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Letters

Fatal necrotising pneumonia due to community-acquired methicillin-resistant Staphylococcus aureus (MRSA)

MJA 2004; 181 (4): 228-229

Anton Y Peleg,* Wendy J Munckhof†

* Infectious Diseases Registrar, Alfred Hospital, Prahran, VIC 3181; † Specialist in Infectious Diseases and Microbiology, Infection Management Service, Princess Alexandra Hospital, Brisbane, QLD. A.PelegATalfred.org.au

To the Editor: Infection with community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is emerging in many countries, including Australia.1 We report the first case of fatal necrotising pneumonia caused by CA-MRSA in Australia.

A previously well 21-year-old Aboriginal man presented to the emergency department with fever and a productive cough. He had no known risk factors for sepsis (such as immunosuppression, diabetes, HIV infection, alcoholism, asplenia or recent influenza) and no history of hospitalisation in the previous 12 months. Chest x-ray revealed left mid-zone consolidation. He was prescribed amoxycillin–clavulanate and discharged.

Two days later, the patient re-presented, with rigors, haemoptysis and agitation. Examination revealed a respiratory rate of 38 breaths per minute, oxygen saturation of 79% breathing room air, temperature of 38.7°C, sinus tachycardia (135 beats per minute), and a systolic blood pressure of 80 mmHg. Respiratory examination revealed diffuse coarse crepitations. No other source of infection was identified.

The patient required intubation, mechanical ventilation and inotropic support. Sputum and blood samples were taken for culture, and empirical treatment was begun with intravenous ceftriaxone, erythromycin and a single dose of gentamicin and rifampicin. Initial investigations showed leukopenia (2.3 × 109/L; reference range [RR], 3.9–12.7 × 109/L), acute renal failure with a serum creatinine level of 0.18 mmol/L (RR, 0.06–0.11 mmol/L), and severe metabolic and respiratory acidosis (pH, 7.19; RR, 7.38–7.43).

The following day, blood and sputum cultures showed gram-positive cocci resembling staphylococci, and intravenous flucloxacillin was added to the antibiotic regimen. Repeat chest x-ray revealed bilateral necrotising pneumonia. Despite resuscitation efforts, the patient died 48 hours after admission.

Susceptibility testing of blood and sputum isolates subsequently confirmed MRSA. The isolate was sensitive to erythromycin, clindamycin, gentamicin, ciprofloxacin, tetracycline, vancomycin, rifampicin and fusidic acid. Methicillin resistance was confirmed by detection of the mecA gene by polymerase chain reaction (PCR).

Further PCR testing of the isolate revealed the Panton–Valentine leukocidin (pvl) gene, an important virulence factor that has been associated with necrotising pneumonia2 and death,3 and is rarely found in methicillin-susceptible S. aureus or hospital-acquired MRSA isolates.1,2,5 Typing of the isolate by pulsed-field gel electrophoresis showed that it was the recently described “R” pulsotype of CA-MRSA, or “Queensland clone”.4 This clone was first noted in the white population in south-east Queensland in 2000, and is uncommon in Aboriginal people.4 Most CA-MRSA infection in Aboriginal people is caused by WA-MRSA, which may be less virulent than the Queensland clone of CAMRSA as it lacks the Panton–Valentine leukocidin.5

This is the first reported case of fatal necrotising pneumonia caused by CA-MRSA in Australia and illustrates the invasive nature of this infection. Thus far, CA-MRSA has predominantly caused skin and soft tissue infections, but the incidence of life-threatening sepsis is increasing. The first case of severe pneumonia caused by CA-MRSA in Australia was reported in early 2003.6 Fatal cases of necrotising pneumonia caused by CA-MRSA have also been described in the United States3 and France,7 and this presentation is becoming a particular feature of this organism.

Clinicians should consider the possibility of CA-MRSA in any patient presenting to hospital with severe staphylococcal sepsis or pneumonia and should consider including parenteral vancomycin in the initial empirical therapy, particularly in geographic locations where CA-MRSA has been reported and in ethnic groups at increased risk.

Acknowledgements: We thank the staff of the Microbiology Department at the Royal Brisbane and Women’s Hospital for the isolate. We also thank Sharon Kleinschmidt for performing the pulsed field gel electrophoresis and Alex Stephens for performing the polymerase chain reaction test for the pvl gene.

  1. Vandenesch F, Naimi T, Enright MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis 2003; 9: 978-984. <PubMed>
  2. Gillet Y, Issartel B, Vanhems P, et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Lancet 2002; 359: 753-759. <PubMed>
  3. Centers for Disease Control and Prevention. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus — Minnesota and North Dakota, 1997-1999. JAMA 1999; 282: 1123-1125. <PubMed>
  4. Munckhof WJ, Schooneveldt J, Coombs GW, et al. Emergence of community-acquired methicillin-resistant Staphylococcus aureus (MRSA) infection in Queensland, Australia. Int J Infect Dis 2003; 7: 259-264. <PubMed>
  5. Okuma K, Iwakawa K, Turnidge JD, et al. Dissemination of new methicillin-resistant Staphylococcus aureus clones in the community. J Clin Microbiol 2002; 40: 4289-4294. <PubMed>
  6. Nimmo GR, Playford EG. Community-acquired MRSA bacteraemia: four additional cases including one associated with severe pneumonia [letter]. Med J Aust 2003; 178: 245. <eMJA full text> <PubMed>
  7. Dufour P, Gillet Y, Bes M, et al. Community-acquired methicillin-resistant Staphylococcus aureus infections in France: emergence of a single clone that produces Panton-Valentine leukocidin. Clin Infect Dis 2002; 35: 819-824. <PubMed>

©The Medical Journal of Australia 2004 www.mja.com.au ISSN: 0025-729X


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