Bacteria localization and chorion thinning among preterm premature rupture of membranes.
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OBJECTIVE: Bacterial colonization of the fetal membranes and its role in pathogenesis of membrane rupture is poorly understood. Prior retrospective work revealed chorion layer thinning in preterm premature rupture of membranes (PPROM) subjects. Our objective was to prospectively examine fetal membrane chorion thinning and to correlate to bacterial presence in PPROM, preterm, and term subjects. STUDY DESIGN: Paired membrane samples (membrane rupture and membrane distant) were prospectively collected from: PPROM = 14, preterm labor (PTL = 8), preterm no labor (PTNL = 8), term labor (TL = 10), and term no labor (TNL = 8), subjects. Sections were probed with cytokeratin to identify fetal trophoblast layer of the chorion using immunohistochemistry. Fluorescence in situ hybridization was performed using broad range 16 s ribosomal RNA probe. Images were evaluated, chorion and choriodecidua were measured, and bacterial fluorescence scored. Chorion thinning and bacterial presence were compared among and between groups using Student's t-test, linear mixed effect model, and Poisson regression model (SAS Cary, NC). RESULTS: In all groups, the fetal chorion cellular layer was thinner at rupture compared to distant site (147.2 vs. 253.7 µm, p<0.0001). Further, chorion thinning was greatest among PPROM subjects compared to all other groups combined, regardless of site sampled [PPROM(114.9) vs. PTL(246.0) vs. PTNL(200.8) vs. TL(217.9) vs. TNL(246.5)]. Bacteria counts were highest among PPROM subjects compared to all other groups regardless of site sampled or histologic infection [PPROM(31) vs. PTL(9) vs. PTNL(7) vs. TL(7) vs. TNL(6)]. Among all subjects at both sites, bacterial counts were inversely correlated with chorion thinning, even excluding histologic chorioamnionitis (p<0.0001 and p = 0.05). CONCLUSIONS: Fetal chorion was uniformly thinner at rupture site compared to distant sites. In PPROM fetal chorion, we demonstrated pronounced global thinning. Although cause or consequence is uncertain, bacterial presence is greatest and inversely correlated with chorion thinning among PPROM subjects.
Colony Count, Microbial
Fetal Membranes, Premature Rupture
In Situ Hybridization, Fluorescence
Published Version (Please cite this version)10.1371/journal.pone.0083338
Publication InfoBentley, RC; Feng, L; Fortner, KB; Grotegut, Chad Aaron; Heine, RP; Lan, L; ... Seed, Patrick C (2014). Bacteria localization and chorion thinning among preterm premature rupture of membranes. PLoS One, 9(1). pp. e83338. 10.1371/journal.pone.0083338. Retrieved from http://hdl.handle.net/10161/8299.
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Associate Professor of Obstetrics and Gynecology
Professor of Obstetrics and Gynecology
Dr. Amy Murtha is a Professor in the Department of Obstetrics and Gynecology and Department of Pediatrics, and past Vice Chair for Research in Obstetrics and Gynecology. After graduating from the Medical College of Pennsylvania in 1992 she completed her residency in OB-GYN and fellowship in Maternal Fetal Medicine (MFM) at Duke University then joined the faculty at Duke in 1998. Dr. Murtha served as interim Chair for the Department of OB-GYN and Fellowship Director for the mater
Associate Professor of Pediatrics
We are studying human microbial ecology and the molecular basis for different bacterial infections that are of relevance to both children and adults. Summaries of the research areas are described below: 1. THE MOLECULAR BASIS FOR VIRULENCE OF UROPATHOGENIC ESCHERICHIA COLI AND URINARY TRACT INFECTIONS. Uropathogenic Escherichia coli (UPEC) is the leading cause of community-acquired urinary tract infections (UTIs). Over 100 million UTIs occur annually throughout the world inclu
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