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CJD: update for dental staff
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. Scully C, Smith AJ, Bagg J. Eastman Dental Institute, University of London. It is almost a decade since the recognition of the emergence of a new infectious disease termed variant Creutzfeldt-Jakob disease (vCJD) caused by prions (PrPTSE), abnormal variants of a normal human cell surface protein (PrP).This disease has a number of similarities to other forms of CJD--lethal disorders characterized by a prolonged incubation period, and progressive mental deterioration. In relation to oral tissues, PrPTSE have been found in neural, gingival, pulpal, lingual, lymphoreticular and salivary gland tissue in animal models. In both sporadic and variant CJD, PrPTSE is detectable in the trigeminal ganglion and, in vCJD, in lymphoreticular tissues, but infectivity has not been tested in other human oral tissues. CLINICAL RELEVANCE: PrPTSE is much more resistant to the common methods of inactivation than conventional pathogens, and it adheres avidly to steel whilst retaining its infectivity. Particular attention must be paid to cleaning and sterilizing re-usable dental instruments. Single-use devices, such as endodontic files and matrix bands, must never be re-used. Advice on the reprocessing of dental instruments used on known CJD patients must be obtained from local infection control teams. Research into effective methods of prion inactivation appears promising, although further work on the applicability to general dental practice is required. PMID: 17087448 [PubMed - in process] http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum CJD WATCH MESSAGE BOARD TSS 2005 SEAC Position statement vCJD and Endodontic dentistry Mon May 8, 2006 09:08 68.238.108.206 SEAC Position Statement -------------------------------------------------------------------------------- Position statement vCJD and Endodontic dentistry Issue 1. The Department of Health (DH) asked SEAC to advise on the findings and implications of a preliminary risk assessment of potential vCJD transmission via endodontic procedures (dental procedures involved in the maintenance of dental pulp and the treatment of the pulp cavity) 1. This is particularly pertinent because of the large number of endodontic procedures undertaken in the UK. Background 2. There are no reported definite or suspected cases of vCJD transmission arising from dental procedures. However, prions are more resistant than other types of infectious agent to the conventional cleaning and sterilisation practices used to decontaminate dental instruments 2. Therefore, should dental instruments become contaminated from tissues in the oral cavity of infected individuals, there is a risk of transmission to subsequent patients. 3. A quantitative DH risk assessment 3, accepted by SEAC in 2003, considered two possible mechanisms for the transfer of vCJD infectivity via dental instruments: (i) accidental abrasion of the lingual tonsil, known to carry infectivity in vCJD cases; and (ii) contact with dental pulp that evidence from animal studies suggested may be infective. On the basis of the information available, the DH analysis suggested that the risk of transmission to individual patients via accidental abrasion of the lingual tonsil is very low. Furthermore, should dental pulp be infective, the risk of transmission via endodontic procedures, although higher, is also low. Although a very large number of dental procedures are conducted, the relative risk to public health from potential transmission via dental, compared with hospital, surgery was considered to be relatively low. 4. In 2006, SEAC considered a new preliminary risk assessment by DH of the risks of vCJD transmission via endodontic procedures, taking into account new information on decontamination of dental instruments, the potential infectivity of dental pulp, and the possible existence of subclinical vCJD carrier cases. Endodontic instruments 5. Evidence suggests that the files and reamers used in endodontic procedures are reused and are difficult to reliably decontaminate 4. Appreciable quantities of residual material remain adherent to the surface after normal cleaning and sterilisation 5. Thus, there is potential for transfer of dental pulp between patients undergoing endodontic procedures. vCJD infectivity in dental tissues 6. There are no data on vCJD infectivity in dental pulp. Although no abnormal prions were found in a study of dental tissues, including dental pulp, from vCJD cases 6, dental pulp includes blood and peripheral nerve tissue known to carry vCJD infectivity 7,8. In addition, appreciable infectivity has been found in the dental pulp of hamsters with hamster scrapie 9. Although it is possible that the peripheral nerve may only become infective close to, or after, the onset of clinical vCJD, inflammation may promote the propagation of prions 10. Thus, although the data are limited and indirect, it is reasonable to assume that the dental pulp of individuals subclinically-infected with vCJD may be infectious although the level of infectivity is unknown. Studies underway will provide direct data on the infectivity in dental tissues from vCJD cases. Subclinical carrier state 7. A study of humanised mice showed that vCJD infections may not always progress to clinical disease within the normal lifespan of the animals 11. Another study suggested that prion infections in mice that remain at a subclinical level can be transmitted to other mice, resulting in clinical disease 12. Thus, there is evidence to suggest that individuals infected with the BSE / vCJD agent may remain in a subclinical infection carrier state instead of developing vCJD. A discrepancy between prevalence estimates based on a survey of abnormal prion protein in appendix and tonsil tissue and data on vCJD cases supports this hypothesis 13. As no diagnostic test exists to identify such individuals, they could over the course of their lives be potential sources of numerous secondary infections arising from invasive medical or dental procedures. 8. The prevalence of subclinical infection in the UK population is uncertain. A recent estimate suggests the number of subclinical carriers may be of the order of several thousand 14. SEAC has strongly recommended that further studies to ascertain better the prevalence of vCJD infection be urgently considered 15. Transmission risks 9. The new DH analysis suggests that, on the basis that residual dental pulp on endodontic files and reamers is transferred relatively efficiently to patients on reuse, dental pulp is as infective as peripheral nerve tissue and a subclinical carrier population for vCJD exists, a self-sustaining vCJD epidemic arising from endodontic surgery is plausible. There are uncertainties about the efficiency of vCJD transmission via endodontic procedures, the vCJD infectivity of dental pulp and the existence of a subclinical infection carrier state. However, even if a self-sustaining epidemic were not possible, clusters of vCJD infections could arise from the use of instruments contaminated with the vCJD agent from endodontic procedures on infected patients. Interactions between this and other routes of secondary transmission, such as blood transfusion and hospital surgery, would make a self-sustaining epidemic more likely. Potential risk reduction measures 10. Endodontic files and reamers have a limited lifespan, restricting the number of possible secondary transmissions. Improving the effectiveness of procedures used to decontaminate dental instruments would reduce the risk of transmission. Restricting endodontic files and reamers to single use would prevent potential secondary transmission via these instruments. Conclusions 11. A preliminary risk assessment produced by DH suggests that vCJD transmission via endodontic dentistry may, under certain hypothetical but plausible scenarios, be sufficient to sustain a secondary vCJD epidemic. However, there are uncertainties around the data and assumptions underpinning the assessment. Research underway will address some of these uncertainties and allow the risk assessment to be refined. Once the research is complete and / or other data become available, the risks should be reassessed. A watching brief should be maintained. 12. It is unclear whether or not vCJD infectivity can be transmitted via endodontic files and reamers. However, given the plausibility of such a scenario and the large number of procedures undertaken annually, it would be prudent to consider restricting these instruments to single use as a precautionary measure. Since sufficiently rigorous decontamination of these instruments is difficult, single use of these instruments would eliminate this risk, should it exist. SEAC May 2006 -------------------------------------------------------------------------------- 1. Department of Health. Dentistry and vCJD: the implications of a “carrier state” for a self-sustaining epidemic due to endodontic dentistry. A Preliminary Risk Assessment. Unpublished. 2. Smith et al. (2003) Prions and the oral cavity. J. Dent. Res. 82, 769-775. 3. Department of Health. (2003) Risk assessment for vCJD and dentistry. 4. Letters et al. (2005) A study of visual and blood contamination on reprocessed endodontic files from general dental practice. Br. Dent. J. 199, 522-525. 5. Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241. 6. Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 7. SEAC 91 minutes paragraph 9. www.seac.gov.uk/papers/papers.htm 8. Department of Health (2005) Assessing the risk of vCJD transmission via surgery: an interim view. Unpublished. 9. Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047. 10. Heikenwalder et al. (2005) Chronic lymphocytic inflammation specifies the organ tropism of prions. Science. 307, 1107-1110. 11. Bishop et al. (2006) Predicting susceptibility and incubation time of human-to-human transmission of vCJD. Lancet Neurology. 12. Hill et al. (2000) Species-barrier-independent prion replication in apparently resistant species. Proc. Natl. Acad. Sci. USA. 97, 10248-10253. 13. SEAC Epidemiology Subgroup (2005) Position statement on the vCJD epidemic. http://www.seac.gov.uk/statements/st...06subgroup.htm 14. Clarke & Ghani. (2005) Projections of future course of the primary vCJD epidemic in the UK: inclusion of subclinical infection and the possibility of wider genetic susceptibility. R. J. Soc. Interface. 15. SEAC (2005) SEAC response to the SEAC Epidemiology Subgroup statement on the vCJD epidemic. www.seac.gov.uk/statements/state260106.htm Page updated: 8th May 2006 http://www.seac.gov.uk/statements/statement0506.htm Evidence For CJD/TSE Transmission Via Dental Instruments From Terry S. Singletary, Sr flounder@wt.net 1-24-3 J Hosp Infect 2002 Jul;51(3):233-5 Related Articles, Links [Click here to read] Contaminated dental instruments. Smith A, Dickson M, Aitken J, Bagg J. Infection Research Group, Glasgow Dental Hospital & School, 378 Sauchiehall Street, Glasgow, UK. a.smith@dental.gla.ac.uk There is current concern in the UK over the possible transmission of prions via contaminated surgical instruments. Some dental instruments (endodontic files) raise particular concerns by virtue of their intimate contact with terminal branches of the trigeminal nerve. A visual assessment using a dissecting light microscope and scanning electron microscopy of endodontic files after clinical use and subsequent decontamination was performed. The instruments examined were collected from general dental practices and from a dental hospital. Seventy-six per cent (22/29) of the files retrieved from general dental practices remained visibly contaminated, compared with 14% (5/37) from the dental hospital. Current methods for decontaminating endodontic instruments used in dentistry may be of an insufficient standard to completely remove biological material. Improved cleaning methods and the feasibility of single use endodontic instruments require further investigation. PMID: 12144804 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/q...i?cmd=Retrieve &db=PubMed&list_uids=12144804&dopt=Abstract J Gen Virol 1999 Nov;80 ( Pt 11):3043-7 Transmission of the 263K scrapie strain by the dental route. Ingrosso L, Pisani F, Pocchiari M Laboratory of Virology, lstituto Superiore di Sanita, Viale Regina Elena 299, 00161 Rome, Italy. Apart from a few cases of iatrogenic and familial human transmissible spongiform encephalopathies (TSEs) or prion diseases, the cause of Creutzfeldt-Jakob disease (CJD) remains unknown. In this paper we investigated the possibility that dental procedures may represent a potential route of infection. This was assessed by using the experimental model of scrapie in hamster. In the first part of this study we found that after intraperitoneal inoculation, oral tissues commonly involved in dental procedures (gingival and pulp tissues) bore a substantial level of infectivity. We also found high scrapie infectivity in the trigeminal ganglia, suggesting that the scrapie agent had reached the oral tissues through the sensitive terminal endings of the trigeminal nerves. In the second part of the study we inoculated a group of hamsters in the tooth pulp and showed that all of them developed scrapie disease. In these animals, we detected both infectivity and the pathological prion protein (PrPsc) in the trigeminal ganglion homolateral to the site of injection but not in the controlateral one. This finding suggests that the scrapie agent, and likely other TSE agents as well, spreads from the buccal tissues to the central nervous system through trigeminal nerves. Although these findings may not apply to humans affected by TSEs, they do raise concerns about the possible risk of transmitting these disorders through dental procedures. Particular consideration should be taken in regard to new variant CJD patients because they may harbour more infectivity in peripheral tissues than sporadic CJD patients. PMID: 10580068 http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd= Retrieve&db=PubMed&list_uids=10580068&dopt=Abstrac t a simple auto-claving just will not kill this agent, considering the fact this agent can survive ashing to 600 degrees celsius; New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§ * Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France Contributed by D. Carleton Gajdusek, December 22, 1999 Abstract One-gram samples from a pool of crude brain tissue from hamsters infected with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual infectivity in the treated samples was assayed by the intracerebral inoculation of dilution series into healthy weanling hamsters, which were observed for 10 months; disease transmissions were verified by Western blot testing for proteinase-resistant protein in brains from clinically positive hamsters. Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C. These results suggest that an inorganic molecular template with a decomposition point near 600°C is capable of nucleating the biological replication of the scrapie agent. transmissible spongiform encephalopathy | scrapie | prion | medical waste | incineration Introduction The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin. It also has been assumed that the replication of these agents is a strictly biological process (1), although the notion of a "virus" nucleant of an inorganic molecular cast of the infectious beta -pleated peptide also has been advanced (2). In this paper, we address these issues by means of dry heat inactivation studies. see full text: http://www.pnas.org/cgi/content/full/97/7/3418 Greetings again, please believe me when i tell you this goes far far beyond the hamburger/deerburger/elkburger/sheepburger. Pandora's box of the demented has been opened for decades, closing it will be most impossible with current safeguards. until they can perfect a test, not only to confirm TSE agent, but also to differentiate between the many differnt strains (there are over 20 in sheep scrapie, and sheep scrapie is the sole model for CJD studies), they then will have to perfect a test that will differentiate between the many different routes. so, as you can see, this could very well take many more decades to answer these questions. but in the mean time, i will not now or ever accept the 'spontaneous/sporadic' theory without any source and route. i plan to continue to fan the fire until we know what killed our loved ones... CJD/TSEs MUST BE MADE REPORTABLE NATIONALLY, SUPPORTED WITH A CJD QUESTIONNAIRE TO EVERY VICTIM/FAMILY THAT ASK REAL QUESTIONS PERTAINING TO ROUTE/SOURCE...TSS Diagnosis and Reporting of Creutzfeldt-Jakob Disease T. S. Singeltary, Sr; D. E. Kraemer; R. V. Gibbons, R. C. Holman, E. D. Belay, L. B. Schonberger http://jama.ama-assn.org/issues/v285...jlt0214-2.html 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available. snip... 64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. snip... http://www.seac.gov.uk/minutes/95.pdf 3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. ***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.*** 6:30 Close of Day One http://www.healthtech.com/2007/tse/day1.asp SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ... http://www.cjdsurveillance.com/resou...asereport.html There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection. He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins. http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.htm http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.pdf TSS |
Subject: PrPSc in salivary glands of scrapie-affected sheep
Date: February 15, 2007 at 9:33 am PST J. Virol. doi:10.1128/JVI.02148-06 Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved. PrPSc in salivary glands of scrapie-affected sheep Marta Vascellari*, Romolo Nonno, Franco Mutinelli, Michela Bigolaro, Michele Angelo Di Bari, Erica Melchiotti, Stefano Marcon, Claudia D'Agostino, Gabriele Vaccari, Michela Conte, Luigi De Grossi, Francesca Rosone, Francesco Giordani, and Umberto Agrimi Istituto Zooprofilattico Sperimentale delle Venezie, Histopathology Department, Viale dell'Università 10, 35020 Legnaro (PD), Italy; Istituto Superiore di Sanità, Department of Food Safety and Animal Health, Viale Regina Elena 299, 00161 Roma, Italy; Istituto Zooprofilattico Sperimentale delle Regioni Lazio e Toscana, Strada Terme, 01100 Viterbo, Italy * To whom correspondence should be addressed. Email: mvascellari@izsvenezie.it . Abstract The salivary glands of scrapie-affected sheep and healthy controls were investigated for the presence of the pathological prion protein (PrPSc). PrPSc was detected in major (parotid and mandibular) and minor (buccal, labial and palatine) salivary glands of naturally and experimentally infected sheep. By western blot, PrPSc concentration in glands was estimated as 0.02-0.005% of brain. Immunohistochemistry revealed intracellular deposition of PrPSc in ductal and acinar epithelium and occasional labeling into the lumen of salivary ducts. The presence of PrPSc in salivary glands highlights the possible role of saliva in the horizontal transmission of scrapie. http://jvi.asm.org/cgi/content/abstr...8-06v1?papetoc TSS |
Dental treatment and risk of variant CJD – a case control study
Dental treatment and risk of variant CJD – a case control study
D. Everington,1 A. J. Smith,2 H. J. T. Ward,3 S. Letters,4 R. G. Will5 and J. Bagg6 Objective Knowledge of risk factors for variant CJD (vCJD) remains limited, but transmission of prion proteins via re-useable medical devices, including dental instruments, or enhanced susceptibility following trauma to the oral cavity is a concern. This study aimed to identify whether previous dental treatment is a risk factor for development of vCJD. Design Case control study. Methods Risk factor questionnaires completed by interview with relatives of 130 vCJD patients and with relatives of 66 community and 53 hospital controls were examined by a dental surgeon. Responses regarding dental treatments were analysed. Results We did not find a statistically signifi cant excess of risk of vCJD associated with dental treatments with the exception of extractions in an unmatched analysis of vCJD cases with community controls (p = 0.02). However, this result may be explained by multiple testing. Conclusions This is the first published study to date to examine potential links between vCJD and dental treatment. There was no convincing evidence found of an increased risk of variant CJD associated with reported dental treatment. However, the power of the study is restricted by the number of vCJD cases to date and does not preclude the possibility that some cases have resulted from secondary transmission via dental procedures. Due to the limitations of the data available, more detailed analyses of dental records are required to fully exclude the possibility of transmission via dental treatment. snip... DISCUSSION Many studies have searched for risk factors for the development of different types of CJD, such as diet, exposure to animals, surgical treatment, including dentistry, and occupational exposures. A retrospective case control study15 of 60 definite cases of sporadic CJD, occurring in Japan between 1975 and 1977 found no association with extractions of maxillary or mandibular teeth. An analysis of 26 sporadic CJD cases and 40 matched controls from the United States16 failed to discover a significant odds ratio for endodontic surgery, though these workers did note statistically significant odds ratios for intraocular pressure testing, injury to or surgery on the head, face or neck and trauma to other parts of the body. However, these findings suffer from low statistical power and, in the case of the Japanese paper, information was requested for extractions only during the fi ve year period prior to onset. This paper attempts to identify an association between vCJD and reported dental treatment. Comparison of the reported dental histories of cases and controls found that extractions were the only dental risk factor that reached statistical significance (at the 5% level) in the unmatched analysis with community controls. This may be a result of multiple testing especially as there are fewer extractions in the cases than in the hospital controls. It is likely that the majority of vCJD cases in this cohort were infected through eating BSE contaminated meat products. Therefore, it is diffi - cult to detect a small subgroup that may have been infected by secondary transmission, as in this study, through dentistry. There are a number of limitations to this study, most importantly relying on reported data from relatives and the relatively small numbers of cases and controls resulting in low power to detect statistical differences. Recruitment of controls has been problematic,17 although every effort was made to maximise this group. Selection of controls was not matched for demographic and socio-economic factors for dental attendance and this may have resulted in bias. It is possible that some of the responses of ‘no known treatment’ reflect poor knowledge or recall on the part of the relatives. This would reduce the power of the study to pick up significant differences between groups, but not necessarily introduce bias. Whilst these preliminary data on a topic of great concern for public health do not provide evidence supporting reported dental work as being a major route of transmission of the BSE agent to humans to date, they do not preclude the possibility that some vCJD cases have been infected by this route. Furthermore, the incubation period following infection by a peripheral route may be relatively long and therefore the period of observation to date of potential secondary transmission of vCJD may be too short to detect cases. A more detailed study of previous treatment based on reviewing actual dental records rather than relying on reported treatments is required to gain a wider insight into the dental history of both cases and controls. We are currently investigating the possibility of examining dental records of vCJD cases and a larger group of unmatched controls.18 The National CJD Surveillance Unit is funded by the Department of Health and the Scottish Executive Department of Health. The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, or in the writing of the report. We are also grateful to the families of cases, without whose co-operation this study would not have been possible. FULL TEXT ; http://www.nature.com/bdj/journal/va...j.2007.126.pdf TSS |
(DH) Precautionary advice given to dentists on vCJD
(DH) Precautionary advice given to dentists on vCJD
Thu Apr 19, 2007 11:11 70.110.92.6 19/04/2007 10:14 Department of Health (National) (DH) Precautionary advice given to dentists on re-use of instruments As a precautionary measure the Chief Dental Officer, Dr Barry Cockcroft today issued new guidance to all dentists in England regarding single use of reamers and files, instruments used only in the root filling of teeth. The guidance to dentists follows on from precautionary advice from the Spongiform Encephalopathy Advisory Committee to the Department of Health and early results from ongoing research conducted by the Health Protection Agency, indicating a potential risk of vCJD associated with endodontic procedures. Dr Barry Cockcroft said: "There are no reported definite or suspected cases of vCJD transmission arising from dental procedures - this new guidance to dentists is purely an extra precaution. The public should continue to attend their dentist as normal." Notes to Editors: 1. The guidance applies to all primary and secondary care dentists in England. 2. Endodontics relate to treatment to the dental pulp of a tooth. A major part of this is root canal work. No other aspect of dental work is affected by this precautionary advice. 3. There are approximately 1 million NHS endodontic treatments every year in England and Wales. Since 1996 there have been 165 cases of vCJD. There is no current evidence of vCJD being transmitted by any form of dentistry. 4. Variant Creutzfeldt-Jakob Disease (vCJD) is one of the Transmissible Spongiform Encephalopathies, the group of prion diseases that include Bovine Spongiform Encephalopathy (BSE), Creutzfeldt-Jakob Disease (CJD), and scrapie. 5. This letter reflects precautionary advice from the Spongiform Encephalopathy Advisory Committee (SEAC) and early results on the potential infectivity of dental tissues from research in progress by the Health Protection Agency. This research supports the view that dental instruments (files and reamers) used in root canal treatment could possibly pose an effective route of vCJD transmission. 6. Almost everyone is at some risk of being infected with vCJD due to dietary exposure to BSE. Any additional risk from a root canal treatment could only arise if the instruments had been previously used on an infective patient. The proportion of people carrying infection is highly uncertain. Published information suggests that this may be between 1 in 1,400 and 1 in 20,000 people, though it may well be less for some age groups. It is also not clear how many of those carrying the infection are likely to develop symptoms of vCJD: given the much smaller number of cases actually seen so far, the majority may never do so (Clarke and Ghani, 2005). Even if instruments had been used on someone carrying the infection, it is not clear how great the risk of vCJD being passed on would be. Nevertheless, a precautionary approach is justified in view of the number of endodontic procedures carried out. [ENDS] Client ref 2007/0092 GNN ref 146384P =============================================== PLEASE SEE DENTAL RISK FROM HUMAN AND ANIMAL TSE http://neurotalk.psychcentral.com/ar...p/t-13173.html http://disc.server.com/discussion.cg...USSION%20BOARD http://www.rense.com/general34/evi.htm Subject: MASTER DENTIST FALLS VICTIM TO CJD Date: March 31, 2007 at 1:27 pm PST http://lists.ifas.ufl.edu/cgi-bin/wa...net-mg&P=19835 COULD A CJD QUESTIONNAIRE TO EVERY FAMILY OF A VICTIM HELP ??? http://brain.hastypastry.net/forums/...ead.php?t=2408 USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available. snip... 64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. snip... http://www.seac.gov.uk/minutes/95.pdf 3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. ***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.*** 6:30 Close of Day One http://www.healthtech.com/2007/tse/day1.asp SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ... http://www.cjdsurveillance.com/resou...asereport.html There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection. He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins. http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.htm http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.pdf Thursday, March 15, 2007 Potential Risk of Variant Creutzfeldt-Jakob Disease (vCJD) From Plasma-Derived Products In recent years, questions have been raised concerning the potential risk of variant Creutzfeldt-Jakob disease (vCJD - a rare but fatal brain infection) for recipients of plasma- derived clotting factors, including United States (US) licensed Factor Eight (pdFVIII), Factor Nine (pdFIX), and other plasma-derived products such as immune globulins and albumin. In response to these questions, FDA conducted a risk assessment. Based on the risk assessment, the US Public Health Service believes that the risk of vCJD to patients who receive US licensed pdFVIII products is most likely to be extremely small, although we do not know the risk with certainty. vCJD risk from other plasma derived products, including Factor IX, is likely to be as small or smaller. This web page provides FDA’s risk assessment for US licensed pdFVIII and risk communication materials for this product and other plasma derivatives. Included are Key Points, and Questions and Answers. Additional links are provided to FDA’s current guidance documents on deferral of blood and plasma donors who may be at increased risk of vCJD, and to other sources of information regarding vCJD. Documents Regarding US Licensed pdFVIII, and Other US Licensed Plasma Derivatives Including pdFIX Potential vCJD Risk From US Licensed Plasma-Derived Factor VIII (pdFVIII, Antihemophilic Factor) Products: Summary Information, Key Points Risk Assessment (PDF, 582 KB) Risk Assessment Appendix (PDF, 623 KB) Questions and Answers on vCJD and pdFVIII Questions and Answers on vCJD and Plasma Derivatives Other than pdFVIII Guidance on Donor Deferral Related to CJD and vCJD Draft Guidance for Industry: Amendment (Donor Deferral for Transfusion in France Since 1980) to "Guidance for Industry: Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease (CJD) and Variant Creutzfeldt-Jakob Disease (vCJD) by Blood and Blood Products" - 8/2006 Questions and Answers on FDA Guidance: Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob (CJD) Disease and Variant Creutzfeldt-Jakob Disease (vCJD) by Blood and Blood Products - 1/22/2004 Guidance for Industry: Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease (CJD) and Variant Creutzfeldt-Jakob Disease (vCJD) by Blood and Blood Products - 1/2002 Other Sources of Information Transmissible Spongiform Encephalopathies Advisory Committee Blood Products Advisory Committee Meeting – Summary of Recent TSEAC Meeting and Statement about FXI from the UK, on October 21, 2004 Information on vCJD: Centers for Disease Control and Prevention Information on Bovine Spongiform Encephalopathy (“Mad Cow Disease”): US Department of Agriculture Patient Organizations: Committee of Ten Thousand Hemophilia Federation of America National Hemophilia Foundation and/or HANDI World Federation of Hemophilia http://www.fda.gov/cber/blood/vcjdrisk.htm PRODUCT Recovered Plasma, Recall # B-0854-07 CODE Unit: V10665 RECALLING FIRM/MANUFACTURER Virginia Blood Services, Richmond, VA, by email on August 25, 2004. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Switzerland END OF ENFORCEMENT REPORT FOR MARCH 14, 2007 ### http://www.fda.gov/bbs/topics/enforc.../ENF00995.html nvCJD mad cow blood recalls ENFORCEMENT REPORT FOR MARCH 7, 2007 ___________________________________ PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-0805-07; b) Platelets, Recall # B-0806-07; c) Recovered Plasma, Recall # B-0807-07 CODE a) Units: 4759943, 4677574, 4555912; b) Units: 4759943, 4555912; c) Units: 4677574, 4555912 RECALLING FIRM/MANUFACTURER Oklahoma Blood Institute, Sylvan N. Goldman Center, Oklahoma City, OK, by facsimile on May 20, 2005. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 7 units DISTRIBUTION MA, OK, TX, and Switzerland ___________________________________ PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-0808-07; b) Platelets, Recall # B-0809-07; c) Recovered Plasma, Recall # B-0810-07 CODE a), b), and c) Unit: 5249546 RECALLING FIRM/MANUFACTURER Oklahoma Blood Institute, Sylvan N, Goldman Center, Oklahoma City, OK, by facsimile on August 1, 2005. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION OK, NB, and Switzerland ___________________________________ PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-0811-07; b) Recovered Plasma, Recall # B-0812-07 CODE a) and b) Unit: 5218775 RECALLING FIRM/MANUFACTURER Oklahoma Blood Institute, Sylvan N, Goldman Center, Oklahoma City, OK, by facsimile on July 7, 2005. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION OK and Switzerland ___________________________________ PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-0826-07; b) Platelets, Recall # B-0827-07; c) Fresh Frozen Blood, Recall # B-0828-07; d) Recovered Plasma, Recall # B-0829-07 CODE a) Units: 5250527, 4901850, 4517058; b) Units: 4901850, 4517058; c) Unit: 4517058; d) Units: 5250527, 4901850 RECALLING FIRM/MANUFACTURER Oklahoma Blood Institute, Sylvan N. Goldman Center, Oklahoma City, OK, by facsimile on March 27, 2006. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 8 units DISTRIBUTION OK, TX, Austria, and Switzerland ___________________________________ PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-0843-07; b) Recovered Plasma, Recall # B-0844-07 CODE a) and b) Units: 5738052, 5275313, 4801421 RECALLING FIRM/MANUFACTURER Oklahoma Blood Institute, Sylvan N. Goldman Center, Oklahoma City, OK, by facsimile on January 22, 2006. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 6 units DISTRIBUTION TX, OK, and Switzerland END OF ENFORCEMENT REPORT FOR MARCH 7, 2007 ### http://www.fda.gov/bbs/topics/enforc.../ENF00994.html 4th CASE VCJD VIA BLOOD TRANSFUSION, BSE, BASE, AND SPORADIC CJD By Terry S Singeltary Bacliff, Texas USA Jan 24, 07 http://bloodindex.org/view_news_zone.php?id=206 PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ... http://www.fda.gov/ohrms/dockets/ac/.../3681s2_09.pdf ----- Original Message ----- From: Terry S. Singeltary Sr. To: Terry S. Singeltary Sr. ; [log in to unmask] Cc: [log in to unmask] ; [log in to unmask] Sent: Thursday, November 30, 2006 1:47 PM Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION PART II] http://lists.ifas.ufl.edu/cgi-bin/wa...mg&T=0&P=16159 TSS |
Position Statement vCJD and Dentistry SEAC
SEAC
Position Statement -------------------------------------------------------------------------------- Position Statement vCJD and Dentistry Issue 1. The Department of Health (DH) asked SEAC to advise on the findings of preliminary research aimed at informing estimates of the risk of variant Creutzfeldt-Jakob Disease (vCJD) transmission via dentistry. Background 2. Prions are more resistant than other types of infectious agent to the conventional cleaning and sterilisation practices used to decontaminate dental instruments1. Appreciable quantities of residual material may remain adherent to the surface after normal cleaning and sterilisation2. Therefore, if dental tissues are both infectious and susceptible to infection, then dental instruments are a potential mechanism for the secondary transmission of vCJD. Dentistry could be a particularly significant route of transmission for the population as a whole, due to the large number of routine procedures undertaken and also because dental patients have a normal life expectancy. This is in contrast with other transmission routes, such as blood transfusion and neurosurgery, where procedures are often carried out in response to some life-threatening condition. Additionally, the ubiquity of dental procedures and the lack of central records on dental procedures means that should such transmission occur, then it would be difficult to detect and control. 3. No cases of vCJD transmission arising from dental procedures have been reported to date 3 . Previous DH risk assessments4,5 have focused on two possible mechanisms for the transfer of vCJD infectivity via dental instruments; accidental abrasion of the lingual tonsil and endodontic procedures that involve contact with dental pulp. In considering these assessments, SEAC agreed that the risk of transmission via accidental abrasion of the lingual tonsil appears very low. However, the risk of transmission via endodontic procedures may be higher and give rise to a self sustaining vCJD epidemic under circumstances where (i) dental pulp is infective, (ii) transmission via endodontic instruments is efficient and (iii) a large proportion of vCJD infections remain in a subclinical carrier state (SEAC 91, February 2006). In light of this, SEAC advised that restricting endodontic files and reamers to single use be considered 6. SEAC recommended reassessment of these issues as new data emerge. New research 4. Preliminary, unpublished results of research from the Health Protection Agency, aimed at addressing some of the uncertainties in the risk assessments, were reviewed by SEAC (SEAC 97, May 2007). The prion agent used in these studies is closely related to the vCJD agent. This research, using a mouse model, shows that following inoculation of mouse-adapted bovine spongiform encephalopathy (BSE) directly into the gut, infectivity subsequently becomes widespread in tissues of the oral cavity, including dental pulp, salivary glands and gingiva, during the preclinical as well as clinical stage of disease. 5. It is not known how closely the level and distribution of infectivity in the oral cavity of infected mice reflects those of humans infected with vCJD, as there are no comparable data from oral tissues, in particular dental pulp and gingiva, from human subclinical or clinical vCJD cases7. Although no abnormal prion protein was found in a study of human dental tissues, including dental pulp, salivary glands and gingiva from vCJD cases , the relationship between levels of infectivity and abnormal prion protein is unclear8. Infectivity studies underway using the mouse model and oral tissues that are presently available from human vCJD cases will provide some comparable data. On the basis of what is currently known, there is no reason to suppose that the mouse is not a good model for humans in respect to the distribution of infectivity in oral tissues. Furthermore, the new data are consistent with published results from experiments using a hamster scrapie model9 . 6. A second set of experiments using the same mouse model showed that non-invasive and transient contact between gingival tissue and fine dental files contaminated with mouse-adapted BSE brain homogenate transmits infection very efficiently. It is not known how efficient gingival transmission would be if dental files were contaminated with infectious oral tissues and then subsequently cleaned and sterilised, a situation which would more closely model human dental practice. Further studies using the mouse model that would be more representative of the human situation, comparing oral tissues with a range of doses of infectivity, cleaned and sterilised files and the kind of tissue contact with instruments that occurs during dentistry, should be considered. 7. SEAC considered that the experiments appear well designed and the conclusions justified and reliable, while recognising that the research is incomplete and confirmatory experiments have yet to be completed. It is recommended that the research be completed, submitted for peer-review and widely disseminated as soon as possible so others can consider the implications. Nevertheless, these preliminary data increase the possibility that some oral tissues of humans infected with vCJD may potentially become infective during the preclinical stage of the disease. In addition, they increase the possibility that infection could potentially be transmitted not only via accidental abrasion of the lingual tonsil or endodontic procedures but a variety of routine dental procedures. Implications for transmission risks 8. The new findings help refine assumptions made about the level of infectivity of dental pulp and the stage of incubation period when it becomes infective in the risk assessment of vCJD transmission from the reuse of endodontic files and reamers10. For example, if one patient in 10 000 were to be carrying infection (equivalent to about 6 000 people across the UK – the best current estimate11), the data suggest that in the worst case scenario envisaged in the risk assessment, re-use of endodontic files and reamers might lead to up to 150 new infections per annum. It is not known how many of those infected would go on to develop clinical vCJD. In addition, transmission via the re-use of endodontic files and reamers could be sufficiently efficient to cause a self-sustaining vCJD epidemic arising via this route. 9. These results increase the importance of obtaining reliable estimates of vCJD infection prevalence. Data that will soon be available from the National Anonymous Tonsil Archive may help refine this assessment and provide evidence of the existence and extent of subclinical vCJD infection in tonsillectomy patients. Further data, such as from post mortem tissue or blood donations, will be required to assess prevalence in the general UK population12. 10. Recent guidance issued by DH to dentists to ensure that endodontic files and reamers are treated as single use13 is welcomed and should, as long as it is effectively and quickly implemented, prevent transmission and a self-sustaining epidemic arising via this route. However, the extent and monitoring of compliance with this guidance in private and National Health Service dental practice is unclear. 11. The new research also suggests that dental procedures involving contact with other oral tissues, including gingiva, may also be capable of transmitting vCJD. In the absence of a detailed risk assessment examining the potential for transmission via all dental procedures, it is not possible to come to firm conclusions about the implications of these findings for transmission of vCJD. However, given the potential for transmission by this route serious consideration should be given to assessing the options for reducing transmission risks such as improving decontamination procedures and practice or the implementation of single use instruments. 12. The size of the potential risk from interactions between the dental and other routes of secondary transmission, such as blood transfusion and hospital surgery, to increase the likelihood of a self-sustaining epidemic is unclear. 13. It is likely to be difficult to distinguish clinical vCJD cases arising from dietary exposure to BSE from secondary transmissions via dental procedures, should they arise, as a large proportion of the population is likely both to have consumed contaminated meat and undergone dentistry. However, an analysis of dental procedures by patient age may provide an indication of the age group in which infections, if they occur, would be most likely to be observed. Should the incidence of clinical vCJD cases in this age group increase significantly, this may provide an indication that secondary transmission via dentistry is occurring. Investigation of the dental work for these cases may provide supporting data. There is no clear evidence, to date, based on surveillance or investigations of clinical vCJD cases, that any vCJD cases have been caused by dental procedures but this possibility cannot be excluded. Conclusions 14. Preliminary research findings suggest that the potential risk of transmission of vCJD via dental procedures may be greater than previously anticipated. Although this research is incomplete, uses an animal model exposed to relatively high doses of infectivity, and there are no data from infectivity studies on human oral tissues, these findings suggest an increased possibility that vCJD may be relatively efficiently transmitted via a range of dental procedures. Ongoing infectivity studies using human oral tissues and the other studies suggested here will enable more precise assessment of the risks of vCJD transmission through dental procedures. 15. Guidance was issued to dentists earlier this year recommending that endodontic files and reamers be treated as single use which, provided it is adhered to, will remove any risk of a self-sustaining epidemic arising from re-use of these instruments. To minimise risk it is critical that appropriate management and audit is in place, both for NHS and private dentistry. 16. It is also critical that a detailed and comprehensive assessment of the risks of all dental procedures be conducted as a matter of urgency. While taking into account the continuing scientific uncertainties, this will allow a more thorough consideration of the possible public health implications of vCJD transmission via dentistry and the identification of possible additional precautionary risk reduction measures. The assessment will require continued updating as more evidence becomes available on the transmissibility of vCJD by dental routes, and on the prevalence of infection within the population. A DH proposal to convene an expert group that includes dental professionals to expedite such an assessment is welcomed. Given the potential for transmission via dentistry, consideration should be given to the urgent assessment of new decontamination technologies which, if proved robust and effective, could significantly reduce transmission risks. SEAC June 2007 References 1Smith et al. (2003) Prions and the oral cavity. J. Dent. Res. 82, 769-775. 2Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241. 3Everington et al. (2007) Dental treatment and risk of variant CJD – a case control study. Brit. Den. J. 202, 1-3. 4Department of Health. (2003) Risk assessment for vCJD and dentistry. 5 Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished. 6SEAC (2006) Position statement on vCJD and endodontic dentistry. http://www.seac.gov.uk/statements/statement0506.htm 7Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 8SEAC 90 reserved business minutes. 9Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047. 10Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished. 11Clarke & Ghani (2005) Projections of future course of the primary vCJD epidemic in the UK: inclusion of subclinical infection and the possibility of wider genetic susceptibility R. J. Soc. Interface. 2, 19-31. 12SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic. http://www.seac.gov.uk/statements/st...06subgroup.htm 13DH (2007) Precautionary advice given to dentists on re-use of instruments http://www.gnn.gov.uk/environment/fu...partment=False Page updated: 8 June, 2007 http://www.seac.gov.uk/statements/st...-dentrstry.htm USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available. snip... 64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. snip... http://www.seac.gov.uk/minutes/95.pdf 3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. ***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.*** 6:30 Close of Day One http://www.healthtech.com/2007/tse/day1.asp SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ... http://www.cjdsurveillance.com/resou...asereport.html There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection. He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins. http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.htm http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.pdf Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/http://www....s/60/2/176#535 BRITISH MEDICAL JOURNAL BMJ vCJD in the USA * BSE in U.S. 15 November 1999 http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406 BMJ U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... 2 January 2000 http://www.bmj.com/cgi/eletters/320/7226/8/b#6117 JOURNAL OF NEUROLOGY MARCH 26, 2003 RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: flounder@wt.net I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported 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. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? http://www.neurology.org/cgi/eletters/60/2/176#535 doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk Tracking spongiform encephalopathies in North America Xavier Bosch Available online 29 July 2003. Volume 3, Issue 8, August 2003, Page 463 “My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” ............................ http://www.thelancet.com/journals/la...07151/fulltext http://download.thelancet.com/pdfs/j...9903007151.pdf see history of cjd questionnaire http://brain.hastypastry.net/forums/...ead.php?t=2408 sporadic CJD, the big lie http://lists.ifas.ufl.edu/cgi-bin/wa...mg&T=0&P=25276 TSS |
TSS,
Lots to read! What it truly comes down to is quite simple....... proper sterilization techniques MUST be done under ALL circumstances, ALL of the time, in ALL dental and medical facilities. Precaution should be taken to not just minimize, but eliminate the possibility of contamination to the patients and the staff. Having been in dentistry for 30 yrs......... I can without any doubt say that proper sterilization techniques are not carried out 100% of the time. The only way to do that is to have one very dedicated (or more) staff member whose only job is to clean up and sterilize the operatories/exam rooms and instruments. This cannot be done efficiently or effectively by the staff member who also assists the doctor if she/he is responsible for keeping a tight schedule and has to be in 2 (or more) places at one time. Contamination from a doctor, staff member, dirty instrument or other operatory source is completely avoidable if the proper protocols are put forth, utilized and enforced. Thanks for posting these articles! Bryanna |
Subject: Pre-sterilisation cleaning of re-usable instruments (TSE)
Date: July 13, 2007 at 2:24 pm PST Pre-sterilisation cleaning of re-usable instruments in general dental practice J. Bagg,1 A. J. Smith,2 D. Hurrell,3 S. McHugh4 and G. Irvine5 Objective This study examined the policies, procedures, environment and equipment used for the cleaning of dental instruments in general dental practice. Materials and methods A total of 179 surgeries were surveyed. This was an observational based study in which the cleaning processes were viewed directly by a trained surveyor. Information relating to surgery policies and equipment was also collected by interview and viewing of records. Data were recorded onto a standardised data collection form prepared for automated reading. Results The BDA advice sheet A12 was available in 79% of surgeries visited. The most common method for cleaning dental instruments was manual washing, with or without the use of an ultrasonic bath. Automated washer disinfectors were not used by any surgery visited. The manual wash process was poorly controlled, with 41% of practices using no cleaning agent other than water. Only 2% of surgeries used a detergent formulated for manual washing of instruments. When using ultrasonic baths, the interval that elapsed between changes of the ultrasonic bath cleaning solution ranged from two to 504 hours (median nine hours). Fifty-eight percent of surgeries claimed to have a dedicated area for instrument cleaning, of which 80% were within the patient treatment area. However, in 69% of surgeries the clean and dirty areas were not clearly defi ned. Virtually all cleaning of dental instruments was undertaken by dental nurses. Training for this was provided mainly by demonstration and observed practice of a colleague. There was little documentation associated with training. Whilst most staff wore gloves when undertaking manual cleaning, 51% of staff did not use eye protection, 57% did not use a mask and 7% used waterproof overalls. Conclusions In many dental practices, the cleaning of re-usable dental instruments is undertaken using poorly controlled processes and procedures, which increase the risk of cross infection. Clear and unambiguous advice must be provided to the dental team, especially dental nurses, on appropriate equipment, chemicals and environment for cleaning dental instruments. This should be facilitated by appropriate training programmes and the implementation of quality assurance procedures at each stage of the cleaning process. INTRODUCTION The decontamination of re-usable medical devices is a key element of infection control in clinical settings. The importance of cleaning such devices as a means of preventing cross infection has been reported in relation to diverse items of equipment in many areas of clinical practice. These have included ophthalmology,1 gastroenterology,2 vascular surgery,3 tourniquets4 and dental surgery.5-9 More recently, the emergence of transmissible spongiform encephalopathies (TSEs), such as variant Creutzfeldt-Jakob disease (vCJD), has re-emphasised the importance of thorough cleaning of used devices prior to steam sterilisation10,11 since the abnormal form of prion protein, which is responsible for these diseases, is less susceptible to denaturation by heat. Thus, effi cient cleaning of instruments is believed to be a key procedure for reducing the potential risks of onward transmission of vCJD.10-12 Effective cleaning is also vital to ensure microbial inactivation since retention of organic or inorganic debris may compromise subsequent disinfection or sterilization processes.13-16 The cleaning of re-usable dental instruments is also important to ensure device longevity and functionality, removal of chemical residues and compliance with medicolegal directives.17-19 One mechanism for improving the quality of instrument decontamination is to centralise re-processing in well-equipped sterile services departments, which are operated by highly trained staff, using validated equipment, in an accredited quality management system. In the UK, this approach has been applied in the acute hospital sector. The problem with this centralised model in dentistry is that the high volume of instruments used by dental surgeons provides a signifi cant logistical challenge. It is therefore likely that instrument decontamination in general dental practice will continue to be undertaken at a local level. It is important that all processes involved in decontamination are undertaken to a high standard, but unfortunately there has been little evidence to indicate the robustness of these procedures in dental practice, as highlighted in a systematic review.20 In order to address this problem, a large observational study of decontamination procedures in general dentistry in Scotland was devised and has recently been completed. This paper reports the data generated by the study in relation to procedures used by dentists for pre-cleaning of instruments prior to the sterilisation phase. MATERIALS AND METHODS snip. ... In conclusion, many of the procedures used for the cleaning of re-usable dental instruments in general dental practice do not conform to extant guidance and increase the risk of transmission of infection. This is of particular concern, since cleaning is a key stage in the sterilisation process and in reducing the risk from onward transmission of vCJD. Where possible, practices should review the many options available to them for the reprocessing of dental instruments. In some circumstances this may involve the use of centralised reprocessing facilities35 or single use instruments. Other options may involve a compromise with local reprocessing of expensive devices such as dental handpieces and centralised reprocessing of other instruments. If local reprocessing of dental instruments is to continue in general dental practice, clearly much work is needed to help the dental team improve the cleaning process for dental instruments. This should take the form of education and training programmes and the development of a clearer management process using quality assurance principles. The fi ndings of this survey also have profound fi nancial implications for dental practices, not least in the provision of dedicated decontamination areas and automated washer disinfectors. This also represents an opportunity for improvement, especially with the planning of new dental units. However, if the opportunity is to be fully realised, there is a requirement for suffi cient infrastructure to support practitioners in implementation of improvements in local decontamination,29 for example expert review of new buildings, commissioning and testing of decontamination equipment. Practice-friendly guidance to help practitioners meet the various regulatory requirements for cleaning dental instruments is essential if progress is to be made in this very important area of clinical practice. This research was supported by a grant from the Scottish Executive Health Department. Funding for the training of the survey team members was provided by NHS Education for Scotland. The authors thank Mr Ray Watkins, Chief Dental Offi cer for Scotland and Dr Jim Rennie, Postgraduate Dental Dean for Scotland for support of the study, the members of the survey teams and the dental practitioners and nurses who agreed to be surveyed. snip... full text ; http://www.nature.com/bdj/journal/v2...j.2007.124.pdf It is all about motivation I am occasionally asked by actors and actresses what motivation their characters have for various lines that I have written for them in plays and the like. It is a bit of a cliché but there is usually a good reason for the question as the performer is attempting to understand their character better and provide an improved performance for the audience. But motivation often involves fi nishing the sentence, or at least the sentiment behind it. In acting it is sometimes forgivable, indeed sometimes it adds value for the observer when everything is not spoken or revealed. But there does not seem to be much of a case for it in health care. I have in mind the recent advice issued by the various UK Departments of Health in relation to the single-use of endodontic instruments. One has to assume that the information is imparted in good faith, since why else would a state department issue such advice (it is advice, note, not guidance or direction). Advice nonetheless that ‘dentists are expected to follow’? But the manner in which it was announced and the scientifi c basis on which it is apparently founded both give rise to suspicions and to distrust. It is probably just poor logistics but the result is that it opens the way to questions over motivation. Firstly to the manner in which it was announced; it transpires that all policy developments and guidance in relation to vCJD has to be fi rst reported to Parliament before any other communication can take place. This was a commitment made by John Reid when he was Secretary of State for Health and supported by the then current Ministers. This explains why BDA members contacted us the same morning of the announcement asking why the Association had not let them know. We had to reply that it was because we did not know about it either until we heard it on BBC Radio 2. Important as it is that 630 MPs (or however many were in the Chamber that session) are the fi rst to know, presumably patients in surgeries with the radio on and endodontic instruments in their root canals would also think it a matter of some importance. With hindsight, can our elected representatives really believe that this is the best way to deal with matters of health care? The science on which this advice is based brings forth a further clutch of questions. We are told that, ‘early results from studies in mice suggest that TSE (Transmissible Spongiform Encephalopathies, the group of prion diseases that include BSE, CJD, vCJD and scrapie) infectivity can be found in dental tissues’. The studies, early results or not, are not published so none of us can assess that risk independently. On the one hand this may seem reasonable since we are constantly being entreated ourselves to follow best practice as indicated by evidence-based studies. We have to take the Chief Dental Offi cers’ words at face value, since we have no other base on which to judge them, as indeed presumably they have had to take the words of others above them. But on the other hand this is about calculated risk assessment. Someone, somewhere has taken a decision on the basis of what is known to date and the extent to which they assess that to be a threat to the population. Or in this case a ‘theoretical’ threat. Once again though, we are denied the knowledge of the motivation. Is the advice given on a defensive basis so that if in years to come patients can show that they have contracted a TSE disease from endodontic treatment they will be able to sue the government because it failed to act on the scientifi c advice of the time? Or is the advice given on the basis that such potential litigation is then passed to the individual dentist? Alternatively, is the advice just on the basis of taking good care of the population? It might be all or any of these but we have to guess and it is the guessing that substantially increases the risk of distrust. All of this, sadly, obscures what one hopes is the real motivation behind the advice, which is that if there is a risk then it is wise to take sensible precautions. The issues of who pays the additional costs and the environmental questions of reamer and fi le-mountains all need to be considered in the risk evaluation too. Have they been? Confl icting reports on the possibility or not of fi nancial compensation for those dentists offering NHS dentistry have served only to add further confusion, rumour and annoyance. The handling of the matter as a whole makes one seriously doubt that any kind of global view has been taken before the advice has been rushed out. We may, as a profession, be accused of starting to get paranoid about having matters forced upon us with little or no consultation, little or no notice and precious little respect for our professionalism but is it really surprising? Handled logically, with proper sequencing this development could have been, should have been, a triumph for good sense, measured response and excellence in health care. Instead it is an all too familiar shambles. How many more will there be? Stephen Hancocks OBE Editor-in-Chief DOI: 10.1038/bdj.2007.422 It is all about motivation EDITORIAL BRITISH DENTAL JOURNAL VOLUME 202 NO. 9 MAY 12 2007 http://www.nature.com/bdj/journal/v2...j.2007.422.pdf Dental treatment and risk of variant CJD – a case control study D. Everington,1 A. J. Smith,2 H. J. T. Ward,3 S. Letters,4 R. G. Will5 and J. Bagg6 Objective Knowledge of risk factors for variant CJD (vCJD) remains limited, but transmission of prion proteins via re-useable medical devices, including dental instruments, or enhanced susceptibility following trauma to the oral cavity is a concern. This study aimed to identify whether previous dental treatment is a risk factor for development of vCJD. Design Case control study. Methods Risk factor questionnaires completed by interview with relatives of 130 vCJD patients and with relatives of 66 community and 53 hospital controls were examined by a dental surgeon. Responses regarding dental treatments were analysed. Results We did not fi nd a statistically signifi cant excess of risk of vCJD associated with dental treatments with the exception of extractions in an unmatched analysis of vCJD cases with community controls (p = 0.02). However, this result may be explained by multiple testing. Conclusions This is the fi rst published study to date to examine potential links between vCJD and dental treatment. There was no convincing evidence found of an increased risk of variant CJD associated with reported dental treatment. However, the power of the study is restricted by the number of vCJD cases to date and does not preclude the possibility that some cases have resulted from secondary transmission via dental procedures. Due to the limitations of the data available, more detailed analyses of dental records are required to fully exclude the possibility of transmission via dental treatment. snip... DISCUSSION Many studies have searched for risk factors for the development of different types of CJD, such as diet, exposure to animals, surgical treatment, including dentistry, and occupational exposures. A retrospective case control study15 of 60 defi nite cases of sporadic CJD, occurring in Japan between 1975 and 1977 found no association with extractions of maxillary or mandibular teeth. An analysis of 26 sporadic CJD cases and 40 matched controls from the United States16 failed to discover a signifi cant odds ratio for endodontic surgery, though these workers did note statistically signifi cant odds ratios for intraocular pressure testing, injury to or surgery on the head, face or neck and trauma to other parts of the body. However, these fi ndings suffer from low statistical power and, in the case of the Japanese paper, information was requested for extractions only during the fi ve year period prior to onset. This paper attempts to identify an association between vCJD and reported dental treatment. Comparison of the reported dental histories of cases and controls found that extractions were the only dental risk factor that reached statistical signifi cance (at the 5% level) in the unmatched analysis with community controls. This may be a result of multiple testing especially as there are fewer extractions in the cases than in the hospital controls. It is likely that the majority of vCJD cases in this cohort were infected through eating BSE contaminated meat products. Therefore, it is diffi - cult to detect a small subgroup that may have been infected by secondary transmission, as in this study, through dentistry. There are a number of limitations to this study, most importantly relying on reported data from relatives and the relatively small numbers of cases and controls resulting in low power to detect statistical differences. Recruitment of controls has been problematic,17 although every effort was made to maximise this group. Selection of controls was not matched for demographic and socio-economic factors for dental attendance and this may have resulted in bias. It is possible that some of the responses of ‘no known treatment’ refl ect poor knowledge or recall on the part of the relatives. This would reduce the power of the study to pick up signifi cant differences between groups, but not necessarily introduce bias. Whilst these preliminary data on a topic of great concern for public health do not provide evidence supporting reported dental work as being a major route of transmission of the BSE agent to humans to date, they do not preclude the possibility that some vCJD cases have been infected by this route. Furthermore, the incubation period following infection by a peripheral route may be relatively long and therefore the period of observation to date of potential secondary transmission of vCJD may be too short to detect cases. A more detailed study of previous treatment based on reviewing actual dental records rather than relying on reported treatments is required to gain a wider insight into the dental history of both cases and controls. We are currently investigating the possibility of examining dental records of vCJD cases and a larger group of unmatched controls.18 The National CJD Surveillance Unit is funded by the Department of Health and the Scottish Executive Department of Health. The sponsors of the study had no role in study design, data collection, data analysis, data interpretation, or in the writing of the report. We are also grateful to the families of cases, without whose co-operation this study would not have been possible. http://www.nature.com/bdj/journal/v2...j.2007.126.pdf Subject: Position Statement vCJD and Dentistry SEAC UPDATE DISTURBING Date: June 9, 2007 at 7:52 am PST http://disc.server.com/discussion.cg...RD;pagemark=25 http://disc.server.com/discussion.cg...RD;pagemark=25 TSS |
Prion2007 Abstracts Sporadic Cjd And H Base Mad Cow Alabama And Texas
FC5.3
Assessing the Risk of vCJD Transmission by Dentistry; Distribution of Infectivity in Oral Tissues of VM Mice after Simulated Oral Feeding of BSE-301V Sutton, JM1; Kirby, E1; Dickinson, J1; Dennis, M1; Cornwall, M1; Vassey, MJ1; Smith, A2; Marsh, PD3; Walker, JT1; Raven, NDH1 1Health Protection Agency, Centre for Emergency Preparedness and Response,, TSE Research group, UK; 2University of Glasgow, Dental School, UK; 3Health Protection Agency, Centre for Emergency Preparedness and Response,, UK Background: Ongoing concerns about the prevalence of variant Creutzfeldt Jakob Disease (vCJD) in the UK population has heightened concerns about the risks of iatrogenic transmission of the disease. Although there have been no cases to date of transmission by surgery there have been 4 cases involving blood transfusion. This study aims to assess the potential of transmission of the disease by dental procedures. Whilst the risks are undoubtably low the very large numbers of procedures carried out annually have the potential to amplify the risks considerably and there is very little data in this area to form the basis for accurate risk assessments. Aim(s)/Objective(s): To assess the relative levels of infectivity in oral tissues from a murine model following exposure to BSE-301V through the small intestine. Methods. The study uses a BSE-301V, VM mouse model as a clinically relevant model for assessing iatrogenic vCJD transmission between humans. Infectious mouse brain homogenate was prepared and inoculated into a loop of the duodenum, to prevent direct contamination of the oral tissues. Mice were sacrificed at 3-weekly intervals and at appearance of clinical symptoms. A range of oral tissues, including dental pulp, gingival margin, salivary gland, saliva, lingual tonsil and trigeminal ganglia, together with brain and spleen tissues were removed, processed as homogenates and reinoculated intracranially (ic.) into indicator mice. Results: The primary challenge proved to be a very efficient route of infection with a 100% attack rate and a mean incubation to clinical disease of 157 ± 17 days (compared to 120 days for the same titre inoculum ic.). Infectivity was observed in all oral and control tissues with varying time-courses and titres estimated from incubation period. Discussion: The results throw new light on the potential routes of dissemination and spread of infectivity from the small intestine to the oral cavity and its implications for possible iatrogenic transmission of vCJD via dental, endoscopic or other forms of surgery. Conclusion: The data generated from the study provides support for ongoing risk assessments to look at the potential for vCJD transmission via dental procedures alongside other elements of studies looking at effectiveness of decontamination and re-use of dental instruments. P02.15 Beyond the PrPres Type1/ Type2 dichotomy in Creutzfeldt-Jakob Disease Cassard, H1; Uro-Coste, E2; Simon, S3; Bilheude, JM4; Perret-Liaudet, A5; Ironside, J6; Haik, S7; Basset-Leobon, C2; Lacroux, C1; Peoch’, K8; Stressenberger, N9; Langeveld, J10; Head, M11; Hauw, JJ12; Schecher, F1; Delisle, MB13; Andreoletti, O1 1Ecole Natinale Vétérinaire de Toulouse, France; 22Service d’Anatomie Pathologique and INSERM U466 R, France; 3DRM, CEA/Saclay, France; 4 Bio-Rad, R&D, France; 5 Hôpital Neurologique Service de Neurochimie, France; 6School of Molecular & Clinical Medicine (Pathology),, National Creutzfeldt-Jakob Disease Surveillance Un, UK; 7Pitié Salpetriere Universitary Hospital, France; 8Hôpital Lariboisière, Service de Biochimie et Biologie Moléculaire,, France; 9Hôpital Neurologique -Service de Neurochimie, France; 10CIDC-Lelystad, Netherlands; 11University of Edinburgh, Western General Hospital, UK; 12Pitié Salpetriere Universitary Hospital,, Laboratoire de Neuropathologie, France; 13Rangueil Universitary Hospital, Service d’Anatomie Pathologique, France Creutzfeldt-Jakob disease (CJD) cases are currently classified according to established diagnostic criteria and by the genotype at codon 129 of the PRNP gene and the Western blotting of the proteinase K digested abnormal prion protein that distinguishes a type 1 and a type 2 profile. These biochemically distinct PrPres types have been proposed to represent distinct prion strains. However, since the cooccurence of type 1 and type 2 PrPres in the same patient is common, the rationale of this classification and strain concept as applied to CJD are currently under discussion. Five different brain areas from of 40 sporadic CJD and 11 iatrogenic CJD (both dura matter-, and growth hormone-associated) cases, originating from UK and France, were systematically investigated, using Western blotting typing, and by two others biochemical assays that depend on the behaviour of PrPSc in variable PK digestion conditions. As described previously, co-occurrence of type 1 and type 2 PrPres was found in 30% of the CJD patients examined. However, our novel PK concentration dependent assays identified a single uniform PrP type in cases where both type 1 and type 2 were present. Moreover, in sCJD four distinct biochemical PrPSc signatures were identified by the PK concentration dependent assays and these correlated to the current genotype/clinico-pathological sCJD groups. In iCJD the four similar biochemical signatures were observed, but were not correlated to particular PRNP 129 polymorphism or Western Blot PrPres patterns. Moreover notable differences were observed between PrPSc biochemical properties of French and UK GH-CJD cases, which could reflect, as already suspected, differences in the causative agents. Identification, in sCJD and iCJD, of four different PrPSc phenotypes irrespective of patients PRNP polymorphism at codon 129 and Western blot profile provides new insights into human prion disease aetiology and could reflects an unsuspected diversity of TSE agents in human disease. Further investigations are currently underway using animal transmission to correlate agent strain with our new discriminant biochemical assays. see much more ; PRION2007 ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007 Date: Mon, 24 Sep 2007 21:31:55 -0500 I suggest that you all read the data out about h-BASE and sporadic CJD, GSS, blood, and some of the other abstracts from the PRION2007. ... http://lists.ifas.ufl.edu/cgi-bin/wa...&F=&S=&P=19744 USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS http://lists.ifas.ufl.edu/cgi-bin/wa...mg&T=0&P=19779 see full text 143 pages ; http://www.prion2007.com/pdf/Prion%2...0Abstracts.pdf Terry S. Singeltary Sr. Bacliff, Texas |
Cjd And Blood Update October 2007
P04.49
Case Report of Variant Creutzfeldt-Jakob Disease in a Macaque after Blood Transfusion Lescoutra-Etchegaray, N1; Ruchoux, MM1; Correia, E1; Jolit, A1; Freire, S1; Lasmezas, CI2; Deslys, JP1; Comoy, E1 1CEA/DSV/IMETI/SEPIA, France; 2Scripps Florida, USA A fourth human case of probable transmission of vCJD through transfusion has now been reported but a number of features affecting transfusion-related infection remain imprecise, including infectious dose, length of incubation period and critical infectious window of blood donors. We report here the first case of experimental transmission of vCJD in primates by blood transfusion. Experimental infection of Cynomolgus macaque has been demonstrated to be a sensitive model for the investigation of human prion diseases, inducing similar distribution of infectivity in peripheral lymphoid tissues and equivalent brain pathology. In our study, transfusion was performed with 40 ml of whole blood drawn from a vCJD-infected macaque at the terminal stage of the disease. Clinical symptoms of vCJD appeared in the recipient animal after five years of incubation. The total amount of infectivity in the transfused blood was approximately 106 fold lower than in the brain (titration still in progress). In several animals infected intravenously with brain homogenate, the presence of PrPres in serial lymph nodes biopsies and in other organs at autopsy was examined and results will be presented. http://www.prion2007.com/pdf/Prion%2...0Abstracts.pdf P04.51 Atypical Presentation of Variant Creutzfeldt-Jakob Disease in a 73 Year Old Blood Transfusion Recipient Wroe, S1; Pal, S1; Webb, T1; Alner, K2; Hewitt, P3; Brander, S4; Wadsworth, JD5; Collinge, J1 1National Hospital for Neurology and Neurosurgery, National Prion Clinic, UK; 2National Hospital for Neurology and Neurosurgery, Department of Neuropsychology, UK; 3Health Protection Agency, UK; 4National Hospital for Neurology and Neurosurgery, Department of Neuropathology, UK; 5Institute of Neurology, UCL, UK We report atypical presentation of variant Creutzfeldt-Jakob Disease (vCJD) identified ante-mortem in a 73 year-old recipient of blood products. This patient was transfused following orthopaedic surgery in December 1997. Tracing of blood products identified a single unit of non-leucodepleted red cells from an individual who developed neuropathologically confirmed vCJD eleven months after donation. Nine years post transfusion, this individual was referred to the National Prion Clinic for specialist investigation. Six years post transfusion the recipient complained of fluctuating fatigue and impaired concentration. At this time neurological examination and MRI brain (T1/T2 weighted/DWI) were normal. Progressive symptoms emerged six months later with imbalance and deteriorating cognition. Examination two months after onset of neurological symptoms demonstrated cognitive deficits, dyspraxia or visuospatial dysfunction and normal motor, sensory and gait examination. Six weeks later cognitive impairment was identified alongside tremulousness, impaired manual dexterity and limb ataxia. Serological investigations were normal. MRI (T1/T2 weighted/FLAIR/DWI) demonstrated prominent signal change throughout the dorsal thalamus, consistent with vCJD. PRNP genotyping revealed no mutations and homozygosity for methionine at codon 129. The prolonged incubation period of vCJD and possibility of asymptomatic carrier states pose major public health concerns. This case highlights the significant risk encountered by recipients of contaminated blood products and the necessity for their specialist monitoring. http://www.prion2007.com/pdf/Prion%2...0Abstracts.pdf P04.36 Enhanced Surveillance of Persons Identified as at Increased Risk of CJD Due to Blood Transfusion or Healthcare Procedures Brookes, D1; Chow, Y1; Ward, HJT2; Will, RG2; Hewitt, P3; Gill, ON1 1HPA, CJD, UK; 2National CJD Surveillance Unit, UK; 3Colindale, NHS Blood and Tissue, UK Introduction: Reports of four iatrogenic transmissions of variant-CJD (vCJD) infection in the UK (all due to transfusion of blood from donors who later developed vCJD), evidence from iatrogenic transmissions of sporadic CJD and experimental work on CJD infectivity in tissues and on healthcare instruments have given rise to concern about the risks of iatrogenic transmission of CJD. This risk warrants a) certain public health precautions, and b) follow-up of individuals with identified risks in order to gain evidence about their risks and ensure appropriate management of these risks. Evidence of transmission via iatrogenic routes is important to inform public health measures and so prevent ongoing transmission of CJD. Methods: The Health Protection Agency and Health Protection Scotland holds details of persons identified as ‘at-risk’ of vCJD due to blood transfusion and of persons identified as ‘at-risk’ of CJD (of any type) from other healthcare procedures. The GPs/clinicians of all persons identified as ‘at-risk’ for public health purposes are provided with: information; risk assessment updates; advice on public health precautions and advice on referral to specialist care. Procedures are being established to obtain enhanced surveillance data on these individuals, including: clinical status updates, date and cause of death, surplus tissue and blood specimens, and postmortem investigations. Results: Persons ‘at-risk’ of CJD have experienced a range of exposures. Estimated risks are uncertain and overlapping. Some individuals - recipients of vCJD implicated blood components - are considered to be at a clearly higher risk of infection: active follow-up is currently conducted for these individuals. In time, the enhanced surveillance of persons at increased risk of CJD will provide estimates of transmission risks and of the impact of iatrogenic exposures on mortality. Conclusion: Knowledge about iatrogenic transmission of CJD is being gained by the follow-up of individuals who have been identified as ‘at-risk’ of CJD in the UK. This enhanced surveillance may need to be sustained for many years. http://www.prion2007.com/pdf/Prion%2...0Abstracts.pdf Prions in Plasma of Patients with Sporadic Creutzfeldt-Jakob Disease Safar, J.G1,3, Geschwindm M.D2,3, Letessier, F1, Kuo, A1, Pomeroy, K1, Deering, C1, Serban, A1, Groth, D1, Miller, B.L2,3, DeArmond, S.J1,4, Prusiner, S.B1,3,5 1Institute for Neurodegenerative Diseases, 2Memory and Aging Center, Departments of 3Neurology, 4Pathology, and 5Biochemistry and Biophysics, University of California, San Francisco, California 94143 http://www.prion2007.com/pdf/Prion%20Friday.pdf http://www.prion2007.com/pdf/Prion%20Thursday.pdf http://www.prion2007.com/pdf/Prion%20Wednesday.pdf P04.33 Diagnostic Utility of CSF Biomarkers and General CSF Findings in a U.S Sporadic CJD Cohort Geschwind, MD; Haman, A; Torres-Chae, C; Raudabaugh, BJ; Devereux, G; Miller, BL University of California, San Francisco, USA Background: The diagnostic utility of CSF biomarkers, including 14-3-3 protein, neuron-specific enolase (NSE), AB42, total Tau (T-Tau), and phosphorylated Tau (PTau)/ T-Tau ratio are often are used for sporadic CJD (sCJD) diagnosis is controversial. We have previously reported the CSF 14-3-3 protein to have poor sensitivity for CJD diagnosis. In this study, now report the sensitivity and specificity of several CSF biomarkers and general characteristics in a U.S. cohort of sCJD and non-prion rapidly progressive dementia (RPD) controls (Non-CJD cohort) subjects. Design/Methods: Clinical diagnoses are made through review of medical records, clinical evaluation, and in many cases pathology. Data is stored in a secure clinical relational database, which was queried for various CSF findings, including cell count, protein, IgG index, oligoclonal bands (OCBs), 14-3-3, NSE, T-Tau in patients with probable or definite sporadic CJD and non-prion rapidly progressive dementias (RPD), most of whom were referred to our center with a potential diagnosis of CJD. For probable sCJD diagnosis, we used UCSF criteria that are modified from WHO to substitute MRI for 14-3-3. T-Tau and NSE were considered positive if > 1300 pg/ml and > 35 ng/ml, respectively. For this analysis, ambiguous 14-3-3 results were considered as negative. Results: 14-3-3 protein (n=149) sensitivity was only 48% (47% for definite; 50% for probable sCJD). NSE (n=49) sensitivity was 63% (66% for definite; 59% for probable sCJD). T-Tau (n=28) was the most sensitive at 68% (69% for definite; 67% for probable sCJD). The specificity of these biomarkers among our CJD and RPD controls (n=72) was 66% for 14-3-3 (n=47), 81% for NSE (n=21), and 100% for T-Tau (n=7). The 14-3-3 had the lowest sensitivity and specificity. Mildly elevated CSF protein (<100 mg/dl) is common in sCJD; High WBC; >20, is uncommon in sCJD. Conclusions/Relevance: In a cohort from a major U.S. CJD referral center, the 14-3-3 is neither sensitive nor specific for sCJD. NSE and T-Tau also show poor sensitivity for sCJD. T-Tau may be more specific than 14-3-3 and NSE, but our “n” is small. WHO sCJD criteria should be revised; by eliminating 14-3-3 and including brain MRI into the criteria. We are currently analyzing the effects of disease duration and codon 129 polymorphism on these CSF biomarker results. http://www.prion2007.com/pdf/Prion%2...0Abstracts.pdf USA NVCJD BLOOD RECALLS ONLY ; http://www.google.com/search?hl=en&q...SS&btnG=Search TSS |
Cleanability of dental instruments – implications of residual protein, risks from CJD
Cleanability of dental instruments – implications of residual protein and risks from Creutzfeldt-Jakob disease
J. T. Walker1, J. Dickinson2, J. M. Sutton3, N. D. H. Raven4 & P. D. Marsh5 Dental instruments such as endodontic reamers that are difficult to clean and should be considered as single use. Manual cleaning of dental instruments has a risk of puncture wounds, lacerations and cuts. Ultrasonic cleaners clean well, but the ultrasonic solution can become contaminated with debris. Washer disinfectors provide fully automated and validated cleaning but have yet to be taken up in large numbers of dental practices. Detailed cleaning instructions are required from instrument and washer disinfector manufacturers. -------------------------------------------------------------------------------- AbstractCleaning of dental instruments is the first line of control in reducing the adherent bioburden. The threat of vCJD and the difficulty in removing prion protein has provided a new challenge for cleaning surgical and dental instruments. Prion proteins are also more resistant to many disinfection and sterilisation techniques. A number of different methods are currently available in primary care for cleaning instruments including manual washing, ultrasonic cleaners and washer disinfectors. Manual cleaning of dental instruments is time-consuming, introduces operator error and the risk of puncture wounds, is not reproducible and does not completely remove debris from instruments. Ultrasonic baths are significantly more effective than hand cleaning alone and are currently used by the majority of dental surgeries (often as an adjunct to manual cleaning). Automated washer-disinfectors appear to provide a validated, reliable and reproducible procedure for disinfection and sterilisation of dental instruments to ensure both the safety of patients and dental staff. Dental instruments that are difficult to clean are frequently contaminated with tissue debris after routine reprocessing and cannot be excluded as a potential transmission risk for infectious agents, including prions. The transmission of vCJD via dentistry is considered to be low risk, however, the Department of Health (DoH) has recently advised dentists to ensure that endodontic reamers and files are treated as single-use as a precautionary basis in order to further reduce any risk of vCJD transmission. Top of page -------------------------------------------------------------------------------- HPA Centre for Emergency Preparedness and Response, Porton Down, Salisbury, SP4 0JG HPA Centre for Emergency Preparedness and Response, Porton Down, Salisbury, SP4 0JG HPA Centre for Emergency Preparedness and Response, Porton Down, Salisbury, SP4 0JG HPA Centre for Emergency Preparedness and Response, Porton Down, Salisbury, SP4 0JG HPA Centre for Emergency Preparedness and Response, Porton Down, Salisbury, SP4 0JG; Leeds Dental Institute, Leeds, LS2 9LU Correspondence to: J. T. Walker1 e-mail: jimmy.walker@hpa.org.uk http://www.nature.com/bdj/journal/v2....2007.893.html ***PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase in ''TYPE UNKNOWN''. ...TSS 1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, 26 from 2007) http://www.cjdsurveillance.com/pdf/case-table.pdf USA NVCJD BLOOD RECALLS ONLY ; http://www.google.com/search?hl=en&q...SS&btnG=Search vCJD case study highlights blood transfusion risk http://vcjdblood.blogspot.com/ CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007 http://cjdmadcowbaseoct2007.blogspot.com/ NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007 Tuesday, October 9, 2007 NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 RISES TO 5 DOCUMENTED CASES http://nor-98.blogspot.com/ CREUTZFELDT JAKOB DISEASE MAD COW h-BASE UPDATE USA http://cjdmadcowbaseoct2007.blogspot.com/ ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007 Date: Mon, 24 Sep 2007 21:31:55 -0500 I suggest that you all read the data out about h-BASE and sporadic CJD, GSS, blood, and some of the other abstracts from the PRION2007. ... http://lists.ifas.ufl.edu/cgi-bin/wa...&F=&S=&P=19744 *** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OF POKER INDEED GOES UP. ...TSS USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS http://lists.ifas.ufl.edu/cgi-bin/wa...mg&T=0&P=19779 TSS |
SEAC 99th meeting on Friday 14th December 2007
SEAC 99th meeting on Friday 14th December 2007
snip... © SEAC 2007 New research 4. Preliminary, unpublished results of research from the Health Protection Agency, aimed at addressing some of the uncertainties in the risk assessments, were reviewed by SEAC (SEAC 97, May 2007). The prion agent used in these studies is closely related to the vCJD agent. This research, using a mouse model, shows that following inoculation of mouse-adapted bovine spongiform encephalopathy (BSE) directly into the gut, infectivity subsequently becomes widespread in tissues of the oral cavity, including dental pulp, salivary glands and gingiva, during the preclinical as well as clinical stage of disease. 5. It is not known how closely the level and distribution of infectivity in the oral cavity of infected mice reflects those of humans infected with vCJD, as there are no comparable data from oral tissues, in particular dental pulp and gingiva, from human subclinical or clinical vCJD cases. Although no abnormal prion protein was found in a study of human dental tissues, including dental pulp, salivary glands and gingiva from vCJD cases22, the relationship between levels of infectivity and abnormal prion protein is unclear23. Infectivity studies underway using the mouse model and oral tissues that are presently available from human vCJD cases will provide some comparable data. On the basis of what is currently known, there is no reason to suppose that the mouse is not a good model for humans in respect to the distribution of infectivity in oral tissues. Furthermore, the new data are consistent with published results from experiments using a hamster scrapie model24. 6. A second set of experiments using the same mouse model showed that non-invasive and transient contact between gingival tissue and fine dental files contaminated with mouse-adapted BSE brain homogenate transmits infection very efficiently. It is not known how efficient gingival transmission would be if dental files were contaminated with infectious oral tissues and then subsequently cleaned and sterilised, a situation which would more closely model human dental practice. Further studies using the mouse model that would be more representative of the human situation, comparing oral tissues with a range of doses of infectivity, cleaned and sterilised files and the kind of tissue contact with instruments that occurs during dentistry, should be considered. 7. SEAC considered that the experiments appear well designed and the conclusions justified and reliable, while recognising that the research is incomplete and confirmatory experiments have yet to be completed. It is recommended that the research be completed, submitted for peer-review and widely disseminated as soon as possible so others can consider the implications. Nevertheless, these preliminary data increase the possibility that some oral tissues of humans infected with vCJD may potentially become infective during the preclinical stage of the disease. In addition, they increase the possibility that infection could potentially be transmitted not only via accidental abrasion of the lingual tonsil or endodontic procedures but a variety of routine dental procedures. 20 Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished. 21 SEAC (2006) Position statement on vCJD and endodontic dentistry. http://www.seac.gov.uk/statements/statement0506.htm 22 Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 23 SEAC 90 reserved business minutes. Implications for transmission risks snip...PLEASE SEE DISTURBING FINDINGS FULL TEXT HERE ; http://seac992007.blogspot.com/ TSS |
Risk Assessment of Transmission of sCJD in Endodontic Practice
Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation
Nadège Bourvis1,2, Pierre-Yves Boelle1,2,3, Jean-Yves Cesbron4,5,6, Alain-Jacques Valleron1,2,3* 1 Université Pierre et Marie Curie-Paris6, Unité de Recherche Epidémiologie-Systèmes d'information-Modélisation, UMR S 707, Paris, France, 2 INSERM, U707, Paris, France, 3 Assistance Publique-Hôpitaux de Paris (AP-HP), Unité de Santé Publique, Hôpital St Antoine, Paris, France, 4 Laboratoire Adaptation et de Pathogénie des Micro-organismes, Université Joseph Fourier, UMR 5163, Grenoble, France, 5 Centre National de la Recherche Scientifique (CNRS), UMR 5163, Grenoble, France, 6 Centre hospitalier universitaire (CHU) de Grenoble, Laboratoire d'Immunologie, Grenoble, France Abstract Background Experimental results evidenced the infectious potential of the dental pulp of animals infected with transmissible spongiform encephalopathies (TSE). This route of iatrogenic transmission of sporadic Creutzfeldt-Jakob disease (sCJD) may exist in humans via reused endodontic instruments if inadequate prion decontamination procedures are used. Methodology/Principal Findings To assess this risk, 10 critical parameters in the transmission process were identified, starting with contamination of an endodontic file during treatment of an infectious sCJD patient and ending with possible infection of a subsequent susceptible patient. It was assumed that a dose-risk response existed, with no-risk below threshold values. Plausible ranges of those parameters were obtained through literature search and expert opinions, and a sensitivity analysis was conducted. Without effective prion-deactivation procedures, the risk of being infected during endodontic treatment ranged between 3.4 and 13 per million procedures. The probability that more than one case was infected secondary to endodontic treatment of an infected sCJD patient ranged from 47% to 77% depending on the assumed quantity of infective material necessary for disease transmission. If current official recommendations on endodontic instrument decontamination were strictly followed, the risk of secondary infection would become quasi-null. Conclusion The risk of sCJD transmission through endodontic procedure compares with other health care risks of current concern such as death after liver biopsy or during general anaesthesia. These results show that single instrument use or adequate prion-decontamination procedures like those recently implemented in dental practice must be rigorously enforced. snip... Discussion The results of this modelling approach show that the risk of sCJD transmission due to the reuse of instruments during ET may not be ignored in absence of effective prion-decontamination procedures. How should our conclusions be used in a public health assessment? First note that this risk is already of concern to national health agencies as well as to health professionals [25]–[27]. Our work makes it possible to go beyond a qualitative assessment, towards more quantitative predictions where all hypotheses are clearly stated. The conclusions of this approach may easily be updated as new data accrue. The details of ET were obtained from the latest official reports in France and UK or from experts. We conducted a literature search to collect the best estimates available of the possible quantities of infectious material left on the instruments, and subsequently partially removed by the classical disinfection procedures used until the last years of the 20th century. We obtained similarly estimates of the values of brain infectivity and of the ratio of brain infectivity to pulp infectivity. These parameters were obtained from animal experiments as they are clearly unknown in humans. A comparable approach can be found in the HPA report on vCJD transmission in dentistry with two notable differences [25]. First, the route of instrument contamination and subsequent transmission considered in the HPA report was a very rare accidental process: the abrasion of tonsillar tissue during dental care. On the contrary, we considered the process of accessing the dental pulp during ET as certain, which obviously leads to a higher risk. Second, the HPA report considered infectivity of tonsils to be 106–107 i/c ID50 per gram, while we used dental pulp with a slightly lower range of infectivity from 104-106i/c ID50 per gram ( = BI* BPR). The hypotheses we used concerning the relationship between the estimated inoculums and the probability of infection are obviously critical. In our assessment, we postulated that too small an inoculum (below 10−1 and 10−2 ID50 were considered with functions ϕ1 and ϕ2) would not lead to infection, and that there was a linear dose–response relationship above this threshold. This effectively complies with the “zero risk below a threshold” hypothesis rather than with the “single infectious particle” hypothesis. There is indeed experimental evidence that even very small quantities of infectious material may trigger infection in mice [13], [28], and this hypothesis was previously used in assessing decontamination procedures[29]. However, we adopted a more conservative risk estimate. The duration of the infectious period of CJD is unknown but could be very long. We used as a reference the incubation period estimated from hGH iatrogenic cases [30]. To make comparison easier, and for want of better or more recent evidence, the duration of the infectious period relative to incubation was the same as in the HPA report, i.e. 40% of the incubation period [25]. Our risk assessment should have used the prevalence of infectious sCJD in those undergoing ET instead of that in the general population. Presumably, the former is the largest and the risk was therefore minimized. Indeed, children, who do not develop sCJD are taken into account in the general population estimate, when that in ET patients concerns only adults. The ranges of values of risk assessment generated with our model were broad. They mirror the current lack of knowledge and the uncertainties concerning data and hypotheses. However, our model makes it clear that the ET of the 20th century were not risk-free in terms of CJD. Therefore, our model suggests that patients may well have been contaminated at the end of 20th century, and still be in the latency period and at risk of transmitting the disease. The estimated individual risk of sCJD transmission during ET was low in our assessment. However, these values compared with the mortality rates in general anaesthesia [31], transcutaneous liver biopsy [32] or voluntary abortion [33] which are of concern in the modern health care. We also studied the possible impact of ET at a population level and showed that there was a high probability that the reproduction rate R exceeded 1 in the absence of effective prion decontamination of the instruments: one of the conditions for the initiation of an epidemic process is fulfilled. To date, epidemiological surveillance data did not evidence such an epidemic process. However, would our hypothesis be true, the increase in incidence could remain modest and hard to identify for dozens of years because the incidence of sCJD is low, the incubation period long and in competition with all mortality causes present. CJD surveillance systems is too recent to show such trends. Vacuum autoclaving and porous-load autoclaving for 18 min at 134°C are currently recognised as appropriate methods for prion decontamination, leading to a reduction of the infectivity load by of 3–5 log10 or more. According to our model, this decontamination would prevent CJD transmission in dental practice, even considering that the residual infectivity is not strictly reduced to zero. These methods are recommended in official reports in various countries. However, in a US study conducted in 1996 [34], only 53% of dentists used autoclaves to decontaminate root-canal files. In a survey conducted in France in 2004, only 79% of dentists used an autoclave [35]. The problem of correct use of the autoclaves and regular checking of their efficacy has also been raised by many authors in several countries [34]. A recent survey on dental practice also showed that other elementary precautionary measures against CJD transmission were not widely respected. For example, the vast majority of dentists did not actively seek out patients at-risk for any form of CJD (sporadic, iatrogenic or familial) [36]. Therefore, in the current situation and despite recommended decontamination procedures, the risk of sCJD transmission during dental care might still not be zero. In any case, our findings constitute a strong argument for the strict respect of the official recommendations on decontamination procedures in dentistry, and even suggest that the cost-benefit of single-use endodontic instruments should be re-evaluated. The risk analysis approach we have used relies on a “problem dissection” in which all components to a risk are identified and linked to the available scientific data, knowledge, and expert opinion. It may be of help in other emerging diseases, when data on the natural history of the disease and transmission are still scarce and clinical events cannot be observed directly. In all these cases, the output of the work will always be questionable, because of the lack of data, but the strength of the method is that its results and final statements are refutable as data accrues. snip... end... tss http://www.plosone.org/article/info:...l.pone.0001330 http://www.plosone.org/article/fetch...esentation=PDF Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States http://cjdusa.blogspot.com/ BSE (Mad Cow) Update: Do Reports of sCJD Clusters Matter? snip... see full text ; http://cjdtexas.blogspot.com/ 10 January 1990 NOT FOR PUBLICATION COMMITTEE ON SAFETY OF MEDICINES WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY SURGICAL CATGUT SUTURES 2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to License Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licensed catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K. IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY; snip... see full text ; http://creutzfeldt-jakob-disease.blogspot.com/ CJD QUESTIONNAIRE http://cjdquestionnaire.blogspot.com/ SEAC 99th meeting on Friday 14th December 2007 Greetings, AS one of them _lay_ folks, one must only ponder ; "WITH the Nor-98 now documented in five different states so far in the USA in 2007, and with the TWO atypical BSE H-BASE cases in Texas and Alabama, with both scrapie and CWD running rampant in the USA, IS there any concern from SEAC with the rise of sporadic CJD in the USA from ''UNKNOWN PHENOTYPE'', and what concerns if any, in relations to blood donations, surgery, optical, and dental, do you have with these unknown atypical phenotypes in both humans and animals in the USA ???" "Does it concern SEAC, or is it of no concern to SEAC?" "Should it concern USA animal and human health officials?" snip... ----- Original Message ----- From: xxxxxxxxxx To: flounder9@verizon.net Sent: Thursday, November 22, 2007 5:39 AM Subject: QUESTION FOR SEAC Mr Terry S Singeltary Sr., Bacliff, Texas 77518 USA. Dear Mr Singeltary, "Thank you for your e-mail of yesterday with the question for SEAC. I can confirm that this will be asked at the meeting on your behalf and the question and answer will appear in the minutes of the meeting which will be published on the SEAC Internet site." snip...see full text ; http://seac992007.blogspot.com/ NOR-98 ATYPICAL SCRAPIE CASES USA snip... In FY 2007, 331 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), including 59* Regulatory Scrapie Slaughter Surveillance (RSSS) cases (Figure 5 and Slide 16). In FY 2007, two field cases, one validation case, and two RSSS cases were consistent with Nor-98 scrapie. The Nor98-like cases originated from flocks in California, Minnesota, Colorado, Wyoming and Indiana respectively. Nineteen cases of scrapie in goats have been reported since 1990 (Figure 6). The last goat case was reported in September 2007. snip... see full report here ; http://www.aphis.usda.gov/animal_hea...rly_report.pps P03.141 Aspects of the Cerebellar Neuropathology in Nor98 Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E11National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was firstdescribed in Norway in 1998. Several features of Nor98 were shown to be differentfrom classical scrapie including the distribution of disease associated prion protein(PrPd) accumulation in the brain. The cerebellum is generally the most affected brainarea in Nor98. The study here presented aimed at adding information on theneuropathology in the cerebellum of Nor98 naturally affected sheep of variousgenotypes in Sweden and Norway. A panel of histochemical and immunohistochemical(IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein,amyloid, and cell markers for phagocytic cells were conducted. The type of histologicallesions and tissue reactions were evaluated. The types of PrPd deposition werecharacterized. The cerebellar cortex was regularly affected, even though there was avariation in the severity of the lesions from case to case. Neuropil vacuolation wasmore marked in the molecular layer, but affected also the granular cell layer. There wasa loss of granule cells. Punctate deposition of PrPd was characteristic. It wasmorphologically and in distribution identical with that of synaptophysin, suggestingthat PrPd accumulates in the synaptic structures. PrPd was also observed in thegranule cell layer and in the white matter. The pathology features of Nor98 in thecerebellum of the affected sheep showed similarities with those of sporadicCreutzfeldt-Jakob disease in humans. http://www.prion2007.com/pdf/Prion%2...0Abstracts.pdf It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal. http://www.ars.usda.gov/research/pro...accn_no=408490 snip... [/quote] Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08, 200l 3:03 PM freas@CBS5055530.CBER.FDA.GOV CJDIBSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and Consultants Staff January 2001 Meeting (short version) Greetings again Dr. Freas and Committee Members, snip... with same feeding and rendering practices as that of U.K. for years and years, same scrapie infected sheep used in feed, for years and years, 950 scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known to date. (hmmm, i am thinking why there is not a variant scrapie, that is totally different than all the rest)? just being sarcastic. ... snip...end... see full text Monday, January 08, 200l 3:03 PM ; http://www.fda.gov/ohrms/dockets/ac/.../3681s2_09.pdf http://nor-98.blogspot.com/ Archive Number 20071105.3602 Published Date 05-NOV-2007 Subject PRO/AH/EDR> Prion disease update 2007 (07) PRION DISEASE UPDATE 2007 (07) ****************************** A ProMED-mail post snip... [2] USA: National Prion Disease Pathology Surveillance Center Date: June 2007 Source: National Prion Disease Pathology Surveillance Center (USA) [edited] CJD Cases examined ---------------------- Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD 1996 / 42 / 32 / 26 / 4 / 0 / 0 1997 / 115 / 68 / 57 / 9 / 0 / 0 1998 / 93 / 53 / 45 / 7 / 1 / 0 1999 / 114 / 69 / 61 / 8 / 0 / 0 2000 / 151 / 103 / 89 / 14 / 0 / 0 2001 / 208 / 116 / 106 / 9 / 0 / 0 2002 / 255 / 143 / 118 / 23 / 2 / 0 2003 / 272 / 174 / 132 / 41 / 0 / 0 2004 / 334 / 183 / 157 / 21 / 0 / 1* 2005 / 352 / 195 / 152 / 37 / 1 / 0 2006 / 372 / 186 / 143 / 30 / 0 / 1** 2007 / 120 / 68 / 35 / 7 / 0 / 0 TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2 *Acquired in UK ** Acquired in Saudi Arabia *** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007. **** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006, 26 from 2007). Notes: -- Cases are listed based on the year of death when available. If the year of death is not available, the year of sample receipt is used. -- Referrals: Cases with possible or probable prion disease from which brain tissue or blood in the case of familial disease were submitted. -- Inconclusive: Cases in which the samples were not sufficient to make a diagnosis. -- Non-vCJD type unknown are cases in which the tissue submitted was adequate to establish the presence but not the type; in all cases, vCJD could be excluded. -- Communicated by: Terry S. Singeltary Sr. [In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP] http://www.promedmail.org/pls/askus/..._ID:1010,39963 There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection. He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins. http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.htm http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.pdf JOURNAL OF NEUROLOGY MARCH 26, 2003 RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: flounder@wt.net I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported 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. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? http://www.neurology.org/cgi/eletters/60/2/176#535 THE PATHOLOGICAL PROTEIN Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9 June 2003 BY Philip Yam CHAPTER 14 LAYING ODDS Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population. http://www.thepathologicalprotein.com/ doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk Tracking spongiform encephalopathies in North America Xavier Bosch Available online 29 July 2003. Volume 3, Issue 8, August 2003, Page 463 "My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem." ... http://www.thelancet.com/journals/la...07151/fulltext http://download.thelancet.com/pdfs/j...9903007151.pdf Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/http://www....s/60/2/176#535 Like lambs to the slaughter 31 March 2001 Debora MacKenzie Magazine issue 2284 FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease. Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD. "This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb. ... http://www.newscientist.com/article/...slaughter.html DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehörden sind lax. Link auf diesen Artikel im Archiv: http://service.spiegel.de/digas/find?DID=18578755 "Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ... http://service.spiegel.de/digas/serv...d/DID=18578755 Thu Dec 6, 2007 11:38 FDA IN CRISIS MODE, AMERICAN LIVES AT RISK http://www.cidrap.umn.edu/cidrap/con...ec0407fda.html FDA SCIENCE AND MISSION AT RISK http://www.fda.gov/ohrms/dockets/ac/...Technology.pdf 2 January 2000 British Medical Journal U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well http://www.bmj.com/cgi/eletters/320/7226/8/b#6117 15 November 1999 British Medical Journal vCJD in the USA * BSE in U.S. http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406 TSS |
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