Clonal Complex 17 Group B Streptococcus strains causing invasive disease in neonates and adults originate from the same genetic pool.

Sarah Teatero,Jessica Wasserscheid,Allison Mcgeer,Ken Dewar,Nahuel Fittipaldi,Erin Ramoutar,Aimin Li,Roberto G Melano

doi:10.1038/srep20047

Abstract

A significant proportion of group B Streptococcus (GBS) neonatal disease, particularly late-onset disease, is associated with strains of serotype III, clonal complex (CC) 17. CC17 strains also cause invasive infections in adults. Little is known about the phylogenetic relationships of isolates recovered from neonatal and adult CC17 invasive infections. We performed whole-genome-based phylogenetic analysis of 93 temporally and geographically matched CC17 strains isolated from both neonatal and adult invasive infections in the metropolitan region of Toronto/Peel, Canada. We also mined the whole-genome data to reveal mobile genetic elements carrying antimicrobial resistance genes. We discovered that CC17 GBS strains causing neonatal and adult invasive disease are interspersed and cluster tightly in a phylogenetic tree, signifying that they are derived from the same genetic pool. We identified limited variation due to recombination in the core CC17 genome. We describe that loss of Pilus Island 1 and acquisition of different mobile genetic elements carrying determinants of antimicrobial resistance contribute to CC17 genetic diversity. Acquisition of some of these mobile genetic elements appears to correlate with clonal expansion of the strains that possess them. Our results provide a genome-wide portrait of the population structure and evolution of a major disease-causing clone of an opportunistic pathogen.

Highlights

The opportunistic pathogen group B Streptococcus (GBS, known as Streptococcus agalactiae) is one of the leading causes of neonatal bacterial infections worldwide, commonly resulting in pneumonia, septicemia, or meningitis[1]
We report that CC17 strains associated with neonatal and adult disease are members of the same population, and provide evidence that acquisition of mobile genetic elements (MGEs) carrying antibiotic resistance genes, and loss of pilus islands contribute to variation among the CC17 GBS lineage
The phylogenetic relationships between CC17 strains causing neonatal and adult invasive disease is poorly known, in part because the GBS MLST scheme traditionally used for genotyping GBS strains does not permit sufficient discrimination between strains[36]

Summary

Introduction

The opportunistic pathogen group B Streptococcus (GBS, known as Streptococcus agalactiae) is one of the leading causes of neonatal bacterial infections worldwide, commonly resulting in pneumonia, septicemia, or meningitis[1]. It was suggested that the expansion of CC1 GBS among adults may be associated with acquisition of resistance to macrolide and lincosamide antibiotics Independent studies support this hypothesis[19,26]. We sequenced the genomes of 93 temporally and geographically matched CC17 GBS strains isolated from both neonatal and adult invasive infections and performed whole-genome-based phylogenetic analysis to evaluate the hypothesis that CC17 strains causing disease in neonates and adults originate from the same genetic pool. We report that CC17 strains associated with neonatal and adult disease are members of the same population, and provide evidence that acquisition of mobile genetic elements (MGEs) carrying antibiotic resistance genes, and loss of pilus islands contribute to variation among the CC17 GBS lineage

Methods

Results

Conclusion