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J Infect Dis. 2014 Jul 15;210(2):265-73. doi: 10.1093/infdis/jiu067. Epub 2014 Jan 28.

Group B Streptococcus β-hemolysin/cytolysin breaches maternal-fetal barriers to cause preterm birth and intrauterine fetal demise in vivo.

Author information

1
Department of Pediatrics, Columbia University, New York, New York.
2
Department of Obstetrics and Gynecology, Weill-Cornell Medical Center, New York, New York.
3
Department of Pathology and Cell Biology, Columbia University, New York, New York.
4
Department of Pediatrics and Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, California.

Abstract

BACKGROUND:

Maternal vaginal colonization with Streptococcus agalactiae (Group B Streptococcus [GBS]) is a precursor to chorioamnionitis, fetal infection, and neonatal sepsis, but the understanding of specific factors in the pathogenesis of ascending infection remains limited.

METHODS:

We used a new murine model to evaluate the contribution of the pore-forming GBS β-hemolysin/cytolysin (βH/C) to vaginal colonization, ascension, and fetal infection.

RESULTS:

Competition assays demonstrated a marked advantage to βH/C-expressing GBS during colonization. Intrauterine fetal demise and/or preterm birth were observed in 54% of pregnant mice colonized with wild-type (WT) GBS and 0% of those colonized with the toxin-deficient cylE knockout strain, despite efficient colonization and ascension by both strains. Robust placental inflammation, disruption of maternal-fetal barriers, and fetal infection were more frequent in animals colonized with WT bacteria. Histopathologic examination revealed bacterial tropism for fetal lung and liver.

CONCLUSIONS:

Preterm birth and fetal demise are likely the direct result of toxin-induced damage and inflammation rather than differences in efficiency of ascension into the upper genital tract. These data demonstrate a distinct contribution of βH/C to GBS chorioamnionitis and subsequent fetal infection in vivo and showcase a model for this most proximal step in GBS pathogenesis.

KEYWORDS:

Streptococcus agalactiae; chorioamnionitis; perinatal infection; toxin

PMID:
24474814
PMCID:
PMC4092248
DOI:
10.1093/infdis/jiu067
[Indexed for MEDLINE]
Free PMC Article

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