Genital Mycoplasmas ( Mycoplasma hominis, Mycoplasma genitalium , and Ureaplasma urealyticum )

Etiology

Mycoplasma species are small pleomorphic bacteria that typically lack a cell wall and are bound by a cell membrane. Many of the biologic properties of mycoplasmas are in fact due to the absence of a rigid cell wall, including resistance to β-lactam antibiotics. These ubiquitous organisms are difficult to cultivate and belong to the family Mycoplasmataceae in the class Mollicutes and represent the smallest self-replicating organisms known to date. The entire genome of many of the Mycoplasma species is among the smallest of prokaryotic genomes. The family Mycoplasmataceae is composed of two genera responsible for human infection: Mycoplasma and Ureaplasma. Of those, Mycoplasma hominis, Mycoplasma genitalium, and Ureaplasma spp., which include Ureaplasma urealyticum (biovar 2) and Ureaplasma parvum (biovar 1), are considered human urogenital pathogens and are reviewed in this chapter.

Genital mycoplasmas are often associated with sexually transmitted infections such as cervicitis and nongonococcal urethritis (NGU) or with puerperal infections such as endometritis. M. hominis and Ureaplasma spp. commonly colonize the female genital tract and can cause chorioamnionitis, colonization of neonates, and perinatal infections. Two other genital Mycoplasma species, Mycoplasma fermentans and Mycoplasma penetrans, have been identified in respiratory or genitourinary secretions primarily in HIV-infected patients.

Epidemiology

M. hominis and Ureaplasma spp. are commensal organisms in the lower genital and urinary tract of postpubertal women and men. The prevalence of colonization with these bacteria has been directly associated with low socioeconomic status, hormonal changes, and ethnicity and increases proportionally according to sexual activity, being highest among individuals with multiple sexual partners. Female colonization is greatest in the vagina and lower in the endocervix, urethra, and endometrium, with rates varying from 40% to 80% for Ureaplasma spp. and 21–50% for M. hominis among sexually active asymptomatic women. Ureaplasma is isolated less often from urine than from the cervix, but M. hominis is present in the urine and in the cervix with approximately the same frequency. Male colonization is less common and occurs primarily in the urethra. Among prepubertal children and sexually inactive adults, colonization rates are <10%. M. genitalium is implicated in approximately 15–20% of NGU cases in men and plays a role in cervicitis and pelvic inflammatory disease in women. Studies using polymerase chain reaction (PCR) show that colonization of the female lower urogenital tract with M. genitalium is less common than with M. hominis or Ureaplasma spp.

Transmission

Genital mycoplasmas are transmitted by sexual contact or by vertical transmission from mother to infant. As with other perinatal infections, vertical transmission can occur through ascending intrauterine infection, hematogenous spread from placental infection, or through a colonized birth canal at the time of delivery. Transmission rates among neonates born to women colonized with Ureaplasma spp. range from 18 to 88%. Neonatal colonization rates are higher among infants who weigh <1,000 g, are born in the presence of chorioamnionitis, or are born to mothers of lower socioeconomic status. Neonatal colonization is transient and decreases proportionally with age. Organisms may be recovered from the newborn's throat, vagina, rectum, and, occasionally, conjunctiva for as long as 3 mo after birth.

Pathogenesis

Genital mycoplasmas can cause chronic inflammation of the genitourinary tract and amniotic membranes. These bacteria usually live in a state of adherence to the respiratory or urogenital tract, but can disseminate to other organs when there is a disruption of the mucosa or a weakened or immature immune system, such as in premature infants. Ureaplasma spp. can infect the amniotic sac early in gestation without rupturing the amniotic membranes, resulting in a clinically silent, chronic chorioamnionitis characterized by an intense inflammatory response. Attachment to fetal human tracheal epithelium can cause ciliary disarray, clumping, and loss of epithelial cells. In vitro studies show that Ureaplasma spp. stimulates macrophage production of interleukin (IL)-6 and tumor necrosis factor-α. In addition, high concentrations of proinflammatory cytokines possibly associated with development of bronchopulmonary dysplasia (BPD) of prematurity, such as monocyte chemoattractant protein-1 and IL-8, have been found in tracheal secretions from very-low-birthweight infants colonized with Ureaplasma spp. Immunity appears to require serotype-specific antibody. Thus, lack of maternal antibodies might account for a higher disease risk in premature newborns.

Clinical Manifestations

The main syndromes associated with Ureaplasma spp., M. genitalium, and M. hominis are displayed in Table 251.1 .