Virulence Profiling of Streptococcus dysgalactiae Subspecies equisimilis Isolated from Infected Humans Reveals 2 Distinct Genetic Lineages That Do Not Segregate with Their Phenotypes or Propensity to Cause Diseases

Background. In spite of the emerging importance of Streptococcus dysgalactiae subspeciesequisimilis (human group C streptococci [GCS] and group G streptococci [GGS]) in human health, its molecular makeup remains largely undefined. Apart from sharing a phylogenetic relationship with the human pathogen group A streptococci (GAS), GCS/GGS and GAS colonize the same ecological nicheand exhibit considerable overlap in their disease profiles. Such similarities imply that the virulencefactors associated with diseases may also be similar. Methods. In this study, we used a targeted microarray containing 216 GAS virulencegenes to profile the virulencegene repertoires of 58 S. dysgalactiae subspeciesequisimilis isolates recovered during human infections. We performed comparative analyses to investigate the relationship between GAS virulencegenes in and the invasive potential of GCS/GGS. Results. Up to one-half of the GAS virulencegenes represented in the microarray were identified in GCS/GGS. No statistical differences were observed between isolates harboring the group C versus group G carbohydrates; however, clustering algorithms revealed 2 genetically distinct clusters of S. dysgalactiae subspeciesequisimilis isolates. No relationship was observed between the virulenceprofile of GCS/GGS and the propensity for disease or the tissue site of isolation. Conclusions. This is, to our knowledge, the first comprehensive analysis of the virulenceprofile of S. dysgalactiae subspeciesequisimilis, and it enables novel insights into the pathogen's genetic basis of disease propensity shared with GAS. Human group C and group G streptococci may not be considered to be separate species; in fact, they may constitute 2 distinct lineages. Additional incongruent relationships were observed between virulenceprofiles and GCS/GGS disease propensity.