SUMMARY The genital mycoplasmas represent a complex and unique group of microorganisms that have been associated with a wide array of infectious diseases in adults and infants. The lack of conclusive knowledge regarding the pathogenic potential of Mycoplasma and Ureaplasma spp. in many conditions is due to a general unfamiliarity of physicians and microbiology laboratories with their fastidious growth requirements, leading to difficulty in their detection; their high prevalence in healthy persons; the poor design of research studies attempting to base association with disease on the mere presence of the organisms in the lower urogenital tract; the failure to consider multifactorial aspects of diseases; and considering these genital mycoplasmas only as a last resort. The situation is now changing because of a greater appreciation of the genital mycoplasmas as perinatal pathogens and improvements in laboratory detection, particularly with regard to the development of powerful molecular nucleic acid amplification tests. This review summarizes the epidemiology of genital mycoplasmas as causes of neonatal infections and premature birth; evidence linking ureaplasmas with bronchopulmonary dysplasia; recent changes in the taxonomy of the genus Ureaplasma; the neonatal host response to mycoplasma and ureaplasma infections; advances in laboratory detection, including molecular methods; and therapeutic considerations for treatment of systemic diseases.

Ureaplasma colonization is associated with higher reported rates of BPD, but the greatest reported effect is seen in small studies; reporting bias may be partially responsible for this effect.

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A PCR assay was used to analyze endotracheal aspirates from preterm infants for Ureaplasma parvum versus U. urealyticum. U. parvum was detected more often than U. urealyticum. There was no significant difference or trend in the prevalence of either species between infants with or without bronchopulmonary dysplasia when isolated alone.The major factor leading to high morbidity and mortality of preterm infants is pulmonary immaturity. This manifests as respiratory distress in the early neonatal period and can develop into bronchopulmonary dysplasia (BPD), currently defined as a supplemental oxygen requirement at 36 weeks postmenstrual age, with characteristic radiographic findings (2). A recent survey reported that the incidence of BPD ranged from 67% among infants with birth weights of 500 to 750 g to Ͻ1% in infants weighing 1,250 to 2,500 g (2).Development of BPD is multifactorial and is related to pulmonary immaturity, oxidant injury due to high levels of inspired oxygen, and volutrauma associated with mechanical ventilation. However, recent research has focused on the roles of perinatal infection and the inflammatory response as critical factors influencing chronic lung injury (7, 16). Particular attention has been paid to the role of Ureaplasma species, fastidious bacteria found in the lower genital tracts of 40 to 80% of asymptomatic women (4). Rates of vertical transmission range from 18 to 88%, varying inversely with gestational age (6,8,12,24,25). Ureaplasma spp. are the most common microorganisms isolated from inflamed placentas and the lower respiratory tracts of neonates and are proven causes of neonatal pneumonia (4). Since initial reports associating ureaplasmal colonization and development of BPD were published in 1988 (5, 23, 26), more than 30 studies have been conducted. Most, but not all, have supported this association, despite major changes in the pulmonary management of very-low-birth-weight infants, such as exogenous surfactant, antenatal corticosteroid administration, and high frequency ventilation.

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