파막을 동반하지 않은 임신부의 임신증상이 없는 양수감염 = Subclinical Amniotic Fluid Infection with Intact Membranes

다국어 초록 (Multilingual Abstract)

Subclinical amniotic fluid infection has been proposed to have an important role in the pathogenesis of idiopathic preterm labor and/or premature rupture of the menbranes(PROM). Microbiologic studies of amniotic fluid are positive in 0% to 25% of women with preterm labor in the absence of clinical evidence of infection. Frequently dsolated microorganisms are Ureaplasma urealyticum, Mycoplasma hominis, Fusobacterium species, and other anaerobic bacterias consistent with bacterial vaginosis. Those with positive amniotic fluid cultures are more likely to develop chorioamnionitis subsequently, to be refractory to tocolysis and to rupture their membranes prematurely than are the women with negative amniotic fluid cultures. Histologic examination of placenta and fetal membrane shows that histologic chorioaminioitis are significantly more common in women with preterm deliveries than in women with term deliveries. Histologic chorioaminionitis is observed in 17% to 26% of placentas from preterm deliveries and in 7% to 21% of placentas from term deliveries. Microorganisms have been detected in 51% to 72% of placentas with histologic chorioamnionitis and in 15% to 45% of those without histologic chorioamnionitis. The association between histologic chorioamnionitis and positive culture of the chorioamnion is stronger in preterm deliveries while it is less strong in term placenta. Infants of the mother with histologic chorioamnionitis have increased rates of sepsis. Many studies were done to compare the microbiologic flora of the vagina and cervix in mothers with preterm birth with that of control patients. Possibla lower genital tract microorganisms found in association with preterm birth include Neisseria gonorrheae, Chlamydia trachomatis, group B streptococci, Mycoplasma hominis, Ureplasma urelyticum Trichomonas vaginalis and other aerobic and anaerobic organisms consistent with bacterial vaginosis. Cervicovaginal microorganisms can enter the uterus either by transcervical passage into amniochorion and amniotic fluid or by hematogenous spread to the placenta and membranes. Findings of higher rates of microbial recovery within fetal membranes than in amniotic fluid suggest that cervicovaginal microorganisms more commonly ascend. Host defense mechanism for asending infection have been discussed. Increased uterine contraction and weakened membrane are two possible mechanisms in the pathogenesis of PROM and/or preterm laborRole of anibiotics for prophylaxis for preterm labor and adfuvant therapy for tocolysis have been discussed.