cows, cash, and cover ups, investigating variant CJD
Variant CJD - Documentary
vCJD, the human form of BSE (Mad Cow Disease) has killed nearly 200 people in the UK.
It has been described as a ticking time bomb, a manmade disease, resulting from BSE infected products entering the food chain - it can lay dorment for decades.
This documentary will explore the links between BSE and vCJD, questioning the ethics and actions of the British Farming Industry, the Food Industry and the British Government.
From: Terry S. Singeltary Sr.
Sent: Saturday, June 20, 2015 5:03 PM
Subject: cows, cash, and cover ups, investigating variant
CJD
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and
Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and
Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods. We recently observed the
direct transmission of a natural classical scrapie isolate to macaque after a
10-year silent incubation period, with features similar to some reported for
human cases of sporadic CJD, albeit requiring fourfold longe incubation than
BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third
potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the
origin of human sporadic cases. We will present an updated panorama of our
different transmission studies and discuss the implications of such extended
incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases...TSS
===============
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. ***
ALSO, PLEASE SEE ;
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Saturday, May 30, 2015
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
Wednesday, June 10, 2015
Zoonotic Potential of CWD Prions
LATE-BREAKING ABSTRACTS
please see attached pdf file, with references of breaches in the USA triple
BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS No
documents available. Attachments View All (1) Docket No. APHIS-2014-0107 Bovine
Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary
Submission View Attachment:
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
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
Posted by Terry S. Singeltary Sr. on May 20, 2015 at 9:00am
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
spontaneous atypical BSE ???
if that's the case, then France is having one hell of an epidemic of
atypical BSE, probably why they stopped testing for BSE, problem solved $$$
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
so 20 cases of atypical BSE in France, compared to the remaining 40 cases
in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+
cases per country, besides Frances 20 cases. you cannot explain this away with
any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of
infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical
BSE investigations
Thursday, August 12, 2010
Seven main threats for the future linked to prions
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
Moreover, transmission experiments to non-human primates suggest that some TSE
agents in addition to Classical BSE prions in cattle (namely L-type Atypical
BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
***In addition, non-human primates are specifically susceptible for
atypical BSE as demonstrated by an approximately 50% shortened incubation time
for L-type BSE as compared to C-type. Considering the current scientific
information available, it cannot be assumed that these different BSE types pose
the same human health risks as C-type BSE or that these risks are mitigated by
the same protective measures.
Thursday, June 04, 2015
Catholic Medical Center v. Civil No. 14-cv-180-JL Opinion No. 2015 DNH 110
Fireman’s Fund Insurance Company Creutzfeldt Jakob Disease TSE Prion tainted
medical instruments
UNITED STATES DISTRICT COURT DISTRICT OF NEW HAMPSHIRE
Tuesday, May 26, 2015
Minimise transmission risk of CJD and vCJD in healthcare settings Last
updated 15 May 2015
Saturday, December 13, 2014
Terry S. Singeltary Sr. Publications TSE prion disease
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
snip...
lost my mom to the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD
12/14/97 confirmed. I just made a promise to mom, never forget (I could never
ever forget what I saw), and never let them forget...
layperson
Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
5:05 PM
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