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NAME: Mycoplasma pneumoniae

SYNONYM OR CROSS REFERENCE: Eaton agent, walking pneumonia, primary atypical pneumonia, pleural atypical pneumonia Footnote 1, Footnote 2.

CHARACTERISTICS: M. pneumoniae is a respiratory tract Gram-negative spindle shaped pleomorphic bacterium, which belongs to the Mycoplasmataceae family, in the Mollicutes class Footnote 1, Footnote 3. It measures 1-2 μm long by 0.1-0.2 μm wide Footnote 4. M. pneumoniae is motile, using gliding motility instead of pili or flagella Footnote 5, Footnote 6. This bacterium lacks the cell wall and its three-layered membrane, leading M. pneumoniae to have a parasitic, intracellular, and saprophytic existence Footnote 7. M. pneumoniae colonies are 100 μm in diameter and a stereomicroscope is necessary to be able to observe them. M. pneumoniae is considered an atypical pathogen which metabolizes glucose.


PATHOGENICITY/TOXICITY: M. pneumoniae is the cause of many upper respiratory tract infections (50% of cases), including primary atypical pneumonia and tracheobrontitis Footnote 2. Those infections may be followed or preceded by complication in 25% of patients. The majority of infected patients are asymptomatic. The disease gradually develops, with a disease onset of days to almost one month, and clinical manifestations include sore throat, hoarseness, fever, cough (may be purulent), headaches, coryza, earache, myalgias, chills, and general malaise Footnote 2. There may also be dyspnea and, in some cases, the cough may take on a pertussis-like character. Some children may develop inflammation of the throat, cervical adenopathy, conjunctivitis, and myringitis. Progression to pneumonia is rare for children under five years of age, but common for those between 5 and 15 years old. Adults usually develop mild disease or are asymptomatic; however, infection can be severe in the elderly or immunocompromised. Individuals with co-morbid conditions, such as functional asplenia, sickle cells disease, and other immunosuppressive states are at greater risk to develop more fulminant pneumonia and joint infection Footnote 2. Complications may occur before, during, or after respiratory symptoms, and may also occur without any respiratory syndrome Footnote 2. The most common complications involve the central nervous system, and may include encephalitis (the most common), coma, optic neuritis, diplopia, acute disseminated encephalomyelitis, mental confusion, cerebellar syndrome and polyradiculitis, cranial nerve palsy, aseptic meningitis and meningoencephalitis, and acute psychosis. Complications affecting the motor system include brachial plexus neuropathy, ataxia, chorioathetosis, and ascending paralysis (Guillain-Barré syndrome). Erythematous macropapular and vesicular rashes (25%), nonspecific myalgia, arthralgias and polyarthropathies (14%), cardiac, gastrointestinal, renal complications, and ears symptoms may also occur.

EPIDEMIOLOGY: M. pneumoniae occurs worldwide, but there are more cases in temperate climates Footnote 2, Footnote 8. There is a slight gender difference in certain age groups. Elderly individuals and infants are less susceptible to pneumonia. Outbreaks tend to occur in late summer and early fall, and there are cyclic epidemics every 3-5 years in civilian and military populations Footnote 1, Footnote 8.

HOST RANGE: Humans are the only known host for M. pneumoniae Footnote 2.

INFECTIOUS DOSE: Less than 100 CFU Footnote 8.

MODE OF TRANSMISSION: M. pneumoniae is principally transmitted by large droplet from person-to-person and may be transmitted by fomites to those in close contact with an infected person. As a result, secondary cases among close contacts are frequent, but since the shedding period is long, contamination may take weeks Footnote 2.

INCUBATION PERIOD: 4 to over 23 days Footnote 2.

COMMUNICABILITY: Transmission rates are high and M. pneumoniae will be shed in upper respiratory infections for 2 to 8 days before onset of symptoms, and as long as 14 weeks after infection Footnote 1, Footnote 8.






DRUG SUSCEPTIBILITY: M. pneumoniae is susceptible to most common antibiotics except nalidixic acid, cephalosporins, penicillins, and rifampicin Footnote 5.

SUSCEPTIBILITY TO DISINFECTANTS: Phenolic disinfectants, 1% sodium hypochlorite, 70% ethanol, formaldehyde, glutaraldehyde, iodophore, and peracedic acid are effective against M. pneumoniae Footnote 9.

PHYSICAL INACTIVATION: M. pneumoniae is inactivated by UV, microwave, gamma radiation, moist heat (121°C for at least 20 min) and dry heat (165-170°C for 2 h) Footnote 10-Footnote 13.

SURVIVAL OUTSIDE HOST: If protected from evaporation, M. pneumoniae can survive for one hour in liquid specimen and can survive for at least 4 hours in air Footnote 3, Footnote 14. Airborne survival time is generally higher when relative humidity (RH) is lower. 50% of the sample survives for 4h at 10% RH, 35% at 25% RH, 20% at 90 % RH and less than 10% at 60 and 80% RH.


SURVEILLANCE: Monitor for symptoms. Diagnosis typically done through the complement fixation test, and culture with immunofluorescent antibody (IFA) test and PCR can also confirm negative results Footnote 15. Serologic tests can also be used, however, results varies according to the presence of HIV.

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

FIRST AID/TREATMENT: Administer appropriate drug therapy Footnote 5.

IMMUNIZATION: Different vaccine strains have been used, but none have been successful at protecting against infection Footnote 16.




SOURCES/SPECIMENS: M. pneumoniae may be found in any type of clinical specimen, but more commonly on specimen from the respiratory tract Footnote 2.

PRIMARY HAZARDS: Laboratory workers should pay attention to droplets exposure on mucous membrane, infectious aerosol and ingestion Footnote 2.



RISK GROUP CLASSIFICATION: Risk Group 2 Footnote 18.

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 to splashes Footnote 19.

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 Footnote 19. Additional precautions should be considered with work involving animals and large scale activities.


SPILLS: Allow aerosols to settle. Wearing protective clothing, gently cover spill with paper towels and apply appropriate disinfectant, starting at perimeter and working towards the centre. Allow sufficient contact time before clean up Footnote 19.

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

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


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 2016

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, 2016



Footnote 1
Atkinson, T. P., Balish, M. F., & Waites, K. B. (2008). Epidemiology, clinical manifestations, pathogenesis and laboratory detection of Mycoplasma pneumoniae infections. FEMS Microbiology Reviews, 32(6), 956-973.

Footnote 2
Waites, K. B., & Talkington, D. F. (2004). Mycoplasma pneumoniae and its role as a human pathogen. Clinical Microbiology Reviews, 17(4), 697.

Footnote 3
Waites, K. B., Rikihisa, Y., & Taylor-Robinson, D. (2003). Mycoplasma and Ureaplasma. In P. R. Murray, E. J. Baron, M. A. Pfaller, J. H. Jorgensen & R. H. Yolken (Eds.), Manual of Clinical Microbiology (8th ed., pp. 972-990). Washington, D.C.: ASM Press.

Footnote 4
Taylor-Robinson, D. (2007). The role of mycoplasmas in pregnancy outcome. Best Practice & Research Clinical Obstetrics & Gynaecology, 21(3), 425-438. doi:DOI: 10.1016/j.bpobgyn.2007.01.011

Footnote 5
Taylor-Robinson, D., & Bebear, C. (1997). Antibiotic susceptibilities of mycoplasmas and treatment of mycoplasmal infections. Journal of Antimicrobial Chemotherapy, 40(5), 622.

Footnote 6
Charon, N. W. (2005). Mycoplasma takes a walk. Proceedings of the National Academy of Sciences of the United States of America, 102(39), 13713-13714. doi:10.1073/pnas.0506508102

Footnote 7
Waites, K. B. (2006). Mycoplasma and ureaplasma. Congenital and Perianal Infections (pp. 271-288) Springer.

Footnote 8
Drew, W. L. (2004). Mycoplasma and Ureaplasma. In K. J. Ryan, & C. G. Ray (Eds.), Sherris Medical Microbiology, 4th edition: an introduction to infectious diseases (pp. 409-413). Washington D.C.: ASM press.

Footnote 9
Collins, C. H., & Kennedy, D. A. (1999). Decontamination. Laboratory-Acquired Infections: History, Incidence, Causes and Prevention. (4th ed., pp. 160-186). London, UK: Buttersworth.

Footnote 10
Katara, G., Hemvani, N., Chitnis, S., Chitnis, V., & Chitnis, D. S. (2008). Surface disinfection by exposure to germicidal UV light. Indian Journal of Medical Microbiology, 26(3), 241-242.

Footnote 11
Wu, Y., & Yao, M.Inactivation of bacteria and fungus aerosols using microwave irradiation. Journal of Aerosol Science, In Press, Corrected Proof doi:DOI: 10.1016/j.jaerosci.2010.04.004

Footnote 12
Farkas, J. (1998). Irradiation as a method for decontaminating food. A review. International Journal of Food Microbiology, 44(3), 189-204.

Footnote 13
Csucos, M., & Csucos, C. (1999). Microbiological obseration of water and wastewater. United States: CRC Press.

Footnote 14
Wright, D. N., Bailey, G. D., & Hatch, M. T. (1968). Role of relative humidity in the survival of airborne Mycoplasma pneumoniae. Journal of Bacteriology, 96(4), 970.

Footnote 15
Mundy, L. M., Gaydos, C. A., Summesgill, J., Ramirez, J., Auwaerter, P., Ford, N., Duffy, L., Casseli, G., Charache, P., & Moore, R. D. (1995). Comparison of laboratory diagnostic methods for Mycoplasma pneumoniae in HIV-positive and HIV-negative patients with community-acquired pneumonia. Abstr Gen Meet Am Soc Microbiol, 95, 297.

Footnote 16
Nicholas, R. A. J., Ayling, R. D., & McAuliffe, L. (2009). Vaccines for Mycoplasma Diseases in Animals and Man. Journal of Comparative Pathology, 140(2-3), 85-96. doi:DOI: 10.1016/j.jcpa.2008.08.004

Footnote 17
Kleemola, M., & Jokinen, C. (1992). Outbreak of Mycoplasma pneumoniae infection among hospital personnel studied by a nucleic acid hybridization test. Journal of Hospital Infection, 21(3), 213-221.

Footnote 18
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).

Footnote 19
Office of Laboratory Security, Public Health Agency of Canada. (Ed.). (2004). Laboratory Biosafety Guidelines. (3rd ed.)