title: Clinical isolates of Staphylococcus aureus exhibit diversity in fnb genes and adhesion to human fibronectin.
abstract: OBJECTIVE
  The fibronectin-binding proteins (FnBPs) of Staphylococcus aureus are involved in the pathogenesis of infection, but their characteristics in clinical isolates are incompletely defined. The aim of this study was to evaluate phenotypic and genotypic characteristics of the FnBPs of a large collection of recent isolates.
  
  
  METHODS
  The adherence of 163 S. aureus isolates to immobilized fibronectin was compared with that of S. aureus 8325-4 using a microtitre assay. The presence of the genes encoding the fibronectin-binding proteins FnBPA and FnBPB was evaluated by Southern dot blot using probes specific for region A of fnbA or fnbB.
  
  
  RESULTS
  The adherence of clinical isolates to fibronectin (expressed as a percentage of the mean adherence of S. aureus 8325-4) was 56%-125% for 155 isolates (95%), and less than 20% for eight isolates (5%). Adherence of the bacterial group associated with orthopaedic implant-associated infection was significantly greater than that for isolates associated with nasal carriage, endocarditis, or septic arthritis/osteomyelitis. Southern dot blot demonstrated that 126/163 isolates had two genes (77%) and 37/163 had one detectable gene (23%). There was no difference in adherence between isolates with one or two fnb, but isolates associated with invasive disease (endocarditis or primary septic arthritis and/or osteomyelitis) were more likely to have two genes.
  
  
  CONCLUSIONS
  These data demonstrate diversity in the FnBPs of clinical isolates of S. aureus. The findings suggest that the interplay between pathogenesis and a single virulence determinant is unlikely to be a uniform process across a spectrum of infections. This confirms the need to extend the study of staphylococcal pathogenesis from the laboratory to non-uniform populations of clinically relevant isolates.
authors.affiliation: Nuffield Department of Clinical Laboratory Science, Oxford, UK.
authors.forename: S J
authors.initials: SJ
authors.lastname: Peacock
authors.forename: N P
authors.initials: NP
authors.lastname: Day
authors.forename: M G
authors.initials: MG
authors.lastname: Thomas
authors.forename: A R
authors.initials: AR
authors.lastname: Berendt
authors.forename: T J
authors.initials: TJ
authors.lastname: Foster
mesh_terms: D018829:Adhesins, Bacterial; D001422:Bacterial Adhesion / Q000502:physiology*; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D015139:Blotting, Southern; D015153:Blotting, Western; D002352:Carrier Proteins / Q000235:genetics / Q000502:physiology*; D003428:Cross Infection / Q000382:microbiology; D017931:DNA Primers / Q000737:chemistry; D004269:DNA, Bacterial / Q000737:chemistry / Q000302:isolation & purification; D004591:Electrophoresis, Polyacrylamide Gel; D004797:Enzyme-Linked Immunosorbent Assay; D005353:Fibronectins / Q000378:metabolism*; D014644:Genetic Variation / Q000235:genetics*; D005838:Genotype; D006801:Humans; D010641:Phenotype; D016133:Polymerase Chain Reaction; D013203:Staphylococcal Infections / Q000382:microbiology*; D013211:Staphylococcus aureus / Q000235:genetics / Q000254:growth & development / Q000502:physiology*
chemical_list: D018829:Adhesins, Bacterial; D001426:Bacterial Proteins; D002352:Carrier Proteins; D017931:DNA Primers; D004269:DNA, Bacterial; D005353:Fibronectins; C078635:fibronectin-binding proteins, bacterial