A patent female reproductive tract, although essential for conception and delivery, is theoretically problematic during phase 1 of parturition. Bacteria can gain access to intrauterine tissues through: (1) transplacental transfer of maternal systemic infection, (2) retrograde flow of infection into the peritoneal cavity via the fallopian tubes, or (3) ascending infection with bacteria from the vagina and cervix. Because the lower pole of the fetal membrane-decidual junction is contiguous with the cervical canal oriice, this anatomical arrangement provides a passageway for microorganisms. Ascending infection is considered to be the most common entry route. Ascending microorganisms colonize the cervix, decidua, and possibly the membranes, where they then may enter the amnionic sac.
Intraamnionic infection as a primary cause of preterm labor in pregnancies with intact membranes accounts for 25 to 40 percent of preterm births (Goncalves, 2002; lams, 1987). In some instances, histological evidence of inflammation is found in the fetal membranes, decidua, or umbilical cord. Other cases are deemed "subclinical." Current data suggest that microbial invasion of the reproductive tract is suicient to induce infection-mediated preterm birth. ffected women are more likely to develop clinical chorioamnionitis and PPROM compared with women with sterile cultures. Moreover, their neonates are also more likely to have perinatal complications that include RDS, intraventricular hemorrhage, and necrotizing enterocolitis (Hitti, 2001). Although the clinical course is more severe when intraamnionic infection is obvious, inlammation in the absence of detectable intraamnionic microorganismstermed sterile intraamnionic inlammation-is also a risk factor for an inlammatory response, described in the next section (Lee, 2007, 2008; Romero, 2014). In sum, the earlier the onset of preterm labor, the greater the likelihood of underlying infection (Goldenberg, 2000; Goncalves, 2002; Watts, 1992).
he incidence of culture-positive amnionic luid collected by amniocentesis during spontaneous term labor is similar to that with preterm labor (Gomez, 1994; Romero, 1993). It has been suggested that at term, amnionic luid is iniltrated by bacteria as a consequence oflabor, whereas in preterm pregnancies, bacteria represent an inciting cause of labor. hus, fetal infection, as deined by bacteria detected within the amnionic luid, has both difering etiologies and consequences.
Despite these observations, considerable data associate chorioamnionitis with preterm labor (Goldenberg, 2002; Ustiin, 2001). With chorioamnionitis, microbes may invade maternal tissue only and not amnionic fluid. Despite this, endotoxins can stimulate amnionic cells to secrete cytokines that enter amnionic luid. his scenario may serve to explain the apparently contradictory observations concerning an association between amnionic luid cytokines and preterm labor in cases in which microbes are not detected in the amnionic luid.