Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
Part 4 has been redrafted (February 2010) to clarify how best to manage patients in healthcare and community settings. A number of recent policy decisions have been incorporated into this guidance including:
• Standard infection control precautions should be used to clear up spillages as quickly as possible of all material from patients with, or "at increased risk" of, CJD/vCJD in a healthcare setting. 10,000ppm rather than 20,000ppm sodium hypochlorite is recommended for practical purposes.
• High or medium risk tissues from patients with, or "at increased risk" of, CJD or vCJD, should be incinerated, and low risk tissues or body fluids should follow normal clinical waste disposal.
• Instruments used in high or medium risk procedures on patients with, or "at increased risk" of, CJD/vCJD can be quarantined and re-used exclusively on the same patient, subject to tracking of instruments throughout the decontamination cycle, and ensuring that under no circumstances should quarantined instrument sets be reprocessed for use on other patients unless the diagnosis of CJD or vCJD has been positively excluded.
• Individuals who have been identified prior to high risk surgery as having received blood or blood components from 80 or more donors since January 1980 are now designated as "at increased risk" of vCJD and have been added to Table 4a.
• The anterior eye has been reclassified as low risk with regards to tissue infectivity.
In addition, updated information on other guidance, including dentistry, anaesthesia and intensive care, has been incorporated.
Published: 2 June 2003 Revised and updated: 13 December 2010
• Other relevant guidance
Caring for patients with, or "at increased risk" of, CJD or vCJD
Management arrangements for infection control
• Tissue infectivity
• Iatrogenic transmission
• Patient categorisation
Patients "at increased risk" of CJD or vCJD
• Hospital care of patients
Taking samples and other invasive medical procedures
Surgical procedures and instrument management
Single use instruments
Handling of instruments that are not designated as single-use
Decontamination of instruments
Storage of instruments for research purposes
Incineration of instruments
Use of laser for tonsillectomy – smoke plumes
Anaesthesia and intensive care
• Community healthcare
Caring for symptomatic patients at home
Published: 2 June 2003
Revised and updated: 13 December 2010 Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4
• After death
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Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex A1 ANNEX A1
Distribution of TSE infectivity in human tissues and body fluids
A1.1 There is evidence that the distribution of the disease-specific partially protease-resistant form of prion protein (PrPTSE) in tissues is more widespread in the body in variant CJD (vCJD) patients than in patients affected by sporadic CJD (1, 2, 3). In sporadic CJD, the presence of abnormal prion protein in patients with clinical disease appears to be restricted to the central nervous system (CNS). However, abnormal prion protein has been detected in various lymphoid tissues, including tonsils, spleen, gastrointestinal lymphoid tissue (appendix and rectum), lymph nodes, thymus and adrenal gland of patients with clinical vCJD. Abnormal prion protein has also been detected in lymphoid tissues within the appendix removed from 2 patients some 8 and 24 months before they developed vCJD (4, 5) suggesting that abnormal prion protein could be present in the lymphoid tissue of people incubating vCJD for some time before the onset of clinical disease. In similar tests, abnormal prion protein has not been detected in these tissues from sporadic CJD patients. Infectivity has been demonstrated in tonsil and spleen in vCJD by experimental transmission (6).
A1.2 PrPTSE has been identified in posterior spinal nerve roots in only an occasional case of sporadic CJD and GSS (7), but not in peripheral nerve in vCJD (3, 8). Transmission studies on peripheral nerve samples from cases of sporadic CJD by intracerebral inoculation into primates have shown no evidence of infectivity (9). PrPTSE has been detected in spinal dorsal root ganglia and trigeminal ganglia in vCJD (8), and in trigeminal ganglia in sporadic CJD (10). PrPTSE has also been detected in olfactory epithelium in sporadic CJD patients at post mortem (11), and in the olfactory tract in vCJD (12). Infectivity and PrPTSE have not been detected in dental pulp in a series of sporadic CJD cases (13), and PrPTSE was not detected in the alveolar nerve, dental pulp, gingiva, salivary gland, tongue in a small series of vCJD cases (14).
A1.3 Table A1 presents current information on the distribution of infectivity in tissues and body fluids in CJD other than vCJD, and in vCJD, based on data from experimental studies, where available, and on information from other studies of natural TSE disease in humans and animals. It also shows where PrPTSE has been detected in tissues. Published: 2 June 2003 1
Updated: December 2010 Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex A1
A1.4 The precise relationship between the presence of PrPTSE and infectivity is not certain – for example, the absence of detectable PrPTSE does not necessarily mean absence of infectivity. Conversely, detection of small amounts of PrPTSE in a tissue does not necessarily mean that it will transmit disease in all circumstances. This guidance has been formulated on the basis of likelihood of the presence of infectivity using the identification of PrPTSE as a specific marker. In general terms, there is thought to be a broad correlation between PrPTSE load in a given tissue and the likelihood that the given tissue might present a risk of infection. The relative levels of PrPTSE in different tissues provide useful information for the assessment of relative risks of different procedures.
A1.5 In Table A1, tissue infectivity is classified as high, medium or low, on the basis of infectivity assays in experimental animals. Although such studies are limited in CJD and vCJD tissues, the preliminary data that are available support the findings in tissues from other natural and experimental TSE models. Therefore the relative levels of PrPTSE in different tissues provide useful information for the assessment of relative risks of different surgical and endoscopic procedures.
A1.6 The information given in this Annex describes the position at the time of publication. This will be kept under review and is subject to change as further information becomes available.
Table A1 – Distribution of TSE infectivity in human tissues and body fluids
Key: +ve = tested positive -ve = tested negative
NT = not tested P = infectivity proven in experimental transmission studies
1Spinal ganglia have a high assumed level of infectivity in the WHO Guidelines. However, unpublished results on the infectivity of spinal ganglia indicate that this tissue is of medium infectivity.
Published: 2 June 2003 3 Updated: December 2010 Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex A1 2Dura mater is designated low infectivity as virtually no detectable abnormal prion protein has been found in cases of CJD; however, as grafts of these tissues are associated with CJD transmission, probably as a result of contamination by brain and because of the lengthy period of implantation in the CNS, procedures conducted on intradural tissues (i.e. brain , spinal cord and intracranial sections of cranial nerves) or procedures in which human dura mater was implanted in a patient prior to 1992, remain high risk.
3Although PrPTSE has not been detected in the CSF in either sporadic or variant CJD (15), experimental transmission of infectivity has been achieved from CSF in sporadic CJD in 4 of 27 primates by intracerebral inoculation (9) indicating that levels of infectivity are likely to be much lower than in the central nervous system.
4PrPTSE has been detected in dura mater, skin, kidney, liver, pancreas, ovary and uterus in a case of vCJD in USA with a lengthy duration of illness (16). Earlier studies of these tissues in UK vCJD cases gave negative results (2,8,17).
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Summary of advice (revised January 2010)
Annex J provides a clear and pragmatic way of assessing CJD and vCJD risk prior to surgery or endoscopy. Growing numbers of patients have been informed that they are at increased risk of CJD or vCJD. Therefore it is recommended that all patients about to undergo any surgery or endoscopy should be asked if they have ever been notified as at increased risk of CJD or vCJD. This recommendation is outlined in paragraphs J1 and J2.
In addition, patients undergoing surgery or neuro-endoscopy which may involve contact with tissues of potentially high level TSE infectivity ("high risk tissues") should, through a set of detailed questions, be assessed for their possible CJD/vCJD risk exposure. These questions are outlined in Table J1 and paragraphs J3 to J6.
Annex J has been revised (July 2009) to include a new question to be asked of all patients about to undergo surgery or neuro-endoscopy on high risk tissues. This new question (question 4 in Table J1) has been added to identify those patients who have received blood or blood components from 80or more blood donors. These patients are now designated as at increased risk of vCJD by the CJD Incidents Panel. Table J1 and paragraph J6 provide guidance on how to identify those patients who have received multiple blood transfusions. An algorithm, included as Appendix A, guides health professionals through the process.
Annex J was further revised (January 2010) to encompass recent evidence that patients who underwent intradural neurosurgery or intradural spinal surgeryand received human-derived dura mater before August 1992 are at increased risk of sCJD, but not vCJD. Table J1 has been modified to reflect this change.
Published: 31 July 2006 Revised and updated: 14 December 2010 1Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J
Recommendation for all surgical and endoscopy patients
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Saturday, December 11, 2010
Species-barrier-independent prion replication in apparently resistant species
These results demonstrate the existence of subclinical forms of prion infection with important public health implications, both with respect to iatrogenic transmission from apparently healthy humans and dietary exposure to cattle and other species exposed to bovine spongiform encephalopathy prions, Current definitions of the species barrier, which have been based on clinical endpoints, need to be fundamentally reassessed.
Autor(es): Hill, AF - Joiner, S - Linehan, J - Desbruslais, M - Lantos, PL - Collinge, J -
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Sunday, December 12, 2010
Predominant Involvement of the Cerebellum in Guinea Pigs Infected with Bovine Spongiform Encephalopathy (BSE)
Journal of Comparative Pathology Article in Press
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
Tuesday, December 14, 2010
TAFS1 Position Paper on Relaxation of the Feed Ban in the EU SUMMARY © TAFS, Berne, 2010
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010
Tuesday, November 30, 2010
Council conclusions on the TSE Road Map 2 A Strategy paper on Transmissible Spongiform Encephalopathies for 2010 - 2015
Sunday, November 28, 2010
Variably protease-sensitive prionopathy in a PRNP codon 129 heterozygous UK patient with co-existing tau, a synuclein and AB pathology
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
CHRONIC WASTING DISEASE CWD
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
Advisory Committee on the Safety of Blood, Tissues and Organs
Summary of 3rd Public Meeting - "Organ transplantation - benefits and risks of higher- risk organs" 10am, 26 October 2010 Coin Street Neighbourhood Centre, London, SE1 9NH
WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010
also in the references at bottom i saw ;
12. A single positive marrow in multiple transmission attempts from cattle orally dosed with BSE-infected brain [Wells et al., 1999; Wells et al., 2005; Sohn et al., 2009].
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
Sunday, January 17, 2010
Human tissue, recovered from a donor history indicated increased risk factors for Creutzfeldt-Jacob disease Lions Eye Bank
Saturday, January 16, 2010 Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al
Friday, November 20, 2009
SaBTO Advisory Committee on the Safety of Blood, Tissues and Organs Summary of the Eighth Meeting, 27 October 2009
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
Asante/Collinge et al, that BSE transmission to the 129-methionine
genotype can lead to an alternate phenotype that is indistinguishable
from type 2 PrPSc, the commonest _sporadic_ CJD;
Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater
Comment Number: EC -1
Accepted - Volume 1
Daily Dockets - 04/10/03
00D-1662 Use of Xenotransplantation Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003 - Cached
# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)
Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]
Monday, August 17, 2009
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009
Tuesday, March 16, 2010
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010
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
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
Tuesday, May 11, 2010
Current risk of iatrogenic Creutzfeld-Jakob disease in the UK: efficacy of available cleaning chemistries and reusability of neurosurgical instruments
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
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
Wednesday, June 16, 2010
Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties
DID EVERYONE FILL OUT THEIR CJD QUESIONNAIRE FROM THE CDC AND OR THE CJD FOUNDATION ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518