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  1. Definition.Ureaplasma belongs to the Mycoplasmataceae family. These are small pleomorphic bacteria that characteristically lack a cell wall.

  2. Incidence.Ureaplasma urealyticum is frequently present in the lower genital tract of sexually active women with a colonization rate ranging between 40% and 80%. Vertical transmission to the newborn is high, especially in premature infants <1000 g birthweight where transmission rate approaches 90%.

  3. Pathophysiology.U. urealyticum has been implicated in a variety of obstetric and neonatal diseases including preterm labor, preterm premature rupture of membranes (PPROM), chorioamnionitis, congenital pneumonia, and bronchopulmonary dysplasia (BPD). The presumed mechanisms of infection include fetal exposure to ascending intrauterine infection, passage through an infected birth canal, and hematogenous dissemination through the placenta into umbilical vessels. This exposure leads to colonization of the skin, mucosal membranes, and respiratory tract, and sometimes leads to dissemination into the bloodstream and CNS. Phospholipases and cytokines produced through the inflammatory response can trigger uterine contractions and premature birth. Ureaplasmal infection of the respiratory tract in the newborn promotes a proinflammatory cytokine cascade with increase in tumor necrosis factor alpha, interleukin (IL)-1β, and IL-8. These cytokines recruit neutrophils to the lungs and intensify the inflammatory cascade, which damages the premature lung and impairs future alveolar development.

  4. Risk factors.Ureaplasma colonization is associated with preterm labor, chorioamnionitis, birthweight <1000 g, and gestational age <30 weeks.

  5. Clinical presentation

      1. Preterm labor, PPROM, and chorioamnionitis.Ureaplasmas can invade the amniotic fluid early in pregnancy and are the single most common organisms that can be isolated from inflamed placentas. Ureaplasmas can persist in the amniotic fluid subclinically for several weeks. A recent study showed preterm labor to occur in 58.6% of women with a positive polymerase chain reaction (PCR) assay for Ureaplasmas at 15–17 weeks of gestation as compared with only 4.4% of women with negative results.

      1. Congenital pneumonia. Evidence that suggests Ureaplasma as a cause of congenital pneumonia includes isolation of the organism in pure culture from amniotic fluid and tracheal aspirate of neonates <24 h after birth in the midst of an acute inflammatory response with radiographic changes. These infants develop early interstitial pulmonary infiltrates with cystic/dysplastic changes as early as 10–14 days of age.

      1. Predisposition to chronic lung disease. Multiple cohort studies have linked the development of BPD with colonization of the airways with Ureaplasma.

  6. Diagnosis

      1. Laboratory studies

          1. Culture. Specimens for culture require specific transport media with refrigeration at 4°C. Dacron or calcium alginate swabs should be used instead of cotton swabs.

          1. Other tests. Several sensitive PCR assays have been developed, but they are not available routinely. Serologic assays are of limited value.

  7. Management. Isolation precautions for all infectious diseases, including maternal and neonatal precautions, breast-feeding, and visiting issues, can be found in Appendix F.

      1. Treatment of the colonized pregnant mother. Treatment of pregnant women who present with PPROM with a 10-day course of erythromycin has been shown in a large randomized study to prolong pregnancy, reduce neonatal treatment with surfactant, decrease infant oxygen dependency at ≥28 days of age, and result in fewer major cerebral abnormalities on ultrasonography before discharge. Those same benefits were not accrued if the mother presented with preterm labor but with intact membranes.

      1. Treatment of the colonized newborn infant is controversial. Limited current evidence does not demonstrate a reduction in BPD or other long-term ...

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