Acta Derm Venereol 90
Acta Derm Venereol 2010; 90: 52–57
© 2010 The Authors. doi: 10.2340/00015555-0771
Journal Compilation © 2010 Acta Dermato-Venereologica. ISSN 0001-5555
Fusidic acid-resistant Staphylococcus aureus (FRSA)
has been identified as a causative agent in outbreaks of
impetigo and its emergence has been associated with
increased use of topical fusidic acid. The frequency of
FRSA in atopic dermatitis (AD) has been less extensively
investigated. The aim of this study was to investigate the
bacterial spectrum and frequency of FRSA in patients
with impetigo or secondarily infected AD. A prospective
study in our clinic in 2004 to 2008 included 38 patients
with impetigo and 37 with secondarily infected AD.
S. aureus was the predominant finding in all groups (bul-
lous impetigo 92% (12/13), impetigo 76% (19/25) and
secondarily infected AD 89% (33/37)). Seventy-five per-
cent of S. aureus were fusidic acid resistant in bullous
impetigo, 32% in impetigo and 6.1% in secondarily in-
fected AD (bullous impetigo vs. AD p < 0.0001, impetigo
vs. AD p < 0.05). We then performed a retrospective pa-
tient record review including all patients with impetigo
or secondarily infected AD seen at the clinic during the
first and last year of the prospective study. In the first
year 33% (19/58) of the S. aureus isolates were fusidic
acid-resistant in impetigo and 12% (5/43) in secondarily
infected AD (p < 0.05). In the last year corresponding va-
lues were 24% (6/25) for impetigo and 2.2% (1/45) for
AD (p < 0.01). In summary, the prospective study and the
patient record review both showed higher FRSA levels in
impetigo than in AD. FRSA levels were persistently low
in AD. Continued restrictive use of topical fusidic acid
is advised to limit an increase in FRSA levels in derma-
tology patients. Key words: fusidic acid; Staphylococcus
aureus; impetigo; atopic dermatitis.
(Accepted September 3, 2009.)
Acta Derm Venereol 2010; 90: 52–57.
Mikael Alsterholm, Department of Dermatology and Vene-
reology, Sahlgrenska University Hospital, SE-413 45 Göte-
borg, Sweden. E-mail: email@example.com
Skin and soft tissue infections (SSTIs) are common
conditions managed by dermatologists, general practitio-
ners and other medical professionals, both in outpatient
care and in hospitals. Impetigo contagiosa (in the follo-
wing referred to as impetigo) and secondarily infected
atopic dermatitis (AD) are two SSTIs often caused by
S. aureus. One treatment strategy for these infections has
been the use of a topical preparation of fusidic acid, a
narrow spectrum anti-staphylococcal antibiotic. Fusidic
acid is also used in systemic treatment of conditions
such as osteomyelitis and joint graft infections and can
sometimes be a useful treatment option for methicillin-
resistant S. aureus (MRSA) infection. In vitro exposure
to fusidic acid selects for resistance in S. aureus, which
is why fusidic acid is usually not administered as a single
antimicrobial agent in systemic treatment (1). In cont-
rast, topical preparations of fusidic acid have often been
prescribed as single therapy. Despite this there were few
clinical reports on staphylococcal resistance to fusidic
acid in dermatology from its introduction in the 1960s
and in the three decades that followed (2).
In the last 10 years, a fusidic acid-resistant clone of
S. aureus (FRSA) associated with impetigo has emerged.
The first reports of this shift in the resistance pattern of
S. aureus came from Sweden and Norway in 2002 after
widespread outbreaks of impetigo (3, 4). In 2003, due
to the reports of FRSA, the Swedish Medical Products
Agency recommended avoidance of topical fusidic acid
in the treatment of impetigo (5–7). Instead, cleansing of
crusts with water and a mild soap and, when necessary,
oral antibiotics, was advised.
Later studies have established the presence of the
same FRSA clone in the UK, Ireland and France (8–10).
This particular FRSA has been carefully characterized
and termed the epidemic European fusidic acid-resistant
impetigo clone (EEFIC) (11). The EEFIC chromosome
carries the fusidic acid-resistance determinant fusB
(12, 13). The fusB gene encodes a protein that binds
to elongation factor G (EF-G), a key player in staphy-
lococcal protein synthesis. Fusidic acid targets EF-G
and inhibits translation from RNA to protein. The fusB
protein induces resistance through binding to EF-G,
thereby protecting it from fusidic acid and maintaining
protein synthesis and viability of the bacteria (14).
In addition to fusidic acid, the EEFIC is resistant to
penicillin and, in some cases, erythromycin (11).
While fusidic acid-resistance is an established pro-
blem in impetigo there are fewer reports on FRSA in
AD. The resistance pattern of S. aureus in patients with
AD is of special interest since the skin of these patients
is colonized with S. aureus in up to 90% of cases (15).
In published reports the frequency of FRSA is highly
variable. In 2002 Sule et al. (16) tested 62 patients with
Fusidic Acid-resistant Staphylococcus aureus in Impetigo
Contagiosa and Secondarily Infected Atopic Dermatitis
Mikael ALSTERHOLM, Ingela FLyTSTRöM, Ing-Marie BERGBRANT and Jan FAERGEMANN
Department of Dermatology and Venereology, Sahlgrenska University Hospital, Göteborg, Sweden
Fusidic acid-resistant S. aureus in skin disease
the Department of Clinical Bacteriology for helping us retrieve
The authors declare no conflict of interest.
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Acta Derm Venereol 90