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From: Terry S. Singeltary Sr. (216-119-132-53.ipset12.wt.net)
Subject: Variant Creutzfeldt-Jakob disease: update LETTER GUT/ENDOSCOPY
Date: December 13, 2004 at 8:21 am PST

-------- Original Message --------
Subject: Variant Creutzfeldt-Jakob disease: update LETTER GUT/ENDOSCOPY
Date: Mon, 13 Dec 2004 09:06:33 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


##################### Bovine Spongiform Encephalopathy #####################

© 2005 by BMJ Publishing Group Ltd & British Society of Gastroenterology
------------------------------------------------------------------------


LETTER


Variant Creutzfeldt-Jakob disease: update

M G Bramble1 and J Ironside2

1 James Cook University Hospital, Middlesbrough, UK
2 National CJD Surveillance Unit, Western General Hospital, Edinburgh, UK

Correspondence to:
Professor M G Bramble
James Cook University Hospital, Marton Rd, Middlesbrough TS4 3BW, UK;
mike.bramble@stees.nhs.uk

Keywords: variant Creutzfeldt-Jakob disease; endoscopy

The first 150 words of the full text
of this article
appear below.

Two years ago we reported current thinking on the potential for
gastrointestinal endoscopy to act as a vector for patient to patient
transmission of variant Creutzfeldt-Jakob disease (vCJD).1 In that
article we stressed that the advice would be updated if new evidence
became available. Gastroenterologists may be aware of a recently
published article in the Lancet2 that describes the tissue distribution
of abnormal prion protein (PrPsc) in monkeys that have been inoculated
with brain homogenate from first passage animals with bovine spongiform
encephalopathy (BSE) via the oral route, which is the route by which the
vast majority of patients developing vCJD will have become infected. As
the prion protein responsible for vCJD is found in all lymphoid tissue,
our advice was to reduce "random" biopsies to an absolute minimum and
ensure that re-useable biopsy forceps were meticulously cleaned and
decontaminated according to the strict British Society . . . [Full text
of this article ]

http://gut.bmjjournals.com/cgi/content/extract/54/1/170-a

Something I submitted to GUT previously, but seems all my PhDs hanging
on the wall hindered the publication ............

Subject: Re: gutjnl_el;21 Terry S. Singeltary Sr. (3 Jun 2002)
"CJDs (all human TSEs) and Endoscopy Equipment"
Date: Thu, 20 Jun 2002 16:19:51 -0700
From: "Terry S. Singeltary Sr."
To: Professor Michael Farthing
CC: lcamp@BMJgroup.com

References: <001501c21099$5c8bc620$7c58d182@mfacdean1.cent.gla.ac.uk>

Greetings again Professor Farthing and BMJ,

I was curious why my small rebuttal of the article described below was
not listed in this month's journal of GUT? I had thought it was going to
be published, but I do not have full text access. Will it be published
in the future? Regardless, I thought would pass on a more lengthy
rebuttal of mine on this topic, vCJD vs sCJDs and endoscopy equipment. I
don't expect it to be published, but thought you might find it
interesting, i hope you don't mind and hope to hear back from someone on
the questions I posed...

Here is my short submission I speak of, lengthy one to follow below that:

>> Date submitted: 3 Jun 2002 >> eLetter ID: gutjnl_el;21
>> >> Gut eLetter for Bramble and Ironside 50 (6): 888
>> >>Name: Terry S. Singeltary Sr. >>Email: flounder@wt.net
>>Title/position: disabled {neck injury}
>>Place of work: CJD WATCH
>>IP address: 216.119.162.85
>>Hostname: 216-119-162-85.ipset44.wt.net
>>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4)
>>Gecko/20011019 Netscape6/6.2
>> >>Parent ID: 50/6/888
>>Citation: >> Creutzfeldt-Jakob disease: implications for
gastroenterology
>> M G Bramble and J W Ironside
>> Gut 2002; 50: 888-890 (Occasional viewpoint)
>> http://www.gutjnl.com/cgi/content/abstract/50/6/888 >>
http://www.gutjnl.com/cgi/content/full/50/6/888
>>-----------------------------------------------------------------
>>"CJDs (all human TSEs) and Endoscopy Equipment"
>>-----------------------------------------------------------------
>> >> >> >>

regarding your article; >> >>

Creutzfeldt-Jakob disease: implications for gastroenterology >> >>

I belong to several support groups for victims and relatives of
CJDs. Several years ago, I did a survey regarding endoscopy equipment
and how many victims of CJDs have had any type of this procedure done.
To my surprise, many victims had some kind of endoscopy work done on
them. As this may not be a smoking gun, I think it should warrant a 'red
flag' of sorts, especially since data now suggests a substantial TSE
infectivity in the gut wall of species infected with TSEs. If such
transmissions occur, the ramifications of spreading TSEs from endoscopy
equipment to the general public would be horrible, and could potential
amplify the transmission of TSEs through other surgical procedures in
that persons life, due to long incubation and sub-clinical infection.
Science to date, has well established transmission of sporadic CJDs with
medical/surgical procedures.

>>Terry S. Singeltary Sr. >>CJD WATCH

Again, many thanks, Kindest regards,

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder@wt.net CJD WATCH

[scroll down past article for my comments]

Subject: Creutzfeldt-Jakob disease: implications for gastroenterology &
CJD 38 years after _diagnostic_ use of hGH (Iatrogenic CJDs & sporadic CJDs)
Date: Mon, 17 Jun 2002 16:46:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L

Bovine Spongiform Encephalopathy


OCCASIONAL VIEWPOINTS

Creutzfeldt-Jakob disease' implications for gastroenterology

M G Bramble, J W Ironside

Gut 2002;50:888-890

The current clinical views regarding variant Creutzfeldt-Jakob disease,
and in particular transmission via endoscopy, of those representing both
gastroenterology and the Spongiform Encephalopathy Advisory Committee
are presented in an attempt to guide clinicians as to "best practice"
given the current state of our knowledge.

See end of article for authors' affiliations

Correspondence to: Professor MG Bramble, Endoscopy Centre, James Cook
University Hospital, Marton Rd, Middlesbrough TS4 3BN, UK;

Most gastroenterologists working in the UK have been aware for some time
that endoscopy may be a vector for the transmission of prions from a
patient incubating, but not clinically manifesting, variant
Creutzfeldt-Jakob disease (vCJD) to the next individuals undergoing the
same procedure on the same list. To date there are no recorded cases of
iatrogenic transmission of vCJD via endoscopy but it remains a risk
which will be present for many years to come. Advice to health
authorities on individual cases is through the CJD Incidents Panel.
However, we are aware that advice to health professionals performing
endoscopy needs to be as comprehensive as current evidence will allow,
without making it impossible to perform endoscopic procedures on
patients who will clearly derive long term health benefits from an
accurate endoscopic diagnosis and/or treatment. This article represents
the current clinical views of those representing both gastroenterology
and the Spongiform Encephalopathy Advisory Com-mittee (SEAC). Both
authors sit on the CJD Inci-dents Panel and have been advising the
Depart-ment of Health on individual cases during the last year. It is
important to note that the advice given in this article may be
superseded if additional information or evidence becomes available.

CJD is a member of a group of neurological disorders known as the
transmissible spongilorm encephalopathies or prion diseases, which
affect both animals (such as scrapie in sheep or bovine spongiform
encephalopathy (BSE) in cows) and humans. The precise nature of the
transmissible agents responsible for these disorders is unknown but
there is increasing evidence to support the prion hypothesis, which
states that the agent is composed of an abnormally folded form of a host
encoded protein, prion protein. The normal prion protein (PrPc) is
expressed in many tissues but occurs at the highest levels in neurones
in the central nervous system (CNS) where it may act as a copper binding
protein, although its precise physiological role is unknown. The
abnormal form of the protein (PrPSc) accumulates in the CNS in prion
diseases; the infectious agent is remarkably resistant to most forms of
degradation. The association between PrPSc and the gut has been
eloquently described in a previous lead-ing article1 and
gastroenterologists need to understand where we are in terms of our
present day knowledge of this entity.

In humans, prion diseases occur in three major categories: sporadic,
acquired, and familial. All are currently untreatable and universally
fatal although recent studies have indicated that a combination of drugs
may be effective in experimental prion diseases2: this approach is under
consideration as a clinical trial. The sporadic form of CJD affects
approximately one person per mil-lion per annum in the population on a
worldwide basis. CJD has also occurred as an acquired iatrogenic
disorder, transmitted to other humans through direct (inadvertent)
inoculation of the brain via contaminated neurosurgical instruments, via
corneal and dura mater grafts, or through administration of human
pituitary ex-tracts used to treat growth hormone or gonadotrophin
deficiency. Variant CJD (vCJD) is a new acquired form of CJD which was
first reported in 1996 affecting mainly young adults and with a unique
neuropathological phenotype.3 It is now widely accepted that bovine
prions passed into the human population through consumption of BSE
infected bovine tissues; the transmissible agent responsible for vCJD is
identical to the BSE agent (but different from the agent in sporadic
CJD). The incubation period for vCJD is likely to be lengthy and may
have a mean value of 10-30 years. During this time the affected person
has the potential to transmit the disease to others via surgical
procedures which might result in the transfer of infected tissue into
the next person operated on with the same surgical instruments.

The distribution of PrPSc in the body is different in sporadic and
variant CJD, reflecting the differ-ent pathogenesis of the two forms. In
the case ot sporadic CJD, prion infectivity is largely limited to the
CNS (including the retina) and only opera-tions involving the brain and
eye have resulted in iatrogenic transmission of the disease.
Gastro-intestinal endoscopy is unlikely to be a vector for the
transmission of sporadic CJD as infected tissue is not encountered
during the procedure. No special precautions are necessary during or
after the procedure and the endoscope should be cleaned and disinfected
in the normal thorough way.4

"Endoscopy on patients who are incubating vCJD may result in exposure of
the instrument (and particularly the biopsy forceps) to PrPsc''

In contrast, in vCJD the lymphoreticular system throughout the body
contains PrPSc at the time of death, and experimental evidence suggests
that the lymphoreticular system may contain significant levels of
infectivity for most of the incuba-tion period.5 To support this, in
vCJD abnormal prion protein was found in the germinal centres in the
wall of an appendix from a vCJD patient that was removed eight months
before the onset of neurological disease.6 As lymphoid follicles and
germinal centres are widely distributed in the gastrointestinal tract
(and are often biopsied), it is possible that endoscopy on patients who
are incubating vCJD may result in exposure of the instrument (and
particularly the biopsy forceps) to PrPsc. Consequently, the question
now arises, how great is the risk of secondary (person to person)
transmission in endoscoping a patient incubating vCJD? There are three
scenarios which gastroenterologists are likely to encounter and this
editorial will attempt to guide clinicians as to "best practice" given
the current state of our knowledge.

UPPER GASTROINTESTINAL ENDOSCOPY

Scenario No 1

Occasionally gastroenterologists may be requested to endo-scope a
patient with known or probable sporadic CJD (usually to site a PEG
feeding tube). This can be carried out in the rou-tine way provided vCJD
is not suspected. If inadvertently a patient with suspected vCJD is
endoscoped, the instrument used should be quarantined until the
postmortem diagnosis is known. If sporadic CJD is diagnosed, the
endoscope can be returned to use following thorough cleaning and
decontami-nation, as is normal practice. If vCJD is diagnosed the
endoscope cannot be used again and should be quarantined or sent to the
National CJD Surveillance Unit in Edinburgh for research purposes. The
previous advice to destroy such instru-ments represents a lost
opportunity to study the risks involved in more detail. It would also be
good practice to inform colleagues locally that a quarantined instrument
was available for use in other endoscopy units if they too had a patient
with suspected vCJD requiring endoscopy.

Scenario No 2

For patients with known or probable vCJD,7 endoscopy should only be a
last resort. Ultrasound guided insertion of a gastrostomy feeding tube
would be preferable to a PEG feeding tube if local expertise is
available. If not, endoscopy should be per-formed using an instrument
already set aside for such patients. If no such instrument is available
locally, one can be loaned to any hospital by the National CJD
Surveillance Unit in Edinburgh (contact telephone number 0131 537 1980).
If scenario No 2 becomes more common, endoscopes may need to be held
regionally for this purpose.

Scenario No 3

This scenario covers patients who have been endoscoped by an instrument
previously used on a patient who was not known to be incubating vCJD at
the time of endoscopy but who sub-sequently went on to develop the
disease. This could become the commonest scenario and it must be assumed
that the patient who went on to develop vCJD was incubating the dis-ease
at the time of the original endoscopy. This also means that infectious
material may not have been removed completely by current methods of
decontaminating endoscopes, and that subsequent patients have been
exposed to the prion agent. The instrument used should therefore be
quaran-tined until advice has been sought from the CJD Incidents Panel
(Department of Health, Skipton House, London; contact telephone 0207 972
1761) as to the management of the situa-tion. Local infection control
teams will need to be involved with contact tracing and information
handling.

LOWER GASTROINTESTINAL ENDOSCOPY

It is unlikely that colonoscopy would be clinically justifiable in a
patient known or strongly suspected as suffering from vCJD. However, it
is quite possible that an asymptomatic patient incubating vCJD may
undergo colonoscopy prior to diagnosis and this situation is essentially
the same as in scenario 3. The risks of transmitting prion protein to
the next patient are much greater however, due to a number of factors
which relate to the amount of lymphatic tissue encountered during
endos-copy and the number, site, and size of mucosal biopsies obtained
by this method.

In general the risks of transmitting vCJD from one patient to another
are dependent on the infectivity of the tissues involved, the amount of
tissue contaminating the instrument, the effectiveness of the
decontamination processes, and the susceptibility of subsequently
exposed patients. Experimental studies suggest that levels of
infectivity in prion diseases are highest in the CNS and retina, which
are approximately two logs higher than in the tonsils and other
lymphoreticular tis-sue. A recent study has also detected the abnormal
form of the prion protein in rectal tissue from a patient with vCJD by
western blot examination of autopsy tissues.8 The risk of transmitting
vCJD through the endoscopy procedure itself is likely to be small, but
contamination of the endoscope and forceps as a result of biopsy of
lymphoid tissues may represent a larger (but currently unquantifiable)
risk, even though only small amounts of tissue are involved.

"The risks of transmitting vCJD from one patient to another are
dependent on the infectivity of the tissues involved, the amount of
tissue contaminating the instrument, the effectiveness of the
decontamination processes, and the susceptibility of subsequently
exposed patients"

The greatest risk is undoubtedly that which ensues from biopsy of the
terminal ileum where Peyer's patches may con-tain significant levels of
prion protein for a patient incubating vCJD. The biopsy forceps and the
colonoscope become poten-tial vectors for disease transmission under
these circum-stances. Meticulous manual cleaning of the colonoscope is
probably the best defence against person to person transmis-sion. The
same is true of the biopsy forceps, but as disposable forceps are now
available there is a strong argument for mov-ing towards the universal
use of disposable biopsy forceps for mucosal samples taken at
colonoscopy. Endoscopy units should now work towards a policy of using
disposable biopsy forceps as the only practical way of minimising the
risk which results from ileal biopsy. In addition, "random" biopsies
should be kept to a minimum as lymphoid tissue is distributed widely
throughout the gastrointestinal tract. Although thor-ough cleaning of
flexible endoscopes ensures patient safety for "normal" pathogens, the
same process may not be adequate for the PrPsc. The main benefit of the
decontamination process under these circumstances is undoubtedly
effective manual cleaning, as glutaraldehyde may stabilise PrPSc on the
metal surface of the endoscope, with potentially adverse conse-quences.
It follows that brushes used to clean the channels of the endoscope are
used only once to ensure maximum efficiency and biopsy forceps should
also be functioning opti-mally and discarded as soon as they appear to
be under performing (tearing tissue rather than cutting it). The rubber
valve protecting the biopsy channel is another item which is potentially
disposable and serious consideration should be given to single use
valves. Again, more research is required to determine "best practice".
For rigid endoscopes, autoclaving at the recommended conditions for CJD9
is the best way of attempting decontamination.

What should endoscopists do in the short term? The answer to this
question must be to ensure as far as possible that manual cleaning of
endoscopes and reuseable accessories is of the highest standard.
Endoscopy has a major role in patient care, and this should not be
compromised unless it is absolutely unavoidable in the public interest.
It is also essen-tial that endoscopes should be individually
identifiable and their use traceable in any given patient population.
Random biopsies should be kept to an absolute minimum (particularly of
the ileum in colonoscopy) and endoscopy itself should be as atraumatic
as possible, especially gastroscopy where the instrument is in contact
with the mucosa covering the tonsils. Biopsy forceps should be treated
as "high risk" and undergo thorough ultrasonic cleaning followed by
autoclaving. As research in the UK progresses, it is likely that other
procedures will be developed to inactivate prion infectivity and to
remove proteins from instrument surfaces. The development of such
techniques (along with more sensitive tests for prion detection) may
well have an impact on future advice concern-ing endoscopy and CJD.

Depending on the final numbers of people infected with vCJD, we must
assume that a significant number may undergo endoscopy before
neurological symptoms appear10. It is there-fore up to every endoscopist
to be aware of the dangers and follow the advice set out here. Further
advice on specific cases and possible exposure incidents can be obtained
from the CJD Incidents Panel (Department of Health, Skipton House,
London; contact telephone 0207 972 1761).

Authors' affiliations M G Bramble, Endoscopy Centre, James Cook
University Hospital, Marton Road, Middlesbrough TS4 3BW, UK J W
Ironside, CJD Surveillance Unit, Western General Hospital, Crewe Road,
Edinburgh EH4 2XU, UK

mike.bramble@stees.nhs.uk

Accepted for publication 19 November 2001

REFERENCES

1 Shmakov AN, Ghosh S. Prion proteins and the gut: une liaison
dangereuse? Gut 2001;48:443-7.

2 Korth C, May BCH, Cohen FE, et al. Acridine and phenothiazine
derivatives as pharmacotherapeutics for prion disease. Proc Nail Acad
Sci USA 2001;98:9836-41.

3 Will RG, Ironside JW, Zeidler M, et al. A new variant of
Creutzfeldt-Jakob disease in the UK. Lancet 1996;347:921-5.

4 Report of a Working Party of the British Society of Gastroenterology
Endoscopy Committee. Cleaning and disinfection of equipment for
gastrointestinal endoscopy. Gut 1998;42:585-93.

5 Hill AF, Butterworth R J, Joiner S, et al. Investigation of variant
Creutzfeldt-Jacob disease and other human prion diseases with tonsil
biopsy samples. Lancet 1999;353:183-9.

6 Hilton DA, Fathers E, Edwards P, et al. Prion immunoreactivity in the
appendix before the clinical onset of new variant Creutzfeldt-Jacob
disease. Lancet 1998;352:703-4.

7 Will RG, Zeidler M, Stewart GE, et al. Diagnosis of new variant
Creutzfeldt-Jakob disease. Ann Neuro12000;47:575-82.

8 Wadsworth JD, Joiner S, Hill AF, et al. Tissue distribution of
protease resistant prion protein in variant Creutxfleldt-Jakob disease
using a highly sensitive immunoblotting assay. Lancet 2001 ;358:171-80.

9 Dangerous Pathogens Spongiform Encephalopathy Advisory Committee.
Transmissible spongiform encephalopathy agents: safe working and the
prevention of infection. London: The Stationary Office, 1998.

10 Ironside JW, Hilton DA, Ghani A, et al. Retrospective study of prion
protein accumulation in tonsil and appendix tissue. Lancet
2000;355:1693-94.

http://www.gutjnl.com/cgi/content/abstract/50/6/888
========================================================

Greetings List Members,

This is _very_ disturbing to me:

snip...

The distribution of PrPSc in the body is different in sporadic and
variant CJD, reflecting the different pathogenesis of the two forms. In
the case ot sporadic CJD, prion infectivity is largely limited to the
CNS (including the retina) and only operations involving the brain and
eye have resulted in iatrogenic transmission of the disease.
Gastro-intestinal endoscopy is unlikely to be a vector for the
transmission of sporadic CJD as infected tissue is not encountered
during the procedure. No special precautions are necessary during or
after the procedure and the endoscope should be cleaned and disinfected
in the normal thorough way.4

snip...

i personally believe it is irresponsible for anyone to state in this day
and time, that sporadic CJDs (now at 6 variants) will not transmit the
disease by this route. considering infective dose cannot be quantified,
only speculated, such a statement is thus, irresponsible. to hypothosize
that sporadic CJD just happens spontaneously (with no scientific proof),
that the PrPSc distribution in tissues of all sporadic CJDs is entirely
different than that of vCJD, without being able to quantify the titre of
infection, or even confirm all the different variants yet, again is
_not_ based on all scientific data, then it's only a hypothosis. who is
to say that some of these variants of sporadic CJD were not obtained
_orally_?

also stated:

snip...

Although thorough cleaning of flexible endoscopes ensures patient safety
for ''normal'' pathogens, the same process may not be adequate for the
PrPSc.

snip...

The sporadic form of CJD affects approximately one person per mil-lion
per annum in the population on a worldwide basis.

who is to say how much infectivity are in some of these variants of
sporadic CJDs, without confirming this? if we look at the 6 different
variants of sporadic CJDs, has the infective dose for all 6 _documented_
variants been quantified, and documented as being 'measurable'?

will there be more variants of sporadic CJDs, and what of the
ramifications from them?

what of other strains/variants of TSE in cattle, BSE in sheep, CWD in
cattle, or any of the 20+ strains of Scrapies in deer/elk? i get dizzy
thinking of the different scenerio's. what would the human TSEs from
these species look like and how can anyone quantify any tissue
infectivity from these potential TSE transmissions to humans, and the
risk scenerio described here from this potential route? could not some
of these sporadic CJDs have derived directly or indirectly from one of
these species, and if so, pose a risk by the route described here?

something else to consider, in the recent finding of the incubation
period of 38 years from a _small_ dose of human growth hormone;

snip...

> We describe the second patient with hGH related CJD in the
Netherlands. The patient developed the disease 38 years after hGH
injections. To our knowledge, this is the longest incubation period
described for any form of iatrogentic CJD. Furthermore, our patient was
_not_ treated with hGH, but only received a _low_ dose as part of a
diagnostic procedure. (see full text below).

snip...

so my quesion is, how low is 'low' in quantifing the infectious dose in
vCJD, comparing to _all_ sporadic CJDs, from the different potential
routes, sources, and infectivity dose?

will the titre of infectivity in every tissue and organ of all sporadic
CJDs stay exact or constant, no matter what the infective dose, route
and species may be? this is considering you don't buy the fact that
sporadic CJDs 85%+ of _all_ CJDs, are a happen stance of bad luck,
happen spontaneously without cause, and are one-in-a-million world wide,
with no substantial surveillance to confirm this.

Diagnosis and Reporting of Creutzfeldt-Jakob Disease T. S. Singeltary,
Sr; D. E. Kraemer; R. V. Gibbons, R. C. Holman, E. D. Belay, L. B.
Schonberger

http://jama.ama-assn.org/issues/v285n6/ffull/jlt0214-2.html

and what of Dr. Prusiner et al recent work about tissue infectivity;

Prions in skeletal muscle

snip...

Our data demonstrate that factors in addition to the amount of PrP
expressed determine the tropism of prions for certain tissues. That some
muscles are intrinsically capable of accumulating substantial titers of
prions is of particular concern. Because significant dietary exposure to
prions might occur through the consumption of meat, even if it is
largely free of neural and lymphatic tissue, a comprehensive effort to
map the distribution of prions in the muscle of infected livestock is
needed. Furthermore, muscle may provide a readily biopsied tissue from
which to diagnose prion disease in asymptomatic animals and even humans.

snip...

http://www.pnas.org/cgi/content/abstract/99/6/3812?maxtoshow=&HITS=10&hits=
10&RESULTFORMAT=&author1=prusiner&author2=prusiner&titleabstract=prions+meat+

tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1024346978866_6016&stored_

search=&FIRSTINDEX=0&fdate=1/1/2002

can the science/diagnostic measures used to date, measure this, and at
the same time guarantee that no titre of infectivity exists from
sporadic CJDs (all of the variants), from this potential mode and route
of transmission?

i don't think so, this is just my opinion. this is why i get paid
nothing, and these scientists get the big bucks. i just hope i am wrong
and the big bucks are correct in their _hypothisis_ of this potential
mode/route of transmission with endoscopy equipment, from _all_ human TSEs.

i understand we have to weigh the risks of what we know to what we don't
know, to the disease we _may_ catch to what we are having the procedure
for, but to categorically state at this present time of scientific
knowledge;

snip...

"Gastro-intestinal endoscopy is unlikely to be a vector for the
transmission of sporadic CJD as infected tissue is not encountered
during the procedure. No special precautions are necessary during or
after the procedure and the endoscope should be cleaned and disinfected
in the normal thorough way.4"

snip...

but, to categorically state this, in my opinion, is not only wrong, but
potentially very dangerous to the future of human health...TSS

SHORT REPORT

Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth
hormone

E A Croes, G Roks, G H Jansen, P C G Nijssen, C M van Duijn
...............................................................

J Neurol Neurosurg Psychiatry 2002;72:792-793

A 47 year old man is described who developed pathology proven
Creutzfeldt-Jakob disease (CJD) 38 years after receiving a low dose of
human derived growth hormone (hGH) as part of a diagnostic procedure.
The patient presented with a cerebellar syndrome, which is compatible
with iatrogenic CJD. This is the longest incubation period described so
far for iatrogenic CJD. Furthermore, this is the first report of CJD
after diagnostic use of hGH. Since the patient was one of the first in
the world to receive hGH, other cases of iatrogenic CJD can be expected
in the coming years.

Prion diseases are potentially transmissible. Human to human
transmission was first reported in 1974, when a 55 year old woman was
described who developed symptoms of Creutzfeldt-Jakob disease (CJD) 18
months after a corneal transplant.1 Since then, transmission has been
reported after stereotactic electroencephalographic (EEG) depth
recording, human growth hormone (hGH) and gonadotrophin treatment, and
dura mater transplantation.2-5 More than 267 patients with iatrogenic
CJD are known today and their number is growing.6 The most important
iatrogenic cause of CJD is still contaminated cadaveric hGH. Exposure to
contaminated hGH occurred before 1985, when recombinant growth hormone
became available. In a recent study, incubation periods in 139 patients
with hGH associated CJD were found to range from 5-30 years, with a
median of 12 years.6 One of the factors influencing incubation time is
genotype on polymorphic codon 129 of the prion protein gene.7 The
incubation time is significantly shorter in people who are homozygous
for either methionine or valine on this polymorphism.7

We describe the second patient with hGH related CJD in the Netherlands.
The patient developed the disease 38 years after hGH injections. To our
knowledge, this is the longest incubation period described for any form
of iatrogenic CJD. Further-more, our patient was not treated with hGH
but only received a low dose as part of a diagnostic procedure.

CASE REPORT

This patient presented at the age of 47 years with paraesthesia in both
arms for six months, difficulty with walking for four weeks, and
involuntary movements of mainly the upper extremities of two weeks'
duration. He did not notice any change in cognitive function, although
his twin sister had noticed minor memory disturbances. There was no
family history of neurological disease. During childhood the patient had
experienced a growth delay compared with his twin sister and with the
average in the Netherlands. When he was 9 years old, a nitrogen
retention test with 6 IU hGH over five days was performed to exclude
growth hormone deficiency. Since the result was not decisive, a
quantitative amino acid test was performed, which measures 30 amino
acids during fasting and one, two, and three hours after growth hormone
injection. No abnormal amino acid concentrations were found making the
diagnosis of primordial dwarfism most likely. Therefore, no treatment
with hGH was given.

On neurological examination we found a slight dysarthria without
aphasia. Cranial nerve function was normal. Walking was unstable and
wide based. During movements of the upper extremities myoclonic jerks
were present. Sensation, muscle tone, and strength were normal.
Co-ordination was impaired in all four limbs with a disturbed balance.
Tendon reflexes were brisk at the arms and increased at the legs with a
clonus in the ankle reflex. Plantar responses were both normal. On the
mini mental state examination, the patient scored 30/30. Routine
laboratory investigation, thyroid function, vitamin concentrations (B-1,
B-6, B-12, and E), and copper metabolism were normal. Admission EEG
examination showed generalised arrhythmic slow activity with diffuse
spikes and spike waves. EEG examination two months later showed a
further slowing of the rhythm with bilateral diphasic sharp waves but
was not typical for CJD. Cerebral magnetic resonance imaging was normal.
Cerebrospinal fluid examination showed 1 cell/3 µl, normal glucose and
protein concentrations, and a strongly positive 14-3-3 protein test. The
patient was homozygous for methionine on the PRNP codon 129
polymorphism. On clinical grounds, CJD was diagnosed. Within one month
the patient's condition deteriorated rapidly and because of severe
disturbances in coordination and progressive myoclonus he became
bedridden. An eye movement disorder developed with slow saccadic and
dysmetric eye movements. Temperature became unstable with peaks of 39°C
without an infectious focus, for which a disorder of autoregulation was
presumed. Until a very advanced stage, cognitive function was intact.
The patient died five months after admission. The diagnosis of CJD was
confirmed at necropsy. The brain weighed 990 g and showed clear cortical
and cerebellar atrophy. Spongiosis, neuronal loss, and gliosis were
found predominantly in the putamen, caudate nucleus, and basotemporal
and cerebellar cortex; the cerebellum was the most severely affected of
these. Vacuoles ranged from 2-12 µm. No amyloid or Kuru plaques were
found. Immunohistochemical staining (3F4 antibody 1:1000, Senetek, USA)
was clearly positive for prion protein accumulation in a "synaptic"
distribution. Most deposition was found in the stratum moleculare of the
cerebellum.

DISCUSSION

We describe a 47 year old patient who developed pathology proven CJD 38
years after hGH injections. The patient was never treated with hGH but
received a small dose as part of a diagnostic procedure. The onset of
CJD was signalled by prodromal symptoms of paraesthesia followed by a
rapidly progressive ataxia. The disease presentation and course with
predominantly cerebellar and eye movement disorders are compatible with
iatrogenic CJD caused by hGH treatment.6 8

Growth hormone treatment was first described in 1958 but hGH was not
produced on a larger scale from human pituitary glands until the
beginning of the 1960s. In the Netherlands growth hormone extraction
started in 1963 and was soon centrally coordinated. Until 1979 growth
hormone was extracted non-commercially from pituitaries by a
pharmaceutical company. In 1971 commercial products also became
available. Our patient was one of the first to receive hGH in the
Netherlands but the origin of this product was not recorded. A causal
relation can therefore not be established with full certainty, but
coincidentally receiving growth hormone and developing this very rare
disease is unlikely. Since the clinical course in this relatively young
patient is in accordance with an iatrogenic cause, we think the
probability is high that the hGH injections explain the development of
CJD in this patient.

The first Dutch patient with hGH related CJD died in 1990. 9 During
several periods from 1963 to 1969 she received intramuscular injections
of hGH. During an unknown period the hGH was derived from South America.
At age 39, 27 years after starting the treatment, she developed an
ataxic gait, slurred speech, sensory disorders, and myoclonus, but her
cognitive function remained normal. Postmortem examination of the brain
confirmed the diagnosis of CJD.9 Following the identification of this
patient, a retrospective study was started to trace all 564 registered
hGH recipients who were treated before May 1985. Until January 1995,
none of these was suspected of having CJD.10 Since 1993 prospective
surveillance for all forms of human prion disease has been carried out
in the Netherlands and, apart from the patient described above, a
further two patients with iatrogenic CJD have been identified, who
developed the disease after dura mater transplantation.11

An incubation period as long as 38 years had never been reported for
iatrogenic CJD. Huillard d'Aignaux et al7 studied the incubation period
in 55 patients with hGH related CJD in a cohort of 1361 French hGH
recipients. The median incubation period was between 9 and 10 years.
Under the most pessimistic model, the upper limit of the 95% confidence
interval varied between 17 and 20 years. Although the infecting dose
cannot be quantified, it can be speculated that the long incubation
period in our patient is partly explained by the administration of a
limited amount of hGH. This hypothesis is supported by experimental
models, in which higher infecting doses usually produce shorter
incubation periods.6 Since our patient was one of the first in the world
to receive hGH, this case indicates that still more patients with
iatrogenic CJD can be expected in the coming years. Another implication
of our study is that CJD can develop even after a low dose of hGH. This
case once more testifies that worldwide close monitoring of any form of
iatrogenic CJD is mandatory.

ACKNOWLEDGEMENTS

We are grateful to M Jansen PhD MD for his search for the origin of the
growth hormone and P P Taminiau MD. CJD surveillance in the Netherlands
is carried out as part of the EU Concerted Action on the Epidemiology of
CJD and the the EU Concerted Action on Neuropathology of CJD, both
funded through the BIOMED II programme, and is supported by the Dutch
Ministry of Health. This surveillance would not have been possible
without the cooperation of all Dutch neurologists and geriatricians.
........................................

Authors' affiliations

E A Croes, G Roks*, C M van Duijn, Genetic Epidemiology Unit, Department
of Epidemiology and Biostatistics, Erasmus University Medical Centre
Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands

P C G Nijssen, Department of Neurology, St Elisabeth Hospital, PO Box
90151, 5000 LC Tilburg, Netherlands

G H Jansen, Department of Pathology, University Medical Centre Utrecht,
Heidelberglaan 100, 3584 CX Utrecht, Netherlands

*Also the Department of Neurology, St Elisabeth Hospital

Correspondence to: Professor C M van Duijn, Genetic Epidemiology Unit,
Department of Epidemiology and Biostatistics, Erasmus University Medical
Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands;
vanduijn@epib.fgg.eur.nl

Received 27 December 2001 In revised form 1 March 2002 Accepted 12 March
2002

Competing interests: none declared

REFERENCES

1 Duffy P, Wolf J, Collins G, et al. Possible person-to-person
transmission of Creutzfeldt-Jakob disease. N Engl J Med 1974;290:692-3.

2 Bernoulli C, Siegfried J, Baumgartner G, et al. Danger of accidental
person-to-person transmission of Creutzfeldt-Jakob disease by surgery.
Lancet 1977;i:478-9.

3 Koch TK, Berg BO, De Armond SJ, et al. Creutzfeldt-Jakob disease in a
young adult with idiopathic hypopituitarism: possible relation to the
administration of cadaveric human growth hormone. N Engl J Med
1985;313:731-3.

4 Cochius JI, Burns RJ, Blumbergs PC, et al. Creutzfeldt-Jakob disease
in a recipient of human pituitary-derived gonadotrophin. Aust NZ J Med
1990;20:592-3.

5 Thadani V, Penar PL, Partington J, et al. Creutzfeldt-Jakob disease
probably acquired from a cadaveric dura mater graft: case report. J
Neurosurg 1988;69:766-9.

6 Brown P, Preece M, Brandel JP, et al. Iatrogenic Creutzfeldt-Jakob
disease at the millennium. Neurology 2000;55:1075-81.

7 Huillard d'Aignaux J, Costagliola D, Maccario J, et al. Incubation
period of Creutzfeldt-Jakob disease in human growth hormone recipients
in France. Neurology 1999;53:1197-201.

8 Billette de Villemeur T, Deslys JP, Pradel A, et al. Creutzfeldt-Jakob
disease from contaminated growth hormone extracts in France. Neurology
1996;47:690-5.

9 Roos RA, Wintzen AR, Will RG, et al. Een patiënt met de ziekte van
Creutzfeldt-Jakob na behandeling met humaan groeihormoon. Ned Tijdschr
Geneeskd 1996;140:1190-3.

10 Wientjens DP, Rikken B, Wit JM, et al. A nationwide cohort study on
Creutzfeldt-Jakob disease among human growth hormone recipients.
Neuroepidemiology 2000;19:201-5.

11 Croes EA, Jansen GH, Lemstra AF, et al. The first two patients with
dura mater associated Creutzfeldt-Jakob disease in the Netherlands. J
Neurol 2001;248:877-81.

re-CJD after diagnostic use of human growth hormone

from a donor sourcing aspect, seems the record keeping here has a lot to
be desired for, let us hope it has improved for recipients sake.

also, they speak of 'low dose fitting long incubation'. what about KURU
still existing after some 40 years exposure had ceased. i don't believe
in most instances the dose with kuru is low. just something else to ponder?

TSS

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12023427&dopt=Abstract


1: Ann Neurol 1999 Aug;46(2):224-33

Classification of sporadic Creutzfeldt-Jakob disease based on molecular
and phenotypic analysis of 300 subjects.

Division of Neuropathology, Institute of Pathology, Case Western Reserve
University, Cleveland, OH 44106, USA.

snip...

The present data demonstrate the existence of six phenotypic variants of
sCJD. The physicochemical properties of PrP(Sc) in conjunction with the
PRNP codon 129 genotype largely determine this phenotypic variability,
and allow a molecular classification of the disease variants.

snip...

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10443888&dopt=Abstract


were not all CJDs, even nvCJD, just sporadic, until proven otherwise?

Terry S. Singeltary Sr., P.O. BOX 42, Bacliff, Texas 77518 USA

http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html


Professor Michael Farthing wrote:

Louise Send this to Bramble (author) for a comment before we post. Michael

=======================================================

Subj: Reprocessing of Flexible Endoscopes and Endoscopic Accessories -
an International Comparison of Guidelines
Date: 9/17/02 3:28:43 AM Eastern Daylight Time
From: flounder@WT.NET (Terry S. Singeltary Sr.)
Sender: BSE-L
Reply-to: BSE-L
To: BSE-L

Bovine Spongiform Encephalopathy

Reprocessing of Flexible Endoscopes and Endoscopic Accessories - an
International Comparison of Guidelines

Zeitschrift für Gastroenterologie

© Georg Thieme Verlag Stuttgart New York More about this journal


Endoscopic examinations and procedures are essential for diagnosis and
treatment of gastrointestinal diseases. As a result of poor reprocessing
practice microorganisms can be transmitted via endoscope. The majority
of infection transmissions is due to insufficient performance of
cleaning and disinfection disregarding guidelines of societies of
gastrointestinal endoscopy.

A review of the literature and a comparison of European and American
guidelines for reprocessing flexible endoscopes are given. Differences
in the classification of endoscopic devices, on the possibility of prion
transmission, recommendations on staff training and protection, quality
assurance of reprocessing and evidence-based graduation of guidelines
are stressed and discussed. With respect to the procedure of endoscope
reprocessing, differences concerning the cleaning solution to choose,
necessity of thoroughly manual cleaning and brushing of the accessible
endoscope channels (even in the case of subsequent automatic
reprocessing endoscopes in washers-disinfectors), disinfection solution,
microbiological quality of water for final rinsing and rationale for
alcohol flush of endoscope channels for better drying are mentioned.

The need for experimental investigations of the cleaning and
disinfection process is stressed. In contrast to recent guidelines of
European and American societies of gastrointestinal endoscopy, the now
updated recommendations of the Robert Koch-Institute for reprocessing
flexible endoscopes and endoscopic accessories are evidence-based and
graduated.


Original Article Z Gastroenterol 2002; 40: 531-542 DOI:
10.1055/s-2002-32807 Table of Contents Leitlinien zur Aufbereitung
flexibler Endoskope und endoskopischen Zusatzinstrumentariums im
internationalen Vergleich Reprocessing of Flexible Endoscopes and
Endoscopic Accessories - an International Comparison of Guidelines O.
Leiß1, U. Beilenhoff2, L. Bader3, M. Jung2, M. Exner4 1Fachbereich
Gastroenterologie, Deutsche Klinik für Diagnostik, Wiesbaden 2St.
Hildegardis-Krankenhaus, Mainz 3Max von Pettenkofer-Institut der LMU
München, München 4Hygiene-Institut der Universität Bonn, Bonn

Zusammenfassung

Endoskopische Untersuchungen und Eingriffe sind für Diagnostik und
Therapie gastrointestinaler Erkrankungen unverzichtbar. Durch mangelhaft
aufbereitete Endoskope können Mikroorganismen übertragen werden. Die
Mehrzahl der Infektionsübertragungen bei Endoskopie ist auf
unzureichende Reinigungs- und Desinfektionsmaßnahmen unter Missachtung
aktueller Aufbereitungsrichtlinien der Fachgesellschaften zurückzuführen.

In einer Literaturübersicht werden die Leitlinien europäischer und
amerikanischer Fachgesellschaften zur Aufbereitung flexibler Endoskope
verglichen. Es werden Unterschiede in der Klassifikation des
endoskopischen Instrumentariums, in der Bewertung der
Prionenproblematik, in den Anforderungen an Personalschulung und
Personalschutz, in der Betonung qualitätssichernder Maßnahmen und in der
wissenschaftlichen Untermauerung und Graduierung der ausgesprochenen
Empfehlungen dargestellt und diskutiert. Zu Einzelschritten der
Aufbereitung werden Unterschiede hinsichtlich der einzusetzenden
Reinigungslösung, der Notwendigkeit einer manuellen Bürstenreinigung der
Endoskopkanäle (auch bei nachfolgender maschineller Aufbereitung), der
Wahl des Desinfektionsmittels, der mikrobiologischen Qualität des zur
Schlussspülung verwendeten Wassers und der Empfehlung einer Spülung der
Endoskopkanäle mit Alkohol für eine verbesserte Trocknung herausgestellt
und kritisch bewertet.

Es wird offensichtlich, dass experimentelle Untersuchungen zu
Einzelaspekten der Endoskop-Aufbereitung weitgehend fehlen bzw. erst in
jüngster Zeit bearbeitet wurden. Im Gegensatz zu bisherigen Leitlinien
europäischer und amerikanischer Fachgesellschaften zur
Endoskop-Aufbereitung sind die aktualisierten Empfehlungen des Robert
Koch-Instituts zur Aufbereitung flexibler Endoskope und endoskopischen
Zusatzinstrumentariums mit der verfügbaren Evidenz verknüpft und
graduiert. Schlüsselwörter

Flexible Endoskope - Aufbereitung - Reinigung - Desinfektion -
Personalschulung - Qualitätssicherung - Mikrobiologische Prüfungen -
Hygiene Abstract

http://www.thieme-connect.com/DOI/DOI?10.1055/s-2002-32807

TSS
========================================


-------- Original Message --------
Subject: Re: gutjnl_el;110 Terry S. Singeltary Sr. (22 Aug 2003) ""CJDs
(all human TSEs) and Endoscopy Equipment
Date: Tue, 26 Aug 2003 15:10:51 -0500
From: "Terry S. Singeltary Sr."
To: Robin.Spiller@nottingham.ac.uk

hello Professor Spiller and GUT, this has become a real challenge trying
to raise my concerns to GUT about sporadic CJD. but i will not give up.
you only have to see it once. i hope you take the time to read over all
data below...thank you > unsubstantiated opinion and emotion these are
not my unsubstantiated opinions, they are backed up by science
(transmission studies and or lack of transmissions studies), and i will
try and leave my emotions out. > I feel that we need a proper evidence
based approach to this. > There is too much unsubstantiated opinion i
agree... to categorically state that nv/v CJD is the only risk to
endoscopy equipment, while ignoring all other TSEs, is very
unsubstantiated. i will try and give more evidence for my concerns
below. 1st, there has never been to date any _documented_ transmission
of nv/v CJD via the medical surgical arena. this has only been
hypothesized... 2nd, However, there has been _documented_ evidence of
transmission of sporadic CJD via the medical and surgical arena. TO
continue to hide behind the nv/v CJD only theory, when there are over 20
strains of scrapie, most of which transmits to all mammalian species
that has been tried upon, CWD which no one knows if or if not it can
transmit to humans (to date no transmission studies of any TSEs done on
man), but studies have shown transmission to humans as easy as BSE, and
does transmit to primate. there are now 6 _documented_ phenotypes of
sporadic CJD. with CWD and Scrapie running rampant in the USA, no real
active surveillance in cattle for TSEs and no rapid testing done to find
BSE agent (48,000+ BSE/TSE test in 14 years TOTAL USA), who knows how
these strains of CJD will act and how they will transmit. also, in vitro
experiments have demonstrated that scrapie/cwd prions are as efficient
as BSE prions in transforming normal human prion protein to PrPSc. this
data strongly supports that scrapie/cwd is as infectious as BSE. IN
fact, scrapie seems to be more infectious than BSE due to higher
concentration of TSE infectious agents in ovine muscle meat and other
parts of the sheep, when compared to cattle, and CWD could even be more
infectious than all of them, if you consider how it has rapidly spread
across the USA. but to categorically state that only nv/v CJD to be of
risk to endoscopy equipment when no such documented transmission has
ever been documented, while ignoring such similar medical _documented_
transmissions in sporadic CJD, this is very disturbing and most
unsubstantiated, and potentially risking TSE exposure to millions and
millions due to nothing more than denial and wishful thinking. if i
could deny this and wish it away, i would have done this six years ago.
but we cant, all we can do is warn the public and the medical community
of what we know to date. i am surprised GUT has chosen not to do this,
and only to go with the BSE/nv/v/CJD only theory. 85%+ of all CJDs don't
just happen without route and source. my fear is a great deal are being
mis-diagnosed and un-reported, but being acquired via the medical
surgical arena. but one will never know without making all human TSEs
reportable in every State, and issuing a CJD Questionnaire to all
families of victims of CJD/TSE and asking the _real_ questions that
pertain to route and source of agent...TSS REFERENCES

snip...

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, TEXAS USA 77518

Robin Spiller wrote:

>Your ideas are interesting but I feel that we need a proper evidence
based approach to this. There is too much unsubstantiated opinion and
emotion associated with this issue. I don't wish to publish ideas that
do not have proper scientific basis. If you have such please submit as a
paper for peer review
>Best wishes
>
>Robin Spiller
>
>
>>>>"Terry S. Singeltary Sr." 08/22/03 09:09pm >>>
>>>>
>>>>
>
>
>
>-----------------------------------------------------------------
> Date submitted: 22 Aug 2003
> eLetter ID: gutjnl_el;110
>
>
>
>
>
>
> Gut eLetter for Bramble and Ironside 50 (6): 888
>-----------------------------------------------------------------
>Name: Terry S. Singeltary Sr.
>Email: flounder@wt.net
>Title/position: medically retired
>Place of work: CJD WATCH
>IP address: 216.119.163.28
>Hostname: 216-119-163-28.ipset45.wt.net
>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:1.0.2)
Gecko/20030208 Netscape/7.02
>
>Parent ID: 50/6/888
>Citation:
> Creutzfeldt-Jakob disease: implications for gastroenterology
>
>
> M G Bramble and J W Ironside
>
>
> Gut 2002; 50: 888-890 (Occasional viewpoint)
>
>
> http://www.gutjnl.com/cgi/content/abstract/50/6/888
>
>
> http://www.gutjnl.com/cgi/content/full/50/6/888
>
>
>-----------------------------------------------------------------
>""CJDs (all human TSEs) and Endoscopy Equipment" "
>-----------------------------------------------------------------
>
>
>
>

Greetings GUT and Professor Farthing,
>
>

in my apparent failed attempt to warn you and others
>of all CJD, i see my submission of June 20, 2002
>never got published for whatever reason.
>regardless, since then, further data has come out
>to support just what i have been trying to warn
>the world for 6 years, sporadic CJD has a route
>and source, and that the only proven transmission
>via the surgical/medical arena of CJD that has
>been _documented_ to date is sporadic CJD. with the
>new findings from Asante/Collinge et al, i once again
>put forth my original submission of potential threat
>of endoscopy equipment from _all_ CJD/TSE. i would
>stress this should include the whole medical and
>surgical arena...
>
>

Asante/Collinge et al, that BSE transmission to the 129-methionine
>genotype can lead to an alternate phenotype that is indistinguishable from
>type 2 PrPSc, the commonest _sporadic_ CJD;
>
>

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
>
>

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
>disease in the United States 26 March 2003
>
>

Next Post-Publication Peer Review Top Terry S. Singeltary,
>
>

retired (medically)
>
>

CJD WATCH
>
>

Send Post-Publication Peer Review to journal:
>
>

Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-
>Jakob
>disease in the United States
>
>

Email Terry S. Singeltary:
>flounder@wt.net
>
>

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to
>comment on the CDC's attempts to monitor the occurrence of emerging
>forms of CJD. Asante, Collinge et al [1] have reported that BSE
>transmission to the 129-methionine genotype can lead to an alternate
>phenotype that is indistinguishable from type 2 PrPSc, the commonest
>sporadic CJD. However, CJD and all human TSEs are not reportable
>nationally. CJD and all human TSEs must be made reportable in every
>state and internationally. I hope that the CDC does not continue to
>expect us to still believe that the 85%+ of all CJD cases which are
>sporadic are all spontaneous, without route/source. We have many TSEs in
>the USA in both animal and man. CWD in deer/elk is spreading rapidly and
>CWD does transmit to mink, ferret, cattle, and squirrel monkey by
>intracerebral inoculation. With the known incubation periods in other
>TSEs, oral transmission studies of CWD may take much longer. Every
>victim/family of CJD/TSEs should be asked about route and source of this
>agent. To prolong this will only spread the agent and needlessly expose
>others. In light of the findings of Asante and Collinge et al, there
>should be drastic measures to safeguard the medical and surgical arena
>from sporadic CJDs and all human TSEs. I only ponder how many sporadic
>CJDs in the USA are type 2 PrPSc?
>
>

http://www.neurology.org/cgi/eletters/60/2/176#535
>
>

Subject: Re: gutjnl_el;21 Terry S. Singeltary Sr. (3 Jun 2002) "CJDs
>(all human TSEs) and Endoscopy Equipment" Date: Thu, 20 Jun 2002 16:19:51
>-0700 From: "Terry S. Singeltary Sr." To: Professor Michael Farthing CC:
>lcamp@BMJgroup.com References:
><001501c21099$5c8bc620$7c58d182@mfacdean1.cent.gla.ac.uk>
>
>

Greetings again Professor Farthing and BMJ,
>
>

I was curious why my small rebuttal of the article described below
>was not listed in this month's journal of GUT? I had thought it was going
>to be published, but I do not have full text access. Will it be published
>in the future? Regardless, I thought would pass on a more lengthy rebuttal
>of mine on this topic, vCJD vs sCJDs and endoscopy equipment. I don't
>expect it to be published, but thought you might find it interesting, i
>hope you don't mind and hope to hear back from someone on the questions I
>posed...
>
>

Here is my short submission I speak of, lengthy one to follow below
>that:
>
>

>> Date submitted: 3 Jun 2002 >> eLetter ID: gutjnl_el;21
>>> >> Gut eLetter for Bramble and Ironside 50 (6): 888
>>> >>Name: Terry S. Singeltary Sr. >>Email:
>flounder@wt.net >>Title/position: disabled {neck injury}
>>>Place of work: CJD WATCH >>IP address: 216.119.162.85
>>>Hostname: 216-119-162-85.ipset44.wt.net >>Browser:
>Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4) >>Gecko/20011019
>Netscape6/6.2 >> >>Parent ID: 50/6/888 >>Citation:
>>> Creutzfeldt-Jakob disease: implications for gastroenterology
>>> M G Bramble and J W Ironside >> Gut 2002; 50: 888-890
>(Occasional viewpoint) >>
>http://www.gutjnl.com/cgi/content/abstract/50/6/888 >>
>http://www.gutjnl.com/cgi/content/full/50/6/888 >>------------------
>----------------------------------------------- >>"CJDs (all human
>TSEs) and Endoscopy Equipment" >>-----------------------------------
>------------------------------ >> >> >> >>
>
>

regarding your article; >> >>
>
>

Creutzfeldt-Jakob disease: implications for gastroenterology >>
>>>
>
>

I belong to several support groups for victims and relatives
>>>of CJDs. Several years ago, I did a survey regarding
>>>endoscopy equipment and how many victims of CJDs have >>had
>any type of this procedure done. To my surprise, many >>victims had
>some kind of endoscopy work done on them. >>As this may not be a
>smoking gun, I think it should >>warrant a 'red flag' of sorts,
>especially since data now >>suggests a substantial TSE infectivity
>in the gut wall >>of species infected with TSEs. If such
>transmissions >>occur, the ramifications of spreading TSEs from
>>>endoscopy equipment to the general public would be
>>>horrible, and could potential amplify the transmission >>of
>TSEs through other surgical procedures in that >>persons life, due
>to long incubation and sub-clinical >>infection. Science to date,
>has well established >>transmission of sporadic CJDs with
>medical/surgical >>procedures.
>
>

>>Terry S. Singeltary Sr. >>CJD WATCH
>
>

Again, many thanks, Kindest regards,
>
>

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
>flounder@wt.net CJD WATCH
>
>
>
>
>Robin Spiller
>Professor of Gastroenterology
>Wolfson Digestive Diseases Centre
>C Floor South Block
>University Hospital
>Nottingham NG7 2UH
>UK
>Tel: +44 (0)115 9709352 Direct
>NHS secretary Julie +44 (0)115-9249924 ext 44548
>University Secretary Emma Bradley + 44 (0) 115-9249924 ext 35077
>Fax: +44 (0)115-9422232
>
>
>
>

END...TSS

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