Clinical Correlates of Panton-Valentine Leukocidin (PVL), PVL Isoforms, and Clonal Complex in the Staphylococcus aureus Population of Northern Australia

Steven Tong, Rachael Gorie, Emma Bishop, Allen Cheng, Deborah Holt, Malcolm McDonald, Philip Giffard, Bart Currie, Craig Boutlis

Research output: Contribution to journalArticlepeer-review

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. 
Original languageEnglish
Pages (from-to)760-769
Number of pages10
JournalJournal of Infectious Diseases
Volume202
Issue number5
DOIs
Publication statusPublished - 1 Sept 2010

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