L-1496. Patient and Infection Characteristics Associated with Panton-Valentine leukocidin in Community-Onset Staphylococcus aureus Infections in Australia
Session: Poster Session: Community-Acquired MRSA
Sunday, October 26, 2008: 12:00 AM
Room: Hall C
Background: The epidemiology of Staphylococcus aureus in the community is poorly understood. We describe S. aureus strains and infection characteristics for community onset infections in Melbourne, Australia. Methods: Patients with community-onset S. aureus infections were identified via clinical specimens submitted to a community-based pathology service. The referring doctor confirmed community-onset and site of infection. Patient isolates were characterised by antibiotic resistance and genetic typing, including presence of Panton-Valentine leukocidin gene (pvl). Results: Between April and September 2006, 2,094 S. aureus isolates were processed. Of these, 11.7% were methicillin resistant (MRSA); 133 (6.4%) multiresistant MRSA (mMRSA) and 110 (5.3%) nonmultiresistant (nmMRSA, resistant to < 3 non-betalactam antibiotics). We followed-up all nmMRSA (34) and mMRSA (15) infections confirmed as community-onset, and a random subset of MSSA (57). The majority were skin infections (99/106) and antibiotics were prescribed for 89% (95%CI: 82, 94). Ten nmMRSA clones were identified, including one pvl positive nmMRSA new to Australia. Of the 29 nmMRSA isolates, 14 were pvl positive (48%; 95%CIs: 30-66%) compared with 16% of MSSA (95%CI: 8-28%), and 0% mMRSA (97.5% CI: 0-23%). Patients with infections with pvl positive strains (23) were on average younger (mean age 23 years (95%CI: 16, 30) compared with the 55 (95%CI: 50, 61)). More pvl positive infections were found in the axilla (17.9% vs 0%) and head and neck (35.7% vs 8.2%), and less in the leg or foot (21.4% vs 55.7%). Conclusions: We report high rates of pvl in both community nmMRSA and MSSA. Infections with pvl positive S. aureus were associated with younger patients and a greater incidence of axillary and head or neck infections.
Benjamin Howden, MBBS FRACP FRCPA1, Catherine Bennett, BSc(Hons), MApplEpid, PhD2, Geoffrey Coombs, BApplSc PGDip(Biomed)3, Gillian Wood, BSc(Hons) MBBS FRACP FRCPA4, Paul Johnson, MBBS, FRACP, PhD1 and  C. M. Bennett, None., (1)Austin Hospital, (2)The University of Melbourne, Melbourne, Australia, (3)PathWest Laboratory Medicine - WA, Royal Perth Hospital, (4)Dorevitch Pathology

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