To the Editor: We report a case of severe pneumonia in a previously healthy 3-year-old girl of European background. Non-multiresistant methicillin-resistant Staphylococcus aureus (MRSA) was isolated from her sputum, and she was treated with intravenous vancomycin, followed by oral rifampicin and fusidic acid.

After antibiotic therapy ceased, symptoms recrudesced, and computed tomography of the chest showed bronchiectasis. Sputum again grew MRSA (now also resistant to rifampicin, fusidic acid and erythromycin), as well as Pseudomonas aeruginosa. She was treated with intravenous vancomycin, ceftazidime and tobramycin. As the MRSA persisted, vancomycin was replaced with intravenous linezolid, followed by a course of oral linezolid and trimethoprim–sulfamethoxazole. More than a year after her original illness, she continues to have a productive cough and requires nebulised tobramycin to prevent exacerbations.

The patient’s only risk factor was contact with her mother, who had an MRSA buttock abscess incised several months earlier. Phage typing and pulsed-field gel electrophoresis revealed that the mother’s and daughter’s isolates were identical (Box). They were found to belong to the Queensland strain of community-acquired MRSA (CA-MRSA) and to possess Panton–Valentine leukocidin, a virulence factor which is highly associated with necrotising pneumonitis and invasive primary skin infection. 1

CA-MRSA is a growing problem in Australia, and severe pneumonia due to this organism has recently been reported in adults. 2,3 The isolation of CA-MRSA before prolonged courses of antibiotics, its characterisation as a virulent strain, the response to appropriate treatment and the recrudescence of symptoms on cessation of therapy demonstrate that it was the causative organism in this case. The case is also noteworthy for the documented intrafamilial spread and the fact that the patient did not belong to the Pacific Islander community, in which CA-MRSA infections in south-western Sydney most commonly occur.4

Most S. aureus strains in the community are sensitive to flucloxacillin and dicloxacillin, so these remain the empirical treatments of choice, unless CA-MRSA is isolated or strongly suspected. CA-MRSA strains are non-multiresistant, and oral antibiotic options include clindamycin, trimethoprim–sulfamethoxazole or rifampicin and fusidic acid. 5 Intravenous vancomycin is commonly used in severe infections, but recent evidence suggests that linezolid, an oxazolidinone antibiotic with efficacy against multiply resistant bacteria, including MRSA, penicillin-resistant Streptococcus pneumoniae and vancomycin-resistant enterococci, may be more effective.6 Issues of cost, toxicity, local availability, potential development of resistance and sensitivity of isolates in vitro need to be considered before determining appropriate treatment.

In conclusion, clinicians should be aware of the growing problem of CA-MRSA and the potentially devastating consequences of infection with this organism, even in otherwise healthy children.

Pulsed-field gel electrophoresis (PFGE) of Staphylococcus aureus strains

1. Low-range PFGE marker. 2. Control S. aureus strain (NCTC 8325). 3. S. aureus isolate from patient. 4. S. aureus isolate from mother. 5. Queensland strain of community-acquired methicillin-resistant S. aureus (CA-MRSA).