EBOLA VIRUS – PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/ebola-eng.php

PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

SECTION I – INFECTIOUS AGENT

NAME: Ebolavirus

SYNONYM OR CROSS REFERENCE: African haemorrhagic fever, Ebola haemorrhagic fever (EHF, Ebola HF), filovirus, EBO virus (EBOV), Zaire ebolavirus (ZEBOV), Sudan ebolavirus (SEBOV, SUDV), Ivory Coast ebolavirus (ICEBOV), Tai Forest ebolavirus (TAFV), Ebola-Reston (REBOV, EBO-R, Reston Virus, RESTV), Bundibugyo ebolavirus (BEBOV, BDBV), and Ebola virus disease (EVD) Footnote1 Footnote2 Footnote3 Footnote4.

CHARACTERISTICS: Ebola was discovered in 1976 and is a member of the Filoviridae family (previously part of Rhabdoviridae family, which were later given a family of their own based on their genetic structure). Five Ebola species have been identified: Zaire ebolavirus (ZEBOV), which was first identified in 1976 and is the most virulent; Sudan ebolavirus, (SEBOV); Tai Forest ebolavirus (formerly Ivory Coast ebolavirus); Ebola-Reston (REBOV), originating from the Philippines; and Bundibugyo ebolavirus (BEBOV), the most recent species discovered (2008) Footnote1 Footnote3 Footnote5 Footnote6 Footnote7.

Ebola is an elongated filamentous virus, which can vary between 800 – 1000 nm in length, and can reach up to 14000 nm long (due to concatamerization) with a uniform diameter of 80 nm Footnote2 Footnote5 Footnote8 Footnote9. It contains a helical nucleocapsid (with a central axis), 20 – 30 nm in diameter, and is enveloped by a helical capsid, 40 – 50 nm in diameter, with 5 nm cross-striations Footnote2 Footnote5 Footnote8 Footnote9 Footnote10. The pleomorphic viral fragment may take on several distinct shapes (e.g., in the shape of a “6”, a “U”, or a circle), and are contained within a lipid membraneFootnote2 Footnote5. Each virion contains a single-strand of non-segmented, negative-sense viral genomic RNA Footnote5 Footnote11.

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Ebola virions enter host cells through endocytosis and replication occurs in the cytoplasm. Upon infection, the virus affects the host blood coagulative and immune defence system and leads to severe immunosuppression Footnote10 Footnote12. Early signs of infection are non-specific and flu-like, and may include sudden onset of fever, asthenia, diarrhea, headache, myalgia, arthralgia, vomiting, and abdominal pains Footnote13. Less common early symptoms include conjunctival injection, sore throat, rashes, and bleeding. Shock, cerebral oedema, coagulation disorders, and secondary bacterial infection may co-occur later in infection Footnote8. Haemorrhagic symptoms may begin 4 – 5 days after onset, including hemorrhagic conjunctivitis, pharyngitis, bleeding gums, oral/lip ulceration, hematemesis, melena, hematuria, epistaxis, and vaginal bleeding Footnote14. Hepatocellular damage, marrow suppression (such as thrombocytopenia and leucopenia), serum transaminase elevation, and proteinuria may also occur. Persons that are terminally ill typically present with obtundation, anuria, shock, tachypnea, normothermia to hypothermia, arthralgia, and ocular diseases Footnote15. Haemorrhagic diathesis is often accompanied by hepatic damage and renal failure, central nervous system involvement, and terminal shock with multi-organ failure Footnote1 Footnote2. Contact with the virus may also result in symptoms such as severe acute viral illness, malaise, and maculopapular rash. Pregnant women will usually abort their foetuses and experience copious bleeding Footnote2 Footnote16. Fatality rates range between 50 – 100%, with most dying of hypovolemic shock and multisystem organ failure Footnote17.

Pathogenicity between species of Ebola does not differ greatly in that they have all been associated with hemorrhagic fever outbreaks in humans (excluding Reston) and non-human primates. The Ebola-Zaire and Sudan strains are especially known for their virulence with up to 90% fatality rate Footnote18, with reduced virulence noted in the Tai Forest ebolavirus and the more recently discovered Bundibugyo strain, which caused a single outbreak in Uganda Footnote6 Footnote7. Bundibugyo was the outbreak virus in Isiro, Democratic Republic of Congo, in 2012. Ebola-Reston was isolated from cynomolgus monkeys from the Philippines in 1989 and is less pathogenic in non-human primates. Ebola-Reston virus appears to be non-pathogenic in humans, with reported health effects limited to serological evidence of exposure as identified in 4 animal handlers working with infected non-human primates Footnote19.

EPIDEMIOLOGY: Occurs mainly in areas surrounding rain forests in equatorial Africa Footnote10with the exception of Reston, which has been documented to originate in the Philippines Footnote7. No predispositions to infection have been identified among infected persons.

The largest recorded ebolavirus outbreak to date began in March 2014, with initial cases reported in Guinea and then additional cases identified in the surrounding regions (Liberia, Sierra Leone, Nigeria). A new strain of the ZEBOV species was identified as the causative agent of the outbreak Footnote16 Footnote21 Footnote22.

HOST RANGE: Humans, various monkey species, chimpanzees, gorillas, baboons, and duikers are natural animal hosts for ebolavirus Footnote1 Footnote2 Footnote5 Footnote22 Footnote23 Footnote24 Footnote25 Footnote26 Footnote27 Footnote28 Footnote29 Footnote30 Footnote31. Serological evidence of immunity markers to ebolavirus in serum collected from domesticated dogs suggests asymptomatic infection is plausible, likely following exposure to infected humans or animal carrion Footnote32 Footnote33. The Ebolavirus genome was discovered in two species of rodents and one species of shrew living in forest border areas, raising the possibility that these animals may be intermediary hosts Footnote34. Experimental studies of the virus have been done using mouse, pig, guinea pig, and hamster models, suggesting wild-type ebolavirus has limited pathogenicity in these models Footnote35 Footnote36.

Bats are considered to be a plausible reservoir for the virus. Serological evidence of infection with ebolavirus (antibody detection to EBOV, ZEBOV, and/or REBOV) has been reported in fruit bats collected from woodland and forested areas near Ghana and Gabon, with reduced frequency of isolation from bats collected in mainland China and Bangladesh Footnote37 Footnote38 Footnote39 Footnote40.

INFECTIOUS DOSE: Viral hemorrhagic fevers have an infectious dose of 1 – 10 organisms by aerosol in non-human primates Footnote41.

MODE OF TRANSMISSION: In an outbreak, it is hypothesized that the first patient becomes infected as a result of contact with an infected animal Footnote22. Person-to-person transmission occurs via close personal contact with an infected individual or their body fluids during the late stages of infection or after death Footnote1 Footnote2 Footnote22 Footnote42. Nosocomial infections can occur through contact with infected body fluids for example due to the reuse of unsterilized syringes, needles, or other medical equipment contaminated with these fluids Footnote1 Footnote2. Humans may be infected by handling sick or dead non-human primates and are also at risk when handling the bodies of deceased humans in preparation for funerals Footnote2 Footnote10 Footnote43.

In laboratory settings, non-human primates exposed to aerosolized ebolavirus from pigs have become infected, however, airborne transmission has not been demonstrated between non-human primates Footnote1 Footnote10 Footnote15 Footnote44 Footnote45. Viral shedding has been observed in nasopharyngeal secretions and rectal swabs of pigs following experimental inoculation Footnote29 Footnote30.

INCUBATION PERIOD: Two to 21 days Footnote1 Footnote15 Footnote17.

COMMUNICABILITY: Communicable as long as blood, body fluids or organs, contain the virus. Ebolavirus has been isolated from semen 61 to 82 days after the onset of illness, and transmission through semen has occurred 7 weeks after clinical recovery Footnote1 Footnote2 Footnote59 Footnote60.

SECTION III – DISSEMINATION

RESERVOIR: The natural reservoir of Ebola is unknown Footnote1 Footnote2. Antibodies to the virus have been found in the serum of domestic guinea pigs and wild rodents, with no relation to human transmission Footnote34 Footnote47. Serum antibodies and viral RNA have been identified in some bat species, suggesting bats may be a natural reservoir Footnote37 Footnote38 Footnote39 Footnote40.

ZOONOSIS: Zoonosis between humans and animal is suspected Footnote2 Footnote22 Footnote37.

VECTORS: Unknown.

SECTION IV – STABILITY AND VIABILITY

All information available on stability and viability comes from peer-reviewed literature sources depicting experimental findings and is intended to support local risk assessments in a laboratory setting.

DRUG SUSCEPTIBILITY: Unknown. Although clinical trials have been completed, no vaccine has been approved for treatment of ebolavirus. Similarly, no post-exposure measures have been reported as effective in treating ebolavirus infection in humans although several studies have been completed in animals to determine the efficacy of various treatments.

DRUG RESISTANCE: There are no known antiviral treatments available for human infections.

SUSCEPTIBILITY TO DISINFECTANTS: Ebolavirus is susceptible to 3% acetic acid, 1% glutaraldehyde, alcohol-based products, and dilutions (1:10-1:100 for ≥10 minutes) of 5.25% household bleach (sodium hypochlorite), and calcium hypochlorite (bleach powder)Footnote48 Footnote49 Footnote50 Footnote62 Footnote63. The WHO recommendations for cleaning up spills of blood or body fluids suggest flooding the area with a 1:10 dilutions of 5.25% household bleach for 10 minutes for surfaces that can tolerate stronger bleach solutions (e.g., cement, metal) Footnote62. For surfaces that may corrode or discolour, they recommend careful cleaning to remove visible stains followed by contact with a 1:100 dilution of 5.25% household bleach for more than 10 minutes.

PHYSICAL INACTIVATION: Ebola are moderately thermolabile and can be inactivated by heating for 30 minutes to 60 minutes at 60°C, boiling for 5 minutes, or gamma irradiation (1.2 x106 rads to 1.27 x106 rads) combined with 1% glutaraldehyde Footnote10 Footnote48 Footnote50. Ebolavirus has also been determined to be moderately sensitive to UVC radiation Footnote51.

SURVIVAL OUTSIDE HOST: Filoviruses have been reported capable to survive for weeks in blood and can also survive on contaminated surfaces, particularly at low temperatures (4°C)Footnote52 Footnote61. One study could not recover any Ebolavirus from experimentally contaminated surfaces (plastic, metal or glass) at room temperature Footnote61.  In another study, Ebolavirus dried onto glass, polymeric silicone rubber, or painted aluminum alloy is able to survive in the dark for several hours under ambient conditions (between 20 and 250C and 30–40% relative humidity) (amount of virus reduced to 37% after 15.4 hours), but is less stable than some other viral hemorrhagic fevers (Lassa) Footnote53. When dried in tissue culture media onto glass and stored at 4 °C, Zaire ebolavirus survived for over 50 days Footnote61. This information is based on experimental findings only and not based on observations in nature. This information is intended to be used to support local risk assessments in a laboratory setting.

A study on transmission of ebolavirus from fomites in an isolation ward concludes that the risk of transmission is low when recommended infection control guidelines for viral hemorrhagic fevers are followed Footnote64. Infection control protocols included decontamination of floors with 0.5% bleach daily and decontamination of visibly contaminated surfaces with 0.05% bleach as necessary.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Definitive diagnosis can be reached rapidly in an appropriately equipped laboratory using a multitude of approaches, including RT-PCR to detect viral RNA, ELISA based techniques to detect anti-Ebola antibodies or viral antigens, immunoelectron microscopy to detect ebolavirus particles in tissues and cells, and indirect immunofluorescence to detect antiviral antibodies Footnote1 Footnote2 Footnote14 Footnote41. It is useful to note that the Marburg virus is morphologically indistinguishable from the ebolavirus, and laboratory surveillance of Ebola is extremely hazardous Footnote1 Footnote2 Footnote14 Footnote54. Please see the interim biosafety guidelines for laboratories handling specimens from patients under investigationfor EVD for more information.

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: There is no effective antiviral treatment Footnote27 Footnote37. Instead, treatment is supportive, and is directed at maintaining organ function and electrolyte balance and combating haemorrhage and shock Footnote22 Footnote55.

IMMUNIZATION: None Footnote27.

PROPHYLAXIS: None. Management of the Ebola virus is solely based on isolation and barrier-nursing with symptomatic and supportive treatments Footnote8.

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: One reported near-fatal case following a minute finger prick in an English laboratory (1976) Footnote56. A Swiss zoologist contracted Ebola virus after performing an autopsy on a chimpanzee in 1994 Footnote2 Footnote57. An incident occurred in Germany in 2009 when a laboratory scientist pricked herself with a needle that had just been used on a mouse infected with Ebola; however, human infection was not confirmed. Additional incidents were recorded in the US in 2004, and a fatal case in Russia in 2004 Footnote8.

SOURCES/SPECIMENS: Blood, serum, urine, respiratory and throat secretions, semen, and organs or their homogenates from human or animal hosts Footnote1 Footnote2 Footnote53. Human or animal hosts, including non-human primates, may represent a further source of infection Footnote54.

PRIMARY HAZARDS: Accidental parenteral inoculation, respiratory exposure to infectious aerosols/droplets, and/or direct contact with skin or mucous membranes Footnote54.

SPECIAL HAZARDS: Work with, or exposure to, infected non-human primates, rodents, or their carcasses represents a risk of human infection Footnote54.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 4 Footnote58.

CONTAINMENT REQUIREMENTS: Containment Level 4 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, and cultures. Please see the interim biosafety guidelines for laboratories handling specimens from patients under investigation for EVD for more information.

PROTECTIVE CLOTHING: Personnel entering the laboratory must remove street clothing, including undergarments, and jewellery, and change into dedicated laboratory clothing and shoes, or don full coverage protective clothing (i.e., completely covering all street clothing). Additional protection may be worn over laboratory clothing when infectious materials are directly handled, such as solid-front gowns with tight fitting wrists, gloves, and respiratory protection. Eye protection must be used where there is a known or potential risk of exposure to splashes.

OTHER PRECAUTIONS: All activities with infectious material should be conducted in a biological safety cabinet (BSC) in combination with a positive pressure suit, or within a class III BSC line. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are unloaded in a biological safety cabinet. The integrity of positive pressure suits must be routinely checked for leaks. The use of needles, syringes, and other sharp objects should be strictly limited. Open wounds, cuts, scratches, and grazes should be covered with waterproof dressings. Additional precautions should be considered with work involving animal activities.

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean-up.

DISPOSAL: Decontaminate all materials for disposal from the containment laboratory by steam sterilisation, chemical disinfection, incineration or by gaseous methods. Contaminated materials include both liquid and solid wastes.

STORAGE: In sealed, leak-proof containers that are appropriately labelled and locked in a Containment Level 4 laboratory.

SECTION IX – REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: August 2014.

PREPARED BY: Centre for Biosecurity, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©

Public Health Agency of Canada, 2014
Canada

REFERENCES

Footnote1
Plague. (2004). In R. G. Darling, & J. B. Woods (Eds.), USAMRIID’s Medical Management of Biological Casualties Handbook (5th ed., pp. 40-44). Fort Detrick M.D.: USAMRIID.
Footnote2
Acha, P. N., & Szyfres, B. (2003). In Pan American Health Organization (Ed.), Zoonoses and Communicable Diseases Common to Man and Animals (3rd ed., pp. 142-145). Washington D.C.: Pan American Health Organization.
Footnote3
International Committee on Taxonomy of Viruses (2013 Release). Virus Taxonomy. Ebolavirus. http://www.ictvonline.org/virusTaxonomy.asp
Footnote4
Kuhn, J. H., Becker, S., Ebihara, H., Geisbert, T. W., Johnson, K. M., Kawaoka, Y., Lipkin IW, Negredo AI, Netesov SV, Nichol ST, Palacios G, Peters CJ, Tenorio A, Volchokov VE, & Jahrling, P. B. (2010). Proposal for a revised taxonomy of the family Filoviridae: classification, names of taxa and viruses, and virus abbreviations. Archives of virology, 155(12), 2083-2103.
Footnote5
Sanchez, A. (2001). Filoviridae: Marburg and Ebola Viruses. In D. M. Knipe, & P. M. Howley (Eds.), Fields virology (4th ed., pp. 1279-1304). Philadelphia, PA.: Lippencott-Ravenpp.
Footnote6
Takada, A., & Kawaoka, Y. (2001). The pathogenesis of Ebola hemorrhagic fever. Trends in Microbiology, 9(10), 506-511.
Footnote7
Towner, J. S., Sealy, T. K., Khristova, M. L., Albarino, C. G., Conlan, S., Reeder, S. A., Quan, P. L., Lipkin, W. I., Downing, R., Tappero, J. W., Okware, S., Lutwama, J., Bakamutumaho, B., Kayiwa, J., Comer, J. A., Rollin, P. E., Ksiazek, T. G., & Nichol, S. T. (2008). Newly discovered ebola virus associated with hemorrhagic fever outbreak in Uganda. PLoS Pathogens, 4(11), e1000212.
Footnote8
Feldmann, H. (2010). Are we any closer to combating Ebola infections? Lancet, 375(9729), 1850-1852. doi:10.1016/S0140-6736(10)60597-1.
Footnote9
Beran, G. W. (Ed.). (1994). Handbook of Zoonosis, Section B: Viral (2nd ed.). Boca Raton, Florida: CRC Press, LLC.
Footnote10
Mwanatambwe, M., Yamada, N., Arai, S., Shimizu-Suganuma, M., Shichinohe, K., & Asano, G. (2001). Ebola hemorrhagic fever (EHF): mechanism of transmission and pathogenicity. Journal of Nippon Medical School.68(5), 370-375.
Footnote11
Sanchez, A., Kiley, M. P., Klenk, H. D., & Feldmann, H. (1992). Sequence analysis of the Marburg virus nucleoprotein gene: comparison to Ebola virus and other non-segmented negative-strand RNA viruses. The Journal of General Virology, 73 (Pt 2)(Pt 2), 347-357.
Footnote12
Harcourt, B. H., Sanchez, A., & Offermann, M. K. (1999). Ebola virus selectively inhibits responses to interferons, but not to interleukin-1beta, in endothelial cells. Journal of Virology, 73(4), 3491-3496.
Footnote13
Bwaka, M. A., Bonnet, M. J., Calain, P., Colebunders, R., De Roo, A., Guimard, Y., Katwiki, K. R., Kibadi, K., Kipasa, M. A., Kuvula, K. J., Mapanda, B. B., Massamba, M., Mupapa, K. D., Muyembe-Tamfum, J. J., Ndaberey, E., Peters, C. J., Rollin, P. E., Van den Enden, E., & Van den Enden, E. (1999). Ebola hemorrhagic fever in Kikwit, Democratic Republic of the Congo: clinical observations in 103 patients. The Journal of Infectious Diseases, 179 Suppl 1, S1-7.
Footnote14
Zilinskas, R. A. (Ed.). (2000). Biololgical Warfare – Modern Offense and Defense. Boulder, Colorado, USA: Lynne Rienner Publishers, Inc.
Footnote15
Feigin, R. D. (Ed.). (2004). Textbook of Pediatric Infectious Diseases (5th ed.). Philadelphia, USA: Elsevier, Inc.
Footnote16
Baize, S., Pannetier, D., Oestereich, L., Rieger, T., Koivogui, L., Magassouba, N., Soropogui, B., Sow, M. S., Keita, S., De Clerck, H., Tiffany, A., Dominguez, G., Loua, M., Traore, A., Kolie, M., Malano, E. R., Heleze, E., Bocquin, A., Mely, S., Raoul, H., Caro, V., Cadar, D., Gabriel, M., Pahlmann, M., Tappe, D., Schmidt-Chanasit, J., Impouma, B., Diallo, A.K., Formenty, P., Van Herp, M., & Gunther, S. (2014). Emergence of Zaire Ebola Virus Disease in Guinea – Preliminary Report. The New England Journal of Medicine. Epub ahead of print.
Footnote17
Casillas, A. M., Nyamathi, A. M., Sosa, A., Wilder, C. L., & Sands, H. (2003). A current review of Ebola virus: pathogenesis, clinical presentation, and diagnostic assessment. Biological Research for Nursing, 4(4), 268-275.
Footnote18
World Health Organization. Ebola Virus Disease – Fact Sheet N°103. Updated April 2014.
Footnote19
Centers for Disease Control and Prevention. (1990). Epidemiologic notes and reports updates: filovirus infection in animal handlers. MMWR, 39, 221.
Footnote20
World Health Organization. Global Alert and Response (GAR) – Ebola virus disease update – West Africa. Disease outbreak news. August 6 2014
Footnote21
Centres for Disease Control. 2014 Ebola Outbreak in West Africa (Guinea, Liberia, Sierra Leone and Nigeria. August 6 2014
Footnote22
Bausch, D. G., Jeffs B.S.A.G, & Boumandouki, P. (2008). Treatment of Marburg and Ebola haemorrhagic fevers: a strategy for testing new drugs and vaccines under outbreak conditions. Antiviral Res., 78(1), 150-161.
Footnote23
WHO Disease Outbreak News – Ebola Haemorrhagic Fever in the Democratic Republic of Congo. (2007). 2008
Footnote24
WHO Disease Outbreak News – Ebola Haemorrhagic Fever in Uganda – Update. (2007). 2008
Footnote25
Formenty, P., Boesch, C., Wyers, M., Steiner, C., Donati, F., Dind, F., Walker, F., & Le Guenno, B. (1999). Ebola virus outbreak among wild chimpanzees living in a rain forest of Cote d’Ivoire. The Journal of Infectious Diseases, 179 Suppl 1, S120-6. doi:10.1086/514296.
Footnote26
Bray, M. (2003). Defense against filoviruses used as biological weapons. Antiviral Research, 57(1-2), 53-60.
Footnote27
Leroy, E. M., Rouquet, P., Formenty, P., Souquière, S., Kilbourne, A., Froment, J., Bermejo, M., Smit, S., Karesh, W., Swanepoel, R., Zaki, S. R., & Rollin, P. E. (2004). Multiple Ebola Virus Transmission Events and Rapid Decline of Central African Wildlife. Science, 303(5656), 387-390.
Footnote28
Nfon, C. K., Leung, A., Smith, G., Embury-Hyatt, C., Kobinger, G., & Weingartl, H. M. (2013). Immunopathogenesis of severe acute respiratory disease in Zaire ebolavirus-infected pigs. PloS one, 8(4), e61904.
Footnote29
Kobinger, G. P., Leung, A., Neufeld, J., Richardson, J. S., Falzarano, D., Smith, G., Tierney, K., Patel, A., & Weingartl, H. M. (2011). Replication, pathogenicity, shedding, and transmission of Zaire ebolavirus in pigs. Journal of Infectious Diseases, jir077.
Footnote30
Marsh, G. A., Haining, J., Robinson, R., Foord, A., Yamada, M., Barr, J. A., Payne, J., White, J., Yu, M., Bingham, J., Rollin, P. E., Nichol, S. T., Wang, L-F., & Middleton, D. (2011). Ebola Reston virus infection of pigs: clinical significance and transmission potential. Journal of Infectious Diseases, 204(suppl 3), S804-S809.
Footnote31
Morris, K. (2009). First pig-to-human transmission of Ebola Reston virus.9(3), 148.
Footnote32
Allela, L., Bourry, O., Pouillot, R., Délicat, A., Yaba, P., Kumulungui, B., Rougquet, P., Gonzalez, J-P., & Leroy, E. M. (2005). Ebola virus antibody prevalence in dogs and human risk. Emerg Infect Dis, 11(3), 385-90.
Footnote33
Olson, S. H., Reed, P., Cameron, K. N., Ssebide, B. J., Johnson, C. K., Morse, S. S., Karesh, W. B.., Mazet, J. A. K., & Joly, D. O. (2012). Dead or alive: animal sampling during Ebola hemorrhagic fever outbreaks in humans. Emerging health threats journal, 5.
Footnote34
Morvan, J. M., Nakouné, E., Deubel, V., & Colyn, M. (2000). Ebola virus and forest ecosystem. [Écosystèmes forestiers et virus Ebola] Bulletin De La Societe De Pathologie Exotique, 93(3), 172-175.
Footnote35
Connolly, B. M., Steele, K. E., Davis, K. J., Geisbert, T. W., Kell, W. M., Jaax, N. K., & Jahrling, P. B. (1999). Pathogenesis of experimental Ebola virus infection in guinea pigs. The Journal of Infectious Diseases, 179 Suppl 1, S203-17.
Footnote36
Ebihara, H., Zivcec, M., Gardner, D., Falzarano, D., LaCasse, R., Rosenke, R., Long, D., Haddock, E., Fischer, E., Kawaoka, Y., & Feldmann, H. (2012). A Syrian golden hamster model recapitulating Ebola hemorrhagic fever. Journal of Infectious Diseases, jis626.
Footnote37
Leroy, E. M., Kumulungui, B., Pourrut, X., Rouquet, P., Hassanin, A., Yaba, P., Délicat, A., Paweska, J. T., Gonzalez, J., & Swanepoel, R. (2005). Fruit bats as reservoirs of Ebola virus. Nature, 438(7068), 575-576.
Footnote38
Hayman, D. T., Yu, M., Crameri, G., Wang, L. F., Suu-Ire, R., Wood, J. L., & Cunningham, A. A. (2012). Ebola virus antibodies in fruit bats, Ghana, West Africa. Emerging infectious diseases, 18(7), 1207.
Footnote39
Yuan, J., Zhang, Y., Li, J., Zhang, Y., Wang, L. F., & Shi, Z. (2012). Serological evidence of ebolavirus infection in bats, China. Virol. J, 9, 236.
Footnote40
Olival, K. J., Islam, A., Yu, M., Anthony, S. J., Epstein, J. H., Khan, S. A., Khan, S. U., Crameri, G., Wang, L-F., Lipkin, W. I., Luby, S. P., & Daszak, P. (2013). Ebola virus antibodies in fruit bats, Bangladesh. Emerging infectious diseases, 19(2), 270.
Footnote41
Franz, D. R., Jahrling, P. B., Friedlander, A. M., McClain, D. J., Hoover, D. L., Bryne, W. R., Pavlin, J. A., Christopher, G. W., & Eitzen, E. M. (1997). Clinical recognition and management of patients exposed to biological warfare agents. Jama, 278(5), 399-411.
Footnote42
Arthur, R. R. (2002). Ebola in Africa–discoveries in the past decade. Euro Surveillance : Bulletin Europeen Sur Les Maladies Transmissibles = European Communicable Disease Bulletin, 7(3), 33-36.
Footnote43
Hewlett, B. S., & Amolat, R. P. (2003). Cultural contexts of Ebola in Northern Uganda. Emerging Infectious Diseases, 9(10), 1242-1248.
Footnote44
Reed, D. S., Lackemeyer, M. G., Garza, N. L., Sullivan, L. J., & Nichols, D. K. (2011). Aerosol exposure to Zaire ebolavirus in three nonhuman primate species: differences in disease course and clinical pathology. Microbes and Infection, 13(11), 930-936.
Footnote45
Twenhafel, N. A., Mattix, M. E., Johnson, J. C., Robinson, C. G., Pratt, W. D., Cashman, K. A., Wahl-Jensen, V., Terry, C., Olinger, G. G., Hensley, L. E., & Honko, A. N. (2012). Pathology of experimental aerosol Zaire ebolavirus infection in rhesus macaques. Veterinary Pathology Online, 0300985812469636.
Footnote46
Weingartl, H. M., Embury-Hyatt, C., Nfon, C., Leung, A., Smith, G., & Kobinger, G. (2012). Transmission of Ebola virus from pigs to non-human primates. Scientific reports, 2.
Footnote47
Stansfield, S. K., Scribner, C. L., Kaminski, R. M., Cairns, T., McCormick, J. B., & Johnson, K. M. (1982). Antibody to Ebola virus in guinea pigs: Tandala, Zaire. The Journal of Infectious Diseases, 146(4), 483-486.
Footnote48
Mitchell, S. W., & McCormick, J. B. (1984). Physicochemical inactivation of Lassa, Ebola, and Marburg viruses and effect on clinical laboratory analyses. Journal of Clinical Microbiology, 20(3), 486-489.
Footnote49
Elliott, L. H., McCormick, J. B., & Johnson, K. M. (1982). Inactivation of Lassa, Marburg, and Ebola viruses by gamma irradiation. Journal of Clinical Microbiology, 16(4), 704-708.
Footnote50
World Health Organization. Interim Infection Control Recommendationsfor Care of Patients with Suspected or Confirmed Filovirus (Ebola, Marburg) Haemorrhagic Fever. March 2008
Footnote51
Sagripanti, J. L., & Lytle, C. D. (2011). Sensitivity to ultraviolet radiation of Lassa, vaccinia, and Ebola viruses dried on surfaces. Archives of virology, 156(3), 489-494.
Footnote52
Belanov, E. F., Muntianov, V. P., Kriuk, V., Sokolov, A. V., Bormotov, N. I., P’iankov, O. V., & Sergeev, A. N. (1995). [Survival of Marburg virus infectivity on contaminated surfaces and in aerosols]. Voprosy virusologii, 41(1), 32-34.
Footnote53
Sagripanti, J-L., Rom, A.M., Holland, L.E. (2010) Persistence in darkness of virulent alphaviruses, Ebola virus, and Lass virus deposited on solid surfaces. Arch Virol. 155: 2035-9.
Footnote54
Biosafety in Microbiological and Biomedical Laboratories (BMBL) (2007). In Richmond J. Y., McKinney R. W. (Eds.), . Washington, D.C.: Centers for Disease Control and Prevention.
Footnote55
Clark, D. V., Jahrling, P. B., & Lawler, J. V. (2012). Clinical Management of Filovirus-Infected Patients. Viruses, 4(9), 1668-1686.
Footnote56
Emond, R. T. D., Evans, B., Bowen, E. T. W., & Lloyd, G. (1977). A case of Ebola virus infection. British Medical Journal, 2(6086), 541-544.
Footnote57
Formenty, P., Hatz, C., Le Guenno, B., Stoll, A., Rogenmoser, P., & Widmer, A. (1999). Human infection due to Ebola virus, subtype Cote d’Ivoire: Clinical and biologic presentation. Journal of Infectious Diseases, 179(SUPPL. 1), S48-S53.
Footnote58
Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).
Footnote59
Rowe AK, Bertolli J,Khan AS,et al. Clinical, virologic, and immunologic follow-up of convalescent Ebola hemorrhagic fever patients and their household contacts, Kikwit, Democratic Republic of the Congo. Commission de Lutte contre les Epidemies à Kikwit. J Infect Dis 1999;179 (Suppl 1):S28-35.
Footnote60
Rodriguez LL, De Roo A, Guimard Y, et al. Persistence and genetic stability of Ebola virus during the outbreak in Kikwit, Democratic Republic of the Congo, 1995. J Infect Dis 1999;179 (Suppl 1):S170-6.
Footnote61
Piercy, T.J., Smither, S.J., Steward, J.A., Eastaugh, L., Lever, M.S. (2010) The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. J Appl Microbiol. 109(5): 1531-9.
Footnote62
World Health Organization (2010). WHO best practices for injections and related procedures toolkit. March 2010. http://whqlibdoc.who.int/publications/2010/9789241599252_eng.pdf?ua=1
Footnote63
World Health Organization (2014). Interim infection prevention and control guidance for care of patients with suspected or confirmed filovirus haemorrhagic fever in health-care settings, with focus on Ebola. August 2014.
http://www.who.int/csr/resources/who-ipc-guidance-ebolafinal-09082014.pdf
Footnote64
Baush, D.G., Towner, J.S., Dowell, S.F., Kaducu, F., Lukwiya, M., Sanchez, A., Nichol, S.T., Ksiazek, T.G., Rollin, P.E. (2007) Assessment of the Risk of Ebola virus Transmission from Bodily Fluids and Fomites. JID. 196 (Suppl 2).
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