Ureaplasma belongs to the Mycoplasmataceae family. These are small pleomorphic bacteria that characteristically lack a cell wall. The genus Ureaplasma contains 2 species capable of causing human infection, Ureaplasma urealyticum and Ureaplasma parvum.
Ureaplasma species are 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, in whom the transmission rate approaches 90%.
U urealyticum has been implicated in a variety of obstetric and neonatal diseases including preterm labor, preterm premature rupture of membranes (pPROM), chorioamnionitis, postpartum fever and endometritis, congenital pneumonia, bacteremia, meningitis, intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), 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, gastrointestinal and respiratory tract, and sometimes dissemination into the bloodstream and central nervous system (CNS). Phospholipases and cytokines produced through the inflammatory response can trigger uterine contractions and premature birth. Ureaplasma infection of the respiratory tract in the newborn promotes a proinflammatory cytokine cascade with increase in tumor necrosis factor-α, 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. The same mechanisms may be involved in Ureaplasma-mediated intestinal injury and NEC.
Ureaplasma colonization is associated with preterm labor, chorioamnionitis, birthweight <1000 g, and gestational age (GA) <30 weeks. Respiratory colonization is inversely related to GA at birth (65% in infants <26 weeks vs 31% in infants ≥26 weeks).
Preterm labor, preterm premature rupture of membranes, and chorioamnionitis. Ureaplasma can invade the amniotic fluid early in pregnancy and are the single most common organisms that can be isolated from inflamed placentas. Ureaplasma can persist in the amniotic fluid subclinically for several weeks. Detection of Ureaplasma in second-trimester amniotic fluid by polymerase chain reaction (PCR) correlates with subsequent preterm labor and delivery (58.6% for those with positive PCR vs 4.4% for those with negative results). In addition, Ureaplasma cord blood infections (identified by cultures) are far more common in spontaneous than indicated preterm deliveries and are strongly associated with markers of acute placental inflammation. Positive cord cultures are also associated with neonatal systemic inflammatory response syndrome.
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 hours after birth with specific immunoglobulin M (IgM) response in the midst of an acute inflammatory reaction and radiographic changes. These infants develop early interstitial pulmonary infiltrates with cystic/dysplastic changes as early as 7 to 10 days of age.
Meningitis and intraventricular hemorrhage. Multiple studies have shown Ureaplasma to be isolated from cerebrospinal fluid (CSF) of premature infants with meningitis, IVH, and hydrocephalus. The contribution of Ureaplasma to the outcome of these newborns is uncertain.
Association with necrotizing enterocolitis. One study showed that the incidence of NEC was 3.3-fold higher in Ureaplasma-positive, ≤28 weeks preterm infants with higher cord blood IL-6 and IL-1β.