Mycoplasmal pneumonia is an acute inflammatory change of the respiratory tract and lungs caused by Mycoplasma pneumoniae (MP), often accompanied by pharyngitis and bronchitis. Mycoplasma pneumoniae is an important pathogen causing community acquired pneumonia (CAP) in humans, accounting for approximately 5% - 30% of all CAP pathogens. Airborne oral and nasal secretions can cause sporadic cases and outbreaks, predominantly in children and adolescents, but also in adults. Most patients present with mild symptoms and good prognosis, but Mycoplasma pneumoniae infection can also cause severe bilateral pneumonia and other systemic extrapulmonary complications, such as meningitis, myelitis, myocarditis, pericarditis, immune hemolytic anemia, and nephritis, leading to death.
Etiology and pathogenesis
MP is the smallest, facultatively anaerobic microorganism between bacteria and viruses, and can live independently. Mycoplasma in respiratory secretions is transmitted to close contacts in the form of aerosol particles with droplets, with an incubation period of 2 - 3 weeks and low infectiousness. Mycoplasmal pneumonia is mostly found in children and adolescents, and in infants with interstitial pneumonia, the disease should also be considered. MP can be found in respiratory secretions from 2 - 3 days before onset to several weeks after recovery. After Mycoplasma pneumoniae invades the respiratory tract, it adheres to the neuraminic acid receptors on the surface of respiratory epithelial cells with the help of surface proteins, and moves to the basal cilia, thereby protecting the Mycoplasma from clearance by the ciliary system. Mycoplasma pneumoniae causes mucosal damage of the bronchi and bronchioles by inducing immunologic injury and releasing toxic metabolites such as hydrogen peroxide (H2O2) and superoxide, the ciliary movement weakens and even vanishes, and interstitium and alveolar wall can be involved. In addition to the direct pathogenic effect of pathogens, there are also complex immunopathological mechanisms in the infection and pathogenesis. After MP infection, specific IgM, IgG, and IgA are produced in serum, and corresponding secretory antibodies are also produced locally in the respiratory tract. The latter has a strong protective effect, and can prevent exacerbation of symptoms of reinfection in children or adolescents. IgE reaction is also enhanced after MP infection, and IgE-mediated hypersensitivity reactions may occur, which may cause acute attacks in asthma patients. After infection with Mycoplasma pneumoniae, various non-specific antibodies, such as cold agglutinins, streptococcus MG agglutinins, and anti-brain, anti-heart, anti-lung, anti-liver, and anti-smooth muscle autoantibodies can be produced, which may be related to the occurrence of extrapulmonary complications in patients. In addition, there are reports that immune complexes can be detected in the serum of patients with Mycoplasmal pneumonia, and immune complexes containing Mycoplasma pneumoniae antigens can be detected in the glomeruli of patients with complicated nephritis. Specific cellular immunity can be produced after MP infection, which increases with age. Delayed-type hypersensitivity reactions resembling the tuberculin reaction can also occur. The cell membrane of MP and the host cell membrane have common antigenic components, allowing it to evade the immune surveillance and resulting in long-term colonization.
Pathology
Pulmonary lesions include bronchopneumonia, interstitial pneumonia, and bronchiolitis. The alveoli may contain little exudation, and focal atelectasis may occur. The alveolar walls and septa are infiltrated by neutrophils, monocytes, lymphocytes, and plasma cells. The bronchial mucosa is congested, the epithelial cells are swollen, cytoplasmic vacuoles are formed, and there are necrosis and shedding. There may be fibrin exudation and little exudation in the thoracic cavity. Data from lung biopsy show that Mycoplasma pneumoniae infection can also cause bronchiolitis obliterans with organizing pneumonia.
Clinical manifestations
Mycoplasma pneumoniae infection presents with slow onset, asymptomatic period of several days to a week, fatigue, headache, pharyngeal pain, myalgia, and obvious cough, mostly paroxysmal dry cough. Severe cough is usually at night, and purulent expectoration can occur. Persistent paroxysmal cough is a typical manifestation of mycoplasmal pneumonia. Generally, medium-grade fever is present, but fever may be absent. Nasopharyngeal pain, otalgia, tachypnea, and dyspnea may be accompanied. Congestion can be seen in the pharynx and tympanic membrane, and the cervical lymph nodes may be enlarged. 10% - 20% of patients have maculopapular rash or erythema multiforme. Chest signs are not obvious. Sonorous wheezes, sibilant wheezes, and moist crackles can be heard. There are few signs of pulmonary consolidation, and some patients have no positive signs throughout the course of the disease.
Laboratory and auxiliary examinations
The total count of white blood cells is normal or slightly elevated, mostly neutrophils. About 2/3 of patients have a positive cold agglutination test 2 weeks after onset, with a titer ≥ 1:32. If the titer gradually increases, it has more diagnostic value. If the serum mycoplasma IgM antibody ≥ 1:64, or the antibody titer has a fourfold increase in the convalescent stage, the disease can be confirmed. Direct detection of Mycoplasma pneumoniae antigen in respiratory specimens can be used for early rapid clinical diagnosis. Immunoblotting, nucleic acid hybridization, and PCR have the advantages of high efficiency, specificity, and sensitivity.
X-ray shows various forms of segmental infiltration in the lungs, mostly in the lower lung field, and some extend outward from the vicinity of the hilum. The lesions often subside spontaneously in 3 - 4 weeks. Some patients have little pleural effusion.
Diagnosis and differential diagnosis
On the basis of clinical symptoms, x-ray imaging, and serological test result, a diagnosis can be established. Although the isolation of Mycoplasma pneumoniae in culture is decisively significant for diagnosis, its detection rate is low, the technical conditions are high, and the time required is long. Serological tests have a certain reference value, especially in patients with a fourfold increase in serum antibodies, but mostly in retrospective diagnosis. This disease should be differentiated from viral pneumonia and legionella pneumonia. The count of peripheral eosinophils is normal, which can be used to differentiate from pulmonary eosinophilia.
Treatment
The early use of appropriate antibiotics can alleviate symptoms and shorten the course of the disease. This disease is self-limiting, and most patients can heal without treatment. Macrolides, such as erythromycin, roxithromycin, and azithromycin, are preferred. In patients who are not sensitive to macrolides, respiratory fluoroquinolones, such as levofloxacin and moxifloxacin, can be selected. Tetracyclines are also used to treat Mycoplasmal pneumonia. The course of treatment is generally 2 - 3 weeks. Because Mycoplasma pneumoniae has no cell wall, antibiotics such as penicillin or cephalosporin are ineffective. In patients with severe cough, antitussives should be given appropriately. If bacterial infection is complicated, pertinent antibiotics can be selected based on etiological examination.