Friday, March 21, 2014

Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?

Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?

 

Rancho Recall Explained

 

As of March 20, 2014, FSIS has completed all checks (effectiveness checks and disposition verification checks) for recalls 002-2014 and 013-2014 regarding Rancho Feeding Corporation. FSIS has determined that based on the number of successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses were notified of the recall and removed affected products from commerce that the recall activities were effective.

 

There will be no further additions to the distribution list. Because of widespread interest in both of these recalls, however, FSIS has decided to temporarily leave the recall releases and distribution lists in the “active” section of the recalls website, rather than moving it to the “archive” section, as is usual policy, in an effort to continue to make the information as accessible as possible.

 

Background

 

FSIS inspection personnel were present at Rancho Feeding Corporation during normal operations, as required by law.

 

At this time, USDA’s Office of Inspector General (OIG) is conducting an investigation into activities at the facility. FSIS is partnering with OIG on the investigation and is unable to comment further while the investigation is ongoing.

 

Any meat product that is processed without the full benefit of inspection is considered unwholesome and unfit for human consumption. Therefore, FSIS requested, and the establishment agreed to conduct a Class I recall of all products, including whole carcasses, produced from Jan. 1, 2013 through Jan. 7, 2014.

 

FSIS has received no reports of illness from consumption of these products. Anyone concerned about an illness should contact a healthcare provider.

 

Many of the carcasses that were the subject of the recall were shipped to other establishments where they were processed into smaller cuts and sold. Some of this meat was included in processed products, such as frozen entrees.

 

As part of the recall process, FSIS personnel track down the distribution of the product. Because this recall occurred at the source—the slaughter establishment—FSIS has followed the path of the recalled product as the cuts were sold for processed food.

 

Additional Resources

 

The recall release for Recall 013-2014 is available on the FSIS website.

 

The distribution list for Recall 013-2014 also is available on the FSIS website.

 

Inspection 101 provides an overview of how agency inspectors and veterinarians oversee the safe production of meat, poultry and egg products that enter commerce.

 

To understand the recall process, the FSIS Recall Directive explains how and why the agency conducts recalls.

 

To understand ante-mortem inspection, please read FSIS Directive 6100.1 Ante-Mortem Livestock Inspection.

 

To understand post-mortem inspection, please read FSIS Directive 6100.2 Post-Mortem Livestock Inspection.

 

To learn more about the law that sets the guidelines to ensure the nation’s meat, poultry and egg supply are safe, read the Federal Meat Inspection Act.

 

Follow FSIS through two Twitter feeds: •@USDA Food Safety (English) •@USDA Food Safety_es (Spanish)

 

Sign up for FSIS RSS Feeds and E-mail subscription.

 

To submit a request for information, visit the FSIS Freedom of Information Act page.

 

Where Did Rancho Product Go? Rancho Feeding Corporation to Distribution Centers to Processing Establishments to Retail Establishments

 

 Last Modified Mar 20, 2014

 


 

>>>The page informs consumers that inspection personnel were on-site during normal operations, but due to the ongoing investigation by the USDA Office of the Inspector General, FSIS can’t give any further comment on “the company’s intermittent circumvention of inspection requirements that may have occurred over an extended period of time.” FSIS has received no reports of illness from consumption of these products. <<<

 

holy mad cow, I sure do feel better about the situation now...not. 10 to 50 years incubation period for TSE prion disease, so the line ‘’FSIS has received no reports of illness from consumption of these products’’, in relations to the TSE prion disease, aka mad cow type disease, there would be no reported illness, yet. that’s what they are reporting in the UK around 1985, about all the offal and such over there (UK), that was distributed and consumed, until the incubation period started catching up around 1995. does not mean there will not be any in the future, with regards to the TSE prion disease, from this incident.

 

 

>>> As of March 20, 2014, FSIS has completed all checks and determined that the recall activities were effective. There will be no further additions to the distribution list, but, in an effort to make the information as accessible as possible, it will remain in the “active” section of the FSIS recalls website. <<<

 

 

so, no further additions, end of story, or not ???

 

I am absolutely stunned here as well. just calling it off, the rest of the consumers can fend for themselves ???

 

what about the NSLP, and what our children ???

 

Did any of this recall from Rancho OFFAL from Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014, did any of this go to our children via NSLP like the Westland/Hallmark: 2008 Beef Recall did ?

 

is this why they are calling off the additional list of recipients of the Rancho OFFAL from Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014 ???

 

no one sick yet, famous last words, triple BSE firewall, nothing but ink on paper I tell, nothing but ink on paper. ...tss

 

 

“Cases of vCJD peaked in 2000, leading some scientists to speculate that the disease has an incubation period of about a decade. Yet studies of different forms of CJD suggest that the incubation time of vCJD could be much longer, indicating that many people in Britain could be carrying the infection without symptoms.”

 


 

Monday, October 14, 2013

 

Researchers estimate one in 2,000 people in the UK carry variant CJD proteins

 


 

However, I think that the specific confusion there is that people talk about sporadic CJD occurring at 1 per million. That is not your individual risk. Your risk is 1 per million every year. Actually, it is nearer 2 per million per year of the population will develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about 1 in 30,000. So that has not really changed. When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.

 


 

Cases of vCJD peaked in 2000, leading some scientists to speculate that the disease has an incubation period of about a decade. Yet studies of different forms of CJD suggest that the incubation time of vCJD could be much longer, indicating that many people in Britain could be carrying the infection without symptoms.

 


 

Tuesday, March 11, 2014

 

Science and Technology Committee Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD

 

Actually, it is nearer 2 per million per year of the population will develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about 1 in 30,000. So that has not really changed. When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 

Thursday, March 20, 2014

 

JACK IN THE BOX NOW CAUGHT UP IN MASSIVE RANCHO DEAD STOCK DOWNER CANCER COW RECALL

 


 

Thursday, March 6, 2014

 

TEXAS RECALL LIST MASSIVE FROM DEAD STOCK DOWNER CANCER COWS OFFAL from Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014 shipped to Texas, Florida, and Illinois UPDATE FEBRUARY 14, 2014

 


 

Thursday, February 27, 2014

 

BEEF, CANCER, PRIONS, AND OTHER DANGEROUS AND DEADLY PATHOGENS, APPARENTLY, IT'S WHAT'S FOR DINNER

 


 

Friday, February 14, 2014

 

OFFAL from Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014 shipped to Texas, Florida, and Illinois UPDATE FEBRUARY 14, 2014

 


 

 Thursday, February 13, 2014

 

HSUS VS USDA ET AL BAN DOWNER CALVES FOR HUMAN CONSUMPTION (*veal) and potential BSE risk factor there from

 


 

Tuesday, February 11, 2014

 

*** California Firm Recalls Various Meat Products Produced Without the Benefit of Full Inspection Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014

 


 

Thursday, November 28, 2013

 

Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows

 


 

*** seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???

 

Saturday, September 21, 2013

 

Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT

 


 

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ??? this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)

 


 

try this link ;

 


 

Sunday, November 13, 2011

 

*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock

 


 

Thursday, February 20, 2014

 

*** Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr. Linda Detwiler 2014

 


 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

 Monday, March 3, 2014

 

*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers to eat dead stock downers and whatever else the industry decides

 

see updated Rancho CLASS 1 HIGH RISK dead stock cancer downer recall for IDAHO

 


 


 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 

OAI 2012-2013

 

OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.

 

ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St. Newberry SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y

 

DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN 46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y

 

ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC 28163-7617 OPR FL, TH NP 7/17/2013 OAI N

 

NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007 OPR FR, OF NP 7/16/2013 OAI Y

 

DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N

 

CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y

 

*** DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N

 

Ruminant Feed Inspections Firms Inventory (excel format)

 


 

PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates posted, as in numerical order, you will have to sift through them for yourselves. ...tss

 

snip...see full text ;

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

Saturday, December 15, 2012

 

Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012

 


 

Sunday, February 2, 2014

 

The Presence of Disease-Associated Prion Protein in Skeletal Muscle of Cattle Infected with Classical Bovine Spongiform Encephalopathy

 

NOTE Pathology

 


 

Saturday, December 21, 2013

 

**** Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle ****

 


 

Wednesday, December 4, 2013

 

*** Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 /

 

Wednesday, December 4, 2013

 


 

Saturday, November 2, 2013

 

*** APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe

 


 

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. ***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

 


 

 Thursday, August 12, 2010

 

Seven main threats for the future linked to prions

 

First threat

 

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

 

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

 

Second threat

 

snip...

 


 

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

 

Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.

 


 

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

 

Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD

 

Date: Thu, 28 Nov 2002 10:23:43 -0000

 

From: "Asante, Emmanuel A" e.asante@ic.ac.uk

 

To: "'flounder@wt.net'" flounder@wt.net

 

Dear Terry,

 

I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.

 

Thank you for your interest in the paper.

 

In respect of your first question, the simple answer is, yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.

 

I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.

 

Emmanuel Asante

 

<>

 

____________________________________

 

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)

 

____________________________________

 


 

 Freas, William

 

From: Terry S. Singeltary Sr. [flounder@wt.net]

 

Sent: Monday, January 08,2001 3:03 PM

 

To: freas@CBS5055530.CBER.FDA.GOV

 

Subject: CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)

 

Greetings again Dr. Freas and Committee Members,

 

I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version).

 

I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below).

 

So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here:

 

remember AIDS/HIV, 'no problem to heterosexuals in the U.S.?

 

no need to go into that, you know of this blunder:

 

DO NOT make these same stupid mistakes again with human/animal TSE's aka MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother to sCJD as well (both cases confirmed). I have seen many deaths, from many diseases. I have never seen anything as CJD, I still see my Mom laying helpless, jerking tremendously, and screaming "God, what's wrong with me, why can't I stop this". I still see this, and will never forget. Approximately 10 weeks from 1st of symptoms to death. This is what drives me. I have learned more in 3 years about not only human/animal TSE's but the cattle/rendering/feeding industry/government than i ever wished to.

 

I think you are all aware of CJD vs vCJD, but i don't think you all know the facts of human/animal TSE's as a whole, they are all very very similar, and are all tied to the same thing, GREED and MAN.

 

I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, eyelid test, anything at whatever cost, we need a test FAST.

 

DO NOT let the incubation time period of these TSEs fool you.

 

To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. from the BVA and the URL is posted in my (long version).

 

U.S.A. should make all human/animal TSE's notifiable at all ages, with requirements for a thorough surveillance and post-mortem examinations free of charge, if you are serious about eradicating this horrible disease in man and animal.

 

There is histopathology reports describing “_florid_ plaques" in CJD victims in the USA and some of these victims are getting younger. I have copies of such autopsies, there has to be more. PLUS, sub-clinical human TSE's will most definitely be a problem.

 

THEN think of vaccineCJD in children and the bovine tissues used in the manufacturing process, think of the FACT that this agent surviving 6OO*C. PNAS -- Brown et al. 97 (7): 3418 scrapie agent live at 600*C

 

Then think of the CONFIDENTIAL documents of what was known of human/animal TSE and vaccines in the mid to late 80s, it was all about depletion of stock, to hell with the kids, BUT yet they knew. To think of the recall and worry of TSE's from the polio vaccine, (one taken orally i think?), but yet neglect to act on the other potential TSE vaccines (inoculations, the most effective mode to transmit TSEs) of which thousands of doses were kept and used, to deplete stockpile, again would be foolish.

 

--Oral polio; up to 1988, foetal calf serum was used from UK and New Zealand (pooled); since 1988 foetal calf serum only from New Zealand. Large stocks are held.

 

--Rubella; bulk was made before 1979 from foetal calf serum from UK and New Zealand. None has been made as there are some 15 years stock.

 

--Diphtheria; UK bovine beef muscle and ox heart is used but since the end of 1988 this has been sourced from Eire. There are 1,250 litres of stock.

 

--Tetanus; this involves bovine material from the UK mainly Scottish. There are 21,000 litres of stock.

 

--Pertussis; uses bovine material from the UK. There are 63,000 litres of stock.

 

--They consider that to switch to a non-UK source will take a minimum of 6-18 months and to switch to a non-bovine source will take a minimum of five years.

 

3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are sourced from the USA and the company believes that US material only is used.

 

89/2.14/2.1

 

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

 

BSE3/1 0251

 

4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK. there are 440,000 units of stock. They have also got MMR using bovine serum from the UK.

 

5. XXXXXXXXXXX have influenza, rubella, measles, MMR vaccines likely to be used in children. Of those they think that only MMR contains bovine material which is probably a French origin.

 

6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial. These use veal material, some of which has come from the UK and has been made by XXXXXXXXXXX (see above).

 

I have documents of imports from known BSE Countries, of ferments, whole blood, antiallergenic preparations,

 

2

 

human blood plasma, normal human blood sera, human immune blood sera, fetal bovine serum, and other blood fractions not elsewhere specified or included, imported glands, catgut, vaccines for both human/animal, as late as 1998. Let us not forget about PITUITARY EXTRACT. This was used to help COWS super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease.

 

ANNEX 6

 

MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF BSE TO BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL

 

How much of this was used in the U.S.?

 

Please do not keep making the same mistakes;

 

'Absence of evidence is not evidence of absence'. What are the U.S. rules for importing and manufacturing vaccines, medicines and medical devices?

 

Does the U.S.A. allow sourcing of raw material of ruminants from the U.S.A.?

 

U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds.?

 

The U.S. rendering system would easily amplify T.S.E.'s: Have we increased the stability of the system (improved heat treatments) since the EU SSC report on the U.S.A. was published in july 2000?

 

What is done to avoid cross-contaminations in the U.S.A.?

 

How can the U.S. control absence of cross-contaminations of animal TSE's when pig and horse MBM and even deer and elk are allowed in ruminant feed, as well as bovine blood?

 

I sadly think of the rendering and feeding policy before the Aug. 4, 1997 'partial' feed ban, where anything went, from the city police horse, to the circus elephant, i will not mention all the scrapie infected sheep. I am surprised that we have not included man 'aka soyent green'. It is a disgusting industry and nothing more than greed fuels it.

 

When will the U.S.. start real surveillance of the U.S. bovine population (not passive, this will not work)?

 

When will U.S. start removing SRMs?

 

Have they stopped the use of pneumatic stunners in the U.S.?

 

If so, will we stop it in all U.S. abattoirs or only in those abattoirs exporting to Europe?

 

If not, WHY NOT?

 

same questions for removal of SRM in the U.S.A., or just for export?

 

If not, WHY NOT?

 

How do we now sterilize surgical/dental instruments in the U.S.A.?

 

Where have we been sourcing surgical catgut?

 

(i have copies of imports to U.S., and it would floor you) hen will re-usable surgical instruments be banned?

 

Unregulated "foods" such as 'nutritional supplements' containing various extracts from ruminants, whether imported or derived from

 

3

 

US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or at least very seriously regulated. (neighbors Mom, whom also died from CJD, had been taking bovine based supplement, which contained brain, eye, and many other bovine/ovine tissues for years, 'IPLEX').

 

What is the use of banning blood or tissue donors from Germany, France, etc... when the U.S.A. continues exposing cattle, sheep and people to SRM, refuses to have a serious feed ban, refuses to do systematic BSE-surveillance?

 

The FDA should feel responsible for the safety of what people eat, prohibit the most dangerous foods, not only prohibit a few more donors - the FDA should be responsible for the safe sourcing of medical devices, not only rely on banning donors "from Europe" The 'real' risks are here in the U.S. as well, and nave been for some time.

 

We must not forget the studies that have proven infectivity in blood from TSE's.

 

The Lancet, November 9, 1985

 

Sir, --Professor Manuelidis and his colleagues (Oct 19, p896) report " transmission to animals of Creutzfeldt-Jakob disease (CJD) from the buffy coat from two patients. We also transmitted the disease from whole blood samples of a patient (and of mice) infected with CJD.1 Brain, Cornea, and urine from this patient were also infectious, and the clinicopathological findings2 are summarised as follows.

 

snip...

 

Samples,were taken aseptically at necropsy. 10% crude homogenates of brain and cornea in saline, whole blood (after crushing a clot), and untreated CSF and urine were innoculated intracerebrally into CF1 strain mice (20 ul per animal). Some mice showed emaciation, bradykinesia, rigidity of the body and tail, and sometimes tremor after long incubation periods. Tissues obtained after the animal died (or was killed) were studied histologically (table). Animals infected by various inocula showed common pathological changes, consisting of severe spongiform changes, glial proliferation, and a moderate loss of nerve cells. A few mice inoculated with brain tissue or urine had the same amyloid plaque found in patients and animals with CJD.3

 

snip...

 

Department of Neuropathology, Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka812, Japan

 

JUN TATEISHI (full text-long version)

 

and

 

CWD and transmission to man will be no different than other TSE's.

 

"Clearly, it is premature to draw firm conclusions about CWD assing naturally into humans, cattle and sheep, but the present esults suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has

 

4

 

caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs,"

 

G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O'Rourke3, L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M. Smits2 and B. Caughey1,7

 

or more recently transmission of BSE to sheep via whole blood Research letters Volume 356, Number 9234 16 September 2000

 

Transmission of BSE by blood transfusion in sheep Lancet 2000; 356: 999 – 1000

 

F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock

 

See Commentary

 

"We have shown that it is possible to transmit bovine spongiform encephalopathy (BSE) to a sheep by transfusion with whole blood taken from another sheep during the symptom-free phase of an experimental BSE infection. BSE and variant Creutzfeldt-Jakob disease (vCJD) in human beings are caused by the same infectious agent, and the sheep-BSE experimental model has a similar pathogenesis to that of human vCJD. Although UK blood transfusions are leucodepleted--a possible protective measure against any risk from blood transmission-- this report suggests that blood donated by symptom-free vCJD-infected human beings may represent a risk of spread of vCJD infection among the human population of the UK."

 

"The demonstration that the new variant of Creutzfeldt-Jakob disease (vCJD) is caused by the same agent that causes bovine spongiform encephalopathy (BSE) in cattle1 has raised concerns that blood from human beings in the symptom-free stages of vCJD could transmit infection to recipients of blood transfusions (full text long version)" and...

 

"The large number of cases (1040), temporal clustering of the outbreaks (15 in the first 6 months of 1997), the high in-flock incidence, and the exceptional involvement of goats (390 cases), suggested an accidental infection. The source of the epidemic might have been TSE-contaminated meat and bonemeal, but eight flocks had never been fed any commercial feedstuff. Infection might have risen from the use of a formol-inactivated vaccine against contagious agalactia prepared by a single laboratory with brain and mammary gland homogenates of sheep infected with Mycoplasma agalactiae. Although clinical signs of TSE in the donor sheep have not been found, it is possible that one or more of them were harbouring the infectious agent. Between 1995 and 1996, this vaccine was given subcutaneously to 15 of the affected flocks (to one flock in 1994) ; in these animals the disease appeared between 23 and 35 months after vaccination. No information is available for herd 13 because it was made up of stolen animals. Sheep from the remaining three flocks (1-3, figure) did not receive the vaccine, thus suggesting a naturally occurring disease.” (again, full text long version).

 

IN SHORT, please do under estimate this data and or human/animal TSE's including CWD in the U.S.A.

 

A few last words, please.

 

The cattle industry would love to have us turn our focus to CWD and forget about our own home grown TSE in Bovines. This would be easy to do. Marsh's work was from downer cattle feed, NOT downer deer/elk feed. This has been proven.

 

DO NOT MAKE THAT MISTAKE.

 

There should be NO LESS THAN 1,000,000 tests for BSE/TSE in 2001 for U.S.A. French are testing 20,000 a week. The tests are available. Why wait until we stumble across a case from passive surveillance, by then it is to late. IF we want the truth, this is a must???

 

United States Total ,Bovine Brain Submissions by State,

 

May 10, 1990 thru October 31, 2000

 

Total 11,700

 

FROM 1.5 BILLION HEAD OF CATTLE since 1990 ???

 

with same feeding and rendering practices as that of U.K. for years and years, same scrapie infected sheep used in feed, for years and years, 950 scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known to date. (hmmm, i am thinking why there is not a variant scrapid, that is totally different than all the rest)? just being sarcastic.

 

with only PARTIAL FEED BAN implemented on Aug. 4, 1997??? (you really need to reconsider that blood meal etc. 'TOTAL BAN')

 


 

AND PLEASE FOR GODS SAKE, STOP saying vCJD victims are the only ones tied to this environmental death sentence. "PROVE IT". It's just not true. The 'CHOSEN ONES' are not the only ones dying because of this man-made death sentence. When making regulations for human health from human/animal TSEs, you had better include ALL human TSE's, not just vCJD. Do NOT underestimate sporadic CJD with the 'prehistoric' testing available to date. This could be a deadly mistake. Remember, sCJD kills much faster from 1st onset of symptoms to death, and hvCJD is the fastest. Could it just be a higher titre of infectivity, or route or source, or all three?

 

Last, but not least. The illegal/legal harvesting of body parts and tissues will come back to haunt you. Maybe not morally, but due to NO background checks and human TSEs, again it i will continue to spread.

 

Stupidity, Ignorance and Greed is what fuels this disease. You must stop all of this, and ACT AT ONCE...

 


 


 


 

DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)

 

The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why???? than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!!

 

Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....

 

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!

 

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...

 

Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and aggressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"

 

again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

 

You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)

 

 

Monday, August 9, 2010

 

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?

 

Greetings,

 

I think something is terribly wrong here with this prionpathy debate vs prion debate i.e. Ironside first 10 nvCJD in 1996, compared to Gambetti's first 10+ prionpathy here in the USA in 2010.

 

what does this tell us ???

 

let's compare Gambetti's first 10 in 2010, to Ironside's first 10 in 1996, to a few other cases of this prionpathy in other countries. let' compare clinical and pathological features.

 

we know that the UKBSEnvCJD theory was born from the theory of sheep scrapie, to BSE in cows via feed, to nvCJD to humans via the infectious mad cows that were fed this tainted feed. but we now know that these different strains, cause different symptoms, length of illness from onset of symptoms to death, psychotic vs dementia, kuru type plaques vs no kuru plaques. but yet in 2010, this does not matter.

 

so why did it matter with the first 10 of Ironside?

 

How can we overlook some of the exact same clinical and pathological features from nvCJD (Ironside's first 10) to (Gambetti's first 10), and how can they conclude that in 1996 they meant one thing, but yet in 2010 they mean something else?

 

so how can there be so much change in science from then to now?

 

how can the big pond be such a factor in prion science $

 

why is it that only the UK and other EU countries can have mad cows, and have humans with mad cow disease there from, but here in the USA, where we have the most documented prion disease in different species on the planet, it's all spontaneous, or generic, with no related gene mutation, but a sporadic genetic prion disease, now called prionpathy ?

 

I don't believe it. I believe that it's just more of the same, just different strains.

 

I now call this new prionpathy, 'Prionbaloney'.

 

they cannot have their cake, and eat it too. which is it ? who is right ? Ironside or Gambetti ?

 

Does the USA really have a prion cloaking devise that protects us no matter how much banned mad cow protein is in commerce?

 

WHY is it so hard to believe that these atypical BSE strains were a cause of feed, same as with the c-BSE?

 

This theory was proven by the EU mad cow feed ban and the dramatic drop in mad cow cases across the EU, there from.

 

WHY is it that no one will assess this scientifically with transmission studies $ i.e. will atypical BSE transmit via feed as does/did c-BSE?

 

The only cow documented in the world to date with a Genetic mutation g-h-BSEalabama, the same as Gambetti's first 10+ in humans, and this cow had access to TONS of banned mad cow protein in Alabama during that same time period, and there is no link there, it's all just generic, spontaneous, but there is no related mutation to the humans, only to the cow in Alabama ???

 

something just does not compute here $

 

O.K. let's compare some recent cases of this prionpathy in other countries besides Gambetti's first 10 recently, that he claims is a spontaneous event, from a genetic disorder, that is not genetic, but sporadic, that is related to no animal TSE in North America, or the world. ...

 

 

snip...see full history of this charade here ;

 

 

Monday, August 9, 2010

 

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?

 


 

 

Monday, January 14, 2013

 

Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe

 


 

 

VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $

 

OR-10 15:25 - 15:40 VARIABLY PROTEASE-SENSITIVE PRIONOPATHY IS TRANSMISSIBLE IN BANK VOLES Nonno

 


 

 

OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles

 

Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanit√†; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Universit√† di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA

 

Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.

 

Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.

 

Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases. In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.

 

Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109. The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 

SOURCE PRION2012

 


 


 

“Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease.”

 

Friday, January 10, 2014

 

*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ??? ***

 

Greetings Friends, Neighbors, and Colleagues,

 


 

CJD QUESTIONNAIRE USA

 


 


 

CJD VOICE

 


 

Saturday, November 2, 2013

 

APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe

 


 

Tuesday, March 5, 2013

 

Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)

 

FDA believes current regulation protects the public from BSE but reopens comment period due to new studies

 


 

Tuesday, March 11, 2014

 

Science and Technology Committee Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD

 

Actually, it is nearer 2 per million per year of the population will develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about 1 in 30,000. So that has not really changed. When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.

 


 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 


 

*** And Terry, I promised the editor you would respond so thanks for backing my prediction up. I have read your tripe before so did not reread the whole thing. but your point about the age of the cattle takes on the scientific regulatory bodies of every country but one that exports US beef. They all, but one, agree that meat from cattle under 30 months of age carries zero risk of BSE prions. 1 △ ▽ • Reply • Share ›

 

Terry S. Singeltary Sr. > doc raymond • a month ago

 

Dr. Richard Raymond Sir, I only reply when you are scientifically wrong. I commented today, because again, you were scientifically wrong, and I proved it again, with scientific facts to back it up. sorry if that upsets you. you can fool some of the folks some of the time, but not all of us all the time. you either blatantly lied in your editorial, or you are grossly uninformed, time and time again. I think the public can take their pick on that, and in both cases, and they would be correct in both cases, in my opinion. you have a nice day sir. ...kind regards, terry

 

kind regards, terry

 

What is a Downer Calf?

 

By Dr. Richard Raymond | February 21, 2014

 


 

see full text Dr. Richard Raymond vs Terry S. Singeltary Sr.

 


 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

Thursday, February 20, 2014

 

Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr. Linda Detwiler 2014

 


 

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

 


 

FSIS, USDA, REPLY TO SINGELTARY

 


 

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

 


 

Tuesday, August 18, 2009

 

* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009

 


 

WHAT about the sporadic CJD TSE proteins ?

 

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***

 


 

Sunday, October 13, 2013

 

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 


 

 

 

 kind regards, terry

Thursday, March 20, 2014

JACK IN THE BOX NOW CAUGHT UP IN MASSIVE RANCHO DEAD STOCK DOWNER CANCER COW RECALL

JACK IN THE BOX NOW CAUGHT UP IN MASSIVE RANCHO DEAD STOCK DOWNER CANCER COW RECALL

 

Letter: Rancho Feeding meat went to Jack in the Box

 

Wed, Mar 19, 2014

 

Much of the beef from Rancho Feeding Corp., the Petaluma slaughterhouse that had to recall all the meat it produced last year, ended up in hamburgers sold by fast food giant Jack in the Box, according to a letter from the plant's manager to the federal government.

 

The beef also ended up in the products of other fast food chains. Those companies, as well as Jack in the Box, have recalled the hamburger patties, a top industry consultant said on Tuesday.

 

Also, the company that supplied the food chains has recalled the product, though it is all but certain it has been consumed, said the consultant, Dave Theno.

 

“At this stage, I believe they are all completed,” Theno, a former executive with Jack in the Box, said of the fast food chains' recall actions.

 

In the Oct. 28, 2013, letter to the U.S. Department of Agriculture's Food Safety Inspection Service, Rancho Feeding manager Scott Parks criticized as unfounded a USDA inspector's report that a cow was slaughtered inhumanely.

 

The Press Democrat obtained the letter from a source who asked to remain anonymous because the case is being investigated by the USDA and the U.S. Attorney General. In it, Parks said Rancho would lose customers if it was thought to be treating animals incorrectly.

 

His main concern was with Jack in the Box.

 

“The majority of our carcasses end up at Jack in the Box,” Parks wrote to the USDA's Alameda office, “and if they stop taking our product we will be out of business.”

 

(page 2 of 4)

 

Former Rancho co-owner Robert Singleton said Tuesday that he doubted Parks had actually written such a statement regarding the fast-food company, saying, “He wouldn't know.”

 

Jack in the Box officials did not respond to calls and emails seeking comment.

 

Rancho was forced in February to recall 8.7 million pounds of beef and veal produced in 2013 and sold throughout the United States and Canada. The USDA said it had been produced without being fully inspected.

 

No illnesses have been reported, but thousands of retailers who bought Rancho meat, from Safeway to Wal-Mart, have had to recall products ranging from Hot Pocket sandwiches to beef jerky from Sonoma-based Krave Pure Foods.

 

Also, a number of North Bay custom ranchers have had their beef locked down — unable to sell or retrieve it — even though, they say, the health of their cattle has not been questioned and they were processed separately from the plant's dairy cows.

 

The USDA and the U.S. Attorney General's Office — as well as Rancho's owners — have been tight-lipped about what suspected wrongdoings are being investigated. Sources with knowledge of the investigation have said one issue is that the slaughterhouse was processing cows with cancer. That is illegal.

 

Rancho ceased operations in February and is in the process of being sold to a Marin rancher.

 

Parks, in the seven-page letter that is a catalogue of complaints about the USDA inspector, did not say how much of the slaughterhouse's beef was sold to Jack in the Box, which has 2,250 restaurants and franchises in 21 states, according to its website.

 

(page 3 of 4)

 

Theno said the meat represented “a substantial amount of product” for Jack in the Box.

 

About 40 percent of a typical fast-food hamburger patty consists of fat and fat trimmings. The remainder is the type of lean beef that Rancho produced from dairy cows it purchased, said Theno, who was senior vice president and chief food safety officer for Jack in the Box. The company hired him after a 1993 scandal in which its burgers were blamed for a massive food illness outbreak in which four children died.

 

Depending on the blend of lean to fat beef, and on the size of the hamburger patties, one million pounds of beef could produce 4 million quarter-pound patties to 9 million smaller patties, said Theno, a Meat Industry Hall of Fame member.

 

Rancho did not sell directly to Jack in the Box, but to a meat grinding operation that then sold patties to the fast food firm, said Theno. He said that the grinder, which he would not identify because of his links to the industry, also supplied other fast food chains. All had been affected by the recall, he said.

 

“I know for a fact that these guys (the grinder) produce for both Jack as well as other providers, major fast food people, and you've got to go out to everyone” in a recall, Theno said.

 

The breakdown in the food safety chain in the Rancho case already has caused a reassessment at the major fast-food chains, Theno said.

 

“This is a situation, everyone in the stream takes a look at, 'OK, we aren't having any fun here, what do we need to be doing to make sure this isn't happening on our watch again,'” he said.

 

(page 4 of 4)

 

There likely has been a burst of legal activity in the wake of the recall, said Bill Marler, a Seattle food safety attorney who publishes Food Safety News, an online news service.

 

From end users like Jack in the Box, through the grinders that supply them, through any middlemen, to the original slaughterhouse, each party relies on the actions of the one preceding it in the chain of distribution, Marler said.

 

“Jack in the Box would be the downstream entity making claims upstream,” he said. “I would be shocked at this stage, given the amount of product being recalled and the number of stores and now restaurants being implicated, if there weren't claims being made.”

 

You can reach Staff Writer Jeremy Hay at 521-5212 or jeremy.hay@pressdemocrat.com.

 


 


 


 


 

Thursday, March 6, 2014

 

TEXAS RECALL LIST MASSIVE FROM DEAD STOCK DOWNER CANCER COWS OFFAL from Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014 shipped to Texas, Florida, and Illinois UPDATE FEBRUARY 14, 2014

 


 

 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 


 

Monday, March 3, 2014

 

*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers to eat dead stock downers and whatever else the industry decides

 


 

 Thursday, February 13, 2014

 

HSUS VS USDA ET AL BAN DOWNER CALVES FOR HUMAN CONSUMPTION (*veal) and potential BSE risk factor there from

 


 

 Thursday, February 20, 2014

 

*** Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr. Linda Detwiler 2014

 


 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

Tuesday, March 11, 2014

 

Science and Technology Committee Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD

 

Actually, it is nearer 2 per million per year of the population will develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about 1 in 30,000. So that has not really changed. When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.

 


 

*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.

 


 


 


 


 

*** And Terry, I promised the editor you would respond so thanks for backing my prediction up. I have read your tripe before so did not reread the whole thing. but your point about the age of the cattle takes on the scientific regulatory bodies of every country but one that exports US beef. They all, but one, agree that meat from cattle under 30 months of age carries zero risk of BSE prions. 1 △ ▽ • Reply • Share ›

 

Terry S. Singeltary Sr. > doc raymond • a month ago

 

Dr. Richard Raymond Sir, I only reply when you are scientifically wrong. I commented today, because again, you were scientifically wrong, and I proved it again, with scientific facts to back it up. sorry if that upsets you. you can fool some of the folks some of the time, but not all of us all the time. you either blatantly lied in your editorial, or you are grossly uninformed, time and time again. I think the public can take their pick on that, and in both cases, and they would be correct in both cases, in my opinion. you have a nice day sir. ...kind regards, terry

 

kind regards, terry

 

What is a Downer Calf?

 

By Dr. Richard Raymond | February 21, 2014

 


 

see full text Dr. Richard Raymond vs Terry S. Singeltary Sr.

 


 

Monday, March 10, 2014

 

Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014

 


 

Thursday, February 20, 2014

 

Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr. Linda Detwiler 2014

 


 

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

 


 

FSIS, USDA, REPLY TO SINGELTARY

 


 

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

 


 

Tuesday, August 18, 2009

 

* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009

 


 

WHAT about the sporadic CJD TSE proteins ?

 

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***

 


 

Sunday, October 13, 2013

 

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

TSS