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.
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
http://www.cfsph.iastate.edu/Factsheets/pdfs/bovine_spongiform_encephalopathy.pdf
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 Sanità ; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università 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
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
Sunday, August 09, 2009
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
