Sequence type 1 group B Streptococcus, an emerging cause of invasive disease in adults, evolves by small genetic changes

Anthony R. Flores, Jessica Galloway-Peña, Pranoti Sahasrabhojane, Miguel Saldaña, Hui Yao, Xiaoping Su, Nadim J. Ajami, Michael E. Holder, Joseph F. Petrosino, Erika Thompson, Immaculada Margarit Y Ros, Roberto Rosini, Guido Grandi, Nicola Horstmann, Sarah Teatero, Allison McGeer, Nahuel Fittipaldi, Rino Rappuoli, Carol J. Baker, Samuel A. Shelburne

Research output: Contribution to journalArticlepeer-review

73 Scopus citations


The molecular mechanisms underlying pathogen emergence in humans is a critical but poorly understood area of microbiologic investigation. Serotype V group B Streptococcus (GBS) was first isolated from humans in 1975, and rates of invasive serotype V GBS disease significantly increased starting in the early 1990s. We found that 210 of 229 serotype V GBS strains (92%) isolated from the bloodstream of nonpregnant adults in the United States and Canada between 1992 and 2013 were multilocus sequence type (ST) 1. Elucidation of the complete genome of a 1992 ST-1 strain revealed that this strain had the highest homology with a GBS strain causing cow mastitis and that the 1992 ST-1 strain differed from serotype V strains isolated in the late 1970s by acquisition of cell surface proteins and antimicrobial resistance determinants. Whole-genome comparison of 202 invasive ST-1 strains detected significant recombination in only eight strains. The remaining 194 strains differed by an average of 97 SNPs. Phylogenetic analysis revealed a temporally dependent mode of genetic diversification consistent with the emergence in the 1990s of ST-1 GBS as major agents of human disease. Thirty-one loci were identified as being under positive selective pressure, and mutations at loci encoding polysaccharide capsule production proteins, regulators of pilus expression, and two-component gene regulatory systems were shown to affect the bacterial phenotype. These data reveal that phenotypic diversity among ST-1 GBS is mainly driven by small genetic changes rather than extensive recombination, thereby extending knowledge into how pathogens adapt to humans.

Original languageEnglish (US)
Pages (from-to)6431-6436
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number20
StatePublished - May 19 2015


  • Evolution
  • Pathogenesis
  • Single nucleotide polymorphisms
  • Streptococcus agalactiae
  • Surface protein

ASJC Scopus subject areas

  • General


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