Public Health Agency of Canada
Symbol of the Government of Canada

Share this page

MEASLES VIRUS

PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Measles virus

SYNONYM OR CROSS REFERENCE: MV, measles, morbilli, rubeola, pneumonia, measles inclusion body encephalitis, encephalomyelitis, atypical measles, subacute sclerosing panencephalitis, red measles, 5 or 10-day measles, hard measles (1-3).

CHARACTERISTICS: Measles virus is a negative-sense, single stranded RNA virus, which belongs to morbillivirus genus in the Paramyxoviridae family (1). It consists of a helical nucleocapsid, 100-300 nm in diameter, surrounded by an envelope. The envelope is lined by matrix proteins and carries transmenbrane hemaglutinin and fusion glycoproteins which are the virulence factors.

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: The Measles virus may cause measles, a systemic infection starting in the respiratory epithelium of the nasopharynx (3, 4). Measles may lead to severe complication and can cause death. After an incubation period of 8-12 days, fever (approximately 38.3°C) and malaise develop over 24 hours (3). These symptoms are followed by cough, coryza (inflammation of the nasal mucous membranes) and conjunctivis. After 2-3 days of cough, coryza and conjunctivitis, Koplik spots (white and granular lesions in the lateral buccal mucosa) appear. On the forth day, a macropapular rash appears on the head and neck, behind the ears. The rash then spreads to the rest of the body and persists for 3-5 days before fading (2). Other symptoms include anorexia and dyspnea (5). Subjective improvement can begin 2-4 days after the rash first appears (3). Infants, pregnant women, immunocompromised and malnourished patients are at a greater risk of developing complications, and experience more severe illness (3, 4). Historically, males have had a higher mortality rate than females, but this difference has tended to decrease with modernization of healthcare in western countries. Common complications include bacterial superinfection, which results in otitis media (middle ear infection), bronchitis, croup and pneumonia (3.5-50% cases), lymphadenopathy, diarrhea and encephalitis (1 in 1,000 cases) (3). Pneumonia is the main cause of mortality. Encephalitis may result in coma and brain damage (25%) or death (15%). Rarer complication includes thrombocytopenic purpura, myocarditis, subacute sclerosing panencephalitis, abdominal pain and acute appendicitis. During pregnancy, measles results in increased risk of spontaneous abortion and preterm birth. In industrialized countries, the fatality rate is 1-2 per 1,000 cases (4), while is it 15-25% in developing countries (2). People vaccinated with killed vaccine (used between 1963 and 1968 and abandoned because protection was too short) or who receive immunoglobulin as a prophylactic measure 6 days after infection may develop atypical measles (4) . They may experience higher fever, prominent rash (often with petechia) on the extremities, and are at a greater risk of developing pneumonia.

EPIDEMIOLOGY: Before vaccine introduction in 1963 in United States, 130 million cases and 7-8 million deaths were estimated to be due to measles and 95-98% of children were infected (4, 6). Endemic in metropolitan centers, measles became epidemic every 2-3 years primarily in late winter and early spring and spread by waves to smaller cities and rural area, where it was more severe (1, 7). Mortality declined in the first half of twentieth century due to life quality improvement. In the 1960’s, vaccine introduction allowed substantial reduction of both incidence and mortality due to measles. Resurgence of disease in 1989-1991 was due to low vaccination coverage amongst certain populations in industrialized countries (4) . Measles is considered eliminated in the Americas and Europe, however occasional outbreaks occur due to imported cases and unvaccinated populations (6). Measles is still a common disease in developing countries (1).

HOST RANGE: Humans are the primary host, but non-human primates can also be a host, and measles is a threat to their conservation (6, 8).

INFECTIOUS DOSE: 0.2 units by intranasal spray (9).

MODE OF TRANSMISSION: Measles can be spread by respiratory droplets and by direct contact with secretions from nose and throat of an infected person (7, 8). Direct contact is the primary mode of transmission, and airborne droplet and indirect contact are less common modes of transmission.

INCUBATION PERIOD: 8-12 days (3).

COMMUNICABILITY: Measles is a highly communicable disease (3). Patients are infectious from the onset of prodomal symptoms until 2-4 days after rash development, but communicability is higher before rash appearance.

SECTION III - DISSEMINATION

RESERVOIR: The only known reservoir is human (4, 6). Even if non-human primates can be infected, the overall population is estimated to be too low to maintain transmission (10).

ZOONOSIS: None known (11), but humans may communicate the disease to non-human primates.

VECTORS: None.

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Measles virus has been reported to be susceptible to Ribavirin, but it is not currently approved for therapeutic use against measles (12).

SUSCEPTIBILITY TO DISINFECTANTS: MV is susceptible to povidone iodine, formaldehyde, 1% sodium hypochlorite, 70% ethanol, glutaraldehyde, phenolic disinfectants, peracetic acid, hydrogen peroxide (13-15).

PHYSICAL INACTIVATION: Heat (30 min at 56°C), UV light, acidic pH, and trypsin (7, 10, 16).

SURVIVAL OUTSIDE HOST: Agent may survive less than 2 hours on surfaces or objects (7). Respiratory droplets can remain infective for at least 1 hour in a close space (17).

SECTION V - FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms, microbiological and serological testing for measles virus or anti-measles antibodies (3).

FIRST AID/TREATMENT: There is currently no treatment for measles other than supportive care. In cases of malnourishment or vitamin A deficiency, vitamin A may be prescribed to help avoid complications (12).

IMMUNIZATION: There is a trivalent vaccine using live-attenuated virus of measles, mumps and rubella (MMR), but this vaccine requires constant cold for storage and transport, which is a problem in developing countries (3, 10). The first dose is given in the first year, and the second at the beginning of schooling (4-6 years of age) to allow full coverage (6). In Canada, vaccination is also recommended for all people born after 1957, because first generation killed vaccine was poorly immunogenic. Before 1957, most people had contracted measles and are considered immune. Pregnant women should not take MMR (3).

PROPHYLAXIS: Immunization with live virus vaccine can be given up to 72 hours post-exposure to prevent measles in unvaccinated persons. Passive immunization with measles immunoglobulin (0.25 mL/kg, for a maximum of 15 mL) between 72 hours and 6 days following exposure or in persons for which measles vaccine is contraindicated can be given to prevent or decrease the severity of measles (3).

SECTION VI - LABORATORY HAZARD

LABORATORY-ACQUIRED INFECTIONS: One case of a laboratory acquired infection up to 1974 (11).

SOURCES/SPECIMENS: MV may be isolated from urine, conjunctiva, nasopharynx, and blood (18).

PRIMARY HAZARDS: Splashing, accidental parenteral inoculation and droplet exposure of mucous membrane may cause a laboratory-acquired infection (13).

SPECIAL HAZARDS: None.

SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2 (19).

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes (20).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities (20).

SECTION VIII - HANDLING AND STORAGE

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

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism by autoclave, chemical disinfection, gamma irradiation, or incineration before disposing.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled.

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: September 2011

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, 2011

Canada

REFERENCES:

  1. Griffin, D. E. (2007). Measles virus. In D. M. Knipe, P. M. Howley, D. E. Griffin, R. A. Lamb, M. A. Martin, B. Roizman & S. E. Straus (Eds.), Fields Virology (pp. 1551-1585). Philadelphia: Wolters Kluwer Health and lippincott Williams & Wilkins.

  2. Ray, C. G. (2004). Mumps virus, Measles, Rubella, and other Childhood Exanthems. In K. J. Ryan, & C. G. Ray (Eds.), Sherris Medical Microbiology (4th ed., pp. 513-539). United State of America: McGraw-Hill.

  3. Signore, C. (2001). Rubeola. Primary Care Update for Ob/Gyns, 8(4), 138-140. doi:DOI: 10.1016/S1068-607X(01)00073-7

  4. Perry, R. T., & Halsey, N. A. (2004). The clinical significance of measles: a review. The Journal of Infectious Diseases, 189 Suppl 1, S4-16. doi:10.1086/377712

  5. Shimatsu, Y., & Fujimori, K. (1999). Pulmonary complications in adult measles. Kansenshogaku Zasshi.the Journal of the Japanese Association for Infectious Diseases, 73(7), 640-645.

  6. Moss, W. J. (2009). Measles control and the prospect of eradication. Current Topics in Microbiology and Immunology, 330, 173-189.

  7. Centers for Disease Control and Prevention. (2009). In Atkinson W., Wolfe S., Hamborsky J. and McIntyre L. (Eds.), Epidemiology and Prevention of Vaccine-Preventable Diseases (11th ed.). Washington D.C.: Public Health Foundation.

  8. Jones-Engel, L., Engel, G. A., Schillaci, M. A., Lee, B., Heidrich, J., Chalise, M., & Kyes, R. C. (2006). Considering human-primate transmission of measles virus through the prism of risk analysis. American Journal of Primatology, 68(9), 868-879. doi:10.1002/ajp.20294

  9. Knudsen, R. C. (2001). Risk assessment for working with infectious agents in the biological laboratory. Applied Biosafety, 6, 19-26.

  10. Moss, W. J., & Griffin, D. E. (2006). Global measles elimination. Nature Reviews.Microbiology, 4(12), 900-908. doi:10.1038/nrmicro1550

  11. Sewell, D. L. (1995). Laboratory-associated infections and biosafety. Clinical Microbiology Reviews, 8(3), 389.

  12. Plemper, R. K., & Snyder, J. P. (2009). Measles control--can measles virus inhibitors make a difference? Current Opinion in Investigational Drugs (London, England: 2000), 10(8), 811-820.

  13. Collins, C. H., & Kennedy, D. A. (1999). Laboratory acquired infections. Laboratory acquired infections: History, incidence, causes and prevention (4th ed., pp. 1-37). Woburn, MA: BH.

  14. Cardoso, A. I., Beauverger, P., Gerlier, D., Wild, T. F., & Rabourdin-Combe, C. (1995). Formaldehyde inactivation of measles virus abolishes CD46-dependent presentation of nucleoprotein to murine class I-restricted CTLs but not to class II-restricted helper T cells. Virology, 212(1), 255-258. doi:10.1006/viro.1995.1479

  15. Kawana, R., Kitamura, T., Nakagomi, O., Matsumoto, I., Arita, M., Yoshihara, N., Yanagi, K., Yamada, A., Morita, O., Yoshida, Y., Furuya, Y., & Chiba, S. (1997). Inactivation of human viruses by povidone-iodine in comparison with other antiseptics. Dermatology (Basel, Switzerland), 195 Suppl 2, 29-35.

  16. Tu, R. (2005). UV-inactivated measles virus stimulates human mice naive lymphocytes to proliferate in vitro. Journal of Medical Virology, 46(2), 133-137.

  17. Bloch, A. B., Orenstein, W. A., Ewing, W. M., Spain, W. H., Mallison, G. F., Herrmann, K. L., & Hinman, A. R. (1985). Measles outbreak in a pediatric practice: airborne transmission in an office setting. Pediatrics, 75(4), 676.

  18. Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., Pfaller, M. A., & Yolken, R. H. (Eds.). (2003). Manual of Clinical Microbiology (8th ed.). Herdon, VA, United States of America: American Society for Microbiology.

  19. Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).

  20. 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.