REPORT ON CURRENT & FUTURE SURVEILLANCE FOR BOVINE SPONGIFORM ENCEPHALOPATHY

REPORT ON CURRENT & FUTURE SURVEILLANCE FOR BOVINE SPONGIFORM ENCEPHALOPATHY 4 November 2008 Version 1.1 Patrick Burke BVM&S MRCVS Veterinary Adviser Department for Environment, Food & Rural Affairs


snip...


The TSE Regulation also requires MSs to ensure that any animal suspected of being infected with a TSE is notified immediately for investigation. The adult cattle population in the EU is approximately 43 million (approximately 5 million in UK). Between 2001 and 2007, over 70 million cattle were tested in the EU (over 3.6 million in the UK). From 2001 to 2007, the number of BSE cases detected in the EU fell from 2181 to 175 and the detection rate fell from 2.55 to 0.18 positive BSE cases per 10000 tests carried out (Figure 1). The mean age of BSE cases in the EU15 is increasing as the epidemic declines (Figure 2). Figure 1: BSE Cases Detected per 10,000 Cattle Tested in EU from 2001 to 2007

snip...



http://www.defra.gov.uk/animalh/bse/publications/bse-surveillance.pdf



http://www.defra.gov.uk/animalh/bse/othertses/index.html



http://www.defra.gov.uk/animalh/Bse/publications/index.html



http://www.food.gov.uk/bse/



Sunday, November 23, 2008

PRION October 8th - 10th 2008 Book of Abstracts

http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.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



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



Friday, November 21, 2008

Plasma & Serum Proteins Receive Continued FDA Approval

http://madcowfeed.blogspot.com/2008/11/plasma-serum-proteins-receive-continued.html


http://madcowfeed.blogspot.com/



4/25/08
DEPARTMENT OF HEALTH AND HUMAN SERVICES
Food and Drug Administration
21 CFR Part 589
[Docket No. 2002N-0273] (formerly Docket No. 02N-0273)
RIN 0910-AF46
Substances Prohibited From Use in Animal Food or Feed
AGENCY: Food and Drug Administration, HHS.
ACTION: Final rule.
SUMMARY: The Food and Drug Administration (FDA) is amending the agency's regulations to prohibit the use of certain cattle origin materials in the food or feed of all animals. These materials include the following: The entire carcass of bovine spongiform encephalopathy (BSE)- positive cattle; the brains and spinal cords from cattle 30 months of age and older; the entire carcass of cattle not inspected and passed for human consumption that are 30 months of age or older fiom which brains and spinal cords were not removed; tallow that is derived fiom BSEpositive cattle; tallow that is derived from other materials prohibited by this rule that contains more than 0.15 percent insoluble impurities; and mechanically separated beef that is derived fiom the materials prohibited by this rule. These measures will further strengthen existing safeguards against BSE.


see full text 144 pages ;

http://www.fda.gov/OHRMS/DOCKETS/98fr/FDA-2002-N-0031-nfr.pdf


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


AND as everyone knows, the rest is history, those dead-stock downers, the most high risk cattle, were NOT tested, and in FACT, was a major source of YOUR CHILDRENS SCHOOL LUNCH PROGRAM, all across the Nation. sorry, these are the most high risk cattle for TSE aka mad cow disease, and i am a bit touchy about this topic. ...sorry. ...terry

DOWNER COW SCHOOL LUNCH PROGRAM

http://downercattle.blogspot.com/


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.

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf


Wednesday, July 16, 2008

Implementation of 2008 Feed Ban Enhancements Questions and Answers July 15, 2008

snip...

In 2007, in one weekly enforcement report, the fda recalled 10,000,000+ pounds of BANNED MAD COW FEED, 'in commerce', and i can tell you that most of it was fed out ;

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST REASON Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI

REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html



Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST

snip... see listings and references of enormous amounts of banned mad cow protein 'in commerce' in 2006 and 2005 ;

see full text ;

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


Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials

Recall Release CLASS II RECALL FSIS-RC-021-2008 HEALTH RISK: LOW

Congressional and Public Affairs (202) 720-9113 Amanda Eamich

WASHINGTON, June 26, 2008 – Paradise Locker Meats, a Trimble, Mo., establishment, is voluntarily recalling approximately 120 pounds of fresh cattle heads with tonsils not completely removed, which is not compliant with regulations that require the removal of tonsils from cattle of all ages, the U.S. Department of Agriculture’s Food Safety and Inspection Service announced today.

Tonsils are considered a specified risk material (SRM) and must be removed from cattle of all ages in accordance with FSIS regulations. SRMs are tissues that are known to contain the infective agent in cattle infected with BSE, as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.

The products subject to recall include: Boxes of “BEEF HEAD, PARADISE LOCKER MEATS.” Each shipping package bears the establishment numbers “EST. 31865” inside the USDA mark of inspection.

These products were sent to retail establishments and restaurants in the Kansas City, Kansas, area.

The problem was discovered through routine FSIS inspection that verified there had been incomplete removal of the tonsils by the recalling establishment.

Media and consumers with questions about the recall should contact company Production Supervisor Louis Fantasma at (816) 370-6328.

Consumers with food safety questions can “Ask Karen,” the FSIS virtual representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded food safety messages are available 24 hours a day. #

http://www.fsis.usda.gov/News_&_Events/Recall_021_2008_Release/index.asp


Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

Recall Release CLASS II RECALL FSIS-RC-020-2008 HEALTH RISK: LOW

Congressional and Public Affairs (202) 720-9113 Peggy Riek

WASHINGTON, June 26, 2008 – Beltex Corporation, doing business as Frontier Meats, a Fort Worth, Texas, establishment, is recalling approximately 2,850 pounds of fresh cattle heads which may contain specified risk materials (SRMs), the U.S. Department of Agriculture’s Food Safety and Inspection Service announced today.

SRMs are tissues that are known to contain the infective agent in cattle infected with BSE, as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.

The products subject to recall include: Cases of "BEEF WHOLE HEAD." Each shipping package bears the establishment number "EST. 7041B" inside the USDA mark of inspection, as well as a package code of "51904" or "63922."

The company is recalling all products packed between May 31, 2007, and June 24, 2008. These products were distributed to retail establishments and lunch carts in the Dallas-Ft. Worth, Texas, area.

The problem was discovered by the State of Texas officials during a routine inspection at a retail establishment.

Media and consumers with questions about the recall should contact the company Sales Department at (817) 624-1136.

Consumers with food safety questions can “Ask Karen,” the FSIS virtual representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded food safety messages are available 24 hours a day.

#

http://www.fsis.usda.gov/News_&_Events/Recall_020_2008_Release/index.asp


Thursday, June 26, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

http://madcowfeed.blogspot.com/2008/06/texas-firm-recalls-cattle-heads-that.html



Tuesday, May 27, 2008

FDA BSE/Ruminant Feed Inspections Firms Inventory Report Texas Legend Ranch OAI 05/10/2008

http://madcowfeed.blogspot.com/2008/05/fda-bseruminant-feed-inspections-firms.html



SPECIFIED RISK MATERIALS SRMs

http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html


SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/srm-mad-cow-recall-406-thousand-pounds.html



Tuesday, July 1, 2008

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

http://madcowfeed.blogspot.com/2008/07/missouri-firm-recalls-cattle-heads-that.html


Wednesday, July 9, 2008 [Docket No. FDA-2008-N-0369] Ruminant Feed Ban Support Project; ``Response to RFA-FDA-08-008''

http://madcowfeed.blogspot.com/2008/07/docket-no-fda-2008-n-0369-ruminant-feed.html


snip...see full text ;

http://madcowfeed.blogspot.com/2008/07/implementation-of-2008-feed-ban.html



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

BSE CASE CONFIRMED IN BRITISH COLUMBIA November 17, 2008

OTTAWA, November 17, 2008 - The Canadian Food Inspection Agency (CFIA) has confirmed bovine spongiform encephalopathy (BSE) in a seven-year-old dairy cow from British Columbia. No part of the animal’s carcass entered the human food or animal feed systems.

The animal’s birth farm has been identified, and an investigation is underway. The CFIA is tracing the animal's herdmates at the time of birth and examining possible sources of infection. The age and location of the infected animal are consistent with previous cases detected in Canada.

This case was detected through the national BSE surveillance program, which has been highly successful in demonstrating the low level of BSE in Canada. The program continues to play an important role in Canada’s strategy to manage BSE.

Canada remains a Controlled Risk country for BSE, as recognized by the World Organisation for Animal Health (OIE). Accordingly, this case should not affect exports of Canadian cattle or beef.

- 30 -

For information:

Canadian Food Inspection Agency Media relations: 613-228-6682

http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/bccb2008/15notavie.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

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


Prof Collinge old findings, a key issue, the media always seems to forget about, states that BSE propagates as either variant CJD-like or sporadic CJD-like prion strains. funny how our health officials, governments, and such seem to conveniently ignore these findings, let alone the atypical TSE in cattle and sheep that do NOT look like nvCJD in the lab, but some sub-types of the sporadic CJD. all this goes ignored for one reason, and one reason only $$$ it's why the UKBSEnvCJD only theory was put forth in the first place, and it's why it is still set in stone $$$ to much science has been forth to date that proves that theory wrong.

PLEASE NOTE, the last two mad cows documented in the USA were H-type BSE, then the USDA quickly shut the testing down to a level of non-detection. it would be a miracle to find one case, from testing only 40,000 annually, from some 97,000,000 (that's 97 million head), and of that, some 37 million slaughtered, if i am not mistaken. and these cattle are cherry picked brains too, probably calves from USDA grain fed facilities, and don't think these corrupt people are not capable of doing it either. they are very capable. ...


"REDACTED is alleged to have provided possibly inaccurate test results involving diseased sheep. However, because the results were determined to be inconclusive, no actual violation was actually committed.''

http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html

snip...

Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

snip...

I would note that the sample was taken in April, at which time the protocols allowed for a preservative to be used (protocols changed in June 2005). The sample was not submitted to us until last week, because the veterinarian set aside the sample after preserving it and simply forgot to send it in. On that point, I would like to emphasize that while that time lag is not optimal, it has no implications in terms of the risk to human health. The carcass of this animal was destroyed, therefore there is absolutely no risk to human or animal health from this animal.

snip...

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

snip...

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

http://www.usda.gov/oig/webdocs/sarc070619.pdf

full text ;

http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html

USDA: In 9,200 cases only one type of test could be used

WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.

In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.

The department posted the information on its website because of an inquiry from The Associated Press.

Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.

"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."

Officials intended to report the tests later in an annual report, Clifford said.

These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC.

In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.

Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.

The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.

Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.

"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."

Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.

Date: 8/25/05

http://www.hpj.com/archives/2005/aug05/aug29/BSEtestoptionswerelimited.cfm

""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

THIS WAS DONE FOR A REASON!

THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

USDA 2003

We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip.............

Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip...

FULL TEXT;

Completely Edited Version PRION ROUNDTABLE

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

2005

=============================

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end

http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...

http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm

PLEASE NOTE ;

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 p evious 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

THE SEVEN SCIENTIST REPORT ***

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf

***

WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;

Bio-Rad, TSS phone conversation 12/28/04

Finally spoke with ;

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX

at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.

my question;

Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???

ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.

again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer"

"very political"

"very loaded question"

outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing. said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives? said something about ''just look at the sheep that tested IHC- but were positive''. ...

TSS

-------- Original Message -------- Subject: Your questions Date: Mon, 27 Dec 2004 15:58:11 -0800 From: To: flounder@wt.net

Hi Terry:

............................................snip Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you

Regards

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: =================================

END...TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########

http://madcowtesting.blogspot.com/

Executive Summary

In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.

http://www.aphis.usda.gov/lpa/issues/bse/epi-updates/bse_final_epidemiology_report.pdf



i hope i have not lost you. i know how some don't like to get political, but cwd, mad cow disease (all strains), TME, Scrapie, and cjd i.e. human and animal TSE, that's all they are are political. bush has failed us terribly, clinton before him failed us terribly, and whomever gets in office next will do the same damn thing, in terms of human and animal TSE. it was said long ago ;


In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


PLEASE NOTE, ''FANATICAL INCIDENT TO BE AVOIDED IN THE US AT ALL COSTS.''

and they meant it. ...TSS

The EMBO Journal Vol. 21 No. 23 pp. 6358±6366, 2002

BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein

Emmanuel A.Asante, Jacqueline M.Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L.Wood, Julie Welch, Andrew F.Hill, Sarah E.Lloyd, Jonathan D.F.Wadsworth and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.uk Variant Creutzfeldt±Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSEderived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure. ...snip...end...TSS

Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans. ...end

USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.

snip...

64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. *** A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.

snip...

http://www.seac.gov.uk/minutes/95.pdf

AND WHAT ABOUT THOSE atypical NOR-98 scrapie cases in the USA, now documented at 6 cases in the past two years, and the risk thereof to humans as sporadic CJD ???

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

INFECTED AND SOURCE FLOCKS

There were 20 scrapie infected and source flocks with open statuses (Figure 3) as of April, 30, 2008. Twenty eight new infected and source flocks have been designated in FY 2008 (Figure 4); three source flocks were reported in April. ...snip

POSITIVE SCRAPIE CASES

As of April 30, 2008, 122 new scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2008 (Figure 6). Of these, 103 were field cases and 19* were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected in FY 2008 and reported by May 20, 2008). Positive cases reported for April 2008 are depicted in Figure 7. Eighteen cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 8). The most recent positive goat case was confirmed in February 2008 and originated from the same herd in Michigan as the other FY 2008 goat cases. ...snip

CAPRINE SCRAPIE PREVALENCE STUDY (CSPS)

snip...

However, four positive goats have been identified this fiscal year through field investigations. One was a clinical suspect submitted for testing and the other three originated from the birth herd of the clinical case.

ANIMALS SAMPLED FOR SCRAPIE TESTING

As of April 30, 2008, 26,703 animals have been sampled for scrapie testing: 23,378 RSSS, 1,517 goats for the CSPS study, 1,466 regulatory field cases, 270 regulatory third eyelid biopsies, and 72 regulatory rectal biopsies (chart 8).

TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...

PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps

NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the USA in 2007, in five different states. WHICH pathologically looks like some sub-types of sporadic CJD, of which Stanely Prusiner warns of a public health risk ;

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)

http://www.pnas.org/cgi/content/abstract/0502296102v1

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

NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007

http://nor-98.blogspot.com/2008/04/seac-spongiform-encephalopathy-advisory.html

http://nor-98.blogspot.com/

Nonambulatory Cattle as a Potential Source of TSE

In this study, Wisconsin was the only State in which mink producers were reported to receive nonambulatory cows directly from dairies. However, given the small number of surveyed herds this finding is likely a result of the sampling design. Because mink producers pay a premium for nonambulatory cows, it appears reasonable that the practice of feeding nonambulatory cows to mink could occur wherever both large numbers of dairy cows and mink are found. As many as 2,157(3) nonambulatory cows per million milk cows, or a total of 9,482 nonambulatory cows, could have been fed to mink in the 7 surveyed States in 1992. Based on the sample response, only half of those cows would have had an identifiable reason for being nonambulatory. This equates to an estimated 4,741 nonambulatory cows that were, hypothetically, a potential source of TSE in the surveyed States.

(3)This estimate does not account for any nonambulatory cows received from slaughter plants.

Page 23

The five reported outbreaks of TME in the U.S. reveal no discernable trend. Assuming an average of 2,000 mink farms in the U.S. during the last 50 years, one outbreak of TME has occurred per 20,000 mink farm-years. Extrapolating from the data gathered in this study, 66,374 nonambulatory cows have been fed to mink in the 7 surveyed States since the last reported outbreak of TME in 1985. Of those, 33,187 would have had no identifiable reason for being nonambulatory and were hypothetically a potential source of TSE. Given the severity of signs and number of mink affected by TME it is unlikely that outbreaks have gone unreported. If any form Of a TSE (infectious, spontaneous, or other) occurs in U.S. cattle that is transmissible to mink in the form of TME, then it must be exceedingly rare or the conditions for its transmission must be highly specific and unusual. Nonetheless, studies are underway at the State and Federal levels to further characterize the disposition of nonambulatory cows and usage on mink farms.

snip...

An estimated 4,741 nonambulatory cows hypothetically considered to be potential sources of TSE may have been fed to mink in the 7 surveyed States in 1992. This equates to 33,187 such cows fed to mink since the last reported outbreak of TME in mink. Given this large number of nonambulatory cows fed to mink, the historic and current mink population, and the infrequent occurrence of TME, if TSE exists in cattle in the U.S. it must be very rare or transmissible to mink only under very unusual conditions.

http://downercattle.blogspot.com/2008/08/quantitative-assessment-of-possible.html

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.

snip...

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.***

snip...end

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

Epidemiology Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old. The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In Factsheet Veterinary Services February 2002 APHIS 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.

snip...

The 1985 Stetsonville Outbreak The most recent TME outbreak occurred on one mink ranch in Stetsonville, WI, in 1985. In the herd of 7,300 adult mink, 60 percent of the animals died. Clinical signs included tail arching, incoordination, and hyperexcitability. At the most advanced stages of the disease, the animals were in trancelike states and eventually died. The outbreak lasted 5 months. Microscopic examination of sections of the brain confirmed the spongelike changes characteristic of TME. Diagnostic tests identified the prion protein. The following year, mink born during the outbreak showed no signs of TME. The late Richard Marsh, a veterinary virologist at the University of Wisconsin who studied the transmission of TME and other TSE’s, investigated this outbreak. Marsh learned that the mink were fed a diet composed of fresh meat products from “downer cattle” and commercial sources of fish, poultry, and cereal. Downer cattle are nonambulatory and cannot rise because they are affected with a condition such as a metabolic disease, broken limbs, or a central nervous system disorder. Marsh theorized that the meat from these downer cattle introduced a TSE agent to the mink in which TME resulted. Although Marsh’s hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of more than 20,141 cattle have been examined at APHIS’ National Veterinary Services Laboratories and other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another TSE in cattle.

http://www.aphis.usda.gov/publications/animal_health/content/printable_version/fs_ahtme.pdf

AND as everyone knows, the rest is history, those dead-stock downers, the most high risk cattle, were NOT tested, and in FACT, was a major source of YOUR CHILDRENS SCHOOL LUNCH PROGRAM, all across the Nation. sorry, these are the most high risk cattle for TSE aka mad cow disease, and i am a bit touchy about this topic. ...sorry. ...terry

DOWNER COW SCHOOL LUNCH PROGRAM

http://downercattle.blogspot.com/

IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?

In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.

We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.

snip...

PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986

http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

NOW, back to those mad mink i.e. TME. let me throw a curve ball here ;

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* and Richard A. Bessen† Emerging Infectious

Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine- passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, Htype BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profi les, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME. The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE. Transmissible mink encephalopathy (TME) is a rare prion disease in ranch-raised mink (Mustela vison) in North America and Europe (1–4). Six outbreaks have been reported from 1947 through 1985 in North America, and several have been linked to contaminated commercial feed (1). Although contamination of feed with scrapie-infected sheep parts has been proposed as the cause of TME, the origin of the disease remains elusive. The idea that scrapie in sheep may be a source of TME infection is supported by fi ndings that scrapie-infected mink have a similar distribution of vacuolar pathologic features in the brain and the same clinical signs as mink with natural and experimental TME (5). However, mink are not susceptible to scrapie infection following oral exposure for up to 4 years postinoculation, which suggests that either the scrapie agent may not be the source of natural TME infection or that only specifi c strains of the scrapie agent are able to induce TME (6,7). Epidemiologic investigations in the Stetsonville, Wisconsin, outbreak of TME in 1985 suggested a possible cattle origin, since mink were primarily fed downer or dead dairy cattle but not sheep products (8). Experimental transmission of Stetsonville TME into cattle resulted in transmissible spongiform encephalopathy (TSE) disease with an incubation period of 18.5 months. Back passage of bovine TME into mink resulted in incubation periods of 4 and 7 months after oral or intracerebral inoculation, respectively, which was similar to that found following inoculation of Stetsonville TME into mink by these same routes (8). These fi ndings indicated that cattle are susceptible to TME, and that bovine-passaged TME did not result in a reduced pathogenicity for mink. These studies raised the question as to whether an unknown TSE in cattle was the source of TME infection in the Stetsonville outbreak. Several additional TME outbreaks in the United States have been associated with mink diet that contained downer or dead cattle (9). ...

snip...full text ;

http://www.cdc.gov/EID/content/13/12/pdfs/1887.pdf

http://transmissible-mink-encephalopathy.blogspot.com/

CWD, is but a small piece, of a very big puzzle. and one of the main reasons this puzzle has not been solved, is the secrecy, cover-ups, and such. you must not ignore these facts. i did not want to believe this either. for years i was naive, but the facts speak for themselves.

it goes way back ;

Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

August 20, 2008

http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html


Wednesday, September 03, 2008
Accelerated High Fidelity Prion Amplification Within and Across Prion Species Barriers http://chronic-wasting-disease.blogspot.com/2008/09/accelerated-high-fidelity-prion.html


Resistance of Bovine Spongiform Encephalopathy (BSE) Prions to Inactivation

Kurt Giles1,2, David V. Glidden3, Robyn Beckwith1, Rose Seoanes1, David Peretz1,2¤, Stephen J. DeArmond1,4, Stanley B. Prusiner1,2,5*

1 Institute for Neurodegenerative Diseases, University of California San Francisco, San Francisco, California, United States of America, 2 Department of Neurology, University of California San Francisco, San Francisco, California, United States of America, 3 Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, United States of America, 4 Department of Pathology, University of California San Francisco, San Francisco, California, United States of America, 5 Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California, United States of America

Abstract


Distinct prion strains often exhibit different incubation periods and patterns of neuropathological lesions. Strain characteristics are generally retained upon intraspecies transmission, but may change on transmission to another species. We investigated the inactivation of two related prions strains: BSE prions from cattle and mouse-passaged BSE prions, termed 301V. Inactivation was manipulated by exposure to sodium dodecyl sulfate (SDS), variations in pH, and different temperatures. Infectivity was measured using transgenic mouse lines that are highly susceptible to either BSE or 301V prions. Bioassays demonstrated that BSE prions are up to 1,000-fold more resistant to inactivation than 301V prions while Western immunoblotting showed that short acidic SDS treatments reduced protease-resistant PrPSc from BSE prions and 301V prions at similar rates. Our findings argue that despite being derived from BSE prions, mouse 301V prions are not necessarily a reliable model for cattle BSE prions. Extending these comparisons to human sporadic Creutzfeldt-Jakob disease and hamster Sc237 prions, we found that BSE prions were 10- and 106-fold more resistant to inactivation, respectively. Our studies contend that any prion inactivation procedures must be validated by bioassay against the prion strain for which they are intended to be used.


http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000206


snip...



Greetings,

Considering all the above, and the fact that there are over 20 documented strains of the so called typical scrapie, with new and emerging atypical Scrapie i.e. the NOR-98, and not to forget BSE transmission to sheep and goat. CWD in deer and elk, and just how many strains do we have there? cBSE (typical), hBSE, both documented in North America, and the fact several outbreaks of TME in the USA, no l-BSE ? i question no l-BSE in the USA, due to the fact of the total bungling of the USDA's so called enhanced BSE surveillance program, and then the sudden dramatic decrease in the USDA BSE testing right after being forced to come clean on the negative atypical BSE case in Texas due to the Fong effect, and the Alabama atypical BSE case. i would bet my mothers life on the l-BSE being circulating among the other TSE strains in the USA, just undetected for all the obvious reasons. but how many other strains? now mind you, all of the above strains of TSE transmitting to primates, and mind you, the _typical_ scrapie transmitting to the primate by THERE NON-FORCED ORAL CONSUMPTION. oh yes, but don't forget, typical scrapie has never been documented to transmit to humans. r i g h t ! with the new and emerging human TSEs, some showing up right here in the USA, why is it that the human TSE (all age groups) why are they not all reportable in the USA in every state and Internationally? This must be done. the ramifications from proven transmission studies via the medical and surgical arena's are real, they have been real for some time. Blood now a real issue, now a threat. We must act now, let science take it's course, and put the politics and the industry aside, the conflicts of interest are just to great. these studies take too long due to the incubation period, for partisan, industry, political issues to stand in the way. people are dying. this old study, and some newer ones, always bring it home for me. there is much more to this story than the infamous UKBSEnvCJD hamburger eating adolescents only story. ...TSS




J Neurol Neurosurg Psychiatry. 1994 June; 57(6): 757–758. PMCID: PMC1072988

Copyright notice

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

C J Gibbs, Jr, D M Asher, A Kobrine, H L Amyx, M P Sulima, and D C Gajdusek Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892


Abstract

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

FULL TEXT ;

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1072988&blobtype=pdf



snip...please see full text ;



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


to be continued. ...TSS

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

TSS

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

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