Transmissible Spongiform Encephalopathy

Title: Prion diseases in humans: Oral and dental implications

Author(s): P. Jayanthi , Priya Thomas , P. Bindhu and Rekha Krishnapillai Source: North American Journal of Medical Sciences. 5.7 (July 2013): p399. Document Type: Disease/Disorder overview Copyright : COPYRIGHT 2013 Medknow Publications and Media Pvt. Ltd. http://www.najms.org/aboutus.asp

Full Text: Byline: P. Jayanthi, Priya. Thomas, P. Bindhu, Rekha. Krishnapillai

Prion diseases are a group of neurodegenerative disorders characterized by accumulation of abnormal prion proteins in the central nervous system. The prions resist conventional sterilization procedures especially when infected tissue becomes dried onto metal or glass surfaces. This article, a review of literature collected using Pubmed as search engine, describes the oral manifestations of prion diseases in addition to studying the possibility of cross contamination in the dental office. The article emphasizes the importance for dentists to be aware of these diseases, to identify the high-risk patients by obtaining adequate medical history and to know the appropriate deactivation procedures to be followed.

Introduction

Prion diseases also known as transmissible spongiform encephalopathies (TSEs), are a group of fatal neurodegenerative diseases occurring in both humans and animals. Stanley B. Prusiner was the first person to purify the infectious agent of prion disease and won the 1997 Nobel Prize in Physiology/Medicine. Prusiner defined prions as infectious, transmissible proteinaceous particles that lack nucleic acid. The normal cellular prion protein (PrP [sup]c ) is encoded by PrP [sup]c gene, which is located on the short arm of chromosome 20. PrP [sup]c has predominantly alpha helical structure, is soluble and proteinase sensitive. The normal function of PrP [sup]c is not well-known, but the suggested functions are signal transduction, cell adhesion, regulation and distribution of acetylcholine receptors. [sup][1]

PrP [sup]c is transformed into abnormal isoform of the protein (PrP [sup]Sc ) due to post translational modification or mutation in the PrP [sup]c gene. PrP [sup]Sc has predominantly beta structure, is insoluble and partially proteinase resistant. This mutated PrP [sup]Sc gives rise to TSEs, including bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep and goats and Creutzfeldt-Jakob disease (CJD) in humans. These diseases are characterized by vacuolization of the gray matter and these vacuoles are located in the neuropils between the nerve cell bodies. [sup][2],[3]

Although the risk of transmission of CJD through dental procedures is still unclear, the theoretical possibility of transmission through contaminated dental instruments should be kept in mind. This article aims to give a brief overview of the clinical characteristics, risk of transmission and infection control methods of prion diseases for dentists using data obtained from literature search in Pubmed search engine.

Etiopathogenesis

The infectious agents for prior disease are composed of a 35-kD brain sialoglycoprotein called PrP [sup]Sc that is essential for the transmission and pathogenesis of several neurodegenerative diseases. PrP [sup]Sc is able to propagate itself in the host by stimulating the conversion PrP [sup]c to PrP [sup]Sc , leading to its accumulation. [sup][4]

Accumulation of PrP [sup]Sc can result either from exposure to infectious prions iatrogenically or through ingestion, or because of mutations in the PrP gene. Sporadic CJD has an unknown cause; that is, thus far no apparent infections or mutations of the PrP gene have been found in association with such cases, although the brain in these patients also accumulates PrP [sup]Sc . [sup][2]

Human Transmissible Spongiform Encephalopathies

Based on the etiopathogenesis, different types of human TSEs have been recognized. [Table 1] describes the transmission routes and clinical features of TSEs in humans.{Table 1}

Sporadic Creutzfeldt-Jakob disease

This is the most common type of CJD accounting for 85% of all CJD cases, occurring in middle or older age group. The disease is characterized by progressive dementia, ataxia, myoclonus, cortical blindness, akinesia and speech loss, followed by death within 4 months. [sup][5]

Iatrogenic Creutzfeldt-Jakob disease

The disease occurs following neurosurgery, duramater transplantation, corneal grafting, and injection of pituitary hormones obtained from human cadavers. This type of prion disease is important to dentists due to the risk of cross contamination after the use of infected dental instruments. The incubation period is variable ranging from 2 to 35 years. The clinical features are similar to sporadic form, but cerebellar motor symptoms are predominant in this type. [sup][5]

Variant Creutzfeldt-Jakob disease

vCJD is associated with the intake of BSE-contaminated beef and beef products. The disease is characterized by depression, delirium, hallucinations, paresthesia and dysesthesia in hands, feet and mouth followed by dementia and akinesia. Deposition of amyloid plaques in the lymphatic tissues throughout the body is a prominent feature. [sup][5]

Kuru

Kuru is endemic in Papua New Guinea and is transmitted by intake of infected nervous tissue in cannibalistic practices. The disease is characterized by ataxia, tremors, dysarthria and death. Though cannibalism is banned in 1950, the incubation period is more than 40 years and the chance of appearance of new cases is still possible. [sup][4]

Fatal familial insomnia

The disease presents with progressive insomnia, dysautonomy in the form of hyperthermia, myosis and loss of sphincter control, followed by dysarthria, tremors, motor dysfunction and cognitive deterioration. Death occurs within 7-18 months. [sup][6]

Gerstmann-Straussler-Scheinker syndrome

Gerstmann-Straussler-Scheinker syndrome gives rise to lack of coordination leading to ataxia, dysarthria and nystagmus. Death occurs after 1-10 years. [sup][6]

Oral Manifestations

Oral manifestations are rarely seen in prion diseases. Dysphagia (difficulty in swallowing) and dysarthria (poor articulation of speech) are noticed in all forms of human TSEs. Dysphagia and dysarthria could be early symptoms of the disease and occur as a consequence of pseudobulbar paralysis. [sup][7] In vCJD, parasthesia (tingling, pricking or numbness), orofacial dysesthesia (abnormal sensations in the absence of stimulation) and one case of loss of taste and smell have been reported in the literature. [sup][8],[9]

Infectivity of human oral tissues

Studies on human oral tissues for the presence of PrP [sup]Sc showed positivity in limited number of oral tissues. Various human tissues like tonsil, tongue, submandibular and parotid salivary glands, trigeminal ganglia, inferior alveolar nerve, dental pulp and gingiva taken from different post mortem cases of vCJD were analyzed for the presence of PrP [sup]Sc . Majority of the cases showed positive PrP [sup]Sc in tonsils and trigeminal ganglia, while the other human tissues were negative for PrP [sup]Sc . Western blot, paraffin-embedded tissue blot, and immunohistochemical techniques were used for the study and the sensitivity of these assay indicated that PrP [sup]Sc must have been at the level of less than 1% of that found in the brain tissue. [sup][10]

Presence of PrP [sup]Sc in trigeminal ganglia may raise concerns about the extent of deposition of PrP [sup]Sc along the cranial nerves and possible extension into oral and nasal cavities which are innervated by the ganglia. Guiroy et al., [sup][11] have noted positive PrP immunostaining of axons in the nerve root and around the degenerating ganglion cells of trigeminal ganglion, suggesting centripetal or centrifugal extension of the infectious agent along the axons.

Blanquet-Grossard et al., [sup][12] have investigated the presence of protease-resistant PrP [sup]Sc in pulp tissues from eight patients with sCJD using specific monoclonal antibody by Western blotting. Though the authors were unable to detect protease-resistant PrP [sup]Sc in pulpal tissues, they suggested that the negative results could be due to low sensitivity of the technique used and the potential for transmission of CJD via dental procedures could not be dismissed. The authors have calculated that 1 g of sCJD infected pulp would be expected to contain 40 log [sub]10 LD [sub]50 /g of infectivity, compared to 10 [sub]8-9 LD [sub]50 /g of infectivity in brain tissue.

Prions and Dentistry

There is no evidence to show that TSE is transmissible from one person to other by normal social contact, sexual contact or airborne droplets. Studies have failed to show evidence of transmission of sCJD by blood components or plasma products. On the contrary, there have been four reports of probable transmission of vCJD via blood transfusion, where the donors were at preclinical phase of the disease at the time of blood donation [Table 1]. [sup][13]

Occupational exposure

There is no risk of transmission of TSE to health care workers including medical doctors and dentists through clinical contact or noninvasive clinical investigative procedure. A total of 24 cases of sCJD have been reported in health care workers as of 2005. [sup][14] Theoretically, it is possible that the health care workers may acquire prion diseases from affected patients through needle stick injuries. However, there is no epidemiological evidence to prove an association between occupational exposure and sCJD. The health care personnel should be informed about the nature of the hazard as well as the relevant safety procedures. The World Health Organization (WHO) has recommended "common-sense" actions in case of an occupational exposure while performing dental procedures on TSE patients [Table 2]. [sup][15]{Table 2}

Dental procedures

To date, there are no reported definite or suspected cases of human TSEs arising from dental procedures. Bourvis et al., [sup][16] had theoretically assessed the risk of iatrogenic transmission of sCJD during endodontic treatment. They estimated that the risk of being infected during endodontic treatment ranged from 3.4 to 13 per million procedures, if no effective prior deactivation procedures were used. However, the probability that more than one case was infected secondary to endodontic treatment ranged from 47% to 77% depending on the quantity of the infective material. The results of this study showed that the risk of sCJD transmission is higher because of the reuse of endodontic instruments in the absence of effective prion decontamination procedures.

Achieving appropriate decontamination of endodontic instruments intended for reuse is extremely difficult. Therefore, there is a possibility that these decontaminated instruments that were in contact with dental pulpal tissue may transfer the prion proteins from the infected patients to other patients. [sup][17]

There are two possible mechanisms assessed for the transfer of CJD via dental instruments:

*Accidental abrasion of lingual tonsil during dental procedures. Such a chance is extremely low (10 [sup]4 -10 [sup]9 times less likely than tonsillectomy). *Contact of dental instruments with pulp tissue. As dental pulp originates from richly innervated neural crest cells, it is theoretically possible that the dental pulp of individuals infected with CJD may be infectious. [sup][12] General recommendations for dentists

The role of the dentist is to identify the patients with different forms of CJD and to take appropriate measures to reduce the possible risk of cross contamination. This can be achieved by obtaining: (a) complete medical history of the patient, (b) family history of prion diseases, (c) travel history to know about the possible exposure during visits to endemic areas like United Kingdom. Based on this information, patients can be classified as being at high risk or low risk for developing the disease. [sup][2]

High-risk patients

Patients with diagnosis or suspicion of CJD; asymptomatic patients with a gene mutation; all members of the family with a case of hereditary CJD ; all members of a family with a case of vCJD.

Low-risk patients

Patients with undiagnosed progressive neurological disease with or without dementia; members of a family with history of undiagnosed dementia or neurological disease; recipients of human pituitary hormone or duramater; patients undergoing transdural surgery between 1972 and 1989 as infectious agent could be transmitted during those procedures.

Prion inactivation methods

The routine physical and chemical sterilizing procedures are ineffective against prion agents, as they are heat resistant and bind tightly to surgical steel instruments. The prions also become more resistant to inactivation when dried and have shown to transmit disease experimentally and clinically, even after disinfection. [sup][18]

It is advisable to use disposable instruments whenever possible and incinerate reusable instruments that are difficult to clean (endodontic files, broaches, carbide and diamond burs and dental matrix bands). Endodontic files used in the treatment of pulp cavity contain blood and peripheral nerves known to carry the prion proteins and their intricate surface topography enable to trap the proteins. Therefore, a recent communication in 2007 titled "Advise for dentists on re use of endodontic instruments and variant Creutzfeldt-Jakob Disease" issued by UK Department of Health, has advised dentists to ensure single use of endodontic reamers and files as a precaution to reduce any potential risk of transmission of vCJD. The nondisposable instruments should be mechanically cleaned and passed thorough stringent decontamination protocols before reuse, as recommended by WHO in 2000 [Table 3]. [sup][15]{Table 3}

The handling of instruments depends on the risk of the patient being treated. When treating high-risk patients, all materials must be incinerated. The source of refrigeration and aspiration system should be external to the equipment due to the possibility that some residues might pass via internal systems and compromise sterilization. The patient should never use the normal spittoon but a disposable receptacle that is later incinerated. The histological samples of high-risk patients must be handled by specialized staffs that are aware of the risk. As routine formalin fixation does not inactivate prion proteins, the samples must be immediately immersed in 98% formic acid for 1 h prior to paraffin embedding and labelled as biohazardous. [sup][5]

In patients with suspicion of CJD, all the instruments must be stored separately in a rigid container labelled with data of the patient, type of treatment provided and details of the attending clinician until a definitive diagnosis is arrived. The instruments are incinerated if the diagnosis is confirmed or sterilized by conventional methods like autoclaving if diagnosis is ruled out. [sup][5]

Conclusion

TSEs are a group of fatal neurodegenerative disorders with no approved cure. The prion proteins resist conventional sterilization methods used in dental clinics and laboratories. Although there appears to be very low risk of CJD transmission during dental procedures, account must be taken of this possibility. As a general rule, appropriate medical and family history should be taken from all the patients before dental procedures. The dental professionals should have up to date knowledge about transmission, diagnosis, infection control and decontamination procedures regarding prion diseases.

References

1. Azarpazhooh A, Leake JL. Prions in dentistry-what are they, should we be concerned and what can we do? J Can Den Assoc 2006;72:53-60.

2. Bebermeyer RD, Powell JF, Hobdell MH, Durban EM. Dental practice implications in prion diseases. Quintesence Int 2003;34:38-44.

3. Azarpazhooh A, Fillery ED. Prion disease: The implications for dentistry. J Endod 2008;34:1158-66.

4. Pruisner SB, Miller B. Prion Diseases. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, editors. Harrison's Principles of Internal Medicine. New York: McGraw Hill 2005; p. 2495-8.

5. Scully C, Smith AJ, Bagg J. Prions and the human transmissible spongiform encephalopathies. Dent Clin North Am 2003;47:493-516.

6. Palacios-Sanchez B, Esparza-Gomez GC, Campo-Trapero J, Cerero-Lapiedra R. Implications of prion disease for dentistry: An update. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:316-20.

7. Porter SR. Prion disease: Possible implications for oral health care. J Am Dent Assoc 2003;134:1486-91.

8. Zeidler M, Johnstone EC, Bamber RK, Dicken CM, Fisher CJ, Francis AF, et al . New variant Creutzfeldt-Jakob disease: Psychiatric features. Lancet 1997;350:908-10.

9. Reuber M, Al-Din AS, Baborie A, Chakrabraty A. New variant Creutzfeldt-Jakob disease presenting with loss of taste and smell. J Neurol Neurosurg Psychiatry 2001;71:412-8.

10. Head MW, Ritchie D, McLoughlin V, Ironside JN. Investigation of PrP [sup]res in dental tissues in variant CJD. Br Dent J 2003;195:339-43.

11. Guiroy DC, Shankar SK, Gibbs CJ Jr, Messenheimer JA, Das S, Gajdusek DC. Neuronal degeneration and neurofilament accumulation in the trigeminal ganglia in Creutzfeldt-Jakob disease. Ann Neurol 1989;25:102-6.

12. Blanquet-Grossard F, Sazdovitch V, Jean A, Deslys JP, Formant D, Hauw JJ, et al . Prion protein is not detectable in dental pulp from patients with Creutzfeldt-Jakob disease. J Dent Res 2000;79:700.

13. Ludlam CA, Turner ML. Managing the risk of transmission of variant Creutzfeldt-Jakob disease by blood products. Br J Hematol 2006;132:13-24.

14. Ena J. Prions: Who should worry about them? Arch Med Res 2005;36:622-7.

15. WHO Consultation: WHO infection control guidelines for transmissible spongiform encephalopathy. Geneva, Switzerland: World Health Organization Communicable Disease Surveillance and Control; 2000. Report No: WHO/CDS/CSR/APH/2000.

16. Bourvis N, Boelle PY, Cesbron JY, Valleron AJ. Risk assessment of transmission of sporadic Creutzfeldt-Jakob disease in endodontic practice in absence of adequate prion inactivation. PLoS One 2007;2:e1330.

17. Letters S, Smith AJ, McHugh S, Bagg J. A study of visual and blood contamination on reprocessed endodontic files from general dental practice. Br Dent J 2005;199:522-5.

18. Dello Russo N. Understanding prions. J Am Dent Assoc 2004;135:278.

P. Jayanthi, Priya. Thomas, P. Bindhu, Rekha. Krishnapillai

Source Citation (MLA 7th Edition) Jayanthi, P., et al. "Prion diseases in humans: Oral and dental implications." North American Journal of Medical Sciences 5.7 (2013): 399. Academic OneFile. Web. 4 Nov. 2013. Document URL

Gale Document Number: GALE|A340744668

http://go.galegroup.com/ps/i.do?id=GALE%7CA340744668&v=2.1&u=capes58&it=r&p=AONE&sw=w&asid=c1f2cb9a722e0f64d416e2c62a58a10f

Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review

Yeoungsug Kim DDS1, Hessam Nowzari DDS; PhD2,*, Sandra K. Rich MPH, PhD3

Article first published online: 15 DEC 2011

DOI: 10.1111/j.1708-8208.2011.00407.x

Issue

Clinical Implant Dentistry and Related Research

Volume 15, Issue 5, pages 645–653, October 2013

Additional Information(Hide All)

How to CiteAuthor InformationPublication History

How to Cite

Kim, Y., Nowzari, H. and Rich, S. K. (2013), Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review. Clinical Implant Dentistry and Related Research, 15: 645–653. doi: 10.1111/j.1708-8208.2011.00407.x

Author Information 1 Resident, Advanced Education in Periodontics Program, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA

2 professor, Clinical Dentistry and director, Advanced Education in Periodontics Program, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA

3 associate professor, Advanced Education in Periodontics Program, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA

*Dr. Hessam Nowzari, Herman Ostrow School of Dentistry, University of Southern California, Norris Dental Science Center-DEN, 925W. 34th Street, Room 119, Los Angeles, CA 90089-0641, USA; e-mail: nowzari@usc.edu

Publication History Issue published online: 7 OCT 2013 Article first published online: 15 DEC 2011

Keywords:

anorganic bovine bone substitutes; BSE diagnostic test; BSE prion inactivation; BSE prion infectivity; protein; PrP(27-30); PrPSc

ABSTRACT

Background: Despite the causal association between variant Creutzfeldt – Jakob disease and bovine spongiform encephalopathy (BSE), bovine origin graft materials are widely used during dental surgical procedures. The aim of this study was to assess the risk of BSE transmission through anorganic bovine bone substitutes.

Methods: Electronic database of MEDLINE was searched to identify relevant studies regarding our focused questions, presence of BSE prion infectivity in raw bovine bone, BSE prion inactivation by bone substitute manufacturing process, protein contents in anorganic bovine bone substitutes, and validity of current BSE diagnostic methods. Search terms yielded 1,704 titles. After title/abstract screening and duplicates removal, 36 full-text articles were screened for inclusion.

Results: A total of 16 studies were included in the final analysis. No eligible studies were identified regarding the efficacy of BSE prion inactivation by the treatments used for anorganic bovine bone manufacturing. BSE infectivity and PrPSc, pathological prion, were detected in bovine bone marrow and serum samples. Proteins were detected in Tutoplast® (bovine), Bio-Oss®, and tibia samples treated at the similar condition for Bio-Oss deproteinization. Inconsistent results of different BSE diagnostic tests were not unusual findings (Iwata et al. 2006; Arnold et al. 2007; Murayama et al. 2010), and a study by Balkema-Buschmann and colleagues showed an apparent discrepancy between BSE infectivity and detection of PrP(27-30), the current surrogate marker for prion disease infectivity.

Conclusion: This review indicates that bovine-derived graft biomaterials may carry a risk of prion transmission to patients.

http://onlinelibrary.wiley.com/doi/10.1111/j.1708-8208.2011.00407.x/abstract

Saturday, November 2, 2013

*** Recommendation of the Swiss Expert Committee for Biosafety on the classification of activities using prion genes and prion protein January 2013

http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/recommendation-of-swiss-expert.html

Tuesday, October 29, 2013

Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review

http://transmissiblespongiformencephalopathy.blogspot.com/2013/10/risk-of-prion-disease-transmission.html

Sunday, September 08, 2013

*** Iatrogenic Creutzfeldt-Jakob disease via surgical instruments and decontamination possibilities for the TSE prion

http://creutzfeldt-jakob-disease.blogspot.com/2013/09/iatrogenic-creutzfeldt-jakob-disease.html

Sunday, February 10, 2013

Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection report/CJD

http://creutzfeldt-jakob-disease.blogspot.com/2013/02/creutzfeldt-jakob-disease-cjd-biannual.html

Thursday, January 17, 2013

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

4.19 All people who are “at increased risk” of CJD/vCJD are asked to help prevent any further possible transmission to other patients by following this advice: Don’t donate blood. No-one who is “at increased risk” of CJD/vCJD, or who has received blood donated in the United Kingdom since 1980, should donate blood; Don’t donate organs or tissues, including bone marrow, sperm, eggs or breast milk; If you are going to have any medical, dental or surgical procedures, tell whoever is treating you beforehand so they can make special arrangements for the instruments used to treat you if you need certain types of surgery or investigation; You are advised to tell your family about your increased risk. Your family can tell the people who are treating you about your increased risk of CJD/vCJD if you need medical or surgical procedures in the future and you are unable to tell them yourself.

4.20 GPs are asked to record their patient’s CJD/vCJD risk status in their primary care records. The GP should also include this information in any referral letter should the patient require surgical, medical or dental procedures.

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

4.68 The risks of transmission of infection from dental instruments are thought to be very low provided satisfactory standards of infection control and decontamination are maintained. There is no reason why any patient with, or “at increased risk” of, CJD or vCJD, should be refused routine dental treatment. Such people can be treated in the same way as any member of the general public.

4.69 Information for dentists about the management of patients with, or “at increased risk” of, CJD/vCJD can be found here. Advice for dentists on re-use of endodontic instruments and vCJD can be found here. An advice note concerning problems with dental care for individuals 'at-risk' of CJD for public health purposes can be found here.

Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 Published: 2 June 2003 Amended: January 2013

4.70 Dental instruments used on patients with, or “at increased risk” of, CJD or vCJD can be handled in the same way as those used in any other low risk surgery, i.e. these instruments can be reprocessed according to best practice and returned to use. Dentists are reminded that any instruments labelled by manufacturers as ‘single-use’ should not be re-used under any circumstances.

4.71 Advice on the decontamination of dental instruments can be found in the Department of Health guidance HTM01-05 ‘Dental decontamination’. This guidance has been produced to reflect a reasonable and rational response to emerging evidence around the effectiveness of decontamination in primary care dental practices, and the possibility of prion transmission through protein contamination of dental instruments. It is available here. After death

4.72 Guidance on dealing with the bodies of patients with, or “at increased risk” of, CJD or vCJD, is contained in Annex H. This includes advice on carrying out post mortem examinations and transportation of bodies, and advice for undertakers on embalming, funerals and cremations.

http://www.dh.gov.uk/health/files/2012/11/Part-4-Infection-Control-Jan13.pdf.pdf

Greetings again HPA et al,

I repeat, what I have said all along, all these human and animal TSE prion strains must all be made reportable, and there should be no age restrictions tied to any reporting criteria. TSE prion disease knows no borders, they know no age groups.

Finally, the infamous UKBSEnvCJD only theory should be put to rest once and for all.

For the scientific communities to continue to endorse such fallacious, and misleading science as the UKBSEnvCJD only theory, this will only lead to other, needless and countless exposures, and I can only guess as to how many in the future will go clinical and die.

These needless and countless exposures and deaths, in the near future, years, decades to come, from the Transmissible Spongiform Encephalopathy TSE prion disease, the Prionpathy, the Prionopathies, the VPSPr’s, the sporadic CJD and all it’s sub-types, the sporadic FFI’s and all it’s potential sub-types, what about GSS, what about a case of sporadic Creutzfeldt-Jakob disease with a Gerstmann-Sträussler-Scheinker phenotype but no alterations in the PRNP gene, and don’t forget VPSPr. VPSPr, has introduced a novel and very different prion strain to sporadic human prion diseases which may have similarities with those associated with GSS.

none of this is possibly tied to iatrogenic TSE in humans and or a zoonosis source, and or both?

TO continue to base iatrogenic TSE prion safety protocols and guidelines, and continue to base this only on the UKBSEnvCJD theory, and all the rest a spontaneous happenstance of bad luck, is NOT scientific in my opinion, and I and the world will hold you all responsible for future needless exposure and deaths by basing your scientific advice, on corporate and political science, bought and paid for by the the livestock industry, and enforced by the OIE, USDA, CFIA, DEFRA, et al. ...

Ladies and Gentlemen, source references at the bottom of these comments with links, for anyone that is still interested in the rest of this nightmare. ...

thank you,

with kindest regards,

I am sincerely and respectfully,

Terry S. Singeltary Sr.

layperson

see full text ;

http://transmissiblespongiformencephalopathy.blogspot.com/2013/01/tse-guidance-surgical-dental-blood-risk.html

Tuesday, December 18, 2012

Bioassay Studies Support the Potential for Iatrogenic Transmission of Variant Creutzfeldt Jakob Disease through Dental Procedures

http://vcjd.blogspot.com/2012/12/bioassay-studies-support-potential-for.html

Bioassay Studies Support the Potential for Iatrogenic Transmission of Variant Creutzfeldt Jakob Disease through Dental Procedures

Elizabeth Kirby1#, Joanne Dickinson1#, Matthew Vassey1, Mike Dennis1, Mark Cornwall1, Neil McLeod1, Andrew Smith2, Philip D. Marsh1,3, James T. Walker1, J. Mark Sutton1*, Neil D. H. Raven1

1 Health Protection Agency - Porton Down, Salisbury, Wiltshire, United Kingdom, 2 College of Medical, Veterinary & Life Sciences, Glasgow Dental Hospital & School, University of Glasgow, Glasgow, United Kingdom, 3 Leeds Dental Institute, Leeds, West Yorkshire, United Kingdom

Abstract

Background

Evidence is required to quantify the potential risks of transmission of variant Creutzfeldt Jakob (vCJD) through dental procedures. Studies, using animal models relevant to vCJD, were performed to address two questions. Firstly, whether oral tissues could become infectious following dietary exposure to BSE? Secondly, would a vCJD-contaminated dental instrument be able to transmit disease to another patient?

Methods

BSE-301V was used as a clinically relevant model for vCJD. VM-mice were challenged by injection of infected brain homogenate into the small intestine (Q1) or by five minute contact between a deliberately-contaminated dental file and the gingival margin (Q2). Ten tissues were collected from groups of challenged mice at three or four weekly intervals, respectively. Each tissue was pooled, homogenised and bioassayed in indicator mice.

Findings

Challenge via the small intestine gave a transmission rate of 100% (mean incubation 157±17 days). Infectivity was found in both dental pulp and the gingival margin within 3 weeks of challenge and was observed in all tissues tested within the oral cavity before the appearance of clinical symptoms. Following exposure to deliberately contaminated dental files, 97% of mice developed clinical disease (mean incubation 234±33 days).

Interpretation

Infectivity was higher than expected, in a wider range of oral tissues, than was allowed for in previous risk assessments. Disease was transmitted following transient exposure of the gingiva to a contaminated dental file. These observations provide evidence that dental procedures could be a route of cross-infection for vCJD and support the enforcement of single-use for certain dental instruments.

Citation: Kirby E, Dickinson J, Vassey M, Dennis M, Cornwall M, et al. (2012) Bioassay Studies Support the Potential for Iatrogenic Transmission of Variant Creutzfeldt Jakob Disease through Dental Procedures. PLoS ONE 7(11): e49850. doi:10.1371/journal.pone.0049850

Editor: Noriyuki Nishida, Nagasaki University Graduate School of Biomedical Sciences, Japan

Received: March 23, 2012; Accepted: October 15, 2012; Published: November 30, 2012

Copyright: © 2012 Kirby et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The study was funded by the Department of Health (England), contract number 007/0099. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: AS has received lecture fees and funding for a PhD studentship from W&H Ltd, lecture fees from Steris Ltd and travel expenses for attending a meeting from Schulke and Mayr. PM identified consultancy work for Johnson and Johnson, UK and Unilever, UK. JMS identified consultancy work for Advanced Sterilisation Products and funding for research involving TSO3, CISA SpaA, BES Decon, BiotAK, and Genencor International. JMS also received travel money to attend a meeting of the British Association for the Study of Community Dentistry. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.

* E-mail: mark.sutton@hpa.org.uk

# These authors contributed equally to this work.

snip...

Implications for public health

Currently there is no evidence for vCJD transmission through either surgery or dentistry. Transmission of vCJD by blood transfusion [5], [9] highlights that any procedure contacting nervous or lymphoid tissue must also be considered a risk given the wider tissue distribution of vCJD infectivity compared to sporadic CJD [19]–[21]. The highly efficient transmission of BSE strain 301 V infection through direct inoculation into the murine small intestine in this study raises similar concerns for vCJD transmission through endoscopic procedures in man.

The observations in the current study also provide theoretical grounds for concern in respect to dental procedures. The levels of infectivity observed in all oral tissues tested (most notably gingival margin with up to ~1000 ID per mg) were higher than previously considered.

A further element of the study assessed residual protein contamination on a range of dental instruments after routine cleaning and disinfection in general dental practice in England [22]). The study showed a number of instrument types and cleaning procedures where the upper interquartile range for residual protein was in excess of 100 µg. This could equate to up to 100 ID per instrument in the case of gingival tissue. Autoclaving has been shown to achieve only a 3-log inactivation of various TSE agents [23] and an autoclave designed for the dental market has been tested recently and shown to provide only a 100-fold reduction in infectivity in the BSE301V/VM model used here (134°C, 18 minutes; Sutton et al unpublished). A dental instrument soiled with infectious gingival tissue and disinfected under this regimen would have an inadequate safety margin.

The gingival challenge was designed as a worse-case scenario in respect to the infectious load on a dental instrument, but to be of limited invasiveness. The procedure resulted in very high levels of transmission with short incubation periods indicating that a much lower titre challenge material would also have caused some transmission. Even if a relatively rare event, the large number of dental interventions taking place in a younger age profile population (c.f. surgical procedures) and a carrier population of unknown size means these risks are not negligible. This would seem to be at odds with the absence of any reported cases of clinical vCJD transmission linked to dental procedures. This might be explained by a number of factors, including difficulties in linking dental records to known vCJD patients [24], asymptomatic cases [5] and extended incubation periods for patients exposed by blood transfusion (up to 7.8 years; [25]). As a worse case study, the incubation periods described here would be expected to be the most rapid giving rise to prion-disease symptoms in this model, and as a novel low-dose, peripheral model of infection, the incubation periods might be expected to be considerably longer than those observed for blood transfusion cases. Given the difficulties in linking dental procedure case histories to vCJD, such cases may not yet be evident.

Preliminary data from this study have already been provided to the UK Department of Health as part of the revision of the dental risk assessment (http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/dh/en/documents/digitalasset/dh_081217.pdf; accessed 12th November 2011).

Additional control measures have been incorporated into guidance on decontamination in dental settings in England (http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_109363; accessed 12th November 2011). The emphasis on standardised decontamination methods and single use instruments for difficult to clean devices appear sensible and proportionate given the experimental observations described and discussed here.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0049850

see full text and more ;

Tuesday, December 18, 2012

Bioassay Studies Support the Potential for Iatrogenic Transmission of Variant Creutzfeldt Jakob Disease through Dental Procedures

http://vcjd.blogspot.com/2012/12/bioassay-studies-support-potential-for.html

Friday, August 10, 2012

Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual update (July 2012)

http://creutzfeldt-jakob-disease.blogspot.com/2012/08/incidents-of-potential-iatrogenic.html

Thursday, April 12, 2012

Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010

Eurosurveillance, Volume 17, Issue 15, 12 April 2012

Research articles

http://creutzfeldt-jakob-disease.blogspot.com/2012/04/health-professions-and-risk-of-sporadic.html

Thursday, December 22, 2011

Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review Clin Implant Dent Relat Res. 2011 Dec 15. doi: 10.1111/j.1708-8208.2011.00407.x. [Epub ahead of print]

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/risk-of-prion-disease-transmission.html

Sunday, October 23, 2011

The oral secretion of infectious scrapie prions occurs in pre-clinical sheep with a range of PRNP genotypes

JVI Accepts, published online ahead of print on 19 October 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/oral-secretion-of-infectious-scrapie.html

Monday, May 16, 2011

Does Poor Dental Health Have a Role in the Emergence of Variant Creutzfeldt Jakob Disease in the United Kingdom?

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/does-poor-dental-health-have-role-in.html

Thursday, October 23, 2008

ONE HUNDRED AND FIRST MEETING OF THE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE

http://seac992007.blogspot.com/2008/10/one-hundred-and-first-meeting-of_23.html

http://seac992007.blogspot.com/2008/01/spongiform-encephalopathy-advisory.html

MASTER DENTISTS FALLS VICTIM TO CJD

Subject: MASTER DENTIST FALLS VICTIM TO CJD

From: "Terry S. Singeltary Sr." <[log in to unmask]>

Reply-To: Sustainable Agriculture Network Discussion Group <[log in to unmask]>

Date: Sat, 31 Mar 2007 15:51:24 –0600

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&F=&S=&P=106052

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A3=ind0703&L=SANET-MG&E=quoted-printable&P=3426823&B=------%3D_NextPart_000_00BB_01C773AC.6F8F9B40&T=text%2Fplain;%20charset=Windows-1252&header=1

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A3=ind0703&L=SANET-MG&E=quoted-printable&P=3492412&B=------%3D_NextPart_000_00BB_01C773AC.6F8F9B40&T=text%2Fhtml;%20charset=Windows-1252&XSS=3&header=1

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

Page updated: 8th May 2006

http://www.seac.gov.uk/statements/statement0506.htm

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/vaop/ncurrent/pdf/bdj.2007.126.pdf

SNIP...

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/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17087448&query_hl=1&itool=pubmed_docsum

SNIP...

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

SNIP...

SECTION 7: THE RISK TO PATIENTS UNDERGOING DENTAL

TREATMENT

It is of great concern that there may be a risk of becoming infected with nv-CJD in the dental

surgery due to cross infection from either the dentist or another patient. The two main sources of

infectious material in the dental surgery are blood and saliva. As shown in Table 7 these are of

relatively low infectivity compared to the tissues of the CNS.

As nv-CJD has only recently been discovered, few experiments have been carried out to discover

whether it can be transmitted. Therefore, we must look at the other TSEs to get an indication of

likely risk.

The risk of transmission via saliva

Studies to ascertain levels of PrP have shown that salivary gland tissue contains high levels of

infectivity, much earlier than in brain tissue (Sakaguchi 1993, Eklund 1967). Replication of the

infectious agent first appears in salivary tissue soon after inoculation, possibly indicating that the

salivary glands are one of the primary sites of replication, rather than the brain. It was also found

that infectivity declines with time, suggesting that greatest risk from transmission is likely to be

early in the disease, before clinical signs are present.

There has been no research into the risk of transmission from saliva, however we must assume

that if salivary gland is infected then so is the saliva it produces.

The effect of gingival scarification on transmission

If it is found that BSE has been transmitted to humans via the oral route it is essential to ascertain

any factors that may have increased susceptibility and therefore may have implications for

human to human transmission. Studies into the effect of gingival scarification on the

transmission of Scrapie (Carp 1982) have shown that a higher proportion of mice succumbed to

infection if their gingivae had been scarified compared to the controls (100% and 71%

respectively). It was also shown that the incubation period was significantly shorter.

Although it has not been possible to transmit Scrapie using dental burs (Adams 1978) it was

found that the gingivae of infected mice do contain a low level of Scrapie infection that can be

transmitted using an intra-cerebral approach.

The risk of transmission via blood products

Although most forms of CJD have been considered infectious by the mid-1960s its

transmissibility through the use of blood products is still controversial.

Sporadic CJD has been reported to be transmitted to mice by injecting blood from human

patients directly into mouse brain (Brown, 1994, Manuelidis, 1985). However this evidence has

not been reproduced and another review of research with non-human primates indicated that

sporadic CJD-infected human blood did not transmit the disease to primates (Tateishi, 1985).

Some evidence indicates that blood of experimentally infected animals contains an infective

agent. PrP infectivity resides predominately or exclusively in lymphocytes and monocytes rather

than granulocytes (Lavelle, 1972). There has been no evidence of infectivity in erythrocytes,

platelets or plasma, but low infectivity cannot be excluded. Animal studies have demonstrated

that the scrapie-agent replicates first in the spleen and other lymphoid tissues but reaches the

highest concentration in the brain, where it results in the clinical appearance of the disease

(Kurudail 1983). Hence, peripheral tissues in contact with blood also harbour PrP infectivity.

Animal transmission data indicate that human spleen, lymph nodes, serum and cord blood are

irregularly infective for animals, although few cord blood samples have been tested (Manuelidis,

1979). Studies of experimental sporadic CJD in guinea pigs and mice have shown that the

infectious agent is present in the brain, viscera and blood before clinical disease develops

(Lavelle, 1972 & Czub 1986).

Several factors must be considered in reviewing the animal evidence regarding transmission of

human TSEs in blood: the type of human TSE being tested, the level of PrP infectivity of the

study tissue, the species barrier, and the route of transmission.

The evidence from animal studies is inconclusive regarding transmission of sporadic CJD

between humans by transfusion.

Although case reports have provided evidence linking CJD to the receipt of dura mater and

human growth hormone, no human cases have yet been causatively linked to blood transfusion.

A number of cases have been seen where patients have undergone organ transplant and then

developed CJD. It is, however, impossible to determine whether the organ was the source of the

infection as insufficient information about each case is available.

If CJD is transmissible in blood, cases should occur in young patients, particularly if the

incubation period is short as in the other iatrogenic cases. Even if the incubation period were

many years, one would expect to see cases in young persons because of the transfusions given to

infants and young children. If CJD is transmitted in blood, a detectable increase in cases in blood

transfusion patients may be expected. There is a ban on the use and export of blood and blood

products from the UK (February 1998) as a precautionary measure and for the past two years any

donor with a family history of CJD has been prevented from donating blood. However this may

be unreliable, as many patients will not know the accurate diagnoses of a family member's

illness.

As noted by Brown (1996) in reference to blood products, "iatrogenic disease from this source

would dwarf in importance all other sources by virtue of the sheer numbers of people who

theoretically have been or could be at risk". The appearance of nvCJD raises new concerns. Due

to a possible oral route of infection and a novel strain of agent, the distribution of tissue

infectivity may differ from other forms of CJD. This is supported by evidence that suggested that

at the palatine tonsil might harbour PrP in nvCJD but not in sporadic CJD.

In view of the theoretical possibility that blood from patients incubating a TSE may harbour the

infective TSE agent the World Health Organisation recommends that the following groups

should be excluded as blood donors:

· Recipients of extracts derived from human pituitary glands (growth hormone and

gonadotropin).

· Those with a family history of CJD, GSS or FFI.

· Those who have received a human dura mater graft.

Animal studies indicate that the infective agent of human TSEs is present in blood in low titres,

and sufficient evidence of animal transmission suggests that the disease has the potential to be

transmitted through blood (Heye 1994). However, to date, epidemiological evidence indicates

that if blood transmission occurs it is likely to be rare. This may be due to polymorphism at

codon 129, which could restrict susceptibility. It is also possible that most transfusions may not

contain sufficient dose to cause infection.

There is no specific scientific evidence to date that nv-CJD will transmit through blood products.

This is due to the incubation period being many months in laboratory animals. As infectivity has

only been detected in white blood cells the potential risk from donated blood can be decreased by

a process known as leuko-depletion, removal white blood cells.

The knowledge that blood may be infected could change the views of both the medical

profession and patients. Transfusions may only be used if absolutely necessary and patients may

be given the option of donating their own blood for scheduled operations.

If CJD were transmitted in pooled blood products or saliva, clusters would be detected. Most

clusters have usually been attributed to familial disease (Masters, 1979 & Reingold 1996).

Surveillance systems have found cases of CJD among persons who have received blood

transfusions but none have been linked to blood transmission.

It must be remembered, however, that surveillance systems may not detect cases when unique

epidemiological or clinical features are present.

SECTION 8: CONCLUSIONS

A number of factors must be taken into consideration when assessing the risk of transmission of

nvCJD during dental treatment. Dental patients are at risk of infection from a number of sources,

the most significant being the consumption of infected animal products during the 1980s. A

small minority of patients will also be at increased risk in their place of work, such as

neuropathologists, neurosurgeons and laboratory technicians.

The most likely route of infection is via ineffectively sterilised instruments. If a patient is

suspected of having or has been diagnosed with nv-CJD further precautions can be taken. The

patient is likely to be showing clinical signs, which are likely to make dental treatment difficult,

therefore only emergency treatment is going to be appropriate. Where possible, a treatment

option that involves the least cross infection risk should be undertaken. . To reduce this risk, all

instruments that have been used on a patient with nvCJD should be disposable or discarded. This

includes oral surgery equipment, root planing hand instruments and ultrasonic tips in addition to

needles and blades. In the case of accidental inoculation it is unlikely that sufficient infective

material will be involved to transmit the disease. As discussed previously, the peripheral route of

infection is ineffective compared with intracerebral inoculation, and blood or saliva contains

little infectivity compared to central nervous tissue. All patients should be treated using universal

precautions, which should be employed in all dental practices as a matter of routine, providing

the maximum protection equally to clinical staff and patients. This includes the use of gloves,

masks and eye protection at all times. After each patient all instruments should be autoclaved and

disposable alternatives should be used where appropriate.

The number of patients likely to be incubating nv-CJD is impossible to predict at present. Much

depends on the average incubation time, the longer the time, the higher the figure is likely to be.

At present the average incubation time can not be calculated nor is it possible to estimate the

dose required to infect a human. With the possibility of a nationwide epidemic investigation

must be carried out to determine the risk from cross infection. Research has yet to prove that

there is a risk, however, until all possibility of this can be discounted caution must prevail.

The resistance of the TSE agent to standard medical sterilisation procedures is noteworthy.

Experimental evidence demonstrates that the agent shows resistance to the following: exposure

to boiling, freezing, ethanol, H2O2, permanganate, iodine, ethylene oxide vapour, detergents,

organic solvents, formaldehyde, UV and gamma irradiation, and standard autoclaving.

Since conventional methods of sterilisation and disinfection do not decontaminate the CJD

infectious agent, specific measures must be used, however, many of these are impractical in the

dental practice.

Although the TSE agent is known to be infectious it is not contagious in the usual sense.

Individuals exposed to patients with CJD: their spouses, nurses and doctors, do not appear to

have an increased risk of developing the disease. Furthermore, professionals who might be

considered 'high risk' in relation to exposure to TSE agents: e.g. pathologists, neurosurgeons,

butchers etc. also do not appear to be at an increased risk of developing CJD. No proven instance

of CJD contracted occupationally has yet been identified. However, over 170 cases of iatrogenic

CJD contracted through inoculation of contaminated CNS tissue or corneal transplantation serve

to remind those of us involved in the management of all CJD patients of the importance of safety

procedures in relation to the TSE agents.

REFERENCES

snip...

http://www.bseinquiry.gov.uk/files/ws/s201a.pdf

snip...

SOURCE

Subject: MASTER DENTIST FALLS VICTIM TO CJD

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

Date: Sat, 31 Mar 2007 15:51:24 -0600

Content-Type: text/plain

Parts/Attachments: Parts/Attachments text/plain (1440 lines)

https://lists.aegee.org/cgi-bin/wa?A2=ind0703&L=BSE-L&F=&S=&X=38299B57C43460E456&Y=flounder9%40verizon.net&P=9279

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.

http://seac992007.blogspot.com/2008/06/seac-2008-one-hundredth-meeting-of.html

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.

PMID: 17087448 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17087448&query_hl=1&itool=pubmed_docsum

Subject: PrPSc in salivary glands of scrapie-affected sheep

Date: February 15, 2007 at 9:33 am PST

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/abstract/JVI.02148-06v1?papetoc

http://seac992007.blogspot.com/2008/06/seac-2008-one-hundredth-meeting-of.html

http://seac992007.blogspot.com/2007/12/seac-99th-meeting-on-friday-14th.html

SEAC 99th meeting on Friday 14th December 2007

snip...

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/

A RE-ASSESSMENT OF THE POTENTIAL RISK OF VCJD TRANSMISSION VIA DENTISTRY ISSUE

1. The Department of Health (DH) has asked SEAC to consider an interim assessment of the potential risk of vCJD transmission via dental procedures. This work builds on previous risk assessments on possible dental transmission considered by SEAC.

BACKGROUND

Previous SEAC considerations of vCJD transmission via dentistry

snip...

The New DH Risk Assessment

8. The research on infectivity just noted forms one strand of a wider programme at the HPA, which is also intended to quantify protein residues found on dental instruments and the effectiveness of sterilisation in reducing infectivity. Following SEAC 97 (May 2007), DH commissioned a comprehensive re-assessment of the potential risks of vCJD transmission associated with dentistry to take account of research at the HPA and elsewhere. The assessment aims to clarify the range of plausible scenarios for vCJD transmission via dental instruments that could occur, given what is currently known, and to identify the most important factors affecting this risk. The assessment will be used to identify the most important areas of further work to address the uncertainties and any robust ways of cost effectively reducing risks further.

9. This new interim risk assessment has been produced by DH analysts (annex 3) in collaboration with a Scientific Reference Group of independent experts (Chaired by Professor Graham Medley). Members of the Group have expertise in dentistry, instrument decontamination, human and animal prion diseases, anatomy, public health, risk assessment modelling and epidemiology. This group met three times to review and refine the modelling framework and agree the risk assessment. The group provided advice on the inputs and assumptions incorporated into the risk assessment, particularly where expert judgement was required due to a lack of hard data. Under circumstances where key data are absent, precautionary assumptions were agreed. As a number of large uncertainties that strongly influence the quantification of risk remain, the risk assessment is considered as interim and will be updated in the future when new scientific evidence becomes available.

10. The assessment examines the risk that vCJD may be transmitted via dental procedures by establishing plausible ranges for key parameters, including (see sections 2 and 3 of the risk assessment):

• the vCJD infectivity of tissues of the oral cavity of infected patients

• the deposition of that material onto different types of dental instruments and the effectiveness of standard cleaning and sterilisation processes used in dental practice

• the mechanisms and efficiency of transfer of vCJD infectivity from contaminated instruments used on subsequent patients

• the probability of transmission based on assessments of the number and types of dental procedure conducted and the number of people who might be carrying an asymptomatic vCJD infection.

Findings 11.

As there is lack of substantial data with which to accurately quantify many of these parameters, plausible ranges for these parameters have been established to take account of the often large uncertainties in the data. The large uncertainties in many of these parameters strongly influence the quantification of the risk.

12. Plausible scenarios built up using ranges for each of these factors include many in which dental transmission would have no detectable effect on the course of the vCJD outbreak (see section 4 of the risk assessment). However, there are some which include a combination of pessimistic assumptions as regards the infectivity of dental / oral tissues and the effects of instrument decontamination which suggest that:

• there could be some hundreds of vCJD transmissions per annum via dentistry - albeit against a background of several thousand existing vCJD infections (not clinical cases of vCJD), or where

• dental transmission could generate a self-sustaining reservoir of vCJD infection within the population.

13. The distinction between vCJD infections and clinical cases of vCJD is important. If a large proportion of secondary transmissions result in subclinical infections (either never developing into clinical disease or doing so over an extended time-scale) and those infected are infectious, the likelihood of a self-sustaining epidemic increases. The proportion of individuals who might enter such a subclinical “carrier state” is unknown. Key Assumptions and areas of uncertainty

14. Work on the risk assessment is on-going and new data should enable some of the inputs and assumptions underpinning these scenarios to be revised. Key areas of uncertainty are:

• Infectivity in relevant tissues. Of all the unknowns, that of overriding importance is whether dental/oral tissues in patients incubating vCJD would be infective, and if so at what level.

There are as yet no results of studies using human gingival and dental pulp tissues, and these studies may extend into 2009 and 2010 respectively. This is examined in section 2.3 of the risk assessment.

• Protein Residues on dental instruments. This is examined in section 2.2 of the risk assessment.

• Efficacy of Autoclaving. This is examined in section 2.3 of the risk assessment.

• Current prevalence of vCJD infection. This is examined in section 3.3 of the risk assessment.

• Epidemiology of vCJD. This is examined in section 4 of the risk assessment.

15. Suggested areas of further work to reduce the uncertainty in these key areas are described in section 5 of the risk assessment together with a preliminary analysis of possible interventions and risk reduction measures.

ADVICE SOUGHT FROM THE COMMITTEE

snip...

POSITION STATEMENT vCJD AND ENDODONTIC DENTISTRY

snip...

Endodontic instruments

5. Evidence suggests that the files and reamers used in endodontic procedures are reused and are difficult to reliably decontaminate4. Appreciable quantities of residual material remain adherent to the surface after normal cleaning and sterilisation5. 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 cases6, dental pulp includes blood and peripheral nerve tissue known to carry vCJD infectivity7,8. In addition, appreciable infectivity has been found in the dental pulp of hamsters with hamster scrapie9. 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 prions10. 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. level of infectivity is unknown.

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.

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 animals11. Another study suggested that prion infections in mice that remain at a subclinical level can be transmitted to other mice, resulting in clinical disease12. 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 hypothesis13. 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 thousand14. SEAC has strongly recommended that further studies to ascertain better the prevalence of vCJD infection be urgently considered15.

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

SEAC May 2006

===================================

New research

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...

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

27 SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic.

http://www.seac.gov.uk/statements/state260106subgroup.htm

http://seac992007.blogspot.com/2007/12/seac-99th-meeting-on-friday-14th.html

http://seac992007.blogspot.com/

28 DH (2007) Precautionary advice given to dentists on re-use of instruments

http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAreaID=2&NavigatedFromDepartment=False

see full text 17 pages ;

http://www.seac.gov.uk/papers/99-7.pdf

13 DH (2007) Precautionary advice given to dentists on re-use of instruments

http://www.gnn.gov.uk/environment/fullDetail.asp?ReleaseID=279256&NewsAreaID=2&NavigatedFromDepartment=False

http://www.seac.gov.uk/statements/state-vcjd-dentrstry.htm

http://seac992007.blogspot.com/2007/12/seac-99th-meeting-on-friday-14th.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

PLEASE REMEMBER, ALL IATROGENIC CJD IS, IS SPORADIC CJD, UNTIL ROUTE AND SOURCE OF THE IATROGENIC EVENT, IT’S ROUTE, IT’S SOURCE, DOCUMENTED, AND PUT INTO THE PUBLIC DOMAIN, DOES ANY EVENT BECOME DOCUMENTED AS IATROGENIC, AND WITH THE INCUBATION PERIOD SO LONG, THESE EVENTS ARE MOSTLY NEVER CONFIRMED, THUS ALL IATROGENIC EVENTS GO DOWN AS SPORADIC CJD, problem solved $$$

WHAT about the sporadic CJD TSE proteins ?

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

Sunday, August 11, 2013

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010

http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html

Sunday, October 13, 2013

CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html

Sunday, October 27, 2013

A Kiss of a Prion: New Implications for Oral Transmissibility

http://transmissiblespongiformencephalopathy.blogspot.com/2013/10/a-kiss-of-prion-new-implications-for.html

Tuesday, September 24, 2013

NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)

Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15

http://creutzfeldt-jakob-disease.blogspot.com/2013/09/nordion-us-inc-and-bioaxone-biosciences.html

Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

"BSE-L in North America may have existed for decades"

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

*** Saturday, November 2, 2013 ***

Exploring the risks of a putative transmission of BSE to new species

http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/exploring-risks-of-putative.html

Wednesday, October 30, 2013

SPECIFIED RISK MATERIAL (SRM) CONTROL VERIFICATION TASK FSIS NOTICE 70-13 10/30/13

http://madcowusda.blogspot.com/2013/10/specified-risk-material-srm-control.html

***Together with previous experiments performed in ovinized and bovinized transgenic mice and hamsters [8,9] indicating similarities between TME and L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME outbreaks in North America and Europe during the mid-1900s.

http://transmissiblespongiformencephalopathy.blogspot.com/2013/09/evaluation-of-zoonotic-potential-of.html

with great sadness and disgust, I must inform you that our federal government has failed us again, and chose the industry over sound science, with regards to TSE prion disease, aka mad cow type disease...tss

Saturday, November 2, 2013

APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe

http://madcowusda.blogspot.com/2013/11/aphis-finalizes-bovine-import.html

Monday, November 4, 2013

R-CALF Bullard new BSE rule represents the abrogation of USDA’s responsibility to protect U.S. consumers and the U.S. cattle herd from the introduction of foreign animal disease

http://madcowusda.blogspot.com/2013/11/r-calf-bullard-new-bse-rule-represents.html

CWD TSE prion disease in cervids, humans, iatrogenic, 85%+ sporadic CJD, ???

PRION2013 CONGRESSIONAL ABSTRACTS CWD

Sunday, August 25, 2013

HD.13: CWD infection in the spleen of humanized transgenic mice

Liuting Qing and Qingzhong Kong

Case Western Reserve University; Cleveland, OH USA

Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals.

***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system

Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1

1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK

Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.

Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.

Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.

Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay.

***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.

PRION2013 CONGRESSIONAL ABSTRACTS CWD

Sunday, August 25, 2013

***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html

I thought your readers and hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there from...like deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. ...

the prion gods at the cdc state that there is ;

''no strong evidence''

but let's see exactly what the authors of this cwd to human at the cdc state ;

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????

“Our conclusion stating that we found no strong evidence of CWD transmission to humans”

From: TSS (216-119-163-189.ipset45.wt.net)

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"

To:

Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

Sent: Monday, September 30, 2002 9:22 AM

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam,

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

Ermias Belay, M.D. Centers for Disease Control and Prevention

-----Original Message-----

From:

Sent: Sunday, September 29, 2002 10:15 AM

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html

http://chronic-wasting-disease.blogspot.com/2006_12_01_archive.html

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD

Accepted 15 November 2010. Abstract Full Text PDF References .

Abstract

The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.

http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract

"These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent."

Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007

Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov

The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

Monday, May 23, 2011 CDC

Assesses Potential Human Exposure to Prion Diseases Travel Warning

Public release date: 23-May-2011

Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences

CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.

"While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases," commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta."But it's also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents."

Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.

CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.

Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.

The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.

The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.

According to Abrams, "The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health."

###

The article is "Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.

In an accompanying podcast CDC's Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast.

http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php

also, they did not call this CWD postive meat back for the well being of the ELK ;

Wednesday, March 18, 2009

Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

___________________________________

PRODUCT

a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;

CODE

Elk Meats with production dates of December 29, 30, and 31

RECALLING FIRM/MANUFACTURER

Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009.

Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.

REASON

Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).

VOLUME OF PRODUCT IN COMMERCE

Unknown

DISTRIBUTION

NV, CA, TX, CO, NY, UT, FL, OK

___________________________________

http://www.fda.gov/bbs/topics/ENFORCE/2009/ENF01099.html

CJD REPORT 1994 increased risk for consumption of veal and venison and lamb

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

Table 9 presents the results of an analysis of these data.

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf

Thursday, October 10, 2013

CJD REPORT 1994 increased risk for consumption of veal and venison and lamb

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html

CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf

CWD transmission to humans.

NEVER ???

never say never with the TSE prion.

PRION2013 CONGRESSIONAL ABSTRACTS CWD

Sunday, August 25, 2013

HD.13: CWD infection in the spleen of humanized transgenic mice

Liuting Qing and Qingzhong Kong

Case Western Reserve University; Cleveland, OH USA

Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1

Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.

PRION2013 CONGRESSIONAL ABSTRACTS CWD

Sunday, August 25, 2013

***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html

Sunday, July 21, 2013

*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?

http://chronic-wasting-disease.blogspot.com/2013/07/as-chronic-wasting-disease-cwd-rises-in.html

I’m just saying. ...

TSS

Transmissible Spongiform Encephalopathy

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Thursday, November 14, 2013

Prion diseases in humans: Oral and dental implications