To the Editor: A 37-year-old man was referred to our emergency department with an acute 7 cm abscess of the buttock. The abscess was incised, and the patient was prescribed oral β-lactam antibiotics and discharged.

After 48 hours, culture of samples from the abscess showed methicillin-resistant Staphylococcus aureus with a community-acquired antibiotic resistance pattern (CA-MRSA). The isolate was resistant to β-lactam antibiotics, but sensitive to trimethoprim, gentamicin, and tetracycline. Unusually for an Australian CA-MRSA strain,1 the isolate was also resistant to erythromycin and ciprofloxacin.

On reviewing the patient’s history, it was noted that he was a previously well United States resident who had visited Australia and New Zealand as part of the support team for an international rock band. Further testing was undertaken, and the isolate tested positive for genes coding for the Panton–Valentine leukocidin toxin, associated with staphylococcal virulence (eg, recurrent furunculosis, abscess formation, and necrotising pneumonia).2 Pulsed-field gel electrophoresis (performed by the Gram-Positive Bacteria Typing and Research Unit, Department of Microbiology and Infectious Diseases, Royal Perth Hospital, WA) confirmed the isolate as the ST8-MRSA-IV strain, also known as USA300.

Most CA-MRSA strains remain susceptible to a majority of non-β-lactam antibiotics, including clindamycin, trimethoprim–sulfamethoxazole, tetracyclines and fluoroquinolones. This helps distinguish CA-MRSA isolates from the typically multiresistant hospital strains, and facilitates oral outpatient therapy. USA300 is the dominant strain causing CA-MRSA infections in the US.3 Among 422 patients with soft-tissue infections presenting to 11 US emergency departments in 2004, 59% of cases were caused by CA-MRSA, of which 99% were USA300. Recent reports indicate that multiresistance is emerging within this strain, with acquisition of resistance to erythromycin, clindamycin, mupirocin and fluoroquinolones. An increasing association of USA300 infections with buttock and perineal infections is also reported, as well as potential sexual transmission, particularly among men who have sex with men.

Our case highlights the ease of international spread of microorganisms. Arguably, a “one-night stand” tour could be an ideal vehicle for microbial dissemination. CA-MRSA was not considered in the patient’s initial assessment, and the patient was discharged with oral β-lactam antibiotics and no planned follow-up. Moreover, the isolate may not have been identified as the “epidemic” USA300 strain without more involved tests. A recent study documented a rising incidence of USA300 isolates in Western Australia between 2003 and 2007. Of 61 patient isolates, 35 were diagnosed in 2007 (Pearson J, Coombs G, Christiansen K, et al. USA300 MRSA identified in the Australian community [abstract PP3.2]. Abstract presented at the Australian Society for Antimicrobials 9th Annual Scientific Meeting; 2008; Feb 21–23; Sydney).

Our case suggests we should be more alert to CA-MRSA infection presenting with furunculosis and soft tissue infections, not only in Indigenous communities and young people, but also in international travellers and patients whose infections fail to respond to usual therapy. It also reinforces the value of incision and drainage. As β-lactam susceptibility is no longer assured, such specimens should routinely undergo culture and susceptibility testing.