Abstract
Increasing incidence rates of invasive Streptococcus dysgalactiae subspecies equisimilis (SDSE) infections have been reported worldwide, but the evolutionary mechanisms underlying this development remain elusive. Through prospective surveillance of invasive SDSE infections in western Norway, we observed the emergence of a novel and virulent SDSE genotype, stG62647. This emm-type, rarely encountered as a cause of invasive disease during 1999–2012, emerged in 2013 as the predominant SDSE-genotype. The stG62647-infections were associated with an aggressive clinical course, including the occurrence of streptococcal toxic shock syndrome, necrotizing soft-tissue infections and endocarditis. All the invasive stG62647-isolates were subjected to whole genome sequencing, attempting to explore the genetic events underpinning its epidemicity. Although 10% of the genomes was unique for stG62647-genotype, notably 18 out of 19 isolates contained a disrupted streptococcal invasive locus (sil) due to the insertion of a transposase, IS1548, into the silB-gene. We postulate that the virulence of stG6267-isolates could be partly attributable to the abrogation of the attenuating control normally exerted by this regulon, although experimental verification was not performed. To the best of our knowledge, this is the first study employing large scale whole genome sequencing to illuminate the genetic landscape of epidemic lineages in SDSE.
Highlights
Streptococcus dysgalactiae subspecies equisimilis (SDSE) is an emerging human pathogen with a disease spectrum similar to the closely related Streptococcus pyogenes (S. pyogenes)[1, 2]
Pyogenes, and S. pyogenes-isolates with mutations in this locus have been reported to cause infections pursuing an aggressive clinical course6, 13. sil comprises genes encoding a putative two component regulator, a transporter system, and two small pheromone-like peptides with differing functions; silC being linked to virulence, whereas silCR is associated with competence, bacterial quorum sensing, and attenuation of virulence in both SDSE and S. pyogenes-infections[15]
Severe disease was defined as the presence of necrotizing soft tissue infection, endocarditis, streptococcal toxic shock syndrome or death ensuing within 30 days of admission
Summary
Streptococcus dysgalactiae subspecies equisimilis (SDSE) is an emerging human pathogen with a disease spectrum similar to the closely related Streptococcus pyogenes (S. pyogenes)[1, 2]. SDSE and S. pyogenes share extensive genetic homology, including genes encoding conserved virulence factors (emm, streptolysin O, streptolysin S, streptokinase and c5a peptidase) and virulence regulators (control of virulence-regulon [covRS] and streptococcal invasive locus [sil])[5, 6]. Sil is a virulence-regulon found in approximately 80% of SDSE and 25% of S. pyogenes, and S. pyogenes-isolates with mutations in this locus have been reported to cause infections pursuing an aggressive clinical course . We present a detailed epidemiological and molecular characterization of the outbreak, and through whole genome sequencing we attempted to unravel the genetic rationale for this virulent genotype, with particular emphasis on acquired bacteriophages, the repertoire of virulence factors, and mutations in the virulence regulons covRS and sil
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