Vital 6, 48 - 49 (2008) doi:10.1038/vital900
Subject Categories: Clinical Health
vCJD & dental treatment Fiona Ord1 & Pauline Watt1
Fiona and Pauline originally qualified as dental hygienists and currently work for the National CJD Surveillance Unit in Edinburgh.
AbstractFiona Ord and Pauline Watt highlight the existing knowledge of a fatal disease and its possible association with dental treatment.
BSE and CJD In the last 15 years variant CJD (vCJD) emerged in the UK and is thought to have been acquired primarily through consumption of BSE-contaminated meat products. CJD is a fatal disease with no immediate prospect of treatment. Abnormal prion proteins associated with vCJD are found outwith the central nervous system, raising concerns for possible transmission of prion proteins via invasive medical (including dental) procedures from persons in the asymptomatic phase of the disease. This article seeks to highlight the existing knowledge of vCJD, the distribution in oral tissues, the possible association with dental treatment and to raise awareness of current research.
History vCJD is a type of human prion disease that was first identified in the UK in 1996. To date, there have been 166 definite/probable cases of vCJD in the UK. The main route of infection is likely to have been dietary exposure to beef products contaminated with bovine spongiform encephalopathy (BSE). Effective measures were put in place to protect the human food chain from BSE in the UK from 1996 onwards. Although the number of new cases has declined in recent years, it remains unclear how many individuals will develop vCJD as a result of the dietary route. Sporadic CJD has been transmitted by neurosurgical procedures and via contaminated growth hormone. While there have been four instances of blood transfusion transmission of vCJD in the UK, there has been no evidence, to date, of transmission via dental treatment, organ transplantation or surgical intervention. However, it is important to assess whether dental treatment is a potential route of transmission of vCJD, especially as animal studies in the UK have shown evidence of transmission of infectious prion proteins via the oral cavity.
Prions – what are they? Prion proteins (PrP) may exist in two forms – the normal cellular form (PrPc) and the abnormal disease associated isoform (PrPSc) Everyone has the normal type of prion protein within brain cells and in other cells of their body, although its function is unknown. Abnormal prion proteins have many unusual properties: enzymes are unable to break down PrPSc and it forms aggregates and deposits in the brain, sometimes in the form of amyloid that are thought to contribute to the damage of nerve cells in the brain of cases of CJD. PrPSc is also associated with infectivity and is resistant to inactivation by common decontamination methods. The infectious agent is therefore neither bacterial nor viral in nature, but is thought to be a rogue protein.
Inactivation of prions Prion diseases have a variable incubation period depending on the type of disease. The duration of illness of vCJD patients can be over a year. The disease is fatal and, as yet, there is no known cure. A major infection control challenge is that the infectious prions are strongly resistant to the usual forms of bacterial and viral inactivation agents, such as disinfectants and steam sterilisation. Prions can survive autoclaving at 134°C for 18 minutes. However, prions are not readily transmissible by routine physical contact.
Prions and the oral cavity In animal studies, abnormal prion proteins have been found in the trigeminal nerve, tooth pulp, gingival tissue, salivary glands, saliva and the tongue. Syrian hamsters showed infectivity in the trigeminal ganglion, dental pulp and gingival tissue after injection with a strain of scrapie.1 Cattle exposed orally to BSE agent showed signs of infectivity in the trigeminal ganglion2 and also in the trigeminal ganglion of sheep and hamsters with experimental scrapie.2, 3
In vCJD, unlike other types of human TSEs, infective proteins may be present in tissues outside the central nervous system, for example the appendix and other lymphoreticular tissues.4Table 1 shows that positive immunochemistry has been detected in the trigeminal ganglion but not the cranial nerve or salivary gland tissues.5
Table 1: Infectivity in oral tissues from humans with vCJD
In humans, the first patient known to have vCJD died in 1995 and to date (1 June 2008) there have been 166 'definite' or 'probable' vCJD cases in the UK (Table 2). The mortality trend in vCJD suggests that it has slowed but it is too early to know whether this remains or to assess the final size of the epidemic. Of concern is the potential that patients incubating vCJD or those with subclinical infection may receive dental treatment leading to the possibility of iatrogenic transmission from inadequately decontaminated dental instruments (Table 3).
Table 2: Summary of vCJD cases in the UK since 1995
Full table Table 3: Clinical concerns for iatrogenic infection of vCJD
Prions and dental treatment The design and intricacy of many dental instruments makes them difficult to clean, therefore the ability to ensure dental instruments are free from debris is a key factor in reducing the possibility of tissue adhering on used instruments and subsequent possible transmission.
A risk assessment by the Department of Health (2006) concluded that, given the existence of a carrier state, a self sustaining epidemic of vCJD was feasible, but employing single use 'files' and 'reamers' in endodontic treatment could eliminate the risk.6 However, subsequent findings from a mouse model of vCJD infection has led the Spongiform Encephalopathy Advisory Committee (SEAC) to conclude that the potential risk of transmission of vCJD via a range of dental procedures may be greater than previously anticipated.7
Dental treatment and vCJD risk A case control study carried out by the National Creutzfeldt-Jakob Disease Surveillance Unit (NCJDSU) examined the potential links between vCJD and dental treatment.8
This study initially examined information reported by relatives and found no statistically significant associations between dental treatment and vCJD. However, the study was limited to data reported from relatives. Therefore, there is a need to examine dental records to obtain more accurate information. A pilot study has demonstrated the feasibility of collating information from dental records. In an attempt to gain a clearer understanding of how vCJD may be transmitted, a study (funded by the Department of Health) is being carried out by the NCJDSU and the University of Glasgow Dental Hospital & School. This research follows the pilot study methodology for retrieving and recording information from dental treatment records.
The study will review dental treatment for all vCJD cases (n = 166) and controls (up to 650) to determine whether there are temporal or geographic links between vCJD cases, and to compare dental treatment in cases and controls. The study has been given ethical approval by a Multi-Centred Research Ethics Committee. Two dental hygienists will collect treatment information on a standardised data collection form by attending dental practices or requesting copies of full treatment histories. Partial or unavailable dental histories will be accessed through NHS Dental payment schemes. Unique identifiers (eg date of birth) will enable the researchers to access dental treatment for patients provided it was claimed for under the National Health Service.
What do I do? If a patient presents for treatment and reports they have vCJD or are 'at risk', treatment may be carried out as usual. Presently, there are no additional precautions required for these patients provided optimal standards of infection control and decontamination are maintained. General advice on infection control can be obtained from the BDA (Advice Sheet A12), whilst instrument decontamination advice can be obtained from the local decontamination unit guidelines produced by Health Protection Scotland.9 It would be prudent to check with your local infection control team to confirm that your instrument reprocessing procedures are indeed optimal.
Current guidance Infection control guidelines in the UK are produced by the Advisory Committee on Dangerous Pathogens and the Spongiform Encephalopathy Advisory Committee (ACDP/SEAC). The CJD Incidents Panel with secretariat provided by the Health Protection Agency (HPA) provide advice on individual incidents. Seewww.hpa.org.uk/infections/topics_az/cjd/incidents_panel.htm
Top of pageReferences Ingrosso L, Pisani, F, Pocchiari M. Transmission of the 236K scrapie strain by the dental route. J Gen Virol 1999; 61: 3235–3240. Wells G A, Hawkins S A, Green R B, Austin A R et al. Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE); an update. Vet Rec 1998; 142: 103–106. PubMed ISI ChemPort Groschup M H, Beekes M, McBride P A, Hardt M et al. Deposition of disease associated prion protein involves the peripheral nervous system in experimental scrapie. Acta Neuropathol 1999; 98: 453–457. Article PubMed ChemPort Hilton D A, Fathers E, Edwards P, Ironside J W, Zajiceck J. Prion immunoreactivity in appendix before the clinical onset of variant Creutzfeldt-Jakob disease. Lancet 1998; 352: 703–704. Article PubMed ISI ChemPort Ironside J W, McCardle L, Horsburgh A, Lim Z, Head M W. Pathological diagnosis of variant Creutzfeldt-Jakob disease. APMIS 2002; 110: 79–87. Article PubMed ChemPort Department of Health. Dentistry and vCJD: the implications of a carrier state for a self sustaining epidemic. 2006. SEAC (2007) Position statement on vCJD and endodontic dentistry. Porter S R. Dental treatment and risk of vCJD. Br Dent J 2007; 202: E19. Article PubMed The HPS local decontamination unit guidelines – www.hps.scot.nhs.uk Main navigationVital content Vital homehttp://www.nature.com/vital/journal/v6/n1/full/vital900.html
North Yorkshire Community Infection Prevention and Control Policies and Guidance
Creutzfeldt-Jakob Disease (CJD) is one of a group of diseases called Transmissible Spongiform Encephalopathies (TSEs) which can occur in people or animals. The ‘transmissible agent’ is an abnormal protein known as a prion (see below). TSEs are characterised by degeneration of the nervous system and are invariably fatal. In the majority of cases, CJD has no known association. It is then termed ‘sporadic CJD’. However, about 15% of cases are inherited and caused by gene mutations (‘familial CJD’). About 1% of cases are iatrogenic, for instance, following injections of human pituitary derived human growth hormone or following corneal transplants. Very rarely, transmission has complicated brain surgery when the infective agent has been passed on by surgical instruments.
Early in 1996, a form of CJD that differed from previously recognised types was identified. The patients affected were usually younger, symptoms different and the histological appearance of brain tissue was distinct. This disease was called ‘new variant CJD’ (nv-CJD) and is now known as simply ‘variant CJD’ (vCJD).
The precise nature of the agent causing vCJD is not known, but the most likely theory implicates an abnormal form of a protein called a ‘prion’. The Government’s Spongiform Encephalopathy Advisory Committee (SEAC) has concluded that the most likely explanation for the emergence of vCJD was that it has been transmitted to people through exposure to bovine spongiform encephalopathy (BSE).
In this document, the term CJD encompasses sporadic CJD, variant CJD (vCJD), familial CJD, and other TSEs such as fatal familial insomnia and Gerstmann-Straussler-Scheinker disease.
A patient with a clinical diagnosis of CJD or vCJD will have a ‘key worker’ allocated to them. This is a named professional individual who will be constantly involved in the coordination of the care of the patient, with good knowledge of local health and social services. The key worker will be able to provide continuing support to both the patient and their family.
12. Dental treatment
Patients requiring dental care must inform their dental practitioner before treatment. Their status is then recorded in the notes.
The clinical care of known or suspected cases of CJD, or their relatives, must not be compromised in any way. Normal decontamination procedures should be observed. Routine dentistry is understood to be low risk, therefore, no special precautions are required.
There are no reported or suspected cases of CJD arising from dental procedures.
In endodontic (root canal) procedures, where instruments may come into contact with the trigeminal nerve and dental pulp, single patient use or disposable files and reamers should be used. Single use instruments should be disposed of after one use and never reprocessed under any circumstances.
The patients’ ‘at risk’ status must be included in any referrals for surgery as head and neck surgery may involve contact with tissues of high or medium infectivity, for which special infection control precautions will be required.
see full text ;http://www.nyypct.nhs.uk/AdviceInformation/InfectionControl/PoliciesAndGuidance/docs/community/NYYPCT%20&%20NYHHPU%20D4%20Creutzfeldt-Jakob%20Disease%20IPC%20Policy%20-%20version%201.00%20-%20November%202008.pdf
SEAC 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/state260106subgroup.htm
13DH (2007) Precautionary advice given to dentists on re-use of instruments http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAreaID=2&NavigatedFromDepartment=Falsehttp://www.seac.gov.uk/statements/state-vcjd-dentrstry.htm
Sunday, November 16, 2008
Resistance of Bovine Spongiform Encephalopathy (BSE) Prions to Inactivationhttp://bse-atypical.blogspot.com/2008/11/resistance-of-bovine-spongiform.html
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
IF atypical BSE strains are more virulent, then would not human infection from an atypical strain of BSE be more virulent ???
REPORT ON CURRENT & FUTURE SURVEILLANCE FOR BOVINE SPONGIFORM ENCEPHALOPATHYhttp://madcowtesting.blogspot.com/2008/11/report-on-current-future-surveillance.html
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain
Qingzhong Kong,1* Mengjie Zheng,1 Cristina Casalone,2 Liuting Qing,1 Shenghai Huang,1? Bikram Chakraborty,1 Ping Wang,1 Fusong Chen,1 Ignazio Cali,1 Cristiano Corona,2 Francesca Martucci,2 Barbara Iulini,2 Pierluigi Acutis,2 Lan Wang,1 Jingjing Liang,1 Meiling Wang,1 Xinyi Li,1 Salvatore Monaco,3 Gianluigi Zanusso,3 Wen-Quan Zou,1 Maria Caramelli,2 and Pierluigi Gambetti1*
Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106,1 CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy,2 Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy3
*Corresponding author. Mailing address: Department of Pathology, Case Western Reserve University, Cleveland, OH 44106. Phone for Pierluigi Gambetti: (216) 368-0586. Fax: (216) 368-2546. E-mail: email@example.com . Phone for Qingzhong Kong: (216) 368-1756. Fax: (216) 368-2546. E-mail: firstname.lastname@example.org
?Present address: Department of Patient Education and Health Information, Cleveland Clinic Foundation, Cleveland, OH 44195.
Received November 30, 2007; Accepted January 16, 2008.
Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to be caused by only one strain, BSE-C. BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE strains by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE strain-infected cattle. Sixty percent of the inoculated Tg mice became infected after 20 to 22 months of incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE strain-infected Tg mice, but none of the Tg mice infected with prions causing a sporadic human prion disease, showed the presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE strain-infected humanized Tg mouse brains are different from those from the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation times are observed for the BASE strain-infected Tg mice. These results suggest that in humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2268471
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
November 25, 2008
Update On Feed Enforcement Activities To Limit The Spread Of BSEhttp://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.html
"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine."
just another one of those sporadic CJD coincidences i suppose $$$
NOT to forget ;
Thursday, June 05, 2008
Review on the epidemiology and dynamics of BSE epidemics
Vet. Res. (2008) 39:15 www.vetres.org DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward , as well as between L-type BSE and CJD . These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) , Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) , Italy (3 L)18, Japan (1 L) , Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland . It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.
And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward , as well as between L-type BSE and CJD . These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.
full text 18 pages ;http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf
please see full text ;http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html
***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***
Progress Report from the National Prion Disease Pathology Surveillance Center
An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD
April 3, 2008http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
Sunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASEhttp://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
Friday, December 05, 2008
Detection of Prion Infectivity in Fat Tissues of Scrapie-Infected Micehttp://scrapie-usa.blogspot.com/2008/12/detection-of-prion-infectivity-in-fat.html
Labels: CJD, DENTAL TREATMENT