Thursday, January 17, 2013

TSE guidance, surgical, dental, blood risk factors, Part 4 Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings (updated January 2013)

Greetings HPA et al,
a warm greetings from Bacliff, Texas.
in reply to ;
TSE guidance web update
Annex F

This guidance has been revised to align with other national guidance on decontamination of flexible endoscopes (in particular the Choice Framework for local Policy and Procedures 01-06). The main change concerns endoscopic procedures carried out on most asymptomatic patients “at increased risk” of vCJD where contact with medium risk gut associated lymphoid tissues may have occurred. It allows endoscopes to be decontaminated and returned to general use, providing decontamination procedures have been followed as set out in the Annex.
Annex J

Annex J has been revised to remove the pre-surgical assessment of blood transfusion history for those undergoing surgery or neuroendoscopy on high risk tissues. While an alternative means to identify the cohort of patients considered to be at increased risk of vCJD because of their transfusion history is being considered, selective identification through pre-surgical assessment has been stopped as it has proved difficult to implement in practice.
Annex M
This new guidance aims to provide practical advice for handling instruments that come into contact with medium infectivity tissues, involved in liver transplants and general surgical procedures, in order to reduce risk of vCJD transmission. It includes advice for elective and emergency surgery and on streaming instruments into those for incineration/quarantine or those that may be reprocessed.
Part 4

This document has been modified to maintain consistency with the above Annexes.
The updated versions are now available on the website at the following link:


Guidance from the ACDP TSE Risk Management Subgroup (formerly TSE Working Group)
27 November, 2012

As part of its remit the ACDP TSE Risk Management Subgroup produces the guidance document Transmissible spongiform encephalopathy agents: safe working and the prevention of infection. The aim of the guidance is the minimisation of the risk of transmission of CJD, and vCJD. The current guidance was published in June 2003, replacing the March 1998 edition. The guidance has evolved in the years since, with new annexes being added and current guidance being updated as further scientific information becomes available, or future policy decisions need to be reflected.
Latest news Published January 2013
Annex F Endoscopy (updated January 2013)
Annex J Assessment to be carried out before surgery and/or endoscopy to identify patients with, or at risk of, CJD or vCJD (updated January 2013)


Annex M Managing vCJD risk in general surgery and liver transplantation (published January 2013)


Part 4 Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings (updated January 2013)


Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4

Published: 2 June 2003
Amended: January 2013

Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings a. Blood borne transmission of vCJD re-examination of scenarios - 2011 Part 4 has been amended (December 2012) as follows to reflect the blood risk re-assessment carried out by the TSE Risk Assessment Sub Group in 2011a The threshold at which individuals are designated “at increased risk” of vCJD because of their transfusion history has been raised (from 80) to 300. This definition concerns those who have received blood or blood components from 300 or more donors since January 1990. This change has been made to Table 4a.
4.1 This guidance 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.
4.2 The use of the term “CJD” in this guidance encompasses sporadic CJD, genetic CJD, Fatal Familial Insomnia (FFI) and Gerstmann-Straussler-Scheinker Disease (GSS), in order to assist readability.
4.3 In this guidance document, the term ‘patients with, or “at increased risk” of, CJD or vCJD’ is used as a proxy for all patient groups in Table 4a. Where this term is used, the guidance is applicable to all patient groups in this Table. Other relevant guidance Caring for patients with, or “at increased risk” of, CJD or vCJD
4.4 “Creutzfeldt-Jakob Disease: Guidance for Healthcare Workers” advice on the care of patients with CJD/vCJD is available at This document refers to a “key worker” who will be constantly involved in the co-ordination of care of a patient with a clinical diagnosis of CJD/vCJD, in either a hospital or community setting. This is a named professional with a good knowledge of local health and social services, who should be identified as soon as possible after a diagnosis of CJD/vCJD seems likely. The “key worker” will be able to provide continuing support, and the primary source of advice and information, to both the patient and their family, and act as a patient advocate for necessary resources. Practical advice on developing patient care packages can be obtained from the National Care Co-ordinator at the National CJD Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh, Tel 0131 537 2129.
4.5 Guidance from the vCJD Clinical Governance Advisory Group available at, recommends that GPs should remain their clinical Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
guardian and anchor, supported by consultant neurologists and the specialist national centres – the National CJD Surveillance Unit and the National Prion Clinic.
Management arrangements for infection control
4.6 Under the Health and Social Care Act 2008, NHS bodies have to register with the Care Quality Commission (CQC), and as a requirement of registration they must protect patients, workers and others who may be at risk of acquiring a healthcare associated infection (including CJD/vCJD).
4.7 The 2008 Act enables the Secretary of State for Health to issue a Code of Practice relating to healthcare associated infections and the CQC to assess compliance with registration requirements on cleanliness and infection control by reference to this Code. A ‘Code of Practice for the NHS on the prevention and control of healthcare associated infections and related guidance’ was published in January 2009 and is available here:
4.8 From 1 April 2010, all NHS registered providers and from October 2010 all other registered providers, including independent healthcare providers, should comply with a revised Code of Practice - ‘The Health and Social Care Act 2008 Code of Practice for health and adult social care on the prevention and control of infections and related guidance’ published in December 2009. This requires registered providers to have in place the policies and procedures to meet criteria around infection prevention and control. This Code is available here:
4.9 The Code of Practice supersedes ‘Standards for Better Health’ and Controls Assurance standards. Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
4.10 The Code of Practice does not replace the requirement to comply with any other legislation that applies to health and social care services; for example, the Health and Safety at Work etc. Act 1974, and the Control of Substances Hazardous to Health Regulations 2002.
Tissue infectivity
4.11 Annexes A1 and A2 provide a summary of the distribution of abnormal prion protein in human tissues, a classification of infectivity in human tissues and body fluids in sporadic and vCJD, based (where available) on data from experimental studies, and a summary of information from other studies of natural TSE disease in humans and animals.
Iatrogenic transmission
4.12 There is no evidence to suggest that CJD/vCJD are spread from person-to-person by close contact, though it is known that transmission of CJD/vCJD can occur in specific situations associated with medical interventions – iatrogenic infections. Due to the possibility of iatrogenic transmission of CJD/vCJD, precautions need to be taken for certain procedures in healthcare, to prevent transmission.
4.13 Worldwide, cases of iatrogenic CJD have been associated with the administration of hormones prepared from human pituitary glands and dura mater preparations, and one definite case has been reported associated with a corneal graft (it is possible that the corneal tissue was contaminated by posterior segment tissue during processing). Iatrogenic transmission has also been identified following neurosurgical procedures with inadequately decontaminated instruments or EEG needles.
4.14 There have been no known transmissions of vCJD via surgery or use of tissues or organs. Since 2003, four cases (three clinical and one asymptomatic) of presumed person-to-person transmission of vCJD infection via blood transfusion of non-leucodepleted red blood cells have been reported in the UK. In addition,
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
in 2009, a case of probable asymptomatic vCJD infection via plasma products was reported in a haemophiliac.
4.15 Since 1997, when the theoretical risk of vCJD transmission through blood was first considered, the UK blood services have taken a number of precautionary measures to protect the blood supply and associated plasma products These precautionary measures to reduce the risk include: Blood components, plasma products or tissues obtained from any individual who later develops vCJD are withdrawn/recalled to prevent their use; Plasma for the manufacture of plasma products, such as clotting factors, has been obtained from non-UK sources since 1998; Synthetic (recombinant) clotting factor for treatment of haemophilia has been provided to the under-16s since 1998, and for all patients in whom it is suitable since 2005; Since 1999 white blood cells (which may carry a significant risk of transmitting vCJD) have been reduced in all blood used for transfusion, a process known as leucodepletion; Since 2002, fresh frozen plasma for treating babies and young children born on or after 1 January 1996 has been obtained from the USA. In 2005 its use was extended to all children up to the age of 16; Since 2004, individuals who have received a transfusion of blood components since January 1980, or are unsure if they have had a blood transfusion, are excluded from donating blood or platelets; Since 2009, cryoprecipitate, a special cold-treated plasma preparation, has been imported from the USA for children up to the age of 16.
Patient categorisation
4.16 When considering measures to prevent transmission to patients or staff in the healthcare setting, it is useful to make a distinction between: symptomatic patients, i.e. those who fulfil the diagnostic criteria for definite, probable or possible CJD or vCJD (see Annex B for full diagnostic criteria), and; patients “at increased risk” i.e. those with no clinical symptoms, but who are “at increased risk” of developing CJD or vCJD, because of their family or
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
medical history. For this group of patients, the infection control advice differs in some circumstances for:
o Patients at increased risk of genetic CJD
o Patients at increased risk because they have received blood from an individual who later developed variant CJD
o Other patients at increased risk of iatrogenic CJD
Table 4a details the classification of the risk status of symptomatic patients and patients “at increased risk”.
Patients “at increased risk” of CJD or vCJD
4.17 A number of patients have been identified as “at increased risk” of CJD or vCJD on the recommendation of the CJD Incidents Panel due to a medical or family history which places them “at increased risk” of developing CJD or vCJD. These patient groups are outlined in Table 4a.
4.18 In most routine clinical contact, no additional precautions are needed for the care of patients in the “increased risk” patient groups. However, when certain invasive interventions are performed, there is the potential for exposure to the agents of TSEs. In these situations it is essential that control measures are in place to prevent iatrogenic CJD/vCJD transmission.
4.19 All people who are “at increased risk” of CJD/vCJD are asked to help prevent any further possible transmission to other patients by following this advice: Don’t donate blood. No-one who is “at increased risk” of CJD/vCJD, or who has received blood donated in the United Kingdom since 1980, should donate blood; Don’t donate organs or tissues, including bone marrow, sperm, eggs or breast milk; If you are going to have any medical, dental or surgical procedures, tell whoever is treating you beforehand so they can make special arrangements for the instruments used to treat you if you need certain types of surgery or investigation; You are advised to tell your family about your increased risk. Your family can tell the people who are treating you about your increased risk of CJD/vCJD if
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4

you need medical or surgical procedures in the future and you are unable to tell them yourself.
4.20 GPs are asked to record their patient’s CJD/vCJD risk status in their primary care records. The GP should also include this information in any referral letter should the patient require surgical, medical or dental procedures.
Table 4a: Categorisation of patients by risk

Hospital care of CJD/vCJD patients
4.22 There is no evidence that normal social or routine clinical contact of a CJD/vCJD patient presents a risk to healthcare workers, relatives and others. Isolation of patients with CJD/vCJD is not necessary, and they can be nursed in an open ward using standard infection control precautions in line with those used for all other patients.
Sample taking and other invasive medical procedures
4.23 When taking samples or performing other invasive procedures, the possible infectivity of the tissue(s) involved must be considered, and if necessary suitable precautions taken. Information on tissue infectivities for CJD/vCJD is included in Annex A1 of this guidance. It is important to ensure that only trained staff, who are aware of the hazards, carry out invasive procedures that may lead to contact with medium or high risk tissue.
4.24 Body secretions, body fluids (including saliva, blood and cerebrospinal fluid (CSF) and excreta) are all low risk for CJD/vCJD. It is therefore likely that the majority of samples taken or procedures performed will be low risk. Contact with small volumes of blood (including inoculation injury) is considered low risk, though it is known that transfusion of large volumes of blood and blood components may lead to vCJD transmission.
4.25 Blood and body fluid samples from patients with, or “at increased risk” of, CJD/vCJD, should be treated as potentially infectious for blood-borne viruses and handled with standard infection control precautions as for any other patient, i.e.; use of disposable gloves and eye protection where splashing may occur; avoidance of sharps injuries and other forms of parenteral exposure; safe disposal of sharps and contaminated waste in line with locally approved arrangements; and single-use disposable equipment should be used wherever practicable.
4.26 When taking biopsy specimens of medium or high risk tissue, for example tonsil biopsy in a patient with suspected vCJD, or intestinal biopsy in a patient “at
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
increased risk” of vCJD, every effort should be taken to minimise the risk of infecting the operator or contaminating the environment.
4.27 In the event of needing to consider a brain biopsy, advice from the Department of Health, endorsed by the Chief Medical Officer, is available in Annex I.
4.28 Samples from patients with, or “at increased risk” of, CJD/vCJD should be marked with a ‘Biohazard’ label, and it is advisable to inform the laboratory in advance that a sample is being sent. Spillages
4.29 When a spillage of any fluid (including blood and CSF) from a patient with, or “at increased risk” of, CJD/vCJD occurs in a healthcare setting, the main defence is efficient removal of the contaminating material and thorough cleaning of the surface.
4.30 Standard infection control precautions should be followed for any spillages, which should be cleared up as quickly as possible, keeping contamination to a minimum. Disposable gloves and an apron should be worn when removing such spillages.
4.31 For spillages of large volumes of liquid, absorbent material should be used to absorb the spillage, for which a number of proprietary absorbent granules are available.
4.32 Standard disinfection for spillages (eg. 10,000ppm chlorine-releasing agent) should be used to decontaminate the surface after the spillage has been removed. A full risk assessment may be required. It should be noted that none of the methods currently suggested by WHO for prion inactivation are likely to be fully effective.
4.33 Any waste (including cleaning tools such as mop heads and PPE worn) should be disposed of as clinical waste (see Table 4b).
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013

Clinical waste

4.34 General guidance on the safe management of clinical waste is given in the Department of Health’s guidance document ‘Health Technical Memorandum 07-01: Safe Management of Healthcare Waste’, available at
4.35 According to this guidance, “Waste known or suspected to be contaminated with transmissible spongiform encephalopathy (TSE) agents, including CJD, must be disposed of by high temperature incineration in suitable authorised facilities.” Additional guidance on the management of TSE-infected waste is given in the Department of Health’s ‘Transmissible spongiform encephalopathy: Safe working and the prevention of infection.’
4.36 The ACDP TSE Risk Management Sub Group have considered the disposal of clinical waste, and have agreed that tissues, and contaminated materials such as dressings and sharps, from patients with, or “at increased risk” of, CJD/vCJD, should be disposed of as in the following table:
Table 4b: Disposal of clinical waste from patients with, or “at increased risk” of, CJD or vCJD

pregnant, it is important to ensure that patient confidentiality is properly maintained, and that any action taken to protect public health does not prejudice individual patient care.
4.38 Childbirth should be managed using standard infection control procedures. The placenta and other associated material and fluids are designated as low risk tissues, and should be disposed of as clinical waste, unless they are needed for investigation, in which case the precautions outlined in paragraphs 4.24-4.29 above should be followed. Instruments should be handled following the advice in paragraphs 4.46-4.56 below.

Bed linen
4.39 Used or fouled bed linen (contaminated with body fluids or excreta), should be washed and dried in accordance with current standard practice. No further handling or processing is necessary.
Occupational exposure
4.40 Although cases of CJD/vCJD have been reported in healthcare workers, there have been no confirmed cases linked to occupational exposure. However, it is prudent to take a precautionary approach.
4.41 The highest potential risk in the context of occupational exposure is from exposure to high infectivity tissues through direct inoculation, for example as a result of sharps injuries, puncture wounds or contamination of broken skin, and exposure of the mucous membranes.
4.42 Healthcare personnel who work with patients with definite, probable or possible CJD/vCJD, or with potentially infected tissues, should be appropriately informed about the nature of the risk and relevant safety procedures.
4.43 Compliance with standard infection control precautions, in line with those set out in “Guidance for Clinical Health Care Workers: Protection Against Infection with
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
Blood-borne Viruses” recommended by the Expert Advisory Group on AIDS and the Advisory Group on Hepatitis will help to minimise risks from occupational exposure.
4.44 For any accident involving sharps or contamination of abrasions with blood or body fluids, wounds should be gently encouraged to bleed, gently washed (avoid scrubbing) with warm soapy water, rinsed, dried and covered with a waterproof dressing, or further treatment given appropriate to the type of injury. Splashes into the eyes or mouth should be dealt with by thorough irrigation. The accident should be reported as defined in local practice, and an accident or incident form completed.
Surgical procedures and instrument management
4.45 For all patients with, or “at increased risk” of, CJD or vCJD, the following precautions should be taken for surgical procedures: Wherever appropriate and possible, the intervention should be performed in an operating theatre; Where possible, procedures should be performed at the end of the list, to allow normal cleaning of theatre surfaces before the next session; Only the minimum number of healthcare personnel required should be involved; Protective clothing should be worn, i.e. liquid repellent operating gown, over a plastic apron, gloves, mask and goggles, or full-face visor;
o for symptomatic patients, this protective clothing should be single use and disposed of in line with local policies;
o for patients “at increased risk” of CJD/vCJD, this protective clothing need not be single use and may be reprocessed; Single-use disposable surgical instruments and equipment should be used where possible, and subsequently destroyed

by incineration or sent to the instrument store; Effective tracking of re-usable instruments should be in place, so that instruments can be related to use on a particular patient.
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
Single use instruments

4.46 Single-use instruments are utilised variably across surgical specialities and NHS Trusts. The following should be taken into account when using single-use instruments: The quality and performance of single-use instruments should be equivalent to those of reusable instruments with appropriate procurement, quality control and audit mechanisms in place; Procurement should be quality based not cost based, with the minimum safe functional requirements of each instrument purchased being understood by the purchaser; For reusable instruments there is an internal quality control, with instruments noted as faulty being either repaired or returned to the system manufacturer. A similar process needs to be put in place for any single-use instrument that is purchased; A CE mark is not necessarily a mark of quality of instruments, and quality control of sub-contractors is often difficult when the number of instruments increases. Handling of instruments that are not designated as single-use
4.47 Where single-use instruments are not available, the handling of reusable instruments depends on: how likely the patient is to be carrying the infectious agent (the patient’s risk status); whether the patient has, or is “at increased risk” of, CJD/vCJD; and how likely it is that infection could be transmitted by the procedure being carried out i.e. whether there is contact with tissues of high or medium infectivity. 4.48 Tables 4c and 4d separately set out the actions to be taken for instruments used on patients with, or “at increased risk” of, CJD/vCJD. The differences in instrument management are due to differences in tissue infectivities between CJD/vCJD. These actions are also summarised in the algorithm at the end of this document.
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
Table 4c: Handling of instruments – patients with, or “at increased risk” of, CJD (other than vCJD)

*Although dura mater is designated low infectivity tissue, procedures conducted on intradural tissues (i.e. brain , spinal cord and intracranial sections of cranial nerves) or procedures in which human dura mater has been implanted in a patient prior to 1992, are high risk and instruments should be handled as such.
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
Quarantining instruments
4.49 Annex E provides guidance on the procedures which should be followed when quarantining surgical instruments is considered. Decontamination of instruments
4.50 Effective decontamination is key to reducing the risk of transmission of CJD/vCJD through surgery. Annex C contains advice on the general principles of decontamination for TSE agents, and Table C4 contains a list of selected guidelines and standards related to decontamination.
4.51 It is important that the efficacy, safety, and compatibility with other decontamination processes, of products and technologies claiming to remove or inactivate prion protein from contaminated medical devices in laboratory and clinical practice, is established. Until this occurs, clinicians and laboratory managers should ensure that current guidelines are followed. Incineration of instruments
4.52 The instruments should already be in a combustible sealed container. This should then be disposed of via the clinical waste stream, ensuring that this results in incineration. Complex instruments
4.53 Some expensive items of equipment, such as drills and operating microscopes, may be prevented from being contaminated by using shields, guards or coverings, so that the entire items does not need to be destroyed. In this case, the drill bit, other parts in contact with high or medium risk tissues, and the protective coverings, would then need to be incinerated. However, in practice, it may be difficult to ensure effective protective covering, and advice should be sought from neurosurgical staff and the manufacturer to determine practicality.
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013

Use of laser for tonsillectomy – smoke plumes

4.54 Some ENT surgeons may use laser techniques as an alternative to ‘conventional’ surgery for tonsillectomy. There is no evidence of the transmission of TSEs by the respiratory route. Any risk to surgeons from smoke plumes is thought to be very low, but there are no data on vCJD. General guidance on the safe use of lasers is available from MHRA - Device Bulletin 2008(03) ‘Guidance on the safe use of lasers, IPL systems and LEDs’ – available here.

Anaesthesia and intensive care
4.55 The Association of Anaesthetists of Great Britain and Ireland (AAGBI) in 2008 published an update to their guidance “Infection Control in Anaesthesia.” This guidance includes a section on prion diseases and can be found here. Endoscopy
4.56 Annex F contains advice on the precautions to be taken for endoscopic procedures on patients with, or “at increased risk” of, CJD/vCJD.
4.57 Annex L contains advice on the precautions to be taken for ophthalmic procedures on patients with, or “at increased risk” of, CJD/vCJD.
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013 Community healthcare of CJD/vCJD patients
4.58 People should not be dissuaded from routine contact with CJD/vCJD patients as both CJD and vCJD are not thought to present a risk through normal social or routine clinical contact.
4.59 No special measures over and above standard infection control precautions are generally required for caring for CJD/vCJD patients in the community, as it is unlikely that procedures will be adopted that will lead to contact with high or medium risk tissues.
Caring for symptomatic patients at home
4.60 Those caring for patients at home should be advised of the standard infection control practices that would apply to any patient. They should be provided with disposable gloves, paper towels, waste bags and sharps containers, as appropriate. Provision should be made with the Local Authority for the removal and disposal of clinical waste and sharps from the home.
4.61 Late stage CJD/vCJD patients may experience tissue breakdown and the development of extensive pressure sores. These lesions should be dressed regularly, using standard infection control precautions, and contaminated dressings disposed of as normal clinical waste. Spillages
4.62 It is assumed that all spillages in the community will be of low risk material, for example blood and urine. Standard infection control precautions should be followed to clear up spillages of material from patients with, or “at increased risk” of, CJD/vCJD in the community. Spillages should be cleared up as quickly as possible, keeping contamination to a minimum. Disposable gloves and an apron should be worn when removing such spillages. The surface should then be washed thoroughly with detergent and warm water.
4.63 For spillages of large volumes of liquid, absorbent material should be used to absorb the spillage. A number of proprietary absorbent granules are available for
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013

such use, including those containing sodium dichloroisocyanurate, but it should be noted that these do not deactivate TSE agents.
4.64 Any waste (including cleaning tools such as mop heads and PPE worn) should be disposed of as normal clinical waste. Clinical waste
4.65 Clinical waste should be disposed of as set out in Table 4b.
Bed linen
4.66 Patients’ clothes and bed linen can be washed as normal, although in the interests of general hygiene it may be preferable to wash fouled linen separately. Commercial laundry services can be used as an alternative and, particularly where patients are incontinent, a laundry service can be of great help to carers.
4.67 In the event that a patient with, or “at increased risk” of, CJD or vCJD becomes pregnant, no additional infection control precautions need to be taken during the pregnancy. If a home delivery is decided upon, it is the responsibility of the midwife to ensure that any contaminated material is removed and disposed of in line with the procedures described in paragraph 4. 39.
4.68 The risks of transmission of infection from dental instruments are thought to be very low provided satisfactory standards of infection control and decontamination are maintained. There is no reason why any patient with, or “at increased risk” of, CJD or vCJD, should be refused routine dental treatment. Such people can be treated in the same way as any member of the general public.
4.69 Information for dentists about the management of patients with, or “at increased risk” of, CJD/vCJD can be found here. Advice for dentists on re-use of endodontic instruments and vCJD can be found here. An advice note concerning problems with dental care for individuals 'at-risk' of CJD for public health purposes can be found here.
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013
4.70 Dental instruments used on patients with, or “at increased risk” of, CJD or vCJD can be handled in the same way as those used in any other low risk surgery, i.e. these instruments can be reprocessed according to best practice and returned to use. Dentists are reminded that any instruments labelled by manufacturers as ‘single-use’ should not be re-used under any circumstances.
4.71 Advice on the decontamination of dental instruments can be found in the Department of Health guidance HTM01-05 ‘Dental decontamination’. This guidance has been produced to reflect a reasonable and rational response to emerging evidence around the effectiveness of decontamination in primary care dental practices, and the possibility of prion transmission through protein contamination of dental instruments. It is available here. After death
4.72 Guidance on dealing with the bodies of patients with, or “at increased risk” of, CJD or vCJD, is contained in Annex H. This includes advice on carrying out post mortem examinations and transportation of bodies, and advice for undertakers on embalming, funerals and cremations.
Greetings again HPA et al,
I repeat, what I have said all along, all these human and animal TSE prion strains must all be made reportable, and there should be no age restrictions tied to any reporting criteria. TSE prion disease knows no borders, they know no age groups.
Finally, the infamous UKBSEnvCJD only theory should be put to rest once and for all.
For the scientific communities to continue to endorse such fallacious, and misleading science as the UKBSEnvCJD only theory, this will only lead to other, needless and countless exposures, and I can only guess as to how many in the future will go clinical and die.
These needless and countless exposures and deaths, in the near future, years, decades to come, from the Transmissible Spongiform Encephalopathy TSE prion disease, the Prionpathy, the Prionopathies, the VPSPr’s, the sporadic CJD and all it’s sub-types, the sporadic FFI’s and all it’s potential sub-types, what about GSS, what about a case of sporadic Creutzfeldt-Jakob disease with a Gerstmann-Sträussler-Scheinker phenotype but no alterations in the PRNP gene, and don’t forget VPSPr. VPSPr, has introduced a novel and very different prion strain to sporadic human prion diseases which may have similarities with those associated with GSS.
none of this is possibly tied to iatrogenic TSE in humans and or a zoonosis source, and or both?
TO continue to base iatrogenic TSE prion safety protocols and guidelines, and continue to base this only on the UKBSEnvCJD theory, and all the rest a spontaneous happenstance of bad luck, is NOT scientific in my opinion, and I and the world will hold you all responsible for future needless exposure and deaths by basing your scientific advice, on corporate and political science, bought and paid for by the the livestock industry, and enforced by the OIE, USDA, CFIA, DEFRA, et al. ...
Ladies and Gentlemen, source references at the bottom of these comments with links, for anyone that is still interested in the rest of this nightmare. ...
thank you,
with kindest regards,
I am sincerely and respectfully,

Terry S. Singeltary Sr.

Thursday, January 17, 2013

FSA notified of two breaches of BSE testing regulations 14 January 2013

Monday, January 14, 2013
Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe

Saturday, January 12, 2013

Exposure of RML scrapie agent to a sodium percarbonate-based product and sodium dodecyl sulfate renders PrPSc protease sensitive but does not eliminate infectivity

Tuesday, December 25, 2012
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

Thursday, October 25, 2012
Current limitations about the cleaning of luminal endoscopes and TSE prion risk factors there from
Article in Press

Something I submitted to GUT previously in the year 2002 ;
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
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:
>>Title/position: disabled {neck injury}
>>Place of work: CJD WATCH
>>IP address:
>>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4)
>>Gecko/20011019 Netscape6/6.2
>> >>Parent ID: 50/6/888
>> 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
Terry S. Singeltary Sr.
Again, many thanks, Kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 CJD WATCH
[scroll down past article for my comments]
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.
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
Tuesday, December 18, 2012
Bioassay Studies Support the Potential for Iatrogenic Transmission of Variant Creutzfeldt Jakob Disease through Dental Procedures
Friday, August 24, 2012
Iatrogenic prion diseases in humans: an update
Monday, August 13, 2012
Summary results of the second national survey of abnormal prion prevalence in archived appendix specimens August 2012
Friday, August 10, 2012
Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual update (July 2012)
Friday, June 29, 2012
Highly Efficient Prion Transmission by Blood Transfusion
Thursday, May 17, 2012
Iatrogenic Creutzfeldt-Jakob Disease, Final Assessment
Volume 18, Number 6—June 2012
Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD, and GSS Blood Specimens: the Baxter Study
Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5; Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama, USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General Hospital, UK; 5Baxter BioSience, Austria
Background: Rodent and sheep models of Transmissible Spongiform Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical and clinical phases of disease. Results in a (presumably more appropriate) non-human primate model have not been reported.
Objective: To determine if blood components (red cells, white cells, platelets, and plasma) from various forms of human TSE are infectious.
Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma samples from chimpanzees infected with either sCJD or Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a period of 5 years, and all dying or sacrificed animals had post-mortem neuropathological examinations and Western blots to determine the presence or absence of the misfolded prion protein (PrPTSE).
Results: No transmissions occurred in any of the animals inoculated with blood components from patients with sporadic or variant CJD. All donor chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their pre-clinical phase plasmapheresis, several months earlier than the expected onset of illness. One monkey inoculated with purified leukocytes from a pre-clinical GSS chimpanzee developed disease after 36 months.
Conclusion: No infectivity was found in small volumes of blood components from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a single transmission from a chimpanzee-passaged strain of GSS shows that infectivity may be present in leukocytes, and the shock of general anaesthesia and plasmspheresis appears to have triggered the onset of illness in pre-clinical donor chimpanzees.
Saturday, September 5, 2009
Saturday, September 5, 2009
But the first thing is our own study, and as I mentioned, it's a Baxter primate study, and those are the major participants. And the goal was twofold, and here is the first one: to see whether CJD, either sporadic or familial -- actually it turns out to be the familial CJD is incorrect. It really should be the Fukuoka strain of Gerstmann-Straussler-Scheinker disease. So it's really GSS instead of familial CJD -- when passaged through chimps into squirrel monkeys using purified blood components, very pure blood components.
So this addresses the question that was raised just recently about whether or not red cell infectivity that's been found in rodents is really in the red cells or is it contaminated.
We prepared these samples with exquisite care, and they are ultra-ultra-ultra purified. There's virtually no contamination of any of the components that we looked at ? platelets, red cells, plasma, white cells -- with any other component.
These are a sort of new set of slides, and what I've tried to do is make them less complicated and more clear, but I'm afraid I haven't included the build. So you'll just have to try and follow what I explain with this little red pointer.
There were three initial patients. Two of them had sporadic CJD. One of them had Gerstmann-Straussler-Scheinker syndrome. Brain tissue from each individual patient was inoculated intracerebrally into a pair of chimpanzees. All right?
From those chimps, either plasma or ultra purified -- in fact, everything is ultra-purified. I'll just talk about purified plasma, purified white cells -- were inoculated intracerebrally and intravenously to get the maximum amount of infective load into a pair of squirrel monkeys.
The same thing was done for each of these three sets. This monkey died from non-CJD causes at 34 months post inoculation.
Let me go back for a second. I didn't point out the fact that these were not sacrificed at this point. These chimpanzees were apheresed at 27 weeks when they were still asymptomatic. In this instance, we apheresed them terminally when they were symptomatic.
And before I forget, I want to mention just a little sidelight of this. Chimpanzees in our experience -- and I think we may be the only people that have ever inoculated chimpanzees, and that's no longer a possibility, so this was 20, 30 years ago -- the shortest incubation period of any chimpanzee that we have ever seen with direct intracerebral inoculation is 13 months.
So we chose 27 weeks, which is about seven months, and incidentally typically the incubation period is more like 16 or 18 months. The shortest was 13 months. We chose the 27th week, which is about six and a half months, thinking that this would be about halfway through the incubation period, which we wanted to check for the presence or absence of infectivity.
But within four weeks after the apheresis, which was conducted under general anesthesia for three or four hours apiece, every single one of the six chimpanzees became symptomatic. That is another experiment that I would love to conclude, perhaps because this is simply not heard of, and it very much smells like we triggered clinical illness. We didn't trigger the disease, but it certainly looks like we triggered symptomatic disease at a point that was much earlier than one would have possibly expected.
Maybe it will never be done because it would probably open the floodgates of litigation. There's no end of little things that you can find out from CJD patients after the fact. For example, the neighbor's dog comes over, barks at a patient, makes him fall down, and three weeks later he gets CJD. So you have a lawsuit against the neighbor.
I mean, this is not an unheard of matter, but I do think that physical stress in the form of anesthesia and four hours of whatever goes on with anesthesia, low blood pressure, sometimes a little hypoxemia looks like it's a bad thing.
So here we have the 31st week. All of the chimps are symptomatic, and here what we did was in order to make the most use of the fewest monkeys, which is always a problem in primate research, we took these same three patients and these six chimps. Only now we pooled these components; that is to say, we pooled the plasma from all six chimps. We pooled ultra-purified white cells from all six chimps because here we wanted to see whether or not we could distinguish a difference between intracerebral route of infection and intravenous route of infection.
With respect to platelets and red blood cells, we did not follow that. We inoculated both intracerebral and intravenously, as we had done earlier because nobody has any information on whether or not platelets and red cells are infectious, and so we wanted again to get the maximum.
This is an IV versus IC goal. This one, again, is just getting the maximum load in to see whether there is, in fact, any infectivity in pure platelets, in pure red cells.
And of all of the above, the only transmission of disease related to the inoculation was in a squirrel monkey that received pure leukocytes from the presymptomatic apheresis. So that goes some way to address the question as to whether or not it's a matter of contamination. To date the red cells have not been -- the monkeys that receive red cells have not been observed for more than a year because that was a later experiment.
So we still can't say about red cells, but we're about four and a half years down the road now, and we have a single transmission from purified leukocytes, nothing from plasma and nothing from platelets.
That was the first part of the experiment. The second part was undertaken with the cooperation of Bob Will and others supplying material to us. These were a couple of human, sporadic cases of CJD and three variant cases of CJD from which we obtained buffy coat and plasma separated in a normal way. That is, these are not purified components.
The two cases of sporadic CJD, the plasma was pooled from both patients. The buffy coat was pooled from both patients, and then inoculated intracerebrally and intravenously into three squirrel monkeys each. This is a non-CJD death five years after inoculation. The other animals are still alive.
For variant CJD we decided not to pool. It was more important to eliminate the possibility that there was just a little bit of infectivity in one patient that would have been diluted to extinction, if you like, by mixing them if it were to so occur with two patients, for example, who did not have infectivity. So each one of these was done individually, but the principle was the same: plasma and buffy coat for each patient was inoculated into either two or three squirrel monkeys. This is, again, a non-CJD related death.
In addition to that, we inoculated rain as a positive control from the two sporadic disease cases of human -- from the two human sporadic cases at ten to the minus one and ten to the minus three dilutions. We have done this many, many times in the past with other sporadic patients. So we knew what to expect, and we got exactly what we did expect, namely, after an incubation period not quite two years, all four monkeys developed disease at this dilution and at the minus three dilution, not a whole lot of difference between the two.
Now, these are the crucial monkeys because each one of these monkeys every three to four months was bled and the blood transfused into a new healthy monkey, but the same monkey all the time. So this monkey, for example, would have received in the course of 21 months about six different transfusions of blood from this monkey into this monkey, similarly with this pair, this pair, and this pair. So you can call these buddies. This is sort of the term that was used. These monkeys are still alive.
In the same way, the three human variant CJD specimens, brain, were inoculated into four monkeys, and again, each one of these monkeys has been repeatedly bled at three to four month intervals and that blood transfused into a squirrel monkey, the same one each time. Ideally we would love to have taken bleeding at three months and inoculated a monkey and then let him go, watch him, and then done the same thing at six months. It would have increased the number of monkeys eightfold and just unacceptably expensive. So we did the best we could.
That, again, is a non-CJD death, as is this.
This was of interest mainly to show that the titer of infectivity in brain from variant CJD is just about the same as it from sporadic. We didn't do a minus five and a minus seven in sporadic because we have an enormous experience already with sporadic disease in squirrel monkeys, and we know that this is exactly what happens. It disappears at about ten to the minus five. So the brain titer in monkeys receiving human vCJD is identical to the brain titer in monkeys that have been inoculated with sporadic CJD.
That's the experiment. All of the monkeys in aqua are still alive. They are approaching a five-year observation period, and I think the termination of this experiment will now need to be discussed very seriously in view of a probable six-year incubation period in the U.K. case. The original plan was to terminate the experiment after five years of observation with the understanding that ideally you would keep these animals for their entire life span, which is what we used to do when had unlimited space, money, and facilities. We can't do that anymore.
It's not cheap, but I think in view of the U.K. case, it will be very important to think very seriously about allowing at least these buddies and the buddies from the sporadic CJD to go on for several more years because although you might think that the U.K. case has made experimental work redundant, in point of fact, anything that bears on the risk of this disease in humans is worthwhile knowing, and one of the things we don't know is frequency of infection. We don't know whether this case in the U.K. is going to be unique and never happen again or whether all 13 or 14 patients have received blood components are ultimately going to die. Let's hope not.
The French primate study is primarily directed now by Corinne Lasmezas. As you know, the late Dominique Dromont was the original, originally initiated this work, and they have very active primate laboratory in France, and I'm only going to show two very simple slides to summarize what they did.
The first one is simply to show you the basis of their statement that the IV route of infection looks to be pretty efficient because we all know that the intracerebral route of infection is the most efficient, and if you look at this where they inoculated the same infective load either intracerebrally or intravenously, the incubation periods were not substantially different, which suggests but doesn't prove, but doesn't prove that the route of infection is pretty efficient.
Lower doses of brain material given IV did extend the incubation period and presumably it's because of the usual dose response phenomenon that you see in any infectious disease.
With a whopping dose of brain orally, the incubation period was even lower. Again, just one more example of inefficiency of the route of infection and the necessity to use more infective material to get transmissions.
And they also have blood inoculated IV which is on test, and the final slide or at least the penultimate slide shows you what they have on test and the time of observation, that taken human vCJD and like us inoculated buffy coat, they've also inoculated whole blood which we did not do.
So to a great extent their studies are complementary to ours and makes it all worthwhile.
We have about -- oh, I don't know -- a one to two-year lead time on the French, but they're still getting into pretty good observation periods. Here's three-plus years.
They have variant CJD adapted to the macaque. That is to say this one was passaged in macaque monkeys, the cynomolgus, and they did the same thing. Again, we're talking about a study here in which like ours there are no transmissions. I mean, we have that one transmission from leukocytes, and that's it.
Here is a BSE adapted to the macaque. Whole blood, and then they chose to inoculate leukodepleted whole blood, in both instances IV. Here they are out to five years without a transmission.
And then finally oral dosing of the macaque, which had been infected with -- which was infected with BSE, but a macaque passaged BSE, whole blood buffy coat and plasma, all by the IC route, and they're out to three years.
So with the single exception of the leukocyte transmission from our chimp that was inoculated with a sporadic case of CJD or -- excuse me -- with a GSS, Gerstmann-Straussler, in neither our study nor the French study, which are not yet completed have we yet seen a transmission.
And I will just close with a little cartoon that appeared in the Washington Post that I modified slightly lest you get too wound up with these questions of the risk from blood. This should be a "corrective."
DR. BROWN: Thanks.
CHAIRPERSON PRIOLA: Yes. Any questions for Dr. Brown? Dr. Linden.
DR. LINDEN: I just want to make sure I understand your study design correctly. When you mention the monkeys that have the IV and IC inoculations, the individual monkeys had both or --
DR. BROWN: Yes, yes, yes. That's exactly right.
DR. LINDEN: So an individual monkey had both of those as opposed to some monkeys had one and some had the other?
DR. BROWN: Correct, correct. Where IC and IV are put down together was IC plus IV into a given monkey.
DR. LINDEN: Into a given monkey. Okay.
And the IC inoculations, where were those given?
DR. BROWN: Right parietal cortex, Southern Alabama.
DR. BROWN: Oh, it can't be that clear. Yeah, here, Pierluigi.
DR. BROWN: Pierluigi always damns me with feint praise. He always says that's a very interesting study, but. I'm waiting for that, Pierluigi.
I think Jay Epstein --
DR. GAMBETTI: I will say that there's an interesting study and will say, but I just --
DR. GAMBETTI: -- I just point of review. You talk about a point of information. You say that -- you mention GSS, I guess, and the what, Fukuowa (phonetic) --
DR. BROWN: Yes, Fukuoka 1.
DR. GAMBETTI: Fukuowa, and is that from the 102, if I remember correctly, of the --
DR. BROWN: Yes, that is correct.
DR. GAMBETTI: Because that is the only one that also --
DR. BROWN: No, it's not 102. It's 101. It's the standard. It's a classical GSS. Oh, excuse me. You're right. One, oh, two is classical GSS. It's been so long since I've done genetics. You're right.
DR. GAMBETTI: Because that is the only one I know, I think, that I can remember that has both the seven kv fragment that is characteristic of GSS, but also the PrPsc 2730. So in a sense, it can be stretching a little bit compared to the sporadic CJD.
DR. BROWN: Yeah, I think that's right. That's why I want to be sure that I made you aware on the very first slide that that was not accurate, that it truly was GSS.
There's a GSS strain that has been adapted to mice, and it's a hot strain, and therefore, it may not be translatable to sporadic disease, correct. All we can say for sure is that it is a human TSE, and it is not variant. I think that's about it.
DR. GAMBETTI: I agree, but this is also not perhaps the best --
DR. BROWN: No, it is not the best. We understand --
DR. GAMBETTI: -- of GSS either.
DR. BROWN: Yeah. If we had to do it over again, we'd look around for a -- well, I don't know. We'd probably do it the same way because we have two sporadics already on test they haven't transmitted, and so you can take your pick of what you want to pay attention to.
DR. EPSTEIN: Yes, Paul. Could you just comment? If I understood you correctly, when you did the pooled apheresis plasma from the six chimps when they were symptomatic at 31 weeks, you also put leukocytes into squirrel monkeys in that case separately IV and IC, but in that instance you have not seen an infection come down in squirrel monkey, and the question is whether it's puzzling that you got transmission from the 27-week asymptomatic sampling, whereas you did not see transmission from the 31-week sampling in symptomatic animals.
DR. BROWN: Yes, I think there are two or three possible explanations, and I don't know if any of them are important. The pre-symptomatic animal was almost symptomatic as it turned out so that we were pretty close to the period at which symptoms would being, and whether you can, you know, make much money on saying one was incubation period and the other was symptomatic in this particular case because both bleedings were so close together. That's one possibility.
The other possibility is we're dealing with a very irregular phenomenon and you're not surprised at all by surprises, so to speak so that a single animal, you could see it almost anywhere.
The third is that we, in fact, did just what I suggested we didn't want to do for the preclinical, namely, by pooling we got under the threshold. See?
You can again take that for what it's worth. It is a possible explanation, and again, until we know what the levels of infectivity are and whether by pooling we get under the threshold of transmission, we simply cannot make pronouncements.
DR. DeARMOND: Yeah, it was very interesting data, but the --
DR. BROWN: I just love it. Go ahead.
DR. DeARMOND: Two comments. The first one was that the GSS cases, as I remember from reading your publications -- I think Gibbs was involved with them -- when you transmitted the GSS into animals, into monkeys, perhaps I think it was chimps, the transmission was more typical of CJD rather than GSS. There were no amyloid plaques. It was vacuolar degeneration so that you may be transmitting a peculiar form, as I criticized once in Bali and then you jumped all over me about.
DR. BROWN: I may do it again.
DR. DeARMOND: Calling me a bigot and some other few things like that.

DR. BROWN: Surely not. I wouldn't have said that.
DR. DeARMOND: So there could be something strange about that particular --
DR. BROWN: Yeah. I think you and Pierluigi are on the same page here. This may be an unusual strain from a number of points of view.
DR. DeARMOND: The other question though has to do with species barrier because the data you're showing is kind of very reassuring to us that it's hard to transmit from blood, but the data from the sheep and from the hamsters and some of the work, I think, that has been done by others, that it's easy in some other animals to transmit, hamster to hamster, mouse to mouse.
Could you comment on the --
DR. BROWN: That's exactly why we went to primates. That's exactly it, because a primate is closer to a human than a mouse is, and that's just common sense.
And so to try and get a little closer to the human situation and not totally depend on rodents for transferrable data, that is why you would use a primate. Otherwise you wouldn't use them. They're too expensive and they cause grief to animal care study people and protocol makers and the whole thing.
Primate studies are a real pain.
DR. DeARMOND: But right now it's inconclusive and you need more time on it.
DR. BROWN: I believe that's true. I think if we cut it off at six years you could still say it was inconclusive, and cutting it off at all will be to some degree inconclusive, and that's just the way it is.
DR. DeARMOND: So what has to be done? Who do you have to convince, or who do we all have to convince to keep that going?
DR. BROWN: Thomas?
Without trying to be flip at all, the people that would be the first people to try to convince would be the funders of the original study. If that fails, and it might for purely practical reasons of finance, then we will have to look elsewhere because I really don't want to see those animals sacrificed, not those eight buddies. Those are crucial animals, and they don't cost a whole lot to maintain. You can maintain eight -- well, they cost a lot from my point of view, but 15 to $20,000 a year would keep them going year after year.
DR. JOHNSON: Yeah, Paul, I'm intrigued as you are by the shortening of the incubation period. Have you in all of the other years of handling these animals when they were transfused, when they were flown out to Louisiana at night -- a lot of the stressful things have happened to some of these chimps. Have you ever noticed that before or is this a new observation?
DR. BROWN: Brand new.
MR. JOHNSON: Brand new. Okay.
CHAIRPERSON PRIOLA: Bob, did you want to say something? Dr. Rohwer.
DR. ROHWER: The Frederick fire, wasn't that correlated with a lot of --
DR. BROWN: Not that I k now of, but you may --
DR. ROHWER: Well, that occurred shortly after I came to NIH, and what I remember is that there were a whole bunch of conversions that occurred within the few months following the fire. That was fire that occurred adjacent to the NINDS facility, but in order to protect it, they moved the monkeys out onto the tarmac because they weren't sure it wouldn't burn as well.
DR. BROWN: Well, if you're right, then it's not brand new, but I mean, I'm not sure how we'll ever know because if I call Carlton and ask him, I'm not sure but what I would trust the answer that he gives me, short of records.
You know, Carlot is a very enthusiastic person, and he might say, "Oh, yeah, my God, the whole floor died within three days," but I would want to verify that.
On the other hand, it may be verifiable. There possibly are records that are still extant.
DR. ROHWER: Actually I thought I heard the story from you.
DR. BROWN: You didn't because it's brand new for me. I mean, either that or I'm on the way
DR. BRACEY: I was wondering if some of the variability in terms of the intravenous infection route may be related to intraspecies barriers, that is, the genetic differences, the way the cells, the white leukocytes are processed, whether or not microchimerism is established, et cetera.
DR. BROWN: I don't think that processing is at fault, but the question, the point that you raise is a very good one, and needless to say, we have material with which we can analyze genetically all of the animals, and should it turn out that we get, for example, -- I don't know -- a transmission in one variant monkey and no transmissions in another and a transmission in three sporadic monkeys, we will at that point genetically analyze every single animal that has been used in this study, but we wanted to wait until we could see what would be most useful to analyze.
but the material is there, and if need be, we'll do it.
CHAIRPERSON PRIOLA: Okay. Thank you very much, Dr. Brown.
I think we'll move on to the open public hearing section of the morning.




see full text ;

Saturday, January 20, 2007
Fourth case of transfusion-associated vCJD infection in the United Kingdom
Friday, June 29, 2012
Highly Efficient Prion Transmission by Blood Transfusion
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
Sunday, May 1, 2011
W.H.O. T.S.E. PRION Blood products and related biologicals May 2011
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???

Sunday, August 01, 2010
Blood product, collected from a donors possibly at increased risk for vCJD only, was distributed USA JULY 2010
atypical L-type BASE BSE California 2012
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
(see tons and tons of banned highly suspect mad cow feed in ALABAMA 2006, and 2007, one decade post partial and voluntary mad cow feed ban in the USA, see where 10,000,000 pounds of blood laced banned meat and bone meal was fed out into commerce)
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012
Thursday, June 14, 2012
R-CALF USA Calls USDA Dishonest and Corrupt; Submits Fourth Request for Extension
R-CALF United Stockgrowers of America

Monday, June 18, 2012 R-CALF
Submits Incomplete Comments Under Protest in Bizarre Rulemaking “Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products”
Canada has had a COVER-UP policy of mad cow disease since about the 17th case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored $$$
THIS proves there is indeed an epidemic of mad cow disease in North America, and it has been covered up for years and years, if not for decades, and it’s getting worse $$$
Thursday, February 10, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

Wednesday, August 11, 2010
Thursday, August 19, 2010

Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
Scrapie and atypical Scrapie Nor98
Wednesday, February 16, 2011

Sunday, April 18, 2010
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Thursday, February 23, 2012

Atypical Scrapie NOR-98 confirmed Alberta Canada sheep January 2012
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011 However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40).
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Monday, November 30, 2009
I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS
Chronic Wasting Disease CWD
Thursday, November 29, 2012
Chronic wasting disease on the Canadian prairies
Tuesday, November 13, 2012

Wednesday, November 14, 2012
Friday, November 09, 2012
Chronic Wasting Disease CWD in cervidae and transmission to other species
OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.
Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
Wednesday, March 28, 2012
*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
1 Listed based on the year of death or, if not available, on year of referral; 2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted; 3 Disease acquired in the United Kingdom; 4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case; *** 5 Includes 8 cases in which the diagnosis is pending, and 18 inconclusive cases; *** 6 Includes 10 (9 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded. *** The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2224 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
Friday, November 23, 2012
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA

Greetings BSE-L members et al, and others,
Confucius is confused again on the infamous ‘classification pending sporadic creutzfeldt jakob disease’ cpsCJD, (because nvCJD has been ruled out).

Confucius is confused about why the increase of these cpsCJD cases in the USA and Canada which we have been seeing, but I saw no reports in the UK surveillance reports of the infamous North American Classification Pending Sporadic Creutzfeldt Jakob disease cases.
if truly a supposedly sporadic spontaneous disease, would you not see these cpsCJD cases popping up all over the world in random ???

or, could these cpsCJD cases be of a North American zoonotic or iatrogenic from North American zoonoses sub-clinical source ???
or both ???
with so many documented Transmissible Spongiform Encephalopathy TSE prion disease in so many different species here in North America, and consumption there from, I believe that this should be at the forefront of research. ...

Confused Confucius...flounder
snip...see full text ;

Friday, November 23, 2012
sporadic Creutzfeldt-Jakob Disease update As at 5th November 2012 UK, USA, AND CANADA
Saturday, October 6, 2012

Sunday, December 2, 2012
CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE BLEW IT’
Tuesday, November 6, 2012
Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and Sporadic CJD, November-December 2012 update
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA

Wednesday, June 13, 2012


Tuesday, December 25, 2012
Saturday, December 29, 2012
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012
Tuesday, July 31, 2012
11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital
Thursday, August 02, 2012
CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients
Saturday, January 05, 2013
Immunohistochemical Detection of Disease- Associated Prion Protein in the Peripheral Nervous System in Experimental H-Type Bovine Spongiform Encephalopathy
Comments on technical aspects of the risk assessment were then submitted to FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
Owens, Julie
From: Terry S. Singeltary Sr. []
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Page 1 of 98
Friday, February 10, 2012
Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive
Monday, November 26, 2012
Aerosol Transmission of Chronic Wasting Disease in White-tailed Deer
Thursday, December 29, 2011
Aerosols An underestimated vehicle for transmission of prion diseases?
please see more on Aerosols and TSE prion disease here ;
Saturday, February 12, 2011
Another Pathologists dies from CJD, another potential occupational death ?
another happenstance of bad luck, a spontaneous event from nothing, or friendly fire ???
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J,
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)

Thursday, September 02, 2010
NEUROSURGERY AND CREUTZFELDT-JAKOB DISEASE Health Law, Ethics, and Human Rights The Disclosure Dilemma
Thursday, August 12, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010
Sunday, August 01, 2010
Blood product, collected from a donors possibly at increased risk for vCJD only, was distributed USA JULY 2010

Thursday, July 08, 2010
Nosocomial transmission of sporadic Creutzfeldt–Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010
Thursday, July 08, 2010
Wednesday, June 02, 2010
CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003 Updated: May 2010
Tuesday, May 11, 2010
Current risk of iatrogenic Creutzfeld–Jakob disease in the UK: efficacy of available cleaning chemistries and reusability of neurosurgical instruments
Tuesday, May 04, 2010
Review of the Human Pituitary Trust Account and CJD Issue 20 January 2010
Tuesday, March 16, 2010
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010
Monday, August 17, 2009
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009
Monday, July 20, 2009
Pre-surgical risk assessment for variant Creutzfeldt-Jakob disease (vCJD) risk in neurosurgery and eye surgery units
Friday, July 17, 2009
Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
Thursday, January 29, 2009
Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number 2-February 2009 Research
Wednesday, August 20, 2008
Tonometer disinfection practice in the United Kingdom: A national survey
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
Monday, December 31, 2007
Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation

Subject: CJD: update for dental staff
Date: November 12, 2006 at 3:25 pm PST

1: Dent Update. 2006 Oct;33(8):454-6, 458-60.
CJD: update for dental staff.
Saturday, January 16, 2010
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr 1-24-3
2011 TO 2012 UPDATE
Saturday, December 3, 2011
Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies
Volume 17, Number 12—December 2011

Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis
full text with source references ;
Are some commoner types of neurodegenerative disease (including Alzheimer's disease and Parkinson's disease) also transmissible? Some recent scientific research has suggested this possibility
Singeltary submission ;
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Proposal ID: 29403
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE

Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
Wednesday, January 5, 2011
David W. Colby1,* and Stanley B. Prusiner1,2
mom dod 12/14/97 hvCJD confirmed

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