Mycoplasma pneumonia is an acute inflammatory condition of the respiratory tract and lungs caused by Mycoplasma pneumoniae (MP). It often presents with pharyngitis, bronchitis, and pneumonia simultaneously. Mycoplasma pneumoniae is an important pathogen responsible for community-acquired pneumonia (CAP), accounting for approximately 5%-30% of all CAP cases. It is transmitted via airborne droplets from oral and nasal secretions and occurs sporadically throughout the year, occasionally causing outbreaks of respiratory infections. It primarily affects children and adolescents but is also common in adults. Most cases of Mycoplasma pneumonia are mild and have a good prognosis. However, Mycoplasma pneumoniae infections can lead to severe bilateral pneumonia and extrapulmonary complications involving other systems, such as meningitis, myelitis, myocarditis, pericarditis, immune hemolytic anemia, and nephritis, which may result in death.
Etiology and Pathogenesis
Mycoplasma pneumoniae is the smallest microorganism capable of independent life, existing between bacteria and viruses, and is a facultative anaerobe. It is transmitted to close contacts via aerosolized droplets from respiratory secretions. The incubation period is 2-3 weeks, and its infectivity is relatively low.
Mycoplasma pneumonia is most common in children and young adults. Interstitial pneumonia in infants should also raise suspicion of this disease. MP can be detected in respiratory secretions from 2-3 days before symptom onset until several weeks after recovery. After invading the respiratory tract, Mycoplasma pneumoniae adheres to sialic acid receptors on the surface of respiratory epithelial cells via surface proteins and moves to the base of cilia, protecting itself from clearance by the ciliary system.
Mycoplasma pneumoniae causes bronchial and bronchiolar mucosal damage by inducing immune-mediated injury and releasing toxic metabolic products such as hydrogen peroxide (H2O2) and superoxide radicals. This leads to impaired or absent ciliary motion and may involve the interstitium and alveolar walls. In addition to the direct pathogenic effects of the microorganism, complex immune and pathological mechanisms contribute to the infection and disease development. After MP infection, specific IgM, IgG, and IgA antibodies are produced in the serum, while corresponding secretory antibodies are also produced locally in the respiratory tract. These secretory antibodies provide significant protection, preventing exacerbation of lesions and symptoms during reinfection in children or adolescents. MP infection can also enhance IgE responses, leading to IgE-mediated hypersensitivity reactions and acute asthma exacerbations in patients with asthma.
MP infection can induce the production of various nonspecific antibodies, such as cold agglutinins, MG streptococcal agglutinins, and autoantibodies against the brain, heart, lungs, liver, and smooth muscle, which may contribute to extrapulmonary complications. Additionally, immune complexes containing MP antigens have been detected in the serum of patients with Mycoplasma pneumonia and in the glomeruli of those with nephritis. MP infection can elicit specific cellular immunity, which increases with age, and may also trigger delayed hypersensitivity reactions resembling tuberculin reactions. The presence of shared antigenic components between the MP cell membrane and host cell membranes allows the pathogen to evade immune surveillance, enabling long-term colonization.
Pathology
Pulmonary lesions in Mycoplasma pneumonia include bronchopneumonia, interstitial pneumonia, and bronchiolitis. Alveoli may contain small amounts of exudate, and focal atelectasis may occur. The alveolar walls and septa show infiltration by neutrophils, monocytes, lymphocytes, and plasma cells. Bronchial mucosa is congested, with epithelial cell swelling, cytoplasmic vacuolation, necrosis, and desquamation. Fibrinous exudates and small amounts of pleural effusion may be present in the pleural cavity. Open lung biopsy studies have shown that MP infection can also cause obliterative bronchiolitis with organizing pneumonia.
Clinical Manifestations
The onset of MP infection is gradual, with an asymptomatic period lasting several days to a week, followed by fatigue, headache, sore throat, muscle aches, and a prominent cough. The cough is often paroxysmal and dry, worsening at night, though purulent sputum may occasionally be produced. Persistent paroxysmal severe coughing is a typical feature of Mycoplasma pneumonia. Fever is usually moderate, though it may be absent. Patients may experience pain in the nasopharynx and ears, as well as shortness of breath or dyspnea. Examination may reveal pharyngeal and tympanic membrane congestion, and cervical lymphadenopathy may be present. About 10%-20% of patients develop maculopapular or erythema multiforme rashes. Chest signs are often minimal and do not correlate with the extent of lung involvement. Wheezing, rhonchi, and moist rales may be heard. Lung consolidation signs are rare, and some patients may have no positive findings throughout the course of the disease.
Laboratory and Other Examinations
White blood cell counts are typically normal or slightly elevated, with neutrophil predominance. About 2/3 of patients have a positive cold agglutination test (titer ≥ 1:32) two weeks after disease onset, and a rising titer is more diagnostically significant. A serum MP IgM antibody titer ≥ 1:64 or a fourfold increase in convalescent-phase antibody titers confirms the diagnosis. Direct detection of MP antigens in respiratory specimens allows for early and rapid clinical diagnosis. Techniques such as monoclonal antibody immunoblotting, nucleic acid hybridization, and PCR are highly efficient, specific, and sensitive.
Chest X-rays reveal various infiltrative patterns, often segmentally distributed, with the lower lung fields most commonly affected. Some lesions extend outward from the hilum. The infiltrates typically resolve spontaneously within 3-4 weeks. A small proportion of patients may develop mild pleural effusion.
Diagnosis and Differential Diagnosis
Diagnosis requires a combination of clinical symptoms, chest imaging findings, and serological test results. Although isolating Mycoplasma pneumoniae from cultures is definitive, it has a low detection rate, requires specialized technical conditions, and is time-consuming. Serological tests are of some diagnostic value, particularly when serum antibody titers increase fourfold, though these are often retrospective. Differential diagnosis includes viral pneumonia and Legionella pneumonia. Normal peripheral eosinophil counts help distinguish Mycoplasma pneumonia from eosinophilic lung infiltration.
Treatment
Early administration of appropriate antibiotics can alleviate symptoms and shorten the disease course. Mycoplasma pneumonia is self-limiting, and most cases resolve without treatment. Macrolide antibiotics are the first-line treatment, including erythromycin, roxithromycin, and azithromycin. For patients unresponsive to macrolides, respiratory fluoroquinolones (e.g., levofloxacin, moxifloxacin) or tetracyclines may be used. The typical treatment duration is 2-3 weeks. Since MP lacks a cell wall, antibiotics such as penicillins and cephalosporins are ineffective. For severe coughing, antitussives may be administered. If bacterial co-infection is present, targeted antibiotics should be selected based on microbiological findings.