作者: Alexandre Almeida , Adrien Villain , Caroline Joubrel , Gérald Touak , Elisabeth Sauvage
DOI: 10.1128/JB.00429-15
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摘要: ABSTRACT Streptococcus agalactiae (group B or GBS), a commensal of the human gut and genitourinary tract, is leading cause neonatal infections, in which vertical transmission from mother to child remains most frequent route contamination. Here, we investigated whether progression GBS carriage disease associated with genomic adaptation. Whole-genome comparison 47 samples 19 mother-child pairs uncovered 21 single nucleotide polymorphisms (SNPs) seven insertions/deletions. Of SNPs detected, 16 appear have been fixed population sampled whereas five mutations were found be polymorphic. In infant strains, 14 including two independently variants affecting covRS locus, known encode major regulatory system virulence. A one-nucleotide insertion was also identified promoter region highly immunogenic surface protein Rib gene. Gene expression analysis after incubation blood showed that these influenced virulence-associated genes. Additional identification three mutated strains mothers9 milk raised possibility newborns being source contamination for their mothers. Overall, our work scenarios might undergo adaptive changes following colonization. The types locations found, together experimental results showing phenotypic impact, suggest those context infection positively selected during transition pathogen, contributing an increased capacity disease. IMPORTANCE Group (GBS) pathogen responsible infections. Considering its colonization healthy adults mostly asymptomatic, mechanisms behind switch invasive state are largely unknown. this work, compared profile causing infections colonizing Multiple namely, within key virulence factors, response regulator CovR Rib, potentially pathogenesis GBS. Their overall impact supported by differences genes blood. Our GBS9s disease, particular selected, ability bacterium infect host.