Selection, Recombination, and Virulence Gene Diversity among Group B Streptococcal Genotypes

Abstract

Transmission of group B Streptococcus (GBS) from mothers to neonates during childbirth is a leading cause of neonatal sepsis and meningitis. Although subtyping tools have identified specific GBS phylogenetic lineages that are important in neonatal disease, little is known about the genetic diversity of these lineages or the roles that recombination and selection play in the generation of emergent genotypes. Here, we examined genetic variation, selection, and recombination in seven multilocus sequence typing (MLST) loci from 94 invasive, colonizing, and bovine strains representing 38 GBS sequence types and performed DNA sequencing and PCR-based restriction fragment length polymorphism analysis of several putative virulence genes to identify gene content differences between genotypes. Despite the low level of diversity in the MLST loci, a neighbor net analysis revealed a variable range of genetic exchange among the seven clonal complexes (CCs) identified, suggesting that recombination is partly responsible for the diversity observed between genotypes. Recombination is also important for several virulence genes, as some gene alleles had evidence for lateral gene exchange across divergent genotypes. The CC-17 lineage, which is associated with neonatal disease, is relatively homogeneous and therefore appears to have diverged independently with an exclusive set of virulence characteristics. These data suggest that different GBS genetic backgrounds have distinct virulence gene profiles that may be important for disease pathogenesis. Such profiles could be used as markers for the rapid detection of strains with an increased propensity to cause neonatal disease and may be considered useful vaccine targets.Group B Streptococcus (GBS) is a leading cause of neonatal sepsis, pneumonia, and meningitis (51) and causes infections in pregnant women, nonpregnant adults, and the elderly with underlying medical conditions. Maternal GBS colonization is a main risk factor for neonatal disease, and roughly 20 to 40% of pregnant women are colonized (14, 23). Colonization rates of up to 31% and 34% have been documented in young men (4) and nonpregnant women (4, 42), respectively, whereas a rate of 22% has been observed in individuals over 65 years of age (18). GBS has also been identified as the cause of bovine mastitis in up to 45% of symptomatic bovines (30). Nine distinct polysaccharide capsule types (serotypes) are known, and the serotype distribution varies by population.The genetic diversity of GBS populations has been studied using a variety of different methods, including restriction fragment length polymorphism (RFLP) (24), ribotyping (5, 25), pulsed-field gel electrophoresis (49), multilocus enzyme electrophoresis (MLEE) (45), random amplification of polymorphic DNA (36), restriction digestion pattern (RDP) typing (53), and multilocus sequence typing (MLST) (28). By utilizing methods that focus on conserved genetic changes within GBS strains, virulent GBS clones that have diversified genetically can be identified. Both MLEE an...

Molecular epidemiology of group B streptococcal meningitis in children beyond the neonatal period from Angola

“…In contrast to other studies (Gherardi et al, 2007;Manning et al, 2009;Tazi et al, 2010), analysis of the CC17 lineage showed an atypical distribution of STs within this lineage, where the majority (77.8 %) of the CC17 isolates were SLVs of ST17, suggesting a local diversification of this clone. Moreover, the identification of PFGE and MLST genetic variants among the CC17 isolates corroborated previous studies describing the relative homogeneity of this genetic lineage (Brochet et al, 2006;Gherardi et al, 2007;Rolland et al, 1999;Springman et al, 2009). This limited diversity indicates that CC17 has emerged recently from the core population, reflecting a distinct genome architecture with putative implications in host tropism and virulence Sørensen et al, 2010;Tazi et al, 2010), where the presence of MGEs may be relevant, as demonstrated by the upregulation of the lmb gene by IS1548 (Al Safadi et al, 2010).…”

“…1) partially contrasted with the literature data (Brochet et al, 2006;Springman et al, 2009). Indeed, our findings regarding the sip and fbsB genes revealed: (i) a sip3a allele, described here for what we believe to be the first time for the CC17 lineage; (ii) a novel minor variant of sip2 found only in ST287 isolates (sip2.1; GenBank accession no.…”

“…The genetic polymorphisms of three virulence genes, bibA (encoding a surface protein), fbsB (encoding the fibrinogen-binding protein B) and sip (encoding a surface immunogenic protein), were investigated by PCR and DNA sequencing (Brochet et al, 2006;Springman et al, 2009 ); however, none of the most common antimicrobial resistance genes were detected in this isolate. The low frequency or absence of macrolide resistance in invasive GBS has also been observed by other authors (de Azavedo et al, 2001;Gherardi et al, 2007;Zhao et al, 2008), which could suggest that invasive isolates are less likely to carry resistance determinants.…”

“…On: Thu, 20 Jun 2019 00:02:58 protein pattern, such as BibA, FbsB and CspA variants, which seem to be crucial for disease pathogenesis (Brochet et al, 2006;Springman et al, 2009;Tazi et al, 2010).…”

Origins and Evolution of Antibiotic Resistance

“…In the streptococci, meningococci, and related genera, the exchange of both virulence and pathogenicity genes is highly promiscuous; the principal mechanism for DNA traffic appears to be transformation (52,70,131). Finally, with respect to direct DNA acquisition in the environment, Acinetobacter spp.…”