I have wasted a decade researching this as a lay person, and believe me, there are some in the industry that will make sure you are aware of that, but that's another story. My mother was murdered by what I call corporate and political homicide. whether or not is oral consumption or friendly fire, second, third, or fourth passage, via someone that consumed something years ago, I am here to tell you we have all been exposed to the mad cow agent, no matter what species you wish to speak of, and I am speaking of the Transmissible Spongiform Encephalopathies, and i could not have spelled that ten years ago, much less the Heidenhain Variant of Creutzfeldt Jakob Disease, and my spell checker does not have that one either. IT is an exceedingly rare strain of the CJD i.e. sporadic, spontaneous, of which neither one has ever been proven to be either. There is a route, and source.
Mad Cow disease has been in the USA for some time, of which has been systematically covered up, and I can and have proven this. The media does not care, and I am going to stop beating the drums on the 10 year anniversary of my mothers homicide December 14, 2007. I send this data to you as a last resort of sorts, you use as you wish. I have no PhDs, I am no doctor, and I am President and CEO of nothing. I simply wanted the truth. I have wasted a decade. But i am hear to tell you the UKBSEnvCJD only theory is and was bogus from the beginning. Its a long long story, one you cannot explain in a few minutes, hours, or even days. But you must become aware of the fact that the USA MAD COW STRAIN i.e. the h-BASE, is more virulent to humans, and mirrors that of some sub-types of the sporadic CJD. I have tried to warn the public, industry and health officials for a decade only to be called a high school flunky. but if you would please take the time to read the data, i believe you will see i was proven correct. and that is disturbing.
The following is from someone that wanted to interview me recently but i said ................
well see for yourself, but please take the time///
Thank you,
I am sincerely,
Terry S. Singeltary Sr.
PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase in ''TYPE UNKNOWN''. ...TSS
1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006,
26 from 2007)
http://www.cjdsurveillance.com/pdf/case-table.pdf
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
http://madcowtesting.blogspot.com/
----- Original Message ----- From: Terry S. Singeltary Sr. To: xxxxxxxxxxxx Sent: Saturday, October 06, 2007 4:49 PM Subject: Re: xxxxxxxxxxxxxxxxxxxxx
October 6, 2007 16:40 hours central
Hello Mr. xxxxxx,
Glad to meet you sir. I have to admit, I am a bit shocked at your fact finding mission now, since I am retiring and have not been giving interviews i.e. radio, tv, or anymore people at my house for a while. I am winding down after a decade as of there abouts 12/14/07 i.e. mom's dod of the Heidenhain Variant of Creutzfeldt Jakob disease. you see, this is why I do/did this, maybe you are aware of that. I am/was only vested in one thing, the truth. no, i don't pretend to have all the answers. there's still many unanswered questions, but the answers we do have, we have been ignoring, we must start taking them serious i.e. amplification and transmission of the TSEs, and the list is growing, and they are becoming more virulent. I have answered the questions I needed, and i tried to educate the public and the industries involved the best I could. you must know, I did not choose to do this. it chose me, and it killed my mother. it, i.e. transmissible spongiform encephalopathy. oral route, or friendly fire, both are 100% fatal once clinical, there is much more to this than what I call the UKBSEnvCJD only theory, of a disease, that was supposedly only in one part of the world, in only one geographical location, only involving one group of cattle, and only one group of young humans, when documented BSE farmers and there wives were dropping dead from the sporadic CJDs i.e. one of six phenotypes now documented, but the list is growing there too, and questionable (we will get to all this in a minute). IF you believe in the UKBSEnvCJD only theory, BSE/TSE tainted MBM was imported into the USA and the rest of the world, and or IF you also believe in the fact that the USA and North America have also recycled there own super strain (you do know we shipped the continuous rendering technology to the UK some 5 years, BEFORE WE STARTED USING IT). The USA did both. so, it's a double whammy so to speak, and super strain due to the fact we have been feeding our food producing animals for consumption, not only all the strains of sheep scrapie typical and atypical, but also the cwd and there different phenotypes of deer and elk, along I am afraid with a few TME cases, I dont think you can rule that out. and nobody even checks for TSE in dogs and cats. so the USA is in a Unique situation. I have files for all this if you want it. sorry, I am rambling now. BUT for anyone to think that Canada having a worse BSE problem than the USA, or Mexico, is not looking at all the data. feed alone trading back and forth, cross contamination of vehicles, live cattle, sheep, deer and elk trades, crossing borders, legal and illegal, and yes, we see that now BSE does transmit to red deer. CWD transmitting to cattle and sheep. all this transmitting to primates. I could go on. with that said, i said long ago, the BSE MRR policy is nothing more than a legal tool to trade TSE globally. the BSE GBR risk assessments must be adhered to, the BSE MRR repealed, killed, buried. the OIE even says the BSE MRR ratings are only as good as what the countries supplying the info are giving them to go by. and if you look at what the top TSE scientist have said about the infamous june 2004 enhanced BSE surveillance program, it was flawed from the beginning, and results should not be trusted, as with what was later found out about the Harvard BSE study, but to get to the just of that, you must read the PEER REVIEW of the Harvard BSE study. I have suppled sources for all this below. ...
Mr. xxxxxx wrote;
> I do care and I'm trying to get all sides of the issue covered.
this is good news! it's about time somebody did. 10 YEARS post voluntary feed ban, and were still feeding cows to cows i.e. srm. however, I am afraid my view does not matter much, I am only the messenger. I am not a cattle baron. not educated much, this is what they keep telling me anyway (this is funny really, see below). what needs to happen is that you Sir read and understand the TSE science, and you tell your readers what really is and has been going on. if your waiting on the USDA to tell you, your gonna have a long wait. you have the USDA cowtailing to the big ag buisiness like the big feeders, packers, renders etc. all feeding off one thing, money. i don't really blame the ranchers, most were pretty much oblivious to the long term severity of TSE. the USDA and FDA did, and they failed to enforce there very own rules and to educate. I found this out sitting in on the Jan. 2001 USDA emergency 50 state BSE conference call ;
Subject: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001 Date: Wed, 10 Jan 2001 14:04:21 -0500 From: Gomez, Thomas M. Reply-To:
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To:
######### Bovine Spongiform Encephalopathy #########
Greetings List Members,
I was lucky enough to sit in on this BSE conference call today and even managed to ask a question. that is when the trouble started.
I submitted a version of my notes to Sandra Blakeslee of the New York Times, whom seemed very upset, and rightly so.
"They tell me it is a closed meeting and they will release whatever information they deem fit. Rather infuriating."
and i would have been doing just fine, until i asked my question. i was surprised my time to ask a question so quick.
(understand, these are taken from my notes for now. the spelling of names and such could be off.)
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you,
U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;
[unknown woman] what group are you with?
[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?
at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.
IF i were another Country, I would take heed to my notes, BUT PLEASE do not depend on them. ask for transcript from;
[log in to unmask] 301-827-6906
he would be glad to give you one ;-)
Rockville Maryland, Richard Barns Host
snip...full text ;
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
NOW, almost 7 years later, look where were at, and what about the atypicals and the fact there are now 4 documented blood transfusion related nvCJD cases.
FDA Proposes Barring Certain Cattle Material From Medical Products As BSE Safeguard
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&P=5318
http://bloodindex.org/view_news_zone.php?id=206
http://www.bseinquiry.gov.uk/files/yb/1988/11/04003001.pdf
8. The Secretary of State has a number of licences. We understand that the inactivated polio vaccine is no longer being used. There is a stock of smallpox vaccine. We have not been able to determine the source material. (Made in sheep very unlikely to contain bovine ingredients).
http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf
http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf
although 176 products do _not_ conform to the CSM/VPC guidelines.
http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf
> Looks like you have the facts at hand. Would you mind being the subject of next week's interview?
negative, I do not have all the facts. I only try to stay informed with the up to date sound science. and I try to give this to the public and industry. a great deal of time the industry and most media choose to ignore the ever so evolving science, and they choose take the rubber stamped TSE data that the USDA feeds them, which most of the time is ancient data. again, this is almost 2008, and we are still feeding cows to cows i.e. banned srms ;
October 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE
http://www.phxnews.com/fullstory.php?article=53149
http://www.fda.gov/cvm/BSE1007.htm
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
MORE 2006 FEED BAN VIOLATIONS BELOW, ''IN COMMERCE'' ;
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
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 ______________________________ PRODUCT a) Dairy feed, custom, Recall # V-134-6; b) Custom Dairy Feed with Monensin, Recall # V-135-6. CODE None. Bulk product RECALLING FIRM/MANUFACTURER Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006. Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete. REASON Possible contamination of dairy feeds with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 1,484 tons DISTRIBUTION TN and WV
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS Date: August 16, 2006 at 9:19 am PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II ______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-115-6 CODE None RECALLING FIRM/MANUFACTURER Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE Approximately 2,223 tons DISTRIBUTION KY
______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-116-6 CODE None RECALLING FIRM/MANUFACTURER Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 1,220 tons DISTRIBUTION KY
______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-117-6 CODE None RECALLING FIRM/MANUFACTURER Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 40 tons DISTRIBUTION LA and MS
______________________________ PRODUCT Bulk Dairy Feed, Recall V-118-6 CODE None RECALLING FIRM/MANUFACTURER Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 7,150 tons DISTRIBUTION MS
______________________________ PRODUCT Bulk custom dairy pre-mixes, Recall # V-119-6 CODE None RECALLING FIRM/MANUFACTURER Walthall County Co-op, Tylertown, MS, by telephone on June 26, 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 87 tons DISTRIBUTION MS
______________________________ 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 MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs Date: August 6, 2006 at 6:14 pm PST PRODUCT Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6 CODE All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products. RECALLING FIRM/MANUFACTURER Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete. REASON The feed was manufactured from materials that may have been contaminated with mammalian protein. VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs DISTRIBUTION MI
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.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
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date: August 6, 2006 at 6:19 pm PST PRODUCT Bulk custom made dairy feed, Recall # V-114-6 CODE None RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE ????? DISTRIBUTION KY END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
CJD WATCH MESSAGE BOARD TSS 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
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006 Date: June 27, 2006 at 7:42 am PST Public Health Service Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.
You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.
You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
http://www.fda.gov/foi/warning_letters/g5883d.htm
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must
also have shared Mr Bradley's surprise at the results because all the dose
levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s145d.pdf
2
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100
grams) was probably given with the benefit of hindsight; particularly if one
considers that later in the same answer Mr Bradley expresses his surprise that it
could take as little of 1 gram of brain to cause BSE by the oral route within the
same species. This information did not become available until the "attack rate"
experiment had been completed in 1995/96. This was a titration experiment
designed to ascertain the infective dose. A range of dosages was used to ensure
that the actual result was within both a lower and an upper limit within the study
and the designing scientists would not have expected all the dose levels to trigger
infection. The dose ranges chosen by the most informed scientists at that time
ranged from 1 gram to three times one hundred grams. It is clear that the designing
scientists must have also shared Mr Bradley's surprise at the results because all the
dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts
[BBC radio 4 FARM news]
http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
2) Infectious dose:
To cattle: 1 gram of infected brain material (by oral ingestion)
http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&P=3715
> I'd love to give you the opportunity to point out what you've detailed in your message to me.
DO you know how long that would take, and what it curtails ? I will try to do this below as short as I can, but to understand all this you will have to go back to early days, then work your way to date. ill try, this is long winded, but this is one reason I don't give interviews anymore, for one thing, it's not about me, and another, if you are really looking for the truth, you cannot give it in a 10 minute one page interview. but if you do really want the facts, as I have come to know them, consider this an interview, and I will try to explain below, and you can use as you wish, in part, or whole. I hope you do, I have wasted 10 years trying to explain that there is more to this story than the UKBSEnvCJD hamburger eating adolescent only theory, and the rest of the 85 to 90 % of dead from CJD, i.e. sporadic, well, that just happens, no route, no source, just spontaneous happening of bad luck. THE spontaneous theory has never been proven. THE only spontaneous TSE they developed in the lab, does not look like natural field TSE. IN fact, most scientist say this cannot even be proven i.e spontaneous TSE in humans, cattle, or any other species. AND the few that do believe in it (without proof), are mostly big ag and industry, and they just try to avoid communicating it at all cost, remember that, 'AT ALL COST'. ...
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://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf
Gerald Wells: Report of the Visit to USA, April-May 1989
snip...
The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...
snip...
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
snip...
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
YOU SEE SIR, it never was about sound science.
LETS start with the UKBSEnvCJD only theory, lets look at UK exports to USA, Canada, and Mexico. the imported only theory. ...
1994 UK EXPORTS BEEF VEAL USA , MEXICO $ CANADA ONLY other Countries list in PDF file)
USA -------- TOTALS ''8'' TONS CANADA -- TOTALS ''29'' TONS
1995 UK EXPORT BEEF AND VEAL TO USA AND CANADA
USA ------- TOTALS ''358'' TONS
CANADA --TOTALS ''24'' TONS
BONE-IN BEEF AND VEAL
USA-------- TOTALS ''10'' TONS (i think this is part of the 358 tons above?)
UK EXPORT OF LIKE CATTLE TO USA AND CANADA
1986 TO 1996 USA TOTAL = 1297
1986 TO 1996 CAN TOTAL = 299
http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf
UK EXPORT MEAT OR OFFAL OF BOVINE ANIMALS DEC 1987
CANADA -- 64,526 KG
UK EXPORT OFFALS OF BOVINE ANIMALS FRESH CHILLED OR FROZEN OTHER THAN LIVER DEC 1987 YTD
USA -- 45,943 KG
UK EXPORT MEAT OF BOVINE ANIMAL WITH BONE IN 1988
CANADA -- 4,163 KG
PREP OR PRES MEAT OR OFFAL OF BOVINE ANIMALS CUMULATIVE TO DEC 1988
USA -------- 28,609 KG CANADA -- 22,044 KG
MEAT OF BOVINE ANIMALS WITH BONE IN CUMULATIVE TO ANUAL 1989
USA -------- 17,880 KG MEXICO---- 33,444 KG
BONELESS MEAT OF BOVINE 1989
USA --------111,953 KG CANADA---1,800 KG MEXICO --- 1,143,387 KG
EDIBLE OFFAL OF BOVINE ANIMALS 1989
USA -------- 19,980 KG MEXICO--- 31,244 KG
MORE........
MEAT OF BOVINE ANIMALS BONELESS 1990
USA 146,443
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995
USA 24 TONS
CANADA 83 TONS
http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.??? From: S.J.Pearsall@esg.maff.gsi.gov.uk Date: Tue, 8 Feb 2000 14:03:16 +0000 To: flounder@wt.net (Receipt Notification Requested) (Non Receipt Notification Requested)
Terry Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below: Country Tonnes
1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990
Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222). Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C
====================================== END...TSS
BSE GBR RISK ASSESSMENTS, USA, CANADA, AND MEXICO
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90's when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/573.html
http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/573.Par.0004.File.dat/sr03_biohaz02_usa_report_v2_en1.pdf
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Canada
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked to provide an up-to-date scientific report on the GBR in Canada, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Canada. This scientific report addresses the GBR of Canada as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into the country middle of the eighties and could have reached domestic cattle in the early nineties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s. It is possible that imported meat and bone meal (MBM) into Canada reached domestic cattle and led to an internal challenge in the early 90s.
A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from UK in the mid 80s could have been slaughtered. This risk continued to exist, and grew significantly in the mid 90's when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of Canada is III, i.e. it is confirmed at a lower level that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the system remains unstable, it is expected that the GBR continues to grow, even if no additional external challenges occur.
http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/564.html
http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/564.Par.0001.File.dat/sr02_biohaz02_canada_report_v2_en1.pdf
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Mexico
Last updated: 8 September 2004 Publication Date: 20 August 2004
Adopted July 2004 (Question N° EFSA-Q-2003-083)
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.
It is likely that BSE infectivity entered processing at the time of imported 'at - risk' MBM (1993) and at the time of slaughter of imported live 'at - risk' cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.
EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.
http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/565.Par.0003.File.dat/sr04_biohaz02_mexico_report_summary_en1.pdf
http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/565.Par.0004.File.dat/sr04_biohaz02_mexico_report_v2_en1.pdf
O.K. NOW Mr. xxxxxx, for the North America Home Grown TSE, amplification, and transmission, and what about the atypical h-base bse, and the nor-98 scrapie cases popping up in the USA and why isn't anyone speaking much about it, and what are the potential ramifications, what does the Nobel Prize Winner Stanely Prusiner say about atypical scrapie, lets look at that first ;
Published online before print October 20, 2005
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102 Medical Sciences
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes
( sheep prion transgenic mice )
Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte , Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude * *Virologie Immunologie Moléculaires and Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
---------------------------------------------------------------------------- ----
Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper.
A.L.D. and V.B. contributed equally to this work.
To whom correspondence should be addressed.
Hubert Laude, E-mail: laude@jouy.inra.fr
www.pnas.org/cgi/doi/10.1073/pnas.0502296102
http://www.pnas.org/cgi/content/abstract/0502296102v1
OF COURSE, the USDA et al once was concerned for human health from typical scrapie, and rightly so, typical scrapie transmits to primates by there NON-FORCED ORAL CONSUMPTION ;
76/10.12/4.6
http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
ALSO,
The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate.
http://www.pnas.org/cgi/content/full/041490898v1
SO, in my opinion, the _myth_ that typical scrapie does not transmit to humans, is just that, a myth. there have never been transmission studies done on man, and I would bet my last bottom dollar, anyone making the statement, would not eat a handful of scrapie infected brains. you do know about james alford don't you, whether or not it was the sheep brains he was fed in the middle east, or something else, this war hero has cjd, and he is very young. this was a tragic story too. dont hear much of that now either. ...
http://www.blackfive.net/main/2004/10/a_dying_hero_ss.html
http://www.blackfive.net/main/2004/03/ssg_james_alfor.html
NOW, why in the world is no one much speaking about the lates 3 cases of the NOR-98 case in the USA, and what are the potential ramifications thereof;
Subject: Aspects of the Cerebellar Neuropathology in Nor98 Date: September 26, 2007 at 4:06 pm PST
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway
Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. *** The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
From: "Terry S. Singeltary Sr."
Sent: Tuesday, August 21, 2007 9:50 AM
Subject: TWO MORE Nor98 atypical Scrapie cases detected in USA bringing total to 3 cases to date
Infected and Source Flocks As of June 30, 2007, there were .....
snip...
One field case and one validation case were consistent with Nor-98 scrapie.
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
IN the February 2007 Scrapie report it only mentions ;
''One case was consistent with Nor98 scrapie.''
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/
(please note flocks of origin were in WY, CO, AND CA. PERSONAL COMMUNCATIONS USDA, APHIS, VS ET AL. ...TSS)
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=14553
An evaluation of scrapie surveillance in the United States
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3427
FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=10451
MR. Jolley, you see why this cannot be done in a 10 minute interview, or a one page story,
SO, lets move on from typical and atypical scrapie, to CWD in deer and elk, and why are
either important to the cattle producer and humans? Because they all transmit to each other
in the lab, and there are potential ramifications from the environmental transmission of these
TSE, and as they have mutated, they become more virulent, so the potential for some TSE
to transmit via the environment is very real i.e. casual contact between sheep, goat, deer, elk,
with cattle in the field. This has never been documented in cattle, yet,
to date. lets look at some of the data there to date ;
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.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
P04.01
Chronic Wasting Disease in a Captive White-Tailed Deer Farm
Keane, D1; Barr, D1; Bochsler, P1; Hall, M2; Gidlewski, T3; O'Rourke, K4; Spraker, T5 1University of Wisconsin, USA; 2US Department of Agriculture, USA; 3US Department of Agriculture, USA; 4USDA ARS-ADRU, Washington State University, USA; 5Veterinary Diagnostic Laboratory, Colorado State University, USA
A white-tailed deer farm in Portage, Wisconsin, was depopulated in January 2006, after chronic wasting disease (CWD) had been initially discovered on the property in September 2002. Prior to the depopulation, a total of 22 positive animals had been removed from the property: one in 2002, six in 2003, ten in 2004, four in 2005 and one in 2006. At the time of depopulation a total of 76 animals remained: 47 females and 29 males. Age was assessed by visual examination of teeth at the time of death and revealed 26 adult, 8 fawn and 42 yearling animals. The following tissues were examined by immunohistochemistry for PrPCWD using Ab99/97.6.1: obex, tonsil, retropharyngeal, submandibular, parotid, prescapular, axillary, inguinal, prefemoral and popliteal lymph nodes, recto-anal mucosal tissue and eye. Seventy-nine percent of animals (sixty) were found to be positive in at least one tissue; 49 were obex positive, 58 retropharyngeal positive, 56 tonsil positive, 48 recto-anal mucosal associated lymphoid tissue positive and 4 animals were positive for PrPCWD in the retina. Prion genotype was determined for all animals.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
P01.47
Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in vitro Conversion Assay
Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1 1University of British Columbia, Brain Research Centre, Canada; 2Public Health Agency of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases Research Institute, Canada Food Inspection Agency, National Reference Laboratory for Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical Biophysics, University of Toronto, Canada
Background: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that can affect North American cervids (deer, elk, and moose). Although the risk of CWD crossing the species barrier and causing human disease is still unknown, however, definite bovine spongiform encephalopathy (BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit the exposure of humans to CWD.
Aim: In view of the fact that BSE can be readily transmitted to non-bovid species, it is important to establish the species susceptibility range of CWD.
Methods: In vitro conversion system was performed by incubation of prions with normal brain homogenates as described before, and protease K (PK) resistant PrP was determined by immunoblotting with 6H4 monoclonal prion antibody.
Results: Our results demonstrate that PrPC from cervids (including moose) can be efficiently converted to a protease-resistant form by incubation with elk CWD prions, presumably due to sequence and structural similarities between these species. Interestingly, hamster shows a high conversion ratio by PrPCWD. Moreover, partial denaturation of substrate PrPC can apparently overcome the structural barriers between more distant species.
Conclusions: Our work correctly predicted the transmission of CWD to a wild moose. We find a species barrier for prion protein conversion between cervids and other species, however, this barrier might be overcome if the PrPC substrate has been partially denatured in a cellular environment. Such an environment might also promote CWD transmission to non-cervid species, *** including humans. Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro conversion than PrPC treated at physiological pH. This has implications for the process by which the prion protein is converted in disease.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Subject: Clinical Observations of BSE Infection in Red Deer Date: October 4, 2007 at 9:05 am PST
P04.80
Clinical Observations of BSE Infection in Red Deer
Steele, P1; Martin, S2; Jeffrey, M2; González, L2; Sisó, S2; Finlayson, J1; Hamilton, S1; Eaton, Samatha L1; Reid, Hugh W1; Todd, R1; Pang, Y1; Chianini, F1; Dagleish, MP1 1Moredun Research Institute, UK; 2Veterinary Laboratory Agency, Lasswade, UK
Observation of clinical signs is often the first step in the diagnosis of TSE diseases in experimental, farmed and wild animals. Clinical presentation of chronic wasting disease (CWD) infected deer varies widely as disease progresses and many clinical signs observed can be non-specific to TSE infection, however by terminal stage the majority of cases involve behavioural changes and loss of body condition. We present here the first description of clinical disease in deer experimentally infected with BSE. These data are part of the results of an ongoing project to investigate the susceptibility of UK red deer (Cervus elaphus elaphus) to BSE infection either by alimentary or intra-cerebral infection. Eighteen European red deer calves (mean 64 days old) were challenged intragastrically with 25g of BSE-infected bovine brain. Six challenged and 2 control deer were culled at 6 and 12 month post infection. These animals showed no clinical signs and no disease-specific PrP (PrPd) on immunohistochemistry (IHC) examination of a wide range of tissues collected at post-mortem. Six BSE-dosed and 4 negative control deer are still alive at time of writing (1384 dpi). Subsequently, 6 red deer of the same cohort (mean 341 days old) were challenged with 0.05g of BSE positive bovine brain material and 2 with sterile saline by the intracerebral route. Currently (1106 dpi), five of the six challenged animals have developed clinical signs and terminal disease confirmed by IHC and western blot detection of PrPd. Clinical signs similar to CWD cases have been observed including behavioral change, wide stance, lowered head, and excessive salivation. All animals had significant weight loss attributed to inability or unwillingness to feed, with inhalation pneumonia occurring in the case of one animal which is commonly observed in CWD cases. The first animal to show clinical signs was markedly different to the four subsequent cases. This animal had to be culled following several behavioral episodes causing physical injury. Our results prove for the first time that UK red deer are susceptible to intra-cerebral BSE infection and shows that the clinical presentation of disease shares many similarities to that recorded for CWD.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie McKenzie2, Judd M. Aiken1,2*
1 Program in Cellular and Molecular Biology, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 2 Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 3 Department of Soil Science and Molecular and Environmental Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 4 Biostatistics and Medical Informatics, University of Wisconsin Medical School, Madison, Wisconsin, United States of America
Soil may serve as an environmental reservoir for prion infectivity and contribute to the horizontal transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. Here, we assess the oral infectivity of Mte- and soil-bound prions. We establish that prions bound to Mte are orally bioavailable, and that, unexpectedly, binding to Mte significantly enhances disease penetrance and reduces the incubation period relative to unbound agent. Cox proportional hazards modeling revealed that across the doses of TSE agent tested, Mte increased the effective infectious titer by a factor of 680 relative to unbound agent. Oral exposure to Mte-associated prions led to TSE development in experimental animals even at doses too low to produce clinical symptoms in the absence of the mineral. We tested the oral infectivity of prions bound to three whole soils differing in texture, mineralogy, and organic carbon content and found soil- bound prions to be orally infectious. Two of the three soils increased oral transmission of disease, and the infectivity of agent bound to the third organic carbon-rich soil was equivalent to that of unbound agent. Enhanced transmissibility of soil-bound prions may explain the environmental spread of some TSEs despite the presumably low levels shed into the environment. Association of prions with inorganic microparticles represents a novel means by which their oral transmission is enhanced relative to unbound agent.
snip...
Discussion These experiments address the critical question of whether soil particlebound prions are infectious by an environmentally relevant exposure route, namely, oral ingestion. Oral infectivity of soil particlebound prions is a conditio sine qua non for soil to serve as an environmental reservoir for TSE agent. The maintenance of infectivity and enhanced transmissibility when TSE agent is bound to the common soil mineral Mte is remarkable given the avidity of the PrPTSEMte interaction [22]. One might expect the avid interaction of PrPTSE with Mte to result in the mineral serving as a sink, rather than a reservoir, for TSE infectivity. Our results demonstrate this may not be the case. Furthermore, sorption of prions to complex whole soils did not diminish bioavailability, and in two of three cases promoted disease transmission by the oral route of exposure. While extrapolation of these results to environmental conditions must be made with care, prion sorption to soil particles clearly has the potential to increase disease transmission via the oral route and contribute to the maintenance of TSE epizootics.
Two of three tested soils potentiated oral prion disease transmission. The reason for increased oral transmissibility associated with some, but not all, of the soils remains to be elucidated. One possibility is that components responsible for enhancing oral transmissibility were present at higher levels in the Elliot and Bluestem soils than in the Dodge soil. The major difference between the Dodge soil and the other two soils was the extremely high natural organic matter content of the former (34%, [22]). The Dodge and Elliot soils contained similar levels of mixed-layer illite/smectite, although the contribution of smectite layers was higher in the Dodge soil (14%16%, [22]). The organic matter present in the Dodge soil may have obstructed access of PrPTSE to sorption sites on smectite (or other mineral) surfaces.
The mechanism by which Mte or other soil components enhances the oral transmissibility of particle-bound prions remains to be clarified. Aluminosilicate minerals such as Mte do not provoke inflammation of the intestinal lining [39]. Although such an effect is conceivable for whole soils, soil ingestion is common in ruminants and other mammals [25]. Prion binding to Mte or other soil components may partially protect PrPTSE from denaturation or proteolysis in the digestive tract [22,40] allowing more disease agent to be taken up from the gut than would otherwise be the case. Adsorption of PrPTSE to soil or soil minerals may alter the aggregation state of the protein, shifting the size distribution toward more infectious prion protein particles, thereby increasing the specific titer (i.e., infectious units per mass of protein) [41]. In the intestine, PrPTSE complexed with soil particles may be more readily sampled, endocytosed (e.g., at Peyer's patches), or persorbed than unbound prions. Aluminosilicate (as well as titanium dioxide, starch, and silica) microparticles, similar in size to the Mte used in our experiments, readily undergo endocytotic and persorptive uptake in the small intestine [4244]. Enhanced translocation of the infectious agent from the gut lumen into the body may be responsible for the observed increase in transmission efficiency.
Survival analysis indicated that when bound to Mte, prions from both BH and purified PrPTSE preparations were more orally infectious than unbound agent. Mte addition influenced the effective titer of infected BH to a lesser extent than purified PrPTSE. Several nonmutually exclusive factors may explain this result: (1) other macromolecules present in BH (e.g., lipids, nucleic acids, other proteins) compete with PrPTSE for Mte binding sites; (2) prion protein is more aggregated in the purified PrPTSE preparation than in BH [45], and sorption to Mte reduces PrPTSE aggregate size, increasing specific titer [41]; and (3) sorption of macromolecules present in BH to Mte influences mineral particle uptake in the gut by altering surface charge or size, whereas the approximately 1,000-fold lower total protein concentration in purified PrPTSE preparations did not produce this effect.
We previously showed that other inorganic microparticles (kaolinite and silicon dioxide) also bind PrPTSE [22]. All three types of microparticles are widely used food additives and are typically listed as bentonite (Mte), kaolin (kaolinite), and silica (silicon dioxide). Microparticles are increasingly included in Western diets. Dietary microparticles are typically inert and considered safe for consumption by themselves, do not cause inflammatory responses or other pathologies, even with chronic consumption, and are often sampled in the gut and transferred from the intestinal lumen to lymphoid tissue [39,46,47]. Our data suggest that the binding of PrPTSE to dietary microparticles has the potential to enhance oral prion disease transmission and warrants further investigation.
In conclusion, our results provide compelling support for the hypothesis that soil serves as a biologically relevant reservoir of TSE infectivity. Our data are intriguing in light of reports that naïve animals can contract TSEs following exposure to presumably low doses of agent in the environment [5,79]. We find that Mte enhances the likelihood of TSE manifestation in cases that would otherwise remain subclinical (Figure 3B and 3C), and that prions bound to soil are orally infectious (Figure 5). Our results demonstrate that adsorption of TSE agent to inorganic microparticles and certain soils alter transmission efficiency via the oral route of exposure.
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full text is here:
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030093
http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-L.pdf
http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-S.pdf
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&F=&S=&m=1742&P=7260
From: "Terry S. Singeltary Sr." Subject: CWD UPDATE 88 AUGUST 31, 2007
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&P=450
Date: Wed, 29 Aug 2007 21:13:08 -0500
From: "Terry S. Singeltary Sr."
Subject: CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again)
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=26079
Monitoring the Potential Transmission of Chronic Wasting Disease to Humans Using a Hunter Registry Database in Wyoming (405 lines)
From: Terry S. Singeltary Sr. Date: Thu, 30 Aug 2007 21:23:42 -0500
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&F=&S=&P=27654
J Biol Chem. 2007 Aug 20; : 17709374
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain.
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our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.
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FULL TEXT ;
http://www.jbc.org/cgi/
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=21267
From: TSS (216-119-163-189.ipset45.wt.net) Subject: CWD aka MAD DEER/ELK TO HUMANS ??? Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias" To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias" Sent: Monday, September 30, 2002 9:22 AM Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was
attached
to your email), we did not say CWD in humans will present like variant
CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message----- From: Sent: Sunday, September 29, 2002 10:15 AM To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Aguzzi warns of CWD danger
The TSE family of diseases also includes chronic wasting disease (CWD) in deer, a condition that has spread in the US in recent years (Nature 416, 569; 2002). Speaking at the Days of Molecular Medicine conference in La Jolla in March, prion expert Adriano Aguzzi issued a strong warning against underestimating this form of TSE.
"For more than a decade, the US has by-and-large considered mad cows to be an exquisitely European problem. The perceived need to protect US citizens from this alien threat has even prompted the deferral of blood donors from Europe," he said. "Yet the threat-from-within posed by CWD needs careful consideration, since the evidence that CWD is less dangerous to humans than BSE is less-than-complete. Aguzzi went on to point out that CWD is arguably the most mysterious of all prion diseases.
"Its horizontal spread among the wild population is exceedingly efficient, and appears to have reached a prevalence unprecedented even by BSE in the UK at its peak. The pathogenesis of CWD, therefore, deserves a vigorous research effort. Europeans also need to think about this problem, and it would be timely and appropriate to increase CWD surveillance in Europe too." Aguzzi has secured funding from the National Institutes of Health to investigate CWD, and the effort will be lead by Christina Sigurdson in his department at the University of Zurich. KAREN BIRMINGHAM, LONDON
This quote from Dr. Gambetti is especially significant since he is the rather cautious TSE researcher under contract with the Centers for Disease Control to examine the brains of individuals who have died of CJD. -----------------
Pierluigi Gambetti, director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, said all deer should be tested for chronic wasting disease before any processing is done.
"There is no way around it," he said. "Nobody should touch that meat unless it has been tested." --------------------------------------
http://www.ledger-enquirer.com/mld/...ion/3954298.htm ================================================== ====
'As implied in the Inset 25 we must not assume that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.'
http://www.bse.org.uk/files/yb/1991/01/04004001.pdf
see full text ;
Re: Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES)
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=1165
doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
Available online 29 July 2003.
Volume 3, Issue 8, August 2003, Page 463
"My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem." ............................
http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fulltext
http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf
see history of cjd questionnaire
http://brain.hastypastry.net/forums/showthread.php?t=2408
MR. xxxxxxx, I strongly urge you to read in full and uderstand the following about the TWO atyipcal H-BASE mad cow cases in Texas and Alabama ;
FC5.5.1
BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc C-terminal Truncated Fragments
Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S3 1University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA, France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA
The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human prion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K-resistant prion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility of the unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V) codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE) and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all genotypes,; (ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V- 2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD subtype M/V-2 shared molecular and pathological features with an atypical form of BSE, named BASE, thus suggesting a potential link between the two conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculated with brain homogenates from BASE. Samples were separated by using a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJD MV-2 subtype. These data strongly support the link, or at least a common ancestry, between a sCJD subtype and BASE.
This work was supported by Neuroprion (FOOD-CT-2004-506579)
FC5.5.2
Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease
Zanusso, G1; Lombardi, G2; Casalone, C3; D'Angelo, A4; Gelmetti, D2; Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy
The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease.
P01.34
Pathological Interaction Between Protein Misfolding Disorders: Prions and Alzheimer's Disease
Morales, R; Estrada, L; Castilla, J; Soto, C University of Texas Medical Branch, Neurology, USA
Protein Misfolding Disorders (PMD) include several diverse diseases, such Alzheimer's, Parkinson's, Transmissible Spongiform Encephalopathies, Diabetes Type II and various systemic amyloidosis. The central event in these diseases is the accumulation of a misfolded, ß-sheet rich aggregated form of a naturally expressed protein. In vitro studies have shown that protein misfolding and aggregation follows a seedingnucleation mechanism similar to the process of crystallization. In this model, the limiting step is the formation of small oligomeric intermediates that act as seeds to catalyze the polymerization process. The seeding-nucleation model provides a rationale and plausible explanation for the infectious nature of prions. Infectivity lies on the capacity of preformed stable misfolded oligomeric proteins to act as a seed to catalyze the misfolding and aggregation process. The mechanism of misfolding and aggregation is similar in all PMD suggesting that misfolded aggregates have an inherent capability to be transmissible. Moreover, it has been shown that oligomeric seeds formed by one protein can accelerate the misfolding and aggregation of another protein, by a process termed cross-seeding. Our current study aims to assess the potential molecular cross-talk among PMD in vivo. For this purpose we inoculated with prions a transgenic mice model of Alzheimer's disease (tg2576) that develops typical amyloid plaques over time. 45, 303 and 365 days old transgenic and wild type mice were inoculated intraperitoneally with RML prions. We found significant diminution in prion incubation periods for tg2576 mice compared to age matched wild type controls. Moreover, a time dependent effect was observed, where the shorter incubation period was observed in animals containing larger number of amyloid plaques. Inoculation of tg2576-RML prions into wild type mice showed incubation periods similar to the original infectious material, suggesting that strains characteristics are maintained. In vitro data showed cross-seeding aggregation between PrPSc and Aß. Our findings suggest an interaction between Alzheimer's and prion pathologies, indicating that one protein misfolding process may be an important risk factor for the development of a second perhaps more prevalent disease.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Subject: Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route Date: September 29, 2007 at 12:50 pm PST
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study "BSE in primates" supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Subject: Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC Date: September 29, 2007 at 12:45 pm PST
P03.137
Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan
Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
P04.49
Case Report of Variant Creutzfeldt-Jakob Disease in a Macaque after Blood Transfusion
Lescoutra-Etchegaray, N1; Ruchoux, MM1; Correia, E1; Jolit, A1; Freire, S1; Lasmezas, CI2; Deslys, JP1; Comoy, E1 1CEA/DSV/IMETI/SEPIA, France; 2Scripps Florida, USA
A fourth human case of probable transmission of vCJD through transfusion has now been reported but a number of features affecting transfusion-related infection remain imprecise, including infectious dose, length of incubation period and critical infectious window of blood donors.
We report here the first case of experimental transmission of vCJD in primates by blood transfusion. Experimental infection of Cynomolgus macaque has been demonstrated to be a sensitive model for the investigation of human prion diseases, inducing similar distribution of infectivity in peripheral lymphoid tissues and equivalent brain pathology. In our study, transfusion was performed with 40 ml of whole blood drawn from a vCJD-infected macaque at the terminal stage of the disease. Clinical symptoms of vCJD appeared in the recipient animal after five years of incubation. The total amount of infectivity in the transfused blood was approximately 106 fold lower than in the brain (titration still in progress). In several animals infected intravenously with brain homogenate, the presence of PrPres in serial lymph nodes biopsies and in other organs at autopsy was examined and results will be presented.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
P04.51
Atypical Presentation of Variant Creutzfeldt-Jakob Disease in a 73 Year Old Blood Transfusion Recipient
Wroe, S1; Pal, S1; Webb, T1; Alner, K2; Hewitt, P3; Brander, S4; Wadsworth, JD5; Collinge, J1 1National Hospital for Neurology and Neurosurgery, National Prion Clinic, UK; 2National Hospital for Neurology and Neurosurgery, Department of Neuropsychology, UK; 3Health Protection Agency, UK; 4National Hospital for Neurology and Neurosurgery, Department of Neuropathology, UK; 5Institute of Neurology, UCL, UK
We report atypical presentation of variant Creutzfeldt-Jakob Disease (vCJD) identified ante-mortem in a 73 year-old recipient of blood products. This patient was transfused following orthopaedic surgery in December 1997. Tracing of blood products identified a single unit of non-leucodepleted red cells from an individual who developed neuropathologically confirmed vCJD eleven months after donation. Nine years post transfusion, this individual was referred to the National Prion Clinic for specialist investigation. Six years post transfusion the recipient complained of fluctuating fatigue and impaired concentration. At this time neurological examination and MRI brain (T1/T2 weighted/DWI) were normal. Progressive symptoms emerged six months later with imbalance and deteriorating cognition. Examination two months after onset of neurological symptoms demonstrated cognitive deficits, dyspraxia or visuospatial dysfunction and normal motor, sensory and gait examination. Six weeks later cognitive impairment was identified alongside tremulousness, impaired manual dexterity and limb ataxia. Serological investigations were normal. MRI (T1/T2 weighted/FLAIR/DWI) demonstrated prominent signal change throughout the dorsal thalamus, consistent with vCJD. PRNP genotyping revealed no mutations and homozygosity for methionine at codon 129. The prolonged incubation period of vCJD and possibility of asymptomatic carrier states pose major public health concerns. This case highlights the significant risk encountered by recipients of contaminated blood products and the necessity for their specialist monitoring.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
P04.36
Enhanced Surveillance of Persons Identified as at Increased Risk of CJD Due to Blood Transfusion or Healthcare Procedures
Brookes, D1; Chow, Y1; Ward, HJT2; Will, RG2; Hewitt, P3; Gill, ON1 1HPA, CJD, UK; 2National CJD Surveillance Unit, UK; 3Colindale, NHS Blood and Tissue, UK
Introduction:
Reports of four iatrogenic transmissions of variant-CJD (vCJD) infection in the UK (all due to transfusion of blood from donors who later developed vCJD), evidence from iatrogenic transmissions of sporadic CJD and experimental work on CJD infectivity in tissues and on healthcare instruments have given rise to concern about the risks of iatrogenic transmission of CJD. This risk warrants a) certain public health precautions, and b) follow-up of individuals with identified risks in order to gain evidence about their risks and ensure appropriate management of these risks. Evidence of transmission via iatrogenic routes is important to inform public health measures and so prevent ongoing transmission of CJD.
Methods:
The Health Protection Agency and Health Protection Scotland holds details of persons identified as 'at-risk' of vCJD due to blood transfusion and of persons identified as 'at-risk' of CJD (of any type) from other healthcare procedures. The GPs/clinicians of all persons identified as 'at-risk' for public health purposes are provided with: information; risk assessment updates; advice on
public health precautions and advice on referral to specialist care. Procedures are being established to obtain enhanced surveillance data on these individuals, including: clinical status updates, date and cause of death, surplus tissue and blood specimens, and postmortem investigations.
Results:
Persons 'at-risk' of CJD have experienced a range of exposures. Estimated risks are uncertain and overlapping. Some individuals - recipients of vCJD implicated blood components - are considered to be at a clearly higher risk of infection: active follow-up is currently conducted for these individuals. In time, the enhanced surveillance of persons at increased risk of CJD will provide estimates of transmission risks and of the impact of iatrogenic exposures on mortality. Conclusion: Knowledge about iatrogenic transmission of CJD is being gained by the follow-up of individuals who have been identified as 'at-risk' of CJD in the UK. This enhanced surveillance may need to be sustained for many years.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Prions in Plasma of Patients with Sporadic Creutzfeldt-Jakob Disease Safar, J.G1,3, Geschwindm M.D2,3, Letessier, F1, Kuo, A1, Pomeroy, K1, Deering, C1, Serban, A1, Groth, D1, Miller, B.L2,3, DeArmond, S.J1,4, Prusiner, S.B1,3,5 1Institute for Neurodegenerative Diseases, 2Memory and Aging Center, Departments of 3Neurology, 4Pathology, and 5Biochemistry and Biophysics, University of California, San Francisco, California 94143
http://www.prion2007.com/pdf/Prion%20Friday.pdf
http://www.prion2007.com/pdf/Prion%20Thursday.pdf
http://www.prion2007.com/pdf/Prion%20Wednesday.pdf
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007
Date: Mon, 24 Sep 2007 21:31:55 -0500
I suggest that you all read the data out about h-BASE and sporadic CJD, GSS, blood, and some of the other abstracts from the PRION2007. ...
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744
*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OF POKER INDEED GOES UP. ...TSS
USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779
BRITISH MEDICAL JOURNAL
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... Terry S Singeltary (2 January 2000)
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries." ...snip...END
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
Full Text Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama
Suppressed peer review of Harvard study October 31, 2002.
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
(this is funny really, see below)
a funny thing happened. I was honored with having my name added to this list. they slammed for being an uneducated scientist, on a list with scientists that seemed to be interested in my thoughts, or the data I was putting out, and they also said that I was a high school drop flunky, quoting from an article I had writing and it published in the journal of neurology some years ago, and the sad part is, I was correct. most everything in that article has come to pass. you can take a look here ;
Terry Singletary -- A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to "sporadic" Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother's death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary's life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of "sporadic" cases). Sporadic CJD, unlike its newer "variant," is not linked to meat.
As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the "BSE-L" mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as "Dr. Terry Singletary," apparently an honorary degree as he has yet to finish high school.
Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer's, Parkinson's, and Lou Gehrig 's disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.
http://www.consumerfreedom.com/article_detail.cfm/article/138
ARTICLE IN QUESTION ABOVE FOLLOWS ;
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to
comment on the CDC's attempts to monitor the occurrence of emerging
forms of CJD. Asante, Collinge et al [1] have reported that BSE
transmission to the 129-methionine genotype can lead to an alternate
phenotype that is indistinguishable from type 2 PrPSc, the commonest
sporadic CJD. However, CJD and all human TSEs are not reportable
nationally. CJD and all human TSEs must be made reportable in every
state and internationally. I hope that the CDC does not continue to
expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in
the USA in both animal and man. CWD in deer/elk is spreading rapidly and
CWD does transmit to mink, ferret, cattle, and squirrel monkey by
intracerebral inoculation. With the known incubation periods in other
TSEs, oral transmission studies of CWD may take much longer. Every
victim/family of CJD/TSEs should be asked about route and source of this
agent. To prolong this will only spread the agent and needlessly expose
others. In light of the findings of Asante and Collinge et al, there
should be drastic measures to safeguard the medical and surgical arena
from sporadic CJDs and all human TSEs. I only ponder how many sporadic
CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
3 MONTHS LATER IN A BOOK INTERVIEW, VENDICATION OF SORTS
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations.
ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded
that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
IN REALITY, sporadic CJD is 1 in 9,000 in 50 years of age and above, and that's with a inadequate or what I call passive surveillance system. see below ;
Dr. William Shulaw, a veterinarian with The Ohio State University extension service, is involved in a nationwide program to eradicate scrapie, the form of BSE found in sheep.
Shulaw said the chances of a person getting sporadic Creutzfeldt-Jakob disease is about one in a million. But that's the total population, infants, children, adults and the elderly. Chances increase to one in 9,000 when the group is restricted to those age 50 and older.
http://www.pjstar.com/stories/082207/REG_BE523NH6.049.php
FURTHER into my journal of neurology article, some years later, again, sadly, I was proven correct ;
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...
http://www.cjdsurveillance.com/resources-casereport.html
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
AND YES, to the na Sayers, you are more likely to be killed by a car wreck than by CJD, for now, but my mother, and my neighbors mother, neither one were killed in a car wreck, they both died from CJD, confirmed, my mother dying from an exceedingly, rare phenotype of the sporadic CJDs i.e hvCJD, and there are others, and the numbers are increasing for sporadic CJD. but most all of us have been exposed to the TSE agent, one way or the other. however, the zillion dollar questions are still the same, why do only some humans and animals go clinical and die
from the TSE agent, and of course the origin, which to me is not as important as what we do know, amplification and transmission, i cannot stress this enough, the transmission studies do not lie.
I guess if I could say one thing about this Canadian vs USA mad cow situation, I would say this would have been, should have been resolved long ago. but instead, everyone ignored it, and now, all they want to do is sit around and point fingers at each other. my suggestion, test, test, test, I would say at least 1 million head a year, for five years.
the june 2004 enhanced bse surveillance does not even count (see why bio-rad, tss below). and that's not really enough, i would like to see 100% testing for consumption of either human or pet food for TSE. then you might have an answer to what you really have in relations to BSE and BASE H or L type. but the testing protocols and sampling protocols must be adhered too, this did not happen in the 2004 enhanced cover-up, and they could not even get that right. enforce the feed ban, srm removal (in fact you may have to enhance that with the atypicals, due to more tissue/organs tissue infectivity).
NOW, about that June 2004 enhanced BSE cover-up program ;
United States District Court, District of Arizona
USA v Roland Emerson Farabee 2: 07-wi-0001-01-EHC
Proceeding Type: Waiver/Plea
Judge: Honorable Earl H Carroll Courtroom: Phoenix Courtroom #501, 5th Floor
Date: 01/17/2007 Court Reporter: Candy Potter Time: 01:30 PM Courtroom Deputy: Bobbi Hightower
Counts: (may not reflect all counts) 18:641 and 2 (Theft of Government Money and Adiding and Abetting) 1 18: 1341 and 2 (Mail Fruad and Aiding and Abetting) 2 18:1343 and 2 (Wire Fraud and Aiding and Abetting) - 3
U.S. Attorney: Long, Robert
---------------------------------------------------------------------------- ---- Defense Attorney(s): Attorney Phone: Attorney Designation: McDonald, Jr., A. Melvin retained
http://www.azd.uscourts.gov/azd/callive.nsf/552b822403e5434a07256d6c007cc3ef/256244d68b5f47780725725e006aac31?OpenDocument&Click=
if my siphering is correct, that would be about another 2600 potential mad cows that went into the food chain. add that to these ;
It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing.< href="http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html">http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
and add these in ; UPI previously reported that from 2001 to 2003 the USDA collected the wrong part of the brain in more than 200 cows that were being screened as part of its BSE surveillance program. The USDA documents also indicate the agency never was able to identify or test 52 cows that came into the United States in 2001 along with the Washington cow that tested positive in 2003. Of these, 11 were considered to be "high risk" because they were born within a year and on the same premises as the infected cow. These cows may have gone into the food supply and been consumed by people. The concern is humans can contract a fatal brain disease from eating beef products contaminated with the mad cow pathogen.
http://www.terradaily.com/upi/2005/WWN-UPI-20050721-17422400-bc-us-madcow.html
NOT to forget what Paul Brown TSE expert at CDC said ; THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ; CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006 The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade. The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old. These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen. "The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that." Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive. USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general. "Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE Tuesday, September 12, 2006 11:10 AM "Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ; Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II and Food Safety and Inspection Service Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III Report No. 50601-10-KC January 2006 Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Greetings list members, IF you remember correctly, i posted this ;
Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE DECEMBER 19, 2004 USA Date: Thu, 30 Dec 2004 12:27:06 -0600 From: "Terry S. Singeltary Sr. BSE-L
snip...
OH, i did ask Bio-Rad about this with NO reply to date; -------- Original Message -------- Subject: USA BIO-RADs INCONCLUSIVEs Date: Fri, 17 Dec 2004 15:37:28 -0600 From: "Terry S. Singeltary Sr." To: susan_berg@bio-rad.com
Hello Susan and Bio-Rad, Happy Holidays! I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here? HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'? IS there more politics working here than science in the USA? What am I missing?
-------- Original Message -------- Subject: Re: USDA: More mad cow testing will demonstrate beef's safety Date: Fri, 17 Dec 2004 09:26:19 -0600 From: "Terry S. Singeltary Sr."
snip...end
Experts doubt USDA's mad cow results
snip...END
WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ; Bio-Rad, TSS phone conversation 12/28/04 Finally spoke with ;
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one. my question;
Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ??? ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated. again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer" "very political" "very loaded question" outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing. said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives? said something about ''just look at the sheep that tested IHC- but were positive''. ... TSS
------- Original Message --------
Subject: Your questions Date: Mon, 27 Dec 2004 15:58:11 -0800 From: To: flounder@wt.net
Hi Terry: ............................................snip Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you Regards Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: ================================= END...TSS
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
THE SEVEN SCIENTIST REPORT *** http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle 03-025IFA 03-025IFA-2 Terry S. Singeltary 9/13/2005
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
ALL IN ALL, it's a terribly failed system of TSE surveillance and attempted erradication of this agent in the USA, a failed policy driven by industry greed and ignorance. ...
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&F=P&P=10277
THAT TEJAS MAD COW THAT WAS COVERED-UP FOR ABOUT 7 PLUS MONTHS, i confirmed 7 months previously, but the other Tejas mad cow, got away, went to the render without testing at all ; TSS REPORT ON 2ND TEJAS MAD COW Mon, 22 Nov 2004 17:12:15 -0600 (the one that did NOT get away, thanks to the Honorable Phyllis Fong)
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ??? Date: Mon, 22 Nov 2004 17:12:15 -0600 From: "Terry S. Singeltary Sr." To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???terry
==============================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ??? Date: Fri, 19 Nov 2004 11:38:21 -0600 From: Carla Everett To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no informationabout the animal being in Texas. CarlaAt 09:44 AM 11/19/2004,
you wrote:>Greetings Carla,>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from>TEXAS. can you comment on this either way please?>>thank you,>Terry S. Singeltary Sr.>> ===================
-------- Original Message -------- Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ??? Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett To: "Terry S. Singeltary Sr." References: <[log in to unmask]> <[log in to unmask] us> <[log in to unmask]> <[log in to unmask] us> <[log in to unmask]>
our computer department was working on a place holder we could postUSDA's announcement of any results. There are no results to be announced tonightby NVSL, so we are back in a waiting mode and will post the USDA announcementwhen we hear something.At 06:05 PM 11/22/2004,
you wrote:>why was the announcement on your TAHC site removed?>>Bovine Spongiform Encephalopathy:>November 22: Press Release title here >>star image More BSE information>>>>terry>>Carla Everett wrote:>>>no confirmation on the U.S.' inconclusive test...>>no confirmation on location of animal.>>>>>>========================== ==========================
THEN, 7+ MONTHS OF COVER-UP BY JOHANN ET AL! no doubt about it now $$$
NO, it's not pretty, hell, im not pretty, but these are the facts, take em or leave em, however, you cannot change them.
with kindest regards,
I am still sincerely disgusted and tired in sunny Bacliff, Texas USA 77518
Terry S. Singeltary Sr.
FULL 130 LASHINGS TO USDA BY OIG again
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Link: TSS
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&T=0&P=23557
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&T=0&P=720
MR. xxxxxxxxx, THAT MAD COW IN TEXAS WOULD HAVE NEVER BEEN CONFIRMED IF NOT FOR THE HONORABLE
PHYLLIS FONG OF THE OIG.
I know I have missed something, but not sure what it is. I hope if nothing else, I hope you take the time to read all of this,
I could even go further into this and try and explain about Mission Texas and the late Richard Marsh findings, and the BSE farmers
and there wives with sporadic CJD, and that part of the equation to this long term nightmare, but I am afraid I have been too long
winded already. IF not, and your still with me, i have documented here ;
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
NOW BACK TO THOSE FARMERS WITH BSE HERDS THAT DIED FROM SPORADIC CJD
CJD FARMERS WIFE 1989
http://www.bseinquiry.gov.uk/files/yb/1989/10/13007001.pdf
http://www.bseinquiry.gov.uk/files/yb/1989/10/13003001.pdf
cover-up of 4th farm worker ???
http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/20006001.pdf
CONFIRMATION OF CJD IN FOURTH FARMER
http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.pdf
now story changes from;
SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms.
to;
This is not unexpected...
was another farmer expected?
http://www.bseinquiry.gov.uk/files/yb/1995/11/13010001.pdf
4th farmer, and 1st teenager
http://www.bseinquiry.gov.uk/files/yb/1996/02/27003001.pdf
SEE FULL TEXT ;
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&T=0&P=25276
Mr. xxxxx,
I hope you study this, I hope it helps answer a few questions you might not have answered yourself.
I tried/did help r-calf Dr. Thornsberry et al, but they were only interested in one thing, themselves.
the history of that is here ;
*** http://ranchers.net/forum/viewtopic.php?t=15704&postdays=0&postorder=asc&start=12
http://ranchers.net/forum/viewtopic.php?t=15704&postdays=0&postorder=asc&start=24
http://ranchers.net/forum/viewtopic.php?t=15704&postdays=0&postorder=asc&start=36
http://ranchers.net/forum/viewtopic.php?t=15704&postdays=0&postorder=asc&start=48
EXPORTATION AND IMPORTATION OF ANIMALS AND ANIMAL PRODUCTS: BSE; MRR AND IMPORTATION OF COMMODITIES, 65758-65759 [E6-19042]
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=3854
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&P=3381
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=498
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&T=0&P=10277
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=9972
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=4492
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2583
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2470
BOTTOM LINE ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............
http://www.oie.int/eng/Session2007/RF2006.pdf
----- Original Message -----
From: Terry S. Singeltary Sr. To: Terry S. Singeltary Sr. Sent: Thursday, March 29, 2007 3:44 PM Subject: BSE; MRR; Importation of Live Bovines and Products Derived from Bovines Commodities
Sent: Sunday, January 28, 2007 9:12 PM Subject: BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01 COMMENT SUBMISSION
----- Original Message ----- From: Terry S. Singeltary Sr. To: Terry S. Singeltary Sr. Sent: Thursday, March 29, 2007 3:27 PM Subject: BSE; MRR; Importation of Live Bovines and Products Derived from Bovines Commodities
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=19960
Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type RULE Document ID APHIS-2006-0041-0397
COMMENT FROM TERRY S. SINGELTARY SR. 1/09/2007
snip...
MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???
go figure....
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
see full text ;
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3412&disposition=attachment&contentType=crtext
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8152
ATTACHMENT TO SINGELTARY COMMENT 1/09/2007
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f3412
England worried briefly about infecting other countries 27 Aug 00 confidential correspondence obtained by Terry S. Singeltary Sr. http://www.mad-cow.org/00/aug00_last_news.html#fff
Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas
http://www.mad-cow.org/00/sep00_news.html#hhh
Other US BSE risks: the imported products picture 24 Jul 00 Trade Statistics: UK to US Compiled by Terry S.Singeltary Sr of Bacliff, Texas
http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh
http://www.mad-cow.org/00/may00_news.html
http://www.mad-cow.org/00/may00_news.html#aaa
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&P=21108
THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946
NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND
ANNUAL CONGRESS, 1946
The annual Congress, 1946, was held at the Royal Veterinary College, Royal College Street, London, N.W.I. from September 22nd to September 27th.
Opening Meeting
[skip to scrapie vaccine issue...tss]
Louping-ill vaccine incident ;
http://www.whale.to/v/singeltary.html
To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
R.F. Marsh* and G.R. Hartsough
.Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092
ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.
INTRODUCTION
Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.
DISCUSSION These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy. We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.
ACKNOWLEDGEMENTS These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.
REFERENCES Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.
MARSH
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Mr. xxxxxx SIR,
You will never know how much time and money i........we i.e. myself and my wife, have spent doing this, nobody will. but that's not why i did it. i made a promise to mom, i would find the complete truth, and i would make a promise to myself to get cjd reportable reportable in every state, with a cjd questionnaire asking real questions pertaining to route and source of TSE agent. i failed.
IN close, I hope you find time to study this. see for yourself what i have tried to do is/was in good faith.
YOU might wonder why I have wasted almost a decade, daily, hourly almost, doing this for nothing.
I cannot answer that myself, if you figure it out, let me know, and my wife, she would love to know.
IF nothing else, I hope I have at least brought more awareness to this disease, and helped change the
industries involved that are responsible in the spreading of this TSE agent, to change there ways.
who knows, someone might have listened to some of it.
I have attached a PDF file, that is my hypothesis on the diagnostic criteria differentiating the human TSEs,
and what I have said was wrong with it from day one. IT was never published by Lancet. but I have no PhDs.
I am only a lay person as they say when trying to get something published with no PhD. should have listened
to mom, and stayed in school. ...
kindest regards,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
----- Original Message ----- From: xTo: Terry S. Singeltary Sr. Sent: Friday, October 05, 2007 3:19 PM Subject: x
I do care and I'm trying to get all sides of the issue covered. Looks like you have the facts at hand. Would you mind being the subject of next week's interview? I'd love to give you the opportunity to point out what you've detailed in your message to me.
x
---------------------------------------------------------------------------- ---- Date: Fri, 5 Oct 2007 14:52:23 -0500 From: flounder9@verizon.net Subject: x To: x> CC: x
Jolley: Five Minutes With Ray Rodriguez
A. The US has no reported cases born after the ban was in effect. We have 1 atypical case, 1 imported cow from Canada and another with the same prion type as the Europe-Canada prion.
http://www.cattlenetwork.com/content.asp?contentid=165979
make that 2 H-BASE ATYPICALS. plus, one we will never know in Texas because they sent that stumbling suspect mad cow straight to the render, no test, no nothing, just get rid of it, and the faster the better. FYI, i am not sure if you are aware of this, or even if you care, but some disturbing data coming out about the h-BASE. ...terry
----- Original Message -----
From: xxxxxxxxx To: flounder9@verizon.net Sent: Wednesday, August 22, 2007 11:52 PM Subject: Re: HELLO DR. DETWILER... question please ... TSS
Mr. Singeltary,
Yes, both US cases (TX and AL) were H atypicals. I will check if details on the tests have been published.
Linda
Greetings Dr. Detwiler,
I must be slipping here, but i forget, did both those cows in Texas and Alabama have the H-type atypical TSE i.e. base/bse or whatever the be nice they are calling it now
Has this been documented on paper yet, i cannot find it now?
were both the Texas and Alabama BASE H-type ?
Texas ???
Alabama ???
any pathological reports on both those cows on the web yet ?
i saw those 2 further cases of the Nor-98 like/type/whatever reported in the june scrapie report. interesting!
snip...END...TSS
October 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE
http://www.phxnews.com/fullstory.php?article=53149
Transmissible Spongiform Encephalopathy UPDATE USA OCTOBER 2007
http://www.phxnews.com/fullstory.php?article=53128
http://www.phxnews.com/
***ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007
Date: Mon, 24 Sep 2007 21:31:55 -0500
I suggest that you all read the data out about h-BASE and sporadic CJD, GSS, blood, and some of the other abstracts from the PRION2007. ...
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744
*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OF POKER INDEED GOES UP. ...TSS
USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779
see full text 143 pages ;
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
From: "Terry S. Singeltary Sr." Sent: Tuesday, August 21, 2007 9:50 AM Subject: TWO MORE Nor98 atypical Scrapie cases detected in USA bringing total to 3 cases to date
Infected and Source Flocks
As of June 30, 2007, there were .....
snip...
One field case and one validation case were consistent with Nor-98 scrapie.
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
IN the February 2007 Scrapie report it only mentions ;
''One case was consistent with Nor98 scrapie.''
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/
(please note flocks of origin were in WY, CO, AND CA. PERSONAL COMMUNCATIONS USDA, APHIS, VS ET AL. ...TSS)
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=14553
An evaluation of scrapie surveillance in the United States
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=3427
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............
http://www.oie.int/eng/Session2007/RF2006.pdf
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Report to Congressional Requesters: February 2005: Mad Cow Disease:
FDA's Management of the Feed Ban Has Improved, but Oversight Weaknesses Continue to Limit Program Effectiveness:
[Hyperlink, http://www.gao.gov/cgi-bin/getrpt?GAO-05-101]:
http://www.gao.gov/htext/d05101.html
http://www.gao.gov/highlights/d05101high.pdf
January 2002 MAD COW DISEASE Improvements in the Animal Feed Ban and Other Regulatory Areas Would Strengthen U.S. Prevention Efforts GAO-02-183
http://www.gao.gov/new.items/d02183.pdf
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
####
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&P=720
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
http://www.upi.com/
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
BRITISH MEDICAL JOURNAL
SOMETHING TO CHEW ON
BMJ
http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2
BMJ
http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1
THE PATHOLOGICAL PROTEIN
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
INTRODUCTION
http://www.thepathologicalprotein.com/_wsn/page3.html
Yam Philip Yam News Editor Scientific American www.sciam.com http://www.thepathologicalprotein.com/
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...
http://www.cjdsurveillance.com/resources-casereport.html
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734.
http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535
JOURNAL OF NEUROLOGY
MARCH 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to
comment on the CDC's attempts to monitor the occurrence of emerging
forms of CJD. Asante, Collinge et al [1] have reported that BSE
transmission to the 129-methionine genotype can lead to an alternate
phenotype that is indistinguishable from type 2 PrPSc, the commonest
sporadic CJD. However, CJD and all human TSEs are not reportable
nationally. CJD and all human TSEs must be made reportable in every
state and internationally. I hope that the CDC does not continue to
expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in
the USA in both animal and man. CWD in deer/elk is spreading rapidly and
CWD does transmit to mink, ferret, cattle, and squirrel monkey by
intracerebral inoculation. With the known incubation periods in other
TSEs, oral transmission studies of CWD may take much longer. Every
victim/family of CJD/TSEs should be asked about route and source of this
agent. To prolong this will only spread the agent and needlessly expose
others. In light of the findings of Asante and Collinge et al, there
should be drastic measures to safeguard the medical and surgical arena
from sporadic CJDs and all human TSEs. I only ponder how many sporadic
CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
THE PATHOLOGICAL PROTEIN Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
Available online 29 July 2003.
Volume 3, Issue 8, August 2003, Page 463
"My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem." ............................
http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fulltext
http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf
ya'll gonna miss me ;-)...tss
PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase in ''TYPE UNKNOWN''. ...TSS
1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006,
26 from 2007)
http://www.cjdsurveillance.com/pdf/case-table.pdf
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 Posted by Terry S. Singeltary Sr. at 12:57 PM 3 comments:
Terry S. Singeltary Sr. said... Mr. xxxxxx,
I figured since you were studying this, i thought i might send you this too. i am sure it will be just explained off as another one of those strange coincidences, and i am just biased due to the circumstances i.e. the mom dod hvcjd card, i find it very interesting however that about the same time the atypicals were showing up, the feds were wanting to destroy decades of archives of brains samples of cjd victims and primate victims, donated for research $$$ i know its just another coincidence, and i am tainted/biased, but i thought i might send this to you if you were not aware of this factor. ...terry
Mad Cow Cover-Up: NIH Plans to Destroy Brain Samples of Humans Afflicted with Mad Cow-Like CJD
Steve Mitchell of UPI has been providing excellent, ongoing coverage of mad cow and its threats in the US. Here is his latest piece. One more strong piece of evidence of the cover-up ‹ it now deserves that label ‹ of mad cow risks here in the US under an administration beholden to big beef.
John Stauber -
NIH may destroy human brain collection http://www.washtimes.com/upi-breaking/20050323-053919-8481r.htm
Washington Times - Washington,DC,USA NIH may destroy human brain collection
By Steve Mitchell Medical Correspondent
Washington, DC, Mar. 24 (UPI) -- The National Institutes of Health may discard part or all of a rare collection that includes hundreds of human brain samples from patients that suffered from a disorder similar to mad cow disease -- unless another researcher or institution takes them on, United Press International has learned.
Several scientists said the collection, which is held by the NIH's National Institute for Neurological Disorders and Stroke in Bethesda, Md. -- and includes brains and other tissue samples from people afflicted with the brain-wasting illness Creutzfeldt Jakob disease -- is irreplaceable and could even provide insight into treatments for the fatal disorder.
Currently, there is no cure for CJD and patients typically die within a year after symptoms begin.
However, NIH officials in control of the collection's fate told UPI the remaining samples are of little scientific value and may be disposed of if researchers outside the agency do not claim it. That position stands in sharp contrast with CJD experts who thought the collection should be preserved.
"It's invaluable," said Dr. Paul Brown, former medical director of the NIH's Laboratory for Central Nervous System Studies, whose expertise is in CJD and mad cow disease (also known as bovine spongiform encephalopathy, or BSE).
The collection is badly in need of organization and no one is certain how many brains or other tissue samples it contains, said Brown, who worked with the collection since its inception in the 1960's until his retirement last year. There could be brains, blood, spinal fluid and various other tissues from 1,000 people or more, he said. Some of the specimens would be of scientific use today, he said.
"This collection has the unique value of stretching back to the beginning of when these diseases were discovered," Brown told UPI, noting that the first samples were obtained in 1963. "It would be as though you had in your hands the possibility of finding out when AIDS started."
Bruce Johnson, a former technician at the CNSS lab who worked extensively with the collection before he retired in 2003, told UPI he was told "in two years they (NIH officials)are going to destroy it, if nobody wants it."
Eugene Major, acting director of the basic neuroscience program at the NIH, said no specific timeframe had been established.
"We have not set a firm deadline date," Major told UPI. "We are working very hard with investigators that we know in order to be able to make sure that whatever we deem is valuable is potentially kept here." Some samples already have been determined not to have any research value and have been "removed and disposed of," he said.
Others samples have been given out to Dr. David Asher at the Food and Drug Administration and Pierluigi Gambetti at the National Prion Disease Pathology Surveillance Center in Cleveland, Ohio.
Major maintained the remaining collection was not particularly valuable for research. "Whatever had been collected here that has not already been distributed to responsible investigators who could use them really has very little remaining value," he said.
Neither Asher nor Gambetti returned phone calls from UPI, but Brown said he thought Asher had received only a dozen or two samples at most and Gambetti had not received much at all.
Neil Cashman, a brain-disease researcher at the University of Toronto's Center for Research in Neurodegenerative Diseases -- who has tried to obtain the collection from the NIH -- said it was priceless.
"It would be like destroying an art museum," Cashman told UPI. "There's all this information and insight that's locked up in these tissues and if it's destroyed it will be lost forever."
The Memorial Institute for Neurodegenerative Diseases Inc., a non-profit organization consisting of more than 40 university and institute researchers from the United States, Canada, United Kingdom and France, also thinks the brain collection is invaluable.
"It is the opinion of the Board of Directors ... of The MIND Inc., that the ... brain bank should not be broken up nor destroyed," said Harry E. Peery, MIND's executive director, in a letter to UPI. "We believe that this collection is of inestimable research value and should be kept intact."
The institute, at the University of Saskatchewan in Saskatoon, applied for possession of the collection in early 2004, but received a letter from the NINDS indicating the fate of the collection had not yet been determined.
"We have heard nothing further since that time" and continue to be interested in acquiring the complete collection, Peery said.
CJD belongs to a group of rare, brain-wasting disorders that are little understood, incurable and fatal. This includes mad cow disease in cows, chronic wasting disease in deer and elk. The most infamous of these illnesses in humans is variant CJD, which people can contract from eating beef products infected with the mad-cow pathogen.
Although vCJD has infected more than 154 people worldwide, only one case has ever been detected in the United States -- in a Florida woman who is thought to have contracted the disease while living in the United Kingdom. However, the NIH brain samples have never been screened for vCJD -- something Johnson thinks is critically important.
"No one has ever looked to see if any American (in the collection) in the past had variant CJD," Johnson said. "You think it would be required that they do that. You think it would be a Congressional mandate that they test these brains: 'Let's see if we've got this disease in our country.'"
Johnson noted at least one brain in the collection he personally had examined -- from a French woman collected in 1971 -- showed evidence of possible vCJD infection, but the sample needed further study to be sure.
Other samples in the collection include the brains of patients who were only 16 years old when they were diagnosed with CJD. This would be unusual for sporadic CJD, because generally it strikes those over age 60. Variant CJD, on the other hand, typically occurs in patients in their 20s or younger.
"I thought it was absolutely vital (to test these brains)," Johnson said. "Maybe there's a dozen cases in there of variant CJD."
Major disagreed. "There's really no reason to do that," he said. "The effort it would take to screen those samples ... would not give us any new insights into variant CJD beyond what it is we already know."
Johnson said he was frustrated with the NIH administration's lack of interest in preserving the collection or testing for vCJD. "They don't understand," he said, "they honest-to-god don't understand what it's all about."
Patient advocates also objected to the possible destruction of the brains.
Terry Singeltary, whose mother died of a type of CJD called Heidenhain variant in 1997, said he is outraged and families of other CJD victims probably will be, too.
"A lot of these families went through a lot of heartache and a lot of trouble to get these brain samples to the NIH," Singeltary told UPI. "Now they're just going to discard them because they're not of scientific use? That's just asinine. That stuff is valuable information."
Graham Steel, vice-chair of the Human BSE Foundation in the United Kingdom, told UPI, "The potential loss of such important tissue samples would be a massive blow for TSE (the group of diseases that includes CJD and BSE) research in the United States. This should not be allowed to happen."
Singeltary noted there currently is no cure for these diseases. "If you don't have any answers yet, why would you throw these specimens away?" he asked.
He added that more sensitive tests are just becoming available and could help determine the origin of some of the CJD cases. "We've all been sitting around waiting for more sensitive tests to get validated because we want answers," he said.
"You know, it must be an embarrassment," Johnson said. "Some Senator is going to eventually say 'What is NIH doing about mad cow disease?' And people are going to scratch their heads and say 'not much'." He added, "What's going to happen (is) one of these senators or their wife is going to develop spontaneous CJD one day and ... there's going to be hell raised and they're going to ask, 'Why isn't NIH working on this?'"
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E-mail sciencemail@upi.com
NIH sends mixed signals on CJD brains
By Steve Mitchell Medical Correspondent
Washington, DC, Apr. 7 (UPI) -- A National Institutes of Health official who told United Press International the agency might destroy its collection of brains from human patients afflicted with a condition similar to mad cow disease reportedly has told the head of a patient-advocate group the collection would be preserved.
The official, Eugene Major, acting director of the basic neuroscience program at the NIH, has not responded to e-mail or a phone call from UPI seeking clarification of his remarks, and the official status of the collection remains unknown.
As reported by UPI on March 24, the collection is stored in freezers by the NIH's National Institute for Neurological Disorders and Stroke in Bethesda, Md. It contains brains and other tissue samples from hundreds of people who died from the brain-wasting illness Creutzfeldt Jakob disease, as well as tissues from an untold number of experimental animals.
The consensus of scientists in this field is the collection, which dates back to 1963, is invaluable for research and could even provide insight into treatments for the fatal disorder. Currently, there is no cure for CJD and patients typically die within a year after symptoms begin.
Florence Kranitz, president of the non-profit advocacy group CJD Foundation, told UPI she had "a very long conversation" with Major, in which he told her the remaining tissues in the collection would not be destroyed.
"He reassured me in no uncertain terms," Kranitz said, noting constituents of the foundation and other CJD advocacy groups had been expressing concerns to her the tissues would be destroyed.
Kranitz, who has personal reasons for wanting the collection preserved -- her husband died of CJD in 2000 -- said she plans to meet with Major at the end of April to discuss the issue further.
CJD belongs to a group of diseases collectively known as transmissible spongiform encephalopathies, or TSEs, that includes mad cow disease in cows, chronic wasting disease in deer and elk, and scrapie in sheep. All TSEs are incurable and fatal.
Major previously told UPI some samples already have been destroyed and others have been given to researchers at the Food and Drug Administration and the National Prion Disease Pathology Surveillance Center in Cleveland.
Major said the remaining collection "has very little remaining value" and could be destroyed if another entity does not claim them.
Bruce Johnson, a former NIH scientist who retired at the end of 2003, said he had been told the collection would be destroyed in two years if no one took the samples from the NIH.
In response to hearing that Major had failed to confirm to UPI the brain collection would not be destroyed, Patricia Ewanitz, who lives in Port Jefferson Station, N.Y., and is founder of the advocacy group CJD Voice, said, "The brain tissue might not be indispensable to the National Institutes of Health but it is absolutely necessary to the families who thought enough of science to donate the brains, brain tissue and blood in hopes of someday finding an answer to why their loved one died."
Ewanitz, whose husband died of CJD in 1997, added, "It now seems like such a joke."
Terry Singeltary, whose mother passed away from a type of CJD in 1997, said the NIH should use the samples for scientific research, not just store them in freezers.
Both Singeltary and Ewanitz said they would feel more reassured if Major verified in writing the collection will not be destroyed.
"I would go further and ask Major what he plans to do with them," Singeltary said. "If the samples are just going to sit up there and go bad, then they should give them out to researchers looking for cause and cure."
The revelation the NIH might destroy part or all of the collection sparked an outcry from patient advocates, consumer groups and scientists.
Advocates have been contacting their members of Congress, urging them to investigate and prevent the NIH from destroying the brains. Consumer groups also have gotten involved and scientists have taken steps to obtain the collection or have urged Major not to destroy the samples.
Felicia Nestor, who serves as a consultant to Public Citizen, told UPI she had contacted certain legislators and at least one was considering looking into the situation. Nestor asked the legislator's name be withheld.
Kranitz said Major also told her he plans "to advertise in professional neurological journals and by whatever means necessary to make it known" to researchers in the field the tissues are available.
Major previously said, however, that efforts to inform researchers of the availability of the collection were already underway and included informing NIH grantees. He added he had personally notified researchers at scientific meetings, but no TSE researcher contacted by UPI was aware of this.
"I was never informed," said Laura Manuelidis, an expert on these diseases and section chief of surgery in the neuropathology department at Yale University. She said the first she had heard of the situation was in UPI's March 24 report.
Manuelidis also said she contacted Major, expressing interest in the specimens, but so far has not received a response.
"I sent a letter to (Major) on (March 25) about our interest in these specimens, but he has not replied," she told UPI in an e-mail.
Neil Cashman, a TSE expert at the University of Toronto, who said he was not aware the samples might be destroyed, has lobbied colleagues at the University of British Columbia -- where Cashman is scheduled to move to this summer -- to help draft a letter requesting the collection.
The Memorial Institute for Neurodegenerative Diseases Inc., a non-profit organization consisting of more than 40 university and institute researchers from the United States, Canada, the United Kingdom and France, requested the collection in January, 2004. So far, the institute has not been informed of a decision by the NIH.
Asked if Major had told him whether the collection would be preserved, MIND Executive Director Harry Peery said, "We have heard nothing further from Eugene Major or anyone else at the NIH regarding the brain collection."
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E-mail: sciencemail@upi.com
##################### Bovine Spongiform Encephalopathy #####################
NIH says it will preserve CJD brains By STEVE MITCHELL
WASHINGTON, May 31 (UPI) -- The National Institutes of Health apparently has reversed its position on the fate of an invaluable collection of brains from people afflicted with a condition similar to mad cow disease, saying in a letter to a U.S. senator it will not destroy the collection.
An NIH official had told United Press International previously that the brain collection, which consists of samples from hundreds of people who died from the brain-wasting illness called Creutzfeldt Jakob disease, could be discarded if another entity does not claim them.
That sparked an outcry from patient-advocacy groups, consumer watchdogs and scientists, and the agency now appears to have backed away from that course.
"All the brains and other tissues with potential to help scientists learn about CJD are, and will continue to be, conserved," Story Landis, director of the National Institute of Neurological Disorders and Stroke, which oversees the brain collection, wrote in a May 10 letter to Sen. John Cornyn, R-Texas.
Cornyn had inquired about the status of the collection in April.
Last March, Eugene Major, acting director of the basic neuroscience program at the NIH, told UPI the useful portions of the collection had been doled out to scientists and the remaining samples had "very little remaining value" and could be destroyed.
Landis could not be reached for comment Tuesday. NINDS spokesman Paul Girolami told UPI he had been unable to locate her.
Scientists think the collection, which dates back to 1963, is invaluable for research on CJD and similar diseases and could even provide insight into treatments. There is no cure for CJD and patients typically die within a year after symptoms begin.
"Absolutely, the collection is worth keeping," Bruce Johnson, a former NIH scientist who said he had been told the collection would be destroyed in two years if no one took the samples from the agency, told UPI.
The Memorial Institute for Neurodegenerative Diseases Inc., a non-profit organization consisting of more than 40 researchers from several countries, offered to take the collection off of NIH's hands more than a year ago and so far has not heard anything from the agency, Harry Peery, MIND's executive director, told UPI.
CJD belongs to a group of incurable and fatal diseases collectively known as transmissible spongiform encephalopathies, or TSEs, that includes mad cow disease in cows, chronic wasting disease in deer and elk, and scrapie in sheep.
Variant CJD, or vCJD, is a relatively new TSE, which people can contract from consuming beef products infected with the mad cow pathogen.
Despite Landis' assurance the collection will be preserved, some family members of the patients who donated their brains to the NIH are still skeptical. This is because the wording Landis used in the letter leaves open the possibility that some brain samples are being destroyed.
"The tissues that are discarded are those that have either decayed to an extent that renders them no longer appropriate for research or those for which we do not have sufficient identification," Landis wrote.
"Which ones" are being destroyed? asked Terry Singeltary, who is involved with several CJD patient groups.
"With a system like this, they could destroy whatever and whenever they wanted, for whatever reason they wanted," Singeltary, whose mother died of CJD in 1997, told UPI.
"It's a perfect excuse to discard some suspicious tissue resembling vCJD or some atypical TSE related to animal TSEs in the USA," he added.
Although the collection includes samples from CJD patients as young as 16 that could make them candidates for possible vCJD, the brains have never been screened for evidence of the disease. The only confirmed vCJD case in the United States occurred in a Florida woman who is thought to have contracted the disease in England.
Johnson said he along with renowned CJD expert Paul Brown were in the process of sorting through the samples to match them up with patient identification documents until they both retired. Some of the samples may prove impossible to identify, he said, but he and Brown are the only ones familiar enough with the collection to organize it and neither has been asked back by the agency to aid in the identification process.
Steve Mitchell is UPI's Medical Correspondent. E-mail: sciencemail@upi.com
Copyright 2005 by United Press International. All Rights Reserved.
http://washingtontimes.com/upi-brea...50800-6771r.htm
http://www.sciencedaily.com/upi/ind...s-cjdbrains.xml
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JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 April 26,2005 Mr. Terry SingeltaryP.O. Box 42Bacliff, Texas 77518 Dear Mr. Singeltary: In response to your recent request for my assistance, I have contacted the National Institutes ofHealth. I will write you again as soon as I receive a reply. I appreciate having the opportunity to represent you in the United States Senate and to be ofservice in this matter. Sincerely,
JOHN CORNYN United States Senator JC:djl
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JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 May 18,2005 Mr. Terry SingeltaryP.O. Box 42Bacliff, Texas 77518 Dear Mr. Singeltary: Enclosed is the reply I received from the Department of Health and Human Services in response to my earlier inquiry on your behalf. I hope this will be useful to you. I appreciate having the opportunity to represent you in the United States Senate. Thank you for taking time to contact me. Sincerely,
JOHN CORNYN United States Senate JC:djl Enclosure
DEPARTMENT OF HEALTH & HUMAN SERVICES National Institutes of HealthNational Institute of NeurologicalDisorders and Stroke NINDS Building 31, Room 8A52 31 Center Dr., MSC 2540 Bethesda, Maryland 20892-2540 Phone: 301-496-9746 Fax: 301-496-0296 Email: sll22c@nih.gov
May 10, 2005
The Honorable John CornynUnited States SenatorOccidental Tower5005 LBJ Freeway, Suite 1150Dallas, Texas 75244-6199
Dear Senator Cornyn:
Your letter to the National Institutes of Health (NIH) forwarding correspondence from Mr. Terry S. Singeltary, Sr., has been forwarded to me for reply. Mr. Singeltary is concerned about thepreservation of Creutzfeldt-Jakob disease (CJD) brain samples that have been maintained by theNational Institute of Neurological Disorders and Stroke (NINDS) Intramural Research programfor many years. I am sorry to learn that Mr. Singeltary's mother died of CJD and can certainly understand hisdesire that any tissues that could help investigators unravel the puzzle of this deadly disease arepreserved. I hope he will be pleased to learn that all the brains and other tissues with potential tohelp scientists learn about CJD are, and will continue to be, conserved. (The tissues that arediscarded are those that have either decayed to an extent that renders them no longer appropriatefor research or those for which we do not have sufficient identification.) The purpose of gathering these brains and tissues is to help scientists learn about CJD. To that end, some of the NINDS-held samples are distributed to investigators who can demonstrate thatthey have a compelling research or public health need for such materials. For example, sampleshave been transferred to NIH grantee Dr. Pierluigi Gambetti, who heads the National PrionDiseases Pathology Surveillance Center at Case Western Reserve University in Ohio and workswith the Centers for Disease Control and Prevention to monitor all cases of CJD in the UnitedStates. Dr. Gambetti studies the tissues to learn about the formation, physical and chemicalproperties, and pathogenic mechanisms of prion proteins, which are believed to be involved inthe cause of CJD. Samples have also been transferred to Dr. David Asher, at the U.S. Food andDrug Administration, for use in assessing a potential diagnostic test for CJD.
Page 2 - The Honorable John Cornyn
in closing, we know that donating organs and tissue from loved ones is a very difficult andpersonal choice that must often be made at the most stressful of times. We at the NINDS aregrateful to those stalwart family members who make this choice in the selfless hope that it willhelp others afflicted with CJD. We also know the invaluable contribution such donations maketo the advancement of medical science, and we are dedicated to the preservation of all of thetissue samples that can help in our efforts to overcome CJD.
I hope this information is helpful to you in responding to Mr. Singeltary. Sincerely,
Story C. Landis, Ph.D. Director, National Institute ofNeurological Disorders and Stroke ================================== END...TSS
SEE FULL TEXT where NIH wanted to destroy all CJD brains donated for research after BSE scandal broke in USA ;
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&P=12771
The cow in the 2003 case was born in Canada, but the last two -- ***found in Texas in June 2005, and Alabama in March 2006 -- were born and raised in the U.S. USDA scientists did not find any definite spongiform lesions on the brains of the Texas and Alabama cows. Also, abnormal forms of prion proteins -- which are thought to cause BSE -- were larger in these cows than those described in most European BSE cases, and they reacted differently to antibodies.
http://www.agriculture.com/ag/story.jhtml?storyid=/templatedata/ag/story/data/1150135629418.xml&catref=ag1001
tss
October 24, 2007 1:03 PM Terry S. Singeltary Sr. said... Subject: BSE TSE NORTH AMERICA THE REGULATORY POINT OF VIEW or the lack of Date: October 22, 2007 at 3:12 pm PST
=======================
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
Completely Edited Version
PRION ROUNDTABLE
pages 36 -53. ...tss
THE REGULATORY POINT OF VIEW
Dr. Linda Detwiler: I'm going to take a different approach. I'm going to talk about scientific findings and how they're pertinent and why they're important to regulatory policy. We know there have been about 150 deaths from variant CJD from 1986. These are very tragic indeed, however, there are a lot more deaths from the flu and other diseases, yet this is what's made headlines and created a panic.
The objective is to review the research significant to regulatory issues and what's know and—equally important—what's not known. We'll look at the BSE case in Canada and what happened there and what may have happened in their feed cycle. We'll look at implications for the US and possible next steps.
It's important for us to know the similarities, and equally important to know the differences. The differences between species for control purposes, eradication, and prevention are so critical. If you don't know the differences in regards to transmission, pathogenesis, etc., you won't be able to control the diseases appropriately. For example you cannot control Scrapie like you do BSE with a feed ban.
My mantra is that you have to remember these long incubation diseases with limits to the pre-clinical. You have to be thinking. If you knew the disease was going to be here tomorrow, what should you have done yesterday? If you wait until the first time you find the disease, you are years too late. You might be one incubation cycle too late or multiple incubation cycles too late. The population you're concerned with, be it cows or sheep or elk or humans, it's already been infected and you're just going to live out the clinical manifestation of the disease.
Prevention is best, but if you know it’s been introduced, what can you do to limit the transmission? Europe has had to play it out. The UK in 1988 put the ruminant-to-ruminant feed ban on, but they did not ban the total use. It's banned only for ruminants, so they had too much to use. It's not prohibited to go other places, so the meat and bone meal is sold to the continent. It dumps into France and starts to move throughout Europe. Add another five years incubation period, plus surveillance, and you see the manifestation of clinical detection in the Benelux countries.
Europe then started to restrict the use of meat and bone meal, and sale of it went on to other countries. There are a lot of countries that probably have received product, but are not doing surveillance. This is something the US needs to watch out for. We don't classify countries like we do for other diseases, like foot and mouth. For BSE, we'll stop trade if a country is not okay, which is just the opposite from the policy for foot and mouth. This is something the US needs to change. We need to evaluate the countries of the world. Canada has done this and Canada will trade only if the BSE risk is at an acceptable level.
We can't forget other animal species are susceptible, such as cats. Domestic cats and large zoo cats are susceptible to the BSE agent, as well as TSEs of exotic ruminants. If exposed to the BSE agent, bison are susceptible.
Why is the distribution of infectivity important for us? There are several reasons from a regulatory standpoint. If you know where the infectivity is, it helps you eliminate high risk tissue, especially ones that might be a zoonotic risk. That is, What tissues might be more infectious to humans if it’s a zoonotic disease or out of the rations of other animlas if they’re susceptible. Also, it provides direction as to what tissues you might target for diagnostic purposes. In natural cases of BSE, infectivity was in retina, brain and the spinal cord.
In the experimental challenges, calves were fed 100 grams of BSE-infected brain tissue. At certain intervals, some were sacrificed. Forty-some tissues from these calves were put into mice to be bio-assayed. The British were criticized, saying the mouse bio-assay is not as sensitive because of the species barrier, and that you should go back and repeat this in cattle—at least for the most important tissues. This study in cattle had actually generated some additional data { that is additional tissues where infectivity has been found}. The trigeminal ganglia, the dorsal ganglia, the distal ileum and the bone marrow were all from the original mouse pathogenesis study. Recently, tonsil has been found to have infectivity by a calf bio-assay.
Pre-clinically, the distal ileum was six months post-inoculation, and the tonsil was about 10 months post-inoculation. To date, cattle muscle samples have been put into mice and also back into cattle, and no infectivity has been found.
Scrapie infectivity has been identified in brain, spinal cord, tonsil, the peripheral lymph nodes, nasal mucosa, placenta, liver, and the length of the intestine from the esophagus to the rectum. Nora Hunter has published work where both whole blood and buffy coat were taken from sheep and inoculated back into sheep from New Zealand, and those sheep did come down with TSE.
Dr. Spraker: How did they demonstrate nasal mucosa?
Dr. Detwiler: Bill Hadwell collected nasal mucosa from Suffolk sheep and inoculated it into mice.
In baby ruminants, the cells of the distal ileum are a different cell type up until about nine months of age. The cell type is such that they allow the passage of large molecules to transported across the intestine. By about nine months, that function wanes. It's probably for colostral purposes, for colostral antibodies to transfer over. But some have asked if that's why there's an ease of transmission across the gut at a younger age. Horrigan's work at Mission, Texas, showed that after nine months, it appeared to be more difficult to transmit Scrapie. It may be there's a correlation with the change of cell types.
This is a chart I made for the OIE, the Office of International Epizootics to look at secretions and excretions in sheep and goats where, to date, no infectivity had been found in feces, urine, saliva, colostrum, milk and semen. Intra-cranial inoculation into mice resulted in no infectivity. But I want to point out that I don't think we should stop looking. Even with the blood. If you had asked someone prior to 2000 if infectivity was ever found in sheep's blood, he would have said "no," because work done to that time had not shown infectivity in sheep blood. But that work was all blood intra-cranially into mice. How much blood, feces and saliva can you put intra-cranially into a mouse?
Dr. Bartz: With BSE into mice, they estimated a 104 difference in sensitivity between the cow and the mouse.
Dr. Detwiler: How about nasal discharge? Is that a possibility for shed of the agent? We have to keep asking these questions, even for cattle. If it's in the lymphoid tissue of the distal ileum, the tonsil, or the lymphoid tissue of the third eyelid, would it not make sense that, at least at some low level, there might be some lymphoreticular distribution similar to the other animals with TSE. I think that's a valid question to ask, and the calf pathogenesis studies are not finished. I think we have to be careful definitively in saying it's limited to only two three peripheral tissues.
Dr. Detwiler: Dr. Prusiner is examing muscle from cattle with BSE, and looking for presence of PRP and probably infectivity.
Dr. Thornsberry: He's very concerned about muscle tissue.
Dr. Bartz: There's one comment I'd like to make on the muscle infectivity studies. We need to remember that a lot of these are taking a biopsy. If you take a biopsy of muscle, what's in that? It's obviously muscle cells, but it's also nervous tissue and LRS tissue. It's in a muscle homogenate, which is consumed, but the question remains what cell type in that homogenate is the agent really in?
Dr. Detwiler: I asked that of Dr. Prusiner. How did they ascertain that it was muscle cells versus nerve tissue, etc. He said they were very careful in how they took the biopsy.
Dr. Thornsberry: Doesn't every muscle biopsy have some neural tissue in it?
Dr. Detwiler: There's some innervation going to those muscle groups.
Dr. Detwiler: Parenterally, BSE does go into pigs. It was through three routes: intra-cranial, IV and IP with incubation times of 69 to 150 weeks. Seven out of 10 came down with BSE. Orally, it did not go after 84 months. It's important to note that infectivity was not confined only to the CNS, but also in stomach, jejunum, distal ileum and pancreas.
With chickens, both parenterally and orally, they did not find evidence of disease. They tried to sub-passage the chickens by taking brain from animals that had been exposed, to see if it adapted. I think you may have to do this multiple times. What the research in the UK did do was look at high-risk tissues from pigs and chickens that had been exposed to BSE, and put them into susceptible mice. Again, we have to be careful to say there's no residual infectivity at all. If continually fed to a species over time , there may be some kind of passage or adaptation over time. That's why, in other countries, they take out high-risk tissues and don't allow them to be fed at all. In Europe, they've gone to the extreme of taking out all animal tissue being fed to food-producing animals, to break this cycle.
Lateral Transmission
Scrapie and CWD spread animal to animal. In both embryo and semen studies, infectivity for transmission of BSE was not detected. Two cases of disease with fairly significant numbers have been caused by making vaccines from tissues from animals incubating the disease. Just recently, a Mycoplasma aglacia vaccine that was given to sheep and goats in Italy caused infection in 600 to 700 premises.
Contaminated feed appears to be the primary if not sole source of infectivity. Animals that are incubating the disease get slaughtered, rendered, and fed back to other cattle, and they get sick in an average of three to six years.
This is significant to me when we talk about the British attack rate studies. In this experiment, infected brain was given orally. One gram killed seven of 10, so the British knew that had to go down to lower doses. They've now looked at a tenth of a gram and a hundredth and a thousandth of a gram. This is still underway, but at about 60 months, a tenth of gram has killed three of 15 animals affected with BSE, and a hundredth of a gram has killed one of 15 thus far at a 50-plus-month incubation. It doesn’t take too much brain material. The British message is to not underestimate the possibility of cross-contamination in the feed cycle. In the United States we allow mills and plant to use the same equipment when processing ruminant and non-ruminant material. Although a system of cleaning is required by the FDA, the science questions how effective the flush methodologies could really be. The same trucks may haul ruminant and non-ruminant feeds. Those are potentials for cross-contamination.
Dr. Keller: What about risk from feather meal/poultry litter?
Dr. Detwiler: Feather meal can pick up infectivity from other feeds.
Dr. Keller: Whenever you feed a ruminant product to chickens and then the feathers/litter are collected, they're collecting the ruminant material directly in the spillage.
Dr. Detwiler: Hold on to that thought and I'll address it later. A big unknown for the whole world but important to answer involves sheep. BSE goes into sheep orally and maintains BSE characteristics. In research, it looks like Scrapie clinically and histologically. To date, the only valid way to differentiate BSE and Scrapie in sheep is a mouse bio-assay. Would it spread? If it does go naturally into sheep, would it spread like Scrapie through some kind of contagious nature? So far, the distribution of infectivity is looking identical to Scrapie. The significance of this is that the worst case scenario would be BSE in sheep naturally. You would have a potentially zoonotic disease that could spread from sheep to sheep and could not be differentiated from a common endemic disease, would have a widespread tissue distribution, peripheral nerve, blood, so no tissue of the sheep would really be safe. What would countries do if they found this? That's about 40 million sheep.
Dr. Bartz: Do you know if anyone is taking material from the BSE-infected sheep and inoculating non-human primates, to see if it looks like variant CJD?
Dr. Detwiler: It seems a good idea, but I'm not aware of it.
Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test.
There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don’t get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an ‘official’ test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren’t they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
Why Do We Do Surveillance?
Is the disease present? You absolutely have to do surveillance to find out if the disease is present. It will also tell you if your prevention has been successful. If you have the disease, it will also give you indication that your controls are working. That's how Britain knew the feed ban had a big effect. They continued to monitor disease and they saw it peak and they saw it come down about five years after the implementation of the feed ban.
You also need surveillance for buyer confidence and for trade confidence with our international partners. BSE is found in older animals, over 24 months of age, high risk, those exposed to contaminated feed, neurologically ill cattle, any fallen stock and emergency slaughter. This is important to collect samples through active surveillance as owners will sometimes miss subtle signs.
In regards to inactivation, Paul Brown did some work and had to repeat it because people didn't believe it. He found that, at 600° degrees Celius, there was survival in the ash. However, there was none in air emission or the residue. At 1000° Celius, he found no survival.
Canada has actually had two cases of BSE. The first was an imported case in 1993—a UK import. This animal had a broken leg, but because it was a UK import, the owner called the government veterinary staff and they had it looked it. The Canadians had to do extensive tracings on all their UK imports because of this case.
The native case was, of course, in May 2003. This animal was six years old, an Angus type, presented for slaughter as down with signs of pneumonia. It was condemned at slaughter, so it did not go for human consumption. The head was taken for BSE surveillance, and the rest of the carcass went to rendering. The 2003 animal was not related to any of the imports. Was it spontaneous, or was it a case of chronic wasting disease Epidemiologically, the animal was born in the spring of 1997 and was most likely infected at that time. Canada did import 182 head of cattle from the United Kingdom between 1981 and 1990, and there were 11 in the high-risk period, possibly incorporated into the animal feed chain. They also did a risk assessment, which showed they had a low risk of introduction.
They did trace-backs, and that helped to keep the public calm. There was no crisis. In fact, beef consumption went up in Canada. But they tried to find the herd of birth, which is really key in BSE. They narrowed it down to three herds, and all of these were put under quarantine. The cattle in those groups were pretty much depopulated.
When the positive animal was identified, CFIA did trace-backs, and that helped to keep the public calm. There was no crisis. In fact, beef consumption went up in Canada. But they tried to find the herd of birth, which is really key in BSE. They narrowed it down to three herds, and all of these were put under quarantine. The cattle in those groups were pretty much depopulated.
They do have a national ID system, but it had been in place for only two years. So they had to use other types of identification to trace back the animal. Subsequent to the depopulations, one herd was identified as the herd of birth.
One thing the OIE requires is that, for a country to resume trade in animals and animal products, they should depopulate progeny if it's a BSE-infected cow, along with birth cohorts. They had to depopulate over 100 head in these trace-forward herds.
The positive cow itself went to the slaughter plant and was condemned. The head went to the lab and the remaining carcass went to a renderer. From the renderer, the material could have gone to three farms. Two of these were poultry farms. The poultry farms also had cattle, and there was an admission that the cattle were fed the same material as the poultry. Again this is prohibited by the feed ban, but it happens on the farm. These three farms were depopulated in their eintirety.
This renderer did not have dedicated lines, so he made ruminant feed and non-ruminant, prohibited and non-prohibited. They used a barley flush. After the positive cow was processed, the barley flush went to one of these farms and could have been fed to cattle. That was another breakdown in the feed system. That's not supposed to happen, but it did.
It went to two pet-food plants. Material from the renderer at the time the animal might have been processed also went to a feed mill that had 1800 clients, but none of these was depopulated. There were violations. The message is that there are not a lot of resources for checking on-farm compliance with the feed ban. The rubber hits the road on the farm.
I already talked about the epidemiological investigation, the trace-forwards and the trace-backs. CFIA depopulated 2700 animals. They tested approximately 2000 of those. They also brought in an international review team made up of scientists from Switzerland, the US and New Zealand, who reviewed the epi investigation and found it to be thorough and complete. They made recommendations that Canada really had to get an SRM ban to take the high-risk materials out of the human good chain now. Canada has done that.
The committee told CFIA they needed to increase surveillance which examined high risk cattle in large numbers. The review team also said they had to find mechanisms to prevent this cross contamination in the animal food chain. Take out high-risk materials from the animal food chain period. Have dedicated mills, plants, etc.
The media was kind. There was no panic. However, rendering, slaughter and the producer level impacts are still significant. Initially, there was no place for the meat and bonemeal to go. The whole system started to back up. The renderers couldn’t sell it, so they filled their silos. The feed-mills filled their silos. They stopped slaughtering older cows because the system couldn’t take any more. The government started to help, and some things started to go to landfill. Canada did put the SRM ban in place for public protection, but not yet for a nimals. CFIA is working on increasing surveillance, and they need to look at changes in the feed rule.
More Surveillance
North America needs Canada to increase surveillance. Right now, it's a black box. We need to know if it's a single, isolated case or not. With the way BSE works, that's not likely. Or are the ones that were exposed dead and long gone? If there were to be more cases, how many? And very important, if there are additional cases, how old are they? If they were all born prior to the feed ban, that lets us know the feed ban has been very effective. If not, we have had leaks. This year (2003) for surveillance in Canada, they'll come to about the same level they had last year, about 3700 brains tests. They really need to kick this up. The recommendation by the international committee and even by their own government is up to the level of about 40,000.
Think about the whole task of on-farm compliance. You have hundreds of thousands of farms. How do you get 100% compliance? That's very difficult. You can’t be on all farms at all times. My philosophy is choke infectivity out high. If you take your infectivity out of the system at the highest point, what leaks through on the farm won’t matter. Take your high-risk material, your brains and spinal cords and your deads and downs, and get them completely out of the animal food chain. If people inadvertently feed the wrong material on the farm, it won't have the infectivity to keep the cycle going.
It doesn’t take much to introduce BSE into a country. Identification is extremely important. We don’t have a national ID system in place. We're moving in that direction, but how about if tomorrow we found a case of BSE here and we couldn't trace it back? We couldn’t stand up in front of the American public and say, "We don’t know where this animal came from." What would be the reaction?
Disposal itself can cause emergency situations and we need an infrastructure—not only for TSEs but for all animal diseases. The US and Canada both need some kind of infrastructure for proper animal disposal, for animal health and public health reasons.
Can it happen here in the US? Would we find it? To me, we could not have been more fortunate. We got a warning shot right in our neighbor's back yard. We now know that before May 20, we thought we had escaped the bullet of the agent coming to North America. May 20 showed us we were wrong. We know the agent entered North America in the indigenous population. We now have time to re-evaluate the risk, to look the lessons not only in Canada, but around the world. We can do it without having this crisis upon us.
We have import regulations, feed bans, etc. We've had import regulations in place since 1989 on live ruminants and ruminant products. This shouldn't be down-played. This is significant. Look at the way it spread through Europe. That was from imports of high-risk products.
Surveillance: We've looked at all the groups you're supposed to look at for BSE in all the high-risk categories of the downers, etc. We've looked at about 20,000 for the last two years. We should go higher. We've had the same feed ban date as Canada. We do have a few different exceptions.
We've done formal risk assessments—one by the USDA, one by the European Union, and one by Harvard. Harvard's assessment was the most extensive. They looked at the potential pathways. They found that ,although US is resistant to BSE, there is still a potential for a low animal and human exposure. We still allow the use of high-risk material in the US—brain, spinal cord, and advanced meat recovery. Advanced meat recovery is the process where the bones will go through a machine to remove more muscle tissue. The allows some potential exposure if you have BSE infectivity in the system because the spinal column (even if you remove the spinal cord) still has dorsal ganglia that could be incorporated into AMR. That can still introduce infectivity into the AMR product.
Harvard found the feed ban is key to protection and that the leaks will allow amplification, at least in pockets. Why is the risk not zero? Science, trading patterns, existing regulations and human error all constitute a risk. The US, like Canada, does not have dedicated facilities or transport.
The UK imports into the US. There were 496 total, and 173 of the UK imports could have entered the US feed system. People don't like to hear this, but it's possible that one of the UK imports in the US entered the animal feed system and was exported to Canada. That's a possibility, because they import 50% of their feed from the US.
From 1994, we imported 11 million head of cattle from Canada. Most of these were feedlot animals for slaughter, but there were about 500,000 breeding animals. A number of Canada’s cull cows were slaughtered here and could have introduced infectivity into our system. Even today we have Canadian imports in the country, breeding animals that were brought in prior to the ban and reside here.
We have feed ban exemptions: plate waste, poultry litter. We still allow that if it comes off a human plate, or if it's trimmings, it can be palletized and fed to ruminants. That might be a small amount, but it could allow spinal cord in certain cuts to be fed back to ruminants. Poultry litter or feather meal could be significant. Poultry is getting quite a bit of ruminant material in the US because it cannot go back to ruminants. Poultry and pigs are getting a substantial amount. Poultry litter is not only what passes through the chicken, but think about how chickens eat. They spill a lot on the floor. That stuff is still allowed to be fed back to cattle. That's a direct break in the ban, except that it's legal. Ruminants are getting ruminant material.
Unfiltered tallow: tallow is a lipid material. However, if it's not filtered, there are protein residues. That's meat and bone meal. That's allowed to be fed, so that's another legal exception where you can feed ruminant meat and bone meal through unfiltered tallow. We don't have an SRM ban and the 40 animals are the ones that if you have the agent, they introduce the most infectivity back into the animal food chain when they're rendered.
What's our on-farm compliance? We really don't know.
Dr. Thornsberry: What about blood meal?
Dr. Detwiler: Although there's not been infectivity found in cattle blood, the one thing we have to be concerned about is the stunning method. You can have micro-emboli of brain material in blood, and we do allow the legal feeding of blood meal. You could have a contamination from these emboli. Also the brain drips into the blood.
In the past a stun gun that injected air into the cranium had been used. It was so high pressure that it scrambled the brain, pushed it through the foramen magnum, rippled the spinal cord and went down into the azygous venous system. Big parts of the brain and spinal cord were being found in the heart, the lungs, the liver. The industry has gone away from using this stun gun, but there's no regulation that prohibits it.
Firewalls
Identification and traceability aren’t going to stop the disease, but they are essential for locating herd cohorts and identifying other animals that may have been exposed. OIE requires birth cohorts and progeny of a BSE positive cow to be removed.
Canada implemented what the international scientific committee told them to do: they're taking all these tissues out of the food supply for people. You can't remove the dorsal ganglia, the trigeminal ganglia out of the bony tissues so you have both the skull and veretabral column be SRM. The distal ileum is coming out of all ages.
AMR is one thing the US needs to look at. It's a wide dissemination of nervous tissue in the meat product, especially if the process is not done correctly. Even if you remove the spinal cord, you still have the dorsal ganglia associated with the vertebral column and the dura that protects the spinal cord. It would be prudent for the government to move now on restricting ARM.
Harvard's first model did 1000 runs and found the mean ID-50s to humans was 35. Eleven of these were from brain and spinal cord. Twenty—more than half—were from AMR. In the recent runs with Canada, they had some where the ID-50s were up in the hundreds and, in the worst-case scenario- over 1000. Half of those were from AMR. So even if you remove brain and spinal cord from the human food chain, AMR will still deliver more potential doses of infectivity to the public than brain and spinal cord combined.
Dr. Bartz: Exactly what is AMR? Why does it increase infectivity?
Dr. Detwiler: You put the vertebral column through a machine that beats everything off of it.
Dr. Bartz: So you’re saying that if you pull out the spinal cord, when it goes through the ARM, it's pulling off DRGs and the dura.
Dr. Detwiler: And then that gets incorporated into ground beef and it's widely disseminated. In the United States, food has to be labeled. You wouldn't go to a store and buy something that had brain and spinal cord in it. It would have to be labeled so you would know you were eating it.
Dr. Thornsberry: I don't remember the percentage, but it was over half of all advanced meat recovery material we were manufacturing was going into the commodity-type systems.
Dr. Detwiler: That doesn't have to be labeled AMR, so you don’t know what's in and what's not. That could be incorporated into any mixed meat product. The public would feel betrayed and they wouldn't know what products to avoid because of the labeling requirements. McDonald's has never allowed it in their product, even before BSE risk. They continue to not allow it. I don’t know about the other fast-food chains.
Dr. Thornsberry: It looks like a paste. It doesn't have a consistency and it's got a lot of water in it. It's a paste of junk. You combine that and make a sausage or a salami. The average person wouldn't get a piece of AMR meat, but might get some specialty meat that had AMR in it.
Dr. Detwiler: If it's in ground beef, it has to be done in a smaller percentage. It technically could, in a lower percent, go into some ground beef. Some of these large dairies are looking for protein sources and they mix their own on-farm. Two practitioners in California told me their dairies are feeding pet food. What goes into pet food? A lot of the down cows. It never crosses their mind that this could be ruminant material.
The 4D risk is significant. In the Harvard study the model showed that if BSE was circulating in the cattle production system, 1500 ID-50s would come from healthy cattle at slaughter, and 37,000 from the 4D. Think about it. If a cow dies from BSE it is at the end stage disease where the level of infectivity is highest. If there are leaks in the feed ban, this population re-introduce the highest level of infectivity back to your cattle population.
Dr. Spraker: What are the four Ds?
Dr. Detwiler: Dead, dying, down, diseased. They're a lump sum of the animals that don’t make it for human consumption.
LESSONS LEARNED
We have to be careful that the absence of evidence is not evidence of absence, and when we say there's absolutely no scientific evidence. We need to be very careful when we talk to the public, and even producers, to make sure there is scientific evidence, and if there's not, to tell that to the public. A case in point is the UK with the link to human disease. In 1989, some experts said that there was absolutely no scientific evidence that the disease could go to humans. That was a correct statement then, however, it was not the entire story. What should have followed was that there is no evidence to definitively state that BSE could not cross species. The bottom line was that we don’t have much evidence period. We have to be careful of predictions from TSE’s in other species, as these long incubations dieeases are like wolves in sheep’s clothing.
Prevention with adverse action or significant cost is very difficult to sell. I spent my whole career with APHIS trying to sell prevention—first with Scrapie and then with BSE. If BSE didn't go to humans, I don't think we'd ever have sold the feed ban. Now the industry is glad we did. Failure to prevent is an easy target, but how do you measure success? Regulations: if people believe it will protect them, you don't need much compliance. If people aren't cognizant or don't realize how it will protect them, you need a lot of compliance. Driving is a good example. People believe seat belts will at least reduce fatality. You don't need a cop in your car to wear your seatbelt. But speeding is a different story. How many people drive the speed limit? By statistics, the higher the speed limit, the more you increase your chance of fatality. We need to know how much your producers and clients believe in the feed ban.
Disposal: positive solutions for one problem may create more expensive problems. It's easy to say "ban everything," but then what do you do with it? That's something we need to educate the public on. It's not as easy as it appears. You create environmental problems.
Dr. Keller: Do you know what they're doing with the rendered product? We heard at one time they were using it in the UK to make asphalt.
Dr. Detwiler: There are a lot of different things now. Some places are combining it with concrete and asphalt because it's a binder. Most of it gets rendered first and then the rendered material is used. They're using it as a fuel source—the meat and bone meal and the tallow. The tallow, apparently, burns well. Some of the rendering plants in California converted their systems when energy prices rose and ran off their own tallow. There's a cement company in the US that wants to burn meat and bone meal in their kilns. Temperatures will go up into the thousands of degrees. Regaining scientific credibility and public confidence may require extreme measures. That's why I think it's so important for the countries not to lose public confidence. Japan lost it, and they've had to take extreme measures, like testing every cow for human consumption.
Dr. Thornsberry: Two years ago, I worked as a consultant in Missouri and I had a couple of clients who owned large swine operations. They were cleaning out their swine feed bins and feeding it to their cows. They were feeding for a large corporate entity, and that entity would remove a group of hogs and they might leave two or three tons of hog feed. The hog feed contained meat and bone meal. It wasn't a real high level. Sometimes it was porcine meal and sometimes it was bovine, but it was in there. I got in contact with the state veterinarian and it went up to the FDA level concerning the feeding of this and the feeding of poultry litter. I asked if they'd made any rulings about the feeding of poultry litter because I knew that 5% of our feed is lost without ever being consumed. The FDA veterinarian’s comment to me was, "Dr. Thornsberry, until there are dead bodies lying in the street, you will not see a change made on the feeding of poultry litter." I said, "You know there's a potential epidemiological link between the spread of this disease and the feeding of poultry litter, and you're telling me you have to have dead bodies before you make a ruling on it."
He said yes. What's going on with our government?
Dr. Thornsberry: We need to put the pressure on.
Dr. Detwiler: That's right, and there are different entities that are saying this to the government. The Food Marketing Institute, the chain restaurants, do have a position statement they've put together that say they'd like to see the exemptions gone. They feel there are reasons to close the loopholes.
Dr. Thornsberry: I got a memo this summer that Canada agreed not to use AMR from that point on, but it is not prohibited in Canada.
Dr. Detwiler: Right, and that's crucial. Vertebral column is considered a risk material and it cannot be used. The United States has not done that. We're testing products to see if evidence of nervous tissue can be found, but that's not every product. It's done on a random basis by FSIS. We are still allowing AMR.
THE STATE REGULATORY VIEWPOINT
Dr. Keller: My focus is mainly on questions I have from a state perspective. Although I had about 10 years of veterinary practice experience, my education, with respect to prions, began when I started working for the State of North Dakota in ~1997. Serving as ND’s Designated Scrapie Epidemiologist (DSE) and working with their mandatory Chronic Wasting Disease (CWD) surveillance program, has further increased my appreciation for regulatory challenges associated with TSEs.
Recently, state animal health officials have had the task of drafting comments for the proposed BSE rule, which attempts to address ‘minimal risk countries.’
Background: In ND, the North Dakota Board of Animal Health is charged with protecting the health of domestic animals and also non-traditional livestock. In our state, that includes everything from captive birds to farmed cervids, to lions and tigers and bears. When in a state regulatory position, these responsibilities are not optional, they are required of animal health officials by statute. We are also to prevent escape and release of animals injurious or competitive with agriculture, horticulture, forestry, and other natural resource interests; thereby addressing potential environmental concerns.
We're also charged with taking any steps necessary to control, suppress, eradicate, any and all contagious and infectious diseases. Since prion diseases are indeed considered infectious, they fall under that statute. The State Veterinarian also has the responsibility, if warranted, to quarantine domestic animals and non-traditional livestock. He is to regulate and prohibit arrival or departure from our state of any animals that may be exposed or infected with the disease. Where this could get interesting, is when a state doesn't think the federal regulations are protecting the state’ s animal health or is not responsive enough in addressing urgent concerns. Also, it is very difficult trying to regulate prion diseases when you have limited ‘official live animal tests’ available, such as are available for TB and Brucellosis where you can get more definitive answers quickly. In that situation, prevention is always the best policy.
The industry groups and state agencies need to have a clearer understanding of the prion agent, its pathogenicity, and how it's transmitted so that more useful comments can be submitted on proposed rules.
We need to be concerned about what is an ‘acceptable risk’ of having possible disease transmission to other animals. We also cannot over look the economic damage done by diseases. Look at what one case of BSE did to Canada from an economic standpoint! Another area of responsibility we are charged with, is addressing zoonotic diseases. BSE is one prion disease that is currently considered to be zoonotic.
We have zero tolerance in this country for fecal contamination of our food, so what are we going to determine is an ‘acceptable risk’ for BSE contamination? And if we do allow animals in from countries where there is a risk, what are the mitigating factors or measures that need to be taken? It is my opinion that we need to have extensive measures in place to prevent the introduction of the disease and to maintain the identity of animals from other countries, even if they are only considered to be of ‘minimal risk’.
When we talk about identifying a country as minimal risk because they've had only one case, could this then be extrapolated to other countries? We may end up comparing apples and oranges though. For example, if we have a country in Europe that has one case of BSE, it's not really the same because it's on a different continent with different neighbors. We may not even be fully familiar with the extent of their country’s animal movements or the quality of their surveillance.
Dr. Detwiler: That's a very good point. This rule will allow other countries to apply for minimal-risk status, and I can tell you there are countries other than Canada that have only one case—Greece, Austria, Finland—that have much higher surveillance levels and have had measures in place a lot longer. So this is a reality that this situation could happen.
Dr. Keller: Those countries are watching the situation closely and may be waiting to make their application should the proposed BSE rule be approved as is. So what would happen if the US found one case of BSE? In our department, there would be immediate attention to what we would say to the producers and to the consuming public. We would need to have factual information available to address food safety concerns. How would we do that? We would need to be able to say we were doing a thorough epidemiologic investigation, and quickly get information back to consumers and our international trading partners as it became available. Two critical actions need to be done: country of origin labeling through maintenance of import identification of live animal and products and identification of individual animals. Another question that needs to be posed is which is easier and more cost effective to do first? There is identity on animals that come into this country, but when we've looked into that, there's no requirement for anyone to maintain that identity. In the past, this country has relied on the use of the brucellosis tags, auction-market back tags and brand inspection. But this does not allow for complete tracking of animals. Especially as the Brucellosis program winds down. There is an obvious need for individual animal identification.
The tattoos that have been suggested as a way to track animals long-term are not a fail-safe method. Everyone has their own idea of what a tattoo should be, what type of ink to use, etc. The reality is, you could have a very good tattoo but it’s not user-friendly. We'd have trouble getting compliance if we asked feedlots to rely on running every animal through a chute to read a tattoo. Running multiple animals down an alley and using RFID readers to collect their information as they run by, might be a workable system. A second form of ID will be needed in case of ID failure.
What's the international standard when we talk about BSE? OIE does not necessarily require seven years since the last case before you can move animals, but OIE has certain requirements for regions to qualify as minimal-risk regions in countries where BSE was identified fewer than seven years ago. For a minimal-risk zone or in a country, these are the things that have to be done: It has to have been based on fewer than one case per million during each of the last four consecutive 12-month periods, within the cattle population that’s over 24 months. These are very specific requirements. Whenever we talk about being consistent with OIE, we really need to consider that, since other countries usually recognize the status assigned by the OIE.
What are the consequences of being more lenient than international standards? It could be used in the marketplace against us and thus lead to a loss of consumer confidence. Other countries would be quick to speak up if they have more stringent standards in avoiding SRMs. When we have a case, it may become a marketing tool for another country.
When our standards are lower, we tend to be the country that would be exposed to the movement of animals that are at risk for bringing in BSE. We could have a ripple effect where we would have loss of consumer confidence, loss of markets, and devastation to the US cattle industry. If we have another country that's not using SRM and we're looking at identifying that country as a minimal risk area, but we bring in animals that they're not using SRMs from, and the US is still allowing use of SRMS, will that not possibly affect consumer confidence in this country or give our trading partners a reason to question the rationale?
Dr. Detwiler: How about the animals we have now? As I mentioned, if breeding animals were north of the border and they went to slaughter like the cull dairy cows, they'd have their SRMs removed to protect the Canadian public. Below the border, those same animals do not have their SRMs removed.
Dr. Keller: I agree. The number of Canadian birth cohorts you refer to that have entered the US is significant and has not yet been addressed by APHIS. There again, another country could be quick to point out the lack of attention by our epidemiologists to that group of animals, should we ever have a case of BSE in a US born and raised bovine. The main point is that we need to have a standard. The list of SRMs has expanded through research, and I think we’re hearing today that it’s possible even more SRMs may be added. Whatever the list of SRMs is, it needs to be consistent among countries, and the OIE needs to define what the SRMs are.
Obviously there's going to be resistance to taking additional precautions due to costs, but the costs will be even greater and farther reaching if we don’t. We need to be proactive on this issue, not reactive.
The feeding of feather meal is also a major concern. Does feather meal risk increase when you’re moving animals in that are from minimal-risk countries? I believe it would be a potential route of amplification of the prion in our ruminant feed supply. The Harvard Risk Assessment warned against it.
Dr. Schuler, the ND State Veterinarian discovered that in the proposed BSE rule, where they use the terminology "designated feedlot," that it means only the feedlot name listed on a health certificate. It does not mean that the animals going to a designated feedlot are actually going to go to slaughter immediately under a verified protocol. When animals from another country go to a designated feedlot, there's nothing to prevent their tags from being removed and animals being deviated out of the slaughter channel they were originally intended for.
Dr. Detwiler: How did they ever identify what animals ___________________
Dr. Keller: That's a very good question, and it goes back to "what is a designated feedlot?" and "why doesn’t the ID have to be maintained on those animals?" Actions must be taken to address the need for maintenance of ID.
Dr. Thornsberry: We're required in the state of Nebraska to write on the health certificate that these animals are for feeding purposes only and must go to slaughter. But that doesn’t mean that they do.
Dr. Detwiler: A lot of the feedlots will come in and remove the ear-tags and put their own lot tags in order to make a consistent lot, so you lose that ID. That was a problem when the US wanted to investigate what animals were already in feedlots. There's no regulation for that animal to retail that ID.
Dr. Thornsberry: I thought there was, for disease control.
Dr. Detwiler: There might be for Mexican steers, but not others.
Dr. Keller: Most people are not aware that all state animal health officials know from the health certificates, is the first point of destination. For example, feedlot heifers might be brought in from another country and when the feedlot manager discovers some of them are bred, they may be pulled out to be sold as breeding animals and no one may ever know.
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FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
The roundtable presentations and discussions were recorded. A transcript will be made available to the Academy of Veterinary Consultants, the American Association of Bovine Practitioners, and the Colleges of Veterinary Medicine throughout the United States and Canada. A condensed version translated for the livestock industry will be made available to educate livestock producers about prion related diseases.
http://www.r-calfusa.com/Newsletter/2004January.pdf
2005
National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC) Testing Summary
The BSE enhanced surveillance program involves the use of a rapid screening test, followed by confirmatory testing for any samples that come back "inconclusive." The weekly summary below captures all rapid tests conducted as part of the enhanced surveillance effort. It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing.
http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html
*** Suppressed peer review of Harvard study October 31, 2002 ***
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
Owens, Julie From: Terry S. Singeltary Sr. [flounder9@verizon.net] Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006
Greetings FSIS,
I would kindly like to comment on the following ;
[Federal Register: July 12, 2006 (Volume 71, Number 133)] [Notices] [Page 39282-39283] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr12jy06-35] ----------------------------------------------------------------------- DEPARTMENT OF AGRICULTURE Food Safety and Inspection Service [Docket No. FSIS-2006-0011] Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Update; Notice of Availability and Technical Meeting
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http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-10928.htm
MY comments/questions are as follows ;
1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught with error after the PEER REVIEW assessment assessed this fact, how do you plan on stopping this from happening again, will there be another peer review with top TSE Scientist, an impartial jury so-to-speak, to assess this new and updated Harvard BSE/TSE risk assessment and will this assessment include the Atypical TSE and SRM issues ?
*** Suppressed peer review of Harvard study October 31, 2002 ***
http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf
2. WITH A RECENT NATION WIDE MAD COW FEED BAN RECALL in the past few months that consisted of some 10,878.06 TONS, then another Mad Cow feed ban warning letter in May, IT should seem prudent to ask why our feed bans continue to fail in 2006, and continue to fail today ?
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full text 98 pages ;
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
http://madcowtesting.blogspot.com/
PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase in ''TYPE UNKNOWN''. ...TSS
1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, *** 26 from 2007)
http://www.cjdsurveillance.com/pdf/case-table.pdf
USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN
18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.
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64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.
Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.
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http://www.seac.gov.uk/minutes/95.pdf
3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse
Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University
Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years.
***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***
6:30 Close of Day One
http://www.healthtech.com/2007/tse/day1.asp
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...
http://www.cjdsurveillance.com/resources-casereport.html
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
or this ;
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
####
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
What Do We Feed to Food-Production Animals? A Review of Animal Feed
Ingredients and Their Potential Impacts on Human Health
Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker1 1Johns Hopkins Center for a Livable Future, Bloomberg School of Public Health, Baltimore, Maryland, USA; 2Maryland Institute for Applied Environmental Health, College of Health and Human Performance, University of Maryland, College Park, Maryland, USA; 3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA
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Table 1. Animal feed ingredients that are legally used in U.S. animal feeds
Animal
Rendered animal protein from Meat meal, meat meal tankage, meat and bone meal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products
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Conclusions
Food-animal production in the United States has changed markedly in the past century, and these changes have paralleled major changes in animal feed formulations. While this industrialized system of food-animal production may result in increased production efficiencies, some of the changes in animal feeding practices may result in unintended adverse health consequences for consumers of animal-based food products. Currently, the use of animal feed ingredients, including rendered animal products, animal waste, antibiotics, metals, and fats, could result in higher levels of bacteria, antibioticresistant bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting animal-based food products intended for human consumption. Subsequent human health effects among consumers could include increases in bacterial infections (antibioticresistant and nonresistant) and increases in the risk of developing chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide range of potential human health impacts that could result from animal feeding practices, there are little data collected at the federal or state level concerning the amounts of specific ingredients that are intentionally included in U.S. animal feed. In addition, almost no biological or chemical testing is conducted on complete U.S. animal feeds; insufficient testing is performed on retail meat products; and human health effects data are not appropriately linked to this information. These surveillance inadequacies make it difficult to conduct rigorous epidemiologic studies and risk assessments that could identify the extent to which specific human health risks are ultimately associated with animal feeding practices. For example, as noted above, there are insufficient data to determine whether other human foodborne bacterial illnesses besides those caused by S. enterica serotype Agona are associated with animal feeding practices. Likewise, there are insufficient data to determine the percentage of antibiotic-resistant human bacterial infections that are attributed to the nontherapeutic use of antibiotics in animal feed. Moreover, little research has been conducted to determine whether the use of organoarsenicals in animal feed, which can lead to elevated levels of arsenic in meat products (Lasky et al. 2004), contributes to increases in cancer risk. In order to address these research gaps, the following principal actions are necessary within the United States: a) implementation of a nationwide reporting system of the specific amounts and types of feed ingredients of concern to public health that are incorporated into animal feed, including antibiotics, arsenicals, rendered animal products, fats, and animal waste; b) funding and development of robust surveillance systems that monitor biological, chemical, and other etiologic agents throughout the animal-based food-production chain “from farm to fork” to human health outcomes; and c) increased communication and collaboration among feed professionals, food-animal producers, and veterinary and public health officials.
REFERENCES...snip...end
Sapkota et al. 668 VOLUME 115 NUMBER 5 May 2007 • Environmental Health Perspectives
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf
Brief review on the epidemiology of transmissible spongiform encephalopathies (TSE) Marcus G. Doherr Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bremgartenstrasse 109a, P.O. Box 8466, 3001 Bern, Switzerland Received 25 June 2006; accepted 30 October 2006 Available online 13 November 2006
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As a consequence of the studies linkingMBM use in cattle feed to BSE, the inclusion of MBM into ruminant feed was banned in the UK in July 1988, and in Switzerland in December 1990. These bans in both countries resulted in a significant reduction of new infections in cattle born after their implementation, thereby highlighting the importance of controlling this exposure route [34].However, the relatively large number of BSE cases born after those bans indicated that, despite the feed ban in place, BSE infectivity — to some extent – was still reaching cattle. These cases, subsequently denoted as born-after-the-ban (BAB) and born-after-the-reinforced (UK in 1996) ban (BARB), documented the presence of other infection routes besides direct (legal) inclusion of MBM in cattle concentrates. Cross-contamination of cattle feed with feed for pigs and poultry during production, transportation or storage, and cross-exposure of cattle to pig or poultry feed on mixed-species farms were suspected as additional routes [35–37]. More recently, insufficiently heated bone meal and tallow used in concentrate feeds and milk replacers has been suggested as an additional source of BSE infectivity [38,39]. The measures such as the MBM bans currently implemented in Europe, as shown by intensive surveillance with over 40 million animals (clinical suspects, emergencyslaughtered and fallen cattle as well as healthy-slaughtered adult cattle) tested between January 2002 and September 2005, have resulted in a constant decline of the BSE epidemic at least in the old EU member states (Fig. 2) [18]. It is to be expected that the epidemic will phase out in countries with sufficiently implemented control measures. This, due to the long incubation time of the disease, will require time.
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October 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE
http://www.phxnews.com/fullstory.php?article=53149
http://www.fda.gov/cvm/BSE1007.htm
* GAO-05-51 October 2004 FOOD SAFETY (over 500 customers receiving potentially BSE contaminated beef) - TSS 10/20/04
October 2004 FOOD SAFETY USDA and FDA Need to Better Ensure Prompt and Complete Recalls of Potentially Unsafe Food
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Page 38 GAO-05-51 Food Recall Programs To examine the voluntary recall of beef products associated with the December 2003 discovery of an animal infected with BSE, we analyzed the distribution lists USDA collected from companies and the verification checks it conducted to develop a diagram illustrating the location and volume of recalled beef that reached different levels of the distribution chain. We compared the distribution lists and verification checks to identify how many customers listed on the distribution lists did not receive the recalled beef and the number of customers not listed on distribution lists that received the recalled beef. We interviewed USDA and FDA staff involved with the recall to understand the timing of recall actions and the challenges encountered during the recall. To develop information on the 2002 recall of ground beef by a ConAgra plant in Greeley, Colorado, we reviewed USDA s recall file and other documents on the recall. We also met with the department s Office of Inspector General and reviewed the Inspector General s September 2003 report.1 We conducted our review from May 2003 through August 2004 in accordance with generally accepted government auditing standards. 1U.S. Department of Agriculture, Office of Inspector General, Great Plains Region Audit Report: Food Safety and Inspection Service: Oversight of Production Process and Recall at ConAgra Plant (Establishment 969), Report No. 24601-2-KC (September 2003). Page 39 GAO-05-51 Food Recall Programs Appendix II Federal Actions Associated with the Discovery of an Animal in the United States Infected with BSE Appendix II On December 23, 2003, USDA announced that a cow in the state of Washington had tested positive for BSE commonly referred to as mad cow disease. This appendix describes the actions USDA took to recall the meat and the actions FDA took with respect to FDA-regulated products, such as animal feed and cosmetics, made from rendered parts of the animal. Beef Recall Was Triggered by a BSEPositive Sample from One Cow On December 9, 2003, the recalling company slaughtered 23 cows. USDA, in accordance with its BSE surveillance policy at the time, took a sample of 1 cow that was unable to walk, although the condition of the tested cow is now disputed. USDA did not process the sample in its Ames, Iowa National Veterinary Services Laboratory in an expedited manner because the cow did not show symptoms of neurological disorder. USDA test results indicated a presumptive positive for BSE on December 23, 2003. Recall Begun in December 2003 Was Completed in March 2004 On December 23, 2003, after learning about the positive BSE test, USDA headquarters notified the Boulder District Office, which is the field office with jurisdiction over the recalling firm. The Boulder District began gathering information about the recalling company s product distribution. Field staff telephoned the recalling company and were on-site at 7:00 p.m. The Boulder District initially thought 3 days of the recalling company s production would have to be recalled, but further examination of facility cleanup and shipping records revealed that it was only necessary to recall 1 day of production. USDA recall staff convened at 9:15 p.m. and discussed the science related to BSE and whether the recalling company s cleanup practices were sufficient to limit the recall to 1 day of production. Following USDA s determination to conduct a Class II recall that is, the beef posed a remote possibility of adverse health consequences USDA contacted the recalling company to discuss recall details and the press release. The press release and Recall Notification Report were released that evening. On December 24, 2003, USDA s Food Safety and Inspection Service (FSIS) sent inspectors to the recalling company s primary customers to obtain secondary customer distribution lists and product shipping records. USDA conducted 100 percent verification checks for this recall it contacted every customer that received the recalled meat. This level of verification checks is well above the percentage of checks conducted by USDA district offices for the Class I recalls we reviewed. Appendix II Federal Actions Associated with the Discovery of an Animal in the United States Infected with BSE Page 40 GAO-05-51 Food Recall Programs On December 26, 2003, USDA began checking the primary and secondary customers of the recalling company that it was aware of, although the entire product distribution chain was unknown. During the checks, USDA tried to determine if the product was further distributed, and it used verification checks to acquire distribution lists for secondary and tertiary customers of the recalling company. Verification checks continued until February 25, 2004. Three USDA districts conducted these verification checks. The Boulder District coordinated the checks and assigned checks to the Minneapolis District Office for customers in Montana and to the Alameda District Office for customers in California. USDA required that 100 percent of the primary checks, 50 percent of the secondary checks, and 20 percent of the tertiary checks be conducted on-site. According to USDA, more than 50 percent of the secondary checks were actually conducted on-site. FDA officials helped conduct verification checks. According to USDA, the recall took a long time to complete because USDA contacted each customer at least twice. USDA first contacted each customer to conduct the check and again to verify product disposition. On February 25, 2004, the Boulder District concluded that the recall was conducted in an effective manner. On March 1, 2004, USDA s Recall Management Division recommended that the agency terminate the recall, and USDA sent a letter to the recalling company to document that USDA considered the recall to be complete. Recall Was Complicated by Inaccurate Distribution Lists and Mixing of Potentially Contaminated and Noncontaminated Beef USDA used distribution lists and shipping records to piece together where the recalled product was distributed. According to USDA, one of the recalling company s three primary customers was slow in providing its customer list. USDA could not begin verification activities for that primary customer without this list. Furthermore, some customers of the recalling company provided USDA with imprecise lists that did not specify which customers received the recalled product. As a consequence, USDA could not quickly determine the scope of product distribution and had to take time conducting extra research using shipping invoices to determine which specific customers received the product. Even when USDA determined the amount and location of beef, the agency still had trouble tracking the beef in certain types of establishments, such as grocery store distributors. USDA could not easily track the individual stores where those distributors sent the beef because of product mixing Appendix II Federal Actions Associated with the Discovery of an Animal in the United States Infected with BSE Page 41 GAO-05-51 Food Recall Programs and the distributors record-keeping practices. Generally, distributors purchase beef from multiple sources, mix it in their inventory, and lose track of the source of the beef they send to the stores that they supply. To deal with this problem, USDA first identified the dates when recalled beef was shipped to the distributors and then asked for a list of the stores that were shipped any beef after those dates. Consequently, some stores were included in the recall that may never have received recalled beef. The recall was also complicated by repeated mixing of recalled beef with nonrecalled beef, thereby increasing the amount of meat involved in the recall. The recalling company slaughtered 23 cows on December 9, 2003, and shipped those and 20 other carcasses to a primary customer on December 10, 2003. The recalling company s carcasses were tagged to identify the slaughter date and the individual cow. The primary customer removed the identification tags and mixed the 23 recalled carcasses with the 20 nonrecalled carcasses. Because the carcasses could not be distinguished, the recall included all 43 carcasses at the primary customer. After one round of processing at the primary customer, the meat from the carcasses was shipped to two other processing facilities. Both establishments further mixed the recalled meat from the 43 carcasses with meat from other sources. In all, the mixing of beef from 1 BSE-positive cow resulted in over 500 customers receiving potentially contaminated beef. Imprecise distribution lists and the mixing of recalled beef combined to complicate USDA s identification of where the product went. Specifically, on December 23, 2003, USDA s initial press release stated that the recalling company was located in Washington State. Three days later, on December 26, 2003, USDA announced that the recalled beef was distributed within Washington and Oregon. On December 27, 2003, USDA determined that one of the primary customers of the recalling firm distributed beef to facilities in California and Nevada, in addition to Washington and Oregon, for a total of four states. On December 28, 2003, USDA announced that some of the secondary customers of the recalling company may also have distributed the product to Alaska, Montana, Hawaii, Idaho, and Guam, for a total of eight states and one territory. On January 6, 2004, over 2 weeks from recall initiation, USDA determined that the beef went to only six states Washington, Oregon, California, Nevada, Idaho, and Montana and that no beef went to Alaska, Hawaii, or Guam. To reach that conclusion, USDA used the distribution lists, shipping records, and sales invoices that it received from companies to piece together exactly where the recalled beef may have been sent. The lists Appendix II Federal Actions Associated with the Discovery of an Animal in the United States Infected with BSE Page 42 GAO-05-51 Food Recall Programs showed that 713 customers may have received the recalled beef; 6 of those may have received beef from more than one source. USDA determined that 176 customers on the lists did not actually receive recalled beef, including the customers in Guam and Hawaii. USDA s review also indicated that recalled beef was probably not shipped to Alaska or Utah, and USDA checked 2 retailers in Alaska and 3 retailers in Utah to confirm that was the case. In total, USDA conducted verification checks on 537 of the 713 customers on the lists. USDA s initial checks identified an additional 45 customers that may have received the recalled beef that were not included on the distribution lists, for a total of 582 verification checks. Figure 4 summarizes USDA s verification efforts during the recall. Appendix II Federal Actions Associated with the Discovery of an Animal in the United States Infected with BSE Page 43 GAO-05-51 Food Recall Programs Figure 4: USDA s Recall Verification Checks by Location and Customer Type for Meat Associated with the Animal Infected with BSE Note: USDA checked 15 primary, 40 secondary, and 526 tertiary customers plus the recalling company, for a total of 582 verification checks.
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USDA s press release stated that the recall involved 10,410 pounds of beef products, and the USDA recall coordinator for this recall told us that downstream processors mixed the recalled beef with nonrecalled beef, for a total of more than 38,000 pounds of beef that was distributed at the secondary customer level. According to USDA officials involved with the recall, the precise amount of meat that was sold at the retail level is unknown because retailers at the tertiary level further mixed nonrecalled meat with potentially contaminated meat. USDA told us that more than 64,000 pounds of beef was ultimately returned or destroyed by customers, and that, because of the mixing, it was not able to determine how much of the original 10,410 pounds of recalled beef was contained in the 64,000 pounds that were recovered.
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REPORTS
1. Food Safety: USDA and FDA Need to Better Ensure Prompt and Complete Recalls of Potentially Unsafe Food. GAO-05-51, October 7.tss
http://www.gao.gov/cgi-bin/getrpt?GAO-05-51
Highlights - http://www.gao.gov/highlights/d0551high.pdf
QFC sued over mad cow case
Grocer negligently exposed them to beef, family claims
Friday, March 5, 2004
By LEWIS KAMB SEATTLE POST-INTELLIGENCER REPORTER
An Eastside family who says they ate beef linked to the nation's only known case of mad cow disease yesterday filed a class-action lawsuit against QFC, claiming the grocery store chain negligently exposed them and others to "highly hazardous" meat and did not properly notify them that they had bought it.
Attorneys for Jill Crowson, a 52-year-old interior designer from Clyde Hill, filed the lawsuit in King County Superior Court on behalf of her family and possibly hundreds of other customers who unwittingly bought and consumed beef potentially exposed to mad cow disease.
"I was pretty upset about it," Crowson said. "I've spent all of my kids' lives trying to be a responsible parent for them to keep them safe. I felt badly that the food I served could be harmful to their health."
The lawsuit is believed to be the first stemming from this country's only confirmed case of mad cow disease, or bovine spongiform encephalopathy, which was detected in a slaughtered Holstein from a Yakima Valley ranch on Dec. 23.
Neither officials at Quality Food Centers' Bellevue headquarters, or Kroger -- the company's Ohio-based corporate parent -- could be reached for comment about the lawsuit yesterday.
The suit contends the family bought and later ate ground beef from their local QFC that was part of a batch processed at Vern's Moses Lake Meats on Dec. 9 and included meat from the diseased Holstein.
The beef was later shipped to wholesalers and retailers in Washington, Oregon, California, Idaho, Montana and Nevada.
On Dec. 23 -- after government scientists confirmed the Holstein was infected with BSE -- businesses began pulling potentially affected beef from store shelves under a voluntary recall.
But the family's suit claims that, although QFC was aware of the recall on Dec. 23, the store did not begin pulling the recalled beef from about 40 of its stores that carried it until Dec. 24.
The company also did not try to warn customers about the recalled beef until Dec. 27 -- and only then with small, inconspicuous signs inside the stores, the suit claims.
Steve Berman, the family's attorney, said the company had "a duty to warn" consumers who bought the beef under terms of the Washington Product Liability Act.
QFC could've easily notified customers by taking out TV, radio or newspaper ads, or by tracking and notifying those who bought the beef through customers' QFC Advantage Cards, Berman said.
At Berman's downtown Seattle firm yesterday, Crowson described how on Dec. 22 and Dec. 23 -- the day of the recall -- she bought single packages of "9 percent leanest ground beef" from her local QFC store at Bellevue Village.
Crowson took the beef home, cooked it and made tacos one night and spaghetti the next -- serving the dinners to herself; her daughter, Laura, 22; son, Nicholas, 19; and her niece, Claire De Winter, 23. Members of the family also ate leftovers from those meals for the next several days, Crowson said.
"When the news about mad cow came out, I instantly became concerned," Crowson said. "But the initial stories didn't mention anything about QFC, so I thought we were OK."
While shopping at the grocery store a few days later, Crowson said she asked a store butcher whether QFC stores had sold any of the recalled beef. The butcher assured her they had not, she said.
The family only learned QFC had sold any of the beef in question after reading a news story Jan. 10 about a Mercer Island man who discovered his family had eaten affected beef that he bought at a local QFC store, Crowson said.
Crowson later called QFC and faxed the company a signed letter asking that it track purchases made on her QFC Advantage Card -- a store discount card issued to customers. On Jan. 12, the company notified Crowson that the beef she bought and served to her family was, in fact, part of the recalled batch, she said.
Scientists believe people who eat beef from infected cows can contract a fatal form of the disease.
The family is "now burdened with the possibility that they presently carry (the disease) that may have an incubation period of up to 30 years," the lawsuit says.
Lawyers for the family say they believe hundreds, if not thousands, of QFC customers, and those of other stores, likely ate beef from the recalled batch -- the reason why Berman filed their legal claim as a class-action lawsuit. A USDA official this week said that up to 17,000 pounds of meat affected by the recall likely was eaten or thrown out by customers.
Berman added that an investigator from his firm learned that QFC buys beef for its "9 percent leanest ground beef" products in large tubs that can weigh several hundred pounds, and then regrinds and packages the meat for sale.
Because QFC stores regrind the beef before selling it, Berman contends that makes the store a manufacturer responsible under the Washington Product Liability Act for not selling any unsafe product.
Scientists believe people who eat beef from cows infected with BSE can contract variant Creutzfeldt-Jakob, a fatal brain-wasting disease that has been detected in about 150 people worldwide.
However, officials with the U.S. Agriculture Department have repeatedly said the risk from eating muscle cuts from an infected cow -- the likely cut of meat processed and sold for hamburger in the recalled batch -- is extremely low.
Although Crowson said she tries not to "obsess over it," she is fearful that her family could one day become sick.
"It's pretty scary," she said.
Because no medical test is available to determine whether a living person is infected with the disease, the couple's "stress and fear cannot be allayed," the lawsuit said.
The family seeks unspecified damages for emotional distress and medical monitoring costs.
Crowson said her reason for bringing the lawsuit isn't about money. "The more I've thought about this, the angrier I've gotten," she said.
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http://home.hetnet.nl/~mad.cow/archief/2004/mar04/sued.htm
QFC s Delayed Mad Cow Response Draws Lawsuit Family claims QFC should have used customer database to warn those at risk sooner
March 05, 2004
SEATTLE A Bellevue, Wash. family today filed a proposed class-action lawsuit against Quality Food Centers (QFC), a subsidiary of Kroger (NYSE: KR), claiming the grocery store chain should have used information gathered through its customer loyalty program to warn those who purchased beef potentially tainted with mad cow disease.
The suit, filed in King County Superior Court, seeks to represent all Washington residents who purchased the potentially tainted meat, and asks the court to establish a medical monitoring fund.
Jill Crowson purchased the potentially tainted beef from a Bellevue QFC on Dec. 22 and 23, and used her Advantage Card, QFC s customer loyalty program. She served the meat to her husband over Dec. 25 and 26, and later heard of the recall in the newspaper.
Steve Berman, the attorney representing the Crowsons, asserts that since the company tracks purchases, it should have warned the Crowsons and many other customers who purchased the beef at approximately 40 stores across Washington.
If you lose your keys with an Advantage Card attached, QFC will return them to you free of charge, said Berman. If they can contact you over a lost set of car keys, why couldn t they contact you and tell you that the beef you purchased could kill you?
QFC is among the large number of grocers that track customer purchases through loyalty cards like the Advantage Card. Once a customer shares contact information including name, address and phone number they are given discounts on certain items.
Regardless of any discounts offered, the loyalty card tracks customers every purchase and stores them in a central database, the complaint states.
We contend that QFC knew which Advantage Card customers purchased the suspect meat, and could have easily called to warn them, said Berman. Instead, QFC used a series of spurious excuses to hide their failure to act.
On Dec. 23, the U.S. Department of Agriculture ordered the recall of approximately 10,410 pounds of raw beef that may have been infected with bovine spongiform encephalopathy (BSE), which if consumed by humans can lead to the always-fatal Cruetzfeldt-Jakobs Disease (vCJD).
According to the complaint, QFC at first mistakenly believed it did not have any of the affected beef and took no action to remove the product from its shelves. The store later removed the beef on Dec. 24, but then did little to warn those who earlier purchased the meat, the suit claims.
It wasn t until Dec. 27 that the grocery chain posted small signs with information about the recall, the complaint alleges.
The Crowsons contacted QFC when they suspected they had purchased the potentially tainted meat, but QFC would not confirm their suspicions for two more weeks, the suit states. According to Berman, the family had to file a written request before QFC would confirm their fears.
According to health experts, Cruetzfeldt-Jakobs Disease can have an incubation period of as long as 30 years. There is no test to determine if infection took place after possible exposure, nor is there any treatment once one is infected. The condition is always fatal.
If the court grants the suit class-action status, QFC would likely be compelled to turn over the names of those who purchased the potentially tainted beef.
The proposed class-action claims QFC violated provisions of the Washington Product Liability Act by failing to give adequate warning to consumers about the potentially dangerous meat.
The suit seeks unspecified damages for the plaintiffs, as well as the establishment of a medical monitoring fund.
http://www.hagens-berman.com/frontend?command=PressRelease&task=viewPressReleaseDetail&iPressReleaseId=654
QFC's Delayed Mad Cow Response Draws Lawsuit
... subsidiary of Kroger , claiming the grocery store chain should ... beef potentially tainted with "mad cow disease ... beef at approximately 40 stores across Washington. ... www.forrelease.com/D20040305/sff005.P2.03042004214558.03634.html - 9k -
040307 Woman Sues QFC Over Mad-Cow Recall ... Jakob disease, the human form of mad-cow, from eating ... QFC is subject to the Washington Product Liability ... been found in a slaughtered Yakima County dairy cow. ... www.spcnetwork.com/mii/2004/040307.htm - 6k
http://search.yahoo.com/search?p=QFC+sued+over+mad+cow+case+&fr=yfp-t-501&toggle=1&cop=mss&ei=UTF-8
Subject: GOVERNOR SCHWARZENEGGER PREFERS CALIFORNIANS TO EAT MAD COW BEEF IN SECRECY, VETOED BILL SB 1585 Date: October 1, 2004 at 2:22 pm PST
GOVERNOR SCHWARZENEGGER PREFERS CALIFORNIANS TO EAT MAD COW BEEF IN SECRECY, VETOED BILL SB 1585
Schwarzenegger Vetoes Meat Recall Disclosure Bill
Legislation Would Have Identified Stores that Received Contaminated Meat and Poultry
Governor Arnold Schwarzenegger (R-CA) vetoed a bill yesterday that would have let Californians know whether they ve purchased contaminated meat or poultry. The bill, SB 1585, would have ended a secrecy agreement between the U.S. Department of Agriculture (USDA) and California that prevents the state from disclosing the names and locations of stores that receive shipments of recalled meat.
Consumers have a right to know if they purchased recalled meat or poultry, said Ken Kelly, Staff Attorney at the Center for Science in the Public Interest (CSPI). Why force families to roll the dice when they put food on the table? Governor Schwarzenegger prefers a get-sick-first, ask-questions-later policy.
Earlier this year, California was one of several states that received meat from the Washington State cow that tested positive for mad cow disease. But because California is one of 12 states that have signed a secrecy agreement with USDA, state health officials were prohibited from identifying stores or restaurants that may have received beef from the infected cow. Even recalled meat tainted with deadly E. coli 0157:H7 bacteria would be subject to the secrecy agreement, leaving consumers uncertain as to whether the ground beef in their refrigerator were safe to eat.
In his veto message, Governor Schwarzenegger indicated he would instruct the state s health department to renegotiate an agreement that would allow USDA to share recall information with local public health officials. But according to CSPI, even if USDA agreed to share recall information with local officials, the local officials would be similarly prohibited from disclosing names of retail outlets with consumers. In August, CSPI urged USDA not to force states to sign any such secrecy agreements. Federal and state government should be more concerned with protecting consumers from unnecessary hospitalizations and deaths associated with food-borne illness, and less concerned with protecting grocers and meat producers from bad publicity, Kelly said.
http://cspinet.org/new/200410011.html
SUPERIOR COURT OF THE STATE OF WASHINGTON FOR KING COUNTY
JILL CROWSON, ET AL., PLAINTIFFS
VS
QUALITY FOOD CENTERS, INC., an Ohio corporation Defendent
NO. 04-2-05608-0 SEA
snip...
The Court hereby GRANTS the defendant's motion to dismiss the plaintiff's claims based on a manufacturer's strict liability (Counts I and II) and DENIES the defendant's motion to dismiss the plaintiff's claim of negligence by a product seller (Count III).
DATED this 14th day of June, 2004
snip...
http://www.hagens-berman.com/files/Mad%20Cow%20Order%20Denying%20Motion%20to%20Dismiss1088546283878.pdf
Date Filed: March 5, 2004 Court: King County Superior Court (Washington) Location: Seattle Ticker Symbol: NYSE:KR
Join This Suit Tell a Friend
Consumers filed a proposed class-action lawsuit against Quality Food Centers (QFC), a subsidiary of Kroger (NYSE: KR), claiming the grocery store chain should have used information gathered through its customer loyalty program to warn those who purchased beef potentially tainted with ?mad cow disease.? The USDA issued a recall notice for the meat on December 23, 2003. QFC sold the meat through its approximately 40 stores across Washington.
The suit claims that even though QFC had the ability to quickly warn every customer who purchased the potentially deadly meat if they used the QFC Advantage Card at the time of purchase, the grocery store neglected to do so.
The suit seeks to represent every consumer in Washington state who purchased the recalled meat from QFC.
Recent Updates
June 14, 2004 - the King County Superior Court gave the green light to a suit claiming QFC didn't do enough to warn customers about beef potentially tainted with 'mad cow disease,' finding enough questions about the beef and
QFC's responsibility to explore in the courtroom.
Read the court order.
http://www.hagens-berman.com/frontend?command=Lawsuit&task=viewLawsuitDetail&iLawsuitId=653
QFC - 'Mad Cow' Frequently Asked Questions
The Suit
What is the key issue in this suit? On December 23, 2003, the United States Department of Agriculture (USDA) recalled more than 10,000 pounds of raw beef that could have been exposed to bovine spongiform encephalopathy (BSE). Humans consuming BSE-tainted meat can contract Creutzfeldt-Jakob Disease (vCJD), an always-fatal condition.
QFC sold this meat throughout its stores in Washington. Even though QFC had the ability to quickly warn every customer who purchased the potentially deadly meat if they used the QFC advantage card at the time of purchase, the grocery store neglected to do so, the suit alleges.
Who does the suit seek to represent? The suit seeks to represent all persons who purchased recalled meat from any QFC store in the state of Washington.
Who are the defendants? Quality Food Centers, or QFC. Once a local, Northwest company, QFC is now a wholly owned subsidiary of the grocery chain giant, Kroger.
What does the suit seek? The suit asks the court to order QFC to establish a medical monitoring fund which would allow those who purchased and consumed the meat to seek medical care, checking for ? and if necessary, treating --- the infection of vCJD. The suit also seeks the creation of a medical notification system, allowing those who may have been exposed to the disease to receive periodic updates on research and treatment of vCJD. The suit also seeks unspecified damages for the plaintiffs.
Does the suit claim QFC violated specific laws? Yes. The lawsuit claims QFC violated the Washington Product Liability Act. In addition, the suit claims QFC was negligent by not warning consumers of the dangers associated with the affected meat.
Where was the lawsuit filed? The suit was filed in King County Superior Court on March 4, 2004.
How do I determine if I qualify to join the lawsuit? If you have a QFC Advantage card and believe that you bought recalled meat from a QFC store, you may be eligible to join the lawsuit. Click here to fill out the sign-up request form, or you can contact Hagens Berman attorneys.
QFC
What is the QFC Advantage Card? The Advantage Card is known in the grocery industry as a Customer Loyalty Card. Customers who sign up for QFC?s Advantage Card receive special discounts on selected items, but gives the grocery store chain the ability to track consumers? purchases in order to enhance their marketing efforts. In addition, grocery chains which offer affinity card programs often use the database and shopping pattern data to send users coupons and other marketing material. According to the complaint, QFC tracks every purchase made by consumers presenting the Advantage Card, including product description, date of purchase, store of purchase and the price, and saves that data with customer contact information.
What was QFC?s response to the meat recall? On Dec. 23, 2003, QFC received notice from the U.S. Department of Agriculture (USDA) of a recall of approximately 10,410 lbs. of raw meat that may have been contaminated with the infectious agent that causes ?mad cow? disease. QFC did not act immediately on the recall notice but initially responded by denying that it had any of the tainted meat. On December 24 QFC pulled the meat from its shelves, but the company took no steps to directly warn consumers. It was not until Dec. 27 that QFC posted small signs in its stores recalling the tainted beef, according to the complaint. During that four day period when QFC was silent hundreds of consumers may have eaten the meat.
Can QFC determine if an Advantage Card holder purchased the potentially dangerous meat? Yes. In fact, consumers can now contact QFC directly and the company will provide information about meat purchases ? but only if you ask. Hundreds of other consumers who purchased the meat and are unaware of the situation have not heard from QFC, the complaint states.
Why was QFC sued even though they pulled the meat? Under Washington law since QFC ground the meat it is deemed a manufacturer and is strictly liable for any unsafe product. In addition QFC possessed specific and easily obtainable information on which customers purchased the recalled meat, but did not act to inform customers, the suit states. Considering the potential danger and risk of worry for consumers, and the ease of contacting consumers using database information, simply pulling the meat from the shelves and belatedly posting small signs was not an adequate response, according to the complaint.
What information on customer purchases does QFC track with the Advantage Card? QFC tracks every purchase that a customer with an Advantage Card makes, regardless of whether discounts are offered or not, according to the complaint.
Does the recently announced larger-than-expected recall of beef affect the lawsuit? No. Regardless of the size of the beef recall, attorneys believe the facts in the case remain the same.
How can I find out if I bought recalled meat from QFC? If you believe that you may have purchased recalled meat from a QFC store, and you have an Advantage Card, you can contact QFC and ask if your record shows you purchased recalled beef. You can contact QFC at 866-221-4141.
Isn?t QFC prohibited by privacy laws from contacting consumers with warnings like this? No ? the suit notes that the company will return car keys returned to the store if the keys have an Advantage Card attached. According the complaint, If QFC can return car keys by mail, why can?t they send a notice saying the meat a customer purchased in their store could cause an incurable, fatal disease? Further privacy laws would prevent QFC from disclosing information to third parties, disclosing the information to the customer whose card it is does not violate privacy laws. For example, if a trade group wanted to know the names of consumers who purchased a given drug sold at QFC, disclosure of that private information might be a privacy concern. However, disclosure to a consumer of his own records is not.
?Mad Cow? Disease
What is Mad Cow disease? In cows, mad cow disease is defined as bovine spongiform encephalopathy (BSE), and is a progressive neurological disease. The human disease variant is know as Creutzfeldt-Jakob Disease (vCJD), which is a rare brain disorder that causes a rapid, progressive dementia and is always fatal, according to the complaint.
Where can I get more information on Mad Cow disease? The USDA provides information on the disease at www.usda.gov/.
What should I do if I believe that I?ve eaten recalled meat? According to the complaint, no screening tests or treatments have been found for Creutzfeldt-Jakob disease. Those who suspect they?ve eaten recalled meat should contact their physician for more information.
http://www.hagens-berman.com/files/madcowfaq1-13-051105661006369.html
Do Stores That Offer Loyalty Cards Have a Duty to Notify Customers of Product Safety Recalls? A Recent Suit Raises This Novel Question By ANITA RAMASASTRY ----
Thursday, Aug. 05, 2004
An interesting new Washington state court suit raises an important question: If a retailer benefits from collecting personally identifiable information about its customers, does it have a corresponding duty to use such data to alert its customers that products they've bought have been recalled for health or safety reasons? And if so, could turning over private data to companies actually create benefits, as well as privacy risks, for the consumer?
In the suit, consumer Jill Crowson is suing her grocery store -- Quality Food Center (QFC), a subsidiary of Kroger -- for negligent infliction of emotional distress and disregard of a "duty to warn" under the Washington Product Liability Act. Crowson alleges in her complaint that QFC failed to alert her family that ground beef it had sold them had been recalled in December's mad-cow scare.
Yet, Crowson says, QFC easily could have done so through information it maintained connected with her Advantage card - a "loyalty card" that meant QFC had Crowson's name, address and purchasing information. According to her complaint, QFC tracks every purchase made by consumers presenting the Advantage Card, including product description, date of purchase, store of purchase and the price, and saves that data alongside customer contact information.
Now, Crowson says, her family members "feel like walking time bombs" knowing they may be infected with the human form of mad-cow disease which the complaint states may have an up-to-30-year incubation period. And they are not the only ones: Crowson is seeking class action status for herself and what she believes are "hundreds" of similarly-situated Washington customers at QFC's approximately 40 stores in the state.
Some lawyers think Crowson's suit is a stretch. Federal law does not impose on companies a specific duty to notify consumers when tainted meat is recalled under the direction of the U.S. Department of Agriculture (USDA), as was the case here. Also, Crowson and her family, and the class she seeks to represent, are suing based on fear (and possible future harm), not current illness. Moreover, the chance they will actually get Mad Cow Disease some time in the future are apparently remote.
Nevertheless, the lawsuit has strong intuitive appeal: QFC could have saved the Crowsons and others like them a lot of worry, and perhaps sleepless nights, with what appears would have been minimal effort, using information at its digital fingertips. And the court has already once refused to dismiss it - finding that there were sufficient factual questions about the beef and about QFC's responsibility to the Crowsons, to merit further exploration of the evidence, through discovery and in the courtroom.
Regardless of the outcome of Crowson's suit, it underscores the need for retailers and policymakers to examine what sort of responsibilities come with private data gathering under loyalty card schemes.
The Lawsuit: The Chronology of Facts Alleged, and the Loyalty Card at Issue
On December 22 and 23, 2003, Crowson bought ground beef from a QFC store. Also on December 23, 2003, the USDA recalled Washington beef after it confirmed that a cow slaughtered in Washington had been infected with Mad Cow Disease. But Crowson says QFC did not pull the affected meat from its shelves until December 24, and did not post signs in its stores announcing the recall until December 27. By then, the Crowson family had eaten the meat.
Crowson states that she only learned of the recall by reading an article in her local newspaper. She said she subsequently called the supermarket chain, then faxed QFC a letter asking that her purchase be traced through her QFC Advantage card. On January 10, she was notified that her ground beef purchase was indeed from the recalled batch.
Crowson says that what QFC allegedly did in response to the recall - pulling the beef from shelves the next day, and posting signs three days after that -- was far from enough. She says it should have immediately warned customers who had bought possibly tainted meat through newspaper, radio and television advertising -- and by contacting individually those who, like her, had Advantage cards. Its failure to do so, she says, is what makes the company liable to her and other shoppers.
The Advantage Card is known in the retail industry as a customer "loyalty card" - providing discounts on specific items, in exchange for consumer information that will aid in better tailoring the company's marketing efforts. Combining the data from one's loyalty card application with data from other commercial databases or public records (for examples, mortgage records, or court filings) can often allow a very specific profile of each consumer.
Some states limit the types of information that a grocery store can collect from you when you register for a loyalty card. For example, California state law prohibits a grocery store from requiring that you turn over your social security or your driver's license number.
Companies, of course, stress the potential savings that might result from use of a loyalty card. Consider, for instance, the sales pitch on the QFC website it reads: "If you don't have a QFC Advantage Card, you're missing out! The Advantage Card is a powerful new way to save on the groceries you buy every day. It gives you the best of all possible worlds: premium quality, superb service and lower prices. That's something no other grocery store can match. So make sure you take advantage of the big savings."
Privacy advocates complain that loyalty cards result in the improper use - and, often, sale to third parties - of customers' private information. QFC apparently doesn't sell customers' data to third parties, however. Its website promises that "QFC will not release your name to any list service or manufacturer, and that such information will be held in the strictest of confidence-even within our company."
Privacy advocates also warn, however, that even if third-party sales of data are not allowed, the data compiled can always be accessed with a subpoena or warrant and used against the customer in court proceedings. Meanwhile, consumer advocates claim that certain loyalty cards don't really offer the savings they promise. Nevertheless, numerous stores employ loyalty cards.
Turning the Privacy Debate on Its Head: With Great Information, Comes Great Responsibility?
The Crowson lawsuit turns the privacy debate on its head. Typically, privacy advocates ask retailers to safeguard the personal information they collect about their shoppers. In this case, in contrast, plaintiff is asking that QFC delve into its database to notify her about a meat recall.
QFC does this very thing if a consumer loses his or her keys with an Advantage Card attached to them - returning the keys free of charge. So Crowson's attorney, Steve Berman, asks: "If they can contact you over a lost set of car keys, why couldn't they contact you and tell you that the beef you purchased could kill you?"
According to some news reports, QFC was reluctant to call customers regarding the recall based on privacy concerns. But in this case, the concerns seem misplaced. No privacy law is violated when a consumer communicates with the customer herself regarding private information - indeed, every offer the customer receives is, in a sense, this kind of communication. When the customer is receiving personalized discounts based on her purchase history, why can't she receive personalized health and safety warnings based on that history, too?
Was There a Duty to Warn Here?
From the law's perspective, the question will be not whether QFC ideally should have warned the Crowsons - of course it should have. The question will be if it had a legal duty to do so. Such a duty would come from either the common law of torts, which allows claims where there is a duty to behave reasonably to prevent foreseeable harm to others. . Or it might come from the Washington product liability statute - which, as noted above, creates a "duty to warn" in certain situations.
And of course, if there is no current duty, the legislature may see fit to pass a statute creating such a duty. :It may seem more prudent, however, for retailers to voluntarily assume such a responsibility. When companies benefit from collecting customer information, shouldn't they also assume a duty to protect customers from known risks associated with that very information? Some risks, of course, may be a matter of opinion. But this one was not: The fact of the risk was acknowledged by the USDA recall of the meat. With this kind of clear notice of the risk, it seems that QFC either does - or ought to - have a duty to protect customers from this risk.
Of course, should a retailer not wish to take on this responsibility, it can also change its loyalty program. QFC and other retailers could still track consumer purchases without asking them for personally identifiable information.
http://writ.corporate.findlaw.com/ramasastry/20040805.html
FindLaw's Writ - Ramasastry: Mad Cow in the USA
http://writ.corporate.findlaw.com/ramasastry/20031230.html
Family to sue grocery chain
A Seattle family that ate beef linked to the US's only known case of BSE has filed a classaction
lawsuit against the grocery chain QFC, claiming the company negligently exposed
them and others to "highly hazardous" meat and did not properly notify them that they had
bought it.34 The suit contends that Jill Crowson and her family bought and later ate ground
beef from their local QFC that was part of a batch processed at Vern's Moses Lake Meats on
9 December 2003 and included meat from the diseased Holstein. The beef was later shipped
to wholesalers and retailers in Washington, Oregon, California, Idaho, Montana and Nevada.
After government scientists confirmed on 23 December that the Holstein was infected with
BSE, businesses began pulling potentially affected beef from store shelves under a voluntary
recall. But, the family's suit claims, although QFC was aware of the recall, the store did not
begin pulling the beef from about 40 of its stores until 24 December. The company also did
not try to warn customers about the recalled beef until 27 December – and only then with
small, inconspicuous signs inside the stores, the suit claims. The family only learned QFC had
9
sold any of the beef in question after reading a news story on 10 January about a man who
discovered his family had eaten affected beef that he bought at a local QFC store, Crowson
said. She later called QFC and faxed the company a signed letter asking that it track
purchases made on her QFC Advantage Card, and on 12 January the company notified
Crowson that the beef she bought and served to her family was, in fact, part of the recalled
batch, she said.
The family seeks unspecified damages for emotional distress and medical monitoring costs.
Crowson said her reason for bringing the lawsuit is not about money. "The more I've thought
about this, the angrier I've gotten," she said. Neither the company nor its parent corporation,
Kroger, have commented.
http://www.which.net/campaigns/food/safety/bse_reports/bserep0304.pdf
2006 - 2007 still feeding ban mad cow SRM protein to cows in USA
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html
NEW URL
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
MORE 2006 FEED BAN VIOLATIONS BELOW, ''IN COMMERCE'' ;
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
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 ______________________________ PRODUCT a) Dairy feed, custom, Recall # V-134-6; b) Custom Dairy Feed with Monensin, Recall # V-135-6. CODE None. Bulk product RECALLING FIRM/MANUFACTURER Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006. Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete. REASON Possible contamination of dairy feeds with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 1,484 tons DISTRIBUTION TN and WV
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS Date: August 16, 2006 at 9:19 am PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II ______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-115-6 CODE None RECALLING FIRM/MANUFACTURER Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE Approximately 2,223 tons DISTRIBUTION KY
______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-116-6 CODE None RECALLING FIRM/MANUFACTURER Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 1,220 tons DISTRIBUTION KY
______________________________ PRODUCT Bulk custom made dairy feed, Recall # V-117-6 CODE None RECALLING FIRM/MANUFACTURER Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 40 tons DISTRIBUTION LA and MS
______________________________ PRODUCT Bulk Dairy Feed, Recall V-118-6 CODE None RECALLING FIRM/MANUFACTURER Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete. REASON Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 7,150 tons DISTRIBUTION MS
______________________________ PRODUCT Bulk custom dairy pre-mixes, Recall # V-119-6 CODE None RECALLING FIRM/MANUFACTURER Walthall County Co-op, Tylertown, MS, by telephone on June 26, 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 87 tons DISTRIBUTION MS
______________________________ 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 MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs Date: August 6, 2006 at 6:14 pm PST PRODUCT Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6 CODE All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products. RECALLING FIRM/MANUFACTURER Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete. REASON The feed was manufactured from materials that may have been contaminated with mammalian protein. VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs DISTRIBUTION MI
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.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
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date: August 6, 2006 at 6:19 pm PST PRODUCT Bulk custom made dairy feed, Recall # V-114-6 CODE None RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE ????? DISTRIBUTION KY END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
CJD WATCH MESSAGE BOARD TSS 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
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006 Date: June 27, 2006 at 7:42 am PST Public Health Service Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.
You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.
You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
http://www.fda.gov/foi/warning_letters/g5883d.htm
USDA FSIS SRM TSE QUARTERLY ENFORCEMENT REPORT UPDATE
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&D=1&H=1&P=10713
http://www.prwatch.org/node/4541
Subject: Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route Date: September 29, 2007 at 12:50 pm PST
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
LETS start with the UKBSEnvCJD only theory, lets look at UK exports to USA, Canada, and Mexico. the imported only theory. ...
1994 UK EXPORTS BEEF VEAL USA , MEXICO $ CANADA ONLY other Countries list in PDF file)
USA -------- TOTALS ''8'' TONS CANADA -- TOTALS ''29'' TONS
1995 UK EXPORT BEEF AND VEAL TO USA AND CANADA
USA ------- TOTALS ''358'' TONS
CANADA --TOTALS ''24'' TONS
BONE-IN BEEF AND VEAL
USA-------- TOTALS ''10'' TONS (i think this is part of the 358 tons above?)
UK EXPORT OF LIKE CATTLE TO USA AND CANADA
1986 TO 1996 USA TOTAL = 1297
1986 TO 1996 CAN TOTAL = 299
http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf
UK EXPORT MEAT OR OFFAL OF BOVINE ANIMALS DEC 1987
CANADA -- 64,526 KG
UK EXPORT OFFALS OF BOVINE ANIMALS FRESH CHILLED OR FROZEN OTHER THAN LIVER DEC 1987 YTD
USA -- 45,943 KG
UK EXPORT MEAT OF BOVINE ANIMAL WITH BONE IN 1988
CANADA -- 4,163 KG
PREP OR PRES MEAT OR OFFAL OF BOVINE ANIMALS CUMULATIVE TO DEC 1988
USA -------- 28,609 KG CANADA -- 22,044 KG
MEAT OF BOVINE ANIMALS WITH BONE IN CUMULATIVE TO ANUAL 1989
USA -------- 17,880 KG MEXICO---- 33,444 KG
BONELESS MEAT OF BOVINE 1989
USA --------111,953 KG CANADA---1,800 KG MEXICO --- 1,143,387 KG
EDIBLE OFFAL OF BOVINE ANIMALS 1989
USA -------- 19,980 KG MEXICO--- 31,244 KG
MORE........
MEAT OF BOVINE ANIMALS BONELESS 1990
USA 146,443
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995
USA 24 TONS
CANADA 83 TONS
http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.??? From: S.J.Pearsall@esg.maff.gsi.gov.uk Date: Tue, 8 Feb 2000 14:03:16 +0000 To: flounder@wt.net (Receipt Notification Requested) (Non Receipt Notification Requested)
Terry Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Country Tonnes
1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990
Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222).
Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C
====================================== END...TSS
BSE GBR RISK ASSESSMENTS, USA, CANADA, AND MEXICO
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/573.html
http://www.efsa.europa.eu/
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Canada
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked to provide an up-to-date scientific report on the GBR in Canada, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Canada. This scientific report addresses the GBR of Canada as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into the country middle of the eighties and could have reached domestic cattle in the early nineties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s. It is possible that imported meat and bone meal (MBM) into Canada reached domestic cattle and led to an internal challenge in the early 90s.
A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from UK in the mid 80s could have been slaughtered. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of Canada is III, i.e. it is confirmed at a lower level that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the system remains unstable, it is expected that the GBR continues to grow, even if no additional external challenges occur.
http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/564.html
http://www.efsa.europa.eu/
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Mexico
Last updated: 8 September 2004 Publication Date: 20 August 2004
Adopted July 2004 (Question N° EFSA-Q-2003-083)
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.
It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.
EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.
http://www.efsa.europa.eu/
USA NVCJD BLOOD RECALLS ONLY ;
http://www.google.com/search?hl=en&q=CJD+BLOOD+RECALLS+TSS&btnG=Search
vCJD case study highlights blood transfusion risk
http://vcjdblood.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007
http://cjdmadcowbaseoct2007.blogspot.com/
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
Tuesday, October 9, 2007 NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 RISES TO 5 DOCUMENTED CASES
http://nor-98.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW h-BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/
ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007
Date: Mon, 24 Sep 2007 21:31:55 -0500
I suggest that you all read the data out about h-BASE and sporadic CJD, GSS, blood, and some of the other abstracts from the PRION2007. ...
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744
*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OF POKER INDEED GOES UP. ...TSS
USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779
From: "Terry S. Singeltary Sr." Subject: CWD UPDATE 88 AUGUST 31, 2007
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&P=450
Date: Wed, 29 Aug 2007 21:13:08 -0500 From: "Terry S. Singeltary Sr." Subject: CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again)
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=26079
Monitoring the Potential Transmission of Chronic Wasting Disease to Humans Using a Hunter Registry Database in Wyoming (405 lines) From: Terry S. Singeltary Sr. <[log in to unmask]> Date: Thu, 30 Aug 2007 21:23:42 -0500
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&F=&S=&P=27654
Subject: Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST
Subject: Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain Date: August 25, 2007 at 12:42 pm PST
J Biol Chem. 2007 Aug 20; : 17709374
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain.
[My paper] Atsushi Kobayashi , Masahiro Asano , Shirou Mohri , Tetsuyuki Kitamoto
The genotype (methionine or valine) at polymorphic codon 129 of the human prion protein (PrP) gene and the type (type 1 or type 2) of abnormal isoform of PrP (PrP(Sc)) are major determinants of the clinicopathological phenotypes of sporadic Creutzfeldt-Jakob disease (sCJD). Here we found that transmission of sCJD prions from a patient with valine homozygosity (129V/V) and type 2 PrP(Sc) (sCJD-VV2 prions) to mice expressing human PrP with methionine homozygosity (129M/M) generated unusual PrP(Sc) intermediate in size between type 1 and type 2. The intermediate type PrP(Sc) was seen in all examined dura mater graft-associated CJD cases with 129M/M and plaque-type PrP deposits (p-dCJD). p-dCJD prions and sCJD-VV2 prions exhibited similar transmissibility and neuropathology, and the identical type of PrP(Sc) when inoculated into PrP-humanized mice with 129M/M or 129V/V. These findings suggest that p-dCJD could be caused by cross-sequence transmission of sCJD-VV2 prions.
snip...
In this study, the strain-dependent traits of sCJDMM1 prions were inherited through cross-sequence transmission without any modification. The humanized mice with 129V/V produced type 1 PrPres after inoculation with sCJD-MM1 prions. Because sCJD-VV1 cases are extremely rare (at most 1-2% of the total number of sCJD cases) and characterized by early onset (mean age at onset: 39.3 years) (5),
####################################
our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.
###################################
In conclusion, cross-sequence transmission of sCJD-VV2 prions generates a new prion strain with altered conformational properties and disease phenotypes as p-dCJD prions. Furthermore, the newly generated prions have unique transmissibility including the traceback phenomenon. In the future, if atypical prion strains emerge through cross-sequence transmission, especially from animals, traceback studies will enable us to identify the origin of the prions.
REFERENCES...snip...end
FULL TEXT ;
http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Cross-sequence+transmission+of+sporadic+Creutzfeldt-Jakob+disease+creates+a+new+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=21267
Re: Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES)
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=1165
Subject: MAD COW BASE H-TYPE AND L-TYPE
Date: August 23, 2007 at 11:30 am PST
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779
October 2007 Update on Feed Enforcement Activities to Limit the Spread of BSE
http://www.phxnews.com/fullstory.php?article=53149
Transmissible Spongiform Encephalopathy UPDATE USA OCTOBER 2007
http://www.phxnews.com/fullstory.php?article=53128
http://www.phxnews.com/
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
October 24, 2007 1:07 PM
Terry S. Singeltary Sr. said... NOW, let us look at another BSE ROUNDTABLE DISCUSSION by USDA et al in the year 2003, please note the BSE science on IHC testing then, and then compare to now, and then ponder those other 9,200 cattle of the infamous June 2004 BSE cover-up program, that did not have rapid testing or WB, just IHC, the lease likely to find BSE/TSE ;
USDA 2003
We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.
snip...
Environmental Contamination We're finding out on a smaller scale with CWD and Scrapie that environmental contamination is becoming a big concern. It's something we’ve never had to deal with. Even with anthrax, we never had as much interest like we’re seeing with prions. If potential environmental contamination is a problem, then how do you safely dispose of suspect animals? It takes a lot of time and communication with the health department and the landfill owners in trying to get everybody to a comfort level. Legal concerns do need to be addressed. It is a ripple effect. You may have feedlot contamination, and then you have all the water that ran off. In many of these large feedlots, they're using that water run-off to irrigate fields nearby. Unfortunately, perception often wins over science in these situations, whether it is a real risk or not! Here's an example of a situation we dealt with in our state. A wild deer was shot in a state that has areas endemic with CWD. This animal was harvested just outside of that area. We received a call that this animal had tested positive. The brain had been pulled in that state, but the carcass was allowed to leave with the hunter before the results were reported. By that time, the hunter had taken the meat to a ND processor for final processing and packaging. Then we had to tell the processing plant that they'd had a CWD-positive animal go through their facility and we gave them advice on a recommended cleaning process.
Dr. Bartz: What is the recommended cleaning process?
Dr. Keller: There is no ‘officially approved’ disinfectant for surface cleaning, but strong chlorine solutions, sodium hydroxide or Environ LPH have been recommended.
Dr. Thornsberry: Steam cleaning is part of the process.
Dr. Keller: There has been discussion about the potential approval of Environ LPH for surface cleaning.
Dr. Detwiler: Rick Race has a publication coming out on the different versions of the LPh. The company's supposed to come back out with the old formulation. It's not as corrosive.
Dr. Spraker: When you use it, hold your breath.
Dr. Keller: Another concern I have that's been talked about today already is ‘what is the infectious dose’ and how does that affect the incubation period? We have been focusing on animals, but I know that human health concerns usually supercede animal health concerns in our state. What's at stake? Supposedly an estimate came out of Canada saying they were still losing $10 million per day. Extrapolating that to the number of cattle in our country, you could be looking at up to $50 million a day. I think that's a very conservative estimate. Price of human life: should we be talking money when we're talking about a disease with so many unknowns yet about its pathogenicity and infectivity? It appears we can’t talk about zero tolerance anymore, because prions are here in many forms (normal and abnormal). And we will not ever make all prion diseases just ‘go away’, but we do need to put all the effective mitigating factors in place that we can to decrease the introduction and amplification of prion diseases. We need to look at what we can do to ‘prevent’ and then also be ready to deal with the disease if needed.
Dr. Detwiler: I went through one of the biggest cull cow plants up in Canada. They have to do the full SRM—the vertebral column and everything. I asked what it cost to implement that and it's about two cents per pound. That's really not much when you consider the ramifications.
Dr. Keller: If there are going to be costs, they usually trickle down in the cattle business to the producer. But there's probably not a producer who wouldn't spend a few cents to save his industry and assure his customer about the safety of the final product. From the estimates I’ve read, I don’ t think cost is as big an issue as some would like us to believe.
Dr. Thornsberry: If the USDA decides to open the border the first of March with no restrictions, does North Dakota have the authority to turn away Canadian cattle?
Dr. Keller: We cannot stop animals coming through our state, but we could prevent them from unloading in North Dakota.
Dr. Thornsberry: So some state along the border could put a stop to cattle coming into the state to stay. The interesting thing about Missouri, where I live, is that Canada will not allow us to export any cattle. We are a southern state with endemic Anaplasmosis and we have potential blue tongue virus infection in our cattle herd. They have all these restrictions based on those two disease control programs, but yet the government is going to force us to take cattle from Canada. Our state veterinarian is under the impression that, if they open the border, there's no way we can restrict them coming in. In Missouri, it's a federal rule. My understanding was that the state veterinarian could make a ruling that because of disease control, nothing could come in to Missouri.
Dr. Keller: I'm really not the person to answer this from a legal perspective, but we've always been counseled that state laws could be more restrictive than federal laws.
Dr. Detwiler: If you recall some of the conference calls where the states had more restrictive rules, the federal government said they would challenge those in court.
Dr. Thornsberry: California has always been able to do that for years, and everybody seems to abide by it.
Dr. Detwiler: Our attorney says that's wrong; they can't. I've heard it both ways. I've heard it from the federal side that yes, you can be restrictive on some diseases, and then they say no on others.
Dr. Thornsberry: I'd like Dr. Detwiler and Dr. Keller to comment on the Harvard risk assessment. The USDA is kind of using that as a carte blanche for opening up the border to Canada, and I think they've already made their mind up. Yet the Harvard risk assessment, if you get into the depth of it a little bit, says that yes, there is an inherent risk of bringing prion-related diseases into this country if the border is opened. Nobody can say that risk is not there. What we’re saying is if it does come in, we have enough safe-guards in place to contain it. That one case in Japan created the loss of 40% of their demand for beef products overnight, and it lasted for several months until they instituted the program to test every animal. I'm not sure we'd have that much of a ramification. However, just saying we can identify the case is not sufficient. Our government should be more oriented toward preventing a case from ever coming rather than letting us figure out how to deal with it once it gets here. I have a meat plant in Missouri and I have a zero tolerance for Listeria spp., for E. coli O157:H7, and Salmonella, which are sometimes fatal to children and older people. Everyone else survives. If they find that in my plant, I'm shut down until I can prove to USDA that it's not there. And yet we're going to open up our borders and allow a disease to come through that's 100% fatal if a human being should contract the disease. There's an inconsistency in the regulations concerning these animal diseases. One of the comments we're probably going to make to the USDA as a veterinary group, is that the Harvard risk assessment is fine, but once one case is here and identified, we now have potentially seeded large areas with prions. And we know they exist forever. How should the livestock industry view the Harvard risk assessment?
Dr. Keller: I think we need to look at the big picture. There are bits and pieces that people quote from the HRA, but even if you look at the executive summary of the update, there are significant things it says. It's true that the United States is robust and resistant. If the disease is introduced, it will go away because of the system. Other countries have demonstrated that by feed bans. But it also says we're not totally resistant to the introduction, and that if you look at the possible scenarios, it could potentially be a 20-year decline of the agent. It won’t be like it's here today and gone tomorrow. That's one thing that's very significant—to say that you have to expect a 20-year period to eliminate the agent. The other thing is that there are weaknesses in the system, and it's so important that we don't have high risk SRMs being introduced into our food supply, because if the agent is in the United States, however small there's the perception of a potential public health risk. And, the HRA indicated that there is definitely a potential for further transmission to animals if there are leaks in the feed ban. The most significant item is that, in the worst-case scenario, if the agent comes from Canada, it's below the level of detection of the USDA's current surveillance system.
Dr. Thornsberry: That's very significant. From an epidemiological standpoint, it blares out. It asks, “Why would you make this decision with the current level of surveillance that we have in this country?”
Dr. Detwiler: To me, the concern is to look at what minimum risk is. Unless it's further defined, how do you look at all the other countries? Some have never been evaluated. Where do they fall in the scheme of things? Those are concerns I have. We also really need to be aware that the risk set a precedent for the US.
Dr. Keller: We know we're at risk for having our own case of BSE here in the US, but I don't think two wrongs make a right. We need to be proactive in getting something done to identify animals as they come in, if they do come in. We need to be able to track animals that are considered minimal risk. We need to hold all countries, including ourselves, to a standard to determine prevalency of all diseases, including prion diseases. I don’t see why we would accept animals from other countries until that is done! It's easy to say you're free of something if you're not adequately testing for it. We've seen that happen with other diseases.
Dr. Detwiler: I'll play devil's advocate. If the US found a case tomorrow, what would we ask of the world? I think that's valid to ask. It's valid to turn the mirror back on yourself.
Dr. Thornsberry: I guarantee you that we would immediately have individual animal ID and it wouldn’t be two years later.
Dr. Keller: And it probably would not be ID that's initially acceptable to the industry. Producers need to realize that if they don’t get involved, it will become mandatory and then they will no longer have the opportunity for producer input.
Dr. Thornsberry: It's almost in the process of being mandated now. I sat on that task force. We're just months away. July 1, 2004, we're supposed to issue premise IDs to every farm in the nation. By the first of January, 2005, we're supposed to have some sort of mandatory identification in place, probably electronic. Right now they have no funds to do that, nor have they been given permission, but they say that, because of disease control, they have the right to mandate this program now. The other issue that comes up is the concept of country-of-origin labeling. At the time the Canadian BSE cow was identified, I did some investigation at Sterling, Colorado, and a few other packing plants that were taking in Canadian beef. There were over 500,000 pounds of Canadian-bred meat out of two or three different plants in the Colorado area that were in the food chain and could not be identified. Once the animal was brought into the plant and slaughtered, that carcass just went right down the chain with all the others. There was no way to identify where that meat went. If the government at that time had wanted to put a retention on Canadian meat, they'd have had to retain a whole bunch of our meat at the same time. That's been one of the strong arguments for country-of-origin labeling, at least to maintain some ability to track that carcass past the point that it's slaughtered. Right now we don’t have that capability. Once it receives that USDA stamp, it's over. That's an issue that will have to come into play for disease control concerns. We already have, as of the first of July, a country-of-origin labeling program for Japan and South Korea to guarantee to them that no Canadian meat will make it into their country through our system. But our consumers don’t have the same choice. I think that's a travesty in our industry that we can ’t offer American consumers a choice. If we can offer it to Japan's consumers and South Korea's consumers, it seems only logical we should be able to offer it to US consumers, but we do not.
Dr. Spraker: Does the US import a lot of meat from Argentina and South America?
Dr. Thornsberry: They don’t right now. They do import a lot of cooked product. They have so much foot and mouth disease. I've been in a lot of those countries and I don't see that they'll ever have that problem under control.
Dr. Keller: We've had many foreign exchange students at out ranch, and several from South America. They have insinuated that there is a great deal of unrestricted movement between South American countries.
Dr. Thornsberry: I spent time in Venezuela on a ranch with 50,000 mother cows and they couldn’t tell you where those cows were at any one time, period. They have computers and they keep track of things, but the level of technology is much more primitive.
Dr. Keller: Communication indicated that political pressure kept Argentina animal health officials from reporting the FMD case. It was actually producers who encouraged reporting their own FMD case. I am beginning to wonder if in this country, too, it's going to take industry and producers to encourage our officials to do the right thing for US animal health and US agriculture.
Dr. Thornsberry: One group of people we haven't discussed today is the consumers in this country. Over 90% of the meat in the United States is purchased by women. I don't know if the USDA has allowed any input from consumer groups on this subject.
Dr. Keller: We should not needlessly scare the public, but there is a responsibility to take additional precautions in processing if needed. When the education and research information does catch up with the buying and consuming public, they're going to want to know what’s been done to address concerns regarding SRMs and AMR meat.
Dr. Spraker: With CWD, so many men will turn a head in and say they can't bring the meat in the house because the wife wants it tested first.
Dr. Detwiler: We get asked all the time why does the public react so volatily to this? and the only thing that I can figure is that you can't cook it away, you can't detect it with certainty in the live animal, you can ’t test the product for it. So the consumer relies on the industry and the government. It's an issue where the consumer lacks control. With E. coli, they know: if you cook it right and feed it to your kids, it's going to be okay. They have some control.
Dr. Bartz: With many infectious diseases, in two weeks, you’re over it and you get on with your life. But if you consume BSE-potentially-tainted beef, you're going to be worried for the rest of your life.
Dr. Thornsberry: In 1994, I spent a month in Spain, Portugal and France, and I know I ate beef when I was there..
Dr. Detwiler: You ate mutton.
Dr. Thornsberry: I ate mutton, I ate pork, I ate pig ears. I ate a lot of traditional Spanish and Portuguese meat, and I ate beef. And Portugal and France have had numerous cases of BSE. So have I been exposed to BSE? My son went with me.
Dr. Spraker: We know how many deaths occur from alcohol and we know how many people die from chewing tobacco. But we're not afraid of those. Why not?
Dr. Keller: It's likely because the use is intentional with alcohol and tobacco.
Dr. Detwiler: The risk communicators will tell you that if you make the choice and take the risk, there's a different kind of perception.
Dr. Thornsberry: This has been an excellent round-table. I know I've learned a lot…
[tape change]
…There does not seem to be very much risk of CWD being transferred to other species except cervids. It hasn't been seen and the chances are not great, although with any prion disease, the risk is possible.
Dr. Detwiler: If we let it go unchecked, we increase the biological load. I think it's prudent for the government to keep the biological load down.
Dr. Spraker: Because we don’t know if, 10 years from now, there will be an emergence of a new strain of CWD with a totally different host range.
Dr. Thornsberry: These prions are infective. That's the one thing that we've come to a common knowledge of here today, that's not being released by some of our cattle organizations. They are pushing the idea that a prion disease is an end-stage disease: an animal gets it, he dies, and that's the end of it. Being that these prions survive in the environment basically forever and there's no way to disinfect them, no way to destroy them, no way to get rid of them, the potential for BSE to be infective to any variety of animals does exist. We know that certain risk factors are much more inherent than others, but it is an infectious disease. I have a small feed mill and there's no telling how many people have asked me if they can feed dog food to their show steers to increase the fat in their diet, not understanding that most dog food has some level of meat and bone meal in it.
Dr. Spraker: And people eat dog food and cat food.
Dr. Thornsberry: The association of dog food manufacturers has fought against a meat and bone meal ban and they don't even want to list it in their contents. They believe if it's listed, people will quit buying it. You have to fill out paperwork to buy fish food with meat and bone meal, but I could buy a whole truck load of dog food with meat and bone meal in it and feed it to my cattle. It is illegal. There are some SRMs that are out there in this industry. Blood meal is one of my favorite concerns. We have a lot of big corporations that are using beef tallow in diets to increase the fat content in dairy rations. They're doing it as much as a pound per cow per day.
Dr. Detwiler: The thing that worries me is that those SRM’s are also in calf rations. The calves could have more susceptibility. I worry about the increased amount of blood going into calf rations.
Dr. Thornsberry: The concept of the prions making it through the system is very significant. Another issue we haven't discussed is the people taking the cleanings out of poultry barns and scattering them on their pastures for fertilizer. The prions don't ever go away, and the cattle eat the pasture down to the ground. How many prions are they being exposed to? There are a whole lot of issues there to deal with. Poultry manure can be composted and used as fuel and other things. It has alternative uses. The swine industry has made better strides in telling people not to feed hog food to cattle, although I know it still goes on in my area. Fortunately, most of the swine finishing diets don't have any bone meal. There are some things we need to do in our country to do a better job of surveillance. The veterinary industry needs to be proactive. I hope some of those SRMs are identified and the livestock producers are made aware of them and we get the information out: Don’t be feeding what's left over from your hog feed bin to your cattle.
Dr. Keller: Is there an economic analysis being done on the current situation in Canada, that could be used as an educational tool to encourage immediate consideration of other ways to utilize high risk product?
Dr. Detwiler: They are doing something on economic alternatives and what the costs would be.
Dr. Thornsberry: And there are a number of them. Any fat-soluble product has a number of possibilities and we've identified several of them today. So here's the plan. These proceedings will be made available to the American Association of Bovine Practitioners, the Academy of Veterinary Consultants, to veterinary schools and whoever would like to have them. I will also try to translate and summarize the material into some sort of publication we can give to the livestock industry. They obviously don't want to know all about PRPC and all those things, but there is information in these presentations that they need to know. You may want to add something that you didn’t say that you think might be pertinent. A lot of discussions like this have taken place, but nothing has been made available to the livestock industry—nothing on a practical level that a livestock producer can understand about the potential for CWD spreading, etc. They do not understand what BSE is. I hope, from this, we can give our producers a firm grasp of what the disease is and also let them know how they can participate in the process. And if we do that, we will have accomplished what I wanted to do with this program today.
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
2005
National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC) Testing Summary
The BSE enhanced surveillance program involves the use of a rapid screening test, followed by confirmatory testing for any samples that come back "inconclusive." The weekly summary below captures all rapid tests conducted as part of the enhanced surveillance effort. It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing.
http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html
The roundtable presentations and discussions were recorded. A transcript will be made available to the Academy of Veterinary Consultants, the American Association of Bovine Practitioners, and the Colleges of Veterinary Medicine throughout the United States and Canada. A condensed version translated for the livestock industry will be made available to educate livestock producers about prion related diseases.
http://www.r-calfusa.com/Newsletter/2004January.pdf
BACK TO REALITY OCT 24, 2007
Title: Bovine Spongiform Encephalopathy: what is "Atypical BSE" and can we detect it?
Author
Richt, Juergen
Submitted to: United States Animal Health Association Proceedings Publication Type: Abstract Publication Acceptance Date: October 17, 2006 Publication Date: October 12, 2006 Citation: Richt, J.A. 2006. Bovine spongiform encephalopathy: what is "atypical BSE" and can we detect it [abstract]? United States Animal Health Association. p. 730.
Technical Abstract: Transmissible spongiform encephalopathy (TSE) agents induce fatal neurodegenerative diseases in humans and in some other mammalian species. Human TSEs include Creutzfeldt¿Jakob disease (CJD), Gerstmann-Sträussler-Scheinker (GSS) syndrome, Kuru and Fatal Familial Insomnia (FFI). In animals, several distinct TSE diseases are recognized: scrapie in sheep and goats, transmissible mink encephalopathy (TME) in mink, chronic wasting disease (CWD) in cervids, and bovine spongiform encephalopathy (BSE) in cattle. BSE was first detected in 1986 in the United Kingdom and is the most likely cause of variant CJD in humans. BSE in cattle is a neurological disease with a characteristic molecular pattern of the protease-resistant prion protein, PrP**res. This BSE 'signature' has also been identified in BSE-induced TSEs of both domestic cats and exotic ruminant species. Since 2004, some cases of prion diseases in cattle have been described which show unusual or atypical features as assessed by the molecular characterization of PrP**res and/or histopathology, when compared to the unique features of previously described BSE. These atypical BSE cases have been characterized by Western blot and have been referred to as H- (i.e., high molecular weight) or L-type (i.e., low molecular weight type). These atypical BSE cases have been found mainly in cattle older than 8 years. In the U.S., three cases of BSE have been diagnosed so far. Case 1 represented a typical BSE isolate, identified in an animal imported from Canada. Cases 2 and 3 were identified in animals raised in the U.S. and revealed an unusual molecular PrP**res pattern, consistent with atypical BSE cases described as H-type in Europe. It should be noted that the Western Blot method applied for BSE confirmatory tests in the U.S. has been able to detect both H-type and L-type BSE cases when using known positive European samples.
Last Modified: 10/21/2007
http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=202722
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
http://madcowtesting.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007
http://cjdmadcowbaseoct2007.blogspot.com/
NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007
Tuesday, October 9, 2007 NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 RISES TO 5 DOCUMENTED CASES
http://nor-98.blogspot.com/
TSS
Wednesday, October 24, 2007
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