Sporadic Creutzfeldt-Jakob Disease MM1+2C and MM1 Are Identical in Transmission Properties
Research Article
Sporadic Creutzfeldt-Jakob Disease MM1+2C and MM1 Are Identical in
Transmission Properties
Atsushi Kobayashi1,†, Yuichi Matsuura2, Toru Iwaki3, Yasushi Iwasaki4, Mari
Yoshida4, Hitoshi Takahashi5, Shigeo Murayama6, Masaki Takao6, Shinsuke Kato7,
Masahito Yamada8, Shirou Mohri1 and Tetsuyuki Kitamoto1,*
DOI: 10.1111/bpa.12264
This article is protected by copyright. All rights reserved.
Issue
Cover image for Vol. 25 Issue 2
Brain Pathology
Conflicts of interest: The authors declare that they have no conflict of
interest
This article has been accepted for publication and undergone full peer
review but has not been through the copyediting, typesetting, pagination and
proofreading process, which may lead to differences between this version and the
Version of Record. Please cite this article as doi: 10.1111/bpa.12264
Abstract
Abstract
The genotype (methionine, M or valine, V) at polymorphic codon 129 of the
PRNP gene and the type (1 or 2) of abnormal prion protein in the brain are the
major determinants of the clinicopathological features of sporadic
Creutzfeldt-Jakob disease (CJD), thus providing molecular basis for
classification of sporadic CJD, e.g., MM1, MM2, MV1, MV2, VV1, or VV2. In
addition to these “pure” cases, “mixed” cases presenting mixed neuropathological
and biochemical features have also been recognized. The most frequently observed
mixed form is the co-occurrence of MM1 and MM2, namely MM1+2. However, it has
remained elusive whether MM1+2 could be a causative origin of dura mater
graft-associated CJD (dCJD), one of the largest subgroups of iatrogenic CJD. To
test this possibility, we performed transmission experiments of MM1+2 prions and
a systematic neuropathological examination of dCJD patients in the present
study. The transmission properties of the MM1+2 prions were identical to those
of MM1 prions because MM2 prions lacked transmissibility. In addition, the
neuropathological characteristics of MM2 were totally absent in dCJD patients
examined. These results suggest that MM1+2 can be a causative origin of dCJD and
causes neuropathological phenotype similar to that of MM1.
friendly fire, the pass it forward mode of the TSE prion aka mad cow type
disease, i.e. iatrogenic TSE prion disease.
with the many different species in North America with a TSE prion disease,
and then the others nobody tests for i.e. feline, canine, just for a few
examples, and the exposure there from via consumption, casual contact, or the
many other potential exposure possibilities, what about friendly fire there from
???
it would be nice to be able to start differentiating the many causes of the
sporadic CJDs TSE prion disease, and I believe that to be iatrogenic.
all sporadic CJD Creutzfeldt Jakob Disease Transmissible Spongiform
Encephalopathy TSE Prion disease means, from UNKNOWN CAUSE, simply meaning the
route and source of the TSE prion agent is not known to date. there are many
different strain or phenotype of the so called sporadic or spontaneous CJD.
it will be costly to the industry to differentiate the many potential
causes and sources of sCJD. who will prevail, the industry or the consumer $$$
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...
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...
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
Tuesday, November 04, 2014
Towards an Age-Dependent Transmission Model of Acquired and Sporadic
Creutzfeldt-Jakob Disease
Thursday, September 18, 2014
Development of Dose-Response Models of Creutzfeldt-Jakob Disease Infection
in Nonhuman Primates for Assessing the Risk of Transfusion-Transmitted variant
Creutzfeldt-Jakob Disease
Tuesday, December 30, 2014
TSEAC USA Reason For Recalls Blood products, collected from a donors
considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were
distributed END OF YEAR REPORT 2014
Sunday, February 08, 2015
FDA SCIENCE BOARD TO THE FOOD AND DRUG ADMINISTRATION BOVINE HEPARIN BSE
CJD TSE PRION Wednesday, June 4, 2014
Thursday, March 26, 2015
Variant CJD and blood transfusion: are there additional cases?
Vox Sanguinis (2014) 107, 220–225 ORIGINAL PAPER © 2014 International
Society of Blood Transfusion DOI: 10.1111/vox.12161
Saturday, March 21, 2015
Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence
Rates Increasing
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment Iatrogenic Alzheimer’s, a TSE prion disease, what if ?
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type
prion disease, what it ???
some old history on Endoscopy equipment and CJD TSE Prion concerns ; 1999
Subject: CJD * Olympus Endoscope Date: Sun, 10 Oct 1999 16:41:49 –0500
From: "Terry S. Singeltary Sr."
Saturday, February 21, 2015
Design of Endoscopic Retrograde Cholangiopancreatography (ERCP)
Duodenoscopes May Impede Effective Cleaning: FDA Safety Communication
From: Terry S. Singeltary Sr.
Sent: Tuesday, March 31, 2015 9:59 AM
Subject: re-Design of Endoscopic Retrograde Cholangiopancreatography (ERCP)
Duodenoscopes May Impede Effective Cleaning: FDA Safety Communication
Greetings Miss Storms Ma’am, Olympus et al,
Thank you kindly for the reply.
Miss Storms stated;
>>>Dear Mr. Singeltary - thank you for contacting me and I will
ask an Olympus representative to respond to your question. As duodenoscopes do
not contact tissue at high risk associated with CJD, can you please advise on
specifically what is your request. <<<
My request were stated in my previous email ;
>>>In reference to the latest incident of deaths from the use of
these endoscopy equipment, what is Olympus recommendations, requirements, and
guarantees, for disinfection against the CJD Transmissible Spongiform
Encephalopathy TSE PRION type disease ?
Miss Storms, I was in contact with Olympus around 1999 about my concerns
with endoscopy equipment and CJD TSE prion via iatrogenic mode. we did a crude
questionnaire on CJD and endoscopy, and it was disturbing how many of our loved
ones, had in the past, before dying from CJD, had some sort of endoscopy work
done on them
and then recently, I read a letter from Olympus from January 6, 2012, and
it stated ;
>>>At this time, there have been 6 reported cases of iatrogenic
transmission of the CJD agent associated with contaminated medical equipment,
all of which occurred prior to 1976 before the implementation of standard
sterilization procedures. Of the six cases linked to the use of contaminated
equipment, four were associated with neurosurgical instruments, and two with
stereotactic EEG depth electrodes. In addition, there are no known cases of
iatrogenic transmission of the CJD agent from endoscopy.<<< (see letter
below for reference...tss)
Miss Storms, Olympus et al, this in my opinion, is a red herring, an
oxymoron of sorts. all iatrogenic CJD is, is sporadic cjd, until the iatrogenic
event is discovered, documented, and put in the public domain. this very seldom
happens due to trace back efforts, and the very industry that refuses to do any
trace back for CJD, or any TSE prion disease. so your (Olympus) assumptions on
only 6 _reported_ cases of iatrogenic CJD, is just that, an assumption, gross
negligence of _all_ the facts presented, or kindly left out.
I simply believe that by Olympus omitting all these facts, and not
presenting them to the consumer of your products, in this case endoscopy
equipment, you are misleading your consumers, and in my opinion of the science
to date, Olympus is exposing people around the globe with the Transmissible
Spongiform Encephalopathy TSE prion disease.
Miss Storms, Olympus et al stated ;
>>> As duodenoscopes do not contact tissue at high risk associated
with CJD, ...snip...end <<<
BUT, duodenoscopes DO contact medium to low dose TSE prion infections
tissues, if the person being scoped is silently harboring a CJD TSE prion, thus
exposing everyone after that to the CJD TSE prion disease. I am very well aware
of the old study by Gibbs et al, and those brain electrodes ;
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD
20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
regardless of how many lives endoscopy equipment saves ever year, I
strongly, strenuously, urge Olympus to warn their product users, and consumers,
that there is NO KNOWN way to date, that will completely clean and decontaminate
the endoscopy equipment from the CJD TSE prion disease, and they risk exposure
to this agent when exposed to endoscopy equipment. anything less than that would
be criminal in my opinion, with the documented science to date. these atypical
strains of TSE prion disease are mutating, and as they mutate, they can, and
have, become more virulent.
with the emergence of atypical strains of TSE prion in animals and humans,
we cannot wait to prove a negative, while exposing millions waiting on that
negative to come. the science to date, in my opinion, has shown us that this
negative has not, and is not coming, thus, exposure, and friendly fire, i.e.
iatrogenic, is the key to the 85%+ of all human TSE, i.e. sporadic CJD, and once
the science is finally peeled all the way back, biomarkers of some sorts are
discovered, and trace back of iatrogenic events are finally able to be
documented and traced back to source, I believe that companies like Olympus,
that chose to continue to expose millions, regardless of these facts, will be
left for much litigation.
I strongly urge Olympus et al to state plainly these risk factors of their
equipment to the CJD TSE prion like disease, for all to know and see, ASAP. ...
thank you, with kind regards, terry
OLYMPUS
January 6, 2012
RE: Reprocessing Olympus Flexible Endoscopes Exposed to CJD
Dear Healthcare Professional,
This letter is in response to your recent inquiry regarding the
reprocessing of Olympus flexible endoscopes (medical and surgical) exposed to
the proteinaceous infectious agent, or prion, that causes Creutzfeldt - Jakob
disease (CJD). The CJD agent presents a unique infection control challenge
because it exhibits an unusual resistance to conventional disinfection and
sterilization methods. In an effort to provide our customers with information,
Olympus has reviewed various recommendations for the reprocessing of medical
devices exposed to the CJD agent. However, Olympus has not tested the efficacy
of these proposed methods, and therefore cannot recommend these methods for
reprocessing Olympus flexible endoscopes contaminated with the CJD agent. The
following information is provided for your reference only and should not be
considered a recommendation or endorsement for the reprocessing of Olympus
flexible endoscopes contaminated with the CJD agent.
At this time, there have been 6 reported cases of iatrogenic transmission
of the CJD agent associated with contaminated medical equipment, all of which
occurred prior to 1976 before the implementation of standard sterilization
procedures. Of the six cases linked to the use of contaminated equipment, four
were associated with neurosurgical instruments, and two with stereotactic EEG
depth electrodes. In addition, there are no known cases of iatrogenic
transmission of the CJD agent from endoscopy.
A number of organizations have proposed guidelines for the reprocessing of
medical instruments exposed to the CJD agent. The World Health Organization
(WHO) has developed infection control guidelines for preventing iatrogenic
transmission of the CJD agent. Proposed recommendations for the reprocessing of
heat-sensitive medical instruments, such as endoscopes, exposed to the CJD agent
include immersion in sodium hypochlorite (NaClO) or sodium hydroxide (NaOH) for
one hour. NaOH is extremely corrosive to flexible endoscopes and is not
recommended for use. However, Olympus has performed material compatibility
testing and concluded that Olympus flexible endoscopes can withstand up to 25,
one-hour immersions in sodium hypochlorite (NaClO, 2% available chlorine
concentration). Excessive immersion beyond this may cause corrosion and water
leaks.
OLYMPUS AMERICA INC. 3500 Corporate Parkway Center Valley, PA 18034
Telephone: (484) 896-5000 www.olympusamerica.com
It is important to note that Olympus has not tested the efficacy of
immersion in NaCIO and makes no claims regarding the effectiveness of this
procedure for reprocessing endoscopes contaminated with the CJD agent. Olympus
only confirms the material compatibility of NaClO with Olympus flexible
endoscopes.
To evaluate reprocessing any medical instrument exposed to the CJD agent,
published guidance documents recommend that a comprehensive risk assessment be
performed. The risk assessment is based upon three primary criteria: the CJD
status of the patient (high or low risk), the potential infectivity of the
tissue examined (high, low or no infectivity), and the classification of the
medical device (critical vs. semi-critical). Olympus recommends that you consult
with your infection control department and/or industry experts to determine a
strategy that reduces or eliminates the risk of iatrogenic transmission of the
CJD agent.
Olympus continues to monitor published studies and guidance regarding the
destruction or inactivation of the agents responsible for transmissible
spongiform encephalopathies, including variant CJD (vCJD), and will review its
recommendations as additional information becomes available. Below is a list of
useful references that provide guidance on reprocessing medical instruments
exposed to the CJD agent. If you have any additional questions, please contact
your local Olympus sales representative or the Olympus Technical Assistance
Center at 1-800-848-9024 (United States).
Thank you.
Sincerely,
Mary Ann Drosnock, MS, CIC Scientist, Clinical Affairs
maryann.drosnock@olympus.com OLYMPUS AMERICA INC. 3500 Corporate Parkway Center
Valley, PA 18034 Telephone: (484) 896-5000 www.olympusamerica.com
Alvarado, CJ. APIC guideline for infection prevention and control in
flexible endoscopy. Am J Infect Control 2000; 28: 138-155.
References
Centers for Disease Control and Prevention. Questions and Answers:
Creutzfeldt-Jakob disease infection control practices, available at http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm
Rutala, WA, and Weber DJ. Creutzfeldt-Jakob disease: recommendations for
disinfection and sterilization. Clinical Infectious Diseases 2001: 32:
1348-1356. [accessed 6 January 2012] Rutala, WA, and Weber DJ. Managing the risk
of nosocomial transmission of prion diseases. Current Opinion in Infectious
Diseases 2002 Aug.15 (4): 421-5.
United Kingdom, Department of Health, Advisory Committee on Dangerous
Pathogens and the Spongiform Encephalopathy Advisory Committee. Transmissible
spongiform encephalopathy agents: safe working and the prevention of infection,
Annex F: decontamination of endoscopes: available at
World Health Organization. WHO infection control guidelines for
transmissible spongiform encephalopathies; available at [accessed 6 January
2012].
http://whqlibdoc.who.int/hq/2000/WHO_CDS_CSR_APH_2000.3.pdf
[accessed 6 January 2012].
Research and analysis
Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with updated
guidance on decontamination of gastrointestinal endoscopy equipment
Updated 13 February 2015
Contents 1.Monitoring of patients 'at increased risk' of CJD 2.Updated
guidance on decontamination of equipment for gastrointestinal endoscopy .
This six-monthly report provides an update on the enhanced surveillance of
potential iatrogenic (healthcare-acquired) exposures to Creutzfeldt-Jakob
Disease (CJD). The data is correct as at 30 June 2014. For numbers of CJD case
reports, readers should consult data provided by the National CJD Research and
Surveillance Unit (NCJDRSU) .
Following the enhanced surveillance report, an update on the guidance for
the decontamination of equipment for gastrointestinal endoscopy is
presented.
1. Monitoring of patients ‘at increased risk’ of CJD
Individuals who have been identified as at increased risk of CJD as a
consequence of their medical care are informed of their exposure and asked to
follow public health precautions to avoid potentially transmitting the infection
to others. They are also followed-up to help determine the risks of CJD
transmission to patients through different routes and to ascertain whether any
people who may have been exposed to increased CJD risks go on to develop CJD.
Public health follow-up activities include clinical monitoring, general
practitioner (GP) updates, and post mortem investigations to determine whether
asymptomatic individuals in these groups have been infected with the CJD agent.
Some individuals also provide blood or tissue specimens for research purposes. A
number of different organisations are involved in these activities: Public
Health England (formerly the Health Protection Agency), Health Protection
Scotland (HPS), UCL Institute of Child Health/Great Ormond Street Hospital
(ICH), NHS Blood and Transplant (NHSBT), National CJD Research and Surveillance
Unit (NCJDRSU), National Prion Clinic (NPC), and the UK Haemophilia Centre
Doctors’ Organisation (UKHCDO).
The PHE CJD Section coordinates the collation of data on individuals
identified as at increased risk of CJD, and who have been informed of this.
These individuals are followed up through public health monitoring and research
activities by different organisations.
The PHE CJD Section currently holds data on the following groups of ‘at
risk’ patients: •recipients of blood components from donors who subsequently
developed vCJD •blood donors to individuals who later developed vCJD •other
recipients of blood components from these blood donors •recipients of certain
plasma products between 1990 and 2001 (non-bleeding disorder patients) •certain
surgical contacts of patients diagnosed with CJD •highly transfused recipients.
Data on the following risk groups are not held by PHE, but are held by
other organisations: •bleeding disorder patients who received plasma products
between 1990 and 2001 (UKHCDO) •recipients of human derived growth hormone
before 1985 (ICH) •patients who could have received a dura mater graft before
August 1992 (data not currently collected) •people who have been treated with
gonadotrophin sourced from humans before 1973 (data not currently collected)
•family risk of inherent prion disease (NPC).
The data from the UKHCDO are likely to be an underestimate of the true
number of ‘at risk’ patients with bleeding disorders who received UK-sourced
clotting factors, as there was incomplete reporting of identified ‘at risk’
patients by haemophilia centres to the UKHCDO database. Notified ‘at risk’
patients are given the option of removing their details from the UKHCDO
database, and are then removed from the ‘at risk’ totals.
The data on ‘at risk’ patients who received human-derived human growth
hormone held by the ICH is a slight underestimate of the total as a small number
of these patients are not included in the ICH follow-up.
Table 1. Summary of all ‘at risk’ groups on which data are collected (data
correct as at 30 June 2014)
At risk Group
Identified as ‘at risk’
Number notified as being ‘at risk’
Cases
Asymptomatic infections [b]
All Alive Recipients of blood from donors who later developed vCJD 67 27 14
3 1 Blood donors to individuals who later developed vCJD 112 108 104 – – Other
recipients of blood components from these donors 34 32 [c] 19 [c] – – Plasma
product recipients (non-bleeding disorders) who received UK sourced plasma
products 1980-2001 11 10 4 – – Certain surgical contacts of patients diagnosed
with CJD 196 161 [d] 140 [e] – – Highly transfused patients 11 10 5 – – Total
for ‘at risk’ groups where PHE holds data 431 348 [f] 286 [f] 3 1 Patients with
bleeding disorders who received UK-sourced plasma products 1980-2001 [a] 3,977
National information incomplete National information incomplete – 1 Recipients
of human-derived growth hormone [a] 1,883 1,883 1,503 75 – Total for all ‘at
risk’ groups [a] 6,291 At least 2,231 At least 1,789 78 2
a. These are minimum figures. Central reporting for bleeding disorder
patients is incomplete, and a small number of patients have opted out of the
central UKHCDO database. A small number of ‘at risk’ growth hormone recipients
are not included in the Institute of Child Health study. Not all of ‘at risk’
growth hormone recipients have been notified. There is no central record of who
has been informed.
b. An asymptomatic infection is when an individual does not exhibit any of
the signs and symptoms of CJD in life but abnormal prion protein indicative of
CJD infection has been found in tissue obtained from them. In these cases the
abnormal prion protein was identified at post mortem.
c. One patient was notified by proxy.
d. Five of these notified by proxy.
e. Three of these were notified by proxy.
f. Includes patients notified by proxy.
2. Updated guidance on decontamination of equipment for gastrointestinal
endoscopy
The British Society of Gastroenterology have updated their guidance on
decontamination of equipment for gastrointestinal endoscopy [1]. The update
includes revised advice for management and decontamination of endoscopes after
they have been used for procedures on individuals at risk of variant CJD. This
aligns with Department of Health guidance, CFPP 01-06, published in April 2013
[2], which recommended that: There is no longer a requirement to quarantine
endoscopes following an “invasive” procedure on patients at risk of vCJD (with
very few exceptions); a single quality assured decontamination cycle following
recommended guidelines is considered sufficient, but the endoscope should be
decontaminated separately from others with a single-use disinfectant; routine
traceability data should be available to demonstrate thorough reprocessing;
‘Single use’ accessories should always be used in preference to reusable
accessories.
The ACDP TSE specific guidance on endoscopy, Transmissible Spongiform
Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex F
[3], which builds on the recommendations from the BSG guidance has been updated.
2.1 References 1. SG Guidance on Decontamination of Equipment for
Gastrointestinal Endoscopy (2014) . 2. Management and decontamination of
flexible endoscopes (CFPP 01-06) (2013): Policy and Management. 3. Transmissible
Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection:
Annex F (2014).
This report was published in Health Protection Report volume 8 issue 31.
Wednesday, September 10, 2014
*** Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with
updated guidance on decontamination of gastrointestinal endoscopy equipment
Research and analysis
Monday, July 28, 2014
*** Mitigating the Risk of Transmission and Environmental Contamination of
Transmissible Spongiform Encephalopathies 2013 Annual Report
Thursday, October 25, 2012
Current limitations about the cleaning of luminal endoscopes and TSE prion
risk factors there from
Article in Press
Saturday, January 16, 2010
*** Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary
to Bramble et al ***
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
Terry S. Singeltary Sr., P.O. BOX 42, Bacliff, Texas 77518 USA
Professor Michael Farthing wrote:
Louise Send this to Bramble (author) for a comment before we post. Michael
snip...
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
I have researched human/animal TSEs now for over 5 years due to the death
of my Mother from the Heidenhain Variant Creutzfeldt Jakob disease, one of six -
known - variants of the infamous 'sporadic' CJD.
I did a little survey several years ago about CJD and ENDOSCOPY in 2001,
and then went there again when another article was released recently. However,
they seemed to only be concerned with the vCJD strain and risk from endoscopy
equipment.
My concerns are if vCJD can be transmitted by blood, and there are now 6
variants of the infamous sporadic CJDs that they are documenting to date, how do
they know that none of these 6 variants will not transmit the agent (prion) via
blood?...especially since the sporadic CJDs are the only ones documented to date
to transmit via the surgical arena and now that the CWD is spreading more and
more, who knows about the cattle?
I would always read this study and it would bring me back to reality as to
how serious/dangerous this agent is in the surgical/medical arena. You might
want to read this short abstract from the late, great Dr. Gibbs twice, and let
it really sink in. And please remember while reading some of these transmission
studies, that most all, if not ALL these agents transmit freely to primates.
Humans, of course, are primates.
Regarding claims that:
'Well, it has never been documented to transmit to humans."
There are two critical factors to think about:
A. CJD/TSEs in the USA are NOT reportable in most states and there is NO
CJD/TSE questionnaire for most victims and their families, and the one they are
now issuing asks absolutely nothing about route and source of the (prion) agent,
only how the disease was diagnosed. Furthermore, the elderly are only very
rarely autopsied, ie looking for Alzheimer's or 'FAST Alzheimer's' OR prion
disease-related factors and phenomena, such as heart failure caused by
disease.
B. It is unethical and against the law to do transmission studies of TSEs
to humans, they are 100% FATAL.
I suggest you read these case studies about medical arena CJD transmission
very carefully:
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD
20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Tissue Infectivity and TSEs (brain = high / rectum = medium)
snip...see full text ;
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3
re-Singeltary to Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
EFSA supporting publication 2014:EN-559 Any enquiries related to this
output should be addressed to biohaz@efsa.europa.eu. The TSEi model is available
upon request to biohaz@efsa.europa.eu. Suggested citation: Amie Adkin, Robin
Simmons and Mark Arnold, 2014. TSE infectivity model (TSEi) in animal tissues:
Bovine intestines and mesenteries. EFSA supporting publication 2014:EN-559, 74
pp. Available online: www.efsa.europa.eu/publications © European Food Safety
Authority, 2014 EXTERNAL SCIENTIFIC REPORT TSE infectivity model (TSEi) in
animal tissues: Bovine intestines and mesenteries1 Adkin A, Simons R, and Arnold
M Animal Health and Veterinary Laboratories Agency (AHVLA), Weybridge, United
Kingdom
ABSTRACT A stochastic quantitative risk assessment (QRA) has been developed
to (1) compare the level of infectivity of different TSE agents in animal
tissues, (2) estimate the impact of amendments to the list/age for the removal
of SRM on residual TSE infectivity levels for a single infected animal and at
the country level per year, and (3) estimate the impact of certain processing
technologies on residual TSE infectivity in selected animal tissues or products.
In this report the QRA is focused on bovine intestines and mesentery. The tissue
types identified for quantitative modelling are: ileum, duodenum, jejunum,
caecum, colon, mesenteric lymph nodes, mesenteric nerves and the celiac and
mesenteric ganglion complex (CMGC). Of these tissues processed products include
bovine intestines (duodenum, jejunum, caecum, and colon) used to produce sausage
casings and the rendering of fats from mesentery tissues. The ileum is not
processed for human consumption. This report describes the model approach taken
together with the parameterization for each tissue type conceptually divided
into five different components: surveillance, abattoir, SRM, processing, and
infectivity. Both uncertainty and variability associated with input data have
been included separately in the model where estimates are known. A baseline
model has been completed using surveillance and demographic data from 2012. Two
case studies are also provided, the retrospective analysis of the estimated
amount of infectivity in the healthy slaughter and emergency slaughter streams
by age at slaughter (2007-2011), and the amount of infectivity accumulating
during a theoretical re-emergence of BSE. Results are provided based on the
current parameterization and include associated quantifiable uncertainty and
variability. When developing the risk assessment a number of assumptions were
made which need to be considered when reviewing results.
© Animal Health and Veterinary Laboratories Agency (AHVLA), Weybridge,
United Kingdom, 2014 KEY WORDS Bovine Spongiform Encephalopathies, BSE, risk
assessment, mathematical model, bovine intestines, mesentery tissues DISCLAIMER
The present document has been produced and adopted
snip...
10. Conclusions This report describes the model framework developed to
compare the pattern of BSE infectivity in selected animal tissues (bovine
intestines and mesenteries) for an individual infected animal. The model also
estimates infectivity at the member state, or group of member states level by
age at slaughter over one year, results provided in this report for the EU27,
and includes the impact of certain processing technologies (sausage casing
processing) on residual BSE infectivity. Case studies are provided estimating
the annual infectivity historically and in the situation of a future
re-emergence of disease. Results, where appropriate, are stratified by age at
slaughter, infectivity by meter length (for bovine intestinal tissues), tissue
type, and pre and post processing. ...see full text.
Cattle All ages • The tonsils, the intestines, from the duodenum to the
rectum, and the mesentery;
4. Processes regarding the removal or inactivation of transmissible
spongiform encephalopathy (TSE) agents (i.e., prions) from contaminated medical
devices. Please note that as of the date of this guidance, FDA has not approved
or cleared medical devices, including sterilizers, for the intended use of
reducing the infectivity of TSE agents.
nothing on TSE Prions ;
Interpretation Our findings suggest that the possible risk of vCJD linked
to endoscopic procedures might be currently underestimated. Human iatrogenic
vCJD cases infected intravenously raise the same public-health concerns as
primary cases and need the same precautionary measures with respect to blood and
tissue donations and surgical procedures.
We noted that PrPres was present in lymphoreticular tissues such as spleen
and tonsils and in the entire gut from the duodenum to the rectum.
March 26, 2015
URGENT SAFETY NOTIFICATION IMPORTANT UPDATED LABELING INFORMATION: NEW
REPROCESSING INSTRUCTIONS FOR THE OLYMPUS TJF-Q180V DUODENOSCOPE
ATTENTION: Endoscopy Department, Risk Management and Reprocessing
Units
Dear Health Care Professional:
Dr. Linda Detwiler
03-025IF 03-025IF-631 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-631
Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. Page
9. Page 10. Page 11. Page 12.
Intestine
The scenario describe above is essentially true for the intestine.
Infectivity was readily detectable in the distal ileum of cattle infected with
BSE. While certain additional sections of the intestine were tested with no
infectivity identified, not every section of the intestine was included in the
bioassays. Positive immunostaining for Prpres was identified along the length of
the intestine providing evidence for the entire intestine to be considered as
SRM per EU regulations. (personal communication Danny Matthews, UK, VLA). The
International Advisory Committee appointed by Secretary Veneman also recommended
that the SRM ban in the US be amended to the entire intestine from duodenum to
rectum. I recommend that the USDA adjust the definition of SRM to include the
entire intestine from the duodenum to the rectum .
snip...
see full text ;
03-025IF 03-025IF-634 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-634
Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8.
Linda A. Detwiler, DVM
225 Hwy 35
Red Bank, New Jersey 07701
Phone: 732-741-2290
Cell: 732-580-9391
Fax: 732-741-7751
June 22, 2005
FSIS Docket Clerk
U.S. Department of Agriculture Food Safety and Inspection Service 300 12th
Street, SW. Room 102 Cotton Annex Washington, DC 20250
RE: DEPARTMENT OF AGRICULTURE Food Safety and Inspection Service
9 CFR Parts 301, 309, 310, 311, 313, 318, 319 and 320
Prohibition of the Use of Specified Risk Materials for Human Food and
Requirements for the Disposition of Non-Ambulatory Disabled Cattle; Meat
Produced by Advanced Meat/Bone Separation Machinery and Meat Recovery (AMR)
Systems;
Prohibition of the Use of Certain Stunning Devices Used To Immobilize
Cattle During Slaughter; Bovine Spongiform Encephalopathy (BSE) Surveillance
Program
Docket Number 03-025IF: Prohibition of the Use of Specified Risk Materials
for Human Food and Requirements for the Disposition of Nonambulatory Disabled
Cattle
I am writing to clarify a comment I submitted to the above mentioned docket
on May 7, 2004. I had previously written that the entire length of the intestine
should be excluded as SRM. I still hold this opinion and submit the same
recommendation, however one of the reasons behind this opinion needs to be
further clarified. I had misunderstood comments made by Dr. Danny Matthews in
that immunostaining (of PrPbse) was not found throughout the entire length of
the intestine. There was however immunostaining in the myenteric plexus of the
distal ileum in both naturally infected and experimentally challenged cattle
with BSE. (Terry et al.,2003) Given that the myenteric plexus exists throughout
the intestine one cannot eliminate the possibility of infectivity being in other
sections. In fact this was some of the thought behind the designation of the
entire intestine as SRM in the EU:
In its opinion of 7-8 December 2000 (EC 2000), the SSC concluded that the
entire bovine intestine is a risk issue and Commission Regulation (EC) No.
270/2002 (14th February 2002) ANNEX II designates “the entire intestines
from the duodenum to the rectum and the mesentery of bovine animals of all
ages;” as SRM. Also, in the SSC opinion of 28-29 JUNE 2001, Adipose tissue
associated with the digestive tract of cattle, sheep and goats: an appreciation
of possibleTSE risks (EC 2001) the view was expressed that for cattle, “due to
the infectivity titre that could be theoretically reached in nervous tissues and
in some parts of intestine, and due to the risk of contamination with intestine
tissue….
The International Advisory Committee appointed by Secretary Veneman also
recommended that the SRM ban in the US be amended to the entire intestine from
duodenum to rectum.
Although certain additional sections of the intestine were tested with no
infectivity identified, not every section of the intestine was included in the
bioassays. In addition, the study involving immunostaining was also extremely
limited in regard to the testing of tissues other than the distal ileum.
Specifically, other sections of intestinal tissues (excluding the distal ileum
work) were limited to those collected from 3 calves inoculated with BSE at a
timeframe of 6 months post inoculation. Instead of assuming that the untested
sections are devoid of infectivity, it is my belief that we should err on the
side of caution when it comes to protecting public health. Hence I maintain my
opinion that the entire intestine should be considered SRM.
This clarification is also intended for my comments submitted to the FDA’s
ANPR.
Thank you for the opportunity to clarify my comments.
Linda A. Detwiler, DVM
REFERENCES
Terry, L. A.., Marsh, S., Ryder, S. J., Hawkins, S. A. C., Wells, G. H.,
and Spencer, Y. I. (2003) Detection of disease-specific PrP in the distal ileum
of cattle exposed orally to the agent of bovine spongiform encephalopathy. Vet
Rec., 152, 387-392 Wells G.A.H., Dawson M., Hawkins, S.A.C., Green R. B., Dexter
I., Francis M. E., Simmons M. M., Austin A. R., & Horigan M. W. (1994)
Infectivity in the ileum of cattle challenged orally with bovine spongiform
encephalopathy. Vet. Rec., 135, 40-41. Wells G.A.H., Hawkins, S.A.C., Green R.
B., Austin A. R., Dexter I., Spencer, Y. I., Chaplin, M. J., Stack, M. J., &
Dawson, M. (1998) Preliminary observations on the pathogenesis of experimental
bovine spongiform encephalopathy (BSE): an update. Vet. Rec., 142, 103-106.
snip...
see full text ;
WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform
Encephalopathies Updated 2010
snip...
Table IB: Lower-infectivity tissues Humans Cattle Sheep & goats Elk
& deer vCJD Other TSEs BSE Scrapie CWD Tissues Infectivity1 PrPTSE
Infectivity1 PrPTSE Infectivity1 PrPTSE Infectivity1 PrPTSE Infectivity1 PrPTSE
Table IB: Lower-infectivity tissues
Alimentary tract5
Esophagus NT - NT - - NT [+] + NT +
Fore-stomach6
(ruminants only) NA NA NA NA - NT [+] + NT +
Stomach/
abomasum NT - NT - - NT [+] + NT +
Duodenum NT - NT - - - [+] + NT +
Jejunum7 NT + NT - - + [+] + NT NT
Ileum7 NT + NT - + + + + NT +
Appendix (-) + NT - NA NA NA NA NA NA
Colon/caecum7 NT + NT - - - + + NT +
Rectum [+] + NT NT NT NT NT + NT +
snip...
EFSA Journal 2014;12(7):3798
Suggested citation: European Food Safety Authority, 2014.
Protocol 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 Available
online: www.efsa.europa.eu/efsajournal © European Food Safety Authority, 2014
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
1 On request from the European Commission, Question No EFSA-Q-2013-01015,
approved on 11 July 2014.
2 Correspondence: biohaz@efsa.europa.eu
3 Acknowledgement: 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.
snip...
Atypical BSE study protocol
EFSA Journal 2014;12(7):3798 16
2.3. Additional information on material available
Data available from the literature relating to field case examinations, the
EURL study and the other transmission studies outlined above (Section 2.1) have
been collated to provide a comprehensive list of the tissue samples that have
been collected and examined from natural and experimental cases of H-BSE and
L-BSE. The full list is given in Appendix A and represents a wide range of
tissues from both the central and peripheral nervous systems, the
lymphoreticular system, the musculoskeletal system and the gastrointestinal
tract, together with other principal edible organs. However, none of these
studies was explicitly designed to address the issue of potential infectivity in
the context of the current legislation on SRM, and so there are some SRM tissues
that have not been collected within any of these studies, namely the duodenum,
the jejunum and ileum (without Peyer’s patches), the caecum, the colon and the
mesenteric fat. For these tissues there are therefore no data, and no
possibility to create data without undertaking further experimental challenges.
All of the experimental material is derived from animals that have been
challenged intracerebrally. In total, data are available for 15 experimental
H-BSE and 23 L-BSE cases, representing challenges with 4 donors respectively,
while data on PrP distribution in naturally-occurring field cases have been
published for only three L-BSE-affected cattle.
There are no data for field case H-BSE. Where data exist from both field
cases and experimental animals (i.e. for L-BSE only), there is good agreement
between the data with and abnormal PrP distribution, with the CNS and muscles
both consistently affected. However, these data relate to the presence or
absence of PrPSc, and do not attempt to quantify relative amounts of PrPSc or
levels of infectivity. Overall, disease-related PrP has been reported in CNS
tissues, peripheral ganglia and nerves, muscles (predominantly muscle spindles),
adrenal glands and retina for both H-BSE and L-BSE. By contrast, no lymphoid
tissues or gastrointestinal tissues have tested positive by IHC, WB or bioassay.
Some tissues have been collected, but with no testing outcome explicitly
reported.
Comparative data relating to C-BSE (see Appendix A, Table 12) are to a
large extent fragmented, and have evolved over a long period as different
analytical methods have been developed and applied. Many of the original
infectivity data are based on conventional mouse bioassay rather than transgenic
models so, although positive results are robust, negative results do not
necessarily have the same sensitivity thresholds (see also EFSA BIOHAZ Panel
(2014)). It must also be noted that data available for C-BSE are derived
predominantly from field cases or oral challenge models. There are few data from
i.c. challenge studies that can be directly compared with existing data for
Atypical BSE. However, collective data indicate that C-BSE shares the same
tissue distribution as the Atypical BSE cases, with PrPSc and/or infectivity
detected in the central and peripheral nervous systems, including ganglia and
nerves, and the muscle spindles in skeletal muscle. As in Atypical BSE, the
adrenal glands and the retina are also affected.
Additionally, in C-BSE there is also evidence of involvement of the
lymphoreticular system, particularly, but not exclusively, in those tissues
associated with the gastrointestinal tract. The PrPSc distribution and relative
levels of infectivity in the gastrointestinal tissues were presented in detail
in a previous EFSA Opinion (EFSA BIOHAZ Panel, 2014). Nasal mucosa and bone
marrow have also been shown to contain infectivity.
There are insufficient data at present to be clear about whether these
apparent differences in the distribution of disease-specific markers reflect
absolute differences between C-BSE and the H-BSE and L-BSE variants, whether
they are a consequence of detection threshold limitations, or whether they are a
consequence of the different routes of challenge. Atypical BSE study
protocol
EFSA Journal 2014;12(7):3798 17
2.4. Concluding remarks Where data exist from both field cases and
experimental animals (i.e. for L-BSE only), there is good agreement of the data
with regard to abnormal PrP distribution. There are no data for field case
H-BSE. All data currently available relate to the presence or absence of PrPSc,
but do not quantify relative amounts of PrPSc or levels of infectivity.
Disease-related PrP has been reported consistently in CNS tissues, peripheral
ganglia and nerves, muscles (predominantly muscle spindles), adrenal glands and
retina for both H-BSE and L-BSE. All of these tissues are also positive in
C-BSE. By contrast with C-BSE, at this stage no lymphoid tissues or
gastrointestinal tissues from H-BSE- and L-BSE-affected animals have tested
positive for PrPSc presence (IHC, WB) or infectivity (bioassay). There are
insufficient data at present to be clear about whether these apparent
differences in the distribution of disease-specific markers reflect absolute
differences between C-BSE and the H-BSE and L-BSE variants, whether they are a
consequence of detection threshold limitations, or whether they are a
consequence of the different
Research Article
Prion Protein Gene Variability in Spanish Goats. Inference through
Susceptibility to Classical Scrapie Strains and Pathogenic Distribution of
Peripheral PrPsc Cristina Acín ,
Inmaculada Martín-Burriel,
Eva Monleón,
Jaber Lyahyai,
José Luis Pitarch,
Carmen Serrano,
Marta Monzón,
Pilar Zaragoza,
Juan José Badiola
PLOS
Published: April 8, 2013 •DOI: 10.1371/journal.pone.0061118 Detection of
PrPsc in peripheral organs.
snip...
PrPsc was detected in the tonsils, iliac, axillary, pre-scapular,
submandibular, popliteal, and mammary lymph nodes of the six goats analyzed, but
just in five in the mediastinal and mesenteric lymph nodes, ileal and jejunal
Peyer patches, ileocaecal valve and spleen. The enteric nervous system was
positive throughout the whole intestine, from duodenum to rectum, in the five
animals in which PrPsc was also detected in all the areas of the CNS (see Table
1).
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European ***
Monday, November 3, 2014
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
National Prion Disease Pathology Surveillance Center Cases Examined1
(October 7, 2014)
***6 Includes 11 cases in which the diagnosis is pending, and 19
inconclusive cases;
***7 Includes 12 (11 from 2014) cases with type determination pending in
which the diagnosis of vCJD has been excluded.
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob
disease (sCJD),
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
***and 21 cases of sporadic Fatal Insomnia (sFI).
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE
Prion: Case Report
Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies
diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type
disease
what is CJD ? just ask USDA inc., and the OIE, they are still feeding the
public and the media industry fed junk science that is 30 years old.
why doesn’t some of you try reading the facts, instead of rubber stamping
everything the USDA inc says.
sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and
there is much concern now for CWD and risk factor for humans.
My sincere condolences to the family and friends of the House Speaker Becky
Lockhart. I am deeply saddened hear this.
with that said, with great respect, I must ask each and every one of you
Politicians that are so deeply saddened to hear of this needless death of the
Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am
seriously going to ask you all this...I have been diplomatic for about 17 years
and it has got no where. people are still dying. so, are you all stupid or
what??? how many more need to die ??? how much is global trade of beef and other
meat products that are not tested for the TSE prion disease, how much and how
many bodies is this market worth?
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed
with the extremely rare Creutzfeldt-Jakob disease
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report ***
Tuesday, November 04, 2014
Towards an Age-Dependent Transmission Model of Acquired and Sporadic
Creutzfeldt-Jakob Disease
Thursday, January 22, 2015
Transmission properties of atypical Creutzfeldt-Jakob disease: a clue to
disease etiology?
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.
PLEASE REMEMBER ;
The Akron, Ohio-based CJD Foundation said the Center for Disease Control
revised that number in October of 2004 to about one in 9,000 CJD cases per year
in the population group age 55 and older.
HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO
ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???
if not, why not...
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type
prion disease, what it ???
Sunday, February 08, 2015
FDA SCIENCE BOARD TO THE FOOD AND DRUG ADMINISTRATION BOVINE HEPARIN BSE
CJD TSE PRION Wednesday, June 4, 2014
Tuesday, March 5, 2013
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening
of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
FDA believes current regulation protects the public from BSE but reopens
comment period due to new studies
Wednesday, June 19, 2013
Spreading of tau pathology in Alzheimer's disease by cell-to-cell
transmission
Wednesday, January 28, 2015
Another new prion disease: relationship with central and peripheral
amyloidoses
here we go again...
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment ;
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
From: laura.storms@olympus.com
Sent: Monday, March 30, 2015 8:11 AM
To: Terry S. Singeltary Sr.
Subject: Re: Fw: Design of Endoscopic Retrograde Cholangiopancreatography
(ERCP) Duodenoscopes May Impede Effective Cleaning: FDA Safety
Communication
Dear Mr. Singeltary - thank you for contacting me and I will ask an Olympus
representative to respond to your question. As duodenoscopes do not contact
tissue at high risk associated with CJD, can you please advise on specifically
what is your request.
Regards,
Laura Storms V.P., Regulatory/Clinical Affairs & Quality Assurance
Olympus Corporation of the Americas 3500 Corporate Parkway Center Valley PA
18034 Phone (484) 896-5688 Cell (631) 871-1724 laura.storms@olympus.com
From: "Terry S. Singeltary Sr." flounder9@verizon.net
Date: 03/27/2015 01:44 PM
Subject: Fw: Design of Endoscopic Retrograde Cholangiopancreatography
(ERCP) Duodenoscopes May Impede Effective Cleaning: FDA Safety Communication
--------------------------------------------------------------------------------
Greetings Olympus et al, RE- http://medical.olympusamerica.com/sites/default/files/pdf/150326_TJF-Q180V_Customer_letter.pdf
In reference to the latest incident of deaths from the use of these
endoscopy equipment, what is Olympus recommendations, requirements, and
guarantees, for disinfection against the CJD Transmissible Spongiform
Encephalopathy TSE PRION type disease ? thank you, kind regards, terry snip...
Saturday, December 13, 2014
*** Terry S. Singeltary Sr. Publications TSE prion disease Peer Review ***
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
some old history on Endoscopy equipment and CJD TSE Prion concerns ; 1999
Subject: CJD * Olympus Endoscope
Date: Sun, 10 Oct 1999 16:41:49 –0500
From: "Terry S. Singeltary Sr."
Saturday, February 21, 2015
Design of Endoscopic Retrograde Cholangiopancreatography (ERCP)
Duodenoscopes May Impede Effective Cleaning: FDA Safety Communication
Sunday, April 5, 2015
*** Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed
On-Farm Draft Guidance FDA-2014-D-1180 ***
all iatrogenic CJD TSE prion disease is, is sporadic cjd TSE prion
disease, until the iatrogenic event is discovered, documented, and put in the
public domain. this very seldom happens due to trace back efforts, and the very
industry that refuses to do any trace back for CJD, or any TSE prion disease.
...
kind regards, terry
posted by Terry S. Singeltary Sr. at
10:11 AM
