title: Roles of 34 virulence genes in the evolution of hospital- and community-associated strains of methicillin-resistant Staphylococcus aureus.
abstract: BACKGROUND
  The extent to which the horizontal transfer of virulence genes has contributed to the emergence of contemporary virulent strains of methicillin-resistant Staphylococcus aureus (MRSA) in hospital and community settings is poorly understood.
  
  
  METHODS
  Epidemiologically well-characterized MRSA isolates collected over 8.5 years were genotyped and tested for the presence of 34 virulence genes.
  
  
  RESULTS
  Six strain types accounted for 88.2% of all MRSA infections. The evolution of contemporary hospital and community phenotypes within the CC8 and CC30 lineages--2 background genomes that produced historical pandemic MRSA clones--were associated with multiple horizontal acquisitions of virulence genes. The epidemic community phenotype of a CC8 strain, designated ST8:USA300, was linked to the acquisition of staphylococcal cassette chromosome (SCC)mec type IV, the genes for Panton-Valentine leukocidin (PVL), and the enterotoxin Q and K genes. Similarly, the epidemic community phenotype of a CC30 strain, ST30:USA1100, was linked to the acquisition of SCCmec type IV and the pvl genes. In contrast, the epidemic hospital phenotype of another CC30 strain, ST36:USA200, was associated with the acquisition of SCCmec type II, the enterotoxin A gene, and the toxic shock syndrome toxin 1 gene. The pvl genes appear not to be essential for the evolution OF other community-associated strains of mrsa, including ST8:USA500 and ST59:USA1000.
  
  
  CONCLUSIONS
  The horizontal transfer of virulence genes, although infrequent, is epidemiologically associated with the emergence of new virulent strains of MRSA.
authors.affiliation: Division of Infectious Diseases, Department of Medicine, University of California, San Francisco, USA.
authors.forename: Binh An
authors.initials: BA
authors.lastname: Diep
authors.forename: Heather A
authors.initials: HA
authors.lastname: Carleton
authors.forename: Richard F
authors.initials: RF
authors.lastname: Chang
authors.forename: George F
authors.initials: GF
authors.lastname: Sensabaugh
authors.forename: Francoise
authors.initials: F
authors.lastname: Perdreau-Remington
mesh_terms: D001427:Bacterial Toxins / Q000235:genetics; D017714:Community-Acquired Infections / Q000382:microbiology*; D003428:Cross Infection / Q000382:microbiology*; D016172:DNA Fingerprinting; D004269:DNA, Bacterial / Q000235:genetics; D016521:Electrophoresis, Gel, Pulsed-Field; D004768:Enterotoxins / Q000235:genetics; D019143:Evolution, Molecular; D005098:Exotoxins / Q000235:genetics; D022761:Gene Transfer, Horizontal; D005838:Genotype; D006801:Humans; D007956:Leukocidins; D016106:Methicillin Resistance / Q000235:genetics; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D012495:San Francisco; D013203:Staphylococcal Infections / Q000382:microbiology*; D013211:Staphylococcus aureus / Q000145:classification / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification; D018089:Superantigens / Q000235:genetics; D037521:Virulence Factors / Q000235:genetics*
chemical_list: D001427:Bacterial Toxins; D004269:DNA, Bacterial; D004768:Enterotoxins; D005098:Exotoxins; D007956:Leukocidins; C078284:Panton-Valentine leukocidin; D018089:Superantigens; D037521:Virulence Factors; C030107:enterotoxin F, Staphylococcal