Volume 18, Number 6—June 2012
CME ACTIVITY
Iatrogenic Creutzfeldt-Jakob Disease, Final Assessment
Paul Brown , Jean-Philippe Brandel, Takeshi Sato, Yosikazu Nakamura, Jan
MacKenzie, Robert G. Will, Anna Ladogana, Maurizio Pocchiari, Ellen W. Leschek,
and Lawrence B. Schonberger Author affiliations: Centre à l’Energie Atomique,
Fontenay-aux-Roses, France (P. Brown); Institut National de la Santé et de la
Recherche Médicale, Paris, France (J.-P. Brandel); Nanohana Clinic, Tokyo, Japan
(T. Sato); Jichi Medical University, Yakushiji, Japan (Y. Nakamura); Western
General Hospital, Edinburgh, Scotland, UK (J. MacKenzie, R.G. Will); Istituto
Superiore de Sanità, Rome, Italy (A. Ladogana, M. Pocchiari); National
Institutes of Health, Bethesda, Maryland, USA (E.W. Leschek); Centers for
Disease Control and Prevention, Atlanta, Georgia, USA (L.B. Schonberger)
Abstract
The era of iatrogenic Creutzfeldt-Jakob disease (CJD) has nearly closed;
only occasional cases with exceptionally long incubation periods are still
appearing. The principal sources of these outbreaks are contaminated growth
hormone (226 cases) and dura mater grafts (228 cases) derived from human
cadavers with undiagnosed CJD infections; a small number of additional cases are
caused by neurosurgical instrument contamination, corneal grafts, gonadotrophic
hormone, and secondary infection with variant CJD transmitted by transfusion of
blood products. No new sources of disease have been identified, and current
practices, which combine improved recognition of potentially infected persons
with new disinfection methods for fragile surgical instruments and biological
products, should continue to minimize the risk for iatrogenic disease until a
blood screening test for the detection of preclinical infection is validated for
human use.
The first case of what would eventually become a major outbreak of
iatrogenic Creutzfeldt-Jakob disease (CJD) was reported in 1974; the patient had
received a corneal transplant from an infected cadaver (1). In the years that
followed, other sources of infection were identified: stereotactic
electroencephalogram electrodes, neurosurgical instruments, cadaveric dura mater
and pituitary glands, and, most recently, secondary variant CJD (vCJD) blood
products. The ensemble of iatrogenic cases, including a bibliography of primary
references, was last reviewed in 2006 (2). Today, after nearly 40 years of
surveillance, the chronology and essential characteristics of iatrogenic CJD
have been finalized, and the purpose of this article is to present these data
along with a few brief comments about factors that determined the risk for
infection and how future risks might be foreseen and avoided.
By far the most common sources of iatrogenic disease were human cadavers
from which pituitary hormones and dura mater grafts were obtained (Table 1;
Figure); the other major variety of environmentally acquired disease is vCJD.
The incidence curves of human growth hormone–associated and dura
mater–associated CJD are almost superimposable; a broad peak occurred in the
mid-to-late 1990s, just ahead of the sharper peak incidence of vCJD in the
United Kingdom at the turn of the century. The incidence in other countries
peaked a few years later, in 2004, as a result of the delayed appearance of
bovine spongiform encephalopathy in those countries.
The long incubation periods—years to decades—of these low-dose infections
pose a particularly difficult problem for public health officials, whose
recommendations may diminish the number of new cases but are impotent when it
comes to preventing cases in already-infected persons in the preclinical phase
of disease. It is worth remembering that the early recognition of iatrogenic
sources of CJD was entirely because of a few remarkably astute neurologists,
neurosurgeons, and, astonishingly, a pediatric endocrinologist who pursued the
unlikely (and unpopular) diagnosis of CJD in a growth hormone recipient (3). It
is true that some of these connections had the benefit of comparatively short
intervals between the infecting events and the onset of CJD. It is especially
fortunate from the standpoint of early recognition of the dura mater association
that the interval of 19 months between the operation and onset of symptoms in
the first case-patient was among the shortest on record for this form of
iatrogenic CJD (Table 2).
Human Growth Hormone
The current worldwide total of growth hormone–associated cases of CJD is
226. Most cases occurred in France (119 cases/1,880 recipients; attack rate
6.3%), the United Kingdom (65 cases/1,800 recipients; attack rate 3.6%), and the
United States (29 cases/7,700 recipients; attack rate 0.4%).
In France, further epidemiologic observations have revealed that all 119
cases occurred within a 1,170-patient cohort receiving treatment during a
20-month period, from December 1983 through July 1985, when there seems to have
been substantial contamination resulting from sourcing and processing
deficiencies. According to these numbers, the attack rate for the at-risk cohort
in France increases to 10.2%. No new case has been identified since 2008. In the
United Kingdom, no cohort pattern is evident, and cases continue to occur at an
average rate of about 2 per year (only 1 in 2011). In the United States, CJD has
not occurred in any patient who started treatment after 1977, when a highly
selective column chromatography step was introduced into the purification
protocol. Since 2003, only 2 new cases have been identified (1 in 2007 and 1 in
2009). An estimated ≈2,700 patients received treatment before 1977, so the
attack rate in the United States for this at-risk cohort increases to 1.1% (4).
The revised attack rates therefore become 10.2% in France, 3.6% in the United
Kingdom, and 1.1% in the United States.
The methionine (M)/valine polymorphism at codon 129 of the PRNP gene has
been examined in populations with and without CJD in many countries; results
have varied (Table 3). Overall, it is clear that the M allele bestows
substantial susceptibility to the sporadic and the iatrogenic forms of CJD; in
consequence, the proportion of persons with MM homozygous genotype is
overrepresented in both categories of disease (the sole exception occurred in UK
growth hormone recipients, which led to speculation that a different strain of
the pathogenic agent might have been disseminated) (10). It is also clear that,
as a group, persons with heterozygous genotype had longer incubation periods
than did those with homozygous genotype, particularly in France. Notwithstanding
this statistical conclusion, it is noteworthy that several persons with MM
homozygous genotype had incubation periods >30 years, including a patient
with recently diagnosed CJD, whose incubation period was 42 years, the current
world record for any type of iatrogenic disease.
Incubation periods for the total case population (not just those examined
for the codon 129 genotype) ranged from 5 to 42 years (mean 17 years), based on
the interval between the midpoint date of what was almost always a multiyear
period of treatment and the onset of CJD symptoms; the actual date of infection
is impossible to determine. Mean incubation periods for cases in the United
States and New Zealand (patients received hormone made in the United States)
were 22 and 26 years; United Kingdom, 20 years; and France, 13 years. The
shorter incubation periods in France could have resulted partly from the
narrower limit for the date of infection in France and are in accord with the
mean incubation period of 13.5 years in the 4 gonadotropin recipients from
Australia, for whom there is an even more precise date of infection. However, a
greater contribution probably came from different infectious doses received by
patients in the different countries. Among all patients, the clinical features
were distinctive in that, unlike sporadic CJD, signs and symptoms almost never
included dementia, which, if it occurred at all, was typically a late component
of the clinical course.
Dura Mater
The worldwide tally of dura mater–associated cases is 228, and new cases
still continue to occur here and there, the most recent being individual cases
in Austria, South Korea, and the Netherlands in 2011. If the pharmaceutical
industry (in contrast to government-sponsored laboratories) comes away from the
growth hormone story with an almost untainted record—only 1 case has been
attributed to industrially prepared hormone (11)—the same cannot be said about
the private sector producing dura mater grafts. The source of almost all
infections was a manufacturer in Germany, B. Braun Melsungen AG, which has a
worldwide distribution network, and the incidence of CJD appears to have more or
less paralleled the frequency with which this source of dura mater was used. In
Japan, it is estimated that as many as 20,000 patches may have been used each
year, and the 142 cases in that country constitute two thirds of the global
total. Nevertheless, the overall attack rate in the at-risk patient population
in Japan is <0.03%. For the entire (worldwide) group of dura mater–recipient
patients, incubation periods ranged from 1.3 to 30 years (mean 12 years), and,
except in Japan, the clinical and neuropathologic features were similar to those
of sporadic CJD. In Japan, approximately one third of the cases had atypical
features (slow progression, noncharacteristic electroencephalogram tracings,
plaque deposition, and an atypical prion protein molecular signature on Western
blots), which suggested the possibility of 2 different strains of infecting
agent (12,13). One patient had florid plaques and a pulvinar sign on magnetic
resonance imaging, mimicking vCJD (5).
Evaluation of the influence of the codon 129 genotype is complicated by the
fact that the population in Japan, among whom most cases occurred, has a high
frequency of the M allele (>90%), which dominated sporadic and dura
mater–associated forms of CJD (Table 3) (6–9,14,15). Among the cases in persons
not from Japan, the distribution of genotypes approximated that found among
patients with sporadic CJD, and, as with growth hormone–associated cases,
incubation periods were somewhat longer for persons with heterozygous than with
homozygous genotypes.
Current Prevention Strategies
The best way to abolish secondary iatrogenic infections is, obviously, to
prevent primary infections, but without a test to identify infected but
asymptomatic persons, we cannot entirely eliminate the risk inherent in
human-to-human tissue transfer. We are therefore obliged to rely on the default
strategies of 1) identification and donor deferral of persons at higher than
normal risk for CJD development and 2) inclusion of prion-reduction steps in the
sterilization of penetrating instruments and the processing of therapeutic
tissues and fluids.
Delineation of high-risk categories initially focused on precisely those
groups of persons who were exposed to the known sources of iatrogenic disease:
recipients of cadaveric dura mater grafts or pituitary-derived hormones. When
vCJD started to occur, restrictions were also placed on donor time of residence
in the most heavily infected regions—the United Kingdom and, to a lesser extent,
continental Europe—and embargoes were placed on the importation of biological
products from these regions. These deferral and import restrictions remain in
place today and need some thoughtful reevaluation in view of the near extinction
of all such sources of iatrogenic CJD. In the United States, there have been
only 4 cases of dura mater–associated disease (the most recent in 2005) and no
case of growth hormone–associated CJD for anyone who began treatment after 1977.
On the other hand, the possibility of iatrogenic infection resulting from
transfer of tissues or fluids from persons who have contracted a prion disease
from animals has not disappeared with the abating epidemics of bovine spongiform
encephalopathy and vCJD. A few persons who may be experiencing a long incubation
phase of vCJD still pose an obvious danger in the United Kingdom, but an
underappreciated potential danger lies in 2 other animal diseases: scrapie and
chronic wasting disease (CWD). Although scrapie-infected sheep tissues have been
consumed for long enough (hundreds of years) to be considered harmless for
humans, the same cannot be said about the atypical strains of scrapie that are
beginning to displace the typical strains and with which we do not yet have
enough experience to evaluate human pathogenicity. Similarly, we cannot declare
with certainty that CWD poses no threat to humans, and CWD is continuing its
unchecked spread across the United States and Canada with no guarantee that it
will not become globally distributed in the years to come. One hunter has
already put a group of unwitting persons at risk for infection by donating a
deer, later found to have CWD, for consumption at a rural banquet in New York
State (16); more such exposures are likely to occur as CWD continues its
geographic expansion.
Future Prevention Strategies
The issue of reducing risk by taking steps to inactivate prions is always a
work in progress as new therapeutic products come into production and new
methods to inactivate prions are discovered. The tried-and-true laboratory
method of prion sterilization (1-hour exposures to either undiluted bleach or 1
N sodium hydroxide followed by steam autoclaving at 3 atmospheres pressure for
20 minutes) is applicable only to nonfragile instruments and not at all to
living tissues. The surprising resistance of dura mater to 0.1 N sodium
hydroxide (17) and of growth hormone to 6 M urea (18) led to their incorporation
into processing protocols before being replaced by nondural tissue or synthetic
patches and recombinant hormone. To reduce infectivity, blood, blood products,
and other fluids can be subjected to nanofiltration and prion-affinity ligands
(19–22), which should also be applicable to other biological products, for
example, vaccine and stem cell cultures, should they be susceptible to infection
(23). Fragile instruments such as endoscopes and electrodes remain a challenge,
but new and gentler methods— alkaline cleaning solutions, phenolics, and gaseous
hydrogen peroxide—have proven harmless to instruments and give a high, if not
always complete, degree of prion inactivation (24–26).
The ongoing refinement of a quaking-induced conversion detection of the
misfolded prion protein holds the best prospect of evolving into a sensitive and
practical tool, but it has yet to be validated in blind testing of plasma from
symptomatic patients or in presymptomatic persons, even more rigorous but
necessary (27,28). It may be necessary to use scrapie-infected animals for
presymptomatic validation because only 1 group of humans could furnish
appropriate samples—asymptomatic carriers of CJD-inducing mutations—and putting
together and testing a reasonable number of such samples will take years to
accomplish.
The total numbers of cases for the 2 major causes of iatrogenic CJD during
the past 40 years (226 growth hormone cases and 228 dura mater cases) are
amazingly close and are likely to remain so after the few additional
long-incubating cases finally surface in the next few years. The combination of
appropriate blood donor deferrals and the incorporation of tissue, fluid, and
instrument infectivity–reduction steps should continue to hold the sources of
potential iatrogenic disease to a minimum until such time as a practical
screening test for inapparent infection is validated for human use.
Dr Brown spent his career at the National Institutes of Health in the
Laboratory of Central Nervous System Studies conducting research on the
transmissible spongiform encephalopathies, especially with respect to
epidemiology, iatrogenic CJD, disinfection, and blood infectivity. He currently
chairs a scientific advisory committee for the Laboratoire Français du
Fractionnement et des Biotechnologies in Les Ulis, France, and advises the
Centre à l’Energie Atomique in Fontenay-aux-Roses, France.
Acknowledgment
Our profound thanks go to the physicians responsible for the earliest
identification of iatrogenic CJD infections and to the multitude of unsung
persons in many countries around the world who have worked diligently and
continuously to keep track of its global incidence.
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Figure
Figure. . . . Annual incidence of variant Creutzfeldt-Jakob disease (vCJD)
caused by ingestion of meat products contaminated with bovine spongiform
encephalopathy agent (A) and iatrogenic CJD caused by contaminated dura...
Tables
Table 1. Global distribution of cases of iatrogenic Creutzfeldt-Jakob
disease
Table 2. Incubation periods and clinical presentations of iatrogenic
Creutzfeldt-Jakob disease, according to source of infection
Table 3. Comparison of PRNP codon 129 genotype frequencies and incubation
periods in growth hormone– and dura mater–associated cases of iatrogenic CJD
Suggested citation for this article: Brown P, Brandel J-P, Sato T, Nakamura
Y, MacKenzie J, Will RG, et al. Iatrogenic Creutzfeldt-Jakob disease, final
assessment. Emerg Infect Dis [serial on the Internet]. 2012 Jun [date cited]. http://dx.doi.org/10.3201/eid1806.120116
DOI: 10.3201/eid1806.120116
Volume 18, Number 6—June 2012 CME ACTIVITY Iatrogenic Creutzfeldt-Jakob
Disease, Final Assessment MEDSCAPE CME Medscape, LLC is pleased to provide
online continuing medical education (CME) for this journal article, allowing
clinicians the opportunity to earn CME credit.
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Release date: May 16, 2012; Expiration date: May 16, 2013
Learning Objectives
Upon completion of this activity, participants will be able to:
• Distinguish the principal sources of iatrogenic CJD
• Identify countries with the highest rates of documented CJD
• Analyze the clinical presentation of iatrogenic CJD
• Assess new threats which might promote higher rates of CJD.
CME Editor
P. Lynne Stockton, Technical Writer/Editor, Emerging Infectious Diseases.
Disclosure: P. Lynne Stockton has disclosed no relevant financial relationships.
CME AUTHOR
Charles P. Vega, MD, Health Sciences Clinical Professor; Residency
Director, Department of Family Medicine, University of California, Irvine.
Disclosure: Charles P. Vega, MD, has disclosed no relevant financial
relationships.
AUTHORS
Disclosures: Paul Brown; Jean-Philippe Brandel; Takeshi Sato, MD; Yosikazu
Nakamura, MD, MPH, FFPH; Jan MacKenzie; Anna Ladogana; Ellen W. Leschek, MD; and
Lawrence B. Schonberger, MD, MPH, have disclosed no relevant financial
relationships. Robert G. Will, FRCP, has disclosed the following relevant
financial relationships: served as an advisor or consultant for LFB, Farring.
Maurizio Pocchiari, MD, has disclosed the following relevant financial
relationships: served as an advisor or consultant for LFB, Farring.
I hope and pray that Paul Brown et al rosey outlook is correct, and the
end of iatrogenic Creutzfeldt Jakob Disease is truly over, bbut, I have my
doubts. ...TSS
April 12, 2012
Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to
2010
Eurosurveillance,
Volume 17, Issue 15, 12
April 2012
Research articles
Sunday, May 6, 2012
Bovine Spongiform Encephalopathy Mad Cow Disease, BSE May 2, 2012 IOWA
State University OIE
Friday, May 11, 2012
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
SPONTANEOUS ??? NOT...
How the California cow got the disease remains unknown. Government
officials expressed confidence that contaminated food was not the source, saying
the animal had atypical L-type BSE, a rare variant not generally associated with
an animal consuming infected feed.
However, a BSE expert said that consumption of infected material is the
only known way that cattle get the disease under natural conditons. “In view of
what we know about BSE after almost 20 years experience, contaminated feed has
been the source of the epidemic,” said Paul Brown, a scientist retired from the
National Institute of Neurological Diseases and Stroke.
BSE is not caused by a microbe. It is caused by the misfolding of the
so-called “prion protein” that is a normal constituent of brain and other
tissues. If a diseased version of the protein enters the brain somehow, it can
slowly cause all the normal versions to become misfolded. It is possible the
disease could arise spontaneously, though such an event has never been recorded,
Brown said.
Proposal ID: 29403
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both disease, and it’s variants, in many cases are merely
names of the people that first discovered them. Both diseases are incurable and
debilitating brain disease, that are in the end, 100% fatal, with the
incubation/clinical period of the Alzheimer’s disease being longer than the TSE
prion disease. Symptoms are very similar, and pathology is very similar. I
propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation
disease, and that Alzheimer’s is Transmissible, and is a threat to the public
via the many Iatrogenic routes and sources. It was said long ago that the only
thing that disputes this, is Alzheimer’s disease transmissibility, or the lack
of. today, there is enough documented science (some confidential), that shows
that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and
or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and
one that needs to be addressed immediately.
Methods
Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.
Results
The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you
can take the ash and mix it with saline and inject that ash into a mouse, and
the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still
Infectious after Biodiesel Production as well. the TSE prion agent also survives
Simulated Wastewater Treatment Processes. IN fact, you should also know that the
TSE Prion agent will survive in the environment for years, if not decades. you
can bury it and it will not go away. TSE prion agent is capable of infected your
water table i.e. Detection of protease-resistant cervid prion protein in water
from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it
out and be done with. that’s what’s so worrisome about Iatrogenic mode of
transmission, a simple autoclave will not kill this TSE prion agent.
Conclusions
There should be a Global Congressional Science round table event (one of
scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics let science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already. what’s the use of science progressing human life to
the century mark, if your brain does not work?
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
Friday, February 10, 2012
Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential
iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous
Tonsil Archive
Thursday, December 29, 2011
Aerosols An underestimated vehicle for transmission of prion diseases?
PRION www.landesbioscience.com
please see more on Aerosols and TSE prion disease here ;
Saturday, February 12, 2011
Another Pathologists dies from CJD, another potential occupational death ?
another happenstance of bad luck, a spontaneous event from nothing, or
friendly fire ???
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare
and community settings part 4, Annex A1, Annex J,
UPDATE DECEMBER 2010
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of
Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
Thursday, September 02, 2010
NEUROSURGERY AND CREUTZFELDT-JAKOB DISEASE Health Law, Ethics, and Human
Rights The Disclosure Dilemma
Thursday, August 12, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were
distributed July-August 2010
Sunday, August 01, 2010
Blood product, collected from a donors possibly at increased risk for vCJD
only, was distributed USA JULY 2010
Thursday, July 08, 2010
Nosocomial transmission of sporadic Creutzfeldt–Jakob disease: results
from a risk-based assessment of surgical interventions Public release date:
8-Jul-2010
Thursday, July 08, 2010
GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010
Wednesday, June 02, 2010
CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003 Updated:
May 2010
Tuesday, May 11, 2010
Current risk of iatrogenic Creutzfeld–Jakob disease in the UK: efficacy of
available cleaning chemistries and reusability of neurosurgical instruments
Tuesday, May 04, 2010
Review of the Human Pituitary Trust Account and CJD Issue 20 January 2010
Tuesday, March 16, 2010
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Part 4 REVISED FEB. 2010
Monday, August 17, 2009
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Annex J,K, AND D Published: 2009
Monday, July 20, 2009
Pre-surgical risk assessment for variant Creutzfeldt-Jakob disease (vCJD)
risk in neurosurgery and eye surgery units
Friday, July 17, 2009
Revision to pre-surgical assessment of risk for vCJD in neurosurgery and
eye surgery units Volume 3 No 28; 17 July 2009
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June
12, 2009 (Singeltary submission)
Thursday, January 29, 2009
Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan,
1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number
2-February 2009 Research
Wednesday, August 20, 2008
Tonometer disinfection practice in the United Kingdom: A national survey
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition
2007 (occupational exposure to prion diseases)
Monday, December 31, 2007
Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in
Endodontic Practice in Absence of Adequate Prion Inactivation
Subject: CJD: update for dental staff
Date: November 12, 2006 at 3:25 pm PST
1: Dent Update. 2006 Oct;33(8):454-6, 458-60.
CJD: update for dental staff.
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
2011 TO 2012 UPDATE
Saturday, December 3, 2011
Candidate Cell Substrates, Vaccine Production, and Transmissible
Spongiform Encephalopathies
Volume 17, Number 12—December 2011
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of
Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE
RISE IN NORTH AMERICA
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1
(August 19, 2011) including Texas
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis
full text with source references ;
Subject: Bovine Spongiform Encephalopathy; Importation of Bovines and
Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68
Comment from Terry Singeltary Document ID: APHIS-2008-0010-0008 Document
Type: Public Submission This is comment on Proposed Rule: Bovine Spongiform
Encephalopathy; Importation of Bovines and Bovine Products Docket ID:
APHIS-2008-0010 RIN:0579-AC68
Topics: No Topics associated with this document View Document: More
Document Subtype: Public Comment Status: Posted Received Date: March 22
2012, at 12:00 AM Eastern Daylight Time Date Posted: March 22 2012, at 12:00 AM
Eastern Daylight Time Comment Start Date: March 16 2012, at 12:00 AM Eastern
Daylight Time Comment Due Date: May 15 2012, at 11:59 PM Eastern Daylight Time
Tracking Number: 80fdd617 First Name: Terry Middle Name: S. Last Name:
Singeltary City: Bacliff Country: United States State or Province: TX
Organization Name: CJD TSE PRION Submitter's Representative: CONSUMERS
Comment: comment submission Document ID APHIS-2008-0010-0001 Greetings
USDA, OIE et al, what a difference it makes with science, from one day to the
next. i.e. that mad cow gold card the USA once held. up until that fateful day
in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY.
what a difference a day makes$ now that the shoe is on the other foot, the USDA
via the OIE, wants to change science again, just for trade $ I implore the OIE
decision and policy makers, for the sake of the world, to refuse any status quo
of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE
GBR IV, for the following reasons. North America is awash with many different
TSE Prion strains, in many different species, and they are mutating and
spreading. IF the OIE, and whatever policy makers, do anything but raise the
risk factor for BSE in North America, they I would regard that to be highly
suspicious. IN fact, it would be criminal in my opinion, because the OIE knows
this, and to knowingly expose the rest of the world to this dangerous pathogen,
would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again.
I warned the OIE about all this, including the risk factors for CWD, and the
fact that the zoonosis potential was great, way back in 2002. THE OIE in
collaboration with the USDA, made the legal trading of the atypical Nor-98
Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al,
it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe.
IF you let them, they will do the same thing with atypical BSE and CWD (both
strains to date). This with science showing that indeed these TSE prion strains
are transmissible. I strenuously urge the OIE et al to refuse any weakening to
the USA trade protocols for the BSE TSE prion disease (all strains), and urge
them to reclassify the USA with BSE GBR IV risk factor. SEE REFERENCE SOURCES IN
ATTACHMENTS
SEE Terry S. Singeltary Sr. Attachment WORD FILE ;
Sunday, March 11, 2012
APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in
Line with International Animal Health Standards Proposal Aims to Ensure Health
of the U.S. Beef Herd, Assist in Negotiations
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE
in these countries.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
Sunday, May 6, 2012
Bovine Spongiform Encephalopathy Mad Cow Disease, BSE May 2, 2012 IOWA
State University OIE
Friday, May 11, 2012
Experimental H-type bovine spongiform encephalopathy characterized by
plaques and glial- and stellate-type prion protein deposits
TSS
