Department of Agriculture, Food and the Marine Identifies Suspected BSE
Case
The Department today announced the identification of a suspected BSE case
in county Louth. The case was identified through the Department’s on-going
surveillance system on fallen animals (that is animals which die on farm). The
animal was not presented for slaughter and did not enter the food chain.
Confirmatory tests are being undertaken and results will be available in
approximately one week. If confirmed, this will be the first BSE case found in
Ireland since 2013.
DAFM is now undertaking a full investigation into all relevant factors in
this case - including a full epidemiological examination.
DAFM is informing the relevant national and international reference
organisations and the European Commission, and will be liaising with trading
partners.
Note for editors
If, as expected, the tests confirm this to be a classical case of BSE,
this may impact on Ireland’s recently awarded “negligible risk status” from the
World Organisation for Animal Health (OIE). In this case Ireland will revert to
“controlled risk status” which applied up to last week and which facilitated
trade to a wide range of international markets. It will also result in the
continuation of the existing range of controls for a further number of years.
The full range of risk mitigating measures continue in place at slaughter
plants, including the following:
All animals presented for slaughter are systematically subjected to
ante-mortem examination by veterinary inspectors to ensure that only healthy
animals are allowed into the food chain.
A range of tissues - identified as ‘specified risk material’ - where the
BSE infectivity resides in potentially infected animals are systematically
removed from all slaughtered bovines of differing ages as follows:
All ages: tonsils, intestines and mesentery
Over 12 months: skull (including eyes and brain) and spinal cord
Over 30 months: the vertebral column and associated tissues
The animal involved is a five year old cow on a dairy farm in county Louth.
The investigation will include an examination of the birth cohort and progeny of
the cow involved.
BSE IRELAND
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
ruminant feed ban for cervids in the United States ?
31 Jan 2015 at 20:14 GMT
Thursday, May 28, 2015
*** OIE cuts six European countries' mad cow risk level, while increasing
risk factors for humans to the BSE TSE PRION DISEASE around the globe
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. We recently observed the
direct transmission of a natural classical scrapie isolate to macaque after a
10-year silent incubation period, with features similar to some reported for
human cases of sporadic CJD, albeit requiring fourfold longe incubation than
BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third
potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the
origin of human sporadic cases. We will present an updated panorama of our
different transmission studies and discuss the implications of such extended
incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases...TSS
===============
Saturday, May 30, 2015
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
LATE-BREAKING ABSTRACTS
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
Chronic wasting disease (CWD) is a widespread and expanding prion disease
in free-ranging and captive cervid species in North America. The zoonotic
potential of CWD prions is a serious public health concern. Current literature
generated with in vitro methods and in vivo animal models (transgenic mice,
macaques and squirrel monkeys) reports conflicting results. The susceptibility
of human CNS and peripheral organs to CWD prions remains largely unresolved. In
our earlier bioassay experiments using several humanized transgenic mouse lines,
we detected protease-resistant PrPSc in the spleen of two out of 140 mice that
were intracerebrally inoculated with natural CWD isolates, but PrPSc was not
detected in the brain of the same mice. Secondary passages with such
PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient
prion transmission with clear clinical and pathological signs in both humanized
and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD
isolates in a new humanized transgenic mouse line led to clinical prion
infection in 2 out of 20 mice. These results indicate that the CWD prion has the
potential to infect human CNS and peripheral lymphoid tissues and that there
might be asymptomatic human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Friday, May 22, 2015
*** Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual
Meeting 12-14 May 2014 ***
Saturday, May 30, 2015
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
Wednesday, June 10, 2015
Zoonotic Potential of CWD Prions
LATE-BREAKING ABSTRACTS
Tuesday, May 26, 2015
Minimise transmission risk of CJD and vCJD in healthcare settings Last
updated 15 May 2015
PLEASE SEE FRANCE atypical BSE cases ;
it’s all about trade now, nothing else matters $$$
>>>PARIS -- The World Organization for Animal Health said on
Wednesday it had lowered to the safest level the official risk of six countries
for mad cow disease, a move expected to open international market access for
their beef exports. These countries are France, Ireland, Switzerland, the Czech
Republic, Cyprus and the Lichtenstein.<<<
THIS move is _not_ based on science, but on corporate profits and big ag.
to say now that France is a "negligible risk", would be like saying North
America is a "negligible risk", which is preposterous. not based on sound
science, but on greed and special interest. the only _move_ this ‘’BSE mad cow
negligible risk’’ assessment makes, is a move to increase global Transmissible
Spongiform Encephalopathy prion mad cow type disease, via the legal trading of
the TSE prion aka mad cow type disease via the BSE MRR i.e. Minimal Risk Region
policy, a policy set up to fail from the start. please, for whatever God you
pray to sake, please be warned.
‘’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.’’
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
Wednesday, March 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
Friday, April 4, 2014
China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South
Africa and Saudi Arabia still retain BSE-related closures
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
The OIE is nothing more than a trading brokerage for the Transmissible
Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is
still in the midst of a mad cow disease outbreak with atypical BSE cases still
growing. mad cow disease is so bad in France, as with the USA, they stopped
testing for mad cow disease (France altogether and the USA to figures so low,
you would only detect a case of mad cow disease, only by chance).
from the inside looking out ;
Quote: Maybe familirise yourself with the OIE. The primary concern is
animal health of the world they are the animal version of the WHO. It is a long
way down from that ivory tower but here we go, until pressured by the USA
repesentatives a country could not export animals for 6 years after finding a
BSE/BASE positive animal so under the old rules the US would not be able to
export anywhere in the world for another 4 1/2 years. Who got the risk levels
system put in to allow some trade - your US representatives. You guys want to
change rules - OK , but you do not get special rules that only apply to the US.
As i have told you before Sand h I market all my own slaughter animals and you
know that, so don't do the whole holier than thow act.
With all due respect, it is obvious that you know little about the OIE and
how it actually works. Having been to their offices in Paris and talked
personally with the Head of the Animal Test Section, you would choke if you knew
how many lobby groups attend that office daily. There is a steady stream of paid
lobby groups that have one goal in life and that is to sway the Section Heads of
each department within the OIE to suit the needs of different juristictions
around the world, which curiously enough, also includes the USA and Canada.
Anyone can go there and chat with them - providing they can privide valid cause
to be let in. To say that the only goal of the OIE is animal health is actually
only part of their function. They are more than that and my discussions with Dr.
Diaz there has showed me that. But to blindly make a statement regarding what
they do when you have no idea what they actually do is like eating the skin of
the orange and not knowing what is actually under.
Interstingly you state that the US Government applied pressure (to the OIE)
I assume and that is a great example of the lobby groups doing their job. So, at
the end of the day, one can safely assume that it is the pressure applied by
certain influential lobby groups that will determine a likely aoutcome to an
apparent OIE directive. Man alive, isn't it great to live in a democracy wherein
the people get to make the choices and not just some "other" interested party or
group - say like........Cargyll or Tyson for example?
So, one last question, question?
Who wags the tail of that dog?? And for what reason other than one that is
purely associated with trade and international agreements and greed?
And you think it is so simply explainable.
end...tss
please see ;
spontaneous atypical BSE ???
don’t let anyone fool you. spontaneous TSE prion disease is a hoax in
natural cases, never proven.
all one has to do is look at France. France is having one hell of an
epidemic of atypical BSE, probably why they stopped testing for BSE, problem
solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow
disease in numbers they could find any with, after those atypical BSE cases
started showing up. shut down the testing to numbers set up by OIE that are so
low, you could only by accident find a case of BSE aka mad cow disease. and this
brilliant idea by the WHO et al, to change the name of mad cow disease, thinking
that might change things is preposterous. it’s all about money now folks, when
the OIE, USDA and everyone else went along and made the TSE prion disease aka
mad cow type disease a legal trading commodity by the BSE MRR policy, I would
say everyone bit off more then they can chew, and they will just have to digest
those TSE Prions coming from North America, and like it, and just prey you don’t
get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE
prion disease in the decades to come, and or pass it to some other poor soul via
the iatrogenic medical surgical tissue friendly fire mode of transmission i.e.
second hand transmission. it’s real folks, just not documented much, due to lack
of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the
iatrogenic event is tracked down and documented, and put into the academic and
public domain, which very seldom happens. ...
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
so 20 cases of atypical BSE in France, compared to the remaining 40 cases
in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+
cases per country, besides Frances 20 cases. you cannot explain this away with
any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Saturday, May 09, 2015
Expression of genes involved in the T cell signalling pathway in
circulating immune cells of cattle 24 months following oral challenge with
Bovine Amyloidotic Spongiform Encephalopathy (BASE)
(c) The commonest form of CJD occurs as a sporadic disease, the cause of
which is unknown, although genetic factors (particularly the codon 129
polymorphism in the prion protein gene (PRNP)) influence disease susceptibility.
The familial forms of human TSEs (see Box 1) appear to have a solely genetic
origin and are closely associated with mutations or insertions in the PRNP gene.
Most, but not all, of the familial forms of human TSEs have been transmitted
experimentally to animals. There are no known familial or genetic TSEs of
animals, although polymorphisms in the PRNP gene of some species (sheep for
example) may influence the length of the incubation period and occurrence of
disease. (
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Wednesday, May 27, 2015
BSE Case Associated with Prion Protein Gene Mutation
Saturday, May 09, 2015
Expression of genes involved in the T cell signalling pathway in
circulating immune cells of cattle 24 months following oral challenge with
Bovine Amyloidotic Spongiform Encephalopathy (BASE)
Tuesday, May 19, 2015
COUNTRY OF ORIGIN LABELING COOL H.R. 2393 Agriculture Chairman K. Michael
Conaway (R-TX) Fears of US imports infected with mad cow disease is emerging as
an issue in trans-Pacific trade talks
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
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
O.08: H-type bovine spongiform encephalopathy associated with E211K prion
protein polymorphism: Clinical and pathologic features in wild-type and E211K
cattle following intracranial inoculation
S Jo Moore, M Heather West Greenlee, Jodi Smith, Eric Nicholson, Cathy
Vrentas, and Justin Greenlee United States Department of Agriculture; Ames, IA
USA
In 2006 an H-type bovine spongiform encephalopathy (BSE) case was reported
in an animal with an unusual polymorphism (E211K) in the prion protein gene.
Although the prevalence of this polymorphism is low, cattle carrying the K211
allele are predisposed to rapid onset of H-type BSE when exposed. The purpose of
this study was to investigate the phenotype of this BSE strain in wild-type
(E211E) and E211K heterozygous cattle. One calf carrying the wild-type allele
and one E211K calf were inoculated intracranially with H-type BSE brain
homogenate from the US 2006 case that also carried one K211 allelle. In
addition, one wild-type calf and one E211K calf were inoculated intracranially
with brain homogenate from a US 2003 classical BSE case. All animals succumbed
to clinical disease. Survival times for E211K H-type BSE inoculated catttle (10
and 18 months) were shorter than the classical BSE inoculated cattle (both 26
months). Significant changes in retinal function were observed in H-type BSE
challenged cattle only. Animals challenged with the same inoculum showed similar
severity and neuroanatomical distribution of vacuolation and disease-associated
prion protein deposition in the brain, though differences in neuropathology were
observed between E211K H-type BSE and classical BSE inoculated animals. Western
blot results for brain tissue from challenged animals were consistent with the
inoculum strains. ***This study demonstrates that the phenotype of E211K H-type
BSE remains stable when transmitted to cattle without the E211K polymorphism,
and exhibits a number of features that differ from classical BSE in both
wild-type and E211K cattle.
==============
***This study demonstrates that the phenotype of E211K H-type BSE remains
stable when transmitted to cattle without the E211K polymorphism, and exhibits a
number of features that differ from classical BSE in both wild-type and E211K
cattle.***
PLEASE SEE ;
Wednesday, May 27, 2015
BSE Case Associated with Prion Protein Gene Mutation
==============
P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine
Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge;
Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology
Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and
food-borne fatal neurological disease which can be orally transmitted to cattle
and humans. Due to the presence of contaminated milk replacer, it is generally
assumed that cattle become infected early in life as calves and then succumb to
disease as adults.
Here we challenged three 14 months old cattle per-orally with 100 grams of
C-type BSE brain to investigate age-related susceptibility or resistance. During
incubation, the animals were sampled monthly for blood and feces and subjected
to standardized testing to identify changes related to neurological
disease.
At 53 months post exposure, progressive signs of central nervous system
disease were observed in these 3 animals, and they were euthanized. Two of the
C-BSE animals tested strongly positive using standard BSE rapid tests, however
in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not
detected using rapid tests for BSE. Subsequent testing resulted in the detection
of pathologic lesion in unusual brain location and PrPsc detection by PMCA
only.
Our study demonstrates susceptibility of adult cattle to oral transmission
of classical BSE. We are further examining explanations for the unusual disease
presentation in the third challenged animal.
========================
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
Saturday, May 30, 2015
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
Wednesday, June 10, 2015
Zoonotic Potential of CWD Prions
LATE-BREAKING ABSTRACTS
Thursday, June 11, 2015
Ireland Department of Agriculture, Food and the Marine Identifies Suspected
BSE Case
Terry S. Singeltary SR. Texas USA
Terry S. Singeltary Sr.
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