M. pneumoniae is transmitted by respiratory droplets and causes a lower respiratory tract infection (atypical pneumonia, so named because the signs and symptoms are unlike typical lobar pneumonia). The organism accounts for approximately 20 percent of pneumonia cases as well as causing milder infections such as bronchitis, pharyngitis, and nonpurulent otitis media. Infections occur worldwide and year round, with increased incidence in late fall and winter. Cases are usually sporadic, although occasional epidemics among individuals in close contact are reported in both civilian settings (for example, schools and prisons) and among military populations. The highest incidence of clinical disease is seen in older children and young adults (ages 6 to 20 years).

A. Pathogenesis

M. pneumoniae possesses a membrane-associated protein, P1, which functions as a cytoadhesin. It is concentrated in a specialized organelle visible under electron microscopy, which binds sialic acid rich glycolipids found on certain host cell membranes. Among susceptible cell types are ciliated bronchial epithelial cells. The organisms grow closely attached to the host cell luminal surface and inhibit ciliary action. Eventually, patches of affected mucosa desquamate, and an inflammatory response develops in bronchial and adjacent tissues involving lymphocytes and other mononuclear cells. M. pneumoniae produces an exotoxin that is similar to pertussis toxin. The toxin is an adenosine diphosphate–ribosylase and results in extensive vacuolization and death of host cells. In infected individuals, organisms are shed in saliva for several days before onset of clinical illness. Reinfection is common, and symptoms are more severe in older children and young adults who have previously encountered the organism.

B. Clinical significance

Atypical pneumonia (lower respiratory tract disease) is the best-known form of M. pneumoniae infection. However, this disease accounts for a minority of the infectious episodes with this organism, upper respiratory tract and ear infection being much more frequent. Atypical pneumonia clinically resembles pneumonia caused by a number of viruses and bacteria such as Chlamydia species. The incubation period averages 3 weeks. Onset is usually gradual, beginning with nonspecific symptoms such as unrelenting headache, accompanied by fever, chills, and malaise. After 2 to 4 days, a dry or scantily productive cough develops. Earache is sometimes an accompanying complaint. Chest radiographs reveal a patchy, diffuse bronchopneumonia involving one or more lobes (Figure 1). Patients often remain ambulatory throughout the ill ness (hence, “walking pneumonia”). In the absence of preexisting compromise (for example, immunodeficiency or emphysema), the disease remits after 3 to 10 days without specific treatment. X-ray abnormalities resolve more slowly in 2 weeks to 2 months. Complications are rare, but include central nervous system (CNS) disturbances; a rash (erythema multiforme); and mild, hemolytic anemia (the latter associated with production of cold agglutinins, see below). The patient may complain of significant illness despite minimal abnormalities on physical examination.

Fig1. Radiograph of lung of an individual with M. pneumoniae–induced atypical pneumonia.

C. Immunity

Infection with M. pneumoniae elicits both local and systemic immune responses. Only one M. pneumoniae serotype has been described. Serum antibody to outer membrane glycolipids and to the P1 adhesin can be demonstrated, with antibody peaking 2 to 4 weeks after infection and gradually disappearing over the following year. An immunoglobulin M antibody, the cold agglutinin, is produced by approximately 60 percent of infected patients. [Note: This antibody’s name derives from the fact that it reacts with the human erythrocyte antigen I, reversibly agglutinating I⁺ red blood cells at temperatures of 0oC to 4oC but not at 37oC.] Some patients develop very high titers of cold agglutinins. With exposure to cold temperatures this may result in ischemia and even necrosis of distal extremities [hands and feet] because of in vivo clumping of red blood cells.

D. Laboratory identification

Direct microscopic examination of clinical material for M. pneumoniae is of limited value. Sputum is scanty and nonpurulent, and the pathogen stains poorly or not at all using standard bacteriologic stains. Sputum samples or throat swabs can be cultured on special media, but, because isolation of the organism usually requires 8 to 15 days, they cannot aid in early treatment decisions. M. pneumoniae grows under both aerobic and anaerobic conditions and can be isolated on specialized media supplemented with serum. However, the organism is fastidious, and isolation is not commonly performed in clinical laboratories. Serologic tests are the most widely used procedures for establishing a diagnosis of atypical pneumonia due to M. pneumoniae. Specific antibody can be detected by complement fixation, using an extract of mycoplasmal glycolipids. A diagnosis is established by a fourfold rise in titer between acute and convalescent samples. Because symptoms of illness develop slowly, the initial serum sample may be positive. Molecular diagnostics, including polymerase chain reaction (PCR) amplification, are replacing serological tests.

E. Treatment

M. pneumoniae is sensitive to doxycycline, azithromycin, or levofoxacin (see Figure2). When given early, antibiotic treatment shortens the course of disease, although symptoms may be eliminated only gradually. The organisms, however, may persist in the convalescent upper respiratory tract for weeks. Because there is no rapid way to make the diagnosis of M. pneumoniae pneumonia, treatment begins with empiric therapy (most often with macrolide antibiotics) for atypical pneumonia.

Fig2. Summary of Mycoplasma species. 1 Indicates first-line drugs.

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