Subject: RANCHO “He did not know that they were placing healthy cow heads
next to suspect carcasses,” Singleton’s defense team wrote.
LMAO!
Yardman only one not paid in Rancho diseased cow scheme
By Dan Flynn | March 1, 2016
Sentencing continues tomorrow in the criminal prosecution of the four men
whose scheme to circumvent USDA inspection in 2013 caused diseased cattle to end
up as human food.
The owner of Rancho Veal, Robert “Bob” Singleton, and Rancho Feeding Corp.
yardman Eugene Corda will appear for sentencing on Wednesday in U.S. District
Court for Northern California in San Francisco. Felix Sandoval Cabrera, foreman
at the Petaluma, CA, slaughterhouse, will be the last to be sentenced on March
9.
Rancho owner Jesse “Babe” Amaral was the first to be sentenced. On Feb. 10
Amaral was sentenced to a year and day in federal prison to be followed by two
years of supervised released including one year at a half-way house.
four men agreed to plead guilty to a single count of conspiracy to
distribute adulterated, misbranded, and un-inspected meat. In exchange, the
government agreed to drop multiple charges brought in an August 2014 indictment,
including fraud and conspiracy.
Their scheme to process diseased cattle, mostly with eye cancers, caused a
massive 8.7-million-pound meat recall in February 2014. The slaughterhouse was
closed and eventually sold. Recall expenses and other damages cost Rancho’s
business associates millions.
The need for a trial went away when the defendants all pleaded guilty.
Sentencing documents, however, are beginning to fill in some of the details that
would have come out at trial.
Singleton and Amaral met at cattle auctions in the early 1970s and decided
to become business partners.
The real property of the Petaluma slaughterhouse was owned by Singleton
Investments Inc., and was managed by both the Rancho Veal Corp., also owned by
Singleton, and the Rancho Feeding Corp,, owned by Amaral.
Singleton was the cattle buyer at auctions, and also sold processed meat to
vendors though his Rancho Veal Corp. Amara’s Rancho Feeding Corp. was the “USDA
establishment,” permitted to slaughter and process cattle for human
consumption.
Rancho Feeding had “custom slaughter agreements” with Rancho Veal,
contracts where it agreed to manage the slaughterhouse and comply with all USDA
regulations.
Cabrera, Rancho’s foreman who’d studied to be a USDA inspector, worked for
Amaral for more than 30 years.
The 79-year old Singleton claims to have heard about the scheme from the
78-year old Amaral sometime in early 2013. Shortly thereafter, Singleton learned
from Amaral that he’d directed Cabrera to bypass ante mortem (before death)
inspection procedures if the foreman believed a cow was likely to be marked by
an inspector as a “suspect” for condemnation.
Singleton claims not to have known that Amaral and Cabrera had employees
carving the “USDA Condemned” stamps out of cattle that had been condemned. Nor
did he know that, at Amaral’s direction, Corda was swapping un-inspected cattle
showing symptoms of eye cancer for cattle that had already passed ante mortem
inspection.
“He did not know that they were placing healthy cow heads next to suspect
carcasses,” Singleton’s defense team wrote.
However, there was much Singleton did know.
He “knew Amaral, Cabrera, and Corda were somehow effectively circumventing
inspection, and (Singleton) failed to ask questions or take responsibility for
putting a stop to the unlawful scheme,” according to court documents. Amaral
instructed Singleton to pay Cabrera $50 for every cow he “slipped” past USDA
inspection.
“The evidence shows that Corda did not know his codefendants were also
processing condemned cattle, or that Ranch’s owners were defrauding farmers in a
separate scheme, and he was not charged with those counts in the indictment,”
according to the sentencing memorandum filed by Assistant U.S. Attorney Hartley
M.K. West.
“Corda also did not profit from his role beyond his regular paycheck,
whereas Rancho’s owners and the kill floor foreman, Cabrera, did.”
West says Amaral and Singleton profited from the sale of the “eye cows” and
condemned cattle and Amaral from a separate false invoicing scheme.
“Corda was not paid and did not seek compensation.” West wrote. “He was
simply trying to keep his job by doing what Amaral told him.”
The government is recommending that the 65-year old Corda be sentenced to
three years probation including six months of home confinement, which will
apparently allow him to work and take his wife to chemotherapy for treatment of
a re-occurrent breast cancer.
Corda worked for Amaral for 30 years, a man he described as “strong-minded”
and “dominant and forceful.” Singleton became another of his boss’s in 1997, and
like Amaral was known for his lifetime in the cattle business.
“At no time did I ever believe the two men would involve me in a scheme
that would threaten the food supply,” Corda said in his pre-sentencing letter to
the judge. He eventually realized Amaral and Cabrera had come up with a way to
get cattle through without inspection.
Singleton admits he trusted Amaral and Cabrera. Amaral had run the kill
floor of the small slaughterhouse for 45 years and Singleton believed his
business partner could “distinguish between safe and unsafe conduct,”according
to Singleton’s lawyers. They said Singleton especially trusted Cabrera’s
expertise in meat inspection.
“Quite frankly, Bob did not trust the federal inspectors working at Rancho
at the time, and believed that Cabrera had a better idea of what was a passable
cow than those inspectors.” His attorneys said they offered that perspective “to
illustrate the Bob at the time never believed that dangerous meat would ever be
passed through to consumers.”
“Today Bob deeply regrets his conduct and the significant harm it caused,”
wrote the attorneys from Orrick, Herrington & Sutcliffe LLP in San
Francisco.
Due largely due to his being the first to fully cooperate in the
investigation, the government is recommending Singleton be sentenced to three
months in prison and three months of home detention followed by two years of
supervised release with 50 hours of community service.
Singleton wants a “non-custodial sentence of probation.”
Whether he stays out of jail may depend upon whether the judge accepts
Singleton’s view of the “loss calculation.” The recall of 8.7 million pounds of
meat included the production of an estimated 15,600 head of cattle processed by
Rancho over the course of a year.
That resulted in a loss of more than $2.5 million.
However, Singleton’s defense argues that the government’s investigation
found 180 cows were affected by the criminal conduct and from that number, they
could have “profited no more than $90,000.” There is a ten-fold increase in the
impact on the sentencing calculation between the two numbers ($90,000 versus
$2.5 million)
Singleton has also reached settlement agreements with all but one of
companies that were financial harmed by Rancho’s scheme and resulting recall.
The payments he has agreed to include: •RBR Meats/Riteway, $1.5 million; •BN
Ranch, $450,000; •Tillamook Country Smoker, $7,720; and •Argus, $3,000.
Singleton’s attorneys have been unable to get a response from Advance
Pierre Foods, the only remaining “victim entity.”
“Quite simply, Bob has no more money left, and no ability to pay a fine or
further restitution,” his attorneys wrote. “After he pays agreed-to restitution
and legal fees, Bob will be in debt.”
The government wants a separate restitution hearing scheduled after
tomorrow if any unresolved issues remain after sentencing.
© Food Safety News
UPDATED ...SEE VERDICT ;
Three month sentence imposed on Rancho’s other owner
By Dan Flynn | March 3, 2016
Ranchocow_406x250U.S. District Court Judge Charles R. Breyer has sentenced
79-year old Robert W. Singleton to a “custodial term” of three months to be
followed by one year of supervised probation for his role in a scheme to process
cattle condemned by USDA, usually for cancerous eyes.
In a 15-minute sentencing hearing, Singleton was also ordered to pay a $100
court assessment. The judge did not impose any fine, and put restitution off to
May 31.
Breyer ordered Singleton to self-surrender to the U.S. Marshals on or
before May 31, but granted him permission to attend a family reunion in Reno,
NV, before reporting. Singleton has been under instructions not to leave the
jurisdiction of the U.S. District Court for Northern California.
Singleton was the first to cooperate with the government investigation of
infractions at the Petaluma slaughterhouse. His business partner of more than 30
years, Jesse “Babe” Amaral operated the slaughterhouse as the Rancho Feeding
Corp., while Singleton’s Rancho Veal Corp. purchased cattle at auctions and sale
barns. Amaral came up with the idea of moving condemned animals past USDA
inspectors and pocketing the money.
Breyer also sentenced a Rancho yardman, 65-year old Eugene D. Corda, to
three months probation with a $100 assessment. Corda moved cattle into place as
directed by a foreman, but eventually figured out what was going on. The judge
granted Corda permission to continue feeding cattle for Amaral.
Amaral was sentenced last month to a year and day in federal prison. After
that he will be on supervised probation for two years with the first year spent
in a re-entry or half way house.
Only Rancho foreman Felix Cabrera remains to be sentenced. He will appear
before Judge Breyer next week.
In lieu of a trial, all four defendants negotiated agreements with the
government to plead guilty to distributing adulterated, misbranded, and
un-inspected meat. All were also required to cooperate with investigators.
Rancho recalled 8.7 million pounds of meat in early February 2014, covering
more than 13 months production back to Jan. 1, 2013.
>>> *** “He did not know that they were placing healthy cow heads
next to suspect carcasses,” Singleton’s defense team wrote.
***<<<
where have I heard this before ???
THE NEVER ENDING SAGA OF USDA MAD COW INC.
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92
BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
Galen Niehues, an inspector for the Nebraska Department of Agriculture,
(NDA), was convicted of mail fraud for submitting falsified reports to his
employer concerning inspections he was supposed to perform at Nebraska cattle
operations. Niehues was tasked with performing inspections of Nebraska ranches,
cattle and feed for the presence of neurological diseases in cattle including
Bovine Spongiform Encephalopathy (BSE), also known as “Mad Cow Disease”. Niehues
was to identify cattle producers, perform on-site inspections of the farm sites
and cattle operations, ask producers specific questions about feed, and take
samples of the feed. Niehues was to then submit feed samples for laboratory
analysis, and complete reports of his inspections and submit them to the NDA and
to the Federal Food and Drug Administration (FDA). An investigation by the FDA
and NDA revealed Niehues had fabricated approximately 100 BSE inspections and
inspection reports. When confronted, Niehues admitted his reports were
fraudulent, and that had fabricated the reports and feed samples he submitted to
the NDA. Niehues received a sentence of 5 years probation, a 3-year term of
supervised release, and was required to pay $42,812.10 in restitution.
OR THE OLD OBEX ONLY TESTING TSE TESTING ;
ATYPICAL LESION DISTRIBUTION (RBSE 92/21367)
A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in
Aberdeenshirer submitted as a suspect BSE case in the negative study (SE0203),
has been diagnosed as BSE negative on standard, statutory (obex only),
diagnostic criteria at CVL.
Further examination by Dr Jeffrey at Lasswade, as required by the project
design, has revealed vacuolar change in the septal nucleus and putamen which
co-localised with PrP immunoreactivity. No significant lesions were found in any
other part of the brain, neither was PrP found in the medulla.
It is important to note that examination of four brain blocks used earlier
in the epidemic would not have detected the lesion but a 16 block study (as used
in the very days of BSE) would.
FURTHER INFORMATION
The herd of origin has had 15, HB, suspect cases of BSE since July 1989 and
a further case is still alive.
2. Of the 15, eight have been confirmed by standard histopathology and
seven diagnosed negative (including the above case).
3. Fixed brain tissue from the negative cases exists at Lasswade (because
they always collect whole brain in Scotland) but has not so far been examined
further. No frozen tissue was collected so neither SAF nor PrP detection (by
immunoblotting) has been attempted.
4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.
FURTHER ACTION IN PROGRESS
1. The brain tissue from the negative cases will be examined in detail by
conventional histopathology and ICC.
2. Kevin Taylor and his veterinary colleagues have been alerted to the
situation.
OTHER RECOMMENDED ACTIONS
1. TRANSMISSION Attempt transmission from the 'case' to standard mice
strains. (Note: In regard to strain typing, formalin may have modified strain
phenotype - we need to discuss with NPU). Further transmission studies (eg in
cattle) might be suggested if primary transmission in mice fails. These
proposals have funding implications.
CODE 18-77
93/2.17/1.1
2. PrP GENOTYPING - Although only fixed brain tissue is available we are
considering genotyping from parents/offspring/fixed brain. As a first step we
are attempting to extract DNA from the fixed brain and to amplify the PrP gene
by PCR.
3. John Wilesmith has interrogated the data base for the herd history.
Other than the high proportion of negative cases nothing significant is
apparent.
4. Familial relationships between suspect (including positive and negative)
cases in this herd could be examined and tracings of breeding animals
initiated.
5. Consideration might be given to collecting frozen spinal cord from new
cases in this herd or in dispersals from it for (SAF/PrP examination).
CONCLUSIONS
1. At present it is unclear whether or not this is a singleton incident or
whether the other negative cases in this herd show a similar lesion.
2. The discovery might indicate the existence of a different strain of BSE
from that present in the general epidemic or an unusual response by an
individual host.
3. If further atypical lesion distribution cases are revealed in this herd
then implications of misdiagnosis of 'negative' cases in other herds may not be
insignificant.
4. If this is a new strain all the implications need to be considered
including whether or not to proceed with the further investigation of future
cases negative for BSE on obex examination alone and from which whole brains are
available (as in Scotland) or collected in the future. Also perhaps
investigation of the tissue distribution of infectivity in these animals might
be considered.
5. Animal and public health controls in place should be sufficient since
all tissues (other than brain for diagnosis) are incinerated.
We observe that Dr Tyrrell would wish to be informed of this at an early
opportunity and that the SEAC would wish to discuss it at their meeting in
April.
R BRADLEY
M DAWSON
17 February 1993
CVO - for information and comment on further action please
cc Mr K C Taylor
Dr B J Shreeve
93/2.17/1.2
This minute is re-issued with a wider distribution.
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
Mr Scudamore
Mr R C Lowson
Dr D Matthews
Mr I Robertson
Dr K MacOwan
Mr C Randall
Mr J W Wilesmith
Mr G A H Wells
Dr M Jeffrey
Dr M Simmons
93/2.17/1.3
IN CONFIDENCE
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)
1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF
CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS
SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN HISTOPATHOLOGY AND
INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS _NOT_ BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT ?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN
ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE,
AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE
AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. ...
PLEASE NOTE *
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
AND THE USDA ET AL KNEW IT TOO ;
"These 9,200 cases were different because brain tissue samples were
preserved with formalin, which makes them suitable for only one type of
test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in
the bovine, and these were probably from the most high risk cattle pool, the
ones the USDA et al, SHOULD have been testing. ...TSS
USDA 2003
We have to be careful that we don't get so set in the way we do things that
we forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain stem
and we're looking in only one area. In Norway, they were doing a project and
looking at cases of Scrapie, and they found this where they did not find lesions
or PRP in the area of the obex. They found it in the cerebellum and the
cerebrum. It's a good lesson for us. Ames had to go back and change the
procedure for looking at Scrapie samples. In the USDA, we had routinely looked
at all the sections of the brain, and then we got away from it. They've recently
gone back. Dr. Keller: Tissues are routinely tested, based on which tissue
provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another
important thing to get across to the public is that the negatives do not
guarantee absence of infectivity. The animal could be early in the disease and
the incubation period. Even sample collection is so important. If you're not
collecting the right area of the brain in sheep, or if collecting
lymphoreticular tissue, and you don't get a good biopsy, you could miss the area
with the PRP in it and come up with a negative test. There's a new, unusual form
of Scrapie that's been detected in Norway. We have to be careful that we don't
get so set in the way we do things that we forget to look for different emerging
variations of disease. We've gotten away from collecting the whole brain in our
systems. We're using the brain stem and we're looking in only one area. In
Norway, they were doing a project and looking at cases of Scrapie, and they
found this where they did not find lesions or PRP in the area of the obex. They
found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had
to go back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got away
from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
END...TSS
==========
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE
sampling FROM HEALTHY USDA CATTLE)
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services.
In addition to the targeted sample population (those cattle that were more
than 30 months old or had other risk factors for BSE),
*** the owner submitted to USDA, or caused to be submitted, BSE obex (brain
stem) samples from healthy USDA-inspected cattle.
As a result, the owner fraudulently received approximately $390,000.
Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1
include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for
specified risk material (SRM) violations and improved inspection controls over
SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in
future semiannual reports as the relevant audits and investigations are
completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67
PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in
unusual brain location and PrPsc detection by PMCA only.
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
*** Needless conflict ***
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
Terry S. Singeltary Sr. said:
I kindly wish to submit the following please ;
INDICTMENT
see more on Rancho history here;
Friday, March 21, 2014
Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014
?
“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.”
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
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
Saturday, September 21, 2013
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry
Center January 2010 THE FLIM-FLAM REPORT
>>>“Cabrera knocked the cancer eye cows, and he or another kill
floor employee at his instruction slaughtered them and deposited their heads in
the gut bin,” the indictment states. “Cabrera, or another kill floor employee at
his instruction, placed heads from apparently healthy cows, which had been
previously reserved, next to the cancer eye cow carcasses. <<<
where have I heard something similar before ?
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services. In addition to the targeted sample population (those
cattle that were more than 30 months old or had other risk factors for BSE),
***the owner submitted to USDA, or caused to be submitted, BSE obex (brain
stem) samples from healthy USDA-inspected cattle.
As a result, the owner fraudulently received approximately $390,000.
Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1
include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for
specified risk material (SRM) violations and improved inspection controls over
SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in
future semiannual reports as the relevant audits and investigations are
completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
-MORE Office of the United States Attorney District of Arizona
FOR IMMEDIATE RELEASE For Information Contact Public Affairs
February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602)
525-2681
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD
COW DISEASE SURVEILLANCE PROGRAM
PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of
Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail
fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel
Knauss stated, “The integrity of the system that tests for mad cow disease
relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without
that honest cooperation, consumers both in the U.S. and internationally are at
risk. We want to thank the USDA’s Office of Inspector General for their
continuing efforts to safeguard the public health and enforce the law.” Farm
Fresh Meats and Farabee were charged by Information with theft of government
funds, mail fraud and wire fraud. According to the Information, on June 7, 2004,
Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S.
Department of Agriculture (the “USDA Agreement”) to collect obex samples from
cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The
Targeted Cattle Population consisted of the following cattle: cattle over thirty
months of age; nonambulatory cattle; cattle exhibiting signs of central nervous
system disorders; cattle exhibiting signs of mad cow disease; and dead cattle.
Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per
obex sample for collecting obex samples from cattle within the Targeted Cattle
Population, and submitting the obex samples to a USDA laboratory for mad cow
disease testing. Farm Fresh Meats further agreed to maintain in cold storage the
sampled cattle carcasses and heads until the test results were received by Farm
Fresh Meats.
Evidence uncovered during the government’s investigation established that
Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted
Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or
caused to be submitted, obex samples from healthy, USDA inspected cattle, in
order to steal government moneys.
Evidence collected also demonstrated that Farm Fresh Meats and Farabee
failed to maintain cattle carcasses and heads pending test results and falsified
corporate books and records to conceal their malfeasance. Such actions, to the
extent an obex sample tested positive (fortunately, none did), could have
jeopardized the USDA’s ability to identify the diseased animal and pinpoint its
place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee
pleaded guilty to stealing government funds and using the mails and wires to
effect the scheme. According to their guilty pleas:
(a) Farm Fresh Meats collected, and Farabee directed others to collect,
obex samples from cattle outside the Targeted Cattle Population, which were not
subject to payment by the USDA;
(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests
to the USDA knowing that the requests were based on obex samples that were not
subject to payment under the USDA Agreement;
(c) Farm Fresh Meats completed and submitted, and Farabee directed others
to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s
testing laboratory that were false and misleading;
(d) Farm Fresh Meats completed and submitted, and Farabee directed others
to complete and submit, BSE Surveillance Submission Forms filed with the USDA
that were false and misleading;
(e) Farm Fresh Meats falsified, and Farabee directed others to falsify,
internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats
was seeking and obtaining payment from the USDA for obex samples obtained from
cattle outside the Targeted Cattle Population; and
(f) Farm Fresh Meats failed to comply with, and Farabee directed others to
fail to comply with, the USDA Agreement by discarding cattle carcasses and heads
prior to receiving BSE test results. A conviction for theft of government funds
carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud
convictions carry a maximum penalty of 20 years imprisonment. Convictions for
the above referenced violations also carry a maximum fine of $250,000 for
individuals and $500,000 for organizations. In determining an actual sentence,
Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide
appropriate sentencing ranges. The judge, however, is not bound by those
guidelines in determining a sentence.
Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The
investigation in this case was conducted by Assistant Special Agent in Charge
Alejandro Quintero, United States Department of Agriculture, Office of Inspector
General. The prosecution is being handled by Robert Long, Assistant U.S.
Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE
NUMBER: 2007-051(Farabee) # # #
WE can only hope that this is a single incident. BUT i have my doubts. I
remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5
grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and
the FDA was bragging at the time that the amount of potentially BANNED product
was so little and the cattle were so big ;
"It is important to note that the prohibited material was domestic in
origin (therefore not likely to contain infected material because there is no
evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The
potential risk of BSE to such cattle is therefore exceedingly low, even if the
feed were contaminated."
On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to a
processor for rendering into animal protein for use in animal feed. ... FDA's
investigation showed that the animal in question had already been rendered into
"meat and bone meal" (a type of protein animal feed). Over the weekend FDA was
able to track down all the implicated material. That material is being held by
the firm, which is cooperating fully with FDA.
WE now know all that was a lie. WE know that literally Thousands of TONS of
BANNED and most likely tainted product is still going out to commerce. WE know
now and we knew then that .005 to a gram was lethal. WE know that CWD infected
deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been
rendered and fed back to livestock (including cattle) for human and animal
consumption.
Paul Brown, known and respected TSE scientist, former TSE expert for the
CDC said he had ''absolutely no confidence in USDA tests before one year ago'',
and this was on March 15, 2006 ;
"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before one
year ago" because of the agency's reluctance to retest the Texas cow that
initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul
Brown is Senior Research Scientist in the Laboratory of Central Nervous System
... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain
Table 1. Animal feed ingredients that are legally used in U.S. animal feeds
Animal
Rendered animal protein from Meat meal, meat meal tankage, meat and bone
meal, poultry meal, animal the slaughter of food by-product meal, dried animal
blood, blood meal, feather meal, egg-shell production animals and other meal,
hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals
digest from dead, dying, diseased, or disabled animals including deer and elk
Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and
undried processed animal waste products
snip...
Conclusions
Food-animal production in the United States has changed markedly in the
past century, and these changes have paralleled major changes in animal feed
formulations. While this industrialized system of food-animal production may
result in increased production efficiencies, some of the changes in animal
feeding practices may result in unintended adverse health consequences for
consumers of animal-based food products. Currently, the use of animal feed
ingredients, including rendered animal products, animal waste, antibiotics,
metals, and fats, could result in higher levels of bacteria, antibioticresistant
bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting
animal-based food products intended for human consumption. Subsequent human
health effects among consumers could include increases in bacterial infections
(antibioticresistant and nonresistant) and increases in the risk of developing
chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide
range of potential human health impacts that could result from animal feeding
practices, there are little data collected at the federal or state level
concerning the amounts of specific ingredients that are intentionally included
in U.S. animal feed. In addition, almost no biological or chemical testing is
conducted on complete U.S. animal feeds; insufficient testing is performed on
retail meat products; and human health effects data are not appropriately linked
to this information. These surveillance inadequacies make it difficult to
conduct rigorous epidemiologic studies and risk assessments that could identify
the extent to which specific human health risks are ultimately associated with
animal feeding practices. For example, as noted above, there are insufficient
data to determine whether other human foodborne bacterial illnesses besides
those caused by S. enterica serotype Agona are associated with animal feeding
practices. Likewise, there are insufficient data to determine the percentage of
antibiotic-resistant human bacterial infections that are attributed to the
nontherapeutic use of antibiotics in animal feed. Moreover, little research has
been conducted to determine whether the use of organoarsenicals in animal feed,
which can lead to elevated levels of arsenic in meat products (Lasky et al.
2004), contributes to increases in cancer risk. In order to address these
research gaps, the following principal actions are necessary within the United
States: a) implementation of a nationwide reporting system of the specific
amounts and types of feed ingredients of concern to public health that are
incorporated into animal feed, including antibiotics, arsenicals, rendered
animal products, fats, and animal waste; b) funding and development of robust
surveillance systems that monitor biological, chemical, and other etiologic
agents throughout the animal-based food-production chain “from farm to fork” to
human health outcomes; and c) increased communication and collaboration among
feed professionals, food-animal producers, and veterinary and public health
officials.
REFERENCES...snip...end
Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health
Perspectives
NOW, what about the product that is not reported ?
HOW many more Farm Fresh Meats, Inc. and Roland Emerson Farabee's are out
there that submitted bogus samples for the infamous June 2004 ENHANCED BSE MAD
COW COVER-UP, but did not get caught ?
IT was not bad enough to have the USDA et al bungle there own BSE Testing
Protocols up so bad, it took Weybridge and a year of hounding by s o m e, and
finally an act of Congress to finally get that cow confirmed, but once caught
there, i guess the next best thing would be to have bogus BSE testing samples
submitted for testing from healthy USDA cattle, what next ? not to forget about
the other stumbling and staggering Tejas mad cow they rendered without any test
at all, and the other Tejas mad cow that took 7+ months and an act of Congress
to finally get confirmed from Weybridge. my God, even the three stooges, laural
and hardy put all together could have thought up all this. $$$
The beef import forecast for the second quarter was unchanged from last
month’s, despite pressure from higher-than-expected domestic cow slaughter that
has remained high through most of this period. Beef imports into the United
States from Australia, New Zealand, and Uruguay provide additional processing
beef that, along with domestic cow and bull beef, is mixed with 50-percent trim
from fed cattle to make ground beef. Forecast beef exports were raised slightly,
mainly on continued (though gradual) improvements in sales to major Asian
markets. In late May the World Animal Health Organization – known by its French
acronym, OIE – designated the United States as having “controlled risk status”
for bovine spongiform encephalopathy, or BSE. This designation reflects the
OIE’s view that beef produced in the United States is safe for export, since BSE
control measures such as feed bans and removal of specified risk materials
result in negligible risk to consumers. However, the OIE standards are only
guidelines. Individual countries may adopt differing standards, and those
countries that do accept OIE standards must still undertake the bureaucratic
processes to revise their rules and procedures.
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to then Central
Bureau............
P.S. Thank You Honorable Phyllis Fong for trying to keep them straight
anyway. ...TSS
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05
Study of Atypical Bse
infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et
al TRIPLE MAD COW FIREWALL, 10 YEARS AFTER ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS:
VETERINARY MEDICINES -- CLASS II PRODUCT Bulk cattle feed made with recalled
Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed
delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing. REASON Blood meal used to make cattle
feed was recalled because it was cross- contaminated with prohibited bovine meat
and bone meal that had been manufactured on common equipment and labeling did
not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL
Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,
TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY
Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST
POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY
Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC
MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR,
V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML
W/SMARTA, Recall # V-025-2007 CODE The firm does not utilize a code - only
shipping documentation with commodity and weights identified. RECALLING
FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete. REASON Products manufactured from bulk
feed containing blood meal that was cross contaminated with prohibited meat and
bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et
al TRIPLE MAD COW FIREWALL, 16 YEARS AFTER ;
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE
Wednesday, September 25, 2013
Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE
PRION 2013
SUMMARY REPORT CALIFORNIA ATYPICAL L-TYPE BOVINE SPONGIFORM ENCEPHALOPATHY
CASE INVESTIGATION JULY 2012 CALIFORNIA
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Final Feed Investigation Summary - California atypical L-type BSE Case -
July 2012
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
LET'S take a closer look at this new prionpathy or prionopathy, and then
let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the
genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_
mad cow in the world to date like this, ......wait, it get's better. this new
prionpathy is killing young and old humans, with LONG DURATION from onset of
symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and
the plaques are very similar in some cases too, bbbut, it's not related to the
g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that
they claim is a genetic TSE, has no relation to any gene mutation in that
family. daaa, ya think it could be related to that mad cow with the same genetic
make-up ??? there were literally tons and tons of banned mad cow protein in
Alabama in commerce, and none of it transmitted to cows, and the cows to humans
there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we
identified a novel mutation in the bovine prion protein gene (Prnp), called
E211K, of a confirmed BSE positive cow from Alabama, United States of America.
This mutation is identical to the E200K pathogenic mutation found in humans with
a genetic form of CJD. This finding represents the first report of a confirmed
case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We
hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in
"the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation
(J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic
in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the
UK epidemic had most likely originated from such a mutation and argued against
the scrapierelated assumption. Such rare potential pathogenic PRNP mutations
could occur in countries at present considered to be free of BSE, such as
Australia and New Zealand. So it is important to maintain strict surveillance
for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many
countries still feed ruminant proteins to pigs). Removal of specified risk
material, such as brain and spinal cord, from cattle at slaughter prevents
infected material from entering the human food chain. Routine genetic screening
of cattle for PRNP mutations, which is now available, could provide additional
data on the risk to the public. Because the point mutation identified in the
Alabama animals is identical to that responsible for the commonest type of
familial (genetic) CJD in humans, it is possible that the resulting infective
prion protein might cross the bovine-human species barrier more easily. Patients
with vCJD continue to be identified. The fact that this is happening less often
should not lead to relaxation of the controls necessary to prevent future
outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary
Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen
A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier
Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
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
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 13, 2014
HSUS VS USDA ET AL BAN DOWNER CALVES FOR HUMAN CONSUMPTION (*veal) and
potential BSE risk factor there from
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been
discovered in a wide verity of species across North America. typical C-BSE,
atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine,
typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98
Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD
in cervid is slowly spreading without any stopping it in Canada and the USA and
now has mutated into many different strains. Transmissible Mink Encephalopathy
TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease
have been silently mutating and spreading in different species in North America
for decades.
The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion
Firewall, of which we now know without a doubt, that it was nothing but ink on
paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of
banned mad cow feed has been put out into commerce, never to return, as late as
December of 2013, serious, serious breaches in the FDA mad cow feed ban have
been documented. The 2004 enhanced BSE surveillance program was so flawed, that
one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown,
who is preparing a scientific paper based on the latest two mad cow cases to
estimate the maximum number of infected cows that occurred in the United States,
said he has "absolutely no confidence in USDA tests before one year ago" because
of the agency's reluctance to retest the Texas cow that initially tested
positive.
see ;
The BSE surveillance and testing have also been proven to be flawed, and
the GAO and OIG have both raised serious question as to just how flawed it has
been (see GAO and OIG reports). North America has more documented TSE prion
disease, in different documented species (excluding the Zoo BSE animals in the
EU), then any other place on the Globe. This does not include the very
likelihood that TSE prion disease in the domestic feline and canine have been
exposed to high doses of the TSE prion disease vid pet food. To date, it’s still
legal to include deer from cwd zone into pet food or deer food. Specified Risk
Material i.e. SRM bans still being breach, as recently as just last month.
nvCJD or what they now call vCJD, another case documented in Texas last
month, with very little information being released to the public on about this
case? with still the same line of thought from federal officials, ‘it can’t
happen here’, so another vCJD blamed on travel of a foreign animal disease from
another country, while ignoring all the BSE TSE Prion risk factors we have here
in the USA and Canada, and the time that this victim and others, do spend in the
USA, and exposed to these risk factors, apparently do not count in any way with
regard to risk factor. a flawed process of risk assessment.
sporadic CJD, along with new TSE prion disease in humans, of which the
young are dying, of which long duration of illness from onset of symptoms to
death have been documented, only to have a new name added to the pot of prion
disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a
familial type disease could be sporadic with no genetic link to any family
member? when the USA is the only documented Country in the world to have
documented two different cases of atypical H-type BSE, with one case being
called atypical H-G BSE with the G meaning Genetic, with new science now showing
that indeed atypical H-type BSE is very possible transmitted to cattle via oral
transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada,
USA, and the UK, with the same old excuse, better surveillance. You can only use
that excuse for so many years, for so many decades, until one must conclude that
CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a
blip or a reason of better surveillance, it is a mathematical rise in numbers.
More and more we are seeing more humans exposed in various circumstance in the
Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same
time in North America, more and more humans are becoming exposed to the TSE
prion disease via consumption of the TSE prion via deer and elk, cattle, sheep
and goats, and for those that are exposed via or consumption, go on to further
expose many others via the iatrogenic modes of transmission of the TSE prion
disease i.e. friendly fire. I pondered this mode of transmission via the victims
of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone
sub-clinical with sFFI or sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten
nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first
ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is
transmissible. yet all these TSE prion disease and victims in the USA and Canada
are being pawned off as a spontaneous event, yet science has shown, the
spontaneous theory has never been proven in any natural case of TSE prion
disease, and scientist have warned, that they have now linked some sporadic CJD
cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about
this in the public domain. We must make all human and animal TSE prion disease
reportable in every age group, in ever state and internationally, we must have a
serious re-evaluation and testing of the USA cattle herds, and we must ban
interstate movement of all cervids. Any voluntary effort to do any of this will
fail. Folks, we have let the industry run science far too long with regards to
the TSE prion disease. While the industry and their lobbyist continues to funnel
junk science to our decision policy makers, Rome burns. ...end
REFERENCES
Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Saturday, June 14, 2014
Rep. Rosa DeLauro (D-CT) Calls for Briefing on Beef Recalled for Mad Cow
Potential Rep. Rosa DeLauro (D-CT)
Thursday, June 12, 2014
Missouri Firm Recalls Ribeye and Carcass Products That May Contain
Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal
root ganglia may not have been completely removed
Monday, July 28, 2014
Mitigating the Risk of Transmission and Environmental Contamination of
Transmissible Spongiform Encephalopathies 2013 Annual Report
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
PEO752/2 0097
CONFIDENTIAL-POLICY MARKET SENSITIVE-LIMITED DISTRIBUTION
BSE AND CJD
RECEIVED
25 MAR 1996
BSE AND CJD
The Prime Minister held a meeting on Tuesday 19 March to discuss the latest
scientific information on Bovine Spongiform Encephalopathy (BSE) and Creutzfeldt
Jacob Disease (CJD), The Deputy Prime Minister, the Lord President, Chief
Secretary, Lord Privy Seal, the Secretary of State for Health, the Secretary of
State for Scotland, the Minister for Agriculture. the Financial Secretary, the
Attorney General, the Minister for Food, the Chief Whip, Sir Robin Butler, Keith
Meldrum (Chief Veterinary Officer), Professor Pattison (Chairman of SEAC), Dr
Eileen Rubery (Department of Health), Richard Packer (MAFF), Lord McColl, John
Ward, Howell James, Alex Allan, Jonathan Haslam, Robert Culpin (HM Treasury),
Kenneth Mackenzie (Cabinet Office), Tim Sutton (HM Treasury) were also present.
The Deputy Prime Minister, the Chief Secretary to the Treasury and the Lord
Privy Seal all announced that they had relevant interests in the form of cattle
herds.
The Prime Minister began the meeting by commenting that some very difficult
decisions needed to be taken to ensure that the correct balance was struck
between treating this matter seriously and over-reacting. Colleagues needed to
recall that there were many issues which remained unknown.
Professor Pattison said that his committee had considered the new
information which had become available very carefully and had examined in detail
all the possible options. ***The situation was that there were now nine cases of
CJD which appeared to be different from classical CJD. There were, in addition,
three other possibJe cases. The cases tended to be among the young but varied
from those aged 18 to age 41. The new variant CJD showed. an atypical clinical
picture with an unknown pathology. This had persuaded SEAC that the variant was
distinct. No cases in the UK or abroad had been seen before which matched to
this pattern. The Committee had considered the new methods of monitoring the
occurrence of the disease and were aware lab techniques had improved, but they
bad drawn the conclusion that they could not persuade themselves that it was
more careful observation alone which had brought these cases to light.
This implied that there might be a new risk factor and in the view of the
Committee the most likely explanation was that BSE was that risk factor. To date
however the evidence was not available which proved that BSE could be linked to
these cases. It appeared to the Committee to be the most likely explanation but
they might be wrong. It might, for example, be that the new form had always been
present in a low incidence but had remained unreported or there-might be an
entirely separate new environmental factor. However, the committee was of the
view that the most likely cause was something new in the cattle population in
the mid-1980s which was causing something new in the human population in the
mid-1990s. This was in their view likely to be exposure to BSE before the
introduction of the SBO controls.
Professor Pattison noted that it was impossible to predict how many more
cases there might be and it might well be eighteen months before the full extent
of the problem could be ascertained. A dozen or so might be the limit or it
might remain at a relatively low level as in cats and unlike in the cattle
population it had not escalated. The cattle epidemic with escalating numbers was
probably due to feeding cattle remains back to cattle. This had not happened
with cats nor of course with humans.
The committee believed it was increasingly impossible to keep this
information confidential. Members of the Committee had already had to attend two
expert meetings where they had not been able to provide colleagues with the full
story. Given the increasingly high risk of a leak it was the Committee's view
that a controlled statement by the Government would be more appropriate. The
Committee had considered whether extra restrictions on human consumption of beef
or beef products would be necessary. They had not concluded that immediate
measures were necessary other than to stress the importance of implementing
existing controls as nearly perfectly as possible. The Committee would consider
again at the weekend what more might be done. ranging from a do nothing option
to the slaughter of the national herd.
Personally. Professor Pattison did not think that extreme measures would be
necessary. In his view the committee was more likely to focus on controls
concerning older cattle, together with further controls on mechanically
recovered meat. ...snip...end...tss
96/03.19/16.2
CONFIDENTIAL – POLICY MARKET SENSITIVE - LIMITED DISTRIBUTION
CONFIDENTIAL – POLICY
SEAC
Since there were indications that the news was about to break, there was no
reason to prevent all members of the Committee joining the meeting in
London...
Sunday, July 06, 2014
Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory
Case-Control Study
Conclusions—The a priori hypotheses were supported.
*Consumption of various meat products may be one method of transmission of
the infectious agent for sCJD.
Seven main threats for the future linked to prions
***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...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
Moreover, transmission experiments to non-human primates suggest that some TSE
agents in addition to Classical BSE prions in cattle (namely L-type Atypical
BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
***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.
***Infectivity in skeletal muscle of BASE-infected cattle
Friday, December 19, 2014
Rancho Alleged Cancerous Eyeball Case Going To Trial
2015-2016
***********OCTOBER 2015*************
*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***
THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and
Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and
Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. ***We recently observed
the direct transmission of a natural classical scrapie isolate to macaque after
a 10-year silent incubation period, with features similar to some reported for
human cases of sporadic CJD, albeit requiring fourfold longe incubation than
BSE. ***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the
third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the
origin of human sporadic cases. We will present an updated panorama of our
different transmission studies and discuss the implications of such extended
incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases...
===============
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
================
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary:
The transmissible spongiform encephalopathies (also called prion diseases)
are fatal neurodegenerative diseases that affect animals and humans. The agent
of prion diseases is a misfolded form of the prion protein that is resistant to
breakdown by the host cells. Since all mammals express prion protein on the
surface of various cells such as neurons, all mammals are, in theory, capable of
replicating prion diseases. One example of a prion disease, bovine spongiform
encephalopathy (BSE; also called mad cow disease), has been shown to infect
cattle, sheep, exotic undulates, cats, non-human primates, and humans when the
new host is exposed to feeds or foods contaminated with the disease agent. The
purpose of this study was to test whether non-human primates (cynomologous
macaque) are susceptible to the agent of sheep scrapie. After an incubation
period of approximately 10 years a macaque developed progressive clinical signs
suggestive of neurologic disease. Upon postmortem examination and microscopic
examination of tissues, there was a widespread distribution of lesions
consistent with a transmissible spongiform encephalopathy. This information will
have a scientific impact since it is the first study that demonstrates the
transmission of scrapie to a non-human primate with a close genetic relationship
to humans. This information is especially useful to regulatory officials and
those involved with risk assessment of the potential transmission of animal
prion diseases to humans.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health. In
complement to the recent demonstration that humanized mice are susceptible to
scrapie, we report here the first observation of direct transmission of a
natural classical scrapie isolate to a macaque after a 10-year incubation
period. Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
98 | Veterinary Record | January 24, 2015
EDITORIAL
Scrapie: a particularly persistent pathogen
Cristina Acín
Resistant prions in the environment have been the sword of Damocles for
scrapie control and eradication. Attempts to establish which physical and
chemical agents could be applied to inactivate or moderate scrapie infectivity
were initiated in the 1960s and 1970s,with the first study of this type focusing
on the effect of heat treatment in reducing prion infectivity (Hunter and
Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate
the prion protein are based on the method developed by Kimberlin and
collaborators (1983). This procedure consists of treatment with 20,000 parts per
million free chlorine solution, for a minimum of one hour, of all surfaces that
need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so
on). Despite this, veterinarians and farmers may still ask a range of questions,
such as ‘Is there an official procedure published somewhere?’ and ‘Is there an
international organisation which recommends and defines the exact method of
scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could
be applied, especially in relation to the disinfection of surfaces in lambing
pens of affected flocks. A 999/2001 EU regulation on controlling spongiform
encephalopathies (European Parliament and Council 2001) did not specify a
particular decontamination measure to be used when an outbreak of scrapie is
diagnosed. There is only a brief recommendation in Annex VII concerning the
control and eradication of transmissible spongiform encephalopathies (TSE
s).
Chapter B of the regulation explains the measures that must be applied if
new caprine animals are to be introduced to a holding where a scrapie outbreak
has previously been diagnosed. In that case, the statement indicates that
caprine animals can be introduced ‘provided that a cleaning and disinfection of
all animal housing on the premises has been carried out following
destocking’.
Issues around cleaning and disinfection are common in prion prevention
recommendations, but relevant authorities, veterinarians and farmers may have
difficulties in finding the specific protocol which applies. The European Food
and Safety Authority (EFSA ) published a detailed report about the efficacy of
certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and
even a formulation of copper or iron metal ions in combination with hydrogen
peroxide, against prions (EFSA 2009). The report was based on scientific
evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006,
Solassol and others 2006) but unfortunately the decontamination measures were
not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on
the scrapie situation in the EU after 10 years of monitoring and control of the
disease in sheep and goats (EFSA 2014), and one of the most interesting findings
was the Icelandic experience regarding the effect of disinfection in scrapie
control. The Icelandic plan consisted of: culling scrapie-affected sheep or the
whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of
stables, sheds, barns and equipment with high pressure washing followed by
cleaning with 500 parts per million of hypochlorite; drying and treatment with
300 ppm of iodophor; and restocking was not permitted for at least two years.
Even when all of these measures were implemented, scrapie recurred on several
farms, indicating that the infectious agent survived for years in the
environment, even as many as 16 years after restocking (Georgsson and others
2006).
In the rest of the countries considered in the EFSA (2014) report,
recommendations for disinfection measures were not specifically defined at the
government level. In the report, the only recommendation that is made for sheep
is repopulation with sheep with scrapie-resistant genotypes. This reduces the
risk of scrapie recurrence but it is difficult to know its effect on the
infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE
s were provided by the Scientific Steering Committee (SSC) of the EC, whose
advice regarding inactivation procedures focused on treating animal waste at
high temperatures (150°C for three hours) and high pressure alkaline hydrolysis
(SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory
Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe
working and the prevention of TSE infection. Annex C of the ACDP report
established that sodium hypochlorite was considered to be effective, but only if
20,000 ppm of available chlorine was present for at least one hour, which has
practical limitations such as the release of chlorine gas, corrosion,
incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its
active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE)
does not recommend a specific disinfection protocol for prion agents in its
Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General
recommendations on disinfection and disinsection (OIE 2014), focuses on
foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on
prion disinfection. Nevertheless, the last update published by the OIE on bovine
spongiform encephalopathy (OIE 2012) indicates that few effective
decontamination techniques are available to inactivate the agent on surfaces,
and recommends the removal of all organic material and the use of sodium
hydroxide, or a sodium hypochlorite solution containing 2 per cent available
chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s,
and also emphasises the importance of mechanically cleaning surfaces before
disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO
1999).
Finally, the relevant agencies in both Canada and the USA suggest that the
best treatments for surfaces potentially contaminated with prions are sodium
hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution,
while most commercial household bleaches contain 5.25 per cent sodium
hypochlorite. It is therefore recommended to dilute one part 5.25 per cent
bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency
2013).
So what should we do about disinfection against prions? First, it is
suggested that a single protocol be created by international authorities to
homogenise inactivation procedures and enable their application in all
scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available
chlorine seems to be the procedure used in most countries, as noted in a paper
summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015).
But are we totally sure of its effectiveness as a preventive measure in a
scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease
be needed?
What we can conclude is that, if we want to fight prion diseases, and
specifically classical scrapie, we must focus on the accuracy of diagnosis,
monitoring and surveillance; appropriate animal identification and control of
movements; and, in the end, have homogeneous and suitable protocols to
decontaminate and disinfect lambing barns, sheds and equipment available to
veterinarians and farmers. Finally, further investigations into the resistance
of prion proteins in the diversity of environmental surfaces are required.
References
snip...
98 | Veterinary Record | January 24, 2015
*** These results suggest that AA fibrils are relatively heat stable and
that similar to prions, autoclaving at 135 °C is required to destroy the
pathogenicity of AA fibrils.
*** These findings may contribute to the prevention of AA fibril
transmission through food materials to different animals and especially to
humans.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Monday, January 4, 2016
Long live the OIE, or time to close the doors on a failed entity?
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Thursday, October 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad
cow disease USDA and what really happened
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-β pathology and cerebral
amyloid angiopathy
2015-12-07 02:27 AM
Terry S. Singeltary Sr. said: re-Evidence for human transmission of
amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for
bringing this important finding to the attention of the public domain, and the
media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of
more important Transmissible Spongiform Encephalopathy TSE Prion scientific
findings. findings that could have great implications for human health, and
great implications for the medical surgical arena. but apparently, the
government peer review process, of the peer review science, tries to intervene
again to water down said disturbing findings.
where have we all heard this before? it’s been well documented via the BSE
Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country’s) with
the BSE mad cow TSE Prion debacle.
That ‘anonymous' Lancet editorial was disgraceful. The editor, Dick Horton
is not a scientist.
The pituitary cadavers were very likely elderly and among them some were on
their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients who got
pooled extracts injected from thousands of cadavers were 100% certain to have
been injected with both seeds. No surprise that they got both diseases going
after thirty year incubations.
That the UK has a "system in place to assist science journalists" to squash
embargoed science reports they find ‘alarming’ is pathetic.
Sounds like the journalists had it right in the first place: ‘Alzheimer’s
may be a transmissible infection’ in The Independent to ’You can catch
Alzheimer’s’ in The Daily Mirror or ‘Alzheimer’s bombshell" in The Daily
Express.
if not for the journalist, the layperson would not know about these
important findings.
where would we be today with sound science, from where we were 30 years
ago, if not for the cloak of secrecy and save the industry at all cost
mentality?
when you have a peer review system for science, from which a government
constantly circumvents, then you have a problem with science, and humans die.
to date, as far as documented body bag count, with all TSE prion named to
date, that count is still relatively low (one was too many in my case, Mom
hvCJD), however that changes drastically once the TSE Prion link is made with
Alzheimer’s, the price of poker goes up drastically.
so, who makes that final decision, and how many more decades do we have to
wait?
the iatrogenic mode of transmission of TSE prion, the many routes there
from, load factor, threshold from said load factor to sub-clinical disease, to
clinical disease, to death, much time is there to spread a TSE Prion to
anywhere, but whom, by whom, and when, do we make that final decision to do
something about it globally? how many documented body bags does it take? how
many more decades do we wait? how many names can we make up for one disease, TSE
prion?
Professor Collinge et al, and others, have had troubles in the past with
the Government meddling in scientific findings, that might in some way involve
industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain,
fear factor, or any reason, shame, shame on you.
in my opinion, it’s one of the reasons we are at where we are at to date,
with regards to the TSE Prion disease science i.e. money, industry, politics,
then comes science, in that order.
greed, corporate, lobbyist there from, and government, must be removed from
the peer review process of sound science, it’s bad enough having them in the
pharmaceutical aspect of healthcare policy making, in my opinion.
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer’s
of some type (no autopsy?). just made a promise, never forget, and never let
them forget, before I do.
I kindly wish to remind the public of the past, and a possible future we
all hopes never happens again. ...
[9. Whilst this matter is not at the moment directly concerned with the
iatrogenic CJD cases from hgH, there remains a possibility of litigation here,
and this presents an added complication. There are also results to be made
available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on
the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention
of iatrogenic CJD transmission in neurosurgery, all of which will serve to
increase media interest.]
snip...see full Singeltary Nature comment here;
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the
intra- and cross-species transmission of AA amyloidosis Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by
extracellular deposition of AA fibrils. AA fibrils are found in several tissues
from food animals with AA amyloidosis. For hygienic purposes, heating is widely
used to inactivate microbes in food, but it is uncertain whether heating is
sufficient to inactivate AA fibrils and prevent intra- or cross-species
transmission. We examined the effect of heating (at 60 °C or 100 °C) and
autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western
blot analysis, transmission electron microscopy (TEM), and mouse model
transmission experiments. TEM revealed that a mixture of AA fibrils and
amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at
135 °C produced large amorphous aggregates. AA fibrils retained antigen
specificity in Western blot analysis when heated at 100 °C or autoclaved at 121
°C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and
bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly
stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA
fibrils at 121 °C or 135 °C significantly decreased amyloid deposition.
Moreover, amyloid deposition in mice injected with murine AA fibrils was more
severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils
autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These
results suggest that AA fibrils are relatively heat stable and that similar to
prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA
fibrils. These findings may contribute to the prevention of AA fibril
transmission through food materials to different animals and especially to
humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD
54.00
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Tuesday, February 23, 2016
Parks and Wildlife begins reducing deer population at Texas Mountain Ranch
Chronic Wasting Disease CWD TSE Prion Update
*** I kindly would like to comment on a few statements from the TPWD et al
;
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
Tuesday, February 23, 2016
ARKANSAS Detects First Chronic Wasting Disease CWD in a wild elk
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Saturday, February 6, 2016
*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No.
APHIS-2016-0007] Singeltary Submission ***
USDA JUSTIFIES SCIENTIFIC SUPPRESSION AS ITS POLICY Confidential Agency
Panel Approves Censorship and Media Gag Orders Posted on Feb 29, 2016 | Tags:
Scientific Integrity, USDA
--------------------------------------------------------------------------------
Washington, DC — Under its policy purporting to protect scientific
integrity, the U.S. Department of Agriculture is entitled to do just the
opposite, according to confidential findings by an internal agency panel
released today by Public Employees for Environmental Responsibility (PEER). The
panel rejected a complaint by one of its top entomologists that USDA purged
controversial findings, blocked publication of research papers with policy
implications, and forbade scientists from being interviewed by reporters. These
conclusions come from a report by a five-member “Scientific Integrity Review
Panel” convened to review the dismissal of a complaint filed by Dr. Jonathan
Lundgren, a Senior Research Entomologist and Lab Supervisor for the USDA
Agriculture Research Service based in South Dakota who has published research
about adverse effects on monarch butterflies from widely-used neonicotinoid
insecticides (or “neonics”). The panel agreed that Dr. Lundgren’s complaint
should not be pursued because – The panel was told that charges of “reprisal”
and retaliatory investigations were outside the scope of its review;
The panel found that USDA is entitled to prohibit scientists from speaking
with reporters or even answering questions at conferences about the significance
or ramifications of published studies; and
USDA’s Scientific Integrity Policy explicitly authorizes it to block
publication of research containing “statements that could be construed as being
judgments of or recommendations on USDA or any other federal government policy.”
“This review confirms that what occurs inside USDA does not resemble what anyone
else would consider ‘scientific integrity,’” stated Jeff Ruch, Executive
Director of PEER which is suing USDA for its refusal to even consider a
rulemaking petition seeking to strengthen the agency’s Scientific Integrity
Policy. “Inside USDA, politics determines what scientific work will see the
light of day.”
On February 12th, USDA Inspector General Phyllis Fong announced that her
office had opened an investigation into a “significant volume” of complaints by
agency scientists about censorship and interference with research on subjects
that USDA upper management deemed sensitive.
The review panel report on the Lundgren complaint arises out of the first
appeal of any USDA scientific integrity complaint. Dr. Lundgren filed his formal
scientific integrity complaint in September of 2014. One month later, it was
rejected as not even meriting an investigation. Dr. Lundgren immediately
appealed but since USDA had never received an appeal on a scientific integrity
complaint decision, the agency took an entire year to determine how to handle
it. Yet under the guidelines finally developed – The panel does not investigate
the complaint but instead simply reviews materials provided by agency
management. In this case, no panel member even attempted to speak with Dr.
Lundgren or any of the witnesses he identified;
There is no process for remedying any alleged scientific misconduct if it
is ever confirmed; and
The panel findings are confidential and USDA will not release them under
the Freedom of Information Act by maintaining that even final reports are
“deliberative.”
“How will public confidence in the integrity of USDA science be enhanced
when all of the reviews are kept secret?” asked Ruch, noting that a stated
objective of the policy is to “ensure public confidence.” “Given how this
complaint was handled, no wonder scientific integrity lapses inside USDA are
never resolved and simply fester. Something now unmistakably clear is that no
scientist in their right mind should report political manipulation of science
inside USDA.”
###
Read the Scientific Integrity Review Panel report and approvals
See ruling that reprisal is outside the scope of USDA Scientific Integrity
Policy
Examine USDA scientific integrity appeal guidelines
View transmittal letter to Dr. Lundgren asking him to keep it
confidential
Look at Dr. Lundgren’s scientific integrity and whistleblower
complaints
Revisit USDA refusal to consider strengthening its scientific integrity
policy
Jonathan Latham, PhD
Executive Director The Bioscience Resource Project Ithaca, NY 14850
USA
www.independentsciencenews.org
and
www.bioscienceresource.org
jrlatham@bioscienceresource.org
Skype: jonathanlatham2 Tel: 1-607-319-0279
“The conscious and intelligent manipulation of the organized habits and
opinions of the masses is an important element in democratic society. Those who
manipulate this unseen mechanism of society constitute an invisible government
which is the true ruling power of our country.”—Edward Bernays, Propaganda
-- end///
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
