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EASTERN EQUINE ENCEPHALITIS

PATHOGEN SAFETY DATA SHEET- INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Eastern equine encephalitis (EEEV), Western equine encephalitis (WEEV)

SYNONYM OR CROSS REFERENCE: Alphaviruses, sleeping sickness, encephalitis, EEE, WEE, equine or western equine encephalomyelitis(1-3).

CHARACTERISTICS: EEEV and WEEV belong to the genus Alphavirus within the family Togaviradae(1). They are 65-70 nm in diameter, small, spherical, and enveloped viruses with an icosahedral symmetry and triangulation number of 4(1,4). Their genome is comprised of a single stranded positive sense ssRNA of 11.5 kb(1). They replicate in the cytoplasm, with budding from the plasma membrane(4).

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Eastern equine encephalitis (EEE) is the most severe of the arboviral encephalitides and has a mortality of 50 to 75 %(5). Symptoms of the disease include fever, headache, vomiting, respiratory symptoms, leucocytosis, dizziness, decreasing level of consciousness, tremors, seizures, and focal neurological signs(3,5). Death can occur within 3 to 5 days of infection(5). Those who survive suffer from neurological sequel, including convulsions, paralysis, and mental retardation (5). Brain edema, ischemia, and hypoperfusion are present in early stages of the disease(3). WEEV causes asymptomatic or mild infections in humans, with non-specific symptoms such as sudden onset of fever, headache, nausea, vomiting, anorexia, and malaise(3). Some patients may also present with altered mental status and weakness, with signs of meningeal irritation(3). In rare cases, WEEV infection may cause encephalitis or encephalomyelitis, resulting in neck stiffness, confusion, visual disturbances, photophobia, tonic-clonic seizures, somnolence, coma, and death(2,3). Fifteen to fifty percent of the encephalitis survivors, especially young children, suffer from permanent neurological damage (mental retardation, emotional instability, and spastic paresis)(2,3). Western equine encephalitis virus has mortality range of 3-7 %(3).

EPIDEMIOLOGY: EEEV is widely distributed throughout North, Central, and South America; the Caribbean; coastal region of eastern Canada; Poland; former USSR; Thailand; Philippines; andthe former Czechoslovakia(2,5). In the United States, human infections due to EEEV are usually sporadic, with small outbreaks occurring each summer, mostly along the Atlantic and Gulf coasts(5). Furthermore, the Centers for Disease Control and Prevention reported that 220 confirmed human cases of EEE occurred in the U.S. between the years 1964 to 2004(3). In Canada, infections due EEEV occur mainly in spring and are associated with birds migrating from southern United States to northern Canada(2). WEEV virus is widely distributed along North and South America, but is absent from Central America(2). The Centers for Disease Control and Prevention reported that 639 confirmed human cases of WEE occurred in the U.S. between the years 1964 to 2004(3). Children greater than 14 years of age have a higher chance of acquiring WEEV infection(3).

HOST RANGE: Humans, reptiles, bats, pheasants, wild birds, mosquitoes, horses, dogs, and rodents(2,3).

INFECTIOUS DOSE: Unknown.

MODE OF TRANSMISSION: The primary EEEV and WEEV transmission cycle occurs between birds and mosquitoes (Culiseta melanura for EEEV and Culex tarsalis for WEEV)(2,3). Both viruses are transmitted naturally to humans from bites of arthropods (such as Aedes , Coquillettidia , and Culex spps. for EEEV; and Ochlerotatus melanimon , and Aedes dorsalis for WEEV) which feed on both birds and humans(2,3).

INCUBATION PERIOD: The incubation period exceeds 1 week for EEEV (range of 4-10 days)(3,5). The incubation period for WEEV is 2-7 days(3).

COMMUNICABILITY: Person-to-person transmission has not been reported for EEEV or WEEV viruses. Direct bird-to-human infection can occur although humans and horses are not amplifying hosts as virus titers in their bodies are insufficient to infect mosquitoes(2). Eggs of mosquitoes can be infected by the female(6).

SECTION III - DISSEMINATION

RESERVOIR: Wild birds are the main reservoir for transmission of both EEEV and WEEV virus(2). Humans, horses, and other animals (domestic fowl, feral pigs, cattle and rodents) are not significant reservoir hosts(2). Amphibians and reptiles are a possible reservoir for the virus to overwinter. Mosquitoes and infected eggs are also a reservoir for the viruses(6).

ZOONOSIS: Yes(2). The virus can be transmitted from birds to humans via mosquitoes(2).

VECTOR: Both viruses can be transmitted from pheasants to humans by insect vectors, usually, mosquitoes(7). Aedes sollicitans , Aedes vexans , Coquillettidia , and Culex spps are vectors responsible for transmission of EEEV from birds to humans(2,3). Ochlerotatus melanimon (California), Aedes dorsalis (Utah and New Mexico), and Aedes campestris (New Mexico) are responsible for transmission of WEEV to humans(3).

SECTION IV: STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY/RESISTANCE: None.

SUSCEPTIBILITY TO DISINFECTANTS: EEEV can be inactivated by exposure to 50% ethanol at concentration for 60 minutes(8). Most enveloped viruses are also susceptible to 1% sodium hypochlorite, 2% glutaraldehyde, quaternary ammonium compounds, and phenolics(9,10).

PHYSICAL INACTIVATION: Microbial inactivation is possible using moist and dry heat(11). EEEV can be inactivated by UV rays(12).

SURVIVAL OUTSIDE HOST: Unknown.

SECTION V- FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Both EEEV and WEEV infection can be diagnosed using serological assays such as ELISA to detect IgM antibodies in serum and CSF(2,3). The viruses can be isolated from clinical specimens on Vero cells (African Green Monkey kidney cells)(3). Molecular biology methods such as reverse transcription-polymerase chain reaction (RT-PCR) and real-time RT-PCR can also be used to detect WEEV/EEEV-specific RNA in clinical specimens(2,3). Virus can also be detected in clinical specimens or tissues with direct IFA(2).

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

FIRST AID TREATMENT: Currently no treatment is available for EEEV or WEEV infections(2,5). Symptomatic treatment is given to maintain vital functions of the body(2). Passive and active physiotherapy is used during the recovery phase(2).

IMMUNIZATION: None currently available(13).

PROPHYLAXIS: None.

SECTION VI - LABORATORY HAZARD

LABORATORY ACQUIRED INFECTIONS: Four laboratory-acquired cases of EEEV and sixteen cases of WEEV (with 4 deaths) have been reported(14,15).

SOURCES / SPECIMENS: Infected wild birds; infected mosquitoes; infected pheasants; clinical samples such as blood, CSF, central nervous systems, other tissues(2,3,14).

PRIMARY HAZARDS: Accidental parenteral inoculation, contact of the virus with broken skin or mucous membranes, and bites from infected laboratory arthropods or rodents are the primary hazards associated while working with these viruses(14). Exposure to infectious aerosols may also be a potential hazard(14).

SPECIAL HAZARDS: Infection of newly hatched chickens is hazardous(15).

SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 3(16).

CONTAINMENT REQUIREMENTS: Containment Level 3 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Personnel entering the laboratory should remove street clothing 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(17).

OTHER PRECAUTIONS: All activities with infectious material should be conducted in a biological safety cabinet (BSC) or other appropriate primary containment device in combination with personal protective equipment. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are loaded or unloaded in a biological safety cabinet. 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 animals or large scale activities(17).

SECTION VIII - HANDLING AND STORAGE

SPILLS: Allow aerosols to settle, then, wearing protective clothing, gently cover the spill with absorbent paper towel and apply appropriate disinfectant starting at the perimeter and working towards the center. Allow sufficient contact time before starting the clean up(17).

DISPOSAL: All wastes should be decontaminated before disposal either by steam sterilization, incineration or chemical disinfection(17).

STORAGE: The infectious agent should be stored in a sealed and identified container(17).

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: October 2010

PREPARED BY: Pathogen Regulation Directorate, 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, 2010 Canada

REFERENCES:

  1. Jose, J., Snyder, J. E., & Kuhn, R. (2009). A structural and functional perspective of alphavirus replication and assembly. Future Microbiology, 4 (7), 837-856.
  2. Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., Graevenitz, A. V., & Zahner, H. (2003). Viral Zoonoses: Zoonoses caused by Alphaviruses. Zoonoses: Infectious diseases tranmissible from animals to humans (3rd ed., pp. 6-24). Washington, D.C.: ASM press.
  3. Zacks, M. A., & Paessler, S. (2010). Encephalitic alphaviruses. Veterinary Microbiology, 140 (3-4), 281-286.
  4. Dimmock, N. J., Easton, A. J., & Leppard, K. N. (2007). Appendixes: survey of virus properties. Introduction to modern virology (6th ed., pp. 444-479). Malden, MA: Blackwell publishing.
  5. Petersen, L. R., & Gubler, D. J. (2003). Infection: Viruses: Alphaviruses. In D. A. Warrel, T. M. Cox, J. D. Firth & E. J. Benz (Eds.), Oxford Text Book of Medicine (4th ed., pp. 377- 379). Oxford, New York: Oxford University Press. Retrieved from online.statref.com/Document/Document.aspx?FxId=94&DocId=1&SessionId=121DA8BAMRVOHFWX This link will take you to another Web site (external site)
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  7. Kalluri, S., Gilruth, P., Rogers, D., & Szczur, M. (2007). Surveillance of arthropod vector- borne infectious diseases using remote sensing techniques: A review. PLoS Pathogens, 3(10), 1361-1371.
  8. Ali, Y., Dolan, M. J., Fendler, E. J., & Larson, E. L. (2001). Alcohols. In S. S. Block (Ed.), Disinfection, Sterlization, and Preservation (5th ed., pp. 229-240, 253). Philadephia, PA: Lippincott Williams & Wilkins.
  9. Prince, H. N., & Prince, D. L. (2001). Principles of viral control and transmission. In S. S. Block (Ed.), Disinfection, sterilization and preservation (5th ed., pp. 543-571). Philadelphia, PA: Lippincott Williams & Wilkins.
  10. Collins, C.H., and Kennedy, D.A. (1999). Decontamination. . Laboratory-Acquired Infections: History, Incidence, Causes and Prevention. (4th ed., pp. 160-186, 170-176). London, UK.: Buttersworth.
  11. Joslyn, L. J. (2001). Sterilization by Heat. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 695). Philadelphia: Lippincott Williams & Wilkins.
  12. Aguilar, P. V., Paessler, S., Carrara, A. S., Baron, S., Poast, J., Wang, E., Moncayo, A. C., Anishchenko, M., Watts, D., Tesh, R. B., & Weaver, S. C. (2005). Variation in interferon sensitivity and induction among strains of eastern equine encephalitis virus. Journal of Virology, 79 (17), 11300-11310. doi:10.1128/JVI.79.17.11300-11310.2005
  13. Steele, K. E., & Twenhafel, N. A. (2010). REVIEW PAPER: pathology of animal models of alphavirus encephalitis. Veterinary Pathology, 47 (5), 790-805. doi:10.1177/0300985810372508
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  16. Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57- 58 Elizabeth II, 2009. (2009).
  17. Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.