Ureaplasma urealyticum is commonly isolated from the amniotic fluid of unselected individuals with intact membranes at the time of cesarean section even prior to onset of labor. The risk of placental infection increases with onset of labor, rupture of membranes and number of vaginal examinations. Qualitative cultures of women with clinical signs of intraamniotic infection and matched controls indicate that U. urealyticum can be found in 50% of amniotic fluid samples of both groups thus suggesting that it may not be a cause of clinical amnionitis. To gain further understanding of the potential role of this organism, we performed amniotic fluid and blood cultures and measured serologic responses by enzyme-linked immunosorbent assay in women with clinical intraamniotic infection and matched controls. U. urealyticum was the single most common bacterial species isolated from maternal blood and amniotic fluid but the isolation rate did not differ between symptomatic and asymptomatic women. Also other known pathogenic bacteria were often isolated from amniotic fluids containing ureaplasmas. However, the marked difference in serologic response between symptomatic and asymptomatic women and the occurrence of ureaplasmemia in some suggest that in certain individuals U. urealyticum may be a cause of clinical amnionitis. Serologic responsiveness, ureaplasmemia and isolation of urea-plasmas in pure culture from amniotic fluid of some asymptomatic women suggest that U. urealyticum may also be a cause of clinically silent amnionitis. Previous studies have shown a significant association between chorioamnio-nitis documented by histopathology and isolation of U. urealyticum from the placenta or infant but not the maternal cervix. While these studies are not conclusive because of failure to consider the presence of other microorganisms and/or failure to take into account not only membrane rupture but also duration of labor, studies reported elsewhere in this Symposium indicate that U. urealyticum is significantly associated with chorioamnionitis even when all of these factors are taken into account. Furthermore studies performed at 16 to 20 weeks of gestation indicate that in a subpopulation of individuals infected with U. urealyticum in the lower genital tract, the organism can infect amniotic fluid in the absence of labor, membrane rupture and other microorganisms and that ureaplasmas can under these conditions elicit an inflammatory response. In fact in these studies U. urealyticum was shown to persist in amniotic fluid for as long as 2 months in the presence of an intense inflammatory response in the absence of discernible clinical signs or symptoms of amnionitis. We conclude therefore that U. urealyticum is a cause of amnionitis early in gestation and possibly in later stages of pregnancy with or without clinical symptoms. © 1986 by Williams & Wilkins.