Greetings Professor Farthing, Professor Ironside, and GUT et al,
I hate to say I told em so, but sadly, I told em so.
you said you would print my concerns back in 2003, then, you never did, and
now look where we are ?
disturbing...
kind regards,
terry
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Part 4
1
Published: June 2003
Revised and updated: January 2014
PART 4
INFECTION PREVENTION AND CONTROL OF CJD, VCJD AND OTHER HUMAN PRION
DISEASES IN HEALTHCARE AND COMMUNITY SETTINGS
Summary of advice
Part 4 provides advice on safe working practices with the aim of preventing
the transmission of CJD, variant CJD (vCJD) and other human prion diseases in
hospital and community healthcare settings
Variably Protease-Sensitive Prionopathy (VPSPr)
i) VPSPr is a recently described human prion disease, which appears to be a
rare sporadic disorder affecting patients in an age range similar to those
affected by sporadic CJD.
ii) The transmissibility of VPSPr is currently under investigation;
preliminary results appear to indicate that it is transmissible experimentally
to rodents, but the transmission characteristics are still being
determined.
iii) There is very little data on the detection of abnormal prion protein
outside the CNS in VPSPr, so as for other prion diseases where these data are
lacking (eg many genetic forms of prion disease) it seems reasonable to assume a
similar tissue distribution to sporadic CJD, since there is no evidence to
indicate that VPSPr is a BSE-related disorder.
iv) Further advice on VPSPr can be obtained from NCJDRSU (Professor James
Ironside or Dr Anna Molesworth).
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Part 4
2
see full text ;
· Annex F – Endoscopy
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Annex F
1
Published: September 2004
Revised and updated: January 2014
Annex F
ENDOSCOPY
Summary of advice
Annex F provides the definitive UK guidance on decontamination of flexible
endoscopes for TSE infection prevention and control.
The specific recommendations in this guidance are complementary to national
guidance on all aspects of endoscope decontamination such as Choice Framework
for local Policy and Procedures 01-06 and the British Society of
Gastroenterology (BSG) Guidelines for Decontamination of Equipment for
Gastrointestinal Endoscopy.
Annex F provides specific advice for the management of instruments used in
all types of endoscopic procedures. This advice differs depending on the type of
CJD that a patient has been diagnosed with, or for which symptoms are being
investigated, and for those who are asymptomatic but for whom an increased risk
of developing disease has been identified.
Paragraphs F4 to F27 set out the guidance for each circumstance in detail,
while summary advice is provided in table F1 and table F2a.
Endoscopes currently in quarantine
Advice is given below regarding endoscopes that have been held in
quarantine following previous use on patients who are at increased risk of
vCJD.
Endoscopes that have been placed into quarantine on or after 1 January
2010, assuming not used to treat one of the patient categories described at
paragraphs F20 to F23 should be reviewed as follows:
1) Was the endoscope properly decontaminated using a validated process
prior to quarantine?
2) Is there tracking to demonstrate the above?
3) Has the scope been stored properly whilst in quarantine (in a drying
cabinet or at least positioned vertically, not coiled up in a case)?
If all the above are met, the endoscope can be returned to use. If the
endoscope has been out of use for more than a few months it is recommended that
it is returned to the manufacturer for service and a check of handling
characteristics before returning to use.
Previous revision date: December 2012
Changes new to this edition:
Date
Change
Notes
January 2014
Slightly modified text to reflect the wording of Table F1 and F2a
This change affects paragraphs: F8, F17, F18, F22 and F26
January 2014
Changes to table F1 and F2a to align with policy
January 2014
Changes to notes of table F2a to align with policy
January 2014
Change of terminology from “infection control” to “infection prevention and
control”
Changed throughout the document as appropriate
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Annex F
· Annex J - Assessment to be carried out before surgery and/or endoscopy to
identify patients with, or at increased risk of, CJD or vCJD
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Annex J
Published: 31 July 2006
Revised and updated: January 2014
1
ANNEX J
Assessment to be carried out before surgery and/or endoscopy to identify
patients with, or at increased risk of, CJD or vCJD
Summary of advice (revised January 2014)
Annex J provides a clear and pragmatic way of assessing CJD and vCJD risk
prior to surgery or endoscopy. Certain groups of patients have been informed
that they are at increased risk of CJD or vCJD.
*** Therefore it is recommended that all patients about to undergo any
surgery or endoscopy should be asked if they have ever been notified as at
increased risk of CJD or vCJD. This recommendation is outlined in paragraphs J1
and J2.
In addition, patients undergoing surgery or neuro-endoscopy which may
involve contact with tissues of potentially high level TSE infectivity (“high
risk tissues”) should, through a set of detailed questions, be assessed for
their possible CJD/vCJD risk exposure. These questions are outlined in Table J1
and paragraphs J3 to J6.
Previous revision date: January 2013
Changes new to this edition:
Date
Change
Notes
January 2014
Alignment of the list of people considered at increased risk of vCJD with
that contained in Part 4.
This change affects paragraph J14.
January 2014
Change of terminology from “infection control” to “infection prevention and
control”
Changed throughout the document as appropriate
These annexes have table at the start setting out the changes that have
been included in the new version.
· FAQs – a new question has been added regarding blood transfusion
My patient has a history of blood transfusion. Should my patient be
considered at increased risk of CJD and/or vCJD?
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease
Monday, January 13, 2014
*** Prions in Variably Protease-Sensitive Prionopathy: An Update Pathogens
2013 Pathogens 2013, 2, 457-471; doi:10.3390/pathogens2030457
Friday, January 10, 2014
*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ???
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
Saturday, November 16, 2013
Management of neurosurgical instruments and patients exposed to
creutzfeldt-jakob disease 2013 December
Infect Control Hosp Epidemiol.
Thursday, November 14, 2013
Prion diseases in humans: Oral and dental implications
Saturday, November 2, 2013
Recommendation of the Swiss Expert Committee for Biosafety on the
classification of activities using prion genes and prion protein January 2013
January 24, 2003
*** 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
Something I submitted to GUT previously;
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 c58d182="" c8bc620="" 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)
"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
snip...
were not all CJDs, even nvCJD, just sporadic, until proven otherwise?
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... my concerns were never posted and or published, in fact they were
CENSORED. ...tss
see full text ;
2003
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
[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@uni-karlsruhe.de
snip...end
PLEASE UNDERSTAND, THIS NEVER WENT TO PRINT LIKE BRAMBLE ET AL SAID IT
WOULD ???
CENSORSHIP ???
After approximately 100 hours work for this review, an editorial decision
was taken not to publish.
Ironically, this book contained the very paper by Gerald Wells and myself
over which "censorship" has been alleged.
Prolonged delay during "Refereeing/Scrutineering" of manuscripts submitted
for publication 1997 Wood McGill Done and Bradley (ref 12). 31. This work was
started in 1990 to screen for putative BSE in sheep, by James Wood, a colleague
in the Pathology Department at CVL, although it was not finally published until
1997. James sought my assistance in light of my greater experience in TSE
pathology. I worked many many months to get this paper into print
(YB95/6.29/2.1; YB96/9.19/2.1)
6 refereeing process took two years, hardly an acceptable delay for crucial
work in this field. The referees’ comments (YB95/6.29/2.2)
themselves require scrutiny. One scrutineer seemed to referee the paper in
a balanced way, whilst the other seemed more intent on pushing his/her own
opinions onto the paper.
32. Publication was finally expedited in the summer of 1996, when the
politically sensitive question of whether or not BSE had indeed gone into the
sheep population started to be asked in the public domain. This paper finally
appeared (with some important omissions and watering down) in 1997, seven years
after it was started, and two years after it was submitted. It was jointly
funded by MAFF and the Prion Interest Group.
33. Had my ongoing research into sheep scrapie been funded and/or the
McGill and Wood 1992 paper been published, stimulating debate and further
investigations, this paper would most certainly have appeared by 1995. Further
work based on it could have determined by 1997 whether or not, and if so to what
extent, BSE had gone into sheep.
34. In addition, the work may by now have led to a rapid diagnostic test
and a great deal of information on the actual (as opposed to the
theoretical/experimental) causes of sheep scrapie and the fundamental biology of
this entire group of diseases. Some of the work suggested in 1991 has still not
been started. Aspects of TSE work with which I was involved Analysis of the
astrocytic response in BSE and its comparison with natural scrapie.
35. I worked as a neuropathologist with Gerald Wells to establish that
astrocytic reaction, one of the fundamental triad of neuropathological changes
occurring in TSEs, was indeed present in BSE. This work was accomplished using
antibodies to GFAP (a structural component characteristic of astrocytes) to
quantify previously qualitative interpretations that an astrocytic reaction was
present. The astrocytic reaction in natural sheep scrapie was assessed in
parallel. Published: 1988 RVC library. 1991 (Wells, Wilesmith and McGill) -
details of astrocytic response in BSE 1997 (Wood, McGill, Done and Bradley) -
details of astrocytic response in natural sheep scrapie Surveillance for
emerging scrapie-like diseases in animals in the UK
36. Working with Gerald Wells and other pathologists from the State
Veterinary Service, I was involved with surveillance for neurological disease of
animals in the UK. This was with particular reference to surveillance for, and
subsequent confirmation of TSEs. During my time of employment, novel TSEs arose
in domestic cats and in exotic ungulates in zoological collections. I also
became involved in the investigation of a putative TSE in hound packs detected
by Robert Higgins. FSE, and BSE in exotic ungulates published in reviews: 1991
(Wells and McGill) ref 5 7 1992 (Wells and McGill) ref 7 FSE discussed in para
15.
37. Putative TSE in hounds - work started 1990 –(see para 41) Robert
Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a
hound survey in 1990. Gerald Wells and I myself received histological sections
from this survey along with the accompanying letter (YB90/11.28/1.1)
dated November 1990. This letter details spongiform changes found in brains
from hunt hounds failing to keep up with the rest of the pack, along with the
results of SAF extractions from fresh brain material from these same animals.
SAFs were not found in brains unless spongiform changes were also present. The
spongiform changes were not pathognomonic (ie. conclusive proof) for prion
disease, as they were atypical, being largely present in white matter rather
than grey matter in the brain and spinal cord. However, Tony Scott, then head of
electron microscopy work on TSEs, had no doubt that these SAFs were genuine and
that these hounds therefore must have had a scrapie-like disease. I reviewed all
the sections myself (original notes appended) and although the pathology was not
typical, I could not exclude the possibility that this was a scrapie-like
disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration
was also present in the white matter of the hounds, another feature of scrapie.
38. I reviewed the literature on hound neuropathology, and discovered that
micrographs and descriptive neuropathology from papers on ‘hound ataxia’
mirrored those in material from Robert Higgins’ hound survey. Dr Tony Palmer
(Cambridge) had done much of this work, and I obtained original sections from
hound ataxia cases from him. This enabled me provisionally to conclude that
Robert Higgins had in all probability detected hound ataxia, but also that hound
ataxia itself was possibly a TSE. Gerald Wells confirmed in ‘blind’ examination
of single restricted microscopic fields that there was no distinction between
the white matter vacuolation present in BSE and scrapie cases, and that
occurring in hound ataxia and the hound survey cases.
39. Hound ataxia had reportedly been occurring since the 1930’s, and a
known risk factor for its development was the feeding to hounds of downer cows,
and particularly bovine offal. Circumstantial evidence suggests that bovine
offal may also be causal in FSE, and TME in mink. Despite the inconclusive
nature of the neuropathology, it was clearly evident that this putative canine
spongiform encephalopathy merited further investigation.
40. The inconclusive results in hounds were never confirmed, nor was the
link with hound ataxia pursued. I telephoned Robert Higgins six years after he
first sent the slides to CVL. I was informed that despite his submitting a
yearly report to the CVO including the suggestion that the hound work be
continued, no further work had been done since 1991. This was surprising, to say
the very least.
41. The hound work could have provided valuable evidence that a
scrapie-like agent may have been present in cattle offal long before the BSE
epidemic was recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments 8
42. These included neuropathological examination of material from
experiments studying the attempted transmission of BSE to chickens and pigs (CVL
1991) and to mice (RVC 1994). Neuropathological findings in cattle with
clinically suspect but histologically unconfirmed bovine spongiform
encephalopathy
43. This was my main project during my employment at MAFF.
44. At this time, approximately 10% of cattle suspected of having BSE were
not being diagnosed as BSE-positive. The purpose of this work was to establish
what other diseases were being clinically mistaken for BSE and causing these
cattle to be taken as suspects under the BSE Order.
45. Upon closer examination, three of the 200 ‘BSE-negative’ brains proved
positive for spongiform changes diagnostic of BSE (see YB87/12.14/1.2;
YB87/12.15/2.1).
This represents an overall diagnostic accuracy of 99.85%, exceeding the
99.6% previously published for the same standard diagnostic technique. Despite
this, at the behest of MAFF managers, the emphasis of the study and its
provisional title had to be changed, from accurately representing the whole
negative 10%, to a study examining this 10% minus any mention whatsoever of
BSE-affected cattle going undiagnosed. I therefore had to reluctantly locate and
analyse three new BSE-negative suspect brains.
46. Discussion of this would according to MAFF officials have resulted in
‘lack of clarity’ and opened up debate as to the accuracy of diagnosis.
47. Although this may seem a minor consideration, it illustrates the
kneejerk and perhaps unnecessary culture of secrecy operating within MAFF at
that time.
48. As it was also a theoretical possibility that cases of BSE might exist
without the characteristic spongiform changes, a further purpose of this work
was to examine selected cases using immunocytochemistry for PrP to determine if
any had BSE but lacked the characteristic pathology. Although the sensitivity of
the technique used has increased dramatically since then, none were found at
this time, and this was one of the important findings of the paper which was
published.
49. In a number of informal conversations at that time, managers within
MAFF let me know that the upper echelons of MAFF “had had it up to here with you
scientists finding out about new diseases”. As a Veterinary Research Officer
employed in disease surveillance, I had considered that to be my job. Published
1993 (McGill and Wells) ref 10 Theoretical models of TSE diseases
50. Published in the Veterinary Record 1991 (J/VR/128/368) as editorial of
AVTRW conference. In 1991 Martin Alder, new editor of the. Veterinary Record ,
published a very favourable account of my theoretical paper presented at AVTRW
1991 in Scarborough under the heading “Heretical Model of Scrapie”. The Chairman
of this session was Bill 9 Blakemore, Cambridge Vet School. It was printed
(after consultation with me) in an editorial article “Fruits of Research On Show
in Scarborough”. He devoted considerably more column inches to work by myself
and Kenton Morgan than to work reported by NPU, although they had presented far
more papers. It was to be the last time my name would appear in the Veterinary
Record until 1997. Unpublished 1988, 1992 Establishing that human prion disease
can exist without characteristic pathology.
51. This was the first conclusive proof that prion diseases can indeed
exist without any of the characteristic pathology, extending the phenotypic
diversity of prion disease. Published 1992 (Lantos, McGill et al) ref. 6 Setting
up in vitro models of human prion diseases (GSS, familial CJD) in neuroblastoma
cells in culture (Resigned half way through project) Neuropathology of natural
sheep scrapie. Started 1990, submitted 1995, published 1997 (Wood, McGill et al)
ref 12 See para 11 for details of this work. Contact with / Advice to Government
Contact with CVL / MAFF
52. I maintained regular contact with scientists at the CVL until 1997.
53. I cannot catalogue all the information, advice or recommendations I
offered to MAFF or CVL between 1988 and 1997, as there is too much to include.
However, I could illustrate with the following summary of two substantive
suggestions for research. Research on the biochemical/physical nature of
“strains”
54. Prior to their publication as an editorial in the Veterinary Record, a
summary of these ideas was presented to the CVL management for funding as a
‘blue sky’ PhD project in Spring 1991. The proposal was not taken up. This was
the first occasion on which I proposed research to the Government in writing. An
abattoir survey for incidence of BSE
55. I suggested in 1990 that to improve the provision of control material I
should collect 20 cattle heads from a local abattoir.The purpose of this was to
provide BSE-negative material to act as controls for our (CVL’s) BSE work.
However, neuropathological examination of these brains might also have given an
indication of the number of cattle incubating BSE which were entering the human
food chain. This research had actually been recommended in the Interim Report of
the Tyrrell Committee, June 89. 10
56. I was instructed a few days after suggesting this to my head of
department that I was not the first person to have thought of that, and that a
decision had been taken not to do that research. I was also instructed, for some
reason, not to put it in writing.
57. Budgets could hardly have been an issue contributing to the rejection
of this proposal, as tongueless cattle heads were free, being banned from human
consumption. Contact with AFRC
58. I had contact with the AFRC in several capacities: My work at the
Institute of Psychiatry was funded by an AFRC grant. Attending BSE Programme
conferences in 1992 and 1994. Submitted a further grant application to the AFRC
in 1991.
59. This proposal was to continue research on natural scrapie, with which I
had been involved at CVL (eventually published 1997; ref 12). I was to
collaborate with John Powell (molecular neurobiologist) and David Male
(co-author of the standard Immunology text worldwide: Roitt, Brostoff and Male).
All five referees gave positive statements about the proposal, which was
alpha-rated (see YB92/12.10/1.1 and YB92/12.17/1.1).
60. This was the second time that I suggested substantial investigations on
the TSEs to the government in writing. Once more the proposal was not taken up.
61. In view of the continuing uncertainties as to the degree to which BSE
has affected the sheep population, it would perhaps have been wise to fund this
application at that time.
62. Some of this work has still not been initiated, although the paper
(Wood, McGill et al 1997), after a two year delay from submission to
publication, and the original 1992 AFRC grant submission, both described a
unique series of characterised sheep brains affected with naturally occuring
TSEs. The majority of them are natural scrapie although further work on this
series of brains would give an indication of whether BSE was also occurring in
sheep in the 1980s and early 1990s. Events have moved forward since this grant
application was submitted, both in the nvCJD and scrapie fields, but this still
represents a crucial question in the epidemiology of both scrapie and BSE which
remains unanswered. This work should, in my opinion, be initiated forthwith, and
further work based on these results pursued vigorously as results are
obtained.Refer to discussion also at para 31. Additional Comments
63. I could perhaps sum up MAFF’s approach to BSE with an observation which
is by no means original: “Absence of evidence” is not the same as “evidence of
absence” Publications 1. McGill IS (1986) The Shortcut to Elitism.
The Guardian, December 1st, p12. 11 2. Wells GAH, Wilesmith, JW &
McGill IS (1991) Bovine spongiform encephalopathy - a neuropathological
perspective. Brain Pathology, 1, 69-78 3. McGill IS (1991) Bovine Spongiform
Encephalopathy. In: Practical Food Hygiene, Ed. Dickens T, Croner Publications
Ltd, Kingston, UK, pp. 435-436 4. McGill IS & Whatley SA (1991)
Understanding the causes of brain disease. The Independent, August 16th, p. 20
5. Wells GAH & McGill IS (1991) Recently described scrapie-like
encephalopathies of animals - case definitions. In: Sub-acute Spongiform
Encephalopathies, Eds. Bradley R, Savey M & Marchant B, Kluwer Academic
Publishers, Dorchelt, pp. 11-24. 6. Lantos P, McGill IS, Janota I, Doey J,
Collinge J, Bruce M, Whatley SA, Anderton BH, Clinton J, Roberts GW & Rosser
N (1992) Prion protein immunocytochemistry helps to establish the true incidence
of prion disease. Neuroscience Letters, 147, 67-71 7. Wells GAH & McGill IS
(1992) Recently described scrapie-like encephalopathies of animals - case
definitions. Research in Veterinary Science, 53, 1-10 8. Pollin MM, McGill IS
& Wells GAH (1992) The differential neurohistological diagnoses of
clinically suspect but unconfirmed BSE. Neuropathology and Applied Neurobiology,
18, 633 (abstract) 9. Guha M & McGill IS (1992) Book review of Black's
Veterinary Dictionary (17th Edition), Ed, West GP, A & C Black, London.
Reference Reviews, 6, 26 10. McGill IS & Wells GAH (1993). Neuropathological
findings in cattle with clinically suspect but histologically unconfirmed bovine
spongiform encephalopathy (BSE). Journal of Comparative Pathology, 108, 241-260
11. McGill IS (1995) Ayurvedic Medicine - The Documentary. Natural Medicine
Society News, Spring 1995 12. Wood LJN, McGill IS, Done SH and Bradley R (1997)
Neuropathology of scrapie: a study of the distribution patterns of brain lesions
in 222 cases of natural scrapie in sheep, 1982-1991. Veterinary Record 140,
167-174 13. McGill IS, Hobson J (1998) Multi-centre evaluation of a herbal skin
gel for veterinary practice - a questionnaire survey. Veterinary Times, 28, 1,
20-21 14. McGill IS (1998) BSE and Censorship. The Independent January 26th
1998, p14 (YB98/1.26/1.1). 12 ANNEX 1: CURRICULUM VITAE: IAIN STEWART McGILL
Education & Qualifications 1975 - 1982 Southend High School for Boys GCE
O-Levels (1980): 9 (6 A, 3 B) GCE A-Levels (1982): Biology (A), Physics (A),
Chemistry (A) GCE S-Level (1982): Biology (2) 1982 - 1984 Royal Veterinary
College, University of London 1984 - 1985 Kings College, University of London
B.Sc(Hons), II(i) Neuroscience and Immunology 1985 - 1988 Royal Veterinary
College, University of London B.Vet.Med., MRCVS. Distinctions : Medicine ,
Clinical Pathology (Elective Subject) First place for research project Cecil
Aulden Second Prize Professional Experience 1988 - 1989 Veterinary Surgeon --
Blue Cross Animal Hospital, Victoria, London In addition to clinical duties, I
upgraded clinical pathology services within the hospital and established an
interpretive service for laboratory data for other clinicians. 1990 - 1991
Veterinary Research Officer -- MAFF Central Veterinary Laboratory, Weybridge,
Surrey. In this post I worked as a neuropathologist with Gerald Wells and
William Hadlow, in a large interdisciplinary team researching the prion diseases
of animals. My work concentrated on the neuropathological characterisation of
Bovine Spongiform Encephalopathy (BSE), the prion diseases of other animals and
their differential diagnosis. This gave me good general experience of
neurological disease, its diagnosis and pathological characteristics in a wide
range of animals and an introduction to many fields of neuroscience research.
Although broad-based, my research in these varying disciplines was centred on
the Prion protein and its gene, and associated molecular pathology in the prion
diseases. I described, amongst other things, the first cases in the UK of a
chlamydial disease of cattle putatively equivalent to Sporadic Bovine
Encephalomyelitis (see McGill and Wells, 1993). 13 Additional responsibilities
included: Liaison with the Consultant Pathology Unit for neuropathological
surveillance, including rabies diagnosis for the British Isles and
characterisation of novel diseases such as blue eared pig disease. Conducting
occasional seminars introducing scrapie and BSE diagnosis for visiting
scientists from abroad. Rapporteur for The Gibbs Committee on Subacute
Spongiform Encephalopathies (held at CVL in summer 1990). Papers presented at
AVTRW conferences at Scarborough (1990 & 1991), at European Community
Seminar on Spongiform Encephalopathies, Brussels, (1991) and International Pig
Veterinary Society, Holland, (1991). Aug 91 - Dec 92 Research Worker
(post-doctoral level) Department of Neuroscience, Institute of Psychiatry,
London In this post I continued to follow my interest in the prion diseases, and
gained a good grounding in both theoretical and practical molecular biology. I
cloned PrP genes from blood samples taken from individuals with PrP mutations
causal of familial CJD or GSS and transfected them into neuroblastoma cells in
culture to investigate the disease process in vitro. I continued to work with
colleagues from other disciplines, particularly Neurology and Neuropathology,
and with Professor Peter Lantos and others established for the first time that
prion disease can exist without its characteristic pathology (Lantos, McGill et
al, 1992). Positions of responsibility included: Lecturing on a course entitled
"Molecular Mechanisms of Neurodegeneration", to both internal and external
scientists, and as part of the London University M.Sc. Neuroscience course.
Lecturing on scrapie-like diseases as part of the London University M.Sc. in
Animal Health at the RVC. Liaison and research collaboration between the IOP and
my previous employers at CVL, Weybridge. Sole responsibility for the
organisation and funding of the 1992/1993 seminar series for the Department of
Neuroscience, in which leading researchers from around the UK were invited to
give seminars. Paper presented at AFRC BSEP meeting, Reading, April 1992. 1994 -
Present Scientific and Veterinary Consultant 14 (Spring 94) Acted as
neuropathological consultant for research on the transmissibility of BSE in
collaboration with Dr David White and Professor Neil Eddington at the Royal
Veterinary College, University of London. (Summer 94) Veterinary Surgeon, Blue
Cross Animal Hospital (Victoria, London) (Oct 94 - Dec 94) Lecturer in anatomy
and histology, Optics Department, City and Islington College (London). (1995)
Re-established the Prion Interest Group (originally founded at the Institute of
Psychiatry in 1991) as a private organisation, continuing research on prions.
Filmed and directed a documentary in India/Europe about Ayurvedic medicine.
Acted as a locum veterinarian for the PDSA and the Veterinary Centre Caterham.
(Jan 96 - Present) Veterinary Consultant to Ayuvet (UK) Ltd., co-ordinating
clinical and laboratory research into the Ayurvedic system of medicine and its
application in European veterinary medicine. Continued co-ordination of the
Prion Interest Group. Issued on behalf of the witness by: The BSE Inquiry Press
Office 6th Floor Hercules House Hercules Road London SE1 7DU Tel: 0171 261 8377
/ 8383 Fax: 0171 803 0893 Website:
http://www.bse.org.uk email: inquiry@bse.org.uk
DEFRA COMMENT BACK TO SINGELTARY ON HOUND STUDY AND BSE
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
Monday, March 26, 2012 CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF
ANIMAL PRION DISEASE
OR-09 15:10 - 15:25 CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL
PRION DISEASE David
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an
unrecognized sporadic or genetic case of bovine prion disease incorporated into
cattle feed or even cattle feed contaminated with prion-infected human remains.1
However, strong support for a genetic origin of BSE has recently been
demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2
Furthermore, a specific prion protein strain causing BSE in cattle is believed
to be the etiological agent responsible for the novel human prion disease,
variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in
a number countries, including France, Italy, Ireland, the Netherlands, Canada,
Japan, US and the UK with the largest number of cases. Naturally occurring
feline spongiform encephalopathy of domestic cats4 and spongiform
encephalopathies of a number of zoo animals so-called exotic ungulate
encephalopathies5,6 are also recognized as animal prion diseases, and are
thought to have resulted from the same BSE-contaminated food given to cattle and
humans, although and at least in some of these cases, a sporadic and/or genetic
etiology cannot be ruled out. The canine species seems to display resistance to
prion disease and no single case has so far been reported.7,8
Here, we describe a case of a 9 week old male Rottweiler puppy presenting
neurological deficits; and histological examination revealed spongiform
vacuolation characteristic of those associated with prion diseases.9 Initial
biochemical studies using anti-PrP antibodies revealed the presence of partially
proteinase K-resistant fragment by western blotting. Furthermore,
immunohistochemistry revealed spongiform degeneration consistent with those
found in prion disease and displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross
the species barrier transmitted to hamster in vitro with PMCA and in vivo (one
hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100%
attack rate (n = 4) and animals displayed untypical lesional profile and shorter
incubation period.
In this study, we show that the canine species might be sensitive to prion
disease and that PrPSc isolated from a dog can be transmitted to dogs and
hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major
impact on animal and public health and would certainly lead to implementing new
control measures for ‘canine spongiform encephalopathy’ (CSE).
References
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation.
PLoS Pathog 2008; 4:e1000156; PMID:18787697;
http://dx.doi.org/10.1371/journal.
ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy
(BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662;
http://dx.doi.org/10.1093/ hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith
JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic
cats. Vet Rec 1991; 129:233-6; PMID:1957458;
http://dx.doi.org/10.1136/vr.129.11.233.
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu
(Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink
encephalopathy species barrier effect between ferret and mink: PrP gene and
protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604;
http://dx.doi.org/10.1099/0022-1317-
75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et
al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad
Sci U S A 2005; 102:640-5; PMID:15647367;
http://dx.doi.org/10.1073/pnas.0408937102.
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Thursday, January 2, 2014
CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob
Disease MM1 genotype, and iatrogenic CJD ???
kind regards, terry
LAYPERSON
