11: Fetal membrane microbiota is altered in preterm premature rupture of membranes


      Infection is a frequent and important mechanism in preterm birth. Presence of bacteria in fetal membranes throughout gestation has been previously confirmed. The objective is to determine if the microbiota present in fetal membranes vary by clinical phenotype or site of collection.

      Study Design

      Uniform paired membrane samples (rupture and distant) were prospectively collected from: PPROM (22), preterm labor (PTL=11), preterm no labor (PTNL=9), term labor (TL=18), and term no labor (TNL=12) subjects. With intact membranes, fetal membranes overlying the cervix were marked and a section collected. The bacterial 16s rDNA V3 region was amplified by PCR from membrane total DNA and multiplex sequenced by Ion Torrent PGM. Qiime, R, and additional python scripts were employed for analysis.


      TL and PTL membranes had similar compositions with Ureaplasma as the dominant genus (83.4% and 89%). TNL and PTNL had greater diversity than TL and PTL [Chao1 (280+74l, 251+-65) vs. (199+-69, 207+-94) p<0.01). PPROM membranes had lower diversity than PTNL and TNL and were dominated by Pseudomonas, Mycoplasma, Streptococcus, and an uncultivatible gammaproteobacterium (36.5%, 41.0%, 5.2%, and 7.5%). Distant membrane was dominated by Pseudomonas, Streptococcus, and uncultivatible gammaproteobacteria (33.3%, 14.1%, and 20.7%, respectively); rupture sites were dominated by Mycoplasma, Ureaplasma, and Pseudomonas (42.0%, 24.8%, 27.7%). A taxa among Lachnospiraceae distinguished no labor from labor and PPROM samples (p=0.001). Additional taxa in Lachnospiracea and Mycoplasmataceae differentiated PPROM and other groups. Unweighted beta diversity was significantly different between PPROM vs. PTL and TL (p=0.001, p=0.003) but not PPROM vs. PTNL and TNL.


      PPROM membranes have a distinct microbiota in diversity and composition relative to other phenotypes. The microbiota at the rupture site is distinct from distant membrane sites. Future work will elucidate the role of the microbiota and its geodiversity in pathophysiology of PPROM.
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