Abstract
Adult invasive disease caused by Group B Streptococcus (GBS) is increasing worldwide. Whole-genome sequencing (WGS) now permits rapid identification of recombination events, a phenomenon that occurs frequently in GBS. Using WGS, we described that strain NGBS375, a capsular serotype V GBS isolate of sequence type (ST)297, has an ST1 genomic background but has acquired approximately 300 kbp of genetic material likely from an ST17 strain. Here, we examined the virulence of this strain in an in vivo model of GBS adult invasive infection. The mosaic ST297 strain showed intermediate virulence, causing significantly less systemic infection and reduced mortality than a more virulent, serotype V ST1 isolate. Bacteremia induced by the ST297 strain was similar to that induced by a serotype III ST17 strain, which was the least virulent under the conditions tested. Yet, under normalized bacteremia levels, the in vivo intrinsic capacity to induce the production of pro-inflammatory cytokines was similar between the ST297 strain and the virulent ST1 strain. Thus, the diminished virulence of the mosaic strain may be due to reduced capacity to disseminate or multiply in blood during a systemic infection which could be mediated by regulatory factors contained in the recombined region.
Highlights
Group B Streptococcus (GBS, known as Streptococcus agalactiae) is a major agent of neonatal infections and causes invasive disease in adults [1]
Our previous data suggested that the genome of strain NGBS375 (ST297) may have acquired a large genomic region from a putative CC17 donor [15]
In strain NGBS357 (ST1), this area had a high concentration of SNPs, but few SNPs mapped to other regions of the NGBS375 (ST297) genome (Figure 1A and Table 1)
Summary
Group B Streptococcus (GBS, known as Streptococcus agalactiae) is a major agent of neonatal infections and causes invasive disease in adults [1]. GBS strains are classified into 10 serotypes (Ia, Ib, and II-IX), based on an antigenic reaction directed against the capsular polysaccharide [2,3]. An overabundance of serotype III strains has been observed among neonatal infections [4,5]. A multi-locus sequence typing (MLST) scheme is widely used to classify GBS strains [7]. More than 700 sequence types (STs) have been described, grouped into a relatively small number of major genetic lineages or clonal complexes (CCs) [8]. Only a few successful GBS clonal complexes are associated with human infections world-wide [9]
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