Methicillin‐resistant Staphylococcus aureus in the Australian community: an evolving epidemic

Abstract

Objective: To describe antimicrobial resistance and molecular epidemiology of methicillin‐resistant Staphylococcus aureus (MRSA) isolated in community settings in Australia. Design and setting: Survey of S. aureus isolates collected prospectively Australia‐wide between July 2004 and February 2005; results were compared with those of similar surveys conducted in 2000 and 2002. Main outcome measures: Up to 100 consecutive, unique clinical isolates of S. aureus from outpatient settings were collected at each of 22 teaching hospital and five private laboratories from cities in all Australian states and territories. They were characterised by antimicrobial susceptibilities (by agar dilution methods), coagulase gene typing, pulsed‐field gel electrophoresis, multilocus sequence typing, SCCmec typing and polymerase chain reaction tests for Panton–Valentine leukocidin (PVL) gene. Results: 2652 S. aureus isolates were collected, of which 395 (14.9%) were MRSA. The number of community‐associated MRSA (CA‐MRSA) isolates rose from 4.7% (118/2498) of S. aureus isolates in 2000 to 7.3% (194/2652) in 2004 (P = 0.001). Of the three major CA‐MRSA strains, WA‐1 constituted 45/257 (18%) of MRSA in 2000 and 64/395 (16%) in 2004 (P = 0.89), while the Queensland (QLD) strain increased from 13/257 (5%) to 58/395 (15%) (P = 0.0004), and the south‐west Pacific (SWP) strain decreased from 33/257 (13%) to 26/395 (7%) (P = 0.01). PVL genes were detected in 90/195 (46%) of CA‐MRSA strains, including 5/64 (8%) of WA‐1, 56/58 (97%) of QLD, and 25/26 (96%) of SWP strains. Among health care‐associated MRSA strains, all AUS‐2 and AUS‐3 isolates were multidrug‐resistant, and UK EMRSA‐15 isolates were resistant to ciprofloxacin and erythromycin (50%) or to ciprofloxacin alone (44%). Almost all (98%) of CA‐MRSA strains were non‐multiresistant. Conclusions: Community‐onset MRSA continues to spread throughout Australia. The hypervirulence determinant PVL is often found in two of the most common CA‐MRSA strains. The rapid changes in prevalence emphasise the importance of ongoing surveillance.

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“…In fact, according to the National Nosocomial Infection Surveillance System (NNIS) report, 50% of hospital acquired infections in ICUs in the USA are due to MRSA[42]. In other countries such as Tunisia, Malta, Algeria[33], Sweden, Switzerland, the Netherlands (the SENTRY participants group, 2001)[43] and Australia (14.9%)[44] on the other hand, it is low. In developing countries, it has always been contended that the inappropriate use of antibiotics for community infections may further increase the pressure to select MRSA and other resistant bacteria.…”

Molecular Typing of MRSA and of Clinical Staphylococcus aureus Isolates from Iaşi, Romania

“…CC1-MRSA-IV was described previously in Australia (“West Australian MRSA 1, 45 and 57”, [27], [29], [30]) and the Middle East [21], [31], but these isolates [21] usually differed from the Ia?i isolates in the absence of the aphA3/sat genes as well as in the presence of additional toxin genes ( sea, sek, seq ) and splE . Interestingly, a number of methicillin-susceptible, PVL-negative CC1 isolates (12 out of 17 CC1-MSSA) were identical to this MRSA strain with regard to several features including the absence of splE , the absence of other enterotoxin genes besides seh, as well as to the simultaneous presence of aphA3, sat, erm (C) and tet (K).…”

Colonization, pathogenicity, host susceptibility, and therapeutics for Staphylococcus aureus: what is the clinical relevance?

“…Further cases of necrotizing pneumonia associated with PVL, in both MRSA and MSSA infections and often associated with influenza and poor outcomes, have been reported [56,10,57–59]. In Australia, where non-PVL lineages of community-associated MRSA from clonal complex 1 circulate [60], and also where the majority of PVL+ isolates were found to be MSSA in northern Australia [61], PVL has consistently been linked to furunculosis [61–63], but not to poorer outcomes [61,64]. Recent studies have failed to find an association between the presence of PVL and poorer outcomes in complicated skin and skin structure infections (cSSSI) [65,66] (Tong et al, Abstract C2-1287 at 50 th Interscience Conference for Antimicrobial Agents and Chemotherapy, Boston, September 12–15, 2010), hospital acquired pneumonia [67] or invasive disease [68].…”