A high presence of bacteria at the site where fetal membranes rupture may be the key to understanding why some pregnant women experience their "water breaking" prematurely, researchers at Duke Medicine report.
The findings, published online Jan. 8, 2014, in the journal PLOS ONE, suggest that the bacterial presence is associated with thinning of the fetal membranes. More research is needed to understand whether bacterial presence is a cause or consequence of fetal membrane weakening.
"Complications of preterm births can have long-term health effects for both mothers and children," said study author Amy P. Murtha, M.D., associate professor of obstetrics and gynecology at Duke University School of Medicine. "Our research focuses on why the fetal membranes, or water sac, break early in some women, with the overall goal of better understanding the mechanisms of preterm membrane rupture."
Composed of two fetal cell layers, the amnion and chorion, fetal membranes play an important role in maintaining pregnancy through gestation. Nearly one-third of all early deliveries are associated with the water breaking in what's known as preterm premature rupture of membranes, or PPROM.
Previous research from Murtha and her colleagues demonstrated that the chorion has more cell death when infection is present, and that this cell layer may be thinner in women who experience PPROM. Among PPROM patients with infection in the fetal membranes (chorioamnionitis), the cell death within the chorion layer was highest, suggesting that infection may play a role in causing PPROM.
In the current study, the researchers prospectively examined chorion membrane samples to identify a pattern of bacterial presence and association with chorion thinning. They collected membrane samples from a total of 48 women -- including PPROM, preterm and term patients -- after they gave birth. The researchers measured chorion thinning and bacterial presence in membrane samples collected from both near and far from the rupture site.
In all women, the chorion membrane was thinner at the rupture site than at the distant site. However, chorion thinning was greatest among PPROM patients and was not isolated to the rupture site, as the researchers observed a global chorion thinning even distant from where the membrane ruptured.
The researchers then looked to see if bacteria were present in the membranes and whether bacteria levels correlated with the thinning of the cell layers in the membranes. Interestingly, bacteria were present in all fetal membranes, refuting the traditional understanding that fetal membranes are sterile environments. The amount of bacteria present at the rupture site was higher, which the researchers were not surprised to find.
