New research from the US has found a link between preterm births where the water sac around the baby breaks prematurely, and bacteria near where the walls of the sac are thinner.
The researchers, including Amy P. Murtha, associate professor of obstetrics and gynecology at Duke University School of Medicine, report their work in a recent online issue of PLOS ONE.
Prof. Murtha says:
“Complications of preterm births can have long-term health effects for both mothers and children. 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.”
She and her colleagues caution that the study only establishes a link between bacteria and early rupturing, and that more research is needed to determine if one causes the other.
The water sac comprises two transparent membranes that hold the embryo, and later the fetus, as it grows until just before birth.
The inner membrane, the amnion, contains the amniotic fluid and the fetus, while the outer membrane, the chorion, contains the amnion and is part of the placenta.
Nearly a third of early deliveries are associated with water breaking, in what is referred to as premature preterm rupture of membranes (PPROM).
In earlier work, Prof. Murtha and colleagues had shown infection is linked to a higher rate of cell death in the chorion.
They found that women who experience PPROM tend to have a thinner chorion layer, and those with chorioamnionitis, where this layer is infected, had the highest rate of chorion cell deaths.
In this latest study, the team examined samples of chorion membranes to see if there were any patterns between presence of bacteria and membrane thinning.
Altogether they collected samples from 48 women after they gave birth. These included women who gave birth at term and preterm and patients with PPROM.
For each sample they measured the amount of thinning in the chorion membrane, and the presence of bacteria, both near and far from where the membrane ruptured.
In all cases they found the chorion membrane was thinner at the rupture site than the distant site.
But in samples from patients who experienced PPROM, they found chorion thinning was not restricted to the rupture site. The membrane was also thinner at sites distant from the rupture site, indicating that in PPROM, the chorion is thinner all over the water sac.
The researchers were surprised to find that bacteria were present in all the samples, contrary to the common-held view that fetal membranes are sterile environments.
However, they were not surprised to find bacteria levels were higher at the rupture site.
But in the samples from women who experienced PPROM, they found the highest levels of bacteria, both at the rupture site and the sites distant from it.
They also found that for all samples, the thinner the chorion membrane, the more bacteria that were present.
While the study was not designed to find out whether the presence of bacteria causes the chorion thinning, or the thinning increases the level of bacteria, the researchers suggest their findings offer valuable insights into the mechanisms underlying PPROM.
Prof. Murtha says their results “suggest the chorion and its thinning may be the battleground” for the changes that occur inside the fetal membrane when bacteria are present.
She and her colleagues now plan to find out if specific bacteria are involved in PPROM.
If they can find precisely which bacteria are involved, this could open routes to preventive treatments and screening tools.
Prof. Murtha adds:
“We then might be able to treat affected women with antibiotics and reduce their risk for PPROM. Our research is several steps away from this, but it gives us opportunities to explore potential targeted therapeutic interventions, which we lack in obstetrics.”
In 2011, researchers at Yale School of Medicine also found a clue to the mystery of preterm delivery – excessive build up of calcium crystal deposits in the amniotic fluid – offering another possible explanation for PPROM.