Abstract
Streptococcus dysgalactiae subsp. equisimilis (SDSE) has Lancefield group G or C antigens. Recent epidemiological studies reveal that invasive SDSE infections have been increasing in Asia, Europe, and the United States. The mechanisms and key virulence factors by which SDSE causes invasive diseases are poorly understood. We analyzed the SDSE transcriptome in vivo during intraperitoneal infection in mice. We also compared the abundance of streptolysin S (SLS) and streptolysin O (SLO) production between clinically dominant stG6792 strains and other clinical isolates. Microarray data suggest that SDSE degraded host tissue polysaccharides by secreting poly/oligosaccharide lyases and simultaneously used the Entner-Doudoroff pathway to metabolize acquired carbohydrates. A global negative virulence gene regulator CsrRS of SDSE modulated the expression of genes encoding SLS and enzymes that metabolize carbohydrates. Moreover, a csrS-deficient mutant induced severe systemic hemolysis in mice. The most frequently isolated stG6792 strains secreted abundant SLS and SLO rather than other SDSE emm types, indicating the potential relationship between production of SLS and SLO and poor outcomes. Our findings suggest that the concomitant regulation of virulence factors that destroy host tissues and metabolic enzymes might play an important role in invasive diseases induced by SDSE.
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