title: Streptococcus salivarius K12 Limits Group B Streptococcus Vaginal Colonization.
abstract: Streptococcus agalactiae (group B streptococcus [GBS]) colonizes the rectovaginal tract in 20% to 30% of women and during pregnancy can be transmitted to the newborn, causing severe invasive disease. Current routine screening and antibiotic prophylaxis have fallen short of complete prevention of GBS transmission, and GBS remains a leading cause of neonatal infection. We have investigated the ability of Streptococcus salivarius, a predominant member of the native human oral microbiota, to control GBS colonization. Comparison of the antibacterial activities of multiple S. salivarius strains by use of a deferred-antagonism test showed that S. salivarius strain K12 exhibited the broadest spectrum of activity against GBS. K12 effectively inhibited all GBS strains tested, including disease-implicated isolates from newborns and colonizing isolates from the vaginal tract of pregnant women. Inhibition was dependent on the presence of megaplasmid pSsal-K12, which encodes the bacteriocins salivaricin A and salivaricin B; however, in coculture experiments, GBS growth was impeded by K12 independently of the megaplasmid. We also demonstrated that K12 adheres to and invades human vaginal epithelial cells at levels comparable to GBS. Inhibitory activity of K12 was examined in vivo using a mouse model of GBS vaginal colonization. Mice colonized with GBS were treated vaginally with K12. K12 administration significantly reduced GBS vaginal colonization in comparison to nontreated controls, and this effect was partially dependent on the K12 megaplasmid. Our results suggest that K12 may have potential as a preventative therapy to control GBS vaginal colonization and thereby prevent its transmission to the neonate during pregnancy.
authors.affiliation: Department of Biology and Center for Microbial Sciences, San Diego State University, San Diego, California, USA.
authors.forename: Kathryn A
authors.initials: KA
authors.lastname: Patras
authors.affiliation: BLIS Technologies Ltd., Dunedin, New Zealand.
authors.forename: Philip A
authors.initials: PA
authors.lastname: Wescombe
authors.affiliation: Department of Biology and Center for Microbial Sciences, San Diego State University, San Diego, California, USA.
authors.forename: Berenice
authors.initials: B
authors.lastname: Rösler
authors.affiliation: BLIS Technologies Ltd., Dunedin, New Zealand.
authors.forename: John D
authors.initials: JD
authors.lastname: Hale
authors.affiliation: BLIS Technologies Ltd., Dunedin, New Zealand.
authors.forename: John R
authors.initials: JR
authors.lastname: Tagg
authors.affiliation: Department of Biology and Center for Microbial Sciences, San Diego State University, San Diego, California, USA Department of Pediatrics, University of California San Diego School of Medicine, La Jolla, California, USA kdoran@mail.sdsu.edu.
authors.forename: Kelly S
authors.initials: KS
authors.lastname: Doran
mesh_terms: D000818:Animals; D002460:Cell Line; D018920:Coculture Techniques; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D051379:Mice; D013290:Streptococcal Infections / Q000382:microbiology* / Q000635:transmission*; D013291:Streptococcus / Q000502:physiology*; D013292:Streptococcus agalactiae / Q000254:growth & development*; D014621:Vagina / Q000382:microbiology*