BILLING CODE: 3410-34-P DEPARTMENT OF AGRICULTURE Animal and Plant Health
Inspection Service
[Docket No. APHIS-2015-0055]
Concurrence with OIE Risk Designations for Bovine Spongiform
Encephalopathy
AGENCY: Animal and Plant Health Inspection Service, USDA.
ACTION: Notice.
SUMMARY: We are advising the public of our decision to concur with the
World Organization for Animal Health’s (OIE) bovine spongiform encephalopathy
(BSE) risk designations for 14 regions. The OIE recognizes these regions as
being of negligible risk for BSE. We are taking this action based on our review
of information supporting the OIE’s risk designations for these regions.
FOR FURTHER INFORMATION CONTACT: Dr. Roberta Morales, Senior Staff
Veterinarian, Regionalization Evaluation Services, National Import Export
Services, VS, APHIS, 920 Main Campus Drive, Suite 200, Raleigh, NC 27606; (919)
855-7735.
SUPPLEMENTARY INFORMATION:
The regulations in 9 CFR part 92 subpart B, “Importation of Animals and
Animal Products; Procedures for Requesting BSE Risk Status Classification With
Regard to Bovines” (referred to below as the regulations), set forth the process
by which the Animal and Plant Health Inspection Service (APHIS) classifies
regions for bovine spongiform encephalopathy (BSE) risk. Section 92.5 of the
regulations provides that all countries of the world are considered by APHIS to
be in one of three BSE risk categories: Negligible risk, controlled risk, or
undetermined risk. These risk categories are defined in § 92.1. Any region that
is not classified by APHIS as 2 presenting either negligible risk or controlled
risk for BSE is considered to present an undetermined risk. The list of those
regions classified by APHIS as having either negligible risk or controlled risk
can be accessed on the APHIS Web site at
The list can also be obtained by writing to APHIS at National Import Export
Services, 4700 River Road Unit 38, Riverdale, MD 20737. Under the regulations,
APHIS may classify a region for BSE in one of two ways. One way is for countries
that have not received a risk classification from the World Organization for
Animal Health (OIE) to request classification by APHIS. The other way is for
APHIS to concur with the classification given to a country by the OIE.
If the OIE has recognized a country as either BSE negligible risk or BSE
controlled risk, APHIS will seek information to support our concurrence with the
OIE classification. This information may be publicly available information, or
APHIS may request that countries supply the same information given to the OIE.
APHIS will announce in the Federal Register, subject to public comment, its
intent to concur with an OIE classification.
In accordance with that process, we published a notice1 in the Federal
Register on December 4, 2015 (80 FR 75849, Docket No. APHIS-2015-0055), in which
we announced our intent to concur with the OIE risk designations for 16 regions.
The OIE recognizes these regions as being of negligible risk for BSE. We
solicited comments on the notice for 60 days ending on February 2, 2016. We
received two comments by that date, from a private citizen and a representative
of a foreign government.
1 To view the notice and the comments we received, go to
3 One commenter stated that if a product is being imported only for use in
pet food, then the BSE risk status of the exporting region should not be an
issue.
We disagree that bovine products imported for use in pet food do not pose a
risk for introducing or spreading BSE in the United States. It is possible that
pet foods could be used for cattle feed, either by accidental misfeeding of pet
foods to cattle or by misusing salvage pet food for cattle. Farms that raise
multiple species (e.g. dogs, swine, and cattle) present a particular risk for
misfeeding.
The other commenter stated that the United States does not recognize all
the OIE’s risk designations for BSE, noting that the United States still
considers several countries as controlled risk regions though the OIE has
classified them as negligible risk.
As we explained above, § 92.5 of the regulations provides two ways that
APHIS may classify a region for BSE. One way is for countries that have not
received a risk classification from the OIE to request classification by APHIS.
The other way is for APHIS to concur with the classification given to a country
by the OIE. If the OIE has recognized a country as either BSE negligible risk or
BSE controlled risk, APHIS will seek information to support our concurrence with
the OIE classification. This information may be publicly available information,
or APHIS may request that countries supply the same information given to the
OIE.
The length of APHIS’s review of information in support of concurrence
depends on a number of factors, including whether the information is publicly
available, and, if it is not publicly available, how quickly a country responds
to our request for information. This notice updates APHIS’ list of regions
recognized as negligible risk for BSE to include all the regions for which we
have been able to review information. We intend to announce concurrence with
additional countries recognized by the OIE in a future notice.
4
One commenter noted that while the OIE guidelines call for removal of
specified risk materials (SRMs) from animals older than 30 months of age, our
regulations require the removal of SRMs from animals 30 months of age or older.
The commenter stated that while this is not a significant difference from an
epidemiological perspective, it creates a major problem for certification
through the veterinary services of exporting countries and presents a barrier to
trade. APHIS notes that the wording “30 months of age or older” is consistent
with Food Safety and Inspection Service (FSIS) and U.S. Food and Drug
Administration (FDA) regulations as well as with Canadian regulations. We also
note that anyone wishing to import bovine products into the United States must
also meet FSIS or FDA requirements as well as APHIS requirements. We do not
anticipate that this difference will have a significant impact on trade.
In the December 2015 notice, we mistakenly announced our intent to
recognize Romania as a region of negligible risk for BSE. In December 2014, the
OIE suspended Romania’s status as a negligible risk region because Romania
reported a case of atypical BSE. Since then, the OIE has announced its intent to
reinstate Romania’s status as a region of negligible risk for BSE. We will be
seeking information to verify Romania’s status and will announce our intent to
concur with the OIE’s designation in a future notice.
Also in the December 2015 notice, we announced our intent to recognize
France as a region of negligible risk for BSE in concurrence with the OIE. Since
then, France has confirmed a case of classical BSE in a 5-year-old cow.
Accordingly, the OIE has suspended France’s status as a region of negligible
risk for BSE and reinstated its status as a region of controlled risk effective
March 25, 2016. For this reason we have removed France from the list of regions
of negligible risk for BSE in this document. We will continue to recognize
France as a region of controlled risk for BSE.
5
Therefore, in accordance with the regulations in § 92.5, we are announcing
our decision to concur with the OIE risk classifications of the following
countries:
Regions of negligible risk for BSE: Bulgaria, Cyprus, Czech Republic,
Estonia, Hungary, India, Korea (Republic of), Latvia, Liechtenstein, Luxembourg,
Malta, Portugal, Slovakia, and Switzerland.
Authority: 7 U.S.C. 1622 and 8301-8317; 21 U.S.C. 136 and 136a; 31 U.S.C.
9701; 7 CFR 2.22, 2.80, and 371.4.
Done in Washington, DC, this 4th day of August 2016.
Kevin Shea,
Administrator, Animal and Plant Health Inspection Service.
[FR Doc. 2016-18985 Filed: 8/9/2016 8:45 am; Publication Date:
8/10/2016]
> Concurrence with OIE Risk Designations for Bovine Spongiform
Encephalopathy [Docket No. APHIS-2015-0055]
LAUGH OUT LOUD LOL !
THE OIE and USDA BSE MRR policy is the biggest piece of junk science
propaganda I have every seen, which will be sure to continue to spread the
Transmissible Spongiform Encephalopathy TSE PRION disease (all strains), around
the globe, just for trade and the almighty dollar...terry
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND
SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Saturday, July 16, 2016
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Thursday, August 4, 2016
Secretary's Advisory Committee on Animal Health [Docket No.
APHIS-2016-0046] TSE PRION DISEASE
Friday, June 3, 2016
The epidemiological evolution of prion infection on bovine in Romania, in
the period of 2010 – 2015
PRION 2016 TOKYO JAPAN
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
http://scrapie-usa.blogspot.com/2016/05/usda-aphis-national-scrapie-tse-prion.html
***UPDATE ON CWD ZOONOSIS***
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential TOKYO
CONFERENCE 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
Thursday, August 04, 2016
*** MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
***
LEFTOVERS FOR LIVESTOCK: A Legal Guide for Using Food Scraps as Animal Feed
and a recipe for Another TSE Prion Disaster
While using food scraps as animal feed was once a common practice in the
U.S., it has declined since the 1980s because of disease outbreaks linked to
animal products like food-and-mouth and bovine spongiform encephalopathy, also
known as mad cow disease. Stricter state laws and federal regulations were
enacted to prevent outbreaks; 15 states currently ban any animal-derived scraps
from being used in swine feed, and nine of those 15 also ban feeding vegetable
waste to pigs. But the practice can be done responsibly, the report says, and
there is a renewed enthusiasm among farmers, food entrepreneurs and consumers
looking to address the environmental and economic problems related to food
waste. Read it here...
LEFTOVERS FOR LIVESTOCK: A Legal Guide for Using Food Scraps as Animal
Feed
snip...
The use of food scraps as animal feed has been a common practice worldwide
for centuries.5 The vision of a classic agrarian homestead often features the
farmer’s children bringing dinner scraps out to “slop the pigs” and feed the
chickens. Yet the practice of feeding food scraps to animals has declined
precipitously since the 1980s, when several disease outbreaks were linked to
animal feed (specifically, animal products in livestock feed), including
foot-and-mouth disease in swine and bovine spongiform encephalopathy (BSE),
commonly referred to as mad cow disease, in cattle. In an attempt to prevent the
spread of such diseases, federal and state laws and regulations that restricted
what is often pejoratively referred to as “garbage feeding” were enacted. Some
of these policies were overly restrictive, and many of them impose conflicting
requirements among neighboring states. Thus, they contributed to a decline in
the amount of leftover food being used in animal feed. Indeed, by 2007, just
three percent of U.S. hog farms fed food scraps to their livestock.6
snip...
b. Ruminant Feed Ban Rule The Food and Drug Administration’s (FDA) Bovine
Spongiform Encephalopathy (BSE)/Ruminant Feed Ban Rule36 prohibits the use of
mammalian protein (i.e., animal tissue) in feeds for ruminant animals. This ban
covers all “ruminants,” meaning animals that have a stomach with four chambers
through which feed passes during digestion, such as cattle, sheep, goats, deer,
elk, and antelopes, among others (Swine and fowl are not ruminants.).37 The
regulations apply to any “protein derived from mammalian tissue.”38 The ban
specifically lays out the types of products that can and cannot be fed to
particular types of ruminants.39 Producers of waste-based ruminant feed must
certify compliance and keep detailed records of inputs and processes; they are
also subject to inspection by FDA.40 The regulations require any company or
individual that processes animal products unfit for human consumption or meat
scraps to
1) follow specified labeling guidelines indicating that the products are
not to be fed to other ruminants and
2) maintain records tracking the receipt, processing, and distribution of
the products.41 Alternatively, processors can use manufacturing and testing
methods approved by FDA to prevent transmissible spongiform encephalopathy
August 2016 Leftovers for Livestock: A Legal Guide for Using Excess Food as
Animal Feed |4 (BSE)/Ruminant Feed Ban Rule prohibits the use of almost all
mammalian protein (i.e., animal tissue) in feeds for ruminant animals.
diseases, including BSE.42 Those who intend to separate qualifying protein
products from other food scraps are subject to additional processing and
inspection guidelines.43 Finally, ruminant-feeding operations must maintain
copies of purchase invoices and labeling for all feeds containing animal protein
products, which may be subject to FDA inspection.44
snip...
FDA has described such byproducts as portions of processed food that may
not be nutritious, suitable, or desirable for human consumption, but that still
may be a source of energy and nutrition for certain species of animals.47
Examples include culls, peels, trimmings, and pulp from vegetable
manufacturing/processing; chaff, bran, and middlings from grain milling; wet
brewer’s grains from beverage brewing operations; and liquid whey from dairy
facilities.48 This definition embraces food unfit for human consumption, which
might include animal meat, but recall that the SHPA and the BSE/Ruminant Feed
Ban Rule respectively prohibit the feeding of meat containing active disease
organisms to swine49 and the feeding of mammalian protein to ruminant animals
such as cows, sheep, and goats.50 A facility that wishes to use human food
byproducts as animal feed must ensure it complies with these regulations—as well
as any relevant state laws and regulations—in addition to the Preventive
Controls rule for animal food.
seriously ?
you do know that the infamous August 1997 bse mad cow feed ban was a
colossal failure?
you do know that the surveillance and testing for bse was a colossal
failure?
you do know that the bse srm ban was also a colossal failure?
you do know that ***CWD-Detection of infectivity in orally challenged
pigs.
you do know that these plants and grains that mix with feed, could be a
potential source of the cwd tse prion.
please use this as you wish. be careful though, it’s sound science,
something not used anymore...
kind regards, terry
Priority Interim Position Paper PROTECTING THE FOOD CHAIN FROM PRIONS
Perspectives 2016
snip...
5. Proposed Recommendations
a. The question of re-introduction of ruminant protein into the food-chain
The opinion of the members of PRIORITY is that the sustainment of an
absolute feed ban for ruminant protein to ruminants is the essential
requirement, especially since the impact of non-classical forms of scrapie in
sheep and goats is not fully understood or cannot be fully estimated. Therefore,
the consortium strongly recommends prohibiting re-introduction of processed
ruminant protein into the feed-chain. Arguments in support of this opinion are:
the large (and still uncharacterized) diversity of prion agents that
circulate in animal populations;
the uncertainties related to prion epidemiology in animal populations;
the unknown efficacy of industrial processes applied to reduce
microbiological risk during processed animal protein (PAP) production on most
prion agents;
the intrinsic capacity of prions to cross interspecies transmission
barriers;
the lack of sensitive methodology for identifying cross contamination in
food.
The consortium is also hesitant to introduce processed ruminant proteins
into fish food considering the paucity of data on prion infections in fishes and
sea animals, and the risk of establishing an environmental contamination of the
oceans that cannot be controlled.
b. Atypical prion agents
Atypical prion agents will probably in the next future represent the
dominant form of prion diseases. Type L atypical BSE has clear zoonotic
potential. Similarly, there are now some data that seem to indicate that
atypical scrapie agent can cross various species barriers. Moreover, the current
EU policy for eradicating scrapie (genetic selection in affected flocks) is
inefficient to prevent atypical scrapie. In that context it would appear
valuable
to develop knowledge related to pathogenesis and inter-individual
transmission of atypical prion agents in ruminants (both intraspecies and
interspecies)
to investigate for potential PrP resistance allele to the infection by
atypical prion agents
to improve the sensitivity of detection assay that are applied in the field
towards this type of agent
to maintain a robust surveillance of both animal and human populations
c. Species transmission barriers
Intensified search for a molecular signature of the species barrier is
recommended, since this barrier is a key for many important policy areas - risk
assessment, proportional policies, the need for screening of human products and
food.
d. Prion structure
Prion strain structural language will remain an important issue for public
health for the foreseeable future. Understanding the structural basis for
strains and the basis for adaptation of a strain to a new host will require
continued fundamental research.
e. Detection and therapy
Early detection of prion infection, ideally at preclinical stage, will
remain crucial for development of effective treatment strategies in humans
affected by the disease.
Tuesday, May 31, 2016
Priority Interim Position Paper PROTECTING THE FOOD CHAIN FROM PRIONS
Perspectives
PRION 2016 CONFERENCE TOKYO
***CWD-Detection of infectivity in orally challenged pigs
P-154 Prion infectivity detected in swine challenged with chronic wasting
disease via the intracerebral or oral route
S Jo Moore, Robert A Kunkle, Jodi D Smith, M Heather West-Greenlee, Justin
J Greenlee Virus and Prion Research Unit, National Animal Disease Center; ARS,
USDA, United States
Chronic wasting disease (CWD) is a naturally-occurring, fatal
neurodegenerative disease of North American cervids. The potential for swine to
serve as a host for the agent of chronic wasting disease is unknown. In the US,
feeding of ruminant by-products to ruminants is prohibited, but feeding of
ruminant materials to swine, mink, and poultry still occurs. In addition,
scavenging of CWD-affected cervid carcasses by feral pigs presents a potential
risk for CWD exposure. The purpose of this study was to investigate the
susceptibility of swine to the CWD agent following oral or intracranial
experimental challenge.
At 8 weeks of age, crossbred pigs were challenged by the intracranial route
(n=20), oral route (n= 19), or were left unchallenged (n=9). At approximately 6
months of age, the time at which commercial pigs reach market weight, half of
the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months
post challenge (mpc). At death a complete necropsy examination was performed,
including testing of tissues for misfolded prion protein (PrPcwd) by western
blotting (WB), enzyme-linked immunosorbent assay (ELISA), and
immunohistochemistry (IHC).
None of the pigs developed clinical signs consistent with prion disease.
Four >6 month intracranially challenged pigs (survival times 45-73 mpc) were
positive by ELISA, two were also positive by WB, and one was positive by IHC.
One >6 month orally challenged pig (64 mpc) was positive by ELISA.
To further investigate the potential for infectivity, brain tissue from
selected pigs was bioassayed in mice expressing porcine PRNP. Tissue from the
two WB-positive >6 month intracranially challenged pigs produced positive
bioassay results, albeit with low attack rates and variable incubation periods.
Interestingly, bioassay of material from the longest surviving >6 month
orally challenged pig (72 mpc), which was negative for PrPcwd by all other
tests, produced a positive bioassay result. Bioassay of material from additional
animals is currently underway.
This study demonstrates that pigs can serve as potential hosts for CWD,
although with low attack rates and scant PrPcwd accumulation. Detection of
infectivity in orally challenged pigs using mouse bioassay raises the
possibility that naturally exposed pigs act as a reservoir of CWD infectivity,
even though affected pigs do not develop overt clinical signs or readily
detectable PrPcwd.
WS-02
Scrapie in swine: A diagnostic challenge
Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2
1National Animal Disease Center, US Dept. of Agriculture, Agricultural
Research Service, United States; 2Iowa State University College of Veterinary
Medicine
A naturally occurring prion disease has not been recognized in swine, but
the agent of bovine spongiform encephalopathy does transmit to swine by
experimental routes. Swine are thought to have a robust species barrier when
exposed to the naturally occurring prion diseases of other species, but the
susceptibility of swine to the agent of sheep scrapie has not been thoroughly
tested.
Since swine can be fed rations containing ruminant derived components in
the United States and many other countries, we conducted this experiment to test
the susceptibility of swine to U.S. scrapie isolates by intracranial and oral
inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the
brains of clinically ill sheep from the 4th passage of a serial passage study of
the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous
ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were
inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24)
with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of
animals at approximately six months post inoculation (PI), at the time the pigs
were expected to reach market weight. Remaining pigs were maintained and
monitored for clinical signs of TSE until study termination at 80 months PI or
when removed due to intercurrent disease (primarily lameness). Brain samples
were examined by immunohistochemistry (IHC), western blot (WB), and
enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in
each inoculation group was used for bioassay in mice expressing porcine PRNP.
At six-months PI, no evidence of scrapie infection was noted by any
diagnostic method. However, at 51 months of incubation or greater, 5 animals
were positive by one or more methods: IHC (n=4), WB (n=3), or ELISA (n=5).
Interestingly, positive bioassay results were obtained from all inoculated
groups (oral and intracranial; market weight and end of study).
Swine inoculated with the agent of scrapie by the intracranial and oral
routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by
IHC or WB by the time they reach typical market age and weight. However, strong
support for the fact that swine are potential hosts for the agent of scrapie
comes from positive bioassay from both intracranially and orally inoculated pigs
and multiple diagnostic methods demonstrating abnormal prion protein in
intracranially inoculated pigs with long incubation times.
Curriculum Vitae
Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion
Research Unit at the National Animal Disease Center, US Department of
Agriculture, Agricultural Research Service. He applies his specialty in
veterinary anatomic pathology to focused research on the intra- and interspecies
transmission of prion diseases in livestock and the development of antemortem
diagnostic assays for prion diseases. In addition, knockout and transgenic mouse
models are used to complement ongoing experiments in livestock species. Dr.
Greenlee has publications in a number of topic areas including prion agent
decontamination, effects of PRNP genotype on susceptibility to the agent of
sheep scrapie, characterization of US scrapie strains, transmission of chronic
wasting disease to cervids and cattle, features of H-BSE associated with the
E211 K polymorphism, and the development of retinal assessment for antemortem
screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM
degree and completed the PhD/residency program in Veterinary Pathology at Iowa
State University. He is a Diplomate of the American College of Veterinary
Pathologists.
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral
Inoculation
snip...
In the US, feeding of ruminant by-products to ruminants is prohibited, but
feeding of ruminant materials to swine, mink and poultry still occurs. Although
unlikely, the potential for swine to have access to TSE-contaminated feedstuffs
exists.
snip...
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral
Inoculation (see tonnage of mad cow feed in commerce USA...tss)
In an experimental study of the transmissibility of BSE to the pig, seven
of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral
inoculation with a homogenate of bovine brain from natural BSE cases developed
lesions typical of spongiform encephalopathy.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract
Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine:
Preliminary Report
In the United States, feeding of ruminant by-products to ruminants is
prohibited, but feeding of ruminant materials to swine and poultry still occurs.
The potential for swine to have access to scrapie-contaminated feedstuffs
exists, but the potential for swine to serve as a host for
replication/accumulation of the agent of scrapie is unknown. The purpose of this
study was to perform oral and intracerebral inoculation of the U.S. scrapie
agent to determine the potential of swine as a host for the scrapie agent and
their clinical susceptibility. snip... snip... In the United States, feeding of
ruminant by-products to ruminants is prohibited, but feeding of ruminant
materials to swine and poultry still occurs. The potential for swine to have
access to scrapie-contaminated feedstuffs exists, but the potential for swine to
serve as a host for replication/accumulation of the agent of scrapie is unknown.
The purpose of this study was to perform oral and intracerebral inoculation of
the U.S. scrapie agent to determine the potential of swine as a host for the
scrapie agent and their clinical susceptibility.
see full text and more transmission studies here ;
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 176 of 201 pages...tss
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, Valerie 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 long 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***
===============
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
PRION 2016 TOKYO CONFERENCE
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
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.
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
Saturday, April 23, 2016
Prion 2016 Tokyo Update
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
***UPDATE ON CWD ZOONOSIS***
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
Saturday, July 23, 2016
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING,
AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY
2016
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
Thursday, August 04, 2016
*** MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON
CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL
SCJD
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie. ***
I will post several links below, some of you may find interest in, others
will want to disclaim it. the latest science with link source and references are
all there, you will have to make your own minds up. I have wasted a third of my
life chasing this damn disease. I am only vested in the truth. ...thank you, and
good luck!
kindest regards, terry
Greetings Dr. Dagleish and Veterinary Record et al,
we can only pray that Europe is not lost to cwd tse prion.
I read with great interest, but only could read the short abstract, that is
all I have access to as lay person. if you could please send me full text pdf
that would be great. regardless, I wish to forward the latest from the USA, and
some thoughts on where and how cwd was brought to Norway. I do know that there
are no export papers needed for hay and such to be exported to Norway, and we
now know there is a potential risk factor for TSE Prion and plants.
please see ;
***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.
snip...
CELL REPORTS
Report
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
56. Members considered that there is no evidence that crops grown on the
land which received composted excreta from BSE-challenged animals pose a TSE
risk to humans or animals. One member suggested that, as some of these animals
are orally challenged with high doses of BSE-infected materials, and the
distribution of infectivity in the digestive system is not completely
understood, it might be premature to conclude that there is no infective agent
in the manure.
Furthermore, an unpublished study had indicated low level absorption of PrP
from soil by tomato plants although it should be noted that this study had not
been repeated. Details of this work would be sent to the SEAC Secretary. Dr
Matthews explained that most of the manure from animals challenged with high
doses of BSE had already been composted and used for coppicing. Members agreed
that the risks from disposal of residual manure from experimental animals would
be much less than historic risks of on farm contamination from naturally
infected animals at the height of the BSE epidemic. ...SNIP...END
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester
Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE
BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences &
Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s
Hospital London and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the environment.
A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep,
after they had grazed on land which had previously been grazed by
scrapie-infected sheep, even though the land had lain fallow for three years
before the healthy sheep were introduced. Brown also quoted an early experiment
of his own (1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later near where
the material had been placed. 89. Potential environmental routes of infection:
Brown discusses the various possible scenarios, including surface or subsurface
deposits of TSE-contaminated material, which would lead to a build-up of
long-lasting infectivity. Birds feeding on animal remains (such as gulls
visiting landfill sites) could disperse infectivity. Other animals could become
vectors if they later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface water
channels, by effluents and discarded solid wastes from treatment plants. A
reasonable conclusion is that there is a potential for human infection to result
from environmental contamination by BSE-infected tissue residues. The potential
cannot be quantified because of the huge numbers of uncertainties and
assumptions that attend each stage of the disposal process". These comments,
from a long established authority on TSEs, closely echo my own statements which
were based on a recent examination of all the evidence. 90. Susceptibility: It
is likely that transmissibility of the disease to humans in vivo is probably
low, because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no definitive data
are available.
91. Recommendations for disposal procedures: Brown recommends that material
which is actually or potentially contaminated by BSE should be: 1) exposed to
caustic soda; 2) thoroughly incinerated under carefully inspected conditions;
and 3) that any residue should be buried in landfill, to a depth which would
minimise any subsequent animal or human exposure, in areas that would not
intersect with any potable water-table source.
92. This review and recommendations from Brown have particular importance.
Brown is one of the world's foremost authorities on TSEs and is a senior
researcher in the US National Institutes of Health (NIH). It is notable that
such a respected authority is forthright in acknowledging the existence of
potential risks, and in identifying the appropriate measures necessary to
safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M
Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will,
"Geographical distribution of variant CJD in the UK (excluding Northern
Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD
(variant CJD) might live closer to rendering factories than would be expected by
chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were
studied. The incubation period of vCJD is not known but by analogy with other
human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure
to rendering products, such exposure might plausibly have occurred 8-10 years
before the onset of symptoms. The authors were able to obtain the addresses of
all rendering plants in the UK which were in production in 1988. For each case
of vCJD, the distance from the place of residence on 1st January 1998 to the
nearest rendering plant was calculated
snip...
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
snip...
***SO, my question, why is it the OIE and other trade officials and policy
making there from, knowing that the USA and Canada, with not a clue about
Mexico, why is it that nobody has Declared an EXTRAORDINARY EMERGENCY DUE TO A
FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC
WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA ?
well, since no one else will, than I must.
Terry S. Singeltary Sr. Declares a DECLARATION OF EXTRAORDINARY EMERGENCY
DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE
PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA.
The elephant in the room I was speaking of that we all have missed was the
feed, yes we all know of ruminant and non ruminant protein and risk factors
there from with TSE Prion disease, but we missed the rest of the feed i.e. FEED
GRAINS. YES, science has shown in the past, and now recently, the shedding of
the CWD TSE Prion into the environment is indeed a risk factor, and for all the
grains and such that goes into feed, even hay, hell, Norway does not require any
APHIS-Veterinary Services certification for the import of hay/straw. see for
yourself ;
Hay/Straw
Norway does not require any APHIS-Veterinary Services certification for the
import of hay/straw.
you add up all the other grains in feed, and then wonder about exposure to
the CWD TSE PRION from cervid and risk factor from the CWD there from via
shedding or right down to the soil these grains were grown in, and you have a
world of problems. see ;
Feed Grains Data: Yearbook Tables Created March 10, 2016 Updates of this
data, and data covering more years and countries, can be found at http://www.ers.usda.gov/data-products/feed-grains-database/feed-grains-yearbook-tables.aspx
U.S. Acreage, Production, Yield, and Farm Price Table 1--Corn, sorghum, barley,
and oats: Planted acreage, harvested acreage, production, yield, and farm price
World Production, Supply, and Disappearance Table 2--Foreign coarse grains:
Supply and disappearance Table 3--Feed grains (corn, sorghum, barley, and oats):
Supply and disappearance U.S. Supply and Disappearance Table 4--Corn: Supply and
disappearance Table 5--Sorghum: Supply and disappearance Table 6--Barley: Supply
and disappearance Table 7--Oats: Supply and disappearance U.S. Production,
Yield, and Stocks Table 8--Hay: Production, harvested acreage, yield, and stocks
Domestic and International Prices Table 9--Corn and sorghum: Average prices
received by farmers, United States Table 10--Barley and oats: Average prices
received by farmers, United States Table 11--Hay: Average prices received by
farmers, United States Table 12--Corn: Cash prices at principal markets Table
13--Sorghum: Cash prices at principal markets Table 14--Barley and oats: Cash
prices at principal markets Table 15--Feed-price ratios for livestock, poultry,
and milk Table 16--Byproduct feeds: Average wholesale price, bulk, specified
markets Table 17--Processed corn products: Quoted market prices Exports and
Imports Table 18--U.S. corn and sorghum exports Table 19--U.S. barley and oats
exports Table 20--U.S. corn and sorghum imports Table 21--U.S. barley and oats
imports Table 22--U.S. corn and sorghum exports by selected destinations Table
23--U.S. barley and oats exports by selected destinations Table 24--U.S. corn
and sorghum imports by selected sources Table 25--U.S. barley and oats imports
by selected sources Table 26--U.S. white corn exports by selected destinations
Table 27--World coarse grain trade: Selected exporters and importers by
commodity Rail rates and shipments Table 28--Rail rates and grain shipments
Processed feeds and animal unit indexes Table 29--Processed feeds: Quantities
fed and feed per grain-consuming animal unit Table 30--Indexes of feed consuming
animal units Feed, seed, and industrial uses Table 31—Corn: Feed, seed, and
industrial uses Exports and imports for ethyl alcohol and brewers’ and
distillers’ dregs and waste Table 32—U.S. exports of ethyl alcohol by selected
destinations Table 33—U.S. imports of ethyl alcohol by selected sources Table
34—U.S. exports of brewers’ and distillers’ dregs and waste by selected
commodities Table 35—U.S. imports of brewers’ and distillers’ dregs and waste by
selected sources Contact: Thomas Capehart at tcapehart+A25@ers.usda.gov
‘’The statement you were concerned about was corrected to "One sorghum DDGS
out of 168 DG samples was contaminated with animal protein prohibited for use in
ruminant feed and was channeled to poultry feed."
Subject: Re: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE
PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
***UDATED CORRECTION BY AUTHOR...SEE EMAIL TO ME...terry
From: Kyung-Min Lee Sent: Thursday, October 01, 2015 1:39 PM To: Terry S.
Singeltary Sr. ; BSE-L@LISTS.AEGEE.ORG Cc: CJD-L@LISTS.AEGEE.ORG ;
cjdvoice@yahoogroups.com ; bloodcjd@yahoogroups.com ;
jcattanach@foodprotection.org ; cnc3@psu.edu ; dloynachan@foodprotection.org ;
lhovey@foodprotection.org ; Timothy J. Herrman Subject: RE: TEXAS CONFIRMATION
OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE SAMPLE OF SORGHUM DDGS
OUT OF 168 DG SAMPLES
Dear Terry S. Singeltary Sr.
Thank for your interest and concern about our published article entitled
“Evaluation of Selected Nutrients and Contaminants in Distillers Grains from
Ethanol Production in Texas”. I should apologize you and others that there were
some errors and misleading statements in this article due to inappropriate
terminology. The statement you were concerned about was corrected to "One
sorghum DDGS out of 168 DG samples was contaminated with animal protein
prohibited for use in ruminant feed and was channeled to poultry feed." We
requested the journal editor to correct some errors and the relevant statements,
or to withdraw the article from the journal.
Again I sincerely apologize for any confusion and inconvenience this may
cause. Thanks.
best wishes,
Kyung-Min
Kyung-Min Lee, Ph. D. Research Scientist Office of the Texas State Chemist
Texas A&M AgriLife Research P.O. Box 3160, College Station, TX
77841-3160 Phone: 979-845-4113 (ext 132) Email:kml@otsc.tamu.edu Fax:
979-845-1389
snip...end...tss
my link corrected
Sunday, September 27, 2015
TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN ONE
SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
kind regards, terry
Subject: Fw: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE
PRION IN ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
From: Terry S. Singeltary Sr. Sent: Sunday, September 27, 2015 4:39 PM To:
BSE-L@LISTS.AEGEE.ORG Cc: CJD-L@LISTS.AEGEE.ORG ; cjdvoice@yahoogroups.com ;
bloodcjd@yahoogroups.com ; jcattanach@foodprotection.org ; cnc3@psu.edu ;
dloynachan@foodprotection.org ; lhovey@foodprotection.org ; kml@otsc.tamu.edu
Subject: TEXAS CONFIRMATION OF BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION IN
ONE SAMPLE OF SORGHUM DDGS OUT OF 168 DG SAMPLES
TEXAS One sorghum DDGS sample out of 168 DG samples was contaminated with
bovine spongiform encephalopathy, but the transmission route of the bovine
spongiform encephalopathy agent could not be clearly defined.
J Food Prot. 2015 Oct;78(10):1861-9. doi: 10.4315/0362-028X.JFP-15-157.
Evaluation of Selected Nutrients and Contaminants in Distillers Grains from
Ethanol Production in Texas.
Lee KM1, Herrman TJ2. Author information 1Office of the Texas State
Chemist, Texas A&M AgriLife Research, Texas A&M University System,
College Station, Texas 77841, USA. kml@otsc.tamu.edu. 2Office of the Texas State
Chemist, Texas A&M AgriLife Research, Texas A&M University System,
College Station, Texas 77841, USA.
Abstract
This study evaluated distillers grain (DG) by-products produced in
different ethanol plants and supplemented in animal diets in Texas, based on
samples analyzed from 2008 to 2014. The samples were assessed for concentration,
occurrence, and prevalence of selected nutrients and contaminants. Protein and
sulfur contents of DG were largely different between corn and sorghum
by-products as well as wet distillers grain with solubles and dry distillers
grain with solubles (DDGS), indicating a significant effect of grain feedstock
and dry-grind process stream on DG composition and quality. Salmonella was
isolated in 4 DDGS samples out of a total of 157 DG samples, a percentage (2.5%)
that is much lower than the percentage of Salmonella-positive samples found in
other feed samples analyzed during the same period. A small amount of
virginiamycin residue was found in 24 corn DDGS, 1 corn wet distillers grain
with solubles, and 2 sorghum DDGS samples out of 242 samples in total. One
sorghum DDGS sample out of 168 DG samples was contaminated with bovine
spongiform encephalopathy, but the transmission route of the bovine spongiform
encephalopathy agent could not be clearly defined. The concentrations of
aflatoxin and fumonisin DG by-products averaged 3.4 μg/kg and 0.7 mg/kg,
respectively. Among contaminated corn DG samples, five DDGS samples for
aflatoxin contained a higher concentration than the U.S. Food and Drug
Administration action level for use in animal feed, whereas no sample for
fumonisin was found above the action level. The study results raised some
important issues associated with the quality and use of DG by-products,
suggesting several approaches and strategies for their effective and safe use as
a feed ingredient to promote animal and human health and welfare.
PMID: 26408135 [PubMed - in process]
Terry S. Singeltary Sr. Declares a DECLARATION OF EXTRAORDINARY EMERGENCY
DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE
PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA.
it’s time someone steps up to the plate (OIE ...LMAO!), and declare an
extraordinary emergency for foreign animal disease due to Chronic Wasting
Disease or Cervid Spongiform Encephalopathy TSE Prion disease from the United
States of America, Canada, and Mexico i.e. North America, before this damn
disease is spread to hell and back, and you can just throw in there BSE and
Scrapie just for grins. ...and I ain’t grinning Sad smile OIE, you have
floundered too long with mad cow type TSE Prion disease...
snip...see full text ;
Tuesday, August 02, 2016
*** Chronic wasting disease of deer – is the battle to keep Europe free
already lost?
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging
reindeer from the Nordfjella population in South-Norway.
Tuesday, June 14, 2016
*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag
Norway ***
Thursday, July 07, 2016
Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd
Norwegian moose
14/06/2016 - Norway reports a third case
Saturday, July 16, 2016
Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The
British Deer Society 07/04/2016
Red Deer Ataxia or Chronic Wasting Disease CWD TSE PRION?
could this have been cwd in the UK back in 1970’S ???
SEE FULL TEXT ;
Saturday, July 09, 2016
Texas Intrastate – within state movement of all Cervid or Trucking Chronic
Wasting Disease CWD TSE Prion Moratorium
Wednesday, July 27, 2016
Arkansas CWD 101 positive cases documented to date, Biologists to take
additional samples in in southern Pope County, Aug. 1-5
Friday, July 01, 2016
*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were
confirmed at a Medina County captive white-tailed deer breeding facility on June
29, 2016***
*** How Did CWD Get Way Down In Medina County, Texas?
DISCUSSION Observations of natural outbreaks of scrapie indicated that the
disease spread from flock to flock by the movement of infected, but apparently
normal, sheep which were incubating the disease.
There was no evidence that the disease spread to adjacent flocks in the
absent of such movements or that vectors or other host species were involved in
the spread of scrapie to sheep or goats; however, these possibilities should be
kept open...
Tuesday, August 02, 2016
TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas
with CWD Rule Terry S. Singeltary Sr. comment submission
Friday, July 29, 2016
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND
CAPTIVE REPORT UPDATE JULY 2016
Friday, August 05, 2016
MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION
UPDATE
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE
Sunday, July 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
***
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
Saturday, July 16, 2016
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Tuesday, April 19, 2016
Thursday, August 4, 2016
Secretary's Advisory Committee on Animal Health [Docket No.
APHIS-2016-0046] TSE PRION DISEASE
USDA BSE TSE PRION SURVEILLANCE, FEED, TESTING, SRM FIREWALLS...LMAO!
THE USDA FDA TRIPLE MAD COW DISEASE FIREWALL, WERE NOTHING MORE THAN INK ON
PAPER !
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
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
*** Monday, October 26, 2015 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL,
TN, AND WV
Date: September 6, 2006 at 7:58 am PST
PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter,
Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance
Pheasant Finisher, Recall # V-133-6.
CODE None
RECALLING FIRM/MANUFACTURER
Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by
telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated
recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based
protein.
VOLUME OF PRODUCT IN COMMERCE
477.72 tons
DISTRIBUTION
AL
______________________________
PRODUCT
a) Dairy feed, custom, Recall # V-134-6; b) Custom Dairy Feed with
Monensin, Recall # V-135-6. CODE None. Bulk product
RECALLING FIRM/MANUFACTURER
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on
June 28, 2006.
Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated
recall is complete.
REASON
Possible contamination of dairy feeds with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
1,484 tons
DISTRIBUTION
TN and WV
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA,
MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-115-6
CODE None
RECALLING FIRM/MANUFACTURER
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or
about July 14, 2006. FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
Approximately 2,223 tons
DISTRIBUTION
KY
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-116-6
CODE None
RECALLING FIRM/MANUFACTURER
Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006.
FDA initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
1,220 tons
DISTRIBUTION
KY
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-117-6
CODE None
RECALLING FIRM/MANUFACTURER
Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated
recall is completed.
REASON
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
40 tons
DISTRIBUTION
LA and MS
______________________________
PRODUCT
Bulk Dairy Feed, Recall V-118-6
CODE None
RECALLING FIRM/MANUFACTURER
Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA
initiated recall is complete.
REASON
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
7,150 tons
DISTRIBUTION
MS
______________________________
PRODUCT
Bulk custom dairy pre-mixes, Recall # V-119-6
CODE None
RECALLING FIRM/MANUFACTURER
Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm
initiated recall is complete.
REASON
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE
87 tons
DISTRIBUTION
MS
______________________________
PRODUCT
Bulk custom dairy pre-mixes, Recall # V-120-6
CODE None
RECALLING FIRM/MANUFACTURER
Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm
initiated recall is complete.
REASON
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
VOLUME OF PRODUCT IN COMMERCE
350 tons
DISTRIBUTION
AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb.
bags, Recall # V-121-6; b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,
50 lb. bags, Recall # V-122-6; c) Tucker Milling, LLC #31232 Game Bird Grower,
50 lb. bags, Recall # V-123-6; d) Tucker Milling, LLC 31227-Crumble, Game Bird
Starter, BMD Medicated, 50 lb bags, Recall # V-124-6; e) Tucker Milling, LLC
#31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6; f) Tucker Milling, LLC
#30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6; g) Tucker Milling,
LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE
All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER
Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and
visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J.
Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON
Poultry and fish feeds which were possibly contaminated with ruminant based
protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
7,541-50 lb bags
DISTRIBUTION
AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
Subject: MAD COW FEED RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN
COMMERCE 27,694,240 lbs
Date: August 6, 2006 at 6:14 pm PST
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall #
V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J.
Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm
initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated
with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6; b) Performance Sheep Pell
W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc
Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6; e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall #
V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton,
50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated
282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES,
Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin
Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; i) CO-OP LAYING
PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j) CO-OP LAYING
CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt
50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall #
V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email
and visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date:
August 6, 2006 at 6:19 pm PST
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated
recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain
ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
?????
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
CJD WATCH MESSAGE BOARD TSS
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22
71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6; b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight
50lb (22.6 kg), Recall # V-080-6; c) PRO-PAK, MARINE & ANIMAL PROTEIN
CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; d) Feather Meal, Recall #
V-082-6 CODE a) Bulk b) None c) Bulk d) Bulk
RECALLING FIRM/MANUFACTURER
H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15,
2006 and by press release on June 16, 2006. Firm initiated recall is
ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
10,878.06 tons
DISTRIBUTION
Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006
Date: June 27, 2006 at 7:42 am PST
Public Health Service
Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State
Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration
(FDA) investigator inspected your rendering plant, located at 509 Fortson
Street, Shreveport, Louisiana. The inspection revealed significant deviations
from the requirements set forth in Title 21, Code of Federal Regulations, Part
589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This
regulation is intended to prevent the establishment and amplification of Bovine
Spongiform Encephalopathy (BSE). You failed to follow the requirements of this
regulation; products being manufactured and distributed by your facility are
misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the
Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including
sufficient written procedures, to prevent commingling or cross-contamination and
to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent
carryover of protein derived from mammalian tissues into animal protein or feeds
which may be used for ruminants. For example, your facility uses the same
equipment to process mammalian and poultry tissues. However, you use only hot
water to clean the cookers between processing tissues from each species. You do
not clean the auger, hammer mill, grinder, and spouts after processing mammalian
tissues.
You failed to maintain written procedures specifying the clean-out
procedures or other means to prevent carryover of protein derived from mammalian
tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived
from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR
589.2000(e)(1)(i), any products containing or may contain protein derived from
mammalian tissues must be labeled, "Do not feed to cattle or other ruminants."
Since you failed to label a product which may contain protein derived from
mammalian tissues with the required cautionary statement. the poultry meal is
misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your
facility. As a manufacturer of materials intended for animal feed use, you are
responsible for ensuring your overall operation and the products you manufacture
and distribute are in compliance with the law. You should take prompt action to
correct these violations, and you should establish a system whereby violations
do not recur. Failure to promptly correct these violations may result in
regulatory action, such as seizure and/or injunction, without further
notice.
You should notify this office in writing within 15 working days of
receiving this letter, outlining the specific steps you have taken to bring your
firm into compliance with the law. Your response should include an explanation
of each step taken to correct the violations and prevent their recurrence. If
corrective action cannot be completed within 15 working days, state the reason
for the delay and the date by which the corrections will be completed. Include
copies of any available documentation demonstrating corrections have been
made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S.
Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie,
Louisiana 70001. If you have questions regarding any issue in this letter,
please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
SINCE THE LAST TIME I REPORTED :
Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through
September 30, 2005
Date: March 20, 2006 at 12:58 pm PST
YOU can see that report at the bottom of this update.
UPDATEs AS FOLLOWS ;
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT July 1, 2006 through September 30, 2006
snip...
Table 5. Administrative Actions: Large HACCP Plants (7/01/06 to
9/30/06)
Administrative Actions Pending or Taken at Large HACCP Plants [includes
actions initiated in prior quarters]
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS
On 6/15/06, a withholding action concerning labels for Advanced Meat
Recovery System product was taken in accordance with 9 CFR Part 500.8.
snip...
EXCEL CORP 00086R M FORT MORGAN, CO
On 8/11/04, a withholding action concerning labels for Advanced Meat
Recovery System product was taken in accordance with 9 CFR Part 500.8. On
12/22/04, plant appealed the withholding action. Appeal was denied on
1/25/05.
snip...
TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action
concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245L M LEXINGTON, NE X On 3/10/05, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
Table 6. Administrative Actions: Small HACCP Plants (7/01/06 to
9/30/06)
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
SSOP HACCP SPS INH INT Other LOI LOW
BOOKER PACKING COMPANY 07162 M BOOKER, TX 6/2/06 6/5/06 X 9/19/06 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
SSOP HACCP SPS INH INT Other LOI LOW
GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X
8/31/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
HI COUNTRY BEEF JERKY 01248 M01248 P LINCOLN, MT 3/24/06 4/14/06 X 8/31/06
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X
8/15/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
GIBSON PACKING COMPANY 05843 M05843 P SEYMOUR, MO 9/21/06 X Plant failed to
meet regulatory requirements for Escherichia coli Biotype 1 (E. coli). The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
SSOP HACCP SPS INH INT Other LOI LOW
HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X
9/26/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06
4/14/06 6/30/06 7/5/06 X 8/11/06 On 3/16/06, an enforcement action concerning
failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli)
was issued. The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X
7/25/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT April 1, 2006 through June 30, 2006
Table 5. Administrative Actions: Large HACCP Plants (4/01/06 to
6/30/06)
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X On 6/15/06, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X On 8/11/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8. On
12/22/04, plant appealed the withholding action. Appeal was denied on
1/25/05.
snip...
TYSON FRESH MEATS INC 00245L M LEXINGTON, NE X On 3/10/05, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
SSOP HACCP SPS INH INT Other LOI LOW
TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action
concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
BOOKER PACKING COMPANY 07162 M BOOKER, TX 4/13/06 4/19/06 X Plant failed to
meet regulatory requirements for Escherichia coli Biotype 1 (E. coli).
6/2/06 6/5/06 X The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
???
3/24/06 4/14/06
X
The enforcement action included, as basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
C & C MEAT SALES, INC., 18494 M18494 P, DURHAM, NC ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL.
snip...
FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X 4/13/06 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
FRONTIER FOODS & COLD STORAGE, INC 20741 M20741 P EL PASO, TX 5/31/06 X
On 6/8/06, DM closed case by firm’s requested voluntary withdrawal. The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05
10/24/05 X 5/19/06 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06
4/14/06 6/30/06 X On 3/16/06, an enforcement action concerning failure to meet
regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
SAVORY CONNECTION, INC., 31764 M31764 P, SELINGSGROVE, PA. ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL.
snip...
STEAK MASTER, 21159 M21159 P, ELWOOD, NE. ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL.
snip...
THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X 4/4/06 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05
X 5/4/06 The enforcement action included, as basis, failure of the establishment
to comply with Agency requirements concerning specified risk material.
snip...
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT January 1, 2006 through March 31, 2006
Table 5. Administrative Actions: Large HACCP Plants (1/01/06 to
3/31/06)
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X 3/13/06 On 10/11/05, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
snip...
EXCEL CORP. 00086R M FORT MORGAN, CO 8/11/04 2/22/05 X On 8/11/04, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
On 12/22/04, plant appealed the withholding action. Appeal was denied on
1/25/05.
snip...
TYSON FRESH MEATS INC. 00245L M 3/12/04 3/18/04 X
LEXINGTON, NE
X On 3/10/05, a withholding action concerning labels for Advanced Meat
Recovery System product was taken in accordance with 9 CFR Part 500.8.
snip...
TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action
concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
GULF PACKING COMPANY, 00696 M00696 P, SAN BENITO, TX, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
HI COUNTRY BEEF JERKY, 01248 M01248 P, LINCOLN, MT, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
HITCHIN POST STEAK COMPANY, 20773 M20773 P, KANSAS CITY, KS, ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL
snip...
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The
enforcement action included, as basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
snip...
ROCK CREEK SLAUGHTER CO., 09150 M09150 P, FAIRBURY, NE, ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL
snip...
WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 X The enforcement
action included, as basis, failure of the establishment to comply with Agency
requirements concerning specified risk material.
snip...
Table 7. Administrative Actions: Very Small HACCP Plants (1/01/06 to
3/31/06)
A.J. CEKAK'S MEAT MARKET 21562 M ORD. NE, ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL
snip...
ALTA VISTA LOCKER 31931 M ALTA VISTA, KS, ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL
snip...
C&C MEAT SALES, INC. 18494 M18494 P UPPER MARLBORO, MD 2/27/06 3/16/06
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X The enforcement
action included, as a basis, failure of the establishment to comply with Agency
requirements concerning specified risk material.
snip...
H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X
3/6/06 The enforcement action included, as a basis, failure of the establishment
to comply with Agency requirements concerning specified risk material.
snip...
PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X 1/13/06
The enforcement action included, as basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
PARAGON SPRAY DRYING, L.L.C. 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X
2/9/06 The enforcement action included, as basis, failure of the establishment
to comply with Agency requirements concerning specified risk material.
snip...
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05
10/24/05 X The enforcement action included, as basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
snip...
SAVORY CONNECTION, INC. 31764 M31764 P SELINGSGROVE, PA 3/14/06 3/31/06 X
The enforcement action included, as basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
STEAK MASTER, 21159 M21159 P, ELWOOD, NW, ... FAILURE TO COMPLY CONCERNING
SRM MATERIAL
snip...
TEARS MARKET, 04535 M04535 P, PENN YAN, NY, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
THE MEAT SHOP, 31561 M BENSON, VT, ... FAILURE TO COMPLY CONCERNING SRM
MATERIAL
snip...
THEURER'S QUALITY MEATS, INC. 31647 M31647 P, LEWISTON, UT, ... FAILURE TO
COMPLY CONCERNING SRM MATERIAL
snip...
TOOELE VALLEY MEATS 20594 M20594 P, GRANTSVILLE, UT, ... FAILURE TO COMPLY
CONCERNING SRM MATERIAL
snip...
WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
WILLIAM. G. MEST PACKING CO. 04431 M STRYKERSVILLE, NY 2/2/06 2/23/06 X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material. On 3/21/06, NOIE
was modified and reissued. On 6/29/06, NOIE was rescinded.
YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X 2/23/06
The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
snip...
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005
SRM REMOVAL USA
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005
snip....
CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X X On 10/11/05, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X X On 8/11/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding
action. Appeal was denied on 1/25/05.
00245L M LEXINGTON, NE 3/12/04 3/18/04 X 5/4/05 X X On 3/10/05, a
withholding action concerning labels for Advanced Meat Recovery System product
was taken in accordance with 9 CFR Part 500.8.
9/16/05 9/29/05 X X TYSON FRESH MEATS INC. 09268 M PASCO, WA X X On
7/28/04, a withholding action concerning labels for Advanced Meat Recovery
System product was taken in accordance with 9 CFR Part 500.8.
TYSON FRESH MEATS INC. X X 00245D M EMPORIA, KS On 12/23/04, a withholding
action concerning labels for Advanced Meat Recovery System product was taken in
accordance with 9 CFR Part 500.8.
DESERET MEAT 04852 M SPANISH FORK, UT 7/20/05 8/1/05 X X 12/29/05 The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X X X
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
A.J. CEKAK'S MEAT MARKET 9/1/05 9/20/05 X X X On 9/1/05, an enforcement
action 21562 M concerning failure to meet regulatory ORD, NE requirements for
Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included,
as a basis, failure of the establishment to comply with Agency requirements
concerning specified risk material.
ALTA VISTA LOCKER 10/5/05 10/26/05 X X The enforcement action included, as
a 31931 M basis, failure of the establishment toALTA VISTA, KS comply with
Agency requirements concerning specified risk material.
BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 8/8/05 8/16/05 X X X
11/16/05 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
CHAMPLAIN BEEF INC 2/28/05 3/4/05 3/8/05 X X X 08547 M WHITEHALL, NY
10/17/05 X X X The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
FIVE STAR PACK INC. 9/1/05 9/9/05 X X 12/29/05 On 9/1/05, an enforcement
action 08725 M08725 P concerning failure to meet regulatory GOLDEN CITY, MO
requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement
action included, as a basis, failure of the establishment to comply with Agency
requirements concerning specified risk material. FRESH FARMS BEEF 12/16/05
12/28/05 X X X The enforcement action included, as a 18579 M basis, failure of
the establishment toRUTLAND, VT comply with Agency requirements concerning
specified risk material.
GOETZ AND SONS WESTERN 11/15/05 11/23/05 12/1/05 X X MEATS INC 06245 M06245
P EVERETT, WA 12/17/05 12/28/05 X X X On 12/17/05, firm violated a regulatory
control action by selling U.S.D.A retained product.
H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 7/28/05 8/1/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 7/26/05 7/29/05 X X
11/15/05 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material. PARAGON SPRAY
DRYING, LLC 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X X X The enforcement
action included, as a basis, failure of the establishment to comply with Agency
requirements concerning specified risk material.
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05
10/24/05 X X X The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
S & S MEAT COMPANY 01046 M01046 P KANSAS CITY, MO 8/4/05 8/19/05 X X
11/16/05 The enforcement action included, as a basis, failure of the
establishment to comply with Agency requirements concerning specified risk
material.
STEAK MASTER 21159 M21159 P ELWOOD, NE 11/4/05 11/17/05 X X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X X X X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
THEURER'S QUALITY MEATS, INC 31647 M31647 P LEWISTON, UT 7/27/05 7/29/05 X
X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
TOOELE VALLEY MEATS 20594 M20594 P GRANTSVILLE, UT 7/25/05 8/1/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
WALNUT VALLEY PACKING LLC 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X
X X The enforcement action included, as a basis, failure of the establishment to
comply with Agency requirements concerning specified risk material.
YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X X The
enforcement action included, as a basis, failure of the establishment to comply
with Agency requirements concerning specified risk material.
full text 54 pages ;
Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through
September 30, 2005 Date: March 20, 2006 at 12:58 pm PST
UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE
QUARTERLY ENFORCEMENT REPORT July 1, 2005 through September 30, 2005
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
snip...
DESERET MEAT 04852 M SPANISH FORK, UT 07/27/05 08/01/05 X On 7/27/05, a
suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk
Material was taken in accordance with 9 CFR Part 500.3.
snip...
Administrative Actions Pending or Taken at Small HACCP Plants [includes
actions initiated in prior quarters]
snip...
MONTEBELLO MEAT PROCESSING, INC 19075 M19075 P MANATI, PR 08/01/05 08/18/05
X 09/26/05 On 8/1/05, an enforcement action concerning Bovine Spongiform
Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR
Part 500.4.
snip...
Table 7. Administrative Actions: Very Small HACCP Plants (7/01/05 to
9/30/05)
snip...
A.J. CEKAK'S MEAT MARKET 09/01/05 09/20/05 On 9/1/05, an enforcement
action
21562 M
concerning failure to meet regulatory ORD, NE requirements for Escherichia
coli X X X Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified
Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 08/08/05 08/16/05 X On
8/8/05, an enforcement action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
FIVE STAR PACK INC. 08725 M08725 P GOLDEN CITY, MO 09/01/05 09/09/05 X X On
9/1/05, an enforcement action concerning failure to meet regulatory requirements
for Escherichia coli Biotype 1 (E. coli) and Bovine Spongiform
Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part
500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
H AND P MEATS 21352 M SOUTH PITTSBURG, TN 07/28/05 08/08/05 08/17/05
08/19/05 X X On 8/17/05, a suspension action concerning Bovine Spongiform
Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR
Part 500.3.
snip...
HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 07/28/05 08/01/05 X On
7/28/05, a suspension action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.3.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 07/26/05 07/29/05 X X
On 7/26/05, a suspension action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.3.
snip...
PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 09/21/05 X On 9/21/05, an
enforcement action concerning Bovine Spongiform Encephalopathy and Specified
Risk Material was taken in accordance with 9 CFR Part 500.4.
PARAGON SPRAY DRYING, LLC 31792 M31792 P WAUKON, IA 09/06/05 09/12/05 X On
9/6/05, an enforcement action concerning Bovine Spongiform Encephalopathy and
Specified Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 07/01/05 07/28/05 X On 7/1/05,
an enforcement action concerning Bovine Spongiform Encephalopathy and Specified
Risk Material was taken in accordance with 9 CFR Part 500.4.
snip...
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
08/04/05
08/19/05
On 8/4/05,
an enforcement action 01046 M01046 P concerning Bovine SpongiformKANSAS
CITY, MO X X Encephalopathy and Specified Risk Material was taken in accordance
with 9 CFR Part 500.4.
Administrative Actions Pending or Taken at Very Small HACCP Plants
[includes actions initiated in prior quarters]
snip...
THE MEAT SHOP 08/18/05 09/06/05
09/09/05
On 9/6/05, a suspension action 31561 M concerning Bovine SpongiformBENSON,
VT Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR
Part 500.3. XX X X X
THEURER'S QUALITY MEATS, 07/27/05 07/29/05
On 7/27/05, a suspension action INC concerning Bovine Spongiform31647
M31647 P Encephalopathy and Specified Risk X X
LEWISTON, UT Material was taken in accordance with 9 CFR Part 500.3.
TOOELE VALLEY MEATS 07/25/05 08/01/05
On 7/25/05, a suspension action 20594 M20594 Pconcerning Bovine
Spongiform
GRANTSVILLE, UT X X Encephalopathy and Specified Risk Material was taken in
accordance with 9 CFR Part 500.3.
snip...
52 pages
PREVIOUS
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim
McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre,
Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of
Calgary, Canada
Background: Three BSE types (classical and two atypical) have been
identified on the basis of molecular characteristics of the misfolded protein
associated with the disease. To date, each of these three types have been
detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16
Canadian BSE cases based on the biochemical properties of there associated
PrPres.
Methods: Immuno-reactivity, molecular weight, glycoform profiles and
relative proteinase K sensitivity of the PrPres from each of the 16 confirmed
Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type
and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and
changes in glycosylation similar to other atypical BSE cases. PK digestion under
mild and stringent conditions revealed a reduced protease resistance of the
atypical cases compared to the C-type cases. N terminal- specific antibodies
bound to PrPres from H type but not from C or L type. The C-terminal-specific
antibodies resulted in a shift in the glycoform profile and detected a fourth
band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. *This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. ***It also
suggests a similar cause or source for atypical BSE in these countries.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 176 of 201 pages...tss
SEE THE DRASTIC REDUCTION OF CONFIRMED BSE CASES IN THE UK ONCE THE FEED
BAN TOOK HOLD FROM THE TOP YEAR DOWN TO THE FIRST ZERO YEAR ;
1992 36680 SLAUGHTERED SUSPECTS IN WHICH BSE CONFIRMED
2013 0 0 0 0 0 0 0 0
Saturday, January 31, 2015
RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings
in countries with a “negligible risk status for BSE” and on the risk of
modification of the list of specified risk materials (SRM) with regard to BSE
In the USA, USDA et al sometimes serves SRM’s up as appetizers or
horderves.
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
Wednesday, March 2, 2016
RANCHO He did not know that they were placing healthy cow heads next to
suspect carcasses BSE TSE Prion
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
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
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk
Materials Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK
MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM
WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to
lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the
tongue and nasal mucosa of terminally diseased cattle
Comment from Terry Singeltary Sr.
The is a Comment on the Animal and Plant Health Inspection Service (APHIS)
Notice: Agency Information Collection Activities; Proposals, Submissions, and
Approvals: Bovine Spongiform Encephalopathy; Importation of Animals and Animal
Products
For related information, Open Docket Folder
--------------------------------------------------------------------------------
Show agency attachment(s) AttachmentsView All (0)
--------------------------------------------------------------------------------
Comment View document:Docket No. APHIS-2014-0107 Bovine Spongiform
Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
;
I believe that there is more risk to the world from Transmissible
Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from
the United States and all of North America, than there is risk coming to the USA
and North America, from other Countries. I am NOT saying I dont think there is
any risk for the BSE type TSE prion coming from other Countries, I am just
saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present
mad cow risk factors in North America like they are not here?
North America has more strains of TSE prion disease, in more species
(excluding zoo animals in the early BSE days, and excluding the Feline TSE and
or Canine TSE, because they dont look, and yes, there has been documented
evidence and scientific studies, and DEFRA Hound study, that shows the canine
spongiform encephalopathy is very possible, if it has not already happened, just
not documented), then any other Country in the world. Mink TME, Deer Elk cervid
CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type
BSE cattle, atyical HG type BSE cow (the only cow documented in the world to
date with this strain), typical sheep goat Scrapie (multiple strains), and the
atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical
Scrapie has spread from coast to coast. sporadic CJD on the rise, with different
strains mounting, victims becoming younger, with the latest nvCJD human mad cow
case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL
CDC.
typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al),
and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical
Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid
populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk
assessments for each country, and then made BSE confirmed countries legal to
trade mad cow disease, which was all brought forth AFTER that fateful day
December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats
the day it all started. once the BSE MRR policy was shoved down every countries
throat by USDA inc and the OIE, then the legal trading of Scrapie was validated
to be a legal trading commodity, also shoved through by the USDA inc and the
OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion
disease typical and atypical strains, and the BSE TSE Prion aka mad cow type
disease was thus made a legal trading commodity, like it or not. its all about
money now folks, trade, to hell with human health with a slow incubating
disease, that is 100% fatal once clinical, and forget the fact of exposure,
sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion
disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its
all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the
infamous VPSPr. ...problem solved $$$
the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing
but ink on paper.
for this very reason I believe the BSE MRR policy is a total failure, and
that this policy should be immediately withdrawn, and set back in place the BSE
GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all
TSE PRION disease in all species of animals, and that the BSE GBR risk
assessments be made stronger than before.
lets start with the recent notice that beef from Ireland will be coming to
America.
Ireland confirmed around 1655 cases of mad cow disease. with the highest
year confirming about 333 cases in 2002, with numbers of BSE confirmed cases
dropping from that point on, to a documentation of 1 confirmed case in 2013, to
date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad
cow feed ban, and the enforcement of that ban, has drastically reduced the
number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the
USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in
2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD
COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in
my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow
disease in the USA, we still have no clue as to the true number of cases of BSE
mad cow disease in the USA or North America as a whole. ...just saying.
Number of reported cases of bovine spongiform encephalopathy (BSE) in
farmed cattle worldwide* (excluding the United Kingdom)
Country/Year
snip...please see attached pdf file, with references of breaches in the USA
triple BSE mad cow firewalls, and recent science on the TSE prion disease.
...TSS No documents available. AttachmentsView All (1) Docket No.
APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and
Animal Products Singeltary Submission View Attachment:
Terry S. Singeltary Sr. submission ;
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
Posted: 12/30/2014ID: APHIS-2014-0107-0001
Notice: Environmental Impact Statements; Availability, etc.: Animal Carcass
Management
Document ID: APHIS-2013-0044-0001 Docket ID: APHIS-2013-0044 Comment ID:
APHIS-2013-0044-0002
(APHIS) Notice: Agency Information Collection Activities; Proposals,
Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program
Agency Information Collection Activities; Proposals, Submissions, and Approvals:
Chronic Wasting Disease Herd Certification Program (Document ID
APHIS-2011-0032-0001)
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 Harvard BSE Risk Assessment ?
From:Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent:Thursday, September 08, 2005 6:17 PM
To:fsis.regulationscomments@fsis.usda.gov
Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified
Risk Materials for Human Food and Requirements for the Disposition of
Non-Ambulatory Disabled Cattle
APHIS-2006-0118-0096 CWD
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 0500 EMC 1
Terry S. Singeltary Sr. Vol #: 1
PLEASE SEE FULL TEXT SUBMISSION ;
*** 2001 Terry S. Singeltary Sr. comment submission ***
when USDA inc. contracts out for someone to pick up suspect BSE mad cow
cattle heads for testing, you would hope they would be from suspect BSE mad cow
cattle. NOT WITH THE USDA INC., they hired someone to pick up HEALTHY CATTLE
THEY KNEW DID NOT HAVE MAD COW DISEASE BSE TO BE TESTED FOR MAD COW DISEASE BSE.
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
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and
BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
From: Terry S. Singeltary Sr. (216-119-138-129.ipset18.wt.net)
Subject: Emergency Operations...BSE Red Book Date: March 13, 2000 at 1:30
pm PST
BSE Red Book 2.1-35
7.0 Emergency Operations
The section below would be implemented only after a first case of BSE is
confirmed in the United States.
7.1 READEO Activation
Prelimanary Notification
The director of NVSL is responsible for immediately notifying the APHIS,
Veterinary Services (VS) deputy administrator when tests suggest a presumptive
diagnosis of BSE. Once NVSL has made a presumptive diagnosis of BSE, APHIS and
FSIS field activities will also be initiated. APHIS will receive notification
(either confirming or not confirming NVSL's diagnosis) from the United Kingdom
anywhere between 24 and 96 hours
IT TOOK 7 MONTHS AND AN ACT OF CONGRESS TO GET THIS 2ND TEXAS BSE MAD COW
CONFIRMED !
now, someone please tell me why I should expect anything different with
Chronic Wasting Disease CWD TSE Prion testing in Texas $$$
the good old boy system is still alive and well in Texas i.e. shoot,
shovel, and shut the hell up i.e. SSS POLICY...
Tuesday, April 24, 2012
MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA
Wednesday, April 25, 2012
4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
Qualitative Analysis of BSE Risk Factors in the United States February 13,
2000 at 3:37 pm PST (BSE red book)
Thursday, April 26, 2012
FDA Statement on USDA Announcement of Positive BSE Test Result For
Immediate Release: April 26, 2012
Monday, June 23, 2014
PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES
***P.170: Potential detection of oral transmission of H type atypical BSE
in cattle using in vitro conversion
Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food
Inspection Agency; Lethbridge, AB Canada
Keywords: Atypical BSE, oral transmission, RT-QuIC
The detection of bovine spongiform encephalopathy (BSE) has had a
significant negative impact on the cattle industry worldwide. In response,
governments took actions to prevent transmission and additional threats to
animal health and food safety. While these measures seem to be effective for
controlling classical BSE, the more recently discovered atypical BSE has
presented a new challenge. To generate data for risk assessment and control
measures, we have challenged cattle orally with atypical BSE to determine
transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon
presentation of clinical symptoms, animals were euthanized and tested for
characteristic histopathological changes as well as PrPSc deposition.
The H-type challenged animal displayed vacuolation exclusively in rostral
brain areas but the L-type challenged animal showed no evidence thereof. To our
surprise, neither of the animals euthanized, which were displaying clinical
signs indicative of BSE, showed conclusive mis-folded prion accumulation in the
brain or gut using standard molecular or immunohistochemical assays. To confirm
presence or absence of prion infectivity, we employed an optimized real-time
quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain
Laboratory, Hamilton, USA.
Detection of PrPSc was unsuccessful for brain samples tests from the orally
inoculated L type animal using the RT-QuIC. It is possible that these negative
results were related to the tissue sampling locations or that type specific
optimization is needed to detect PrPSc in this animal. We were however able to
consistently detect the presence of mis-folded prions in the brain of the H-type
inoculated animal. Considering the negative and inconclusive results with other
PrPSc detection methods, positive results using the optimized RT-QuIC suggests
the method is extremely sensitive for H-type BSE detection. This may be evidence
of the first successful oral transmission of H type atypical BSE in cattle and
additional investigation of samples from these animals are ongoing.
P.126: Successful transmission of chronic wasting disease (CWD) into mice
over-expressing bovine prion protein (TgSB3985)
Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana
Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1
1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of
California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA
Keywords: chronic wasting disease, transmission, transgenic mouse, bovine
prion protein
Background. CWD is a disease affecting wild and farmraised cervids in North
America. Epidemiological studies provide no evidence of CWD transmission to
humans. Multiple attempts have failed to infect transgenic mice expressing human
PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal
human PrPC in vitro provides additional evidence that transmission of CWD to
humans cannot be easily achieved. However, a concern about the risk of CWD
transmission to humans still exists. This study aimed to establish and
characterize an experimental model of CWD in TgSB3985 mice with the following
attempt of transmission to TgHu mice.
Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were
intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse
(CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly
injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD)
or elk (CWD/Elk). Animals were observed for clinical signs of neurological
disease and were euthanized when moribund. Brains and spleens were removed from
all mice for PrPCWD detection by Western blotting (WB). A histological analysis
of brains from selected animals was performed: brains were scored for the
severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain
regions.
Results. Clinical presentation was consistent with TSE. More than 90% of
TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres
in the brain but only mice in the latter group carried PrPCWD in their spleens.
We found evidence for co-existence or divergence of two CWD/ Tga20 strains based
on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk
or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen
by WB. However, on neuropathological examination we found presence of amyloid
plaques that stained positive for PrPCWD in three CWD/WTD- and two
CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and
CWD/Elkinfected mice were similar but unique as compared to profiles of BSE,
BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM
mice tested positive for PrPCWD by WB or by immunohistochemical detection.
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
P.150: Zoonotic potential of L-type BSE prions: A new prion disease in
humans?
Emilie Jaumain,1 Stéphane Haïk,2 Isabelle Quadrio,3 Laetitia Herzog,1
Fabienne Reine,1 Armand Perret-Liaudet,3 Human Rezaei,1 Hubert Laude,1 Jean-Luc
Vilotte,4 and Vincent Béringue1 1INR A (Institut National de la Recherche
Agronomique); UR892; Virologie Immunologie Moléculaires; Jouy-en-Josas, France;
2IN SERM; Equipe maladie d’Alzheimer et maladies à Prions; CRicm; UMRS 1127; CNR
S; UPMC. R.; ICM, Hôpital de la Salpêtrière; Paris, France; 3Neurobiologie, CMRR
, Gériatrie, Hospices Civils de Lyon, Université Lyon 1-CNR S UMR5292-IN SERM
U1028; Lyon, France; 3INR A; UMR1313; Génétique Animale et Biologie Intégrative;
Jouy-en-Josas, France
In summary, L-type prions can be passaged on the human PrP sequence without
any obvious transmission barrier. The phenotype obtained differs from the
classical CJD prion types known so far. Careful extrapolation would suggest that
the zoonotic transmission of this agent could establish a new prion disease type
in humans.
Wednesday, May 30, 2012
PO-028: Oral transmission of L-type bovine spongiform encephalopathy
(L-BSE) in primate model Microcebus murinus
Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle
Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel
Verdier1
1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils
de Lyon; Lyon, France
Here, we demonstrate that the L-BSE agent can be transmitted by oral route
from cattle to young and adult mouse lemurs. In comparison to IC inoculated
animals, orally challenged lemurs were characterized by longer survival periods
as expected with this route of infection.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral
Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6;
Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique,
France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious
Disease control, Sweden; 5Georg August University, Germany; 6German Primate
Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to
contract BSE through contaminated food. For this purpose, BSE brain was titrated
in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this, to
assess the risk for humans. Secondly, we aimed at examining the course of the
disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE
brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals
were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the onset of
the clinical phase. However, there are differences in the clinical course
between orally and intracerebrally infected animals that may influence the
detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years).
However, there are rapid progressors among orally dosed monkeys that develop
simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE
in primates“ supported by the EU (QLK1-2002-01096).
>>> Both of the atypical BSE subtypes are believed to occur
spontaneously,<<<
LOL!
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Atypical BSE...Spontaneous...LOL
BSE identified in France
Posted May 2, 2016
A cow in northern France has been confirmed to have bovine spongiform
encephalopathy, according to the World Organisation for Animal Health
(OIE).
The cow had developed partial paralysis and was euthanized March 1, a March
25 OIE report states.
BSE is a fatal neurologic prion disease with a typical incubation period of
four to five years. The cow in France was almost 5 years old.
The affected cow had the classic form of BSE, which is most often
associated with feed containing neurologic tissue from infected animals. It is
distinct from atypical BSE, which may develop spontaneously, according to
information from the U.S. Centers for Disease Control and Prevention.
Investigators were trying to identify the source of infection and other
animals at risk for BSE at the time the report was published.
The affected bovine, a Salers female born on April, 8th 2011, showed
paresis and was euthanized on March, 1st 2016. Samples made on March, 4th 2016
during rendering were analyzed at the Department Laboratory of La Somme. The
rapid test proved positive on March, 8th 2016 and the samples were then sent for
further analysis to the National Reference Laboratory, ANSES, which confirmed a
case of classical BSE on March, 21st 2016. The European Union Reference
Laboratory confirmed those results on the basis of documentation on March, 23rd
2016.
>>> It is distinct from atypical BSE, which may develop
spontaneously, according to information from the U.S. Centers for Disease
Control and Prevention.
THIS IS A MYTH $$$
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40
cases in the remaining 12 Countries, divided by the remaining 12 Countries,
about 3+ cases per country, besides Frances 20 cases. you cannot explain this
away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Thursday, March 24, 2016
FRANCE CONFIRMS BOVINE SPONGIFORM ENCEPHALOPATHY BSE MAD COW (ESB) chez une
vache dans les Ardennes
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
If you Compare France to other Countries with atypical BSE, in my opinion,
you cannot explain this with ‘spontaneous’.
Table 1: Number of Atypical BSE cases reported by EU Member States in the
period 2001–2014 by country and by type (L- and H-BSE) (extracted from EU BSE
databases on 1 July 2014). By 2015, these data might be more comprehensive
following a request from the European Commission to Member States for re-testing
and retrospective classification of all positive bovine isolates in the EU in
the years 2003–2009
BSE type
Country 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013(a)
2014(a) Total
H-BSE Austria 1 1
France(b) 1 2 3 1 2 2 2 2 15
Germany 1 1 2
Ireland 1 1 2 1 5
The Netherlands 1 1
Poland 1 1 2
Portugal 1 1
Spain 1 1 2
Sweden 1 1
United Kingdom 1 1 1 1 1 5
Total 2 3 3 1 1 2 2 2 4 4 5 1 4 1 35
L-BSE Austria 1 1 2
Denmark 1 1
France(b) 1 1 1 1 2 1 3 2 1 1 14
Germany 1 1 2
Italy 1 1 1 1 1 5
The Netherlands 1 1 1 3
Poland 1 2 2 1 2 1 2 1 12
Spain 2 2
United Kingdom 1 1 1 1 4
Total 0 5 3 4 3 3 6 3 3 4 3 6 1 1 45
Total Atypical cases (H + L)
2 8 6 5 4 5 8 5 7 8 8 7 5 2 80
(a): Data for 2013-2014 are incomplete and may not include all
cases/countries reported.
(b): France has performed extensive retrospective testing to classify BSE
cases, which is probably the explanation for the higher number of Atypical BSE
cases reported in this country.
The number of Atypical BSE cases detected in countries that have already
identified them seems to be similar from year to year. In France, a
retrospective study of all TSE-positive cattle identified through the compulsory
EU surveillance between 2001 and 2007 indicated that the prevalence of H-BSE and
L-BSE was 0.35 and 0.41 cases per million adult cattle tested, respectively,
which increased to 1.9 and 1.7 cases per million, respectively, in tested
animals over eight years old (Biacabe et al., 2008). No comprehensive study on
the prevalence of Atypical BSE cases has yet been carried out in other EU Member
States. All cases of Atypical BSE reported in the EU BSE databases have been
identified by active surveillance testing (59 % in fallen stock, 38 % in healthy
slaughtered cattle and 4 % in emergency slaughtered cattle). Cases were reported
in animals over eight years of age, with the exception of two cases (one H-BSE
and one L-BSE) detected in Spain in 2011/2012. One additional case of H-BSE was
detected in Switzerland in 2012 in a cow born in Germany in 2005 (Guldimann et
al., 2012).
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 8
Table 1: Number of Atypical BSE cases reported by EU Member States in the
period 2001–2014 by country and by type (L- and H-BSE) (extracted from EU BSE
databases on 1 July 2014). By 2015, these data might be more comprehensive
following a request from the European Commission to Member States for re-testing
and retrospective classification of all positive bovine isolates in the EU in
the years 2003–2009
BSE type Country 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011
2012 2013(a) 2014(a) Total
H-BSE
Austria 1 1
France(b) 1 2 3 1 2 2 2 2 15
Germany 1 1 2 Ireland 1 1 2 1 5
The Netherlands 1 1
Poland 1 1 2
Portugal 1 1
Spain 1 1 2
Sweden 1 1
United Kingdom 1 1 1 1 1 5
Total 2 3 3 1 1 2 2 2 4 4 5 1 4 1 35
L-BSE
Austria 1 1 2
Denmark 1 1
France(b) 1 1 1 1 2 1 3 2 1 1 14
Germany 1 1 2 Italy 1 1 1 1 1 5
The Netherlands 1 1 1 3
Poland 1 2 2 1 2 1 2 1 12
Spain 2 2
United Kingdom 1 1 1 1 4
Total 0 5 3 4 3 3 6 3 3 4 3 6 1 1 45
Total Atypical cases (H + L) 2 8 6 5 4 5 8 5 7 8 8 7 5 2 80
(a): Data for 2013-2014 are incomplete and may not include all
cases/countries reported.
(b): France has performed extensive retrospective testing to classify BSE
cases, which is probably the explanation for the higher number of Atypical BSE
cases reported in this country.
SNIP...
The current lack of information on the distribution of infectivity in
tissues from Atypical BSE-infected cattle does not allow judgement of whether
the current list of bovine SRM, set by EU Atypical BSE study protocol
legislation based on data relating to the pathogenesis and tissue distribution
of C-BSE, is fit for the purpose of removing most of the Atypical BSE
infectivity from bovine carcasses. As is the case for C-BSE, Atypical BSE (H-BSE
and/or L-BSE) agents are able to propagate in experimentally challenged foreign
species such as mice, sheep, voles, primates and hamsters, and in transgenic
mice expressing heterologous, i.e. non-bovine, PrP sequences.
EFSA Journal 2014;12(7):3798 13
SNIP...
2.4. Concluding remarks
Where data exist from both field cases and experimental animals (i.e. for
L-BSE only), there is good agreement of the data with regard to abnormal PrP
distribution. There are no data for field case H-BSE.
All data currently available relate to the presence or absence of PrPSc,
but do not quantify relative amounts of PrPSc or levels of infectivity.
Disease-related PrP has been reported consistently in CNS tissues,
peripheral ganglia and nerves, muscles (predominantly muscle spindles), adrenal
glands and retina for both H-BSE and L-BSE. All of these tissues are also
positive in C-BSE.
By contrast with C-BSE, at this stage no lymphoid tissues or
gastrointestinal tissues from H-BSE- and L-BSE-affected animals have tested
positive for PrPSc presence (IHC, WB) or infectivity (bioassay).
There are insufficient data at present to be clear about whether these
apparent differences in the distribution of disease-specific markers reflect
absolute differences between C-BSE and the H-BSE and L-BSE variants, whether
they are a consequence of detection threshold limitations, or whether they are a
consequence of the different routes of challenge.
No studies have been explicitly designed to address the issue of Atypical
BSE with respect to SRM regulations. Without further experimental challenges or
tissue collection from ongoing studies it will not be possible to obtain any
data on duodenum, the jejunum and ileum (without Peyer’s patches), the caecum,
the colon and the mesenteric fat.
SNIP...
4.1. Selection of tissues
4.1.1. BSE infectivity in bovine tissues
The current SRM list in cattle (see Table 5) has been established and
amended in accordance with current knowledge related to C-BSE agent distribution
in the tissues of infected cattle.
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 24
The SRM measure is aimed at preventing the entry into the food chain of
tissues and anatomical structures that might contain significant amounts of
infectivity. In the framework of C-BSE infection in cattle, these measures are
extremely efficient. However, certain tissues that might contain low amounts of
infectivity in certain BSE-infected cattle are not included in the cattle SRM
list (Table 6).
Table 5: Bovine SRM list, as defined in Regulation (EC) No 999/2001
Bovine SRM list
The skull excluding the mandible and including the brain and eyes, and the
spinal cord of animals aged over 12 months
The vertebral column excluding the vertebrae of the tail, the spinous and
transverse processes of the cervical, thoracic and lumbar vertebrae and the
median sacral crest and wings of the sacrum, but including the dorsal root
ganglia, of animals aged over 30 months
The tonsils, the intestines from the duodenum to the rectum and the
mesentery of animals of all ages
Table 6: Cattle tissues with known infectivity or PrPSc presence for C-BSE
according to WHO (2010), and their inclusion or not in the current SRM
list
Higher-infectivity tissues
SRM
Brain
Dura mater
Spinal cord
Optic nerve
Retina
Spinal ganglia
Trigeminal ganglia
Lower-infectivity tissues
Nictitating membrane
Autonomic ganglia
Tonsil
Ileum
Jejunum
Non-SRM
Peripheral nerves
Adrenal glands
Bone marrow
Skeletal muscle
All the TSE agents replicate and accumulate at a high level in the CNS and
can disseminate (centrifugally and centripetally) along the peripheral
(autonomic and motor) nervous system. However, in a given host the agent
distribution and the relative level of infectivity in other tissues can vary
substantially according to the TSE strain.
For instance, in humans, although sCJD infectivity is mostly confined to
the CNS, numerous lymphoid organs have been shown to be infectious in patients
affected with variant CJD (vCJD) (Gill et al., 2013).
Similarly, in sheep infected with Classical scrapie, a significant level of
infectivity can be found in lymphoid organs (about 103 times less than in the
same weight of brain tissue), whereas in animals affected with Atypical scrapie
lymphoid organs contain either very low (about 107 times less than in the same
weight of brain tissue) or no detectable infectivity (Andreoletti et al.,
2011).
There are currently no quantitative data on the distribution of H-BSE and
L-BSE in cattle tissues.
4.1.2. Prioritisation of tissues to be included in further studies
In order to assess the adequacy and the relative effectiveness of the
current SRM measures for mitigating human dietary exposure to H-BSE and L-BSE, a
large number of tissues/anatomical structures need to be tested for the presence
of PrPSc and/or infectivity.
Considering the potential number of samples and the requirement for
bioassay, the choice of tissues to be tested should be prioritised according to
three criteria:
the level of infectivity they contain in C-BSE-infected cattle (SRM list);
the presence of infectivity, or PrPSc presence, demonstrated in Atypical
BSEs or other TSEs in ruminants;
the importance in terms of input into the food chain in the EU.
SNIP...
CONCLUSIONS AND RECOMMENDATIONS
CONCLUSIONS
Data relating to the prevalence and geographical distribution of Atypical
BSE are incomplete.
The recent cessation of the testing of healthy slaughtered cattle in some
EU Member States will lead to a loss of capacity of the monitoring system to
detect Atypical BSE cases.
For transmission studies, i.c. challenge would be an appropriate proxy for
studying the distribution of the agent if the origin of the disease was
spontaneous, and originating in the brain, while oral challenge would be more
appropriate if the origin of the disease was through ingestion of infected
material.
The current lack of information on the distribution of infectivity in
tissues of Atypical BSE-infected cattle does not allow judgement of whether the
current list of bovine SRM, set by EU legislation based on data relating to the
pathogenesis and tissue distribution of C-BSE, is fit for the purpose of
removing most of the Atypical BSE infectivity from bovine carcasses.
Where data exist from both field cases and experimental animals (i.e. for
L-BSE only), there is good agreement of the data with regard to abnormal PrP
distribution. There are no data for field case H-BSE.
Disease-related PrP has been reported consistently in CNS tissues,
peripheral ganglia and nerves, muscles (predominantly muscle spindles), adrenal
glands and retina for both H-BSE and L-BSE. All of these tissues are also
positive in C-BSE.
By contrast with C-BSE, at this stage no lymphoid tissues or
gastrointestinal tissues from H-BSE- and L-BSE-affected animals have tested
positive for PrPSc presence (IHC, WB) or infectivity (bioassay).
The reference method for the estimation of prion infectious titre in
tissues is endpoint dilution titration in animals. To achieve maximum
sensitivity regarding Atypical H-BSE and L-BSE, this bioassay should ideally be
done in mouse lines over-expressing bovine PrPC. Several mouse lines
over-expressing bovine PrPC are available worldwide.
In vitro amplification techniques can be used to determine whether a tissue
contains any prion seeding activity. A correlation must be made between the
sensitivity achieved by the cell-free assays and bioassays using reference
material such as brain tissue from animals at the terminal stage of disease.
The application of the proposed protocol would provide elements allowing
the assessment of the relative infectious titre, PrPSc accumulation and prion
seeding activity in the tissues of cattle that developed H-BSE or L-BSE (using
posterior brainstem as a reference).
Tissues to be covered by further studies are categorised in three
priorities, based on their inclusion in the cattle SRM list, on the presence of
infectivity, or PrPSc presence, demonstrated in Atypical BSEs or other TSEs in
ruminants, and on the importance in terms of input into the food chain in the
EU.
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 32
Applying the protocol only to the tissues obtained through the EURL study
would provide information on some but not all the tissues from the cattle SRM
list. It would also provide information on some additional tissues not included
in the cattle SRM list, but relevant for the food chain.
Material from other studies could be used to augment the range of SRM and
non-SRM tissues available.
There is no identified source able to provide all the samples necessary to
assess infectivity in tissues belonging to the full cattle SRM list in H- and
L-BSE-infected animals. Therefore, to complete this objective, new inoculations
of cattle would have to be considered.
RECOMMENDATIONS
In accordance with former EFSA recommendations, through the implementation
of the protocol information should also be obtained on the performance of
currently validated rapid tests for TSE active surveillance in cattle/bioassay
for detecting H-BSE and L-BSE agents.
If new inoculation experiments are carried out in cattle with H-BSE and
L-BSE, the following should be considered:
- inoculation through both the i.c. and oral route (despite the potential
length of the oral route experiment);
- inclusion of C-BSE controls in the i.c. route experiment;
- sequential time killing of animals;
- collection of all tissues listed in Table 7.
DOCUMENTATION PROVIDED TO EFSA
1. Summary of the samples available and the tests already carried out by
the EURL-TSE. Submitted by the European Commission as Annex 1 to the
mandate.
2. Information on protocols and tests results provided by the EURL-TSE.
Submitted by the European Commission as Annex 2 to the mandate.
REFERENCES
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical
BSE investigations
>>>(b): France has performed extensive retrospective testing to
classify BSE cases, which is probably the explanation for the higher number of
Atypical BSE cases reported in this country.<<<
LMAO!!!
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
we have seen the spontaneous BSE epidemic in France, what about the other
HIGH INCIDENCE ATYPICAL BSE COUNTRY OF POLAND, another atypical spontaneous
event of high incidence. how can this be blamed on a happenstance of nothing,
i.e. old age? goes against all junk science to date on the spontaneous atypical
BSE i.e.
see more ;
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND
SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
*** 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 ;
What Do We Feed to Food-Production Animals? A Review of Animal
FeedIngredients and Their Potential Impacts on Human Health
Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly
Walker11Johns Hopkins Center for a Livable Future, Bloomberg School of
PublicHealth, Baltimore, Maryland, USA; 2Maryland Institute forApplied
Environmental Health, College of Health and Human Performance,University of
Maryland, College Park, Maryland, USA;3Lisa Y. Lefferts Consulting, Nellysford,
Virginia, USA
snip...
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
bonemeal, poultry meal, animal the slaughter of food by-product meal, dried
animal blood, blood meal, feather meal, egg-shell production animals andother
meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, andanimal 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, antibiotic
resistant bacteria, prions, arsenic, and dioxin like 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 (antibiotic resistant 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
Calves were challenged by mouth with homogenised brain from confirmed cases
of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were
then left to develop BSE, but were not subjected to the normal stresses that
they might have encountered in a dairy herd. Animals in all four groups
developed BSE. There has been a considerable spread of incubation period in some
of the groups, but it appears as if those in the 1 and 10g challenge groups most
closely fit the picture of incubation periods seen in the epidemic. Experiments
in progress indicate that oral infection can occur in some animals with doses as
low as 0.01g and 0.001g. ......... http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose
look at the table and you'll see that as little as 1 mg (or 0.001 gm)
caused7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in
primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian
Herzog,Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia,
NathalieLescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown,
Jean-PhilippeDeslysSummary The uncertain extent of human exposure to bovine
spongiformencephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob
disease(vCJD)--is compounded by incomplete knowledge about the efficiency of
oralinfection and the magnitude of any bovine-to-human biological barrier
totransmission. We therefore investigated oral transmission of BSE tonon-human
primates. We gave two macaques a 5 g oral dose of brain homogenatefrom a
BSE-infected cow. One macaque developed vCJD-like neurologicaldisease 60 months
after exposure, whereas the other remained free of diseaseat 76 months. On the
basis of these findings and data from other studies, wemade a preliminary
estimate of the food exposure risk for man, whichprovides additional assurance
that existing public health measures canprevent transmission of BSE to
man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15
(7%)1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine
inoculumused in our study with primates against a bovine brain inoculum with
asimilar PrPres concentration that was inoculated into mice and cattle.8 *Data
are number of animals positive/number of animals surviving at the time of
clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log.
icip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle
infectedorally with similar BSE brain inocula
Published online January 27, 2005
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
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...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
CONFIDENTIAL
>>> 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 ?
SWISS MEDICAL WEEKLY
Alzheimer-type brain pathology may be transmitted by grafts of dura mater
26/01/2016 Singeltary comment ;
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)
snip...see full Singeltary Nature comment here;
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
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
2016 PRION CONFERENCE TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
snip...
Do our transmission results in tgHu imply that sheep scrapie is the cause
of sCJD cases in humans? This question challenges well-established dogma that
sCJD is a spontaneous disorder unrelated to animal prion disease. In our
opinion, our data on their own do not unequivocally establish a causative link
between natural exposure to sheep scrapie and the subsequent appearance of sCJD
in humans. However, our studies clearly point out the need to re-consider this
possibility. Clarification on this topic will be aided by informed and modern
epidemiological studies to up-date previous analysis that was performed at the
end of the last century3, 4. The value of such an approach is highlighted by the
implementation in the year 2000 of large-scale active animal TSE surveillance
programs around the world that provided an informed epidemiological-based view
of the occurrence and geographical spread of prion disease in small ruminant
populations51. The fact that both Australia and New-Zealand, two countries that
had been considered for more than 50 years as TSE-free territories, were finally
identified positive for atypical scrapie in their sheep flocks provides an
example of how prion dogma can be reversed52. However, the incubation period for
prion disease in humans after exposure to prions via the peripheral route, such
as in iatrogenic CJD transmission and Kuru, can exceed several decades53, 54. In
this context, it will be a challenge to combine epidemiological data collected
contemporarily in animal populations and humans to investigate the existence of
a causative link between prion disease occurrence in these different hosts.
Furthermore, it is crucial to bear in mind that sporadic sCJD in humans is a
rare disease (1–2 individuals per million of the population per year) and that
scrapie has been circulating in small ruminants populations used for food
purposes for centuries. Consequently, it is our opinion that even if a causative
link was established between sheep scrapie exposure and the occurrence of
certain sCJD cases, it would be wrong to consider small ruminant TSE agents as a
new major threat for public health. Despite this, it remains clear that our data
provide a new impetus to establish the true zoonotic potential of sheep scrapie
prions.
Subject terms: Biological sciences• Medical research At a glance
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.
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, Valerie 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 long 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***
===============
2016
CHRONIC WASTING DISEASE TSE PRION
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining
a significant number of brain samples from prion-affected human subjects in the
USA and Canada who have consumed venison from CWD-endemic areas utilizing the
criteria and essays established in Aim 3. The findings from this proposal will
greatly advance our understandings on the potential and characteristics of
cervid prion transmission in humans, establish reliable essays for CWD zoonosis
and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure
to cervid prions because chronic wasting disease (CWD, a widespread and highly
infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) *** CWD transmission to humans has already occurred. *** We will test
these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary
in vitro approaches.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs),
are fatal neurodegenerative diseases affecting humans, cervids, bovids, and
ovids. The absolute requirement of PrPC expression to generate prion diseases
and the lack of instructional nucleic acid define prions as unique infectious
agents. Prions exhibit species-specific tropism, inferring that unique prion
strains exist that preferentially infct certain host species and confront
transmission barriers to heterologous host species. However, transmission
barriers are not absolute. Scientific consensus agrees that the sheep TSE
scrapie probably breached the transmission barrier to cattle causing bovine
spongiform encephalopathy that subsequently breached the human transmission
barrier and likely caused several hundred deaths by a new-variant form of the
human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human
health, emotion and economies can still be felt in areas like farming, blood and
organ donations and the threat of a latent TSE epidemic. This precedent raises
the real possibility of other TSEs, like chronic wasting disease of cervids,
overcoming similar human transmission barriers. A groundbreaking discovery made
last year revealed that mice infected with heterologous prion strains facing
significant transmission barriers replicated prions far more readily in spleens
than brains6. Furthermore, these splenic prions exhibited weakened transmission
barriers and expanded host ranges compared to neurogenic prions. These data
question conventional wisdom of avoiding neural tissue to avoid prion
xenotransmission, when more promiscuous prions may lurk in extraneural tissues.
Data derived from work previously funded by NIH demonstrate that Complement
receptors CD21/35 bind prions and high density PrPC and differentially impact
prion disease depending on the prion isolate or strain used. Recent advances in
live animal and whole organ imaging have led us to generate preliminary data to
support novel, innovative approaches to assessing prion capture and transport.
We plan to test our unifying hypothesis for this proposal that CD21/35 control
the processes of peripheral prion capture, transport, strain selection and
xenotransmission in the following specific aims.
1. Assess the role of CD21/35 in splenic prion strain selection and host
range expansion.
2. Determine whether CD21/35 and C1q differentially bind distinct prion
strains
3. Monitor the effects of CD21/35 on prion trafficking in real time and
space
4. Assess the role of CD21/35 in incunabular prion trafficking
Public Health Relevance Transmissible spongiform encephalopathies, or prion
diseases, are devastating illnesses that greatly impact public health,
agriculture and wildlife in North America and around the world. The impact to
human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease (CWD) of cervids, overcoming similar human transmission barriers. Early
this year Canada reported its first case of BSE in over a decade audits first
case of CWD in farmed elk in three years, underscoring the need for continued
vigilance and research. Identifying mechanisms of transmission and zoonoses
remains an extremely important and intense area of research that will benefit
human and other animal populations.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Allergy and Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly
transmissible prion disease now recognized in 18 States, 2 Canadian provinces,
and Korea. We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination. We have also shown that CWD
can infect some non-cervid species, thus the potential risk CWD represents to
domestic animal species and to humans remains unknown. Whether prions borne in
blood, saliva, nasal fluids, milk, or excreta are generated or modified in the
proximate peripheral tissue sites, may differ in subtle ways from those
generated in brain, or may be adapted for mucosal infection remain open
questions. The increasing parallels in the pathogenesis between prion diseases
and human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, add relevance to CWD as a transmissible protein misfolding disease.
The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an
emergent highly transmissible prion disease now recognized throughout the USA as
well as in Canada and Korea. We have shown that infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces thereby
leading to transmission by direct contact and environmental contamination. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado State University-Fort
Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** 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).***
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.
***********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 ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** 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.
*** now, let’s see what the authors said about this casual link, personal
communications years ago, and then the latest on the zoonotic potential from CWD
to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS
casual evidence ???? “Our conclusion stating that we found no strong evidence of
CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
IN A NUT SHELL ;
(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 the Central Bureau,
Wednesday, March 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
Friday, April 4, 2014
China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa
and Saudi Arabia still retain BSE-related closures
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
The OIE is nothing more than a trading brokerage for the Transmissible
Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is
still in the midst of a mad cow disease outbreak with atypical BSE cases still
growing. mad cow disease is so bad in France, as with the USA, they stopped
testing for mad cow disease (France altogether and the USA to figures so low,
you would only detect a case of mad cow disease, only by chance).
from the inside looking out ;
Quote: Maybe familirise yourself with the OIE. The primary concern is
animal health of the world they are the animal version of the WHO. It is a long
way down from that ivory tower but here we go, until pressured by the USA
representatives a country could not export animals for 6 years after finding a
BSE/BASE positive animal so under the old rules the US would not be able to
export anywhere in the world for another 4 1/2 years. Who got the risk levels
system put in to allow some trade - your US representatives. You guys want to
change rules - OK , but you do not get special rules that only apply to the US.
As i have told you before Sand h I market all my own slaughter animals and you
know that, so don't do the whole holier than thow act.
With all due respect, it is obvious that you know little about the OIE and
how it actually works. Having been to their offices in Paris and talked
personally with the Head of the Animal Test Section, you would choke if you knew
how many lobby groups attend that office daily. There is a steady stream of paid
lobby groups that have one goal in life and that is to sway the Section Heads of
each department within the OIE to suit the needs of different jurisdictions
around the world, which curiously enough, also includes the USA and Canada.
Anyone can go there and chat with them - providing they can provide valid cause
to be let in. To say that the only goal of the OIE is animal health is actually
only part of their function. They are more than that and my discussions with Dr.
Diaz there has showed me that. But to blindly make a statement regarding what
they do when you have no idea what they actually do is like eating the skin of
the orange and not knowing what is actually under.
Interestingly you state that the US Government applied pressure (to the
OIE) I assume and that is a great example of the lobby groups doing their job.
So, at the end of the day, one can safely assume that it is the pressure applied
by certain influential lobby groups that will determine a likely outcome to an
apparent OIE directive. Man alive, isn't it great to live in a democracy wherein
the people get to make the choices and not just some "other" interested party or
group - say like........Cargill or Tyson for example?
So, one last question, question?
Who wags the tail of that dog?? And for what reason other than one that is
purely associated with trade and international agreements and greed?
And you think it is so simply explainable.
end...tss
Subject: UPDATED WHO Guidelines include tissues from Cervidae affected with
Chronic Wasting Disease (CWD)
snip...see full text ;
Sunday, October 18, 2015
*** World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
SSS SHOOT SHOVEL AND SHUT UP !
*** you can find some history of the BSE cases in Canada and Klein’s BSE
SSS policy comment here ;
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Saturday, December 12, 2015
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 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 ***
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
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...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
Terry S. Singeltary Sr.
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