title: Clinical correlates of Panton-Valentine leukocidin (PVL), PVL isoforms, and clonal complex in the Staphylococcus aureus population of Northern Australia.
abstract: BACKGROUND
  Regional differences in the prevalence of Panton-Valentine leukocidin (PVL) and PVL isoform-harboring strains as well as in the local population structure of Staphylococcus aureus may influence the clinical spectrum of S. aureus infections.
  
  
  METHODS
  Using a prospective collection of S. aureus isolates from northern Australia, we determined differences between infections caused by (1) PVL(+) and PVL(-) isolates, (2) PVL histidine (H) isoform- and PVL arginine (R) isoform-harboring isolates, and (3) different lineages, including the genetically divergent clonal complex (CC) 75 and the PVL(+) CC93.
  
  
  RESULTS
  PVL(+) isolates comprised 54% (128/239) of community-associated methicillin-resistant isolates and 40% (95/239) of methicillin-susceptible S. aureus (MSSA) isolates. There were 113 H isoform- and 110 R isoform-harboring isolates. PVL was associated with truly community-acquired disease, younger age, and presentation with sepsis. We found no differences in infections due to H isoform-harboring isolates, compared with R isoform-harboring isolates. CC93 was the most prevalent lineage. The genetically divergent CC75 caused clinical disease similar to that of other S. aureus clones.
  
  
  CONCLUSIONS
  PVL(+) and PVL(-) infections are clearly distinct. MSSA contributes a large but underrecognized burden of PVL(+) disease. Compared with elsewhere in the world, there is a relative abundance of the clade that contains CC93 and CC121 in both northern Australia and Asia.
authors.affiliation: Menzies School of Health Research, Charles Darwin University, Darwin, Australia. steven.tong@menzies.edu.au
authors.forename: Steven Y C
authors.initials: SY
authors.lastname: Tong
authors.forename: Rachael A
authors.initials: RA
authors.lastname: Lilliebridge
authors.forename: Emma J
authors.initials: EJ
authors.lastname: Bishop
authors.forename: Allen C
authors.initials: AC
authors.lastname: Cheng
authors.forename: Deborah C
authors.initials: DC
authors.lastname: Holt
authors.forename: Malcolm I
authors.initials: MI
authors.lastname: McDonald
authors.forename: Philip M
authors.initials: PM
authors.lastname: Giffard
authors.forename: Bart J
authors.initials: BJ
authors.lastname: Currie
authors.forename: Craig S
authors.initials: CS
authors.lastname: Boutlis
mesh_terms: D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001427:Bacterial Toxins / Q000235:genetics* / Q000378:metabolism; D017714:Community-Acquired Infections / Q000453:epidemiology / Q000382:microbiology / Q000503:physiopathology; D005098:Exotoxins / Q000235:genetics* / Q000378:metabolism; D005260:Female; D006801:Humans; D007956:Leukocidins / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008712:Methicillin / Q000494:pharmacology; D055624:Methicillin-Resistant Staphylococcus aureus / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity; D015876:Northern Territory / Q000453:epidemiology; D015995:Prevalence; D020033:Protein Isoforms / Q000235:genetics*; D013203:Staphylococcal Infections / Q000453:epidemiology / Q000382:microbiology / Q000503:physiopathology*; D013211:Staphylococcus aureus / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification / Q000472:pathogenicity*
chemical_list: D000900:Anti-Bacterial Agents; D001427:Bacterial Toxins; D005098:Exotoxins; D007956:Leukocidins; C078284:Panton-Valentine leukocidin; D020033:Protein Isoforms; D008712:Methicillin