-use-in.html

Review on the epidemiology and dynamics of BSE epidemics

Cases of atypical BSE have only been found in countries having implemented
large active surveillance programs. As of 1st September 2007, 36 cases (16
H, 20 L) have been described all over the world in cattle: Belgium (1 L)
[23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1
L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland
(1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23.
Another H-type case has been found in a 19 year old miniature zebu in a
zoological park in Switzerland [56]. It is noteworthy that atypical cases
have been found in countries that did not experience classical BSE so far,
like Sweden, or in which only few cases of classical BSE have been found,
like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human
prion diseases like CJD or GSS have been put forward [10], as well as
between L-type BSE and CJD [17]. These findings raise questions about the
origin and inter species transmission of these prion diseases that were
discovered through the BSE active surveillance.

full text 18 pages ;

http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf


USA BSE ACTIVE SURVEILLANCE ???

http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html


Please remember, the last two mad cows documented in the USA i.e. Alabama
and Texas, both were of the 'atypical' BSE strain, and immediately after
that, the USDA shut down the testing from 470,000 to 40,000 in the U.S. in
2007 out of about 35 million cattle slaughtered. also, science is showing
that some of these atypical cases are more virulent to humans than the
typical UK BSE strain ;

***Atypical forms of BSE have emerged which, although rare, appear to be
more virulent than the classical BSE that causes vCJD.***

Progress Report from the National Prion Disease Pathology Surveillance
Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008

http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45

In this context, a word is in order about the US testing program. After the
discovery of the first (imported) cow in 2003, the magnitude of testing was
much increased, reaching a level of >400,000 tests in 2005 (Figure 4).
Neither of the 2 more recently indigenously infected older animals with
nonspecific clinical features would have been detected without such testing,
and neither would have been identified as atypical without confirmatory
Western blots. Despite these facts, surveillance has now been decimated to
40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and
invites the accusation that the United States will never know the true
status of its involvement with BSE.

In short, a great deal of further work will need to be done before the
phenotypic features and prevalence of atypical BSE are understood. More than
a single strain may have been present from the beginning of the epidemic,
but this possibility has been overlooked by virtue of the absence of
widespread Western blot confirmatory testing of positive screening test
results; or these new phenotypes may be found, at least in part, to result
from infections at an older age by a typical BSE agent, rather than neonatal
infections with new "strains" of BSE. Neither alternative has yet been
investigated.

http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm


Tuesday, June 3, 2008

SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA

http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518


TSS


-------------------- BSE-L@LISTS.AEGEE.ORG --------------------





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