Epidemiology

The mycoplasmas usually considered as commensals are listed in Table 45-1, along with their respective sites of colonization. These organisms may be transmitted by direct sexual contact, transplanted tissue from donor to recipient, or from mother to fetus during childbirth or in utero. M. pneumoniae may be transmitted by respiratory secretions. One species of Acholeplasma (these organisms are widely disseminated in animals), Acholeplasma laidlawii, has been isolated from the oral cavity of humans a limited number of times; however, the significance of these mycoplasmas and their colonization of humans remains uncertain.

Of the other mycoplasmas that have been isolated from humans, the possible role that M. pirum, M. amphoriforme, M. fermentans, and M. penetrans might play in human disease is uncertain at this time. M. pirum, M. fermentans, and M. penetrans have been isolated from patients infected with the human immunodeficiency virus (HIV). It now appears that M. genitalium may account for as much as 15% to 20% of nongonococcal urethritis. M. genitalium is not associated with the presence of other mycoplasmas and ureaplasmas. In women, this organism may also cause cervicitis and endometritis. M. fermentans has been isolated from specimens such as bronchoalveolar lavage, bone marrow, peripheral blood, and the throats of children with pneumonia. The organism has been associated with infection in children and immunocompromised individuals. M. amphoriforme has been detected in the lower respiratory tract in patients with chronic respiratory disease and antibody deficiencies. The incidence of various Mycoplasma spp. infections in immunocompromised patients has been demonstrated following genital or respiratory tract colonization as well as medical procedures such as renal transplantation, genitourinary manipulations, or following trauma resulting in wound infections.

Finally, the remaining three species of mycoplasmas that have been isolated from humans—M. pneumoniae, U. urealyticum, and M. hominis—have well-established roles in human infections. Both U. urealyticum and M. hominis have been isolated from the genitourinary tract of humans, and M. pneumoniae has been isolated from the respiratory tract. Both Ureaplasma species have been isolated from the internal organs of stillborn, premature, and spontaneously aborted fetuses. However, the literature contains conflicting opinions as to the importance of U. urealyticum in comparison to U. parvum.

Infants are commonly colonized with U. urealyticum and M. hominis. Once an individual reaches puberty, colonization with these mycoplasmas can occur primarily as a result of sexual contact. In situations in which these agents cause disease in neonates, organisms are transmitted from a colonized mother to her newborn infant by an ascending route from colonization of the mother’s urogenital tract, by crossing the placenta from the mother’s blood, by delivery through a colonized birth canal, or postnatally from mother to infant.

M. pneumoniae is a cause of community-acquired atypical pneumonia, often referred to as walking pneumonia (see Chapter 69); infections caused by this agent are distributed worldwide, with an estimated 2 million cases per year in the United States. M. pneumoniae infection may also result in bronchitis or pharyngitis. M. pneumoniae may be transmitted person-to-person by respiratory secretions as previously stated or indirectly by inanimate objects contaminated with respiratory secretions (fomites). Infections can occur singly or as outbreaks in closed populations such as families and military recruit camps. Pneumonia caused by M. pneumoniae may present as asymptomatic to mild disease, with early nonspecific symptoms including malaise, fever, headache, sore throat, earache, and nonproductive cough. This differs significantly from the classic symptoms associated with pneumonia as a result of infection with Streptococcus pneumoniae (see Chapters 15 and 69). M. pneumoniae strongly attaches to the mucosal cells and may reside intracellularly within host cells, resulting in a chronic persistent infection that may last for months to years. The infections do not follow seasonal patterns as seen with influenzae and other respiratory pathogens. Besides respiratory infection, M. pneumoniae can cause extrapulmonary manifestations such as pericarditis, hemolytic anemia, arthritis, nephritis, Bell’s palsy, and meningoencephalitis resulting in various additional forms of paralysis.

Pathogenesis

In general, mycoplasmas colonize mucosal surfaces of the respiratory and urogenital tracts. Except for those mycoplasmas noted, most rarely produce invasive disease except in immunocompromised hosts or instrumentation. Of the mycoplasmas that are established as causes of human infections, these agents predominantly reside extracellularly, attaching with great affinity to ciliated and nonciliated epithelial cells. Recently, M. fermentans, M. penetrans, M. genitalium, and M. pneumoniae have been identified intracellularly. Intracellular invasion in bacterial infections is generally considered a means for immune evasion and may contribute to the persistent nature of infections and difficulties in cultivation or isolation of Mycoplasma spp. M. pneumoniae has a complex and specialized attachment organelle to accomplish this process that includes a P1 adhesin protein that primarily interacts with host cells. With respect to the mycoplasmas that are clearly able to cause disease, many of the disease processes are thought to be immunologically mediated. In addition to adherence properties and possibly immune-mediated injury, the ability to cause localized cell injury appears to contribute to their pathogenicity.

Of interest, the mycoplasmas associated with patients with HIV (M. fermentans, M. penetrans, and M. pirum) are all capable of invading human cells and modulating the immune system. Based on these findings, some investigators have proposed that these mycoplasmas might play a role in certain disease processes in these patients.

Specimen Collection, Transport, and Processing

Various specimens are appropriate for the diagnosis of mycoplasma infections by culture or other means of detection. Acceptable specimens include body fluids (e.g., blood, joint fluid, amniotic fluid, urine, prostatic secretions, semen, pleural secretions, sputum, bronchoalveolar lavage specimens), tissues, wound aspirates and swabs of wounds, the throat, nasopharynx, urethra, cervix, or vagina. Blood for culture of genital mycoplasmas should be collected without anticoagulants and immediately inoculated into an appropriate broth culture medium. Mycoplasmas are inhibited by sodium polyanethol sulfonate (SPS), the anticoagulant typically found in commercial blood culture media. This may be overcome by the addition of 1% wt/vol of gelatin; however, commercial blood culture media and automated instruments are not adequate for the detection of Mycoplasma spp. Swab specimens should be obtained without the application of any disinfectants, analgesics, or lubricant; Dacron or polyester swabs on aluminum or plastic shafts should be used. Care must be taken to collect urine samples to avoid contamination with lubricants and antiseptics used during gynecologic examination.

Because mycoplasmas have no cell wall, they are highly susceptible to drying; therefore, transport media are necessary, particularly when specimens are collected on swabs. Liquid specimens such as body fluids do not require transport media if inoculated to appropriate media within 1 hour of collection. Tissues should be kept moist; if a delay in processing is anticipated, they should also be placed in transport media. Specific media for the isolation of Mycoplasma