To the Editor: Panton–Valentine leukocidin (PVL) is a potent necrotising toxin, which, although produced by less than 5% of all Staphylococcus aureus strains, is strongly associated with pathogenic isolates that cause recurrent furunculosis and severe necrotising pneumonia.1 The virulence of PVL-positive community-associated methicillin-resistant S. aureus (CA-MRSA) causing necrotising pneumonia was recently highlighted in the Journal.2 Conversely, PVL produced by methicillin-sensitive S. aureus (MSSA) is uncommon.1 Here, we describe a case of fulminant necrotising pneumonia caused by PVL-positive MSSA, which, to our knowledge, is the first reported case in Australia.

A previously well 33-year-old man presented to the emergency department with a 48-hour history of pleuritic chest pain, fever and productive cough. On presentation, the patient was hypotensive, and in acute renal failure and hypoxemic respiratory failure (type I). Chest x-ray showed bilateral widespread air space consolidation.

Despite treatment with intravenous fluid resuscitation and early broad-spectrum antibiotics (ceftriaxone, azithromycin, vancomycin and co-trimoxazole), the patient’s condition rapidly deteriorated, requiring intubation and inotropic support.

Multiple blood and sputum cultures isolated MSSA. Bronchoscopy revealed widespread airway haemorrhage. A trans-oesophageal echocardiogram excluded endocarditis.

Progressive leukopenia developed. Septic shock and respiratory failure worsened, despite treatment with flucloxacillin as well as maximal inotropic and ventilatory support. The patient died 72 hours after presentation from fulminant pneumonia. Polymerase chain reaction testing subsequently identified the PVL gene in the isolated MSSA.

Rising rates of CA-MRSA causing recurrent furunculosis and severe necrotising pneumonia have been reported worldwide.3 Necrotising pneumonia often affects children and young adults,1 and, despite current treatments, mortality rates are over 50%.4 Our patient exhibited two major factors predictive of increased lethality: leukopenia and airway bleeding.4

PVL has been well described in CA-MRSA; it is present in at least 96% of the two predominant strains in south-east Australia.3 There is some evidence that PVL is the major pathogenic factor of CA-MRSA, although this remains controversial.5 The precise pathogenesis of PVL has not yet been discovered; however, a severe inflammatory response secondary to PVL’s cytolytic effects on polymorphonuclear leukocytes, as well as the induction of other bacterial virulence factors, are possibilities.1 Therapies directed against the PVL toxin, including antibiotics such as clindamycin that target the bacterial ribosome, or intravenous immunoglobulin, have been suggested but have little supportive data.2,3,6,7

In contrast to CA-MRSA, the PVL gene is found much less frequently in MSSA, being present in only 2% of isolates in one French study.1 Specific Australian prevalence data are lacking, but PVL-positive MSSA isolates have similar potential to cause severe invasive disease.1,6

Most cases of severe necrotising staphylococcal pneumonia and recurrent furunculosis are caused by CA-MRSA, and empirical therapy for these conditions should cover this organism. This case involving MSSA highlights the role that PVL may play in the pathogenicity of these conditions, and shows that the development of novel therapeutics directed at PVL may be of value.