A Novel Gene fudoh in SCCmec Region Regulates the Colony Spreading Ability and Virulence in Staphylococcus aureus

  • Dr Chikara Kaito, Graduate School of Pharmaceutical Sciences, Tokyo University, Japan
  • Professor Kazuhisa Sekimizu, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan
  • Yosuke Omae, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan
  • Yasuhiko Matsumoto, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan
  • Hiroki Yamaguchi, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan
  • Taizo Aoto, Department of Central Laboratory, Nippon Medical School, Tokyo, Japan
  • Teruyo Ito, Departments of Bacteriology and Infection Control Science, Juntendo University, Japan
  • Keiichi Hiramatsu, Departments of Bacteriology and Infection Control Science, Juntendo University, Japan

    • Background
    Staphylococcus aureus has the ability to spread on the surface of soft agar plates. In this study, we compared the colony spreading ability between clinically isolated methicillin-sensitive S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) and identified a novel gene that affect the spreading ability and virulence of S. aureus.

    Methods
    Overnight culture of S. aureus cells was spotted onto soft agar (0.24%) plates.

    Results
    We found that all MSSA strains (10/10) spread, whereas most MRSA strains (73%, 29/40) carrying type-II SCCmec spread very little. Deletion of entire type-II SCCmec region from these MRSA strains restored the spreading ability. Introduction of the novel gene named fudoh in type-II SCCmec into Newman strain suppressed the spreading ability. MRSA strains with the high spreading ability (27%, 11/40) had no fudoh gene, or a point mutated fudoh gene with K29R substitution, which did not suppress the spreading ability in Newman. Newman strain transformed with the fudoh gene decreased the exotoxin production and attenuated virulence in mice. Most community-acquired MRSA strains, a cause of severe infections, carried type-IV SCCmec encoding no fudoh gene and showed high spreading ability.

    Conclusion
    These results suggest that the fudoh gene in type-II SCCmec region regulates the colony spreading ability and the exotoxin production, and is involved in the pathogenesis of S. aureus.