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:
NIAID/Flickr CC BY NC ND
- PVL positive Staphylococcus aureus skin infections (2011)
- US Centers for Disease Control and Prevention: Necrotizing fasciitis – a rare disease, especially for the healthy