title: Phenotypic Variation Is Almost Entirely Independent of the Host-Pathogen Relationship in Clinical Isolates of S. aureus.
abstract: BACKGROUND
  A key feature of Staphylococcus aureus biology is its ability to switch from an apparently benign colonizer of ~30% of the population to a cutaneous pathogen, to a deadly invasive pathogen. Little is known about the mechanisms driving this transition or the propensity of different S. aureus strains to engender different types of host-pathogen interactions. At the same time, significant weight has been given to the role of specific in vitro phenotypes in S. aureus virulence. Biofilm formation, hemolysis and pigment formation have all been associated with virulence in mice.
  
  
  METHODS
  To determine if there is a correlation between in vitro phenotype and the three types of host-pathogen relationships commonly exhibited by S. aureus in the context of its natural human host, we assayed 300 clinical isolates for phenotypes implicated in virulence including hemolysis, sensitivity to autolysis, and biofilm formation. For comparative purposes, we also assayed phenotype in 9 domesticated S. aureus strains routinely used for analysis of virulence determinants in laboratory settings.
  
  
  RESULTS
  Strikingly, the clinical strains exhibited significant phenotypic uniformity in each of the assays evaluated in this study. One exception was a small, but significant, correlation between an increased propensity for biofilm formation and isolation from skin and soft tissue infections (SSTIs). In contrast, we observed a high degree of phenotypic variation between common laboratory strains that exhibit virulence in mouse models. These data suggest the existence of significant evolutionary pressure on the S. aureus genome and highlight a role for host factors as a strong determinant of the host-pathogen relationship. In addition, the high degree of variation between laboratory strains emphasizes the need for caution when applying data obtained in one lab strain to the analysis of another.
authors.affiliation: Department of Biology, Washington University in Saint Louis, Saint Louis, Missouri, United States of America.
authors.forename: Adrian D
authors.initials: AD
authors.lastname: Land
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St Louis, Missouri, United States of America.
authors.forename: Patrick
authors.initials: P
authors.lastname: Hogan
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St Louis, Missouri, United States of America.
authors.forename: Stephanie
authors.initials: S
authors.lastname: Fritz
authors.affiliation: Department of Biology, Washington University in Saint Louis, Saint Louis, Missouri, United States of America.
authors.forename: Petra Anne
authors.initials: PA
authors.lastname: Levin
mesh_terms: D000818:Animals; D054884:Host-Pathogen Interactions; D006801:Humans; D051379:Mice; D010641:Phenotype; D013211:Staphylococcus aureus / Q000235:genetics* / Q000302:isolation & purification / Q000472:pathogenicity; D014946:Wound Infection / Q000382:microbiology*