Compliance Guidelines for Use of Video or Other Electronic Monitoring or Recording Equipment in Federally Inspected Establishments

Compliance Guidelines for Use of Video or Other Electronic Monitoring or Recording Equipment in Federally Inspected Establishments

Food Safety and Inspection Service U.S. Department of Agriculture

Note: The Food Safety and Inspection Service (FSIS) is publishing this final compliance guideline after receiving Office of Management and Budget (OMB) approval of information collection under the Paperwork Reduction Act related to Hazard Analysis and Critical Control Point (HACCP) and Sanitation Standard Operating Procedures (Sanitation SOP) video records. FSIS has revised these final compliance guidelines to reflect comments received.

A total of 1,217 comments were received. Of those, 813 were a campaign form letter requesting that video be mandated in establishments. Another 400 comments were general statements that video should be made mandatory in establishments, concerns about worker safety, and concerns about inhumane handling. An additional comment was to require an accredited third party to audit mandatory video use in establishments.

Requiring video cameras in establishments is not necessary to ensure that animals are handled humanely in conjunction with slaughter. FSIS inspectors are required to conduct hands-on inspection to verify establishments are meeting regulatory requirements for humane handling in livestock and good commercial practices in poultry.

FSIS incorporated the three other comments into the final guidelines. This includes more clearly explaining these items:

video records not subject to routine access by FSIS: video records not designated by the establishment for use in HACCP plans or Sanitation SOPs, video records that are used for food defense security, or video records used for other purposes that do not require recordkeeping; such records would be subject to FSIS access during an investigation of food safety, food security, or any unlawful actions

use of video technology as a tool to supplement establishments’ hands-on humane handling and good commercial practice activities; video technology cannot replace FSIS hands-on inspection activities

the importance of effective implementation of video monitoring to result in trustworthy and accurate information that helps to prevent inhumane treatment or poor commercial practices; video cameras should be positioned and operate in such a way to allow continuous viewing of all steps from unloading to stunning

see full text ;

http://www.fsis.usda.gov/PDF/Compliance_Guidelines_for_Use_of_Video_082611.pdf



Hallmark/Westland Beef Recall – Information for School Officials & Parents

On Feb. 17, 2008, the USDA notified States that beef produced by the Hallmark/Westland Meat Packing Company from Feb. 1, 2006, to Feb. 4, 2008 was voluntarily recalled due to regulatory noncompliance. Some of the USDA commodity beef supplied to the National School Lunch Program was produced by Hallmark/Westland. In addition, schools may have purchased Hallmark/Westland beef commercially. On Jan. 30, 2008, USDA instructed all school districts to hold and immediately discontinue use of any Hallmark/Westland commodity beef products in their inventory. Products affected by the recall are no longer being served in schools. To minimize disruption to school food service operations, USDA is working closely with States to quickly provide replacement commodity product from validated sources or credit their commodity entitlement accounts. USDA has given assurance that the health risk of consuming the affected beef is negligible. USDA remains confident in the safety of the food supply, including beef and other products available through the National School Lunch Program. No reports of illness have been associated with the affected product.

For more information, please visit www.usda.gov/actions.

Last updated: 10/29/2008

http://www.fns.usda.gov/fns/safety/hw-information.htm


human mad cow disease i.e. CJD (sporadic CJD has now been linked to atypical BSE in North America), and any exposure there from, i.e. human CJD in children, could take up to 5 decades (50 YEARS), so to state that ''USDA has given assurance that the health risk of consuming the affected beef is negligible.'' is very reckless, and in fact, not accurate.

seems the feds have a camera on every street corner, of every street now, some city's put them up, turn them off, then turn them back on again, just to turn them off again. Houston can't seem to make it's mind up. but if we put cameras up on every street to protect those pesky drivers from running red lights, why not put them up in slaughter houses. why not? what could it hurt? a slaughter house that the end product is going to a consumer, seems to me the consumer should be able to see how that process works, or not.

seems to me, that is how the Nation found out about the USDA NSLP dead stock downer cow school lunch program, through the video taping of animals being abused, course during that blunder, the only one the public was worried about were the animals being abused, just because the most high risk cattle for mad cow disease BSE i.e. the dead stock downer cow were being fed to their children, never seemed to matter to them. my God, look at the children that were exposed, was this not child abuse ???


DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???

you can check and see here ;

http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf


CALIFORNIA FIRM RECALLS BEEF PRODUCTS DERIVED FROM NON-AMBULATORY CATTLE WITHOUT THE BENEFIT OF PROPER INSPECTION WASHINGTON, Feb. 17, 2008 –

Hallmark/Westland Meat Packing Co., a Chino, Calif., establishment, is voluntarily recalling approximately 143,383,823 pounds of raw and frozen beef products that FSIS has determined to be unfit for human food because the cattle did not receive complete and proper inspection. Through evidence obtained by FSIS, the establishment did not consistently contact the FSIS public health veterinarian in situations in which cattle became non-ambulatory after passing ante-mortem inspection, which is not compliant with FSIS regulations.

Such circumstances require that an FSIS public health veterinarian reassess the non-ambulatory cattle which are either condemned and prohibited from the food supply, or tagged as suspect. Suspect cattle receive a more thorough inspection after slaughter than is customary.

This noncompliant activity occurred occasionally over the past two years and therefore all beef product produced during the period of time for which evidence indicates such activity occurred has been determined by FSIS to be unfit for human consumption, and is, therefore, adulterated.

This recall is designated as Class II due to the remote probability that the beef being recalled would cause adverse health effects if consumed. FSIS made this determination because the animals passed ante-mortem inspection but should have been identified as suspect requiring additional inspection after slaughter to determine if there is evidence of disease, injury, or other signs of abnormalities that may have occurred after ante-mortem inspection.

In July 2007, FSIS issued a final rule “Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle.” This rule requires that a case by case disposition must be made by an FSIS Public Health Veterinarian for every animal that becomes non-ambulatory disabled (“downer”) after passing ante-mortem inspection.

The prohibition of downer cattle from entering the food supply is only one measure in an interlocking system of controls the federal government has in place to protect the food supply. The government has multiple safeguards regarding BSE in place and the prevalence of the disease in the United States is extremely low. Other BSE security measures include the feed ban that prohibits feeding ruminant protein to other ruminants and an ongoing BSE surveillance program that began before the confirmation of the first BSE positive cow in the U.S. in 2003.

As another measure to reduce the risk of potential exposure to consumers, FSIS requires the removal of specified risk materials (SRM) so they do not enter the food supply. Several FSIS line inspectors are stationed at designated points along the production line where they are able to directly observe SRM removal activities.

The products subject to this recall were sent to wholesale distributors nationwide in bulk packages and are not available for direct purchase by consumers. All products subject to recall bear the establishment number “EST. 336” inside the USDA mark of inspection. The products were produced on various dates from Feb. 1, 2006 to Feb. 2, 2008. Companies are urged to check their inventories and hold the products until the recalling firm makes arrangements for final disposition of the products.

The following products are subject to recall: [View Labels]

http://www.fsis.usda.gov/images_recalls/005-2008_Labels.pdf



SEE FULL TEXT ;

http://www.fsis.usda.gov/PDF/Recall_005-2008_Release.pdf



PLEASE SEE ALSO ;

Members of The HSUS are also concerned about the meat products provided to their children through the National School Lunch Program. More than 31 million school children receive lunches through the program each school day. To assist states in providing healthful, low-cost or free meals, USDA provides states with various commodities including ground beef. As evidenced by the HallmarkNVestland investigation and recall, the potential for downed animals to make their way into the National School Lunch Program is neither speculative nor hypothetical.

http://biotech.law.lsu.edu/cases/FDA/hsus-v-schafer-usda-complaint.pdf


with an incubation period of up to 50 years or more, we will all just have to wait and see...


SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE

http://downercattle.blogspot.com/2009/05/who-will-watch-children.html


http://downercattle.blogspot.com/



"The prohibition of downer cattle from entering the food supply is only one measure in an interlocking system of controls the federal government has in place to protect the food supply. The government has multiple safeguards regarding BSE in place and the prevalence of the disease in the United States is extremely low."



"Other BSE security measures include the feed ban that prohibits feeding ruminant protein to other ruminants and an ongoing BSE surveillance program that began before the confirmation of the first BSE positive cow in the U.S. in 2003."


let's look as some update science and facts there from ;



*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS

THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$

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/Safety/Recalls/EnforcementReports/2007/ucm120446.htm


Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)

BANNED MAD COW FEED IN COMMERCE IN ALABAMA

Date: September 6, 2006 at 7:58 am PST PRODUCT

a) EVSRC Custom dairy feed, Recall # V-130-6;

b) Performance Chick Starter, Recall # V-131-6;

c) Performance Quail Grower, Recall # V-132-6;

d) Performance Pheasant Finisher, Recall # V-133-6.

CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.

REASON

Dairy and poultry feeds were possibly contaminated with ruminant based protein.

VOLUME OF PRODUCT IN COMMERCE 477.72 tons

DISTRIBUTION AL

______________________________

http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html

PRODUCT Bulk custom dairy pre-mixes,

Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 350 tons

DISTRIBUTION AL and MS

______________________________

PRODUCT

a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;

b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;

c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;

d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;

e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;

f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;

g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6

CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.

REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags

DISTRIBUTION AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###

http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html

Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST PRODUCT

a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;

c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;

e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;

f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;

g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;

h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;

i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;

j) CO-OP LAYING CRUMBLES, Recall # V-109-6;

k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;

l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;

m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE

Product manufactured from 02/01/2005 until 06/06/2006

RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.

REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 125 tons

DISTRIBUTION AL and FL

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html

MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

______________________________

PRODUCT

a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;

b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;

c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;

d) Feather Meal, Recall # V-082-6 CODE

a) Bulk

b) None

c) Bulk

d) Bulk

RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.

REASON

Possible contamination of animal feeds with ruminent derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons

DISTRIBUTION Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html



please see full text ;


http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html


http://www.fda.gov/ICECI/EnforcementActions/EnforcementStory/EnforcementStoryArchive/ucm107472.htm


http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm048448.htm


http://www.gao.gov/new.items/d02183.pdf


http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm048431.htm


http://www.fda.gov/downloads/AnimalVeterinary/NewsEvents/FDAVeterinarianNewsletter/UCM055628.pdf


http://www.fda.gov/AnimalVeterinary/NewsEvents/FDAVeterinarianNewsletter/ucm106105.htm


http://agri.state.nv.us/GAO_FDA%20Mgmt%20Mad%20Cow%20IMprove_Feb05.pdf


http://www.gao.gov/products/GAO-05-101


http://www.gao.gov/new.items/d05101.pdf


http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm115008.htm


http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm048228.htm



Monday, March 1, 2010

ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010

http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html



Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009

http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html



Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html



C O N F I R M E D



----- Original Message -----

From: "Terry S. Singeltary Sr."

To:

Sent: Thursday, November 05, 2009 9:25 PM

Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/11/re-foia-request-on-feed-recall-product.html



PLEASE UNDERSTAND, with a Transmissible Spongiform Encephalopathy, once clinical, the disease is 100% fatal. There should be NO debate of the 'unacceptable risk factor', with any TSE. ...TSS



Sunday, June 26, 2011

Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html




PLEASE be aware, for 4 years, during the BUSH/PERRY era, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens. who will watch our children for CJD for the next 5+ decades ???



DID rick perry and george bush expose your child to mad cow disease via the NSLP ???



http://sciencebushwhacked.blogspot.com/2011/08/rick-perry-texas-bse-aka-mad-cow.html



O.K. SO THE MAD COW FEED BAN FIREWALL WAS JUST BURNT DOWN,
'The Secret Is In The Sauce, Or So They Say' FRIED GREEN TOMATOES...tss


"As another measure to reduce the risk of potential exposure to consumers, FSIS requires the removal of specified risk materials (SRM) so they do not enter the food supply. Several FSIS line inspectors are stationed at designated points along the production line where they are able to directly observe SRM removal activities."

some history on Specified Risk Materials SRM's IN COMMERCE ;



Tuesday, July 1, 2008

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

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


Sunday, October 18, 2009

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009

http://madcowfeed.blogspot.com/2009/10/wisconsin-firm-recalls-beef-tongues.html


Thursday, October 15, 2009

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009

http://madcowfeed.blogspot.com/2009/10/nebraska-firm-recalls-beef-tongues-that.html


Thursday, June 26, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

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


Friday, August 8, 2008

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed

http://madcowfeed.blogspot.com/2008/08/texas-firm-recalls-cattle-heads-that.html


Saturday, April 5, 2008

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

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


Wednesday, April 30, 2008

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/consumption-of-beef-tongue-human-bse.html


Wednesday, April 30, 2008

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

http://cjdmadcowbaseoct2007.blogspot.com/2008/04/consumption-of-beef-tongue-human-bse.html


Friday, October 15, 2010

BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle

http://bseusa.blogspot.com/2010/10/bse-infectivity-in-absence-of.html


SPECIFIED RISK MATERIALS SRMs

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


http://madcowfeed.blogspot.com/


http://madcowspontaneousnot.blogspot.com/


Saturday, July 23, 2011

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html



Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html


Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129




AND NOW THE SPECIFIED RISK MATERIAL (SRM) FIRE WALL BURNT DOWN.



the so called triple mad cow fire wall that the USDA, FSIS, APHIS, FDA, all boast about, in reality was, BSe.


BUT, the mad cow agent continues to spread, and apparently, it's been spreading in North America for decades...tss




Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque



"BSE-L in North America may have existed for decades"


http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html





Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (95%) downer or dead dairy cattle...

http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf


see history of USA mad cow disease blunders here ;

http://sciencebushwhacked.blogspot.com/2011/08/rick-perry-texas-bse-aka-mad-cow.html


Wednesday, March 31, 2010

Atypical BSE in Cattle

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE.

When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2


Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat

snip...

http://www.neuroprion.org/en/np-neuroprion.html


http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html


http://prionpathy.blogspot.com/



Rural and Regional Affairs and Transport References Committee

The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010

2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49

2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50

http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf


Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.

-- Communicated by: Terry S Singeltary Sr

[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.

It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]

******

http://www.promedmail.org/pls/apex/f?p=2400:1202:888892554804923::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,88784



[Terry S. Singeltary Sr. has added the following comment:

"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed

http://whqlibdoc.who.int/publications/2003/9241545887.pdf



http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101



14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

T. Singeltary

Bacliff, TX, USA

Background:

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods:

12 years independent research of available data

Results:

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf



Monday, May 23, 2011

Atypical Prion Diseases in Humans and Animals 2011

Top Curr Chem (2011)

DOI: 10.1007/128_2011_161

# Springer-Verlag Berlin Heidelberg 2011

Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron, and Hans Kretzschmar

http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html


Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease

(see video here)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html


TSS

There Is No Safe Dose of Prions

There Is No Safe Dose of Prions

Helen R. Fryer, Angela R. McLean*

The Institute for Emerging Infections, Oxford Martin School, Department of Zoology, Oxford University, Oxford, United Kingdom

Abstract

Understanding the circumstances under which exposure to transmissible spongiform encephalopathies (TSEs) leads to infection is important for managing risks to public health. Based upon ideas in toxicology and radiology, it is plausible that exposure to harmful agents, including TSEs, is completely safe if the dose is low enough. However, the existence of a threshold, below which infection probability is zero has never been demonstrated experimentally. Here we explore this question by combining data and mathematical models that describe scrapie infections in mice following experimental challenge over a broad range of doses. We analyse data from 4338 mice inoculated at doses ranging over ten orders of magnitude. These data are compared to results from a within-host model in which prions accumulate according to a stochastic birth-death process. Crucially, this model assumes no threshold on the dose required for infection. Our data reveal that infection is possible at the very low dose of a 1000 fold dilution of the dose that infects half the challenged animals (ID50). Furthermore, the dose response curve closely matches that predicted by the model. These findings imply that there is no safe dose of prions and that assessments of the risk from low dose exposure are right to assume a linear relationship between dose and probability of infection. We also refine two common perceptions about TSE incubation periods: that their mean values decrease linearly with logarithmic decreases in dose and that they are highly reproducible between hosts. The model and data both show that the linear decrease in incubation period holds only for doses above the ID50. Furthermore, variability in incubation periods is greater than predicted by the model, not smaller. This result poses new questions about the sources of variability in prion incubation periods. It also provides insight into the limitations of the incubation period assay.

Citation: Fryer HR, McLean AR (2011) There Is No Safe Dose of Prions. PLoS ONE 6(8): e23664. doi:10.1371/journal.pone.0023664

Editor: Noriyuki Nishida, Nagasaki University Graduate School of Biomedical Sciences, Japan

Received May 6, 2011; Accepted July 21, 2011; Published August 15, 2011

Copyright: 2011 Fryer, McLean. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This research was supported by the Oxford Martin School (www.oxfordmartin.ox.ac.uk) and the Foods Standards Agency (www.food.gov.uk), grant number M03027. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interests: The authors have declared that no competing interests exist.

* E-mail: angela.mclean@zoo.ox.ac.uk

SNIP...

Discussion In this study we first asked whether there exists a threshold dose of prions below which the probability of infection is zero. By comparing the scrapie dose-response curve observed in mice to model predictions we found no evidence that such a threshold exists. As the stochastic-birth death model predicts, the probability of infection simply becomes smaller as the dose decreases. Furthermore, we find evidence to support the assumption of a linear relationship between dose and probability of infection in assessing the risk from low dose exposure. Use of a linear relation for doses above the ID50 will lead to overestimation of the risk. Although we find no evidence of a threshold, it must be emphasized that we cannot rule out this possibility. Though it was to be expected because of the limited sample size, no mice were infected at the lowest relative dose tested (–4), therefore a threshold may exist at this dose or lower. However, acquiring data to investigate this question further would require an unfeasibly large number of test animals. Furthermore, the observation of infection at a dose 1000 times more dilute than the ID50 shows that infection is still possible at very low doses. In practical terms this is low enough to regard there to be no safe dose.

Previous modelling work has focussed on understanding the molecular form of a prion and its mechanism of replication. We are not proposing a specific form or replication mechanism, rather we ask whether data on infection probabilities are consistent with the simplest model of replication that assumes no threshold dose. If evidence did emerge of a threshold dose, one could tie it to the hypothesis that the smallest infectious agent involved in TSEs (a prion) is a polymer consisting of multiple PrPSc monomers above a critical polymer length [4-6] . It is thought that such a polymer replicates when it breaks into two or more polymers, each larger than the critical length, before undergoing rapid monomer addition. This is currently the most widely accepted mechanism of prion replication. However, it is noteworthy that a threshold polymer length is not the same as a threshold dose of prions, since a prion is normally regarded as one infectious agent (i.e. a polymer), not one PrPSc monomer. Dilution of infectious substrate would not necessarily split up prion polymers into units lower than the critical polymer length, thus, the polymer breakage-addition model of prion replication is consistent with our finding of no threshold for infectiousness.

In this study we also asked how TSE incubation periods change according to the inoculating dose. First, we asked whether it is true that mean incubation period decreases linearly with logarithmic decrease in dose. The model predicts that this relationship holds only at doses higher than the ID50. For doses below the ID50, mean incubation period is predicted to be invariant to dose. The murine data are consistent with these predictions. This finding delineates the situation in which there is a linear relationship between dose and provides insight into the limitations of the incubation period assay. Specifically, it suggests that the incubation period assay should be unable to distinguish between different doses below the ID50.

Second, we investigated variability in incubation periods and asked whether TSE incubation periods are highly reproducible. We revealed that they are markedly more variable than predicted by the model. Our findings lead us to question why this is so, especially given that the dose response curve and the mean incubation periods are in close agreement with the model. Could the mechanism of prion growth be incorrect or does the inconsistency lie with data collection or the relationship between prion numbers and clinical symptoms? The most popular model for prion growth, based upon polymer breakage and expansion, is underpinned by exponential growth dynamics and would predict the same variability as seen here. That model therefore also cannot explain the effect that we see. In regards to data collection, some variability is likely to arise from the difficulty in spotting symptoms and from small experimental variability in the dose of the inoculum. It must also be noted that some inaccuracies in the data could arise because the duration of the experiments was finite. At the end of each experiment all surviving mice were culled and examined for the presence of pathological lesion without symptoms might have progressed to disease if the experiments had run for longer. However this does not explain the high variability in incubations periods as if the data were not censored in this way, such unusually long incubation periods would only increase variability, not reduce it.

It is not difficult to propose ways in which prion infection is more complex than a stochastic birth-death process in a homogeneous environment. All the heterogeneities of the in vivo situation: spatial, tissue, temporal and genetic [35] could add to the variability in incubation periods. It is indeed remarkable that such a simple model so clearly reproduces the infection probability and mean incubation period across thousands of mice challenged under such a range of experimental conditions. The intellectual challenge posed by this analysis is to understand what processes are driving the observed variability in incubation periods whilst conserving the infection probabilities and mean incubation periods that are so well explained by the simple model presented here.

http://www.plosone.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0023664&representation=PDF

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0023664



Wednesday, August 24, 2011

All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html


Wednesday, June 29, 2011

TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products

http://tseac.blogspot.com/2011/06/tseac-meeting-august-1-2011-donor.html


FC5.1.1

Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD, and GSS Blood Specimens: the Baxter Study

Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5; Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama, USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General Hospital, UK; 5Baxter BioSience, Austria

Background: Rodent and sheep models of Transmissible Spongiform Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical and clinical phases of disease. Results in a (presumably more appropriate) non-human primate model have not been reported.

Objective: To determine if blood components (red cells, white cells, platelets, and plasma) from various forms of human TSE are infectious.

Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma samples from chimpanzees infected with either sCJD or Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a period of 5 years, and all dying or sacrificed animals had post-mortem neuropathological examinations and Western blots to determine the presence or absence of the misfolded prion protein (PrPTSE).

Results: No transmissions occurred in any of the animals inoculated with blood components from patients with sporadic or variant CJD. All donor chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their pre-clinical phase plasmapheresis, several months earlier than the expected onset of illness. One monkey inoculated with purified leukocytes from a pre-clinical GSS chimpanzee developed disease after 36 months.

Conclusion: No infectivity was found in small volumes of blood components from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a single transmission from a chimpanzee-passaged strain of GSS shows that infectivity may be present in leukocytes, and the shock of general anaesthesia and plasmspheresis appears to have triggered the onset of illness in pre-clinical donor chimpanzees.

Saturday, September 5, 2009

TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS

snip...

http://tseac.blogspot.com/2011/06/tseac-meeting-august-1-2011-donor.html


Friday, August 12, 2011

Creutzfeldt-Jakob disease (CJD) biannual update (2011/2), Incidents Panel, National Anonymous Tonsil Archive

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/creutzfeldt-jakob-disease-cjd-biannual.html


Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html


Thursday, August 4, 2011

Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011

see video here ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html



Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque



"BSE-L in North America may have existed for decades"


http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html



Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...



http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf


Sunday, June 26, 2011

Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html



Thursday, June 23, 2011

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html


Thursday, July 21, 2011

A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:

August 2011 - Volume 70 - Issue 8 - pp 698-702

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html


Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html


Wednesday, June 15, 2011

Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html


Saturday, July 23, 2011

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html


Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html


Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129



P.9.21

Molecular characterization of BSE in Canada

Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

*** It also suggests a similar cause or source for atypical BSE in these countries.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

To minimise the risk of farmers' claims for compensation from feed compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.

snip...

THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://web.archive.org/web/20060517074958/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf



Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html


Sunday, August 21, 2011

Classical Bovine Spongiform Encephalopathy by Transmission of H-Type Prion in Homologous Prion Protein Context

Volume 17, Number 9-September 2011

Research

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/classical-bovine-spongiform.html



Thursday, July 28, 2011

An Update on the Animal Disease Traceability Framework July 27, 2011

http://naiscoolyes.blogspot.com/2011/07/update-on-animal-disease-traceability.html


Thursday, July 14, 2011

Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html


Monday, June 20, 2011 2011

Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA

http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html


Thursday, June 2, 2011

USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California

http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html


Monday, June 27, 2011

Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease

http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html




Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html




UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html



Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011

Prions

David W. Colby1,* and Stanley B. Prusiner1,2

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html



Wednesday, July 06, 2011

Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation

http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html



Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html



1989

IN CONFIDENCE

Perceptions of unconventional slow virus diseases of animals in the USA

Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or about that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. Whether they were scrapie infected sheep or not is unclear.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf



http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf


CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf



Sunday, July 03, 2011

Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD Deer

http://chronic-wasting-disease.blogspot.com/2011/07/prion-disease-detection-pmca-kinetics.html



PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html



NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html



Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html



TSS

All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD

All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD

Sandra McCutcheon1., Anthony Richard Alejo Blanco1., E. Fiona Houston2., Christopher de Wolf1, Boon Chin Tan1, Antony Smith3, Martin H. Groschup4, Nora Hunter1, Valerie S. Hornsey5, Ian R. MacGregor5, Christopher V. Prowse5, Marc Turner6, Jean C. Manson1* 1 The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, Edinburgh, United Kingdom, 2 School of Veterinary Medicine, College of Medical, Veterinary and Life Sciences, The University of Glasgow, Glasgow, United Kingdom, 3 The Institute for Animal Health, Compton, Berkshire, United Kingdom, 4 Institute for Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Germany, 5 National Science Laboratory, Scottish National Blood Transfusion Service (SNBTS), Edinburgh, United Kingdom, 6 University of Edinburgh and SNBTS, Edinburgh, United Kingdom

Abstract

Variant CJD (vCJD) is an incurable, infectious human disease, likely arising from the consumption of BSE-contaminated meat products. Whilst the epidemic appears to be waning, there is much concern that vCJD infection may be perpetuated in humans by the transfusion of contaminated blood products. Since 2004, several cases of transfusion-associated vCJD transmission have been reported and linked to blood collected from pre-clinically affected donors. Using an animal model in which the disease manifested resembles that of humans affected with vCJD, we examined which blood components used in human medicine are likely to pose the greatest risk of transmitting vCJD via transfusion. We collected two full units of blood from BSE-infected donor animals during the pre-clinical phase of infection. Using methods employed by transfusion services we prepared red cell concentrates, plasma and platelets units (including leucoreduced equivalents). Following transfusion, we showed that all components contain sufficient levels of infectivity to cause disease following only a single transfusion and also that leucoreduction did not prevent disease transmission. These data suggest that all blood components are vectors for prion disease transmission, and highlight the importance of multiple control measures to minimise the risk of human to human transmission of vCJD by blood transfusion.

Citation: McCutcheon S, Alejo Blanco AR, Houston EF, de Wolf C, Tan BC, et al. (2011) All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD. PLoS ONE 6(8): e23169. doi:10.1371/journal.pone.0023169 Editor: Matthew Baylis, University of Liverpool, United Kingdom Received March 17, 2011; Accepted July 8, 2011; Published August 17, 2011 Copyright:  2011 McCutcheon et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: This is an independent report commissioned and funded by the Policy Research Programme in the Department of Health, UK (007/0162). The views expressed in the publication are those of the authors and not necessarily those of the Department of Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. * E-mail: jean.manson@roslin.ed.ac.uk . These authors contributed equally to this work

snip...

Discussion

We have shown that all of the blood components investigated, whole blood, plasma, red cells, platelets and buffy coat, are capable of transmitting BSE infection following transfusion into susceptible sheep. Although infectivity has consistently been detected in plasma in rodent scrapie models, this is the first time that transmission of prion disease has been demonstrated following transfusion of plasma units collected from pre-clinical donors, and prepared to the same specifications as non-fractionated human plasma. While the results with platelets and leucocytes are similar to that of Mathiason et al. [30], the plasma results are strikingly different. In the previous study, prion infected cell-free plasma appeared not to cause disease following transfusion in deer. The reason for this is not clear and may relate to either a difference in the distribution of PrPSc and/or infectivity in different host species or indeed the strain of infectious agent used.

We also observed a number of cases in which leucoreduced components have caused BSE in recipients following transfusion. Other recipients of leucoreduced components are also now showing early signs of TSE infection and we would therefore expect more positive transmissions of BSE from these components. These data demonstrate that leucoreduction of blood components alone is insufficient to prevent transmission of prion infection via blood transfusion [23]. All four of the documented transfusionrelated transmissions of vCJD infectivity to date have occurred in individuals who received red cells (the most commonly transfused blood component) which were non-leucoreduced, between 1996 and 1999. Eighteen surviving recipients [36] transfused with red blood cells (n= 6), cryodepleted plasma (n =1) and leucoreduced red blood cells (n =11) from donors who were subsequently confirmed to have vCJD are still being followed up (personal communication from Miss J. McKenzie and Prof. R.G. Will, TMER study). There are a small number of cases of clinical vCJD with a history of blood transfusion, where no donor has developed clinical vCJD but where transfusion remains the possible source of infection. The most recent of these cases (2002) received leucoreduced red cells. Our findings would suggest that residual infectivity following leucoreduction may still pose a risk of transmission in a transfusion setting [23,37,38].

These transfusion studies were conducted in sheep, in which many effects of polymorphisms associated with the prnp gene (which modulates susceptibility to prion infection) are well understood. Similarly, the age at which donors and recipients were exposed to BSE prions, the infectious dose (in donor sheep) and the route of infection were relatively well controlled. Despite the control of known variables within this experiment, we observed significant variability in the incubation period of both orally infected donors and transfused recipients. During the course of this study we identified a novel effect of an existing polymorphism in the sheep PRNP gene, which modulates the incubation period of orally infected BSE donors (unpublished observations). While some of the variability in incubation periods of transfused recipients is likely associated with other genetic factors [39,40,41], it is also likely to be influenced by variability in prion titre in blood from donor sheep. It must also be recognised that in this model, incubation period is not considered an indicator of titre of infectivity in blood, since a full titration of infected blood has not yet been undertaken in sheep. However, given that BSE occurred in recipients following a single blood transfusion from donors who were healthy at the time of blood donation, we would suggest that even when or if the infectious load is low, disease can result if the route of transmission, i.e. blood transfusion, is highly efficient. Whilst we have clearly shown that blood collected from donor animals at a single time point is infectious, what remains unclear is when prion-associated infectivity first appears in blood, how it relates to incubation period and how the titre of infection changes as disease progresses. We are investigating these questions by inoculating transgenic mice with blood collected at various time points throughout the incubation period, from the same donor sheep as used in this study. This will allow us to address the duration, pattern and titre of prion infectivity in blood.

Our data raises considerable questions concerning the distribution of infectivity in blood, including its potential association with cell types other than leucocytes i.e. red cells and platelets, and/or other proteins or soluble components of plasma. Our data relating to the current transmission efficiencies of each component suggest whole blood and buffy coat represent the greatest risk in terms of transfusion and blood safety. However, these data may change over the full time course of this study and therefore it is too early to draw definitive conclusions. Furthermore, the blood components used in this study (including leucoreduced equivalents) were not purified cell populations, but also contained plasma and leucocytes to reflect the nature of the components routinely transfused in human patients. This may complicate understanding the process of identifying the relationship between the infectious agent and cell targets. It is also possible that mechanisms such as release of membrane fractions during processing [42] or shedding/transit by plasma membrane-derived microvesicles [43,44] may also contribute to the dissemination of infectivity in blood. It will be critical to understand how prion infectivity associates with particular blood components, and may identify new targets for diagnostics, therapeutics and allow for more refined risk reduction strategies.

Whilst these findings highlight the difficulties in predicting incubation times and the clinical outcomes associated with transfusion-related transmission of vCJD in humans (because of the extensive variability of individuals in terms of age, genetic background, titre and route by which one could be exposed) these data have clear implications for transfusion practices. We demonstrate the potential risk of acquiring vCJD from any blood component used in routine transfusion medicine, following a single transfusion from asymptomatic individuals.

While there has been recent, significant, developments in the quest for a blood-based assay to detect prion infection in symptomatic individuals [45], implementing such assays in the blood transfusion service to detect asymptomatic donors requires extensive validation. Thus there currently remains the potential for human to human transmission of vCJD via blood transfusion from individuals carrying the infectious agent but not showing clinical signs of disease. Our data suggests that leucoreduction alone is inadequate to minimise the risk of transmission of vCJD and to ensure the safety of blood used in transfusions and ultimately to safeguard public health.

http://www.plosone.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0023169&representation=PDF


http://www.plosone.org/article/fetchArticle.action;jsessionid=198F52B91A67C1A9520EB62354DB5D93.ambra01?utm_medium=feed&utm_campaign=Feed%3A+plosone%2FPLoSONE+(PLoS+ONE+Alerts%3A+New+Articles)&utm_source=feedburner&articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0023169


Wednesday, June 29, 2011

TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products

http://tseac.blogspot.com/2011/06/tseac-meeting-august-1-2011-donor.html


FC5.1.1

Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD, and GSS Blood Specimens: the Baxter Study

Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5; Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama, USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General Hospital, UK; 5Baxter BioSience, Austria

Background: Rodent and sheep models of Transmissible Spongiform Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical and clinical phases of disease. Results in a (presumably more appropriate) non-human primate model have not been reported.

Objective: To determine if blood components (red cells, white cells, platelets, and plasma) from various forms of human TSE are infectious.

Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma samples from chimpanzees infected with either sCJD or Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a period of 5 years, and all dying or sacrificed animals had post-mortem neuropathological examinations and Western blots to determine the presence or absence of the misfolded prion protein (PrPTSE).

Results: No transmissions occurred in any of the animals inoculated with blood components from patients with sporadic or variant CJD. All donor chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their pre-clinical phase plasmapheresis, several months earlier than the expected onset of illness. One monkey inoculated with purified leukocytes from a pre-clinical GSS chimpanzee developed disease after 36 months.

Conclusion: No infectivity was found in small volumes of blood components from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a single transmission from a chimpanzee-passaged strain of GSS shows that infectivity may be present in leukocytes, and the shock of general anaesthesia and plasmspheresis appears to have triggered the onset of illness in pre-clinical donor chimpanzees.

Saturday, September 5, 2009

TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS

snip...

http://tseac.blogspot.com/2011/06/tseac-meeting-august-1-2011-donor.html



Friday, August 12, 2011

Creutzfeldt-Jakob disease (CJD) biannual update (2011/2), Incidents Panel, National Anonymous Tonsil Archive

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/creutzfeldt-jakob-disease-cjd-biannual.html


Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html


Thursday, August 4, 2011

Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011

see video here ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html



Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque


"BSE-L in North America may have existed for decades"


http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html



Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...



http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



Sunday, June 26, 2011

Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html



Thursday, June 23, 2011

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html


Thursday, July 21, 2011

A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:

August 2011 - Volume 70 - Issue 8 - pp 698-702

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/second-case-of-gerstmann-straussler.html


Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html


Wednesday, June 15, 2011

Galveston, Texas - Isle port moves through thousands of heifers headed to Russia, none from Texas, Alabama, or Washington, due to BSE risk factor

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/galveston-texas-isle-port-moves-through.html


Saturday, July 23, 2011

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html


Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html


Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129



P.9.21

Molecular characterization of BSE in Canada

Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

*** It also suggests a similar cause or source for atypical BSE in these countries.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

To minimise the risk of farmers' claims for compensation from feed compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.

snip...

THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://web.archive.org/web/20060517074958/http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf



Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html



Sunday, August 21, 2011

Classical Bovine Spongiform Encephalopathy by Transmission of H-Type Prion in Homologous Prion Protein Context

Volume 17, Number 9-September 2011

Research

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/classical-bovine-spongiform.html


Thursday, July 28, 2011

An Update on the Animal Disease Traceability Framework July 27, 2011

http://naiscoolyes.blogspot.com/2011/07/update-on-animal-disease-traceability.html


Thursday, July 14, 2011

Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html


Monday, June 20, 2011 2011

Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA

http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html


Thursday, June 2, 2011

USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California

http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html


Monday, June 27, 2011

Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease

http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html


UPDATE TSE PRION DISEASE NORTH AMERICA...FOR YOU INFORMATION, things you might not be aware of...TSS

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html



UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011

Prions

David W. Colby1,* and Stanley B. Prusiner1,2

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html


Wednesday, July 06, 2011

Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation

http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html


Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html


1989

IN CONFIDENCE

Perceptions of unconventional slow virus diseases of animals in the USA

Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or about that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. Whether they were scrapie infected sheep or not is unclear.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf



http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf


CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf



Sunday, July 03, 2011

Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD Deer

http://chronic-wasting-disease.blogspot.com/2011/07/prion-disease-detection-pmca-kinetics.html



PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html



NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html



Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html



TSS

Creating plastic from beef and what about those pesky prions TSE mad cow agent ?

Creating plastic from beef and what about those pesky prions TSE mad cow agent ?

Creating plastic from beef

By Bev Betkowski

August 12, 2011

(Edmonton) They look a little like fake cookies, the kind you’d find in a child’s toy oven, but the chocolate brown plastic discs created by University of Alberta researcher David Bressler and his lab represent the future of ingenious recycling.

Using the throwaway parts of beef carcasses that were sidelined from the value-added production process after bovine spongiform encephalopathy devastated the industry in 2003, Bressler, an associate professor in the U of A’s Department of Agricultural, Food and Nutritional Science has collaborated with industry, government and other researchers to forge cattle proteins into heavy-duty plastics that could soon be used in everything from car parts to CD cases.

The University of Alberta is the only post-secondary facility to be approved by the Canada Food Inspection Agency to conduct research involving turning high-risk proteins into safe, sustainable materials.

By finding a way to convert these animal byproducts into plastics for industrial use, Bressler and his team, which also includes Phillip Choi, a professor in the U of A’s Faculty of Engineering, hope to divert tonnes of protein waste from landfills across North America, shift to using renewable resources instead of petrochemicals to make plastics, and boost flagging profit levels in the cattle industry.

Beef producers took an economic hit when byproducts such as blood and bone were regulated out of the rendering process after BSE was found in Canada, for fear the material contained deadly prions—infectious proteins that cause BSE, more commonly known as mad cow disease.

“If we can get more fundamental value back into the rendering process, it will help the livestock industry more than any government policy,” Bressler says.

A patent has been filed on the thermal process used to turn protein from bovine byproducts into plastics. Using high temperatures, the proteins are broken into small pieces then cross-linked to other protein molecules to create a network that forms a rigid structure.

The new plastics from Bressler’s lab are currently being tested by The Woodbridge group, a car parts manufacturer. Current funding is focused on research that further experiments with the product, to see if the plastics can be mixed with renewable fibres such as hemp. If successful, the resulting bio-composite material could be used in high-strength materials such as building structural supports.

The bio-friendly plastics, though still in the development stage, are poised to become an innovative addition to the manufacturing industry, Bressler believes. “The plastic industry is under pressure to increase the renewable content in its products. As a result, this project offers the opportunity to do just that, and at the same time help send value back to rural Alberta and the beef sector.”

Bressler’s work is supported by the Alberta Prion Research Institute, PrioNet Canada and the Alberta Livestock and Meat Agency.

http://www.research.ualberta.ca/en/VP%20Research%20News/2011/08/Creatingplasticfrombeef.aspx



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

Cathrin E. Bruederle,1* Robert M. Hnasko,1 Thomas Kraemer,2 Rafael A. Garcia,3 Michael J. Haas,3 William N. Marmer,3 and John Mark Carter1 1USDA-ARS WRRC, Foodborne Contaminants Research Unit, Albany, California, United States of America 2Forensic Toxicology, Institute of Legal Medicine, Saarland University, Homburg/Saar, Germany 3USDA-ARS ERRC, Fats, Oils and Animal Coproducts Research Unit, Wyndmoor, Pennsylvania, United States of America Neil Mabbott, EditorUniversity of Edinburgh, United Kingdom *

E-mail: cathrin.bruederle@gmail.comConceived and designed the experiments: CEB RMH WNM JMC. Performed the experiments: CEB RMH TK. Analyzed the data: CEB TK JMC. Contributed reagents/materials/analysis tools: CEB RMH TK RAG MJH JMC. Wrote the paper: CEB. Received April 21, 2008; Accepted July 24, 2008. Other Sections?

Abstract

The epidemic of bovine spongiform encephalopathy (BSE) has led to a world-wide drop in the market for beef by-products, such as Meat-and-Bone Meal (MBM), a fat-containing but mainly proteinaceaous product traditionally used as an animal feed supplement. While normal rendering is insufficient, the production of biodiesel from MBM has been suggested to destroy infectivity from transmissible spongiform encephalopathies (TSEs). In addition to producing fuel, this method simultaneously generates a nutritious solid residue. In our study we produced biodiesel from MBM under defined conditions using a modified form of alkaline methanolysis. We evaluated the presence of prion in the three resulting phases of the biodiesel reaction (Biodiesel, Glycerol and Solid Residue) in vitro and in vivo. Analysis of the reaction products from 263K scrapie infected MBM led to no detectable immunoreactivity by Western Blot. Importantly, and in contrast to the biochemical results the solid MBM residue from the reaction retained infectivity when tested in an animal bioassay. Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/


New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§ * Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract

One-gram samples from a pool of crude brain tissue from hamsters infected with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual infectivity in the treated samples was assayed by the intracerebral inoculation of dilution series into healthy weanling hamsters, which were observed for 10 months; disease transmissions were verified by Western blot testing for proteinase-resistant protein in brains from clinically positive hamsters. Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C. These results suggest that an inorganic molecular template with a decomposition point near 600°C is capable of nucleating the biological replication of the scrapie agent. transmissible spongiform encephalopathy | scrapie | prion | medical waste | incineration Introduction The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin. It also has been assumed that the replication of these agents is a strictly biological process (1), although the notion of a "virus" nucleant of an inorganic molecular cast of the infectious beta -pleated peptide also has been advanced (2). In this paper, we address these issues by means of dry heat inactivation studies.

see full text:

http://www.pnas.org/cgi/content/full/97/7/3418


P04.61

Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3 1University of Wisconsin, Soil Science/Civil and Environmental Engineering, USA; 2University of Wisconsin, Civil and Environmental Engineering, USA; 3University of Wisconsin, Comparative Biosciences, USA

Concern has been expressed that prions could enter wastewater treatment systems through sewer and/or septic systems (e.g., necropsy laboratories, rural meat processors, private game dressing) or through leachate from landfills that have received TSE-contaminated material. Prions are highly resistant to degradation and many disinfection procedures raising concern that they could survive conventional wastewater treatment. Here, we report the results of experiments examining the partitioning and survival of PrPSc during simulated wastewater treatment processes including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc can be efficiently extracted from activated and anaerobic digester sludges with 1% sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl sarcosinate. Activated sludge digestion does not result in significant degradation of PrPSc. The protein partitions strongly to the activated sludge solids and is expected to enter biosolids treatment processes. A large fraction of PrPSc survived simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions were to enter municipal waste water treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for excluding inputs of prions to municipal wastewater treatment facilities that would result in unacceptable risk of prion disease transmission via contaminated biosolids.

snip...end....NEUROPRION 2007

http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf


PPo4-4:

Survival and Limited Spread of TSE Infectivity after Burial

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

The authors gratefully acknowledge funding from DEFRA.

PPo8-13:

Degradation of Pathogenic Prion Protein and Prion Infectivity by Lichens

Christopher J. Johnson,1 James P. Bennett,1 Steven M. Biro,1,2 Cynthia M. Rodriguez,1,2 Richard A. Bessen3 and Tonie E. Rocke1

1USGS National Wildlife Health Center; 2Department of Bacteriology; University of Wisconsin, Madison; 3Department of Veterinary Molecular Biology; Montana State University; Bozeman, MT USA

Key words: prion, lichen, bioassay, protease, degradation

Few biological systems have been identified that degrade the transmissible spongiform encephalopathy (TSE)-associated form of the prion protein (PrPTSE) and TSE infectivity. Stability of the TSE agent allows scrapie and chronic wasting disease agents to persist in the environment and cause disease for years. Naturally-occurring or engineered processes that reduce infectivity in the environment could aid in limiting environmental TSE transmission. We have previously identified that species of at least three lichens, unusual, symbiotic organisms formed from a fungus and photosynthetic partner, contain a serine protease capable of degrading PrPTSE under gentle conditions. We tested the hypothesis that lichen extracts from these three species reduce TSE infectivity by treating infected brain homogenate with extracts and examining infectivity in mice. We found lichen extracts diminished TSE infectious titer by factors of 100 to 1,000 and that reductions in infectivity were not well-correlated with the extent of PrPTSE degradation observed by immunoblotting. For example, treatment of brain homogenate with Cladonia rangiferina extract caused <100-fold reduction in PrP immunoreactivity but ~1,000-fold decrease in infectivity, suggesting that some PrPTSE remaining after extract treatment was rendered uninfectious or that the lichen protease favors more infectious forms of PrPTSE. Our data also indicate that lichen species closely related to those with prion-degrading protease activity do not necessarily degrade PrPTSE. Characterization of the lichen species-specificity of PrPTSE degradation within the genera Cladonia and Usnea and comparison with known lichen phylogeny has yielded clusters of species on which to focus searches for anti-prion agents.

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf


PAUL BROWN SCRAPIE SOIL TEST

http://collections.europarchive.org/tna/20080102120203/http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf



i suppose my question would be, would any Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease agent survive the production of any said product ??? and then the question of raising one of Gods living, breathing, animals, as a material to build with, as opposed as a gift from God as a source of food, and the ethical or moral aspect of it all, there from...oh hell, never mind, that went out the window a long time ago when factory farming came about. it's all about money now, so heck with it, build a dashboard for your car with prions in it, put a damn boom box in it, and hope for the best, who cares anymore $$$ i am sure that is what God intended...NOT!


stupid is, as stupid does, and some times you just can't fix stupid. ...


TSS


'soyent green'.

see ;

Soylent Green is a 1973 dystopian science fiction movie depicting a future in which overpopulation lead to depleted resources, which in turn leads to widespread unemployment and poverty. Real fruit, vegetables, and meat are rare, commodities are expensive, and much of the population survives on processed food rations, including "soylent green" wafers.

The film overlays the science fiction and police procedural genres as it depicts the efforts of New York City police detective Robert Thorn (Charlton Heston) and elderly police researcher Sol Roth (Edward G. Robinson) to investigate the brutal murder of a wealthy businessman named William R. Simonson (Joseph Cotten). Thorn and Roth uncover clues which suggest that it is more than simply a bungled burglary.

snip...

After Roth dies, Thorn sneaks into the basement of the government-assisted suicide facility, where he sees corpses being loaded onto waste disposal trucks. He secretly hitches a ride on one of the trucks, which is driven to a heavily guarded waste disposal plant. Once inside the plant, Thorn sees how the corpses are processed into Soylent Green wafers. After Thorn escapes from the plant and heads for the supreme exchange with the information, he is ambushed by Fielding and several other gunmen. In the shootout, Thorn kills some of the gunmen, but is himself wounded. He retreats into a cathedral filled with homeless people. After a desperate fight, Thorn stabs and kills Fielding.

When police backup arrives, the seriously wounded and nearly hysterical Thorn confides to Hatcher the horrible secret behind Soylent Green and urges him to spread the word: "Soylent Green is people! We've got to stop them somehow!"

http://en.wikipedia.org/wiki/Soylent_Green



Monday, May 30, 2011

CEPs for gelatin and impact of the revised EU Note for Guidance on the TSE risk EMEA/410/01 Rev.3) will come into force in July 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/ceps-for-gelatin-and-impact-of-revised.html


Saturday, February 26, 2011

Supreme Court Protects Vaccine Manufacturers, Not Injured Children there from Bruesewitz vs Wyeth

http://vcjdtransfusion.blogspot.com/2011/02/supreme-court-protects-vaccine.html



Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease


http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html



Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque



"BSE-L in North America may have existed for decades"


http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html



RE - "BSE-L in North America may have existed for decades" YA THINK ???


Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...



http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf




TSS