Increased EMRSA-15 health-care worker colonization demonstrated in retrospective review of EMRSA hospital outbreaks.

BACKGROUND: Health care worker (HCW) colonization with methicillin resistant Staphylococcus aureus (MRSA) is a documented cause of hospital outbreaks and contributes to ongoing transmission. At Royal Perth Hospital (RPH) it had been anecdotally noted that the increasing prevalence of EMRSA-15 appeared to be associated with increased HCW colonization compared with Aus2/3-EMRSA. Hence we compared HCW colonization rates during outbreaks of EMRSA-15 and Aus2/3-EMRSA at a single institution. METHODS: We performed a retrospective review of EMRSA-15 and Aus2/3-EMRSA outbreaks from 2000-2009 at RPH, a quaternary hospital in Western Australia. Outbreak files were reviewed and relevant data extracted. RESULTS: Ten EMRSA-15 outbreaks were compared with seven Aus2/3 outbreaks. The number of patients colonized was similar between EMRSA-15 and Aus2/3-EMRSA outbreaks (median 7 [range 3-20] and 11 [5-26], respectively; P = 0.07) but the number of HCWs colonized was significantly higher in EMRSA-15 outbreaks compared to Aus2/3-EMRSA outbreaks (median 4 [range 0-15] and 2 [1-3], respectively; P = 0.013). The percentage of HCWs colonized was also higher in EMRSA-15 outbreaks versus Aus2/3-EMRSA outbreaks (median 3.4% [range 0-5.5%] and 0.81% [0.56-2.2%], respectively; P = 0.013). CONCLUSIONS: This study demonstrates a higher level of HCW colonization during EMRSA-15 outbreaks compared with Aus2/3-EMRSA outbreaks. This finding suggests that MRSA vary in their ability to colonize HCWs and contribute to outbreaks. MRSA type should be determined during outbreaks and future research should investigate the mechanisms by which EMRSA-15 contributes to increased HCW colonization.

Antimicrobial susceptibility of Staphylococcus aureus and molecular epidemiology of meticillin-resistant S. aureus isolated from Australian hospital inpatients: Report from the Australian Group on Antimicrobial Resistance 2011 Staphylococcus aureus Surveillance Programme.

The Australian Group on Antimicrobial Resistance (AGAR) performs regular multicentre period prevalence studies to monitor changes in antimicrobial resistance. In 2011, 29 laboratories in Australia participated in the national surveillance of Staphylococcus aureus resistance. The survey only included unique isolates from clinical specimens collected ≥48h after hospital admission. MRSA accounted for 30.3% of S. aureus isolates. MRSA resistance to ciprofloxacin, erythromycin, tetracycline, trimethoprim/sulfamethoxazole, gentamicin and clindamycin (constitutive resistance) varied considerably between regions. Resistance to non-ß-lactam antimicrobials was uncommon in MSSA, with the exception of erythromycin. Regional variation in resistance was due to the differential distribution of MRSA clones between regions. The proportion of S. aureus genetically characterised as healthcare-associated MRSA (HA-MRSA) was significantly lower in this survey (18.2%) compared with the 2005 survey (24.2%) (P<0.0001). Although four HA-MRSA clones were characterised, 98.8% of HA-MRSA were classified as either ST22-MRSA-IV [2B] (EMRSA-15) or ST239-MRSA-III [3A] (Aus-2/3 EMRSA). Multiclonal community-associated MRSA (CA-MRSA) increased markedly from 6.5% in 2005 to 11.7% of all S. aureus in 2011 (P<0.0001). Although the proportion of MRSA resistant to non-ß-lactam antimicrobials has decreased nationally, the proportion of S. aureus that are MRSA has remained stable. This is primarily due to non-multiresistant CA-MRSA becoming more common in Australian hospitals at the expense of the long-established multiresistant ST239-MRSA-III [3A] (Aus-2/3 EMRSA). Given hospital outbreaks of CA-MRSA are thought to be extremely rare, it is most likely that patients colonised at admission with CA-MRSA have become infected with the colonising strain during their hospital stay.

Australian Group on Antimicrobial Resistance Hospital-onset Staphylococcus aureus Surveillance Programme annual report, 2011.

In 2011, the Australian Group on Antimicrobial Resistance (AGAR) conducted a period-prevalence survey of clinical Staphylococcus aureus isolated from hospital inpatients. Twenty-nine microbiology laboratories from all states and mainland territories participated. Specimens were collected more than 48 hours post-admission. Isolates were tested by Vitek2® antimicrobial susceptibility card (AST-P612 card). Nationally, the proportion of S. aureus that were methicillin-resistant S. aureus (MRSA) was 30.3%; ranging from 19.9% in Western Australia to 36.8% in New South Wales/Australian Capital Territory. Resistance to the non-ß-lactam antimicrobials was common except for rifampicin, fusidic acid, high-level mupirocin and daptomycin. No resistance was detected for vancomycin, teicoplanin or linezolid. Antibiotic resistance in methicillin susceptible S. aureus (MSSA) was rare apart from erythromycin (13.2%) and there was no resistance to vancomycin, teicoplanin or linezolid. Inducible clindamycin resistance was the norm for erythromycin resistant, clindamycin intermediate/susceptible S. aureus in Australia with 90.6% of MRSA and 83.1% of MSSA with this phenotype having a positive double disc diffusion test (D-test). The proportion of S. aureus characterised as being healthcare-associated MRSA (HA-MRSA) was 18.2%, ranging from 4.5% in Western Australia to 28.0% in New South Wales/Australian Capital Territory. Four HA-MRSA clones were characterised and 98.8% of HA-MRSA isolates were classified as either ST22-IV [2B] (EMRSA-15) or ST239-III [3A] (Aus-2/3 EMRSA). Multiclonal community-associated MRSA (CA-MRSA) accounted for 11.7% of all S. aureus. In Australia, regional variation in resistance is due to the differential distribution of MRSA clones between regions, particularly for the major HA-MRSA clone, ST239-III [3A] (Aus-2/3 EMRSA), which is resistant to multiple non-ß-lactam antimicrobials.

The molecular epidemiology of the highly virulent ST93 Australian community Staphylococcus aureus strain.

In Australia the PVL-positive ST93-IV [2B], colloquially known as "Queensland CA-MRSA" has become the dominant CA-MRSA clone. First described in the early 2000s, ST93-IV [2B] is associated with skin and severe invasive infections including necrotizing pneumonia. A singleton by multilocus sequence typing (MLST) eBURST analysis ST93 is distinct from other S. aureus clones. To determine if the increased prevalence of ST93-IV [2B] is due to the widespread transmission of a single strain of ST93-IV [2B] the genetic relatedness of 58 S. aureus ST93 isolated throughout Australia over an extended period were studied in detail using a variety of molecular methods including pulsed-field gel electrophoresis, spa typing, MLST, microarray DNA, SCCmec typing and dru typing. Identification of the phage harbouring the lukS-PV/lukF-PV Panton Valentine leucocidin genes, detection of allelic variations in lukS-PV/lukF-PV, and quantification of LukF-PV expression was also performed. Although ST93-IV [2B] is known to have an apparent enhanced clinical virulence, the isolates harboured few known virulence determinants. All PVL-positive isolates carried the PVL-encoding phage ΦSa2USA and the lukS-PV/lukF-PV genes had the same R variant SNP profile. The isolates produced similar expression levels of LukF-PV. Although multiple rearrangements of the spa sequence have occurred, the core genome in ST93 is very stable. The emergence of ST93-MRSA is due to independent acquisitions of different dru-defined type IV and type V SCCmec elements in several spa-defined ST93-MSSA backgrounds. Rearrangement of the spa sequence in ST93-MRSA has subsequently occurred in some of these strains. Although multiple ST93-MRSA strains were characterised, little genetic diversity was identified for most isolates, with PVL-positive ST93-IVa [2B]-t202-dt10 predominant across Australia. Whether ST93-IVa [2B] t202-dt10 arose from one PVL-positive ST93-MSSA-t202, or by independent acquisitions of SCCmec-IVa [2B]-dt10 into multiple PVL-positive ST93-MSSA-t202 strains is not known.

A multidrug-resistant Staphylococcus epidermidis clone (ST2) is an ongoing cause of hospital-acquired infection in a Western Australian hospital.

We report the molecular epidemiology of 27 clinical multidrug-resistant Staphylococcus epidermidis (MDRSE) isolates collected between 2003 and 2007 in an Australian teaching hospital. The dominant genotype (sequence type 2 [ST2]) accounted for 85% of the isolates tested and was indistinguishable from an MDRSE genotype identified in European hospitals, which may indicate that highly adaptable health care-associated genotypes of S. epidermidis have emerged and disseminated worldwide in the health care setting.

Evolution and diversity of community-associated methicillin-resistant Staphylococcus aureus in a geographical region.

BACKGROUND: Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) was first reported in remote regions of Western Australia and is now the predominant MRSA isolated in the state. The objective of this study is to determine the genetic relatedness of Western Australian CA-MRSA clones within different multilocus sequence type (MLST) clonal clusters providing an insight into the frequency of S. aureus SCCmec acquisition within a region. RESULTS: The CA-MRSA population in Western Australia is genetically diverse consisting of 83 unique pulsed-field gel electrophoresis strains from which 46 MLSTs have been characterised. Forty five of these sequence types are from 18 MLST clonal clusters and two singletons. While SCCmec IV and V are the predominant SCCmec elements, SCCmec VIII and several novel and composite SCCmec elements are present. The emergence of MRSA in diverse S. aureus clonal clusters suggests horizontal transmission of the SCCmec element has occurred on multiple occasions. Furthermore DNA microarray and spa typing suggests horizontal transfer of SCCmec elements has also occurred within the same CC. For many single and double locus variant CA-MRSA clones only a few isolates have been detected. CONCLUSIONS: Although multiple CA-MRSA clones have evolved in the Western Australian community only three clones have successfully adapted to the Western Australian community environment. These data suggest the successful evolution of a CA-MRSA clone may not only depend on the mobility of the SCCmec element but also on other genetic determinants.

Antibiotic choice may not explain poorer outcomes in patients with Staphylococcus aureus bacteremia and high vancomycin minimum inhibitory concentrations.

BACKGROUND: There are concerns about reduced efficacy of vancomycin in patients with Staphylococcus aureus bacteremia (SAB), especially when the minimum inhibitory concentration (MIC) nears the upper limit of the susceptible range. METHODS: We examined the relationship between antibiotic treatment, 30-day mortality, and microbiologic parameters in a large Australasian cohort of patients with SAB. RESULTS: We assessed 532 patients with SAB from 8 hospitals. All patients with methicillin-resistant S. aureus (MRSA) bacteremia were treated with vancomycin, and patients with methicillin-susceptible S. aureus (MSSA) bacteremia received either flucloxacillin or vancomycin. Increasing vancomycin MIC was associated with increased mortality in vancomycin-treated patients. However, even in patients with MSSA bacteremia treated with flucloxacillin, mortality was also higher if the vancomycin Etest MIC of their isolate was >1.5 µg/mL, compared with those with lower MIC isolates (26.8% vs 12.2%; P < .001). After adjustment in a multivariate model, age, hospital-onset SAB and vancomycin MIC were independently associated with mortality, but methicillin resistance and antibiotic choice were not. CONCLUSIONS: We have confirmed an association between higher vancomycin MIC and increased mortality in patients with SAB, but surprisingly this relationship was not related to the antibiotic treatment received, suggesting that the use of vancomycin per se is not responsible for the poorer outcome.

Antimicrobial susceptibility of Staphylococcus aureus isolated from hospital inpatients, 2009: report from the Australian Group on Antimicrobial Resistance.

In 2009, the Australian Group on Antimicrobial Resistance (AGAR) conducted a period-prevalence survey of clinical Staphylococcus aureus isolated from hospital inpatients. Thirty medical microbiology laboratories from each state and mainland territory participated. Specimens were collected more than 48 hours post-admission. Isolates were tested by Vitek2 (AST-P579 card) and by Etest for daptomycin. Nationally, the proportion of S. aureus that were MRSA was 33.6%, ranging from 27.3% in South Australia to 41.4% in New South Wales/Australian Capital Territory. Resistance to the non-beta-lactam antimicrobials was common except for rifampicin, fusidic acid, daptomycin and high-level mupirocin. No resistance was detected for vancomycin, teicoplanin, quinupristin-dalfopristin or linezolid. Resistance in the methicillin susceptible S. aureus (MSSA) was rare apart from erythromycin (12%) and absent for vancomycin, teicoplanin, daptomycin, quinupristin-dalfopristin and linezolid. The proportion of methicillin resistant S. aureus (MRSA) has remained stable since the first AGAR inpatient survey in 2005 yet during the same time frame resistance to many antimicrobials, in particular tetracycline, trimethoprim-sulphamethoxazole and gentamicin, has significantly decreased. This suggests that non-multi-resistant community-associated MRSA (CA-MRSA) clones are becoming more common in the hospital setting and replacing the long-established multi-resistant clones such as ST239-III (Aus 2/3 EMRSA). Given hospital outbreaks of CA-MRSA are thought to be extremely rare it is most likely that patients colonised at admission with CA-MRSA have become infected with the colonising strain during their hospital stay.

Differentiation of clonal complex 59 community-associated methicillin-resistant Staphylococcus aureus in Western Australia.

Clonal complex 59 (CC59) community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) strains were characterized using pulsed-field gel electrophoresis, spa typing, multilocus sequence typing, diagnostic DNA microarrays, and PCRs targeting staphylococcal cassette chromosome mec (SCCmec) elements and Panton-Valentine leukocidin (PVL). Six distinct groups within CC59 were characterized. At least seven different variants of SCCmec elements were identified (IVa [2B], IVb [2B], IVd [2B], IV variant [2B], IVa [2B&5], V variant [5C2], and V [5C2&5]). (The structural type is indicated by a Roman numeral, with a lowercase letter indicating the subtype, and the ccr complex and the mec complex are indicated by an Arabic numeral and an uppercase letter, respectively. Where there is an extra ccr element, this is indicated by "&" and an Arabic numeral designating the ccr type.) The first group is similar to the American sequence type 59 (ST59) MRSA-IV CA-MRSA strain USA1000. The second group includes a PVL-negative ST87 strain with an SCCmec element of subtype IVb (2B). The third group comprises PVL-variable ST59 MRSA-IV strains harboring multiple SCCmec IV subtypes. PVL-negative ST59 MRSA strains with multiple or composite SCCmec elements (IVa [2B&5]) form the fourth group. Group 5 corresponds to the internationally known "Taiwan clone," a PVL-positive strain with a variant SCCmec element (V [5C2&5]). This strain proved to be the most common CC59 MRSA strain isolated in Western Australia. Finally, group 6 encompasses the ST59 MRSA-V variant (5C2). The differentiation of CC59 into groups and strains indicates a rapid evolution and spread of SCCmec elements. Observed differences between groups of strains as well as intrastrain variability within a group facilitate the tracing of their spread.

Community-acquired pneumonia due to pandemic A(H1N1)2009 influenzavirus and methicillin resistant Staphylococcus aureus co-infection.

BACKGROUND: Bacterial pneumonia is a well described complication of influenza. In recent years, community-onset methicillin-resistant Staphylococcus aureus (cMRSA) infection has emerged as a contributor to morbidity and mortality in patients with influenza. Since the emergence and rapid dissemination of pandemic A(H1N1)2009 influenzavirus in April 2009, initial descriptions of the clinical features of patients hospitalized with pneumonia have contained few details of patients with bacterial co-infection. METHODOLOGY/PRINCIPAL FINDINGS: Patients with community-acquired pneumonia (CAP) caused by co-infection with pandemic A(H1N1)2009 influenzavirus and cMRSA were prospectively identified at two tertiary hospitals in one Australian city during July to September 2009, the period of intense influenza activity in our region. Detailed characterization of the cMRSA isolates was performed. 252 patients with pandemic A(H1N1)2009 influenzavirus infection were admitted at the two sites during the period of study. Three cases of CAP due to pandemic A(H1N1)2009/cMRSA co-infection were identified. The clinical features of these patients were typical of those with S. aureus co-infection or sequential infection following influenza. The 3 patients received appropriate empiric therapy for influenza, but inappropriate empiric therapy for cMRSA infection; all 3 survived. In addition, 2 fatal cases of CAP caused by pandemic A(H1N1)2009/cMRSA co-infection were identified on post-mortem examination. The cMRSA infections were caused by three different cMRSA clones, only one of which contained genes for Panton-Valentine Leukocidin (PVL). CONCLUSIONS/SIGNIFICANCE: Clinicians managing patients with pandemic A(H1N1)2009 influenzavirus infection should be alert to the possibility of co-infection or sequential infection with virulent, antimicrobial-resistant bacterial pathogens such as cMRSA. PVL toxin is not necessary for the development of cMRSA pneumonia in the setting of pandemic A( H1N1) 2009 influenzavirus co-infection.

Prevalence of MRSA strains among Staphylococcus aureus isolated from outpatients, 2006.

Biennial community-based Staphylococcus aureus antimicrobial surveillance programs have been performed by the Australian Group for Antimicrobial Resistance (AGAR) since 2000. Over this time the percentage of S. aureus identified as methicillin resistant has increased significantly from 10.3% in 2000 to 16% in 2006. This increase has occurred throughout Australia and has been due to the emergence of community-associated MRSA (CA-MRSA) clones. However, healthcare associated MRSA were still predominant in New South Wales/Australian Capital Territory and Victoria/Tasmania. In the 2006 survey CA-MRSA accounted for 8.8% of community-onset S. aureus infections. Although multiple CA-MRSA clones were characterised, the predominate clone identified was Queensland (Qld) MRSA (ST93-MRSA-IV) a Panton-Valentine leukocidin (PVL) positive MRSA that was first reported in Queensland and northern New South Wales in 2003 but has now spread throughout Australia. Several international PVL-positive CA-MRSA clones were also identified including USA300 MRSA (ST8-MRSA-IV). In addition, PVL was detected in an EMRSA-15 (ST22-MRSA-IV) isolate; a hospital associated MRSA clone that is known to be highly transmissible in the healthcare setting. With the introduction of the international clones and the transmission of Qld MRSA throughout the country, over 50% of CA-MRSA in Australia are now PVL positive. This change in the epidemiology of CA-MRSA in the Australian community will potentially result in an increase in skin and soft tissue infections in young Australians. As infections caused by these strains frequently results in hospitalisation their emergence is a major health concern.

SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia.

BACKGROUND: Existing severity assessment tools, such as the pneumonia severity index (PSI) and CURB-65 (tool based on confusion, urea level, respiratory rate, blood pressure, and age >or=65 years), predict 30-day mortality in community-acquired pneumonia (CAP) and have limited ability to predict which patients will require intensive respiratory or vasopressor support (IRVS). METHODS: The Australian CAP Study (ACAPS) was a prospective study of 882 episodes in which each patient had a detailed assessment of severity features, etiology, and treatment outcomes. Multivariate logistic regression was performed to identify features at initial assessment that were associated with receipt of IRVS. These results were converted into a simple points-based severity tool that was validated in 5 external databases, totaling 7464 patients. RESULTS: In ACAPS, 10.3% of patients received IRVS, and the 30-day mortality rate was 5.7%. The features statistically significantly associated with receipt of IRVS were low systolic blood pressure (2 points), multilobar chest radiography involvement (1 point), low albumin level (1 point), high respiratory rate (1 point), tachycardia (1 point), confusion (1 point), poor oxygenation (2 points), and low arterial pH (2 points): SMART-COP. A SMART-COP score of >or=3 points identified 92% of patients who received IRVS, including 84% of patients who did not need immediate admission to the intensive care unit. Accuracy was also high in the 5 validation databases. Sensitivities of PSI and CURB-65 for identifying the need for IRVS were 74% and 39%, respectively. CONCLUSIONS: SMART-COP is a simple, practical clinical tool for accurately predicting the need for IRVS that is likely to assist clinicians in determining CAP severity.

The etiology of community-acquired pneumonia in Australia: why penicillin plus doxycycline or a macrolide is the most appropriate therapy.

BACKGROUND: Available data on the etiology of community-acquired pneumonia (CAP) in Australia are very limited. Local treatment guidelines promote the use of combination therapy with agents such as penicillin or amoxycillin combined with either doxycycline or a macrolide. METHODS: The Australian CAP Study (ACAPS) was a prospective, multicenter study of 885 episodes of CAP in which all patients underwent detailed assessment for bacterial and viral pathogens (cultures, urinary antigen testing, serological methods, and polymerase chain reaction). Antibiotic agents and relevant clinical outcomes were recorded. RESULTS: The etiology was identified in 404 (45.6%) of 885 episodes, with the most frequent causes being Streptococcus pneumoniae (14%), Mycoplasma pneumoniae (9%), and respiratory viruses (15%; influenza, picornavirus, respiratory syncytial virus, parainfluenza virus, and adenovirus). Antibiotic-resistant pathogens were rare: only 5.4% of patients had an infection for which therapy with penicillin plus doxycycline would potentially fail. Concordance with local antibiotic recommendations was high (82.4%), with the most commonly prescribed regimens being a penicillin plus either doxycycline or a macrolide (55.8%) or ceftriaxone plus either doxycycline or a macrolide (36.8%). The 30-day mortality rate was 5.6% (50 of 885 episodes), and mechanical ventilation or vasopressor support were required in 94 episodes (10.6%). Outcomes were not compromised by receipt of narrower-spectrum beta-lactams, and they did not differ on the basis of whether a pathogen was identified. CONCLUSIONS: The vast majority of patients with CAP can be treated successfully with narrow-spectrum beta-lactam treatment, such as penicillin combined with doxycycline or a macrolide. Greater use of such therapy could potentially reduce the emergence of antibiotic resistance among common bacterial pathogens.

Prevalence of MRSA among Staphylococcus aureus isolated from hospital inpatients, 2005: report from the Australian Group for Antimicrobial Resistance.

The Australian Group for Antimicrobial Resistance conducted a survey of the prevalence of antimicrobial resistance in unique clinical isolates of Staphylococcus aureus from patients admitted to hospital for more than 48 hours. Thirty-two laboratories from all states and territories collected 2,908 isolates from 1 May 2005, of which 31.9% were methicillin-resistant Staphylococcus aureus (MRSA). The regional prevalence of MRSA varied significantly (P < 0.0001) from 22.5% in Western Australia to 43.4% in New South Wales/Australian Capital Territory. Prevalence of MRSA from individual laboratories varied even more from 4% to 58%. This variation was explained in part by distribution of age with the risk of MRSA significantly (P < 0.0001) increasing with age. Other unmeasured factors including hospital activity and infection control practices in the individual institution may have also contributed. Further investigation is warranted as reductions in prevalence would reduce morbidity, mortality and healthcare costs.

Prevalence of antimicrobial resistance in Enterococcus isolates in Australia, 2005: report from the Australian Group on Antimicrobial Resistance.

Antibiotic resistance in Enterococcus species causing clinical disease was examined in a point-prevalence study in 2005. Twenty-two sites around Australia collected up to 100 consecutive isolates and tested them for susceptibility to ampicillin, vancomycin, high-level gentamicin and/or high-level streptomycin using standardised methods. Results were compared to similar surveys conducted in 1995, 1999 and 2003. In the 2005 survey, Enterococcus faecalis (1,987 strains) and E. faecium (180 strains) made up 98.6% of the 2,197 isolates tested. Ampicillin resistance was common (77%) in E. faecium, but rare still in E. faecalis (0.2%). Resistance to vancomycin was 7.2% in E. faecium and 0.2% in E. faecalis; the vanB gene was detected in all vancomycin-resistant isolates. High-level resistance to gentamicin was 35.8% in E. faecalis and 52.2% in E. faecium; the figures for high-level streptomycin resistance were 10.3% and 60.2% respectively. Compared to previous Australian Group on Antimicrobial Resistance surveys in 1995, 1999 and 2003, the proportions of vancomycin resistance and high-level gentamicin resistance in enterococci are increasing. It is important to have an understanding of the occurrence of vancomycin resistant enterococci and high level aminoglycoside resistance in Australia to guide infection control practices, antibiotic prescribing policies and drug regulatory decisions.

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

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.

Methicillin-resistant Staphylococcus aureus clones, Western Australia.

Community-associated methicillin-resistant Staphylococcus aureus (MRSA) was first reported in Western Australia in the early 1990s from indigenous peoples living in remote areas. Although a statewide policy of screening all hospital patients and staff who have lived outside the state for MRSA has prevented the establishment of multidrug-resistant epidemic MRSA, the policy has not prevented SCCmec type IV and type V MRSA clones from becoming established. Of the 4,099 MRSA isolates analyzed (referred to the Gram-positive Bacteria Typing and Research Unit) from July 2003 to December 2004, 77.5% were community-associated MRSA (CA-MRSA). Using multilocus sequence/staphylococcal chromosome cassette mec typing, 22 CA-MRSA clones were characterized. Of these isolates, 55.5% were resistant to >1 non-beta-lactam antimicrobial drug. Five Panton-Valentine leukocidin (PVL)-positive CA-MRSA clones were identified. The emergence of multidrug-resistant CA-MRSA clones and the detection of PVL toxin genes in clones previously reported as PVL negative is a major public health concern.