To the Editor: We report the appearance of erythromycin and inducible clindamycin resistance in the south-west Pacific strain of non-multiresistant methicillin-resistant Staphylococcus aureus, which has recently appeared in eastern Australia. Infections occur predominantly in Polynesian people and are usually community-acquired. Most strains belong to Western Samoan phage patterns (WSPP1 or WSPP2) and pulsotype A when typed by pulsed-field gel electrophoresis.1,2 These strains are resistant to all β-lactams, but are usually susceptible to erythromycin, clindamycin, gentamicin, tetracycline, trimethoprim–sulfamethoxazole and ciprofloxacin. Although most of these antibiotics would not be recommended for therapy,3 clindamycin has been recommended for non-parenteral treatment of soft-tissue and bone infections, as it is efficacious in treating similar infections caused by methicillin-susceptible S. aureus.4

Twenty isolates of community-acquired, non-multiresistant pulsotype A MRSA were collected from patients from southern Brisbane and Logan in 1997 and 1998.2 A further 16 isolates were obtained from Ipswich patients between December 1998 and February 2001. We found that all 36 isolates were susceptible in vitro to gentamicin, tetracycline, trimethoprim–sulfamethoxazole, ciprofloxacin, rifampicin, fusidic acid and vancomycin. However, two of the Ipswich isolates had erythromycin and inducible clindamycin resistance. When susceptibility testing was performed using standard disc methods, both isolates appeared resistant to erythromycin but susceptible to clindamycin. However, on testing for inducible macrolide resistance (MLSB phenotype) using a disc-approximation method, both showed inducible clindamycin resistance.5 These isolates were from superficial abscesses in Polynesian people with community-acquired infection. They were indistinguishable by pulsed-field gel electrophoresis, but there were no epidemiological links. As yet, we have found no community-acquired pulsotype A strains of MRSA with erythromycin resistance and constitutive (ie, non-inducible) clindamycin resistance.

Two other recent Australian studies found erythromycin resistance in 13 of 153 and three of 29 isolates of non-multiresistant MRSA, respectively.3,6 These studies did not report clindamycin susceptibilities, and it was not clear what proportion of the isolates belonged to phage patterns WSPP1 or WSPP2, or were community-acquired.

As clindamycin has been recommended as a therapeutic option for soft-tissue and bone infections caused by non-multiresistant MRSA, this finding of inducible clindamycin resistance has important implications. Microbiology laboratories should screen for inducible clindamycin resistance in erythromycin-resistant strains, and, if found, an alternative antibiotic should be used for treatment.7 Alternatively, rather than assessing inducible clindamycin resistance with a disc-approximation test, some laboratories may prefer to report all erythromycin-resistant strains as clindamycin-resistant. Also, given the increasing incidence of community-acquired MRSA infection in Australia, all suspected staphylococcal infections that are not responding to empiric therapy with β-lactam antibiotics should be swabbed for culture.