Mycoplasmas are the smallest free-living organisms. Their genome size is only 10-15% of that of usual bacteria, and they lack the genes necessary for cell wall synthesis. Therefore, antimicrobials that target the cell wall, like beta-lactams, are not effective against mycoplasma.
Mycloplasma pneumoniae is a common cause of acute upper and lower respiratory infections in children and young adults. It is transmitted by respiratory droplets. Previously, pneumonia caused by M. pneumoniae was often referred to as atypical bacterial pneumonia. Before reliable tests became available to accurately diagnose M. pneumoniae, the pneumonia was considered “atypical” because its clinical presentation and response to treatment differed from “typical” bacterial pneumonia.
Mycoplasma pneumoniae infections can occur any time of the year. An estimated 2 million infections are caused by M. pneumoniae each year in the United States. Estimates indicate that approximately 20% of all community-acquired pneumonia is caused by M. pneumoniae.
M. pneumoniae has a lengthy incubation period of 3 weeks, which can result in prolonged outbreaks. Disease onset is insidious. Fever, headache, and malaise occur 2 to 4 days before the onset of respiratory symptoms. Another common clinical syndrome caused by M. pneumoniae is acute or subacute tracheobronchitis.
Extrapulmonary manifestations occur rarely and include erythema nodosum, Stevens-Johnson syndrome, cardiac arrhythmias, pericarditis, myocarditis, coagulopathies, hemolytic anemia and central nervous system involvement. Vascular complications include Raynaud’s phenomenon, which may be associated with the production of cold agglutinins. There is accumulating evidence over the last few years that links M. pneumoniae with chronic asthma in some patients due to persistent infection of the lower respiratory tract.
Most Mycoplasma pneumoniae infections are self-limiting; however, clinicians routinely treat pneumonia caused by M. pneumoniae with antibiotics. Children and adults are usually prescribed a macrolide such as azithromycin.
M. pneumoniae resistance to macrolides has been emerging since the 2000s. Approximately 90% of cases in Asia have become resistant. The United States and Europe have also reported macrolide resistance. Current data suggest that the prevalence of macrolide resistance in M. pneumoniae is approximately 10% in the United States.
Historically, physicians ordered a cold agglutinin titer as a screening test for Mycoplasma infection.. A cold agglutinin titer of 1:32 in the appropriate setting was considered indicative of infection. However, the sensitivity of the cold agglutinin test was low, approximately 50%. The specificity was also low since cold agglutinins are an acute phase reactant and may be seen in a variety of diseases, such as autoimmune disorders, dysproteinemia, lymphoma, legionellosis, and mononucleosis caused by cytomegalovirus or Epstein-Barr virus.
Mycoplasma can be cultured from respiratory tract specimens but it is time consuming because the organism does not grow on routine culture media. Detection usually requires one to two weeks, which limits clinical utility.
M. pneumoniae serology is both sensitive and specific. Enzyme immunoassays are available and have sensitivities and specificities >90%. IgM antibodies are not detectable until approximately 1 week after the onset of illness. Results are reported as negative or positive. The reference value is negative. The presence of IgM antibodies indicates recent infection. The presence of IgG antibody only may indicate recent or past infection and a paired serum sample drawn after 4 weeks may be required to clarify the diagnosis. Specimen requirement is one plain red top tube of blood.
Mycoplasma pneumoniae can be detected much more quickly by polymerase chain reaction (PCR). The test can be performed on a throat swab, saliva, sputum or bronchoalveolar lavage (BAL).
Serologic tests are available but not very specific. Acute and convalescent samples are necessary to diagnose a recent infections.
Preferred specimens for PCR are nasopharyngeal or oropharyngeal swabs. Flocked swabs are preferred. Only sterile Dacron, rayon, or nylon swabs with plastic shafts should be used.
References
Parrott GL, Kinjo T, Fujita J. A compendium for Mycoplasma pneumoniae. Front Microbiol 2016;7:513.
Diaz MH, Benitez AJ, Winchell JM. Investigations of Mycoplasma pneumoniae infections in the United States: trends in molecular typing and macrolide resistance from 2006 to 2013. J Clin Microbiol 2015;53:124–30.