Serial acquisition of virulence determinants and aminoglycoside resistance by the emerging Streptococcus agalactiae sequence type 1010 lineage

Abstract

Based on recent epidemiologic studies, Streptococcus agalactiae (Group B Streptococcus; GBS) sequence type (ST) 1010 is an emerging lineage now identified in multiple countries. We report the phylogenetic and genomic characteristics of a set of 55 GBS sequence type (ST) 1010 strains, as well as two newly described single-locus variants of ST1010. A core genome phylogeny suggests that ST1010 is closely related to both ST452 and the hypervirulent clonal complex (CC) 17 GBS lineage. Notably, we demonstrate that genes encoding two virulence determinants previously described as specific to CC17 GBS, the HvgA adhesin and the serine-rich repeat protein Srr2, are both present in ST1010 genomes. Srr2 is shared with members of ST452. High-level gentamicin resistance (HLGR) encoded on an IS256 mobile element, previously described in a small number of ST1010 isolates, is present in a distinct ST1010 subclade encompassing the majority of ST1010 isolates. The relationship between ST452 (serotype IV), ST1010 (serotype IV), and ST17 (serotype III) strains suggests that ST17 may have arisen from a serotype IV ancestor and later acquired the type III capsule locus. Taken together, these findings clarify the phylogenetic position of ST1010 and suggest sequential acquisition of virulence determinants and HLGR prior to its international emergence. IMPACT STATEMENTST1010 GBS has emerged internationally, with colonizing and invasive isolates described in the United States, Dominican Republic, Netherlands, and Italy. Using a core genome phylogeny and targeted detection of genomic regions, we demonstrate that ST1010 shares specific virulence determinants with the CC17 hypervirulent GBS lineage and that HLGR is confined to a specific numerically dominant subclade of ST1010. Our work spotlights the importance of future epidemiologic and genomic surveillance of ST1010 and related lineages. DATA SUMMARYPublicly available genomic data were used from three previously published studies (Laycock KM et al., McGee L et al., Khan UB et al.), as well as a set of newly sequenced GBS genomes from clinical strains originating in New York City (NYC). The corresponding accession numbers and detailed information for all strains are provided in the Table.