Mycoplasma pneumoniae pneumonia

Clinically apparent M. pneumoniae pneumonia accounts for 3 to 10 per cent of infected persons. However, severe diseases, often mimicking necrotizing bacterial pneumonia, have been described. Peribronchial and perivascular lymphoid infiltrates, and bronchitis and bronchiolitis with variable consolidation of alveoli, have been observed in cases that have gone to autopsy. Infection appears to be acquired via inhalation of infected material after exposure to an acutely ill coughing individual. The incubation period is 2 to 3 weeks.

M. pneumoniae is a short Gram-negative rod with a neuraminic acid receptor site at the end for attachment to the host cell membranes. M. pneumoniae escapes phagocytosis because of this specific attachment to the cell membrane. M. pneumoniae is believed to synthesize superoxide radicals and H 2O2, which are toxic to mucosal cells, on the mucosa. Pathogenicity seems to require both properties.

Several classes of antibodies are produced during M. pneumoniae infection. Some are directed against the agent, but do not necessarily confer lifelong immunity as some reinfection can occur. The other are autoantibodies and include agglutinins to the brain, lung, smooth muscle, and cardiolipins. Cold agglutinins are found in half the cases of M. pneumoniae pneumonias at the beginning of the disease, and have been shown to be oligoclonal IgM autoantibodies directed against an altered I-antigen on the surface of erythrocytes of infected patients. A high titer of cold agglutinins can lead to erythrocyte destruction, presumably by complement activation, but rarely to significant hemolysis.

Many findings suggest that immune mechanisms, rather than actual direct infection, may play a role in the development of clinically apparent M. pneumoniae pneumonia as well as some of the extrapulmonary complications. First, M. pneumoniae is able to cause a wide variety of extrapulmonary symptoms but is never isolated from clinical material except sputum or nasopharyngeal secretions. Second, M. pneumoniae or its antigen have seldom been demonstrated in the lungs of patients with fatal pulmonary infection. Evidence has been reported to support the notion that repeated subclinical M. pneumoniae infections with consequent sensitization of T lymphocytes, and probably other components of the immune system (autoantibodies), may be necessary before manifestations such as pneumonitis occur. Third, antithymocyte globulin abrogates or diminishes the severity of experimental M. pneumoniae infection in animals, and corticosteroids have been used with some beneficial clinical effects in patients with severe M. pneumoniae pneumonia. Moreover, pneumonia failed to develop in a group of children with immunodeficiency syndromes who had acquired severe M. pneumoniae respiratory tract infections.

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