credits bmbl December 7 '06.doc - Central Michigan University

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Agent Summary Statement – Prion Diseases TABLE 1 THE HUMAN PRION DISEASES DISEASE ABBREVIATION MECHANISM OF PATHOGENESIS Kuru Infection through ritualistic cannibalism Creutzfeldt-Jacob disease CJD Unknown mechanism Sporadic CJD sCJD Unknown mechanism; possibly somatic mutation or spontaneous conversion of PrP C to PrP Sc Variant CJD vCJD Infection presumably from consumption of BSE-contaminated cattle products and secondary bloodborne transmission Familial CJD fCJD Germline mutations in PrP gene Iatrogenic CJD iCJD Infection from contaminated corneal and dural grafts, pituitary hormone, or neurosurgical equipment Gerstmann-Sträussler- Scheinker syndrome GSS Germline mutations in PrP gene Fatal familial insomnia FFI Germline mutations in PrP gene TABLE 2 THE ANIMAL PRION DISEASES DISEASE ABBREVIATION NATURAL MECHANISM OF PATHOGENESIS HOST Scrapie Sheep, goats Infection in genetically susceptible sheep and mouflon Bovine spongiform BSE Cattle Infection with prion-contaminated feedstuffs encephalopathy Chronic wasting disease CWD Exotic ungulate encephalopathy Feline spongiform encephalopathy EUE FSE Mule deer, white-tailed deer and Rocky Mountain elk Nyala, greater kudu and oryx Domestic and wild cats in captivity Unknown mechanism; possibly from direct animal contact or indirectly from contaminated feed and water sources Infection with BSE-contaminated feedstuffs Infection with BSE-contaminated feedstuffs Transmissible mink encephalopathy TME Mink (farm raised) Infection with prion-contaminated feedstuffs 300
Agent Summary Statement – Prion Diseases Species-specificity of prions. Most TSE agents, or prions, have a preference for infection of the homologous species, but cross-species infection with a reduced efficiency is also possible. After cross-species infection there is often a gradual adaptation of specificity for the new host; however, infectivity for the original host may also be propagated for several passages over a time-span of years. The process of cross-species adaptation can also vary among individuals in the same species and the rate of adaptation and the final species specificity is difficulty to predict with accuracy. Such considerations help to form the basis for the biosafety classification of different prions. LABORATORY SAFETY Biosafety level classification. In the laboratory setting prions from human tissue and human prions propagated in animals should be manipulated at BSL-2. BSE prions can likewise be manipulated at BSL-2. Due to the high probability that BSE prions have been transmitted to humans, certain circumstances may require the use of BSL-3 facilities. All other animal prions are considered BSL-2 pathogens. However, when a prion from one species is inoculated into another the resultant infected animal should be treated according to the guidelines applying to the source of the inoculum. Contact APHIS National Center for Import and Export at (301) 734- 5960 for specific guidance. Although the exact mechanism of spread of scrapie among sheep and goats developing natural scrapie is unknown, there is considerable evidence that one of the primary sources is oral inoculation with placental membranes from infected ewes. There has been no evidence for transmission of scrapie to humans, even though the disease was recognized in sheep for over 200 years. The diseases TME, BSE, FSE, and EUE are all thought to occur after the consumption of prion-infected foods. 1,2 The exact mechanism of CWD spread among mule deer, white-tailed deer and Rocky Mountain elk is unknown. There is strong evidence that CWD is laterally transmitted and environmental contamination may play an important role in local maintenance of the disease. 2 Human prion diseases. In the care of patients diagnosed with human prion disease, Standard Precautions are adequate. However, the human prion diseases in this setting are not communicable or contagious. 3 There is no evidence of contact or aerosol transmission of prions from one human to another. However, they are infectious under some circumstances, such as ritualistic cannibalism in New Guinea causing kuru, the administration of prion-contaminated growth hormone causing iatrogenic CJD, and the transplantation of prion-contaminated dura mater and corneal grafts. It is highly suspected that variant CJD can also be transmitted by blood transfusion. 4 However, there is no evidence for bloodborne transmission of non-variant forms of CJD. Familial CJD, GSS, and FFI are all dominantly inherited prion diseases; many different mutations of the PrP gene have been shown to be genetically linked to the development of inherited prion disease. Prions from many cases of inherited prion disease have been transmitted to apes, monkeys, and mice, especially those carrying human PrP transgenes. SPECIAL ISSUES 301
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Biosafety in Microbiological and Bi
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SECTION VIII-H: Prion Diseases 299
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Forward Biosafety in Microbiologica
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Editors: L. Casey Chosewood, MD Dir
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Guest Editors: Matthew J. Arduino,
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Charles B. Millard, PhD Lieutenant
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Robert Bull Karen B. Byers Jane Cap
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Thomas L. Miller Douglas M. Moore M
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Robert Yarchoan Uri Yokel Lisa Youn
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Introduction laboratories chose not
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Introduction RISK CRITERIA FOR ESTA
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Introduction BMBL includes an impor
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Section II Biological Risk Assessme
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Biological Risk Assessment informat
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Biological Risk Assessment The NIH
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Biological Risk Assessment effectiv
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Biological Risk Assessment Third, m
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Biological Risk Assessment 14. Oxma
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Principles of Biosafety Safety equi
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Principles of Biosafety Often an in
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Principles of Biosafety Four standa
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Principles of Biosafety 4. Centers
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Laboratory Biosafety Level Criteria
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Section V Vertebrate Animal Biosafe
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Vertebrate Animal Biosafety Level C
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TABLE 1 SUMMARY OF RECOMMENDED BIOS
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Principles of Laboratory Biosecurit
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Occupational Health and Immunoproph
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Agent Summary Statements - Bacteria
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• Section VIII-B: Fungal Agents A
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Agent Summary Statements - Fungal A
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• Section VIII-C: Parasitic Agent
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Agent Summary Statements - Parasiti
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• Section VIII-D: Rickettsial Age
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Agent Summary Statements - Ricketts
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Agent Summary Statements - Ricketts
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• Section VIII-E: Viral Agents Ag
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Agent Summary Statements - Viral Ag
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Agent Summary Statements - Arboviru
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Agent Summary Statements - Arboviru
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Page 307 and 308: Appendix A Proper maintenance of ca
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Page 323 and 324: Appendix A Development of Containme
Page 325 and 326: Appendix A C. Airflow Smoke Pattern
Page 327 and 328: Appendix A TABLES Table 1. Selectio
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Page 343 and 344: Appendix A REFERENCES 1. Centers fo
Page 345 and 346: Appendix B Decontamination and Disi
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Appendix B dioxide gas exits the ge
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Appendix B d The effectiveness of a
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Appendix C Transportation of Infect
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Appendix C 1600 Clifton Road, N.E.,
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Appendix C disease in humans or in
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Appendix C Biological specimen, Cat
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Appendix D Agriculture Pathogen Bio
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Appendix D simultaneous opening of
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Appendix D 14. Pathological inciner
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Appendix D Wastes and other materia
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Appendix D Camelpox virus b a, b, c
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Appendix D SPECIAL ISSUES The impor
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Appendix D required by the USDA and
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Appendix D depression, anorexia, an
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Appendix D laboratory with enhancem
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Appendix D five day period of conta
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Appendix D slaughterhouses or indus
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Appendix D virus does not cause any
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Appendix D NDV is classified in the
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Appendix D movement permit is requi
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Appendix D Spring Viremia of Carp V
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Appendix D REFERENCES 1. Hess WR. A
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Appendix D 37. Alexander DJ. Newcas
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Appendix E Arthropod Containment Gu
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Appendix F Select Agents and Toxins
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Appendix G IPM issues and requireme
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Appendix H Working with Human, NHP
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Appendix I Guidelines for Work with
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decontaminated periodically, for ex
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0.25N, and/or sodium hypochlorite (
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k Irradiation causes a dose-depende
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7. Morin R, Kozlovac J. Biological
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Appendix J NIH Oversight of Researc
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Appendix K Resources for Informatio
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Appendix K E-mail: http://www2.gsu.
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Appendix K and http://www.who.int/c
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Appendix L HEPA High Efficiency Par
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