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

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Chapter 216 Genital Mycoplasmas (Mycoplasma hominis, Mycoplasma genitalium, and Ureaplasma urealyticum)

Dwight A. Powell

Three Mycoplasma species, Mycoplasma hominis, Mycoplasma genitalium, and Ureaplasma urealyticum, are human urogenital pathogens. They are often associated with sexually transmitted infections such as nongonococcal urethritis (NGU) or puerperal infections such as endometritis. M. hominis and U. urealyticum commonly colonize the female genital tract and can cause chorioamnionitis, colonization of neonates, and perinatal infections. Two other genital Mycoplasma species, M. fermentans and M. penetrans, are identified in respiratory or genitourinary secretions more in HIV-infected patients.

Etiology

M. hominis and U. urealyticum require sterols for growth, can grow in cell-free media, and produce characteristic colonies on agar. Colonies of M. hominis are 200-300 µm in diameter with a “fried-egg” appearance, and colonies of U. urealyticum are 16-60 µm in diameter. These organisms are resistant to β-lactams because they lack a cell wall and are resistant to sulfonamides and trimethoprim because they do not produce folic acid. M. hominis is susceptible to clindamycin and quinolones but resistant to macrolides and rifampin. Increasing numbers of tetracycline-resistant strains are being reported. Using 16s ribosomal RNA sequencing, U. urealyticum has been subdivided into two species: U. urealyticum and U. parvum. Most are susceptible to macrolides and advanced generation quinolones but resistant to ciprofloxacin and clindamycin. Susceptibility to aminoglycosides and tetracyclines is variable. M. genitalium can be isolated only in cell culture systems and with difficulty. Identification in most studies has required polymerase chain reaction (PCR).

Epidemiology

M. hominis and U. urealyticum colonize the genital and urinary tracts of postpubertal women and men. Female colonization is maximal in the vagina and less in the endocervix, urethra, and endometrium. Male colonization occurs primarily in the urethra. Colonization rates are directly related to sexual activity and are highest among persons with multiple sexual partners. Colonization rates are <10% among prepubertal children and sexually inactive adults and vary from 40% to 90% among pregnant women.

Transmission

Genital mycoplasmas are transmitted by sexual contact. M. genitalium has been identified predominantly in the male urethra and is capable of attaching to human spermatozoa, suggesting a mechanism for sexual transmissibility.

Vertical transmission rates among neonates born to colonized women are 25-60%. The usual route of neonatal acquisition is contamination from colonized amniotic fluid or during vaginal delivery. However, neonatal colonization can occur in the presence of intact amniotic fluid membranes and with delivery by cesarean section. Neonatal colonization rates are higher among infants who weigh <1,500 g, are born in the presence of chorioamnionitis, and are born to mothers of lower socioeconomic status. Organisms are recovered from the newborn’s throat, vagina, rectum, and, occasionally, eyes for as long as 3 mo after birth.

Pathology and Pathogenesis

Genital mycoplasmas can produce chronic inflammation of the genitourinary tract and amniotic fluid membranes. U. urealyticum 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. U. urealyticum induces macrophages in vitro to increase production of interleukin 6 (IL-6) and tumor necrosis factor 2. Very low birthweight infants colonized with U. urealyticum have increased levels of monocyte chemoattractant protein and IL-8, which are proinflammatory agents possibly associated with development of chronic lung disease of prematurity (CLD). Immunity appears to require serotype-specific antibody. Thus, a lack of maternal antibody might account for a higher risk for disease in premature newborns.

Clinical Manifestations

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