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Ureaplasma spp. is detected in the urogenital tract, including the vagina, cervix, chorioamnion, and placenta. Their colonization is associated with histologic chorioamnionitis (CAM), often observed in placentas from preterm delivery. We isolated Ureaplasma spp. from 63 preterm placentas among 151 specimens, which were delivered at Ͻ32 wk of gestation. Of the 63 placentas, 52 (83%) revealed CAM in cultures positive for Ureaplasma spp., however, CAM was observed only in 30% (26/88) of cultures negative for Ureaplasma spp. (p Ͻ 0.01). Colonization by Ureaplasma spp. was an independent risk factor for CAM (OR, 11.27; 95% CI,). Characteristic neutrophil infiltration was observed in the amnion and subchorion (bistratified pattern) in cultures positive for Ureaplasma spp. FISH analysis of CAM placenta with male infant pregnancy indicated that bistratified infiltrated neutrophils showed the XX karyotype and umbilical vein infiltrated neutrophils showed XY karyotype. The distribution of sulfoglycolipid, the receptor of Ureaplasma spp., was mainly detected in the amnion. Ureaplasmal urease D protein and ureB gene were both detected in the amnion, indicating direct colonization by Ureaplasma spp. U reaplasma spp. is the smallest self-replicating organism, both in genome size and in cellular dimensions. It lacks cell walls and exists in association with eukaryotic cells, mainly colonizing mucosal surfaces of the respiratory and urogenital tracts (1). Ureaplasma spp. is a common inhabitant of the lower genital tract and isolated from 40 to 80% women of child-bearing age (2). However, once Ureaplasma spp. spreads from the lower genital tract into the body, this microorganism exerts widespread pathogenic effects, such as chorioamnionitis (CAM), urinary tract infections, preterm labor, and spontaneous abortion. On the other hand, Ureaplasma spp. infection is also reported as a risk factor for lethal pneumonia, chronic lung disease, and meningitis of fetuses and neonates (3).CAM is a placental finding associated with premature rupture of membranes (PROM) and preterm birth, which are the most important causes of perinatal morbidity and mortality (4,5). Previous studies showed that CAM was positively related to the isolation of Ureaplasma spp (6,7). Although many researchers reported the detection of Ureaplasma spp. from specimens of vagina, cervix, chorioamnion, and placenta using culture or PCR methods (8 -12), the precise pathologic findings of CAM with Ureaplasma spp. remain unclear.A variety of infectious microorganisms use specific host cell surface molecules as receptors. Such receptors provide a mechanism for intimate interaction with the host cell membrane and in some cases may facilitate the subsequent entry of the organism into the cell (13). Ureaplasma spp. and Mycoplasma hominis were shown to specifically recognize host cell surface glycolipids (sulfogalactoglycerolipid and the sphingolipid counterpart, sulfogalactosyl ceramide), which have been implicated in spermegg interactions (14). This glycolipid rec...

The results suggest that abnormal uterine artery flow velocity waveforms may indicate impaired trophoblast migration into the myometrium of the placental bed.

These results suggest that disturbed placental circulation underlies the development of PVL in the majority of cases with prenatal and peripartum brain injury. In chorioamnionitis cases, certain additional factors were suggested in the genesis of PVL. Thus, placental examination is essential for elucidating the pathophysiologic changes leading to PVL in the perinatal process.