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.
Introduction
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 http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4007012.
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
http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_073486,
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: http://webarchive.nationalarchives.gov.uk/+/www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_093762
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: http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_110288
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.
CJD
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.
vCJD
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
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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
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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
SNIP...
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
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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
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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 http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_063274.
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
SNIP....
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
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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
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Table 4c: Handling of instruments – patients with, or “at increased risk”
of, CJD (other than vCJD)
SNIP...
*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
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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.
Ophthalmology
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.
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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
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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.
Pregnancy
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.
Dentistry
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
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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.
layperson
SOURCE REFERENCES
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
References: @mfacdean1.cent.gla.ac.uk
Greetings again Professor Farthing and BMJ,
I was curious why my small rebuttal of the article described below was not
listed in this month's journal of GUT? I had thought it was going to be
published, but I do not have full text access. Will it be published in the
future? Regardless, I thought would pass on a more lengthy rebuttal of mine on
this topic, vCJD vs sCJDs and endoscopy equipment. I don't expect it to be
published, but thought you might find it interesting, i hope you don't mind and
hope to hear back from someone on the questions I posed...
Here is my short submission I speak of, lengthy one to follow below
that:
Date submitted: 3 Jun 2002
>> eLetter ID: gutjnl_el;21
>> >> Gut eLetter for Bramble and Ironside 50 (6): 888
>> >>Name: Terry S. Singeltary Sr. >>Email: flounder@wt.net
>>Title/position: disabled {neck injury}
>>Place of work: CJD WATCH
>>IP address: 216.119.162.85
>>Hostname: 216-119-162-85.ipset44.wt.net
>>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4)
>>Gecko/20011019 Netscape6/6.2
>> >>Parent ID: 50/6/888
>>Citation:
>> Creutzfeldt-Jakob disease: implications for gastroenterology
>> M G Bramble and J W Ironside
>> Gut 2002; 50: 888-890 (Occasional viewpoint)
>>-----------------------------------------------------------------
>>"CJDs (all human TSEs) and Endoscopy Equipment"
>>-----------------------------------------------------------------
>>
>>
>>
>>
regarding your article;
>>
>> Creutzfeldt-Jakob disease: implications for gastroenterology
>>
>>I belong to several support groups for victims and relatives
>>of CJDs. Several years ago, I did a survey regarding
>>endoscopy equipment and how many victims of CJDs have
>>had any type of this procedure done. To my surprise, many
>>victims had some kind of endoscopy work done on them.
>>As this may not be a smoking gun, I think it should
>>warrant a 'red flag' of sorts, especially since data now
>>suggests a substantial TSE infectivity in the gut wall
>>of species infected with TSEs. If such transmissions
>>occur, the ramifications of spreading TSEs from
>>endoscopy equipment to the general public would be
>>horrible, and could potential amplify the transmission
>>of TSEs through other surgical procedures in that
>>persons life, due to long incubation and sub-clinical
>>infection. Science to date, has well established
>>transmission of sporadic CJDs with medical/surgical
>>procedures.
Terry S. Singeltary Sr.
>>CJD WATCH
Again, many thanks, Kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder@wt.net CJD WATCH
[scroll down past article for my comments]
snip...
were not all CJDs, even nvCJD, just sporadic, until proven otherwise?
Terry S. Singeltary Sr., P.O. BOX 42, Bacliff, Texas 77518 USA
Professor Michael Farthing wrote:
Louise Send this to Bramble (author) for a comment before we post.
Michael
=======================================================
snip...
see full text ;
2003
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to
Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
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
FC5.1.1
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
TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS
snip...
Saturday, September 5, 2009
TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS
snip...
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."
(Laughter.)
DR. BROWN: Thanks.
Questions?
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.
(Laughter.)
DR. BROWN: Oh, it can't be that clear. Yeah, here, Pierluigi.
CHAIRPERSON PRIOLA: Dr. Epstein.
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 --
(Laughter.)
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.
Jay?
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.
CHAIRPERSON PRIOLA: Dr. DeArmond.
DR. DeARMOND: Yeah, it was very interesting data, but the --
(Laughter.)
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.
(Laughter.)
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.
CHAIRPERSON PRIOLA: Dr. Johnson.
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.
(Laughter.)
DR. BROWN: You didn't because it's brand new for me. I mean, either that or
I'm on the way
(Laughter.)
CHAIRPERSON PRIOLA: Dr. Bracey.
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.
snip...
snip...
see full text ;
(Laughter.)
Saturday, January 20, 2007
Fourth case of transfusion-associated vCJD infection in the United Kingdom
(Laughter.)
Friday, June 29, 2012
Highly Efficient Prion Transmission by Blood Transfusion
(Laughter.)
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a
Single Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
(Laughter.)
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
(Laughter.)
Sunday, May 1, 2011
W.H.O. T.S.E. PRION Blood products and related biologicals May 2011
(Laughter.)
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 ???
(Laughter.)
Sunday, August 01, 2010
Blood product, collected from a donors possibly at increased risk for vCJD
only, was distributed USA JULY 2010
(Laughter.)
atypical L-type BASE BSE California 2012
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE
INVESTIGATION JULY 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”
CENSORSHIP IS A TERRIBLE THING $$$
Canada has had a COVER-UP policy of mad cow disease since about the 17th
case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored
$$$
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
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
Scrapie and atypical Scrapie Nor98
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 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
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE
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
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA and INDIANA
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
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
*** 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.
AS OF AUGUST 2012 ;
CJD UPDATE USA
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
snip...
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
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES 2011 Annual Report
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
MEXICO IS UNDER or MIS DIAGNOSING CREUTZFELDT JAKOB DISEASE AND OTHER PRION
DISEASE SOME WITH POSSIBLE nvCJD
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25,
2012
Saturday, December 29, 2012
MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT
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
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
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. [flounder9@verizon.net]
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
FSIS, USDA, REPLY TO SINGELTARY
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?
PRION www.landesbioscience.com
please see more on Aerosols and TSE prion disease here ;
Saturday, February 12, 2011
Another Pathologists dies from CJD, another potential occupational death ?
another happenstance of bad luck, a spontaneous event from nothing, or
friendly fire ???
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare
and community settings part 4, Annex A1, Annex J,
UPDATE DECEMBER 2010
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of
Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
Thursday, September 02, 2010
NEUROSURGERY AND CREUTZFELDT-JAKOB DISEASE Health Law, Ethics, and Human
Rights The Disclosure Dilemma
Thursday, August 12, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were
distributed July-August 2010
Sunday, August 01, 2010
Blood product, collected from a donors possibly at increased risk for vCJD
only, was distributed USA JULY 2010
Thursday, July 08, 2010
Nosocomial transmission of sporadic Creutzfeldt–Jakob disease: results from
a risk-based assessment of surgical interventions Public release date:
8-Jul-2010
Thursday, July 08, 2010
GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010
Wednesday, June 02, 2010
CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003 Updated:
May 2010
Tuesday, May 11, 2010
Current risk of iatrogenic Creutzfeld–Jakob disease in the UK: efficacy of
available cleaning chemistries and reusability of neurosurgical instruments
Tuesday, May 04, 2010
Review of the Human Pituitary Trust Account and CJD Issue 20 January 2010
Tuesday, March 16, 2010
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Part 4 REVISED FEB. 2010
Monday, August 17, 2009
Transmissible Spongiform Encephalopathy Agents: Safe Working and the
Prevention of Infection: Annex J,K, AND D Published: 2009
Monday, July 20, 2009
Pre-surgical risk assessment for variant Creutzfeldt-Jakob disease (vCJD)
risk in neurosurgery and eye surgery units
Friday, July 17, 2009
Revision to pre-surgical assessment of risk for vCJD in neurosurgery and
eye surgery units Volume 3 No 28; 17 July 2009
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June
12, 2009 (Singeltary submission)
Thursday, January 29, 2009
Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan,
1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number
2-February 2009 Research
Wednesday, August 20, 2008
Tonometer disinfection practice in the United Kingdom: A national survey
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007
(occupational exposure to prion diseases)
Monday, December 31, 2007
Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in
Endodontic Practice in Absence of Adequate Prion Inactivation
Subject: CJD: update for dental staff
Date: November 12, 2006 at 3:25 pm PST
1: Dent Update. 2006 Oct;33(8):454-6, 458-60.
CJD: update for dental staff.
Saturday, January 16, 2010
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to
Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
2011 TO 2012 UPDATE
Saturday, December 3, 2011
Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform
Encephalopathies
Volume 17, Number 12—December 2011
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of
Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
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
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
layperson
mom dod 12/14/97 hvCJD confirmed
end...TSS
