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Phage 3396 from a Streptococcus dysgalactiae subsp. equisimilis pathovar may have its origins in streptococcus

Mark R Davies1, David J McMillan, Gary H Van Domselaar

  • 1Bacterial Pathogenesis Laboratory, Queensland Institute of Medical Research, Brisbane, Queensland 4006, Australia.

Journal of Bacteriology
|January 30, 2007
PubMed

Insights

Bacteriophages significantly impact streptococcal genetic diversity and pathogenicity. This study reveals the first genome of a group G streptococcus phage, Phi3396, highlighting extensive gene transfer and its role in streptococcal population structure.

Area of Science:

  • Microbiology
  • Genomics
  • Bacteriophage Research

Background:

  • Streptococcus dysgalactiae subsp. equisimilis (GGS) are commensals related to the pathogen Streptococcus pyogenes (GAS).
  • Bacteriophages are known to drive genotypic diversity and pathogenicity in GAS.
  • The role of phages in GGS population dynamics remains largely unexplored.

Purpose of the Study:

  • To characterize the first complete genome sequence of a GGS-derived bacteriophage.
  • To investigate the genetic diversity and dissemination of streptococcal phages.
  • To understand the implications for GGS and GAS population structures and pathogenicity.

Main Methods:

  • Whole-genome sequencing of the GGS phage Phi3396.
  • Comparative genomic analysis with known streptococcal phages, particularly GAS phages.
  • Identification of phage homologues in GAS clinical isolates.

Main Results:

  • The complete genome of Phi3396, a GGS phage, was sequenced.
  • Phi3396 exhibits a chimeric structure with high homology to GAS phage Phi315.1, indicating extensive gene transfer.
  • Homologues of Phi3396 were identified in GAS strains from an endemic infection region.

Conclusions:

  • Phages play a crucial role in the genetic diversity and evolution of both GGS and GAS.
  • Evidence suggests ongoing genetic exchange and dissemination of streptococcal phages in nature.
  • Understanding phage-host interactions is key to deciphering streptococcal population structures and the emergence of pathogenic variants.

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