-------------------- BSE-L@LISTS.AEGEE.ORG --------------------
BSE CASE CONFIRMED IN ALBERTA OTTAWA, May 15, 2009 -
The Canadian Food Inspection Agency (CFIA) has confirmed bovine spongiform encephalopathy (BSE) in an 80-month-old dairy cow from Alberta. 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 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 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: 613-773-6600
http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/ab2009/16notavie.shtml
Sunday, May 10, 2009
Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States
http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html
TSS
-------------------- BSE-L@LISTS.AEGEE.ORG --------------------
The Canadian system is much better than the USA. at least they know. the USA just SHOOTS, SHOVELS, AND SHUTS UP I.E. THE SSS POLICY.
Sunday, May 10, 2009
Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States
http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the United States of America (USA) Question number: EFSA-Q-2003-083 Adopted date: 1 July 2004 Summary (0.1Mb)
Document (0.2Mb)
Summary
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178620779461.htm
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_annex_en1.pdf?ssbinary=true
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1.pdf?ssbinary=true
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_summary_en1.pdf?ssbinary=true
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE-Risk (GBR) of CANADA Question N° EFSA-Q-2003-083 Adopted July 2004 Summary The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC), to provide an up-to-date scientific report on the GBR in Canada, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Canada. This scientific report addresses the GBR of Canada as assessed in 2004 based on data covering the period 1980-2003. The BSE agent was probably imported into the country middle of the eighties and could have reached domestic cattle in the early nineties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s. It is possible that imported meat and bone meal (MBM) into Canada reached domestic cattle and led to an internal challenge in the early 90s. A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from UK in the mid 80s could have been slaughtered. This risk continued to exist, and grew significantly in the mid 90's when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries. EFSA concludes that the current GBR level of Canada is III, i.e. it is confirmed at a lower level that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the system remains unstable, it is expected that the GBR continues to grow, even if no additional external challenges occur.
http://www.mvo.nl/wetgeving-dierlijk-vet/onderzoek/download/EFSA%20on%20BSE%20risk%20Canada%20jul%202004.pdf
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE-Risk (GBR) of MEXICO Question N° EFSA-Q-2003-083 Adopted July 2004 Summary The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003. The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990's. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993. It is likely that BSE infectivity entered processing at the time of imported 'at - risk' MBM (1993) and at the time of slaughter of imported live 'at - risk' cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system. EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSEagent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.
http://www.mvo.nl/wetgeving-dierlijk-vet/onderzoek/download/EFSA%20on%20BSE%20risk%20Mexico%20jul%202004.pdf
Saturday, April 11, 2009
CJD FOUNDATION SIDES WITH R-CALFERS NO BSE OR HUMAN TSE THERE OF IN USA 'don't be fooled'
http://prionunitusaupdate2008.blogspot.com/2009/04/cjd-foundation-sides-with-r-calfers-no.html
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...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
-MORE Office of the United States Attorney District of Arizona FOR IMMEDIATE RELEASE For Information Contact Public Affairs February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT'S MAD COW DISEASE SURVEILLANCE PROGRAM
PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, "The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA's Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law." Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the "USDA Agreement") to collect obex samples from cattle at high risk of mad cow disease (the "Targeted Cattle Population"). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.
Evidence uncovered during the government's investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.
Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA's ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:
(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;
(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;
(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA's testing laboratory that were false and misleading;
(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;
(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and
(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.
Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #
http://www.usdoj.gov/usao/az/press_releases/2007/2007-051(Farabee).pdf
Thu Dec 6, 2007 11:38
FDA IN CRISIS MODE, AMERICAN LIVES AT RISK
http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html
FDA SCIENCE AND MISSION AT RISK
http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study "BSE in primates" supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must
also have shared Mr Bradley's surprise at the results because all the dose
levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s145d.pdf
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate"
experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
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/
Thursday, November 27, 2008 Prion diseases are efficiently transmitted by blood transfusion in sheep
http://vcjdblood.blogspot.com/2008/11/prion-diseases-are-efficiently.html
Scientists warn of first ever case of human mad cow disease from blood plasma
http://vcjdtransfusion.blogspot.com/2009/02/scientists-warn-of-first-ever-case-of.html
Saturday, February 21, 2009 Renderers say industry not prepared for FDA feed ban rule ??? WHAT, IT'S 2009 FOR PETE'S SAKE $$$ Two recent articles caught my eye ;
Renderers say industry not prepared for FDA feed ban rule
Food Chemical News
February 2, 2009
and
BSE, rendering relate to human safety
Emma Struve 02/17/2009
http://madcowfeed.blogspot.com/2009/02/renderers-say-industry-not-prepared-for.html
Monday, May 4, 2009
Back to the Past With New TSE Testing Agricultural Research/May-June 2009
http://madcowtesting.blogspot.com/2009/05/back-to-past-with-new-tse-testing.html
TSS
Showing posts with label North America. Show all posts
Showing posts with label North America. Show all posts
Saturday, May 16, 2009
Friday, April 17, 2009
REPORT ON THE INVESTIGATION OF THE FIFTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
REPORT ON THE INVESTIGATION OF THE FIFTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
BACKGROUND
On November 3, 2008, the Canadian Food Inspection Agency (CFIA) sampled a Holstein cow under Canada's National BSE Surveillance Program. Brain samples were received by the British Columbia Ministry of Agriculture and Lands (BCMAL) Laboratory, where they were screened for BSE using a Prionics rapid test. 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 reaction a second time. Brain samples were then sent to the National BSE Reference Laboratory in Lethbridge, Alberta. Additional testing for BSE (Prionics-Check PrioStrip, BioRad TeSeE ELISA, Prionics-Check Western and Hybrid Western Blot) was conducted at the National BSE Reference Laboratory to validate the result of the screening test and was positive on Nov 6, 2008. The Scrapie Associated Fibril Immunoblot procedure was positive on Nov 7, 2008 and the immunohistochemistry procedure was positive on Nov 14, 2008. The carcass was secured at the sampling site and will subsequently be transferred to CFIA’s Lethbridge laboratory for incineration. No part of the carcass entered the human food supply or animal feed chain.
The CFIA immediately initiated an epidemiological investigation based on the recommended BSE guidelines (Terrestrial Animal Health Code 2008) of the World Organisation for Animal Health, referred to as the OIE. Specifically, the CFIA followed the recommended BSE guidelines for a country with controlled risk status and investigated:
the feed cohort, comprising all cattle which, during their first year of life, were reared with the BSE case during its first year of life, and which investigation showed consumed the same potentially contaminated feed during that period, or the birth cohort, comprising all cattle born in the same herd as, and within 12 months of the birth of the BSE case, if the above cannot be identified and feed to which the animal may have been exposed early in its life. ANIMAL INVESTIGATION The positive animal was a registered Holstein dairy cow born on January 1, 2001, and it was 94 months of age at the time of death. The animal was born, raised and had spent its entire life on the same farm. The producer reported the duration of illness as less than 2 days with the animal exhibiting an abnormal gait (locomotion, change in movement), which was worse on the hind end. The animal had a short stunted gait and exhibited signs of ataxia (uncoordinated movements). The producer elected to have the animal humanely destroyed. Since the inclusion criteria of Canada’s National BSE Surveillance Program were met, arrangements were made to forward appropriate samples for laboratory evaluation.
The birth farm was a dairy operation located in the Fraser Valley area of British Columbia. The feed cohort was determined to comprise 187 animals, which along with the case animal, were raised on the farm. This cohort consisted of female Holsteins. Males sold at less than two weeks of age for fattening and subsequent slaughter without having access to any commercially prepared feeds were excluded from the investigation because they were not exposed to the same potentially contaminated feed as the case animal. No males were retained or raised on the farm. The trace-out investigation of the feed cohort located 22 live animals on the case farm. These animals are quarantined and will be humanely destroyed; their carcasses disposed of by incineration in accordance with the OIE recommendations. The following is the disposition of the remaining animals in the feed cohort:
122 animals were traced and confirmed to have died or been slaughtered; 24 animals were traced and presumed to have died or been slaughtered; 5 animals were traced and confirmed to have been exported for slaughter and the importing country has been notified; and 14 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 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 silages and mixed feed products provided to the farm from one commercial supplier. On-farm mixing equipment consisted of a mixer wagon used to combine forages with commercial products for calves, heifers and lactating cows. Several cats on the farm were fed in the barn and one dog was fed in the house away from the dairy operation. It is reasonable to presume that the cat and dog food did contain prohibited material; however, review of farm feeding practices confirmed that ruminants did not have access to these feeds.
For the first three weeks of life, the case animal was housed individually in a calf pen and fed milk and a commercially prepared calf ration. From 3 to 9 weeks the animal was housed in a series of group pens with animals of similar age and continued to be fed calf ration and milk as well as hay and had access to two kinds of mineral blocks. From 9 weeks to 12 months the animal continued to cycle through several group pens with animals of similar age and continued to be fed calf ration, hay and farm grown corn and grass silages as well as having access to two kinds of mineral blocks. Additionally, a dry cow mineral was added to the animal’s diet at the 3 month stage.
The only other commercial feed products used on the farm included a complete ration for the lactating cows and a dry cow ration. On-farm investigation confirmed that the lactation ration was not fed to the case animal prior to twelve months of age, however, the same on-farm mixer wagon was used to mix rations for both the case animal and the lactating cows. It was also determined that the case animal could not have access to the dry cow ration which was received, stored and fed directly from bags and away from animals less than one year of age.
Investigation at the commercial feed manufacturer, which was the sole supplier of calf ration and lactation ration, identified that this facility handled prohibited material. 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 the commercial feed supplier identified that the two kinds of mineral blocks were manufactured by a separate facility, independent of the main commercial feed manufacturer. Investigation at the manufacturer of these blocks determined that this facility did handle prohibited material during the period of interest; however, no written procedures or production records were available. As the period of interest occurs after the introduction of the 1997 Mammalian Feed Ban, it is unlikely that ruminant meat and bone meal was intentionally used in the formulation of either of these mineral blocks. However, as production records are not available for review, it is not possible to rule out the possibility that contamination during production could have taken place.
The dry cow mineral used on farm was obtained from a specialized facility not handling prohibited material and was packaged in bags. This product was ruled out as a possible source of contamination.
Considering the farm’s feeding regime and specific production records reviewed, a likely source of exposure to BSE infectivity appears to be potentially contaminated heifer ration. However, the risk associated with possible ingestion of small amounts of the lactation ration and either of the mineral blocks 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 15 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.
http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/bccb2008/15investe.shtml
REPORT ON THE INVESTIGATION OF THE FOURTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA BACKGROUND
On July 25, 2008 a commercial beef cow in Northern Alberta was sampled by a private practitioner under Canada's National BSE Surveillance Program. Brain samples from this animal were sent to the Alberta Agriculture and Rural Development (ARD) laboratory where they were screened for BSE using a Bio-Rad rapid test on August 6, 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 reaction a second time. Brain samples were then sent to the National BSE Reference Laboratory in Lethbridge, Alberta. Additional rapid tests for BSE (Prionics-Check PrioStrip and BioRad TeSeE ELISA) were conducted at the National BSE Reference Laboratory to validate the result of the screening test and were positive on August 12, 2008. The Prionics-Check Western and the Hybrid Western Blot was positive on August 14, 2008. Bovine Spongiform Encephalopathy was confirmed on August 14, 2008 using the Scrapie Associated Fibril Immunoblot procedure. The carcass was secured at the sampling site. No part of the carcass entered the human food supply or animal feed chain.
The CFIA immediately initiated an epidemiological investigation based on the recommended BSE guidelines (Terrestrial Animal Health Code 2008) of the World Organisation for Animal Health, referred to as the OIE. Specifically, the CFIA followed the recommended BSE guidelines for a country with controlled risk status and investigated:
the feed cohort, comprising all cattle which, during their first year of life, were reared with the BSE case during its first year of life, and which investigation showed consumed the same potentially contaminated feed during that period, or the birth cohort, comprising all cattle born in the same herd as, and within 12 months of the birth of the BSE case, if the above cannot be identified and feed to which the animal may have been exposed early in its life. ANIMAL INVESTIGATION The positive animal was a commercial beef cow, Gelbvieh cross, born on March 20, 2002 and it was 76 months of age at the time of death. The animal was born, raised and had spent its entire life on the same farm. The producer reported the duration of illness as approximately 6 months with the animal exhibiting gradual deterioration culminating in the animal becoming non-ambulatory (downer). During this period, the animal showed a change in behaviour resulting in the animal becoming apprehensive/nervous. When examined by a private practitioner on July 25, 2008, the animal was recumbent. Physical examination by the practitioner revealed opisthotonus (muscle spasms). The practitioner and producer determined that the animal should be euthanized . A post-mortem examination was conducted, and the kidneys were observed to be smaller than normal with a thickened adherent capsule. A presumptive diagnosis of chronic renal disease was made by the submitting practitioner. Since the inclusion criteria of Canada’s National BSE Surveillance Program were met, arrangements were made to forward appropriate samples for laboratory evaluation.
The birth farm was a commercial beef cow-calf operation. The birth cohort was determined to comprise 72 animals, which along with the case animal, were raised on the farm. Due to the practice of animals being sold in lots from the case premises, 106 animals (including the 72 birth cohorts) were traced. The trace-out investigation of the birth cohort located 6 live animals on the case farm and 3 live animals on a subsequent premises. All of these animals have since been humanely destroyed; their carcasses disposed of by incineration in accordance with the OIE recommendations. The following is the disposition of the remaining animals in the 97 animals:
80 animals were traced and confirmed to have died or been slaughtered, 14 animals were traced and presumed to have died or been slaughtered, 3 animals were determined to be untraceable because of records limitations. FEED INVESTIGATION The feed investigation yielded limited records specific to the animal’s first year of life. All feed products to which the BSE case animal had access were intended for feeding to ruminants.
Routine feeding practices were to provide animals with pasture during the summer months and to provide additional hay and grain during the winter. It was not farm practice to supplement the diets with commercially prepared rations, however due to drought conditions during the animal’s first year of life, three commercially prepared rations were provided in addition to the commonly fed forages, grains, salt and minerals.
For the first seven months of life, the case animal was housed in a cow-calf pen and had pasture access. During this period, the animal received cow’s milk and calf starter and had access to loose mineral, salt blocks and pasture. Beyond seven months to the end of the first year of life, the animal was housed in a calf pen where it received a creep feed, feedlot starter and possibly grain and straw and had access to salt blocks.
The three commercial rations made available to the BSE case animal consisted of a calf starter, a creep feed and a feedlot starter which were manufactured by two different commercial feed manufacturers.
Two forms of salt were used on farm: salt blocks and loose mineral salt. The salt blocks were manufactured by a company which does not handle any prohibited material. The loose mineral salt was manufactured by one of the same facilities which manufactured two of the commercially prepared rations received by the farm.
Neither of the two commercial feed manufacturers has production records dating back to the period of interest. As a result, trace back inspections at the manufacturers of commercial feeds distributed to the birth farm did not yield mixing formulas for the period of interest. As this was subsequent to the implementation of the 1997 Mammalian Feed Ban, it is very unlikely that ruminant meat and bone meal was intentionally used in the formulation of any of the three commercially prepared rations or loose mineral salt distributed to the birth farm.
However, as production records are not available for review, it is not possible to rule out that contamination during production could have taken place. One of the two commercial feed manufacturers did handle ruminant meat and bone meal (prohibited material/PM), however they did have procedures in place to prevent the contamination of ruminant feed with PM. The other commercial feed manufacturer did not handle PM directly, though they did receive a premix used in the manufacture of one of the feeds received by the case farm, from another facility which did handle PM.
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 14 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.
http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/ab2008/14investe.shtml
P26
TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C. The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf
Research Project: GENETIC AND BIOLOGICAL DETERMINANTS OF RESPIRATORY DISEASE SUSCEPTIBILITY Location: Animal Health Systems Research
Title: Association of a bovine prion gene haplotype with atypical BSE
Author
Clawson, Michael
Submitted to: Meeting Abstract Publication Type: Abstract Publication Acceptance Date: December 2, 2008 Publication Date: January 1, 2009 Citation: Clawson, M.L. 2009. Association of a bovine prion gene haplotype with atypical BSE [abstract]. Plant and Animal Genomes XVII Conference. Abstract No. W091. Available: http://www.intl-pag.org/17/abstracts/
Technical Abstract: Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a class of fatal neurodegenerative disorders that occur in humans, ruminants, cats, and mink. Three distinct TSEs afflict cattle: classical bovine spongiform encephalopathy (BSE), atypical H-type BSE, and atypical L-type BSE. Classical BSE was identified in the 1980s and is acquired by cattle through the consumption of feed contaminated with the infectious prion agent. Atypical BSEs have only recently been recognized as distinct cattle prion diseases and are extremely rare. The full extent of genetic susceptibilities to atypical BSEs is unknown; however, one atypical H-type case identified in the United States (2006) was most likely caused by a genetic mutation in the prion gene, E211K. We have identified an association of a bovine prion DNA haplotype with atypical BSE that is independent of E211K. The haplotype spans a portion of the prion gene that includes part of intron 2, the entire coding region of exon 3, and part of the three prime untranslated region of exon 3 (13 kb). Despite the low frequency of this haplotype among general cattle populations, it was present in a majority of H- and L-type atypical BSE cases from Canada, France, and the United States. This result indicates that there is a genetic component to atypical BSE susceptibility in addition to E211K.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=234699
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
P02.35
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.
http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf
Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock
Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement
Start Date: Sep 15, 2004 End Date: Sep 14, 2009
Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490
Wednesday, February 11, 2009
Atypical BSE North America Update February 2009
Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198
snip...end
source :
Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72
Bovine spongiform encephalopathy
Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD
http://avmajournals.avma.org/doi/ref/10.2460/javma.234.1.59
Atypical BSE North America Update February 2009
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
Thursday, April 9, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed
http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html
please see ;
http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html#comments
TSS COMMENT SUBMISSION # 5
Docket ID FDA-2002-N-0031 Docket Title Animal Proteins Prohibited in Ruminant Feed Document ID FDA-2002-N-0031-0132 Document Title Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Delay of Effective Date
Completely Edited Version
PRION ROUNDTABLE
2003
page 29
Dr. Linda Detwiler
The UK imports into the US.
There were 496 total, and 173 of the UK imports could have entered the US feed system. People don't like to hear this, but it's possible that one of the UK imports in the US entered the animal feed system and was exported to Canada. That's a possibility, because they import 50% of their feed from the US.
From 1994, we imported 11 million head of cattle from Canada. Most of these were feedlot animals for slaughter, but there were about 500,000 breeding animals. A number of Canada's cull cows were slaughtered here and could have introduced infectivity into our system. Even today we have Canadian imports in the country, breeding animals that were brought in prior to the ban and reside here.
We have feed ban exemptions: plate waste, poultry litter. We still allow that if it comes off a human plate, or if it's trimmings, it can be palletized and fed to ruminants. That might be a small amount, but it could allow spinal cord in certain cuts to be fed back to ruminants. Poultry litter or feather meal could be significant. Poultry is getting quite a bit of ruminant material in the US because it cannot go back to ruminants. Poultry and pigs are getting a substantial amount. Poultry litter is not only what passes through the chicken, but think about how chickens eat. They spill a lot on the floor. That stuff is still allowed to be fed back to cattle. That's a direct break in the ban, except that it's legal. Ruminants are getting ruminant material.
Unfiltered tallow: tallow is a lipid material. However, if it's not filtered, there are protein residues. That's meat and bone meal. That's allowed to be fed, so that's another legal exception where you can feed ruminant meat and bone meal through unfiltered tallow. We don't have an SRM ban and the 40 animals are the ones that if you have the agent, they introduce the most infectivity back into the animal food chain when they're rendered.
What's our on-farm compliance? We really don't know. ...snip...end...Dr. Linda Detwiler
UK EXPORTS OF MBM TO WORLD
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
OTHERS
BEEF AND VEAL
http://www.bseinquiry.gov.uk/files/mb/m11f/tab08.pdf
http://www.bseinquiry.gov.uk/files/mb/m11f/tab09.pdf
http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf
LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
FATS
http://www.bseinquiry.gov.uk/files/mb/m11g/tab01.pdf
EMBRYOS
http://www.bseinquiry.gov.uk/files/mb/m11g/tab03.pdf
GELATIN ETC
http://www.bseinquiry.gov.uk/files/mb/m11g/tab02.pdf
SEMEN
http://www.bseinquiry.gov.uk/files/mb/m11g/tab04.pdf
MEAT
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
USA BSE GBR
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178620779461.htm
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_annex_en1.pdf?ssbinary=true
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1.pdf?ssbinary=true
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_summary_en1.pdf?ssbinary=true
CANADA BSE GBR
http://www.mvo.nl/wetgeving-dierlijk-vet/onderzoek/download/EFSA%20on%20BSE%20risk%20Canada%20jul%202004.pdf
MEXICO BSE GBR
http://www.mvo.nl/wetgeving-dierlijk-vet/onderzoek/download/EFSA%20on%20BSE%20risk%20Mexico%20jul%202004.pdf
Wednesday, April 16, 2008 MBM, greaves, meat offal, live cattle, imports from UK to USA vs Canada "Three of four possible manufacturers supplying a protein supplement likely fed to the animal could have included meat and bone meal (MBM) as an ingredient in its formulation. One of these manufacturers was able to confirm usage of meat and bone meal in supplements and confirm a source of MBM to be one common to previous BSE investigations."
USA AND CANADA IMPORTS OF UK CATTLE BETWEEN 1981 - 1989
USA = 496
CANADA = 198
*add 14 to 198 as last UK import to Canada, 14 in 1990
http://www.inspection.gc.ca/english/sci/ahra/bseris/bserise.pdf
HERE is another look at all the imports for both the USA and Canada of UK live cattle and greaves exports ;
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995
USA 24 TONS
CANADA 83 TONS
http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.??? From: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000199/!x-usc:mailto:S.J.Pearsall@esg.maff.gsi.gov.uk Date: Tue, 8 Feb 2000 14:03:16 +0000 To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000199/!x-usc:mailto:flounder@wt.net (Receipt Notification Requested) (Non Receipt Notification Requested)
Terry
Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Country Tonnes
1980 1981 12 1982 1983 1984 10 1985 2 1986 1987 1988 1989 20 1990
Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222). Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C
============ END...TSS...2008============
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
snip...full text ;
http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html#comments
Sunday, April 12, 2009 r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada
http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html
http://prionunitusaupdate2008.blogspot.com/2009/04/cjd-foundation-sides-with-r-calfers-no.html#comments
FDA2002N0031
r-calf
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=0900006480952081&disposition=attachment&contentType=pdf
CJD FOUNDATION
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=090000648094d9f9
greetings,
i don't think i interpreted anything about USA mad cow problem, and or USA mad cow feed problem, of which is what this docket was for. in 2007, in one fda warning letter week, two warning letters, where 10,000,000 pounds of suspect banned mad cow feed went into commerce to be fed out. and 2006 was a banner year as well for USA MAD COW FEED that was banned, that went into commerce to be fed out. why does r-calf not mention this $$$ or the failed, flawed, and corrupt 2004 ENHANCED BSE SURVEILLANCE PROGRAM, that was nothing more of another mad cow cover-up. we all know it. OIG said it, in it's own way, and Paul Brown of CDC said it in plain terms. hmmm, no mention there either by r-calf$ that's what the r-calf is all about. they are playing some like a deck of cards.
nothing more of the same, big, big, denial, and that' s what anyone that signed that letter with r-calf ET AL supported, a big denial. ...TSS
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
unday, April 12, 2009
BSE MAD COW TESTING USA 2009 FIGURES
http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html
Saturday, January 24, 2009
Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
2008 Annual Report
http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
see full text ;
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html
Wednesday, February 04, 2009
Creutzfeldt-Jacob disease presenting as severe depression: a case report
http://creutzfeldt-jakob-disease.blogspot.com/2009/02/creutzfeldt-jacob-disease-presenting-as.html
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
BACKGROUND
On November 3, 2008, the Canadian Food Inspection Agency (CFIA) sampled a Holstein cow under Canada's National BSE Surveillance Program. Brain samples were received by the British Columbia Ministry of Agriculture and Lands (BCMAL) Laboratory, where they were screened for BSE using a Prionics rapid test. 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 reaction a second time. Brain samples were then sent to the National BSE Reference Laboratory in Lethbridge, Alberta. Additional testing for BSE (Prionics-Check PrioStrip, BioRad TeSeE ELISA, Prionics-Check Western and Hybrid Western Blot) was conducted at the National BSE Reference Laboratory to validate the result of the screening test and was positive on Nov 6, 2008. The Scrapie Associated Fibril Immunoblot procedure was positive on Nov 7, 2008 and the immunohistochemistry procedure was positive on Nov 14, 2008. The carcass was secured at the sampling site and will subsequently be transferred to CFIA’s Lethbridge laboratory for incineration. No part of the carcass entered the human food supply or animal feed chain.
The CFIA immediately initiated an epidemiological investigation based on the recommended BSE guidelines (Terrestrial Animal Health Code 2008) of the World Organisation for Animal Health, referred to as the OIE. Specifically, the CFIA followed the recommended BSE guidelines for a country with controlled risk status and investigated:
the feed cohort, comprising all cattle which, during their first year of life, were reared with the BSE case during its first year of life, and which investigation showed consumed the same potentially contaminated feed during that period, or the birth cohort, comprising all cattle born in the same herd as, and within 12 months of the birth of the BSE case, if the above cannot be identified and feed to which the animal may have been exposed early in its life. ANIMAL INVESTIGATION The positive animal was a registered Holstein dairy cow born on January 1, 2001, and it was 94 months of age at the time of death. The animal was born, raised and had spent its entire life on the same farm. The producer reported the duration of illness as less than 2 days with the animal exhibiting an abnormal gait (locomotion, change in movement), which was worse on the hind end. The animal had a short stunted gait and exhibited signs of ataxia (uncoordinated movements). The producer elected to have the animal humanely destroyed. Since the inclusion criteria of Canada’s National BSE Surveillance Program were met, arrangements were made to forward appropriate samples for laboratory evaluation.
The birth farm was a dairy operation located in the Fraser Valley area of British Columbia. The feed cohort was determined to comprise 187 animals, which along with the case animal, were raised on the farm. This cohort consisted of female Holsteins. Males sold at less than two weeks of age for fattening and subsequent slaughter without having access to any commercially prepared feeds were excluded from the investigation because they were not exposed to the same potentially contaminated feed as the case animal. No males were retained or raised on the farm. The trace-out investigation of the feed cohort located 22 live animals on the case farm. These animals are quarantined and will be humanely destroyed; their carcasses disposed of by incineration in accordance with the OIE recommendations. The following is the disposition of the remaining animals in the feed cohort:
122 animals were traced and confirmed to have died or been slaughtered; 24 animals were traced and presumed to have died or been slaughtered; 5 animals were traced and confirmed to have been exported for slaughter and the importing country has been notified; and 14 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 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 silages and mixed feed products provided to the farm from one commercial supplier. On-farm mixing equipment consisted of a mixer wagon used to combine forages with commercial products for calves, heifers and lactating cows. Several cats on the farm were fed in the barn and one dog was fed in the house away from the dairy operation. It is reasonable to presume that the cat and dog food did contain prohibited material; however, review of farm feeding practices confirmed that ruminants did not have access to these feeds.
For the first three weeks of life, the case animal was housed individually in a calf pen and fed milk and a commercially prepared calf ration. From 3 to 9 weeks the animal was housed in a series of group pens with animals of similar age and continued to be fed calf ration and milk as well as hay and had access to two kinds of mineral blocks. From 9 weeks to 12 months the animal continued to cycle through several group pens with animals of similar age and continued to be fed calf ration, hay and farm grown corn and grass silages as well as having access to two kinds of mineral blocks. Additionally, a dry cow mineral was added to the animal’s diet at the 3 month stage.
The only other commercial feed products used on the farm included a complete ration for the lactating cows and a dry cow ration. On-farm investigation confirmed that the lactation ration was not fed to the case animal prior to twelve months of age, however, the same on-farm mixer wagon was used to mix rations for both the case animal and the lactating cows. It was also determined that the case animal could not have access to the dry cow ration which was received, stored and fed directly from bags and away from animals less than one year of age.
Investigation at the commercial feed manufacturer, which was the sole supplier of calf ration and lactation ration, identified that this facility handled prohibited material. 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 the commercial feed supplier identified that the two kinds of mineral blocks were manufactured by a separate facility, independent of the main commercial feed manufacturer. Investigation at the manufacturer of these blocks determined that this facility did handle prohibited material during the period of interest; however, no written procedures or production records were available. As the period of interest occurs after the introduction of the 1997 Mammalian Feed Ban, it is unlikely that ruminant meat and bone meal was intentionally used in the formulation of either of these mineral blocks. However, as production records are not available for review, it is not possible to rule out the possibility that contamination during production could have taken place.
The dry cow mineral used on farm was obtained from a specialized facility not handling prohibited material and was packaged in bags. This product was ruled out as a possible source of contamination.
Considering the farm’s feeding regime and specific production records reviewed, a likely source of exposure to BSE infectivity appears to be potentially contaminated heifer ration. However, the risk associated with possible ingestion of small amounts of the lactation ration and either of the mineral blocks 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 15 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.
http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/bccb2008/15investe.shtml
REPORT ON THE INVESTIGATION OF THE FOURTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA BACKGROUND
On July 25, 2008 a commercial beef cow in Northern Alberta was sampled by a private practitioner under Canada's National BSE Surveillance Program. Brain samples from this animal were sent to the Alberta Agriculture and Rural Development (ARD) laboratory where they were screened for BSE using a Bio-Rad rapid test on August 6, 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 reaction a second time. Brain samples were then sent to the National BSE Reference Laboratory in Lethbridge, Alberta. Additional rapid tests for BSE (Prionics-Check PrioStrip and BioRad TeSeE ELISA) were conducted at the National BSE Reference Laboratory to validate the result of the screening test and were positive on August 12, 2008. The Prionics-Check Western and the Hybrid Western Blot was positive on August 14, 2008. Bovine Spongiform Encephalopathy was confirmed on August 14, 2008 using the Scrapie Associated Fibril Immunoblot procedure. The carcass was secured at the sampling site. No part of the carcass entered the human food supply or animal feed chain.
The CFIA immediately initiated an epidemiological investigation based on the recommended BSE guidelines (Terrestrial Animal Health Code 2008) of the World Organisation for Animal Health, referred to as the OIE. Specifically, the CFIA followed the recommended BSE guidelines for a country with controlled risk status and investigated:
the feed cohort, comprising all cattle which, during their first year of life, were reared with the BSE case during its first year of life, and which investigation showed consumed the same potentially contaminated feed during that period, or the birth cohort, comprising all cattle born in the same herd as, and within 12 months of the birth of the BSE case, if the above cannot be identified and feed to which the animal may have been exposed early in its life. ANIMAL INVESTIGATION The positive animal was a commercial beef cow, Gelbvieh cross, born on March 20, 2002 and it was 76 months of age at the time of death. The animal was born, raised and had spent its entire life on the same farm. The producer reported the duration of illness as approximately 6 months with the animal exhibiting gradual deterioration culminating in the animal becoming non-ambulatory (downer). During this period, the animal showed a change in behaviour resulting in the animal becoming apprehensive/nervous. When examined by a private practitioner on July 25, 2008, the animal was recumbent. Physical examination by the practitioner revealed opisthotonus (muscle spasms). The practitioner and producer determined that the animal should be euthanized . A post-mortem examination was conducted, and the kidneys were observed to be smaller than normal with a thickened adherent capsule. A presumptive diagnosis of chronic renal disease was made by the submitting practitioner. Since the inclusion criteria of Canada’s National BSE Surveillance Program were met, arrangements were made to forward appropriate samples for laboratory evaluation.
The birth farm was a commercial beef cow-calf operation. The birth cohort was determined to comprise 72 animals, which along with the case animal, were raised on the farm. Due to the practice of animals being sold in lots from the case premises, 106 animals (including the 72 birth cohorts) were traced. The trace-out investigation of the birth cohort located 6 live animals on the case farm and 3 live animals on a subsequent premises. All of these animals have since been humanely destroyed; their carcasses disposed of by incineration in accordance with the OIE recommendations. The following is the disposition of the remaining animals in the 97 animals:
80 animals were traced and confirmed to have died or been slaughtered, 14 animals were traced and presumed to have died or been slaughtered, 3 animals were determined to be untraceable because of records limitations. FEED INVESTIGATION The feed investigation yielded limited records specific to the animal’s first year of life. All feed products to which the BSE case animal had access were intended for feeding to ruminants.
Routine feeding practices were to provide animals with pasture during the summer months and to provide additional hay and grain during the winter. It was not farm practice to supplement the diets with commercially prepared rations, however due to drought conditions during the animal’s first year of life, three commercially prepared rations were provided in addition to the commonly fed forages, grains, salt and minerals.
For the first seven months of life, the case animal was housed in a cow-calf pen and had pasture access. During this period, the animal received cow’s milk and calf starter and had access to loose mineral, salt blocks and pasture. Beyond seven months to the end of the first year of life, the animal was housed in a calf pen where it received a creep feed, feedlot starter and possibly grain and straw and had access to salt blocks.
The three commercial rations made available to the BSE case animal consisted of a calf starter, a creep feed and a feedlot starter which were manufactured by two different commercial feed manufacturers.
Two forms of salt were used on farm: salt blocks and loose mineral salt. The salt blocks were manufactured by a company which does not handle any prohibited material. The loose mineral salt was manufactured by one of the same facilities which manufactured two of the commercially prepared rations received by the farm.
Neither of the two commercial feed manufacturers has production records dating back to the period of interest. As a result, trace back inspections at the manufacturers of commercial feeds distributed to the birth farm did not yield mixing formulas for the period of interest. As this was subsequent to the implementation of the 1997 Mammalian Feed Ban, it is very unlikely that ruminant meat and bone meal was intentionally used in the formulation of any of the three commercially prepared rations or loose mineral salt distributed to the birth farm.
However, as production records are not available for review, it is not possible to rule out that contamination during production could have taken place. One of the two commercial feed manufacturers did handle ruminant meat and bone meal (prohibited material/PM), however they did have procedures in place to prevent the contamination of ruminant feed with PM. The other commercial feed manufacturer did not handle PM directly, though they did receive a premix used in the manufacture of one of the feeds received by the case farm, from another facility which did handle PM.
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 14 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.
http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/ab2008/14investe.shtml
P26
TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C. The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf
Research Project: GENETIC AND BIOLOGICAL DETERMINANTS OF RESPIRATORY DISEASE SUSCEPTIBILITY Location: Animal Health Systems Research
Title: Association of a bovine prion gene haplotype with atypical BSE
Author
Clawson, Michael
Submitted to: Meeting Abstract Publication Type: Abstract Publication Acceptance Date: December 2, 2008 Publication Date: January 1, 2009 Citation: Clawson, M.L. 2009. Association of a bovine prion gene haplotype with atypical BSE [abstract]. Plant and Animal Genomes XVII Conference. Abstract No. W091. Available: http://www.intl-pag.org/17/abstracts/
Technical Abstract: Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a class of fatal neurodegenerative disorders that occur in humans, ruminants, cats, and mink. Three distinct TSEs afflict cattle: classical bovine spongiform encephalopathy (BSE), atypical H-type BSE, and atypical L-type BSE. Classical BSE was identified in the 1980s and is acquired by cattle through the consumption of feed contaminated with the infectious prion agent. Atypical BSEs have only recently been recognized as distinct cattle prion diseases and are extremely rare. The full extent of genetic susceptibilities to atypical BSEs is unknown; however, one atypical H-type case identified in the United States (2006) was most likely caused by a genetic mutation in the prion gene, E211K. We have identified an association of a bovine prion DNA haplotype with atypical BSE that is independent of E211K. The haplotype spans a portion of the prion gene that includes part of intron 2, the entire coding region of exon 3, and part of the three prime untranslated region of exon 3 (13 kb). Despite the low frequency of this haplotype among general cattle populations, it was present in a majority of H- and L-type atypical BSE cases from Canada, France, and the United States. This result indicates that there is a genetic component to atypical BSE susceptibility in addition to E211K.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=234699
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
P02.35
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.
http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf
Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock
Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement
Start Date: Sep 15, 2004 End Date: Sep 14, 2009
Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.
Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490
Wednesday, February 11, 2009
Atypical BSE North America Update February 2009
Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198
snip...end
source :
Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72
Bovine spongiform encephalopathy
Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD
http://avmajournals.avma.org/doi/ref/10.2460/javma.234.1.59
Atypical BSE North America Update February 2009
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
Thursday, April 9, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed
http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html
please see ;
http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html#comments
TSS COMMENT SUBMISSION # 5
Docket ID FDA-2002-N-0031 Docket Title Animal Proteins Prohibited in Ruminant Feed Document ID FDA-2002-N-0031-0132 Document Title Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Delay of Effective Date
Completely Edited Version
PRION ROUNDTABLE
2003
page 29
Dr. Linda Detwiler
The UK imports into the US.
There were 496 total, and 173 of the UK imports could have entered the US feed system. People don't like to hear this, but it's possible that one of the UK imports in the US entered the animal feed system and was exported to Canada. That's a possibility, because they import 50% of their feed from the US.
From 1994, we imported 11 million head of cattle from Canada. Most of these were feedlot animals for slaughter, but there were about 500,000 breeding animals. A number of Canada's cull cows were slaughtered here and could have introduced infectivity into our system. Even today we have Canadian imports in the country, breeding animals that were brought in prior to the ban and reside here.
We have feed ban exemptions: plate waste, poultry litter. We still allow that if it comes off a human plate, or if it's trimmings, it can be palletized and fed to ruminants. That might be a small amount, but it could allow spinal cord in certain cuts to be fed back to ruminants. Poultry litter or feather meal could be significant. Poultry is getting quite a bit of ruminant material in the US because it cannot go back to ruminants. Poultry and pigs are getting a substantial amount. Poultry litter is not only what passes through the chicken, but think about how chickens eat. They spill a lot on the floor. That stuff is still allowed to be fed back to cattle. That's a direct break in the ban, except that it's legal. Ruminants are getting ruminant material.
Unfiltered tallow: tallow is a lipid material. However, if it's not filtered, there are protein residues. That's meat and bone meal. That's allowed to be fed, so that's another legal exception where you can feed ruminant meat and bone meal through unfiltered tallow. We don't have an SRM ban and the 40 animals are the ones that if you have the agent, they introduce the most infectivity back into the animal food chain when they're rendered.
What's our on-farm compliance? We really don't know. ...snip...end...Dr. Linda Detwiler
UK EXPORTS OF MBM TO WORLD
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
OTHERS
BEEF AND VEAL
http://www.bseinquiry.gov.uk/files/mb/m11f/tab08.pdf
http://www.bseinquiry.gov.uk/files/mb/m11f/tab09.pdf
http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf
LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
FATS
http://www.bseinquiry.gov.uk/files/mb/m11g/tab01.pdf
EMBRYOS
http://www.bseinquiry.gov.uk/files/mb/m11g/tab03.pdf
GELATIN ETC
http://www.bseinquiry.gov.uk/files/mb/m11g/tab02.pdf
SEMEN
http://www.bseinquiry.gov.uk/files/mb/m11g/tab04.pdf
MEAT
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
USA BSE GBR
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178620779461.htm
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_annex_en1.pdf?ssbinary=true
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_v2_en1.pdf?ssbinary=true
http://www.efsa.europa.eu/EFSA/Scientific_Document/sr03_biohaz02_usa_report_summary_en1.pdf?ssbinary=true
CANADA BSE GBR
http://www.mvo.nl/wetgeving-dierlijk-vet/onderzoek/download/EFSA%20on%20BSE%20risk%20Canada%20jul%202004.pdf
MEXICO BSE GBR
http://www.mvo.nl/wetgeving-dierlijk-vet/onderzoek/download/EFSA%20on%20BSE%20risk%20Mexico%20jul%202004.pdf
Wednesday, April 16, 2008 MBM, greaves, meat offal, live cattle, imports from UK to USA vs Canada "Three of four possible manufacturers supplying a protein supplement likely fed to the animal could have included meat and bone meal (MBM) as an ingredient in its formulation. One of these manufacturers was able to confirm usage of meat and bone meal in supplements and confirm a source of MBM to be one common to previous BSE investigations."
USA AND CANADA IMPORTS OF UK CATTLE BETWEEN 1981 - 1989
USA = 496
CANADA = 198
*add 14 to 198 as last UK import to Canada, 14 in 1990
http://www.inspection.gc.ca/english/sci/ahra/bseris/bserise.pdf
HERE is another look at all the imports for both the USA and Canada of UK live cattle and greaves exports ;
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995
USA 24 TONS
CANADA 83 TONS
http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.??? From: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000199/!x-usc:mailto:S.J.Pearsall@esg.maff.gsi.gov.uk Date: Tue, 8 Feb 2000 14:03:16 +0000 To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000199/!x-usc:mailto:flounder@wt.net (Receipt Notification Requested) (Non Receipt Notification Requested)
Terry
Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Country Tonnes
1980 1981 12 1982 1983 1984 10 1985 2 1986 1987 1988 1989 20 1990
Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222). Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C
============ END...TSS...2008============
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
snip...full text ;
http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html#comments
Sunday, April 12, 2009 r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada
http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html
http://prionunitusaupdate2008.blogspot.com/2009/04/cjd-foundation-sides-with-r-calfers-no.html#comments
FDA2002N0031
r-calf
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=0900006480952081&disposition=attachment&contentType=pdf
CJD FOUNDATION
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=090000648094d9f9
greetings,
i don't think i interpreted anything about USA mad cow problem, and or USA mad cow feed problem, of which is what this docket was for. in 2007, in one fda warning letter week, two warning letters, where 10,000,000 pounds of suspect banned mad cow feed went into commerce to be fed out. and 2006 was a banner year as well for USA MAD COW FEED that was banned, that went into commerce to be fed out. why does r-calf not mention this $$$ or the failed, flawed, and corrupt 2004 ENHANCED BSE SURVEILLANCE PROGRAM, that was nothing more of another mad cow cover-up. we all know it. OIG said it, in it's own way, and Paul Brown of CDC said it in plain terms. hmmm, no mention there either by r-calf$ that's what the r-calf is all about. they are playing some like a deck of cards.
nothing more of the same, big, big, denial, and that' s what anyone that signed that letter with r-calf ET AL supported, a big denial. ...TSS
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
unday, April 12, 2009
BSE MAD COW TESTING USA 2009 FIGURES
http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html
Saturday, January 24, 2009
Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
2008 Annual Report
http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
see full text ;
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html
Wednesday, February 04, 2009
Creutzfeldt-Jacob disease presenting as severe depression: a case report
http://creutzfeldt-jakob-disease.blogspot.com/2009/02/creutzfeldt-jacob-disease-presenting-as.html
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
Monday, November 17, 2008
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
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
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