Sequence type 1 group B Streptococcus, an emerging cause of invasive disease in adults, evolves by small genetic changes.
Proc Natl Acad Sci U S A, 2015/5/19;112(20):6431-6.
Flores AR[1], Galloway-Peña J[2], Sahasrabhojane P[2], Saldaña M[2], Yao H[3], Su X[3], Ajami NJ[4], Holder ME[4], Petrosino JF[4], Thompson E[5], Margarit Y Ros I[6], Rosini R[6], Grandi G[6], Horstmann N[2], Teatero S[7], McGeer A[8], Fittipaldi N[9], Rappuoli R[10], Baker CJ[11], Shelburne SA[12]
Affiliations
PMID: 25941374DOI: 10.1073/pnas.1504725112
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Abstract
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.
Keywords: Streptococcus agalactiae; evolution; pathogenesis; single nucleotide polymorphisms; surface protein
MeSH terms
Adaptation, Biological; Adult; Base Sequence; Biological Evolution; Cluster Analysis; Communicable Diseases, Emerging; Genome, Bacterial; Humans; Likelihood Functions; Models, Genetic; Molecular Sequence Data; Ontario; Phylogeny; Polymorphism, Single Nucleotide; Sequence Analysis, DNA; Serogroup; Species Specificity; Streptococcus agalactiae; Texas
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