绒毛膜羊膜炎
解脲支原体
细菌性阴道病
解脲支原体
医学
产科
人型支原体
宫颈环扎术
新生儿败血症
沙眼衣原体
胎膜早破
怀孕
胎儿
支原体
免疫学
胎龄
败血症
生物
微生物学
遗传学
作者
Luís F. Gonçalves,Tinnakorn Chaiworapongsa,Roberto Romero
出处
期刊:Mental Retardation and Developmental Disabilities Research Reviews
[Wiley]
日期:2002-01-01
卷期号:8 (1): 3-13
被引量:592
摘要
Abstract Intrauterine infection is a major cause of premature labor with and without intact membranes. Intrauterine infection is present in approximately 25% of all preterm births and the earlier the gestational age at delivery, the higher the frequency of intra‐amniotic infection. Microorganisms may also gain access to the fetus before delivery. A fetal inflammatory response syndrome elicited in response to microbial products is associated with the impending onset of preterm labor and also with multi‐systemic organ involvement in the human fetus and a higher rate of perinatal morbidity. The most common microorganisms involved in intrauterine infections are Ureaplasma urealyticum , Fusobacterium species and Mycoplasma hominis . The role of Chlamydia trachomatis and viruses in preterm labor remain to be determined. Use of molecular microbiology techniques to diagnose intrauterine infection may uncover the role of fastidious microorganisms that have not yet been discovered. Antibiotic administration to patients with asymptomatic bacteriuria is associated with a significant reduction in the rate of preterm birth. However, such benefit has not been demonstrated for patients with bacterial vaginosis, or women who carry Streptococcus agalactia , Ureaplasma urealyticum or Trichomonas vaginalis . Antibiotic administration to patients with preterm premature rupture of membranes is associated with prolongation of pregnancy and a reduction in the rate of clinical chorioamnionitis and neonatal sepsis. The benefit has not been demonstrated in patients with preterm labor and intact membranes. Major efforts are required to determine why some women develop an ascending intrauterine infection and others do not and also what interventions may reduce the deleterious effect of systemic fetal inflammation. MRDD Research Reviews 2002;8:3–13. © 2002 Wiley‐Liss, Inc.
科研通智能强力驱动
Strongly Powered by AbleSci AI