PVL positive Staphylococcus aureus skin infectionsBMJ 2011; 343 doi: https://doi.org/10.1136/bmj.d5343 (Published 09 September 2011) Cite this as: BMJ 2011;343:d5343
All rapid responses
We applied the HPA guidelines to the management of a series of 32
cases of laboratory confirmed PVL positive Staphylococcus Aureus, (PVLSA)
infection notified to the NHS Tayside Health Protection Team in a two year
Key issues were that close contacts of individual cases comprised not
only those in the same household, but others with lesser degrees of
contact, e.g. grandparents of grandchildren with repeated PVLSA infection. We
concluded that the management of such cases would present a challenge in
primary care, particularly where contacts did not live in the same
locality as the case, and/ or the contacts were registered with another GP
We also observed that simple decolonisation of cases and contacts
often appeared to be insufficient to prevent recurrent infections;
environmental cleaning e.g. of bedlinen and towels, appeared to be a
useful adjunct to decolonisation; a small family outbreak required a multi
-agency approach with access to a daily laundry service. Another
apparently useful measure appeared to be reducing the bacterial load in
household pets, e.g. dogs; this involved seeking veterinary advice in
management of decolonisation. However, formal evidence on the issue of
decontamination appears to be limited.
Contact tracing and co-ordination of decolonisation of close contacts
is resource intensive; we found that an experienced health protection
nurse these activities required several hours of direct patient contact.
The above observations lead us to question whether primary care
professionals may require support from their local health protection unit
in managing case and contact decolonisation for PVLSA.
Competing interests: No competing interests
In this useful overview of PVL positive Staphylococcus aureus skin
infections, and in the accompanying 'practice uncertainties' article,
reference is made to the emergence of these strains and the rapid spread
of multiresistant strains in North America and Australia over the past
decade. The reminder of the morbidity and social and economic cost of
prolonged illness caused by such infections is pertinent and emphasises
the importance of attempting to avoid such spread in the United Kingdom.
Neither article mentions the potential role of household pets in
transmission or as a reservoir of infection. PVL positive Staphylococcus
aureus infections are well recognised by the veterinary profession; MRSA
has been recognised to infect dogs, cats, poultry, pigs, horses and cattle
(1), and there are case reports of apparent transmission of infection
between humans and animals (2). In animals, as in humans, such infections
can be difficult to treat. In most veterinary practices, (animal)
infections would be treated empirically with first and then second line
antibiotics, and PVL/ MRSA would only be looked for if these failed.
Veterinarians are aware of the potential risk to humans of PVL positive
Staphylococcus aureus. They are specifically instructed about the
potential for animals to acquire MRSA from humans; pet owners 'should be
routinely asked if they worked in the healthcare industry', and
veterinarians have been made aware of the risks to vulnerable or
immunocompromised humans from infected animals (3). However, the drugs
recommended for decolonisation in humans are not licensed for use in
animals, and it is unclear what action a concerned veterinarian should
People both like and are intimate with the animals they share
households with; cats sleep on beds, and dogs share sofas; it is not
unknown for humans to kiss animals they are fond of. By the 'close
contact' definition cited by Shallcross et al (4), such contacts would
potentially be close and prolonged. It is far from rare for
immunocompromised or chronically ill and multiply treated animals to share
their living space with humans, and vice versa; this is not something a
human patient would necessarily tell their doctor unless specifically
asked. It may be very worth asking.
Further research looking at the prevalence of carriage of PVL
positive organisms on pets as well as humans sharing a household could
quantify the extent of this potential risk. At what point will we
recognise the need to consider decolonisation of household pets as well as
1) Tackling MRSA in animals and humans: Veterinary Record 2005,
2) E. van Duijkeren, M. J. H. M. Wolfhagen, M. E. O. C. Heck, and W.
J. B. Wannet: Transmission of a Panton-Valentine Leucocidin-Positive,
Methicillin-Resistant Staphylococcus aureus Strain between Humans and a
Dog; J Clin Microbiol. 2005 December; 43(12): 6209-6211.
3) MRSA: what vets need to know: Veterinary Record 2006 158: 579-580
4) L J Shallcross, C N Mbeledogu, A C Hayward Should we screen and
decolonise contacts of patients with Panton Valentine leukocidin
associated Staphylococcus aureus infection? BMJ 2011;343
Competing interests: Partner is a vet
I enjoyed reading Fogo et al's informative article regarding
Staphylococcus aureus skin infections. Panton-valentine leukocidin (PVL)
is a cytotoxin produced by certain strains of S. aureus and such strains
have been linked epidemiologically with virulent community acquired
methicillin resistant S. aureus (CA-MRSA) infection . However, a
definitive role for the presence of the toxin in the pathogenesis of CA-
MRSA skin infections is lacking.
A considerable body of experimental evidence shows that in in vivo
models of soft tissue infection, PVL positive CA-MRSA strains are no more
virulent than isogenic strains lacking PVL [2, 3]. A recent study, using
the prevalent CA-MRSA strain USA-300, identified three virulence factors
with a role in increased virulence in soft tissue infection, but PVL was
not one of these . In addition, this study was carried out in a rabbit
model, which is more sensitive to the effects of PVL than the mouse model
used in the previously cited studies. Another study has shown that CA-MRSA
strain virulence is not related to the amount of PVL produced by the
bacteria . There is some conflicting evidence concerning the role of
PVL in skin infections: a recent study finding a role for PVL in the early
stages of skin infection in a rabbit model . In addition, there is good
in vivo evidence for the role of PVL in CA-MRSA associated necrotizing
pneumonia [7, 8].
In summary, extensive in vivo work characterising the behaviour of S.
aureus strains that produce PVL has consistently failed to find a role for
the toxin in the increased virulence of CA-MRSA soft tissue infection.
This has important implications for clinical practice. Whilst PVL is
currently accepted as a marker of CA-MRSA virulence, better markers likely
exist and should be actively sought.
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Competing interests: No competing interests