Scanning electron micrograph of methicillin-resistant Staphylococcus aureus and a dead human neutrophil.

Community challenge

Infections can come from many sources

In 2004 Richard Campbell-Smith, a fit 18-year-old Royal Marine recruit, grazed his leg on a training run. Within two days he had died, his wound having become infected with a ‘community’ (i.e. non-hospital) form of Staphylococcus aureus – Panton–Valentine leukocidin (PVL) S. aureus.

Identified in the 1930s and common until the 1960s, PVL S. aureus was almost wiped out by the antibiotic methicillin, but antibiotic-resistant forms have emerged in recent decades. It has rapidly become common in skin and soft tissue infections in US hospitals. Although it is less common in the UK, one 2011 study detected PVL-positive S. aureus in 20 per cent of samples from skin or soft tissue infections, compared to only 2 per cent in 2005.

PVL is a toxin produced by the bacteria. Research has shown that it has a double-whammy effect – attacking respiratory tissue and defence cells in the lungs. Tissue destruction is extensive and rapid – PVL S. aureus is one of the causes of necrotising fasciitis, the ‘flesh-eating’ infections that hit the headlines in the 1990s. PVL bacteria seem to have acquired genes from a different species of Staphylococcus, which, although harmless, is better adapted to human skin. These genes may enable community strains to multiply more quickly in people.

The ‘nightmare scenario’ is that these rapidly growing strains take over from the ‘ordinary’ methicillin-resistant S. aureus (MRSA) in healthcare settings.

Lead image:

Scanning electron micrograph of methicillin-resistant Staphylococcus aureus (MRSA) and a dead human neutrophil.



Further reading

About this resource

This resource was first published in ‘Epidemics’ in September 2007 and reviewed and updated in January 2015.

Microbiology, Genetics and genomics, Health, infection and disease, Medicine, Immunology
Education levels:
16–19, Continuing professional development