What is the pathophysiology of chorioamnionitis?

Updated: May 08, 2018
  • Author: Fayez M Bany-Mohammed, MD; Chief Editor: Ted Rosenkrantz, MD  more...
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Answer

Abnormal bacterial colonization of the distal colon during pregnancy may create an abnormal vaginal and cervical microbial environment. [32] Ascending of cervical and vaginal flora through the cervical canal is the most common pathway to chorioamnionitis. Uncommonly, chorioamnionitis may occur via hematogenous spread as a result of maternal bacteremia (eg, Listeria monocytogenes), or via contamination of the amniotic cavity as a result of an invasive procedure (eg, amniocentesis, fetoscopy). Although spread of peritoneal infection to the amniotic cavity via the fallopian tubes has also been suggested, it is very unlikely. [31] Subsequent activation of the maternal and fetal inflammatory response systems generally lead to labor and/or rupture of membranes. [33] More than 3 decades ago, rectovaginal colonization with group B Streptococcus (GBS) during pregnancy was found to be associated with GBS-related infection of the fetus or newborn. [18] Studies have demonstrated that other types of bacteria residing in the vagina, cervix, or both ascend through intact or ruptured fetal membranes and initiate amniotic fluid infection, chorioamnionitis (inflammation), or both. [34]

Urinary tract infection during pregnancy can bathe the vagina with bacterial pathogens and is a recognized risk factor for neonatal sepsis. [35]  This observation is particularly true for untreated asymptomatic GBS-related bacteriuria. [36]

Bacterial vaginosis is associated with premature labor, although overt infection of the neonate with microbes causing bacterial vaginosis is uncommon. Screening for and treatment of bacterial vaginosis and other genital infections may prevent preterm birth, especially if initiated before 20 weeks' gestation. [37]

Many associations related to infection and preterm birth have been made; however, the mechanisms of these relationships are not necessarily understood. These associations include periodontitis, [38]  blood types A and O, [39] alcoholism, [39]  and obesity during pregnancy. [40]

In the mid-trimester of pregnancy (14-24 weeks), ultrasonographic evidence of a short cervix may be the only clinical finding in intraamniotic fluid infection. [11] Cervical insufficiency, regardless of bacterial culture results from amniotic fluid, is associated with intraamniotic inflammation, preterm birth, and other adverse outcomes of pregnancy. [41, 42] Related issues to cervical insufficiency are mechanical methods of cervical ripening that are also suspected of increasing maternal and neonatal infections. [43] A Cochrane review stated that vaginal prostaglandin to initiate labor after premature rupture of membranes may increase maternal and fetal infection and warrants more research. [44] Each of these factors may be associated with altered host defenses that allow ascending infection from the urogenital tract to placental tissues and amniotic fluid. [45]


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