Ureaplasma species: role in diseases of prematurity

Abstract

There is accumulating epidemiologic and experimental evidence that intrauterine or postnatal infection with Ureaplasma species is a significant risk factor for adverse pregnancy outcomes and complications of extreme preterm birth such as bronchopulmonary dysplasia and intraventricular hemorrhage. In a cohort of very low birth weight infants, Ureaplasma spp were detected by culture or polymerase chain reaction in respiratory secretions, blood, or cerebrospinal fluid of almost half of the subjects, suggesting that this organism is the most common pathogen affecting this population. This review summarizes the evidence supporting the hypothesis that Ureaplasma-mediated inflammation in different compartments (intrauterine, lung, blood, or brain) during a common developmental window of vulnerability contributes to preterm labor and lung and brain injury. Appropriate methods for detecting these fastidious organisms and potential strategies to prevent or ameliorate the effects of Ureaplasma infection are discussed.

Figure 1. Overview of potential inflammatory pathways involved in Ureaplasma-mediated preterm labor, and common neonatal morbidities

Intrauterine Ureaplasma infections may develop by ascending infection or transplacental route. Engagement with host pathogen recognition receptors initiates a maternal and fetal inflammatory cascade. In the amniotic cavity, there is sequential upregulation of inflammatory cytokines, recruitment of leukocytes, and release of prostaglandins, and metalloproteinases leading to uterine contractions, cervical dilatation and effacement, and membrane rupture, . In the fetal lung, prolonged exposure to inflammatory cytokines inhibits alveolar development. Systemic invasion via the umbilical cord stimulates a cytokinemia in blood and/or CNS resulting in microglia activation and pre-oligodendrocyte and neuronal injury.

Figure 2. Collagen staining is increased in lungs from antenatal U.parvum-infected baboons

Lung specimens from 125d gestation baboon newborns ventilated for 14d that were either infected antenatally with U. parvum serovar 1 (D) or noninfected (C) were stained with trichome for collagen and compared to stained lung sections from 125d (A) and 140 d (B) gestational controls. The most marked fibrosis occurred in the U. parvum infected lungs (arrows). Magnification x200.