Wednesday, January 15, 2014



Sent: Wednesday, January 15, 2014 11:22 AM

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 ?
kind regards,
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4
Published: June 2003
Revised and updated: January 2014
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
see full text ;
· Annex F – Endoscopy
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex F
Published: September 2004
Revised and updated: January 2014
Annex F
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:
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
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:
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 ???
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 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: References: <001501c21099 c58d182="" c8bc620="""">
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.
Title/position: disabled {neck injury}
Place of work: CJD WATCH
IP address: >>Hostname:
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.
Again, many thanks, Kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 CJD WATCH
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 ;
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 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:
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: email:
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
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
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).
1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http://
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; 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;
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315;
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; 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;
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854;
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Monday, March 26, 2012
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
Thursday, January 2, 2014
CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ???
kind regards, terry
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

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