100 MYCOPLASMA INFECTIONS
Harrison’s Manual of Medicine
Mycoplasmas, which are ubiquitous in nature, are the smallest free-living microorganisms and lack rigid cell walls.
EPIDEMIOLOGY A common cause of upper and lower respiratory tract infection, M. pneumoniae is the most important pathogen of the Mycoplasma group. Infection is acquired by inhalation of aerosols, with an incubation period of 2–3 weeks. Although epidemics can occur in closed populations (e.g., those of schools and military installations), most cases occur sporadically or in families.
CLINICAL MANIFESTATIONS The most common clinical syndrome is acute or subacute tracheobronchitis accompanied by upper respiratory tract symptoms. Pneumonitis is also common. Symptoms generally include headache, malaise, fever [38.9–39.4°C (102–103°F)], sore throat, and a dry paroxysmal cough that later becomes productive. Extrapulmonary manifestations are unusual but may be the only clue that the respiratory infection is mycoplasmal. These manifestations can include otitis media, bullous myringitis, maculopapular rashes, erythema multiforme, and occasionally Stevens-Johnson syndrome. Cardiac abnormalities, including myocarditis and pericarditis, may develop. Neurologic conditions that have been associated with M. pneumoniae include meningoencephalitis, cerebellar ataxia, Guillain-Barré syndrome, transverse myelitis, and peripheral neuropathies. Arthralgias are not unusual, and arthritis can be seen in pts with hypogammaglobulinemia. M. pneumoniae infection may be particularly severe in pts with sickle cell disease, possibly because of functional asplenia.
DIAGNOSIS Clinical, radiologic, and laboratory findings in M. pneumoniae infection are not sufficiently distinctive for diagnostic purposes. The leukocyte count is somewhat elevated. The CXR may show reticulonodular or interstitial infiltrates, primarily in the lower lobes. However, these radiographic abnormalities may be more prominent than would be predicted by auscultation of the chest. Because it lacks a cell wall, M. pneumoniae cannot be seen on Gram’s stain of sputum. Definitive diagnosis is difficult during acute infection, since most clinical laboratories do not have the capability to isolate the organism. Specific antibodies can be detected by ELISA, indirect immunofluorescence, or CF but do not develop early enough to aid in pt management. Examination of paired acute- and convalescent-phase serum specimens taken 2– 4 weeks apart is required for good sensitivity and specificity. Cold agglutinins are nonspecific but develop within the first 7–10 days in >50% of pts with M. pneumoniae pneumonia. In a symptomatic pt, a cold agglutinin titer of ³1:32 supports the diagnosis of mycoplasmal pneumonia.
Because most mycoplasmal infections are not specifically diagnosed, management is directed at one of two syndromes: URI or community-acquired pneumonia. URIs do not require antimicrobial treatment. Community-acquired pneumonia (Chap. 131) should be treated with antibiotics covering common and “atypical” bacteria. Recommended regimens for community- acquired pneumonia include a third-generation cephalosporin (e.g., ceftriaxone, 1 g IV qd) plus erythromycin (500 mg IV or PO qid). Newer agents that may be used as monotherapy include clarithromycin (500 mg PO bid), azithromycin (500 mg PO qd), and levofloxacin (500 mg PO qd). Pneumonia due to M. pneumoniae is usually self-limited, but appropriate antibiotic therapy shortens the course. Treatment of documented M. pneumoniae pneumonia is continued for 14–21 days.
EPIDEMIOLOGY Mycoplasma hominis and Ureaplasma urealyticum are the most prevalent genital mycoplasmas and cause genitourinary syndromes or perinatal infections. Both organisms may colonize the genital tract of healthy, sexually experienced adults without causing disease. Men have somewhat lower rates of genital colonization than women.
CLINICAL MANIFESTATIONS Manifestations include urethritis, epididymitis, prostatitis, and pelvic inflammatory disease. Occasionally, reactive arthritis (Reiter’s disease) may be triggered by ureaplasmas. Pts with agammaglobulinemia develop joint inflammation that can be due to ureaplasmas or mycoplasmas. Infection with M. hominis has been documented in surgical wounds, at sites of trauma, and on prosthetic heart valves. Association of ureaplasmas with infertility in both men and women is controversial.
DIAGNOSIS Diagnosis by culture usually requires that the specimen be sent to a reference laboratory, although M. hominis can be recovered in some routine blood culture systems. There is seldom any reason to examine specimens from the lower genital tract for mycoplasmas since the organisms are ubiquitous.
Treatment for M. hominis infection consists of tetracycline (250 mg PO qid) or clindamycin (150 mg PO qid); erythromycin is not effective. Up to 40% of M. hominis strains may now be resistant to tetracycline. For Ureaplasma infections, erythromycin or tetracycline may be used. Since a microbiologic diagnosis is seldom made, appropriate treatment should provide antimicrobial coverage for all potential pathogens.
For a more detailed discussion, see McCormack WM: Mycoplasma Infections, Chap. 178, p. 1073, in HPIM-15.