Staphylococcus aureus infection with PVL toxin

MRSA or MSSA can express this toxin. By Dr James Powell and Dr Jessica Alcena

PVL-SA is a cause of skin and soft tissue infections (Photograph: SPL)
PVL-SA is a cause of skin and soft tissue infections (Photograph: SPL)

The significance of soft tissue infections such as furuncles has been elevated by their association in the community with strains of Staphylococcus aureus that express Panton-Valentine leucocidin (PVL) toxin,1 regarded as a major virulence factor in Staph aureus infections.2,3

Epidemiology
Staph aureus can be grouped as methicillin-resistant (MRSA) or methicillin-sensitive (MSSA). Both can express PVL toxin.

In 2005-06 the HPA Staphylococcus Reference Unit, which receives samples from England and Wales, identified 720 cases of PVL toxin-associated Staph aureus infections (PVL-SA).3,4

In 2009-10, 4,784 cases of PVL-SA were identified: 58% were MSSA and 42%, MRSA.4

It is not clear if this increase reflects increased awareness and case recognition or is a real rise in PVL-SA. Either way, it seems likely the true burden of PVL-SA is underestimated. It is important to recognise that PVL-SA is relatively rare, representing <2% of all Staph aureus analysed by the HPA.

Of cases identified with PVL-SA in 2005-06, 72% occurred in the community; 26% of patients were aged under 16 years and 35%, 17-40 years.3 Most were skin and soft tissue infections (78%); however, 22% had more serious systemic disease.3 There were 21 deaths, 16 due to PVL-MSSA and five to PVL-MRSA.3

Clinical suspicion
PVL-SA most commonly causes pyogenic skin and soft tissue infections such as furuncles and carbuncles. It should be suspected when these infections are recurrent or fail to respond to standard treatments, or when close contacts are affected.

PVL-SA is identified as causing the 'majority of staphylococcal boils and abscesses' referred to the HPA.5 Other skin and soft tissue infections to suspect include folliculitis, cellulitis and purulent eyelid infections.5

Risk factors for PVL-SA in the UK include compromised skin integrity and close contact to those already colonised, for example, within a household, in gyms, contact sports and prisons.

If infection is suspected, bacterial swabs should be taken for microbiological analysis from lesional skin and from the anterior nares. Information on the sample request form should indicate that PVL-SA infection is suspected, because routine testing for the PVL gene is not performed in the UK.

Management
Personal hygiene measures should be advised, including hand-washing, not sharing towels and bath water, and using appropriate dressings over wounds.6 Some cases may require exclusion from normal work and/or leisure activities.

For those requiring systemic antibiotics, much PVL-SA in the UK remains susceptible to flucloxacillin and erythromycin. Treatment should be altered as required, depending on sensitivity reports from culture, and should last for seven days.

Flucloxacillin is often not used in severe cases because it is thought this may increase PVL toxin production.

Cases of suspected necrotising fasciitis/pneumonia can be fatal and must be referred immediately to secondary care.

Only once the acute infection has resolved should decolonisation be arranged. This aims to reduce transmission of PVL-SA and prevent recurrent infection.

Decolonisation takes five days and involves daily use of chlorhexidine 4% or triclosan 1-2% as a body wash and shampoo, plus mupirocin 2% nasal ointment three times daily.

Post-decolonisation screening is only needed in certain groups, such as healthcare workers and those particularly vulnerable to infection.

Decolonisation is somewhat controversial. The HPA takes an empirical approach while awaiting definitive trials.6 This means close contacts should be decolonised based on a risk assessment, which includes a positive history of suspected PVL-SA in the past year or a positive screen for PVL-SA.

Screening is recommended if the index case has recurrent infection (despite treatment) or a close contact is in a high-risk group for transmitting PVL-SA. All close contacts of a patient with PVL-SA necrotising pneumonia should be offered immediate decolonisation. If patients have an underlying dermatosis, seek a dermatology opinion.

  • Dr Powell is a dermatology registrar and Dr Alcena is an SHO at Worcestershire Royal Hospital

References
1. Lina G, Vandenesch F, Etienne J. A brief history of Staphylococcus aureus Panton Valentine leucocidin. Antimicrobial Therapy database. www.antimicrobe.org/history/PVL-long.asp

2. Boyle-Vavra S, Daum RS. Lab Invest 2007; 87(1): 3-9.

3. Ellington MJ, Ganner M, Smith IM et al. Clin Microbiol Infect 2010; 16: 86-8.

4. HPA. PVL-Staphylococcus aureus infections: an update. Health Protection Report 2011; 5(7).

5. HPA. Improved reporting shows wider prevalence of PVL. Press release, 17 February 2011.

6. HPA. Guidance on the diagnosis and management of PVL-associated Staphylococcus aureus infections (PVL-SA) in England. 2008.

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