Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
New protocol for Atypical BSE investigations
News in brief
21 July 2014
EFSA has developed a laboratory protocol on how to conduct new studies for
investigating the presence of the agent of Atypical Bovine Spongiform
Encephalopathy (BSE) in tissues of infected cattle. Guidance includes the number
of animals to be tested, the tissues to be analysed and the methods to detect
the agent of disease.
BSE belongs to a group of diseases called Transmissible Spongiform
Encephalopathies that affect the brain and nervous system of humans and animals.
BSE can be divided into Classical BSE and Atypical BSE.
Current knowledge on Atypical BSE is limited and the implementation of this
protocol will contribute to fill information gaps.
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE
for further laboratory investigations into the distribution of infectivity
of Atypical BSE EFSA Journal 2014;12(7):3798 [55 pp.].
doi:10.2903/j.efsa.2014.3798 European Food Safety AuthorityAcknowledgment EFSA
wishes to thank the members of the Working Group on Atypical BSE study protocol:
Olivier Andreoletti, Anne Balkema-Buschmann, Vincent Béringue, Marion Simmons
and Juan-Maria Torres for the preparatory work on this scientific output, the
members of the EFSA Panel on Biological Hazards (BIOHAZ) for their endorsement
of the scientific output, and EFSA staff members: Winy Messens and Pietro Stella
for the support provided to this scientific output. Contact
biohaz@efsa.europa.eu
Type: Scientific Report of EFSA On request from: European Commission
Question number: EFSA-Q-2013-01015 Approved: 11 July 2014 Published: 21 July
2014 Affiliation: European Food Safety Authority (EFSA) Parma Italy Article (1.1
Mb) Abstract Information on the pathogenesis and tissue distribution of Atypical
Bovine Spongiform Encephalopathy (BSE) in cattle through the study of field
cases and experimental transmission studies is lacking. The latter are limited
to transmission of Atypical BSE through intracerebral (i.c.) inoculation of
cattle. All data currently available relate to the presence or absence of PrPSc,
but do not quantify relative amounts of PrPSc or levels of infectivity. A
laboratory protocol for further studies is recommended, to allow 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 those studies are
categorised in three priorities, based on their inclusion in the list of
specific risk material in cattle, on the presence of infectivity, or PrPSc
presence, demonstrated in Atypical BSEs or other Transmissible Spongiform
Encephalopathies (TSEs) in ruminants, and on the importance in terms of input
into the food chain in the EU. The protocol provides details in terms of the
minimum number of animals to be tested, processing and preparation of tissues,
and methods to be used to identify abnormal PrP and quantify infectivity, also
depending on the expected level of infectivity and amount of tissue available
for analysis. It is recommended that, 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.
© European Food Safety Authority, 2014
Summary Following a request from the European Commission, EFSA was asked to
provide scientific and technical assistance on a protocol for further laboratory
investigations into the distribution of infectivity of Atypical Bovine
Spongiform Encephalopathy (BSE).
The European Union Reference Laboratory (EURL) for Transmissible Spongifom
Encephalopathies (TSEs) conducted experiments (referred to as the EURL study)
that resulted in the collection and storage of reference material originating
from cattle experimentally infected with Atypical BSE (H-BSE and L-BSE). With
the intention to generate relevant data that could inform further policy options
regarding BSE, in particular as regards rules on specified risk material (SRM),
DG SANCO wished to explore the possibility to submit these tissue samples to
further investigations. EFSA was therefore asked to propose a laboratory
protocol to perform new studies aimed at investigating the presence,
distribution and relative level of infectivity of Atypical BSE (H-BSE and
L-BSE). EFSA was also expected to reflect on whether the tissues available from
the EURL study are sufficient for the purpose and/or suggest that investigations
on other tissues might be possibly needed.
Data relating to the prevalence and geographical distribution of Atypical
BSE in the European Union (EU) are incomplete and subject to variation owing to
the ongoing retrospective typing of BSE cases. So far, 80 cases of Atypical BSE
have been reported by EU Member States from 2001 to 2014. All Atypical BSE cases
have been detected by active surveillance, typically in animals over eight years
of age, with a similar number of cases detected each year.
This report provides an overview of the biological material collected from
field cases of Atypical BSE and transmission studies, both in the framework of
the EURL study and additional published scientific studies. It was concluded
that information on the pathogenesis and tissue distribution of Atypical BSE in
cattle through the study of field cases and experimental transmission studies is
lacking. The latter are limited to transmission of Atypical BSE through
intracerebral (i.c.) inoculation of cattle. 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.
Approaches to quantify Atypical BSE prions in cattle tissues are described
and reviewed, including bioassay and in vitro methods.
A laboratory protocol for further studies is recommended. Its application
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 those studies were 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. The protocol
provides details in terms of the minimum number of animals to be tested,
processing and preparation of tissues, and methods to be used to identify
abnormal PrP and quantify infectivity, also depending on the expected level of
infectivity and amount of tissue available for analysis.
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.
It is acknowledged that 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, and therefore, to complete this
objective, new inoculation experiments with H- and L-BSE agents in cattle would
have to be considered. Recommendations on general principles for such new
experiments are provided.
In accordance with former EFSA recommendations, it is recommended that,
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.
Keywords Atypical BSE, cattle, H-BSE, L-BSE, laboratory protocol,
prion
SCIENTIFIC REPORT OF EFSA
Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE1
European Food Safety Authority2,3
European Food Safety Authority (EFSA), Parma, Italy
ABSTRACT
Information on the pathogenesis and tissue distribution of Atypical Bovine
Spongiform Encephalopathy (BSE) in cattle through the study of field cases and
experimental transmission studies is lacking. The latter are limited to
transmission of Atypical BSE through intracerebral (i.c.) inoculation of cattle.
All data currently available relate to the presence or absence of PrPSc, but do
not quantify relative amounts of PrPSc or levels of infectivity. A laboratory
protocol for further studies is recommended, to allow 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 those studies are categorised in three
priorities, based on their inclusion in the list of specific risk material in
cattle, on the presence of infectivity, or PrPSc presence, demonstrated in
Atypical BSEs or other Transmissible Spongiform Encephalopathies (TSEs) in
ruminants, and on the importance in terms of input into the food chain in the
EU. The protocol provides details in terms of the minimum number of animals to
be tested, processing and preparation of tissues, and methods to be used to
identify abnormal PrP and quantify infectivity, also depending on the expected
level of infectivity and amount of tissue available for analysis. It is
recommended that, 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.
© European Food Safety Authority, 2014
KEY WORDS
Atypical BSE, cattle, H-BSE, L-BSE, laboratory protocol, prion
Saturday, June 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05
Study of Atypical Bse
Friday, December 5, 2014
SPECIAL ALERT The OIE recommends strengthening animal disease surveillance
worldwide
OIE BSE TSE PRION AKA MAD COW DISEASE ?
‘’the silence was deafening’’ ...tss
Wednesday, December 3, 2014
Over 200 Groups Urge Congress to Continue Supporting COOL
For Immediate Release
Tuesday, December 2, 2014
UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion
aka Mad Cow Disease
USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE
WORLD (?) [protected by the BSE MRR policy] $$$
"BSE" - ATYPICAL LESION DISTRIBUTION __ (RBSE 92/21367)
A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in
Aberdeenshire, submitted as a suspect BSE case in the negative study (SE0203),
has been diagnosed as BSE negative on standard, statutory (obex only),
diagnostic criteria at CVL.
Further examination by Dr Jeffrey at Lasswade, as required by the project
design, has revealed vacuolar change in the septal nucleus and putamen which
co-Iocalised with PrP immunoreactivity. No significant lesions were found in any
other part of the brain, neither was PrP found in the medulla.
It is important to note that examination of four brain blocks used earlier
in the epidemic would not have detected the lesion but a 16 block study (as used
in the very early days of BSE) would.
FURTHER INFORMATION
1. The herd of origin has had 15, HB, suspect cases of BSE since July 1989
and a further case is still alive.
2. Of the 15, eight have been confirmed by standard histopathology and
seven diagnosed negative (including the above case).
3. Fixed brain tissue from the negative cases exists at Lasswade (because
they always collect whole brain in Scotland) but has not so far been examined
further. No frozen tissue was collected so neither SAF nor PrP detection (by
immunoblotting) has been attempted.
4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.
FURTHER ACTION IN PROGRESS
1. The brain tissue from the negative cases will be examined in detail by
conventional histopathology and ICC.
2. Kevin Taylor and his veterinary colleagues have been alerted to the
situation.
OTHER RECOMMENDED ACTIONS
TRANSMISSION Attempt transmission from the 'case’ to standard mice strains.
(Note: In regard to strain typing, formalin may have modified strain phenotype -
we need to discuss with NPU). Further transmission studies (eg in cattle) might
be suggested if primary transmission in mice fails. These proposals have funding
implications.
93/2.17/1.1
PrP GENOTYPING-AIthough only fixed brain tissue is available we are
considering genotyping from parents/offspring/fixed brain. As a first step we
are attempting to extract DNA from the fixed brain and to amplify the PrP gene
by PCR.
3. John Wilesmith has interrogated the data base for the herd history.
Other than the high proportion of negative cases nothing significant is
apparent.
4. Familial relationships between suspect (including all positive and
negative) cases in this herd could be examined and tracings of breeding animals
initiated.
5. Consideration might be given to collecting frozen spinal cord from new
cases in this herd or in dispersals from it (for SAF /PrP examination).
CONCLUSIONS
1. At present it is unclear whether or not this is a singleton incident or
whether the other negative cases in this herd show a similar lesion.
2. The discovery might indicate the existence of a different strain of BSE
from that present in the general epidemic or an unusual response by an
individual host.
3. If further atypical lesion distribution cases are revealed in this herd
then implications of misdiagnosis of 'negative' cases in other herds may not be
insignificant.
4. If this is a new strain all the implications need to be considered
including whether or not to proceed with the further investigation of future
cases negative for BSE on obex examination alone and from which whole brains are
available (as in Scotland) or collected in the future. Also perhaps
investigation of the tissue distribution of infectivity in these animals might
be considered.
5. Animal and public health controls in place should be sufficient since
all tissues (other than brain for diagnosis) are incinerated.
We observe that Dr. Tyrrell would wish to be informed of this at an early
opportunity and that the SEAC would wish to discuss it at their meeting in
April.
R BRADLEY M DAWSON 17 February 1993
CVO – for information and comment on further action please
cc Mr K C Taylor Dr B J Shreeve
93/2.17/1.2
This minute is re-issued with a wider distribution. The information
contained herein should be disseminated furhter except on the basis of ‘’need to
know’’.
R BRADLEY 9 March 1993
Mr JM Scudamore Mr RC Lowson Dr D Mattews Mr I Robertson Dr K MacOwan Mr C
Randall Mr J W Wilesmith Mr GAH Wells Dr M Jeffrey Dr. M Simmons
93/2.17/1.3
http://web.archive.org/web/20041226015613/http://www.bseinquiry.gov.uk/files/yb/1993/02/17001001.pdf
USDA 2003 We have to be careful that we don't get so set in the way we do
things that we forget to look for different emerging variations of disease.
We've gotten away from collecting the whole brain in our systems. We're using
the brain stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did not
find lesions or PRP in the area of the obex. They found it in the cerebellum and
the cerebrum. It's a good lesson for us. Ames had to go back and change the
procedure for looking at Scrapie samples. In the USDA, we had routinely looked
at all the sections of the brain, and then we got away from it. They've recently
gone back. Dr. Keller: Tissues are routinely tested, based on which tissue
provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another
important thing to get across to the public is that the negatives do not
guarantee absence of infectivity. The animal could be early in the disease and
the incubation period. Even sample collection is so important. If you're not
collecting the right area of the brain in sheep, or if collecting
lymphoreticular tissue, and you don't get a good biopsy, you could miss the area
with the PRP in it and come up with a negative test. There's a new, unusual form
of Scrapie that's been detected in Norway. We have to be careful that we don't
get so set in the way we do things that we forget to look for different emerging
variations of disease. We've gotten away from collecting the whole brain in our
systems. We're using the brain stem and we're looking in only one area. In
Norway, they were doing a project and looking at cases of Scrapie, and they
found this where they did not find lesions or PRP in the area of the obex. They
found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had
to go back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got away
from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
END...TSS
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING ***
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been
discovered in a wide verity of species across North America. typical C-BSE,
atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine,
typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98
Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD
in cervid is slowly spreading without any stopping it in Canada and the USA and
now has mutated into many different strains. Transmissible Mink Encephalopathy
TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease
have been silently mutating and spreading in different species in North America
for decades.
The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion
Firewall, of which we now know without a doubt, that it was nothing but ink on
paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of
banned mad cow feed has been put out into commerce, never to return, as late as
December of 2013, serious, serious breaches in the FDA mad cow feed ban have
been documented. The 2004 enhanced BSE surveillance program was so flawed, that
one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown,
who is preparing a scientific paper based on the latest two mad cow cases to
estimate the maximum number of infected cows that occurred in the United States,
said he has "absolutely no confidence in USDA tests before one year ago" because
of the agency's reluctance to retest the Texas cow that initially tested
positive. see ; http://www.upi.com/Health_News/2006/03/15/Analysis-What-that-mad-cow-means/UPI-12841142465253/
The BSE surveillance and testing have also been proven to be flawed, and
the GAO and OIG have both raised serious question as to just how flawed it has
been (see GAO and OIG reports). North America has more documented TSE prion
disease, in different documented species (excluding the Zoo BSE animals in the
EU), then any other place on the Globe. This does not include the very
likelihood that TSE prion disease in the domestic feline and canine have been
exposed to high doses of the TSE prion disease vid pet food. To date, it’s still
legal to include deer from cwd zone into pet food or deer food. Specified Risk
Material i.e. SRM bans still being breach, as recently as just last month.
nvCJD or what they now call vCJD, another case documented in Texas last
month, with very little information being released to the public on about this
case? with still the same line of thought from federal officials, ‘it can’t
happen here’, so another vCJD blamed on travel of a foreign animal disease from
another country, while ignoring all the BSE TSE Prion risk factors we have here
in the USA and Canada, and the time that this victim and others, do spend in the
USA, and exposed to these risk factors, apparently do not count in any way with
regard to risk factor. a flawed process of risk assessment.
sporadic CJD, along with new TSE prion disease in humans, of which the
young are dying, of which long duration of illness from onset of symptoms to
death have been documented, only to have a new name added to the pot of prion
disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a
familial type disease could be sporadic with no genetic link to any family
member? when the USA is the only documented Country in the world to have
documented two different cases of atypical H-type BSE, with one case being
called atypical H-G BSE with the G meaning Genetic, with new science now showing
that indeed atypical H-type BSE is very possible transmitted to cattle via oral
transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada,
USA, and the UK, with the same old excuse, better surveillance. You can only use
that excuse for so many years, for so many decades, until one must conclude that
CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a
blip or a reason of better surveillance, it is a mathematical rise in numbers.
More and more we are seeing more humans exposed in various circumstance in the
Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same
time in North America, more and more humans are becoming exposed to the TSE
prion disease via consumption of the TSE prion via deer and elk, cattle, sheep
and goats, and for those that are exposed via or consumption, go on to further
expose many others via the iatrogenic modes of transmission of the TSE prion
disease i.e. friendly fire. I pondered this mode of transmission via the victims
of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone
sub-clinical with sFFI or sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten
nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first
ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is
transmissible. yet all these TSE prion disease and victims in the USA and Canada
are being pawned off as a spontaneous event, yet science has shown, the
spontaneous theory has never been proven in any natural case of TSE prion
disease, and scientist have warned, that they have now linked some sporadic CJD
cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about
this in the public domain. We must make all human and animal TSE prion disease
reportable in every age group, in ever state and internationally, we must have a
serious re-evaluation and testing of the USA cattle herds, and we must ban
interstate movement of all cervids. Any voluntary effort to do any of this will
fail. Folks, we have let the industry run science far too long with regards to
the TSE prion disease. While the industry and their lobbyist continues to funnel
junk science to our decision policy makers, Rome burns. ...end
REFERENCES
[all scientific peer review studies and other scientific information I have
put into blogs, to shorten reference data. I DO NOT advertise or make money from
this, this information is for education use...lost my mom to the hvCJD, and just
made a promise, never forget, and never let them forget. ...TSS]
Saturday, June 14, 2014
Rep. Rosa DeLauro (D-CT) Calls for Briefing on Beef Recalled for Mad Cow
Potential Rep. Rosa DeLauro (D-CT)
Thursday, June 12, 2014
Missouri Firm Recalls Ribeye and Carcass Products That May Contain
Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal
root ganglia may not have been completely removed
Monday, June 02, 2014
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
Monday, June 9, 2014
TEXAS MAD COW COVER UP (human BSE) AGAIN IN TEXAS, Mr. President Sir, we
need your help please
snip...see much more here ;
Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Wednesday, July 23, 2014
After the storm? UK blood safety and the risk of variant Creutzfeldt-Jakob
Disease
Thursday, July 24, 2014
Government must do more to reduce risk of vCJD infection
Monday, June 02, 2014
Confirmed Variant CJD Case in Texas
Saturday, February 01, 2014
*** vCJD With Extremely Low Lymphoreticular Deposition of Prion Protein MAY
NOT HAVE BEEN DETECTABLE
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease ***
Sunday, March 09, 2014
*** A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of
Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease
FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
Thursday, February 20, 2014
*** Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS
Dr. Linda Detwiler 2014
Sunday, July 06, 2014
Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory
Case-Control Study
Conclusions—The a priori hypotheses were supported.
*Consumption of various meat products may be one method of transmission of
the infectious agent for sCJD.
***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.
Monday, June 23, 2014
PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES
Friday, March 09, 2012
Experimental H-type and L-type bovine spongiform encephalopathy in cattle:
observation of two clinical syndromes and diagnostic challenges
Research article
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits
Thursday, June 21, 2012
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy
Associated with E211K Prion Protein Polymorphism
Friday, May 9, 2014
Distinct Transmissibility Features of TSE Sources Derived from Ruminant
Prion Diseases by the Oral Route in a Transgenic Mouse Model (TgOvPrP4)
Overexpressing the Ovine Prion Protein
*** What irks many scientists is the USDA’s April 25 statement that the
rare disease is “not generally associated with an animal consuming infected
feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
The present study demonstrated successful intraspecies transmission of
H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc
in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be
minimally defined by oral transmission of different TSE agents (C-type, L-type,
and H-type BSE agents) [59]. Oral transmission studies with H-type BSE infected
cattle have been initiated and are underway to provide information regarding the
extent of similarity in the immunohistochemical and molecular features before
and after transmission.
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
*** 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. ***
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. ***
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
P.4.23
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw
Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1
1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale,
Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research
Institute, Poland; 5Kansas State University (Previously at USDA National Animal
Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the
classical BSE strain (BSE-C) has led to over 200 cases of clinical human
infection (variant CJD). Atypical BSE cases have been discovered in three
continents since 2004; they include the L-type (also named BASE), the H-type,
and the first reported case of naturally occurring BSE with mutated bovine PRNP
(termed BSE-M). The public health risks posed by atypical BSE were largely
undefined.
Objectives: To investigate these atypical BSE types in terms of their
transmissibility and phenotypes in humanized mice. Methods: Transgenic mice
expressing human PrP were inoculated with several classical (C-type) and
atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation
time, characteristics and distribution of PrPSc, symptoms, and histopathology
were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected
with minimal spongiosis and an average incubation time of 20-22 months, whereas
only one of the C-type BSE-inoculated mice developed prion disease after more
than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse
brains was biochemically different from bovine BASE or sCJD. PrPSc was also
detected in the spleen of 22% of BASE-infected humanized mice, but not in those
infected with sCJD. Secondary transmission of BASE in the humanized mice led to
a small reduction in incubation time.*** The atypical BSE-H strain is also
transmissible with distinct phenotypes in the humanized mice, but no BSE-M
transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than
classical BSE, has a lymphotropic phenotype, and displays a modest transmission
barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg
mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN
HUMANIZED MOUSE MODELS
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina
Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi
Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case
Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto
Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany;
4National Veterinary Research Institute, Poland; 5Kansas State University,
Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous
address: USDA National Animal Disease Center, Ames, IA 50010, USA
Classical BSE is a world-wide prion disease in cattle, and the classical
BSE strain (BSE-C) has led to over 200 cases of clinical human infection
(variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have
been discovered in three continents since 2004. The first case of naturally
occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006
in the USA. The transmissibility and phenotypes of these atypical BSE
strains/isolates in humans were unknown. We have inoculated humanized transgenic
mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M
isolate. We have found that the atypical BSE-L strain is much more virulent than
the classical BSE-C. *** The atypical BSE-H strain is also transmissible in the
humanized transgenic mice with distinct phenotype, but no transmission has been
observed for the BSE-M isolate so far.
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE,
DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
UPDATE
I ask Professor Kong ; Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform
Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE,
or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or
another, but we have found that H-BSE can infect humans. I hope we could publish
these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of
Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
BSE-H is also transmissible in our humanized Tg mice. The possibility of
more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
please see below from PRION2013 ;
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
AD.56: The emergence of novel BSE prions by serial passages of H-type BSE
in bovinized mice
Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki
Okada, Shirou Mohri and Takashi Yokoyama National Institute of Animal Health;
Tsukuba, Japan
H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE,
and has been detected in several European countries, and North America.
Transmission studies of H-type BSE led to the emergence of the classical BSE
(C-BSE) phenotypes during passages in inbred wild type and bovinized
PrP-overexpressing transgenic mice. In this study, we conducted serial passages
of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice
(TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods
of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage
were constant (~= 220 d), no clear differences were observed in their biological
and biochemical properties. However, at the forth passage, 2 different BSE
phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the
other is longer survival times. TgBoPrP mice with longer incubation period
showed the H-type phenotype of PrPsc profile and pathology. However, those of
shorter incubation period were different phenotypes from previously existed BSE
prions (C-BSE, L-type BSE, and H-type BSE).
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
www.landesbioscience.com
please see ;
Thursday, August 15, 2013
The emergence of novel BSE prions by serial passages of H-type BSE in
bovinized mice
LET'S take a closer look at this new prionpathy or prionopathy, and then
let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the
genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_
mad cow in the world to date like this, ......wait, it get's better. this new
prionpathy is killing young and old humans, with LONG DURATION from onset of
symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and
the plaques are very similar in some cases too, bbbut, it's not related to the
g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that
they claim is a genetic TSE, has no relation to any gene mutation in that
family. daaa, ya think it could be related to that mad cow with the same genetic
make-up ??? there were literally tons and tons of banned mad cow protein in
Alabama in commerce, and none of it transmitted to cows, and the cows to humans
there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we
identified a novel mutation in the bovine prion protein gene (Prnp), called
E211K, of a confirmed BSE positive cow from Alabama, United States of America.
This mutation is identical to the E200K pathogenic mutation found in humans with
a genetic form of CJD. This finding represents the first report of a confirmed
case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We
hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in
"the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation
(J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic
in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the
UK epidemic had most likely originated from such a mutation and argued against
the scrapierelated assumption. Such rare potential pathogenic PRNP mutations
could occur in countries at present considered to be free of BSE, such as
Australia and New Zealand. So it is important to maintain strict surveillance
for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many
countries still feed ruminant proteins to pigs). Removal of specified risk
material, such as brain and spinal cord, from cattle at slaughter prevents
infected material from entering the human food chain. Routine genetic screening
of cattle for PRNP mutations, which is now available, could provide additional
data on the risk to the public. Because the point mutation identified in the
Alabama animals is identical to that responsible for the commonest type of
familial (genetic) CJD in humans, it is possible that the resulting infective
prion protein might cross the bovine-human species barrier more easily. Patients
with vCJD continue to be identified. The fact that this is happening less often
should not lead to relaxation of the controls necessary to prevent future
outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary
Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen
A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier
Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE) Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
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.
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and
it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far ***but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
see follow-up here about North America BSE Mad Cow TSE prion risk factors,
and the ever emerging strains of Transmissible Spongiform Encephalopathy in many
species here in the USA, including humans ;
*** 2010-2011 ***
When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.
Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
Risk.12:
Transmission of Atypical Italian sCJD Case to Humanized Mice Reveals a
Novel Infectious Strain
Roberta Galeno,1,† Marco Sbriccoli,1 Loredana Ingrosso,1 Silvia Graziano,1
Angelina Valanzano,1 Anna Poleggi,1 Angela De Pascalis,1 Anna Ladogana,1 Franco
Cardone,1 Maria Puopolo,1 Gianluigi Zanusso2 and Maurizio Pocchiari1
1Istituto Superiore di Sanità; Rome, Italy; 2University of Verona; Verona,
Italy†Presenting author; Email: roberta.galeno@iss.it
Sporadic Creutzfeldt-Jakob disease (sCJD) is a neurodegenerative prion
disorder with uncertain etiology characterized by a typical combination of
clinical symptoms, neuropathological lesions, and by the deposition of the
pathological protein PrPTSE in the brain.
The vast majority of patients affected by sCJD can be categorized according
to the genotype at the polymorphic position www.landesbioscience.com Prion
127
129 of PrP (methionine or valine) and to the molecular mass of PrPTSE (type
1 or 2, corresponding to 21 or 19 kDa), yielding six possible combinations (MM1,
MM2, VV1, VV2, MV1, and MV2) that associate with five clinico-pathological
variants. Transmission studies of these sCJD subtypes into transgenic mice
expressing the human prion protein allowed to identify four different infectious
strains, which can partly explain the heterogeneity observed in sCJD
patients.1
We recently described a novel molecular and pathological phenotype of sCJD
(MV at position 129 of PrP), associated with an unprecedented electrophoretic
pattern of PrPTSE characterized by the absence of the highly glycosylated
isoform. In this work, we sought to characterize the prion strain associated
with this atypical case by intracerebral inoculation into gene-targeted
transgenic mice (HuTg) carrying the human PRNP gene with the three 129 genotype
combinations. For comparison, three Italian sCJD cases heterozygous at position
129 of the prion protein, belonging to different subtypes (MV1, MV1/2, MV2),
were transmitted to the same panel of transgenic mice. Survival times, attack
rates, lesion profiles, and molecular analysis of the PrPTSE type recovered from
mouse brains injected with the atypical case were compared with data from
control animals. Mice inoculated with the atypical case displayed a restricted
host tropism, with only a small number of VV animals that resulted
PrPTSE-positive after an exceedingly long survival time. Interestingly, PrPTSE
accumulated in brains from these mice lacks the diglycosylated band similar to
that in sCJD inoculum, yet dissimilar to any other PrPTSE observed in HuTg mice
by us and by other authors.1,2 Overall, *** these results strongly indicate that
our atypical case associates with a new infectious strain of sCJD. Further
investigations are needed to understand the possible connection with other human
and animal prion diseases.
References
1. Bishop MT, Will RG, Manson JC. Defining sporadic Creutzfeldt-Jakob
disease strains and their transmission properties. Proc Natl Acad Sci USA 2010;
107:12005-10.
2. Bishop MT, Hart P, Aitchison L, Baybutt HN, Plinston C, Thomson V, et
al. Predicting susceptibility and incubation time of human-to-human transmission
of vCJD. Lancet Neurol 2006; 5:393-8.
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque
"BSE-L in North America may have existed for decades"
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
2011 Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
*** The successful transmission of kuru, Creutzfeldt-Jakob disease, and
scrapie by natural feeding to squirrel monkeys that we have reported provides
further grounds for concern that scrapie-infected meat may occasionally give
rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and
VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
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.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CHRONIC WASTING DISEASE CWD
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
***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.169: PrPSc distribution in brain areas of a natural German H-type BSE
case
Anne Balkema-Buschmann, Grit Priemer, Markus Keller, and Martin H Groschup
Friedrich Loeffler Institut, Institute for Novel and Emerging Infectious
Diseases; Greifswald, Insel Riems, Germany
Keywords: BSE H-type, brain, muscle
Ten years after the initial description of atypical BSE cases of the H-type
and L-type, the distribution of PrPSc in different brain areas and peripheral
tissues of natural cases of these BSE forms is still not fully understood.
Intracerebral challenge experiments have been performed with both atypical BSE
forms in cattle, and the distribution of the abnormal prion protein and
infectivity has been analysed in a variety of tissues, confirming the general
restriction to the central nervous system as it was already generally
acknowledged for classical BSE, but showing a slightly earlier and stronger
involvement of the peripheral nervous system and the skeletal muscle.
www.landesbioscience.com Prion 105
However, data from cattle orally challenged with atypical BSE, which might
mimic the natural situation, are not yet available. Unfortunately, for most
natural cases of atypical BSE, only the obex region is available for further
analysis. The PrPSc distribution in the brains of natural L-type BSE cases in
Italy has been described in some detail, but comparably few such data are yet
available for natural H-type cases. Here we describe the analysis of different
brain areas and muscle samples of a natural H-type BSE case diagnosed in Germany
in 2014, and compare these data with those obtained from the respective samples
collected from cattle challenged intracerebrally with H-type BSE.
P.159: Transgenic mice overexpressing rabbit prion protein are susceptible
to BSE, BASE and scrapie prion strains but resistant to CWD and atypical
scrapie
Natalia Fernández-Borges,1 Enric Vidal,2 Belén Pintado,4 Hasier Eraña,1
Montserrat Ordóñez,3 Mercedes Márquez,5 Francesca Chianini,6 Dolors Fondevila,5
Manuel A Sánchez-Martín,7 Olivier Andréoletti,8 Mark P Dagleish,6 Martí
Pumarola,5 and Joaquín Castilla1,3 1CIC bioGUNE; Parque tecnológico de Bizkaia;
Derio; Bizkaia, Spain; 2Centre de Recerca en Sanitat Animal (CReSA); UAB-IR TA,
Campus de la Universitat Autònoma de Barcelona; Bellaterra; Barcelona,
Catalonia, Spain; 3IKERBASQUE; Basque Foundation for Science; Bilbao, Bizkaia,
Spain; 4Centro Nacional de Biotecnología (CNB), Campus de Cantoblanco;
Cantoblanco; Madrid, Spain; 5Department of Animal Medicine and Surgery;
Veterinary faculty; Universitat Autònoma de Barcelona (UAB); Bellaterra
(Cerdanyola del Vallès); Barcelona, Catalonia, Spain; 6Moredun Research
Institute; Bush Loan, Penicuik, Scotland, UK; 7Unidad de Generación de OMGs.
S.E.A. Department of Medicine; University of Salamanca; Salamanca, Spain; 8Ecole
Nationale du Veterinaire; Service de Pathologie du Bétail; Toulouse,
France
Interspecies transmission of prions is a well established phenomenon, both
experimentally and in field conditions. Upon passage through new hosts prion
strains have proven their capacity to change their properties. It is, in fact, a
source of strain diversity which needs to be considered when assessing the
potential risks associated with consumption of prion contaminated protein
sources.
Rabbits were considered for decades a prion resistant species until proven
recently otherwise. To determine the extent of rabbit susceptibility to prions
and to assess their effects on the passage of different prion strains through
this species, a transgenic mouse model overexpressing rabbit PrPC was developed
(TgRab). Intracerebral challenges with prion strains originating from a variety
of species including field isolates (SSBP1 scrapie, Nor98-like scrapie, BSE,
BASE and CWD), experimental murine strains (ME7 and RML), experimentally
obtained strains (sheepBSE) and strains obtained by in vitro crossing of the
species barrier using saPMCA (BSE-RabPrPres, SSBP1-RabPrPres and CWD-RabPrPres)
have been performed.
Interestingly, on first passage, TgRab were susceptible to the majority of
prions tested with the exception of SSBP1 scrapie, CWD and Nor98 scrapie.
Furthermore TgRab were capable of propagating strain-specific features such as
differences in incubation periods, brain lesion and PrPd deposition profiles and
PK resistant western blotting band patterns. Our results confirm previous
studies shattering the myth that rabbits are resistant to prion infection and
this should be taken into account when choosing protein sources to feed rabbits.
P.168: Evolution of the biological properties of L-BSE after passage in
sheep with susceptible and resistant PrP genotypes
Michele A Di Bari, Umberto Agrimi, Claudia D’Agostino, Geraldina Riccardi,
Stefano Marcon, Elena Esposito, Paolo Frassanito, Flavio Torriani, Shimon
Simson, and Romolo Nonno Istituto Superiore di Sanità (ISS) Department of
Veterinary Public Health and Food Safety; Rome, Italy
Background. Cattle L-BSE was efficiently transmitted to sheep with
susceptible (QQ171) and resistant (QR171) PrP genotypes. 1 Notably, the PrPSc
signature of L-BSE was preserved in QQ171 sheep but not in QR171 sheep.2
Notwithstanding, bioassay in transgenic mice expressing bovine or ovine (ARQ)
PrPC showed that L-BSE strain was preserved in both, QQ171 and QR171
sheep-passaged L-BSE.3
Here we studied the biological properties of sheep-passaged L-BSE by
bioassay in bank voles and transgenic mice expressing the ovine VRQ PrP (tg338),
both characterized by a comparatively low susceptibility to cattle L-BSE.
Material and Methods. Voles and tg338 mice were intracerebrally inoculated
with cattle L-BSE and sheep-passaged (QQ171 and QR171) L-BSE isolates. Survival
time, lesion profiles, Pet-blot and WB analysis were used for strain typing.
Results. Cattle L-BSE transmitted quite inefficiently to tg338 mice, with
survival time >400 days post-infection (d.p.i.), while sheep-passaged inocula
were much more efficient and all gave terminal disease by ~140 d.p.i. However,
after sub-passage all inocula converged to a survival time of ~145 d.p.i.. and
showed overlapping pathological phenotypes.
In voles, cattle L-BSE transmitted with very long survival times (~800
d.p.i.) and was accompanied by an upward shift of the PrPSc type. Again, all
sheep-passaged L-BSE isolates transmitted much more efficiently, with similar
survival times of ~360 d.p.i.. Upon second passage, three different strains were
isolated in vole, characterized by distinct pathological phenotypes. This
divergence is epitomized by the different survival times of vole-adapted L-BSE
strains, which were ~400 d.p.i. for cattle L-BSE, ~130 d.p.i. for QQ171-passaged
L-BSE and ~225 d.p.i. for QR171-passaged L-BSE.
Conclusions. These findings, along with previously published data,3 show
that the original L-BSE strain was recovered after passage in sheep when
bioassay was performed in animal models expressing bovine or ovine PrPC. In
contrast, strain changes were observed in both, QQ171- and QR171-passaged L-BSE
by bioassay in vole, a species with divergent PrP sequence compared to
ruminants. Importantly, QQ171- and QR171-passaged L-BSE were characterised by
different PrPSc types and, accordingly, showed different biological properties
when transmitted to voles, but not when transmitted to other animal models.
Overall, our work support the hypothesis that prion isolates are likely
composed of multiple prion components, emphasizes the role of host PrP
polymorphisms on strain selection and mutation, and highlights the risk for new
potentially zoonotic strains that could emerge from prion evolution in animal
reservoirs.
P.172: BSE exposure risk from bovine intestine and mesentery
Fulvio Barizzone,1 Herbert Budka,2 Christine Fast,3 John N Griffin,4
Giuseppe Ru,5 Pietro Stella1 and Olivier Andréoletti6 1European Food Safety
Authority; Parma, Italy; 2Institute of Neuropathology; University Hospital
Zurich; Zurich, Switzerland; 3Friedrich-Loeffler-Institut; Institute of Novel
and Emerging Infectious Diseases; Isle of Riems, Germany; 4Department of
Agriculture, Food and the Marine; Backweston, Celbridge, Co. Kildare, Ireland;
5Istituto Zooprofilattico Sperimentale del Piemonte; Liguria e Valle d’Aosta;
Biostatistics Epidemiology and Analysis of Risk (BEAR) unit; Turin, Italy; 6UMR
Interactions Hôtes Agents Pathogènes; Ecole Nationale Vétérinaire INR A; ENVT;
Toulouse, France
Keywords: Bovine Spongiform Encephalopathy (BSE), cattle, intestine,
mesentery, specified risk material (SRM), quantitative risk assessment
(QRA)
Bovine intestines and mesenteries in the European Union (EU) are considered
among the tissues potentially containing the highest level of BSE infectivity
and have to be removed from the food and feed chain. A quantitative assessment
of the BSE infectious load potentially entering the food and feed chain yearly
in the European Union (EU) was developed. The evolution of the BSE infectious
titre and of the weight of the structures accumulating infectivity was
considered. The number of BSE infected cattle entering undetected in the food
and feed chain yearly was estimated. A model (TSEi) was developed to estimates
the evolution of the BSE infectious load in animals and the total yearly
infectious load that could enter the food and feed chain. In a BSE infected
bovine, the distribution of infectivity in intestines and mesentery varies with
the age. Up to 36 months of age the infectivity is mainly associated (on average
more than 90%) with the last 4 metres of small intestine and the caecum, over 36
and under 60 months of age, there is an inter-individual variability, from 60
months of age the infectivity is mainly associated (on average more than 90%)
with the mesenteric nerves and the celiac and mesenteric ganglion complex. The
total amount of infectivity peaks, about 15 BoID50, in animals younger than 18
months, it declines to 8-9 BoID50 (24–48 months of age) and it drops to 0.7
BoID50 in animals older than 60 months. The ileocaecal plate is the most
infectious part of the intestine and it can be used to estimate the potential
maximum level of exposure for an individual consumer.
In the EU, between 2007 and 2012, the yearly amount of BSE infectivity
associated with intestine and mesentery from animals entering the food and feed
chain was reduced by a factor of 10 (from about 23,000 to about 2,000 BoID50).
However, the maximum level of exposure to the BSE agent from intestine
remained stable (on average about 1.5-1.6 BoID50 per meter).
In case of re-emergence of BSE in the EU there would be an increase of the
potential maximum level of exposure to BSE from intestine. According to the TSEi
model the removal of the last four metres of the small intestine and of the
caecum from the food and feed chain would result in a major reduction of the BSE
exposure risk associated with intestine and mesentery in cattle.
P.131: Transmission of sheep-bovine spongiform encephalopathy in pigs
Carlos Hedman,1 Belén Marín,1 Fabian Corbière,3 Hicham Filali,1 Francisco
Vázquez, José Luis Pitarch,1 William Jirón,1 Rodrigo S Hernandez,1 Bernardino
Moreno,1 Martí Pumarola,2 Olivier Andréoletti,3 Juan José Badiola,1 and Rosa
Bolea1 1University of Zaragoza; Zaragoza, Spain; 2University of Barcelona;
Barcelona, Spain; 3Institut National de la Recherche (INR A); Toulouse,
France
Introduction. The transmissible spongiform encephalopathies (TSE) don´t
occur in swine in natural conditions. However, the bovine spongiform
encephalopathy (BSE) agent, inoculated by 3 simultaneous routes in pigs, is able
to reproduce a neurological disease in these animals. On the other hand, the BSE
agent after passage in sheep under experimental conditions (sheep- BSE) exhibits
altered pathobiologic properties. This new agent is able to cross the cattle-pig
transmission barrier more efficiently than BSE. The potential propagation of TSE
in animals from the human food chain, including pigs, needs to be assessed
regarding the risk for human infection by animals other than TSE-infected
ruminants. The aim of this work was to determine the susceptibility of pigs to
the Sheep-BSE agent and describe the pathological findings and PrPSc deposition
in different tissues.
Material and Methods. Seven minipigs were challenged intracerebrally with
sheep-BSE agent. Clinical observation and postmortem histopathology,
immunohistochemistry (antibody 2G11) and Western blotting were performed on
central nervous system (CNS), peripheral nervous system (PNS) and other
tissues.
Results. One pig was culled in an early incubation stage, and remaining six
were culled at the presence of clinical sings. Pigs developed a clinical disease
with locomotor disorders in an average time of 23 months post inoculation,
showing clinical findings in most of them earlier than those described in the
BSE in pigs experimental infection. TSE wasn´t confirmed in the preclinical pig.
In clinical pigs, the entire cerebral cortex showed severe neuropil vacuolation,
extensive and severe vacuolar changes affecting the thalamus, hippocampus and
cerebellum. PrPSc was found in CNS of all clinical pigs (6/6). Intracellular
(intraneuronal and intraglial) and neuropil-associated PrPSc deposition was
consistently observed in the brainstem, thalamus, and deeper layers of the
cerebral cortex. Also, PrPSc was observed in PNS, mainly in the myenteric plexus
and also in nerves belonging to the skeleton muscle. Moreover, the glycosylation
profile showed a 3 band pattern with a predominant monoglycosylated band in
positive pig samples.
This features concern on the potential risk of utilization of meat and
bound meal of small ruminants in feeding pigs.
P.177: Elements modulating the prion species barrier and its passage
consequences
Juan-Carlos Espinosa,1 Patricia Aguilar-Calvo,1 Ana Villa-Diaz,1 Olivier
Andréoletti,2 and Juan María Torres1 1Centro de Investigación en Sanidad Animal
(CISA-INI A); Valdeolmos, Madrid, Spain; 2UMR INR A-ENVT 1225; Interactions Hôte
Agent Pathogène; École Nationale Vétérinaire de Toulouse; Toulouse, France
The phenotypic features of Transmissible Spongiform Encephalopathy (TSE)
strains may be modified during passage across a species barrier. In this study
we investigated the biochemical and biological characteristics of Bovine
Spongiform Encephalopathy (BSE) infectious agent after transmission in both
natural host species (cattle, sheep, pigs, and mice) and in transgenic mice
overexpressing the corresponding cellular prion protein (PrPC) in comparison
with other non-BSE related prions from the same species. After these passages,
most characteristics of the BSE agent remained unchanged. BSE-derived agents
only showed slight modifications in the biochemical properties of the
accumulated PrPSc, which were demonstrated to be reversible upon re-inoculation
into transgenic mice expressing bovine-PrPC. Transmission experiments in
transgenic mice expressing bovine, porcine or human-PrP revealed that all
BSE-derived agents were transmitted with no or a weak transmission barrier. In
contrast, a high species barrier was observed for the non-BSE related prions
that harboured an identical PrP amino acid sequence such as sheep-scrapie, mouse
RML or human sCJD isolates, supporting the theory that the prion transmission
barrier is modulated by strain properties (presumably conformation-dependent)
rather than by PrP amino acid sequence differences between host and donor.
As identical results were observed with prions propagated either in natural
hosts or in transgenic mouse models, we postulate that the species barrier and
its passage consequences are uniquely governed by the host PrPC sequence and not
influenced by the PrPC expression level or genetic factors other than the PrPC
amino acid sequence. All these findings unequivocally demonstrate that the
species barrier and its passage consequences are uniquely driven by the PrPC
sequence, and not by other host genetic factors, demonstrating the validity of
transgenic PrP animals as models for studies of the species barrier.
The results presented herein reinforce the idea that the BSE agent is
highly promiscuous, infecting other species, maintaining its properties in the
new species, and even increasing its capabilities to jump to other species
including humans. These data are essential for the development of an accurate
risk assessment for BSE.
SNIP...SEE FULL TEXT ;
Monday, June 23, 2014
*** PRION 2014 TYPICAL AND ATYPICAL BSE AND CJD REPORT UPDATES
Sunday, June 29, 2014
*** Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
The most recent assessments (and reassessments) were published in June 2005
(Table I; 18), and included the categorisation of Canada, the USA, and Mexico as
GBR III. Although only Canada and the USA have reported cases, the historically
open system of trade in North America suggests that it is likely that BSE is
present also in Mexico.
Wednesday, February 08, 2012
Scrapie, Israel via OIE 02/02/2012
From: Terry S. Singeltary Sr.
Sent: Wednesday, February 08, 2012 10:28 AM
To: BSE-L BSE-L
Cc: hmb-central@icba.org.il ; delegation-israel@eeas.europa.eu ;
Cvo_vsah@moag.gov.il ; galonn@moag.gov.il ; CJDVOICE CJDVOICE ; bloodcjd
bloodcjd
Subject: Scrapie, Israel via OIE 02/02/2012
Wednesday, May 25, 2011
O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE)
disease reporting 2011
----- Original Message -----
From: Terry S. Singeltary Sr.
To: BSE-L@LISTS.AEGEE.ORG
Cc: trade@oie.int ; oie@oie.int ; f.diaz@oie.int ; scientific.dept@oie.int
; cjdvoice@yahoogroups.com ; BLOODCJD@YAHOOGROUPS.COM
Sent: Tuesday, May 24, 2011 2:24 PM
Subject: O.I.E. Terrestrial Animal Health Standards Commission and prion
(TSE) disease reporting 2011
Greetings OIE et al,
I think that the OIE et al, should explain to the lay public, as to why the
OIE post TSE prion disease reports and incidence there from different species on
their disease reporting reports via email and or on their news feed web site,
daily and or weekly, for just a chosen few Countries, yet other Countries seem
to be exempt from this reporting to the public. WHY is this ?
For instance, Japan just reported another incidence of scrapie, this time
in goat.
however, the USA (Michigan), is awash in scrapie in goat cases, to a point
of epidemic, however, the OIE does not report this, WHY is this ?
the USA and Canada Nor-98 scrapie cases are mounting. NO reports from the
OIE. WHY is this ?
we the lay public deserve an answer. i have ask this question before. i
have ask it about CWD to the OIE a decade ago.
WHY do some Countries get their TSE prion reports posted, and the USA does
not, the USA is exempt from this Global embarrassment?
i am confused.
IF the OIE is going to be a reputable global disease control reporting
agency, then the OIE needs to be honest and trust worthy and equal reporting for
all Countries, not just a chosen few, while others are exempt. This weakens the
animal disease reporting system, and really in all reality, seems to enhance
fraud, and undermines reporting of actual disease, thus, defeats the very
purpose of the O.I.E., thus undermines the very reason the OIE was suppose to be
set up for.
If countries can choose and pick whether or not their different animal
disease are reported, and or NOT reported, then what's the point of the O.I.E.
$$$
MY personal opinion, if a country is going to belong to the OIE, and or
boast about OIE regulations they go by, then they should be made to report
animal disease just as any other country does to the OIE, or they should not be
a part of this OIE, and should not be allowed to be boasting that they go by OIE
guidelines. ...
with sincere regards, terry
snip...see full text ;
Saturday, December 18, 2010
OIE Global Conference on Wildlife Animal Health and Biodiversity -
Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011
I see again that the OIE has done little to help eradicate all animal TSE
from the globe, and in fact in my opinion, have help enhance the spread of BSE
and other animal TSE globally by their industry friendly regulations. I tried to
warn the OIE in 2002 about CWD and the potential, but very real threat of CWD to
humans. I was told that they were seriously considering this. what happened ?
NOW, the OIE and the USDA collaborate to make legal the trading of all strains
of atypical BSE legal, and in fact have done so with the atypical scrapie, when
science has made perfectly clear the risk factors to humans and other species. I
have said it once (see below), and i will say again ;
"THE OIE has now shown they are nothing more than a National Trading
Brokerage for all strains of animal TSE. AS i said before, OIE should hang up
there jock strap now, since it appears they will buckle every time a country
makes some political hay about trade protocol, commodities and futures. IF they
are not going to be science based, they should do everyone a favor and dissolve
there organization."
NOW, some history on the failed OIE BSE/TSE policy, and why the OIE allowed
BSE and other TSE to spread around the globe $$$
snip...see full text ;
Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy;
Animal Identification and Importation of Commodities Docket Type Rulemaking
Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy;
Minimal-Risk Regions, Identification of Ruminants and Processing and Importation
of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title
Comment from Terry S Singletary
Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy;
Minimal-Risk Regions; Importation of Live Bovines and Products Derived from
Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001
Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions;
Importation of Live Bovines and Products Derived From Bovines Public Submission
APHIS-2006-0041-0028 Public Submission Title Comment from Terry S
Singletary
Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY
THE USA is in a most unique situation, one of unknown circumstances with
human and animal TSE. THE USA has the most documented TSE in different species
to date, with substrains growing in those species (BSE/BASE in cattle and CWD in
deer and elk, there is evidence here with different strains), and we know that
sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie
documented and also BSE is very likely to have passed to sheep. all of which
have been rendered and fed back to animals for human and animal consumption, a
frightening scenario. WE do not know the outcome, and to play with human life
around the globe with the very likely TSE tainted products from the USA, in my
opinion is like playing Russian roulette, of long duration, with potential long
and enduring consequences, of which once done, cannot be undone. These are the
facts as I have come to know through daily and extensive research of TSE over 9
years, since 12/14/97. I do not pretend to have all the answers, but i do know
to continue to believe in the ukbsenvcjd only theory of transmission to humans
of only this one strain from only this one TSE from only this one part of the
globe, will only lead to further failures, and needless exposure to humans from
all strains of TSE, and possibly many more needless deaths from TSE via a
multitude of proven routes and sources via many studies with primates and
rodents and other species.
MY personal belief, since you ask, is that not only the Canadian border,
but the USA border, and the Mexican border should be sealed up tighter than a
drum for exporting there TSE tainted products, until a validated, 100% sensitive
test is available, and all animals for human and animal consumption are tested.
all we are doing is the exact same thing the UK did with there mad cow poisoning
when they exported it all over the globe, all the while knowing what they were
doing. this BSE MRR policy is nothing more than a legal tool to do just exactly
what the UK did...
Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy;
Minimal-Risk Regions; Importation of Live Bovines and Products Derived from
Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001
Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions;
Importation of Live Bovines and Products Derived From Bovines Public Submission
APHIS-2006-0041-0028.1 Public Submission Title Attachment to Singletary
comment
January 28, 2007
Greetings APHIS,
I would kindly like to submit the following to ;
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES
[Docket No. APHIS-2006-0041] RIN 0579-AC01
*** REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS
COMMISSION Paris, 19–28 February 2013
In response to a Member Country’s detailed justification for listing of
chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2.,
the Code Commission recommended this disease be reconsidered for listing.
SUMMARY REPORT CALIFORNIA ATYPICAL L-TYPE BOVINE SPONGIFORM ENCEPHALOPATHY
CASE INVESTIGATION JULY 2012 CALIFORNIA
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing ***
IN SHORT, AND 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, February 12, 2014
USDA/APHIS NOTICE: Final Rule Regarding Imports and BSE Effective March 4,
2014
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE
TSS
posted by Terry S. Singeltary Sr. at
2:24 PM
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