Disseminated sepsis due to a Panton‐Valentine leukocidin producing strain of community acquired meticillin resistant Staphylococcus aureus and use of intravenous immunoglobulin therapy

Although unusual in the UK to date, sepsis due to community acquired meticillin resistant Staphylococcus aureus (CA‐MRSA) is an increasing concern globally. CA‐MRSA strains typically produce the exotoxin Panton‐Valentine leukocidin (PVL), a virulence factor associated with severe, rapidly progressive, systemic disease including soft tissue infections and necrotising pneumonia, which has a mortality rate as high as 75%.¹,²

A 14 year old boy presented with septicaemia and disseminated foci of infection including necrotising pneumonia, septic arthritis of the left knee, and deep vein thrombosis of the left leg. Anticoagulants and empirical antibiotics (intravenous cefuroxime, flucloxacillin, and metronidazole) were commenced. At 48 hours he required intensive care for multi‐system organ failure and clindamycin was added. MRSA was isolated from blood cultures, a knee aspirate, and endotracheal secretions. Its origin in the community, the clinical picture, and antibiogram suggested that the MRSA was likely to be a PVL producing CA‐MRSA. This was later confirmed by the staphylococcal reference laboratory in London. Antibiotics were changed to linezolid in combination with rifampicin (to which the isolate was sensitive) and the knee was washed out on three occasions. Despite this at 7 days he had failed to improve clinically.

A French study reported the presence of staphylococcal leukocidin specific antibodies that inhibited the cytopathic effects of PVL in vitro in a commercial intravenous immunoglobulin (IVIG) preparation.³ There is no reported use in human disease. IVIG has been used for its anti‐toxin effects in staphylococcal toxic shock syndrome (TSS) and other causes of septic shock.⁴,⁵

It was felt at this point that the potential benefit outweighed the risk of adverse events, so IVIG at a dose that might be used in TSS was administered (1 g/kg for two days.) This was followed by clinical improvement and a sustained fall in inflammatory markers. There were no immediate adverse effects. The patient was discharged to the ward five days later and has since been discharged home.

Although rare, this case highlights the importance of considering CA‐MRSA in cases with similar presentations, particularly so when disease is rapidly progressive, to enable prompt, appropriate antimicrobial therapy.

It is difficult to determine the extent to which the IVIG contributed to his improvement but given the mortality rate of this condition, the findings in the study cited above, and the possible beneficial effect of IVIG in this case, it is a therapeutic option which should be considered in similar cases in the future.

Acknowledgements

We acknowledge Dr PAF, Dr RT, Dr TW and Mrs CN in the Department of Microbiology, Royal Hallamshire Hospital, Sheffield; and the Staphylococcal Reference Unit, Laboratory of Healthcare Associated Infection, Colindale, London, UK.