M. pneumoniae is a prominent cause of pneumonia, especially in persons 5–20 years of age. Pathogenesis M. pneumoniae is transmitted from person to person by means of infected respiratory secretions. Infection is initiated by attachment of the organism’s tip to a receptor on the sur face of respiratory epithelial cells (Figure 1). Attachment is mediated by a specific adhesin protein on the differentiated terminal structure of the organism. During infection, the organisms remain extracellular.

Fig1. Electron micrograph of M. pneumoniae attached to ciliated respiratory epithelial cells in a sputum sample from a patient with culture-proved M. pneumoniae pneumonia. The organisms (M) are seen on the luminal border attached between cilia (C). (Courtesy AM Collier, Department of Pediatrics, University of North Carolina.)

Clinical Findings

 Mycoplasmal pneumonia is generally a mild disease. The clinical spectrum of M. pneumoniae infection ranges from asymptomatic infection to serious pneumonitis, with occasional neurologic and hematologic (ie, hemolytic anemia) involvement and a variety of possible skin lesions. Bullous myringitis occurs in spontaneous cases and in experimentally inoculated volunteers.

The incubation period varies from 1 to 3 weeks. The onset is usually insidious, with malaise, fever, headache, sore throat, and cough. Initially, the cough is nonproductive, but it is occasionally paroxysmal. Later, there may be blood-streaked sputum and chest pain. Early in the course, the patient appears only moderately ill, and physical signs of pulmonary consolidation are often negligible compared with the striking consolidation seen on radiographs. Later, when the infiltration is at a peak, the illness may be severe. Resolution of pulmonary infiltration and clinical improvement occur slowly over 1–4 weeks. Although the course of the illness is exceedingly variable, death is very rare and is usually attributable to cardiac failure. Complications are uncommon, but hemolytic anemia may occur. The most common pathologic findings in complicated cases are interstitial with peribronchial pneumonitis and necrotizing bronchiolitis. Other diseases less commonly related to M. pneumoniae include erythema multiforme; central nervous system involvement, including meningitis, meningoencepha litis, and mono- and polyneuritis; myocarditis; pericarditis; arthritis; and pancreatitis.

Common causes of community-acquired bacterial pneumonia, in addition to M. pneumoniae, include Streptococcus pneumoniae, Legionella pneumophila, Chlamydia pneumoniae, and Haemophilus influenzae. The clinical presentations of these infections can be very similar, and recognition of the subtleties of signs and symptoms is important. The causative organisms must be determined by sputum examination and culture, blood culture, and other tests.

Laboratory Tests

 The diagnosis of M. pneumoniae pneumonia is largely made by the clinical recognition of the syndrome. Laboratory tests are of secondary value. The white blood cell count may be slightly elevated. A sputum Gram-stain is of value only to identify a non-mycoplasma bacterial pathogen (eg, S. pneumoniae). The causative mycoplasmas can be recovered by culture from the pharynx and from sputum, but culture is a highly specialized test and is almost never done to diagnose M. pneumoniae infection. Cold hemagglutinins for group O human erythrocytes appear in about 50% of untreated patients, in rising titer, with the maximum reached in the third or fourth week after onset. A titer of 1:64 or more supports the diagnosis of M. pneumoniae infection. There is a rise in specific antibodies to M. pneumoniae that is demonstrable by CF tests; acute and convalescent phase sera are necessary to demonstrate a fourfold rise in the CF antibodies. EIA to detect immunoglobulin M (IgM) and IgG antibodies can be highly sensitive and specific and are considered more sensitive than CF tests. Polymerase chain reaction (PCR) assays of specimens from throat swabs or other clinical material can be diagnostic (see earlier discussion).

Treatment

Tetracyclines, macrolides, or fluoroquinolones can produce clinical improvement but do not always eradicate M. pneumoniae, possibly because of their ability to reside intracellularly as well as extracellularly.

Epidemiology, Prevention, and Control

M. pneumoniae infections are endemic all over the world. In populations of children and young adults, where close contact prevails, and in families, the infection rate may be high (50–90%), but the incidence of pneumonitis is variable (3–30%). For every case of frank pneumonitis, there exist several cases of milder respiratory illness. M. pneumoniae is apparently transmitted mainly by direct contact involving respiratory secretions. Second attacks are infrequent. The presence of antibodies to M. pneumoniae has been associated with resistance to infection but may not be responsible for it. Cell-mediated immune reactions occur. The pneumonic process may be attributed in part to an immunologic response rather than only to infection.

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