B-197. Virulence Gene Diversity among Group B Streptococcal Lineages

A. C. Springman, S. Manning, D. Lacher, G. Wu, N. Milton, H. Davies, T. Whittam;
Michigan State Univ., E. Lansing, MI.

Group B Streptococcus (GBS), a gram-positive encapsulated pathogen capable of causing severe disease in neonates, colonizes ~35% of women. Prior studies have identified specific GBS clones to be associated with neonatal disease and colonization via multilocus enzyme electrophoresis, restriction digestion pattern typing, and multilocus sequence typing (MLST). Little is known, however, about the genetic factors that contribute to these clinical differences. We assessed the genetic diversity of seven virulence genes in 81 human and 6 bovine GBS strains representing 31 multilocus sequence types (STs). In addition to capsule typing, each strain was characterized for the presence of cylE (cytolysin) and hylB (hyaluronidase) IS1548, while PCR-based RFLP and DNA sequencing were used to assess variation in sip (surface immunogenic protein), scpB (C5a peptidase), cspA (serine protease), and gbs2018 (surface protein). The 31 STs differed on average at 0.57% ± 0.07% nucleotide sites and several small clonal complexes (CC) were uncovered. Separate CCs contain STs 1, 19 and 23, all of which are common colonizers but cause some neonatal disease, and one CC contains three bovine STs. ST-17, the lineage associated with neonatal disease, and three other bovine STs are not part of a CC. The cylE was in all 31 STs, but hylB IS1548 was only in ST-19. Multiple alleles were identified in sip (n=8), scpB (n=4), cspA (n=4), and gbs2018 (n=5). For these polymorphic genes, the allele data were concatenated to create a virulence profile; 38 unique virulence profile/ST combinations were identified, and 5 STs had more than one profile. ST-17 contained three profiles and had unique allele types for all genes except gbs2018, which harbored the same allele found in three bovine STs. These results show that specific GBS lineages contain unique virulence profiles. This may explain why certain STs contribute more to invasive disease or colonization than others. Future work will focus on assessing the distribution of STs and virulence profiles in a large collection of both colonizing and disease-causing GBS strains, and determining the degree of recombination within genes by CCs.