Monday, January 28, 2013
Brazil BSE ban to stay
XAVIER PORTER27 Jan, 2013 04:00 AM
BRAZIL's issues with bovine spongiform encephalopathy (BSE) are not going
away in a hurry.
Since the announcement of its first case of BSE, describing it as
"atypical" on December 7, 10 countries have imposed full or partial bans.
Many export and import countries were concerned about the two-year delay
between when the BSE cow was first tested and the finding which was only
released in early December, 2012.
The concerns raised by these countries has now resulted in Brazil's
government and the World Organisation for Animal Health (OIE) to further
investigate Brazil's transparency in their BSE surveillance system and testing
processes.
The following are the countries who have introduced partial and full bans
since the announcement South Korea, China, Japan, South Africa, Saudi Arabia,
Peru (full ban for 90 days), Chile, Jordan (only beef from Parana State), Taiwan
(processed beef-only) and Lebanon (Parana State).
The combined export volume of these countries equates to 150,000 tonnes of
beef per year or 12.5 per cent of Brazil's total exports.
The export opportunities for Australia may be limited due to the other
cheaper beef supply countries, with FMD (foot and mouth disease) beef, that
export to the same countries as Brazil.
Russia being the potential exception for Australia due to the heavy tariffs
imposed on countries like India at 31pc duty, its annual import needs of
220,000t of beef could prove to be a boon for Australian exporters.
Brazil makes WTO threat
On December 21, Brazil threatened to take action through the World Trade
Organisation (WTO) unless the countries that have imposed bans on Brazilian beef
reverse their decisions by March.
These actions had the opposite impact, with five additional countries
imposing bans since the WTO threat was announced.
There is no doubt the initial response by Brazil was to try to as quickly
as possible play down the impact of the BSE case and to 'pull into line' the
importers that had banned Brazilian beef by threatening to take them to the WTO.
But instead raised further concerns by more countries about Brazil's BSE
surveillance procedures, with more country's asking the same question why was
there a two-year delay on results being made known?
The US Ranchers-Cattlemen Action Legal Fund (R-CALF) raised directly with
the OIE their additional procedure concerns about the long delay between the
confirmed two positive tests six months to be exact.
After the brain sample tested positive in mid-2012, it was sent to the OIE
reference laboratory in the United Kingdom, where it again tested positive for
BSE on December 6, 2012.
Officials allegedly claim the long delay between the two primary tests was
due to a combination of a work overload at the testing laboratory and OIE rules
that caused Brazil to lower the priority of testing the suspect cow.
BSE audits to be conducted
On January 5, Brazil's agriculture ministry confirmed the country's beef
industry would be thoroughly audited.
State government teams would be sent to beef producers to ensure procedures
to safeguard cows' health were being properly followed.
A review on all operational procedures would be made in accordance with OIE
guidelines.
Ministry of Agriculture international relations secretary Celio Porto said
the audit will start by looking at what possible failures may exist in the fight
against BSE.
This decision seems to be made on the back of the OIE scientific committee
announcing it will examine Brazil's BSE risk status and conduct an audit next
month.
The decision by the OIE to do this audit seems to be related to R-CALF
questioning of not just Brazil's BSE surveillance systems but also the OIE's
procedures.
R-CALF regards the two-year delay as a symptom of the failure of the OIE's
global system that they believe incorrectly assumes foreign countries,
particularly developing countries, have the same means, commitment and
capabilities as the US to control and eradicate diseases.
The OIE annual meeting is to be held in May at which the findings of their
Brazilian audit and any recommendation would be tabled and considered.
In essence, the credibility of not only Brazil's BSE surveillance system
has been questioned but also the OIE's global system.
A negative OIE review would be disastrous for Brazil, which could lead to
potentially more bans from import countries or at best the current bans
remaining in place for an extended period.
It would seem obvious to me that no country is likely to remove bans before
May until the findings of the OIE review are made public.
The message is clear those countries that have imposed bans are needing
transparency in the current Brazil BSE surveillance system and a credible reason
why there was a two-year delay in the findings.
Russia to review its position
Russia's decision to wait and evaluate the situation is based on the
comforting fact that back in 2011 Russia imposed bans on three Brazilian States
Mato Grosso, Parana, Rio and Granda do Sul.
These bans are still in place and Parana, which was the State that the
atypical case was found in, has not shipped beef to Russia in almost 18 months.
The concerns at the time related to sanitary issues and since then 85
export establishments from these three States have been prevented from
exporting.
The need for transparency in any countries BSE surveillance system and
testing processes can not be underestimated and Brazil is no exception.
An independent and credible body, such as the OIE, is critical to ensure
that all importing countries can see correct procedures have been followed and
similar occurrences won't be repeated.
Until these concerns are met, Brazil's beef exports future among the 10
countries with bans in place will remain uncertain.
Friday, December 07, 2012
ATYPICAL BSE BRAZIL 2010 FINALLY CONFIRMED OIE 2012
Wednesday, December 19, 2012
Scientific Report of the European Food Safety Authority on the Assessment
of the Geographical BSE Risk (GBR) of Brazil
Friday, January 25, 2013
Japan may relax US Mad Cow BSE beef import rules in Feb 2013
Monday, January 28, 2013
U.S. Trade Representative Ron Kirk and Agriculture Secretary Tom Vilsack
Announce Agreement to Further Open Japan’s Market to U.S. Beef
Thursday, January 17, 2013
Canada, U.S. agree on animal-disease measures to protect trade, while
reducing human and animal health protection
IT is of my opinion, that the OIE and the USDA et al, are the soul reason,
and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion
diseases, including typical and atypical BSE, typical and atypical Scrapie, and
all strains of CWD, and human TSE there from, spreading around the globe.
I have lost all confidence of this organization as a regulatory authority
on animal disease, and consider it nothing more than a National Trading
Brokerage for all strains of animal TSE, just to satisfy there commodity. 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.
JUST because of low documented human body count with nvCJD and the long
incubation periods, the lack of sound science being replaced by political and
corporate science in relations with the fact that science has now linked some
sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of
CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call
for this organization to be dissolved. ...
Tuesday, July 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th
General Session, 20 - 25 May 2012
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe
WITH BOVINE MAD COW DISEASE
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
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
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE
EUROPEAN COMMUNITIES AND O.I.E. COMMISSION DECISION of 11 November 2009 amending
the Annex to Decision 2007/453/EC as regards the BSE status of Chile, Colombia
and Japan (notified under document C(2009) 8590)
Tuesday, January 1, 2008
BSE OIE USDA
Subject: OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local
cattle dealers i.e. USDA
Date: May 14, 2007 at 9:00 am PST
OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local cattle
dealers i.e. USDA
STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION
March 9, 2007
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012
16 year old with mad cow type TSE prion disease USA, course Gambetti et al
changed the name again...
Monday, January 14, 2013
Gambetti et al USA Prion Unit change another highly suspect USA mad cow
victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes
along with this BSe
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25,
2012
Friday, November 23, 2012
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA,
AND CANADA
Sunday, December 2, 2012
CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE
BLEW IT’
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
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
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
2012 atypical L-type BSE BASE California reports
Saturday, August 4, 2012
Final Feed Investigation Summary - California BSE Case - July 2012
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
CENSORSHIP IS A TERRIBLE THING $$$
Canada has had a COVER-UP policy of mad cow disease since about the 17th
case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored
$$$
THIS proves there is indeed an epidemic of mad cow disease in North
America, and it has been covered up for years and years, if not for decades, and
it’s getting worse $$$
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011
and how to hide mad cow disease in Canada Current as of: 2011-01-31
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
Reasons for the New Regulation Order No. 23 (as well as amending Order No.
149) of the State Committee for Veterinary Medicine name BSE as the reason for
new import requirement. The legal title for Order No. 23 is "On Urgent Measures
Aimed at Prevention and Elimination of BSE and Other Prion Infections in
Cattle”. Neither Order explains how the threat of introduction of BSE can be
addressed through the inspection of producers of all products of animal origin
including fish, dairy products, poultry and pork. It is not clear what other
concerns are addressed through the proposed inspections. Formal Notification of
Trading Partners On August 3rd, Ukraine's Notification and Enquiry Point issued
a legal Notification G/SPS/N/UKR/3/Rev.1 found on the Official WTO Website
(Committee on Sanitary and Phytosanitary Measures)
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011 San Antonio, Texas
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
This is provided by the statistically significant increase in the incidence
of sheep scrape from 1985, as determined from analyses of the submissions made
to VI Centres, and from individual case and flock incident studies. ........
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
12/10/76
AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
Office Note CHAIRMAN: PROFESSOR PETER WILDY
snip...
A The Present Position with respect to Scrapie A] The Problem
Scrapie is a natural disease of sheep and goats. It is a slow and
inexorably progressive degenerative disorder of the nervous system and it ia
fatal. It is enzootic in the United Kingdom but not in all countries.
The field problem has been reviewed by a MAFF working group (ARC 35/77). It
is difficult to assess the incidence in Britain for a variety of reasons but the
disease causes serious financial loss; it is estimated that it cost Swaledale
breeders alone $l.7 M during the five years 1971-1975. A further inestimable
loss arises from the closure of certain export markets, in particular those of
the United States, to British sheep.
It is clear that scrapie in sheep is important commercially and for that
reason alone effective measures to control it should be devised as quickly as
possible.
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca
fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
Epidemiology of Scrapie in the United States 1977
IT'S as obvious as day and night, either Larry, Curley, and Mo have been at
the helm of the USDA/APHIS/FSIS/FDA/CDC/NIH et al for many many years, or the
incompetence of these agencies are so inept, either through ignorance and or
just too overweight with industry reps., they then should be all done away with
and a single agency brought forth, and if not, how will you correct this ongoing
problem ?
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010
Wednesday, January 18, 2012
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural
Scrapie Isolates Similar to CH1641 Experimental Scrapie
Journal of Neuropathology & Experimental Neurology: February 2012 -
Volume 71 - Issue 2 - p 140–147
Thursday, July 14, 2011
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical
Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
Wednesday, January 18, 2012
BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE
February 1, 2012
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible
Spongiform Encephalopathies of Small Ruminants, France, 2002-2009
Volume 17, Number 1 January 2011
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what
otherwise would have been unreported findings of atypical scrapie in sheep. In
2009, five new cases have been reported in Quebec, Ontario, Alberta, and
Saskatchewan. With the exception of Quebec, all cases have been diagnosed as
being the atypical form found in older animals. Canada encourages producers to
join its voluntary surveillance program in order to gain scrapie-free status.
The World Animal Health will not classify Canada as scrapie-free until no new
cases are reported for seven years. The Canadian Sheep Federation is calling on
the government to fund a wider surveillance program in order to establish the
level of prevalence prior to setting an eradication date. Besides long-term
testing, industry is calling for a compensation program for farmers who report
unusual deaths in their flocks.
another atypical Nor-98 Scrapie case documented in Canada for 2012
Date confirmed Location Animal type infected May 31* Quebec Sheep
Sunday, April 29, 2012
Scrapie confirmed at quarantined sheep farm Canada CFIA
Wednesday, April 4, 2012
20120402 - Breach of quarantine/Violation de la mise en quarantaine of an
ongoing Scrapie investigation
Thursday, February 23, 2012
Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012
Tuesday, November 6, 2012
Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and
Sporadic CJD, November-December 2012 update
Monday, March 19, 2012
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform
Encephalopathy
PLoS One. 2012; 7(2): e31449.
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011 However, work with transgenic mice has
demonstrated the potential susceptibility of pigs, with the disturbing finding
that the biochemical properties of the resulting PrPSc have changed on
transmission (40).
***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
*** Intriguingly, these conclusions suggest that some pathological features
of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
*** These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.
Surprisingly the TSE agent characteristics were dramatically different
v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and
biochemical characteristics similar to those of atypical BSE L in the same mouse
model. Moreover, whereas no other TSE agent than BSE were shown to transmit into
Tg porcine mice, atypical scrapie was able to develop into this model, albeit
with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed
similar biological and biochemical characteristics than BSE adapted to this
porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross
species barriers
(ii) the possible capacity of this agent to acquire new characteristics
when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on
the origin of the diversity of the TSE agents and could have consequences on
field TSE control measures.
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE
I strenuously urge the USDA and the OIE et al to revoke the exemption of
the legal global trading of atypical Nor-98 scrapie TSE. ...TSS
Thursday, February 23, 2012
EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE
OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME
TSS
Saturday, January 05, 2013
Immunohistochemical Detection of Disease- Associated Prion Protein in the Peripheral Nervous System in Experimental H-Type Bovine Spongiform Encephalopathy
Immunohistochemical Detection of Disease- Associated Prion Protein in the
Peripheral Nervous System in Experimental H-Type Bovine Spongiform
Encephalopathy
H. Okada1, Y. Iwamaru1, T. Yokoyama1, and S. Mohri1
Abstract
H-type bovine spongiform encephalopathy (BSE) has been identified in aged
cattle in Europe and North America. To determine the localization of
disease-associated prion protein (PrPSc) in the peripheral nerve tissues of
cattle affected with H-type BSE, we employed highly sensitive
immunohistochemical and immunofluorescence techniques with the tyramide signal
amplification (TSA) system. PrPSc deposition was detected in the inferior
ganglia, sympathetic nerve trunk, vagus nerve, spinal nerves, cauda equina, and
adrenal medulla, using this system. Notably, granular PrPSc deposits were
present mainly in the Schwann cells and fibroblastlike cells and occasionally
along certain nerve fibers at the surface of the axons. In the adrenal gland,
PrPSc immunolabeling was observed within the sympathetic nerve fibers and nerve
endings in the adrenal medulla. Although our results were limited to only 3
experimental cases, these results suggest that the TSA system, a highly
sensitive immunohistochemical procedure, may help in elucidating the peripheral
pathogenesis of H-type BSE.
Keywords
atypical bovine spongiform encephalopathy, H-type, prion, tyramide
amplification, peripheral nervous system
snip...
Neuropil, but not neuronal, vacuolation was obvious in all brain areas,
especially in the nuclei of the thalamus and brainstem. Immunolabeled PrPSc was
widely distributed throughout the brain and spinal cord (Fig. 1). Eight patterns
of PrPSc immunolabeling including intraneuronal, perineuronal, intraglial,
linear, fine particulate, coarse granular, stellate, and plaques were identified
in the brain. The most conspicuous pattern of PrPSc was that of fine particulate
and coarse granular deposits in the cerebral and cerebellar cortices and the
nuclei of the thalamus, brainstem, and cerebellum. Stellate-type PrPSc
deposition was detected in the cerebral and cerebellar cortices, basal ganglia,
thalamus, hypothalamus, and hippocampus. Intraglial-type PrPSc deposition was
conspicuous throughout the white matter of the brain and spinal cord. Spherical
PrPSc plaques were sparsely located in the thalamus, basal ganglia, midbrain,
pons, deeper layers of the cerebral cortices, and subcortical white matter.
Immunolabeled PrPSc was observed in the retina, neurohypophysis, and optic
nerve. In the trigeminal and dorsal root ganglia, PrPSc was mainly found
accumulated in both ganglionic and satellite cells, using the conventional
polymer immunodetection method as described previously.9 In addition to the
extracerebral tissues described above, positive PrPSc immunolabeling was
detected in the adrenal gland, cauda equina, cervical spinal nerves, facial
nerve, hypoglossal nerve, vagus nerve, sciatic nerve, and ganglia, such as the
inferior ganglion of the vagus nerve, superior cervical ganglion, stellate
ganglion, ganglia of the sympathetic trunk, and celiac and mesenteric ganglion
complex, with the use of the TSA-biotin system. In these ganglia, not all
neurons of ganglia exhibited intracytoplasmic labeling, but labeling was evident
in the Schwann cells or fibroblast-like cells (Figs. 2, 3). In the cauda equina,
dorsal roots of the cervical spinal nerves, facial nerve, hypoglossal nerve,
vagus nerve, and sciatic nerve, granular PrPSc aggregate was mainly located in
Schwann cells. In the adrenal gland, the PrPSc signal was evident at the
intercellular fine processes of the nerve endings between the chromaffin cells
of the adrenal medulla (Fig. 4). Immunolabeled PrPSc was not detected in the
enteric nervous system such as the myenteric and submucosal plexi of the
digestive tract. No specific immunolabeling was detectable in the lymphoid
tissues with the TSA-biotin system.
Using the dual or triple immunofluorescence technique, localization of
PrPSc was visible in the ganglionic and satellite cells of the ganglia in the
merged images (Fig. 5). In addition, the merged image showed that PrPSc granules
were rarely located at the periphery of axons or within the axons adjacent to
the ganglia (Fig. 6). Moreover, granular PrPSc was observed outside
S100-positive cells (Fig. 7). In the cauda equina and spinal nerves, PrPSc
coexisted mostly in the periphery of Schwann cells labeled with MBP and S100
(Fig. 8). No PrPSc immunolabeling was detected in the compact layers of the
myelin sheath. In addition, no positive signal was detected in the sections from
uninfected controls incubated with mAb F99/97.6.1 by both TSA-biotin and
TSA-fluorescence methods, and no background immunostaining was observed in any
sections of H-type infected animals by both methods when non-immune mouse and
rabbit IgG, or PBS, were applied to the sections instead of the primary
PrP-antibody (Figs. 9, 10).
snip...see full text ;
snip...
Unfortunately, a detailed and all-encompassing analysis of neuropathology
and topographical distribution of immunolabeled PrPSc in H-type BSE-affected
cattle could not be performed, since only the obex region is routinely sampled
for BSE surveillance testing and the remaining brain as well as the carcasses
are not available in most countries [3,10,12,13,24-27]. Recently, clinical signs
and biochemical properties of experimental German H-type BSE cases have been
reported [20]. The primary objective of this study was to investigate the
transmissibility of H-type BSE, using a field isolate detected in the active
surveillance program in Canada [12]. The secondary objective was to extend the
knowledge of the topographical distribution and deposition patterns of
immunolabeled PrPSc in H-type BSE.
snip...
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
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
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)
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.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
SNIP...
Friday, May 11, 2012
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
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
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.
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
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)
Tuesday, November 6, 2012
***Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and
Sporadic CJD, November-December 2012 update
Comments on technical aspects of the risk assessment were then submitted to
FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary.
This document provides itemized replies to the public comments received on
the 2005 updated Harvard BSE risk assessment. Please bear the following points
in mind:
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
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
2012 atypical L-type BSE BASE California reports
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe
WITH BOVINE MAD COW DISEASE
Tuesday, December 25, 2012
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
2011 Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Sunday, December 2, 2012
CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE
BLEW IT’
Monday, July 23, 2012
The National Prion Disease Pathology Surveillance Center July 2012
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25,
2012
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012
TSS