Review article Eur J Dermatol 2010; 20 (1): 6-15

Helmut SCHÖFER Fusidic acid in dermatology: an updated review

Lene SIMONSEN
1
Dept. of Dermatovenereology, Studies on the clinical efficacy of fusidic acid in skin and soft-tissue
University Hospital der
J. W. Goethe-University, infections (SSTIs), notably those due to Staphylococcus aureus, are
Theodor-Stern-Kai 7, reviewed. Oral fusidic acid (tablets dosed at 250 mg twice daily, or a
60590 Frankfurt/Main, Germany suspension for paediatric use at 20 mg/kg/day given as two daily
2
Medical Affairs, LEO Pharma, Ballerup,
Denmark doses) has shown good efficacy and tolerability. Similarly, plain fusi-
dic acid cream or ointment used two or three times daily in SSTIs such
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Reprints: H. Schöfer as impetigo are clinically and bacteriologically effective, with minimal
<schoefer@em.uni-frankfurt.de> adverse events. Combination formulations of fusidic acid with 1%
hydrocortisone or 0.1% betamethasone achieve excellent results in
infected eczema by addressing both inflammation and infection.
A new lipid-rich combination formulation provides an extra moisturiz-
ing effect. Development of resistance to fusidic acid has remained gen-
erally low or short-lived and can be minimized by restricting therapy
to no more than 14 days at a time.
Key words: fusidic acid, impetigo, infected eczema, sodium fusidate,
Article accepted on 23/7/2009 Staphylococcus aureus

usidic acid (Fucidin®; LEO Pharma, Ballerup,

F
also performed on Embase and the Cochrane Database for
Denmark) has been available as an antibiotic for “fusidic acid”. Information on trials published in lan-
use in dermatology for many years: as tablets guages other than English, and in non-indexed journals,
since 1962, a suspension since 1963, an ointment since was obtained from LEO Pharma. This review includes all
1965, and a cream since 1982. It has proved valuable in of the randomized trials that could be identified in which
the treatment of primary and secondary skin infections, the clinical efficacy of fusidic acid in dermatology was
particularly those caused by Staphylococcus aureus. Its studied in comparative trials. Case reports and small stud-
usefulness is further increased by the availability of com- ies on specific aspects other than efficacy were not
bination formulations: fusidic acid/hydrocortisone oint- included. Some reviews and guidelines published in
ment (Fucidin® H) since 1967, fusidic acid/betamethasone 2008, after our main analysis had been performed, and
cream (Fucicort® cream) since 1987 for the treatment of relevant articles from 2009 that came to our notice during
infected eczema, and a new lipid-rich formulation of fusi- the submission process, are also included.
dic acid/betamethasone cream (Fucicort® Lipid), intro-
duced in 2007 for the treatment of infected eczema lesions
where a more lipid-rich formulation is preferred by doc- Properties of fusidic acid
tors or patients.
This review provides an overview of the available evi-
dence for the clinical effectiveness of fusidic acid in der- Fusidic acid is the only commercially available member
matology, as well as new information on changing resis- of the fusidane antibiotic group. It acts by inhibiting bac-
tance patterns. The review is restricted to dermatology; terial protein synthesis through interference with elonga-
ophthalmological use of fusidic acid, and use of the intra- tion factor G in the translocation step [1]. The steroid-like
venous formulation for serious systemic infections are not structure of fusidic acid (figure 1) confers certain advan-
covered. In addition, it should be noted that availability of tages, such as good skin penetration; however, it does not
the different formulations mentioned varies by country. possess either the anti-inflammatory activity or unwanted
The term “fusidic acid” is used to cover both fusidic side effects of steroids [2]. Fusidic acid penetrates normal,
acid (constituent of the cream) and sodium fusidate (con- damaged, and avascular skin [3, 4]. A recent in vitro study
stituent of the ointment and the tablets), as the active prin- also showed high skin permeability to fusidic acid [5].
ciple (fusidate) is the same for both compounds following These significant absorption qualities mean that topical
absorption. administration of fusidic acid results in much higher
local concentrations than can be achieved with systemic
doi: 10.1684/ejd.2010.0833

administration and antimicrobial concentrations of fusidic

Selection of studies for inclusion acid can be achieved even at deeper layers of the epider-
mis or dermis [4].
Searches were performed on PubMed for articles in Administration of oral fusidic acid has also been shown to
English containing “fusidic acid” and classified as “clini- achieve high concentrations in plasma [6], serum, blister
cal trials”, published up to December 2007. Searches were fluid [7], burn crusts [8], and interstitial dermal fluid [9].

6 EJD, vol. 20, n° 1, January-February 2010

 different doses of fusidic acid [15-17]. With doses above
H 3C CH3 250 mg twice daily (BID), cure rates did not increase
greatly, and there were more adverse events at the higher
doses [15, 17]. The most common side effects with sys-
temic fusidic acid are gastrointestinal events such as nau-
sea and diarrhoea. These are reported to occur at a fre-
quency of between > 1% and < 10% [15, 17, 22, 23].
CO2H All other adverse events were reported at a frequency
of < 1% [22, 23]. The recommended dosing in most coun-
H tries is 250 mg BID.
HO OCOCH3
In the studies comparing fusidic acid with flucloxacillin,
pristinamycin, ciprofloxacin, and erythromycin, response
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rates were similar with fusidic acid and the comparator.

Tolerability of fusidic acid was either similar to the com-
parator [18-20] or significantly better, primarily because
H of fewer gastrointestinal adverse events [1, 16, 21]. In
general, systemic fusidic acid has good tolerability, with
HO
few and minor side effects [24].
H Five studies also examined bacteriological efficacy,
defined as eradication of the pre-treatment pathogen or
no swab being taken at the end of treatment because no
Figure 1. Structure of fusidic acid.
pathological material was present. In each case, bacterio-
logical efficacy was high and similar for fusidic acid and
In vitro, fusidic acid has high activity against S. aureus, the comparator: 87% and 91%, 94% and 97%, and 85%
including methicillin-resistant strains (MRSA), and and 83%, respectively, in three studies in which staphylo-
S. epidermidis (table 1) [10-13]. It is also active against cocci were the most common infecting organisms; but
some Corynebacterium species, and is indicated for use in streptococci were also isolated from some patients and
the treatment of mild to moderately severe primary and were included in the bacteriological assessments [18, 19,
secondary skin and soft tissue infections (SSTIs) caused 21]. The remaining two studies reported efficacy against
by sensitive organisms (which in clinical practice are most S. aureus as 96% and 97% for fusidic acid and erythro-
often S. aureus). mycin, respectively [20], and efficacy against all isolated
staphylococci as 92%, 100%, and 97% for fusidic acid
500 mg/day, fusidic acid 1 g/day, and pristinamycin 2 g/
Studies on efficacy and safety day, respectively [16].
Oral fusidic acid is also available in a suspension formu-
Systemic formulations lation suitable for paediatric use. In a recent study of fusi-
Early evidence for the efficacy of fusidic acid tablets was dic acid suspension in 411 children aged 1-12 years with
based largely on case series (for a listing of these, see SSTIs, 91% of those treated with 20 mg/kg/day given in
[14]). Randomized controlled trials have only been two divided doses and 89% of those treated with 50 mg/
reported since 1994. These have shown that fusidic acid kg/day given in three divided doses were cured [25]. The
is at least as effective as other oral antibiotics in SSTIs lower-dose regimen had significantly better tolerability
(table 2) and has similar or greater tolerability [15-21]. (p = 0.025), due to fewer gastrointestinal side effects.
Patients enrolled in these studies were generally suffering Bacteriological efficacy was demonstrated in 100% and
from any of a number of primary or secondary skin infec- 99% of children, respectively.
tions, including abscesses/furuncles, impetigo, acute par- In clinical practice, the systemic formulations of fusidic
onychia, and superficial wound infections. The duration acid are usually used when patients have extensive dis-
of treatment was 5 or 10 days. Response was defined in ease, deeper infections, or evidence of systemic spread
most studies as cure or improvement, as assessed by the of disease or septicaemia, or when topical therapy cannot
investigator; the precise definition of response is given in be used for some reason. Oral fusidic acid is not available
each publication. Some studies compared the effects of in some countries (e.g. Germany, where it serves as a
reserve antibiotic).
Table 1. Minimum inhibitory concentration (MIC) values Topical formulations (plain fusidic acid)
for fusidic acid for common pathogens in skin infections
Numerous studies have shown that both the cream and
Organism MIC 90 Reference ointment formulations of fusidic acid are effective in
(μg/mL) SSTIs. These studies have previously been reviewed by
Staphylococcus aureus 0.25 10 Spelman [14]. Table 3 summarizes the results of all the
MRSA 0.25 10 identified randomized trials in which the efficacy of fusi-
Staphylococcus epidermidis 0.25 10 dic acid cream or ointment in SSTIs was compared with
Corynebacterium minutissimum 0.06 11
that of another agent [26-45]. The cream or ointment was
applied two or three times daily in all of these studies
Propionibacterium acnes 1.0 12
except in the Pakrooh 1977 study [38], which used
Streptococcus pyogenes 8 13
once-daily application.

EJD, vol. 20, n° 1, January-February 2010 7

 Table 2. Studies of fusidic acid tablets in patients with skin and soft tissue infections

Reference Fusidic acid Comparator

Dose Treatment Response rate Dose Treatment Response rate
n = pts treated duration (days) (cure or n = pts treated duration (days) (cure or
improvement) improvement)
(days)a (days)a
Nordin 1994 [15] 250 mg BID 5 93.2% (5) Flucloxacillin 5 90.8% (5)
n = 181 10 93.2% (10) 500 mg TID 10 92.6% (10)
500 mg BID 91.0% (5) n = 178
n = 181 94.5% (10)
Machet 1994 [16] 500 mg/d 9 92.0% (9) Pristinamycin 9 96%
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n = 90 99.0% (9) 2 g/d

1 g/d n = 93
n = 90
Carr 1994 [17] 250 mg BID 5 or 10 90.8% (5) None – –
n = 207 91.3% (10)
500 mg BID 95.0% (5)
n = 206 95.5% (10)
500 mg TID 91.8% (5)
n = 204 92.9% (10)
Newby 1999 [18] 250 mg BID 5 or 10 86.6% Ciprofloxacin 5 or 10 91.5%
n = 94 250 mg BID
n = 92
Morris 2000 [19] 250 mg BID 5 (53% of pts) 75.8% Flucloxacillin 5 (39% of pts) 81.1%
n = 240 10 (47% of pts) 250 mg QDS 10 (61% of pts)
n = 233
Wall 2000 [20] 250 mg BID 5 (52% of pts) 85.3% Erythromycin 5 (57% of pts) 87.3%
n = 225 10 (48% of pts) 1.0 g BID 10 (43% of pts)
n = 229
Claudy 2001 [21] 500 mg BID 7.5 79.7% Pristinamycin 10 76.1%
n = 158 1 g BID
n = 155
BID: twice daily; TID: three times daily; QDS: four times daily; pts: patients.
a
As defined in each study, to include cure or cure/improvement. Cure rates are given for “end of treatment” unless otherwise stated.

As can be seen in table 3, in general, fusidic acid had nasal carriage of MRSA [48-51]. A new antibiotic, reta-
similar clinical and bacteriological efficacy to the com- pamulin, which has recently been approved in the USA
parators in all of the studies. Some advantages of fusidic and Europe for use in impetigo due to S. aureus
acid were apparent. In one study, healing time was signif- (methicillin-susceptible isolates only) or S. pyogenes,
icantly more rapid with topical fusidic acid than with oral was not available when the reviews were conducted. In
antibiotics (p < 0.01) [38]. Fusidic acid ointment was clin- a comparative study, retapamulin and fusidic acid showed
ically as effective as mupirocin ointment in all of the stud- similar efficacy in impetigo, and there were fewer drug-
ies comparing these two agents. However, patients consid- related adverse events with fusidic acid (one adverse
ered fusidic acid ointment more acceptable, primarily event reported in 172 subjects) than with retapamulin
because of the greasiness of mupirocin ointment [41]. (14 adverse events reported in 345 subjects) [45].
Patients also preferred fusidic acid cream to mupirocin The adverse events most commonly noted with topical
ointment [29]. antibiotics relate to the induction of hypersensitivity,
With respect to impetigo, more patients responded to fusi- resulting in local irritation or sensitization. Clinical expe-
dic acid than to neomycin/bacitracin combination cream rience over many years of use has been that plain topical
(p < 0.01), and after 7 days, 69% of patients using fusidic fusidic acid formulations have low sensitizing potential,
acid were healed, versus 47% using neomycin/bacitracin and few and mild side effects. A recent safety overview
[39]. A Cochrane review has concluded that there is good of published and unpublished studies and postmarketing
evidence that topical fusidic acid is equally, or more, surveillance data has confirmed the good tolerability of
effective than oral antibiotics for patients with limited these formulations [52].
impetigo [46]. Similarly, the authors of a recent systematic Specific studies confirm the low allergenic potential of
review concluded that fusidic acid and mupirocin are fusidic acid. A study in the UK showed a low incidence
equally effective, and recommended the use of a topical of positive patch test reactions to fusidic acid (0.3%, com-
agent for 7 days in limited impetigo, noting also that top- pared with 3.6% for neomycin and 0.7% for clioquinol),
ical antibiotics have better tolerability and may achieve and no increase in the frequency of allergic reactions to
better compliance compared with oral antibiotics [47]. In fusidic acid since the early 1980s, despite increasing use
clinical practice, mupirocin is often reserved to eradicate [53]. Patch testing data from Germany showed a low

8 EJD, vol. 20, n° 1, January-February 2010

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Table 3. Studies on healing rates and times with fusidic acid cream (a) and ointment (b) in skin and soft tissue infections

Reference Condition Fusidic acid Comparator

n = pts treated Clinical Treatment n = pts treated Clinical response rate Treatment duration
response rate duration (%)a (days)
(%)a (days)
a) Fusidic acid cream
Pakrooh 1980 [26] Skin sepsis (abscesses, 50 98% 7.9b –c – –
boils, paronychia, infected
wounds)
Baldwin 1981 [27] Superficial localized sepsis 487 92% 7.7b –c – –
(impetigo, abscesses/boils,

EJD, vol. 20, n° 1, January-February 2010

wounds and other
secondary infections)
Macotela Ruiz 1988 [28] Skin infection 19 95% 14 Dicloxacillin 89% 14
500 mg BID
n = 19
Langdon 1990 [29] Acute skin sepsis 104 95% 7 Mupirocin 98% 7
(impetigo, folliculitis, n = 102
infected trauma, infected
dermatosis)
El Mofty 1990 [30] Superficial bacterial 34 78% 14 Trimethoprim-polymixin 84% 14
infections of the skin n = 30
Jaafar 1991 [31] Pyodermas 50 47% 14 Trimethoprim-polymixin 73% 14
n = 50
Hamann 1991 [32] Erythrasma 31 87% 14 Erythromycin tablets 77% 14
n = 31
Sutton 1992 [33] Facial impetigo 93 97% 7 Mupirocin 98% 7
n = 84
Christensen 1994 [34] Impetigo 128 82% 12.4b Hydrogen peroxyde cream 72% 14.4b
[Bact: 93%]d n = 128 [Bact: 88%]d
Koning 2002 [35] Impetigo 78e 95% 14 Povidone/iodine 86% 14
[Bact: 89%]d n = 82 [Bact: 74%]d
b) Fusidic acid ointment
Jackson 1966 [36] Bacterial skin infection 101 93% 6.8b Oral/intramuscular 96% (oral) 5.3 daysb (oral)
penicillin 98% (i.m.) 4.9 daysb (i.m.)
n = 58
Somerville 1971 [37] Erythrasma 66 89% 5d (axillae and 6% benzoic acid + 3% 90% (benzoic acid) 5d (axillae and groins)
groins) salicylic acid, n = 61 32% (base) 14 d (toe webs)
14 d (toe webs) Ointment base n = 59
Pakrooh 1977 [38] Soft tissue infections 49 100% 7.1b Oral antibioticsf 83% 9.7b
(abscesses, boils, n = 41
paronychia, infected
wounds)
Pakrooh 1980 [26] Skin sepsis (abscesses, 51 91% 7.7b –g – –
boils, paronychia, infected
wounds)
(continued)

9
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Table 3 (continued)

10
Reference Condition Fusidic acid Comparator
n = pts treated Clinical Treatment n = pts treated Clinical response rate Treatment duration
response rate duration (%)a (days)
(%)a (days)

Baldwin 1981 [27] Superficial skin sepsis 249 90% 7.1b –g – –

Cassels-Brown 1981 [39] Impetigo 52 70% healed 7 Neomycin/ bacitracin 47% healed 7
100% healed/ n = 58 90% healed/improved
improved
Zelvelder 1984 [40] Skin infections 30 93% 4-7 Oral amoxicillin n = 30 97% 4-7
Oral amoxicillin + FA 90% 4-7
ointment n = 30
Morley 1988 [41] Acute skin infection 191 86% 7 Mupirocin 86% 7
n = 163
White 1989 [42] Superficial skin infections 138 93% 7 Mupirocin 97% 7
[Bact: 89%]d n = 275 [Bact: 93%]d
Gilbert 1989 [43] Primary and secondary 35 94% 7 Mupirocin 94% 7
skin infections [Bact: 87%h]d n = 35 [Bact: 97%h]d
Jasuja 2001 [44] Primary pyodermas 50 84% 7 Mupirocin 90% 7
n = 50
Oranje 2007 [45] Impetigo 172 90% 7 Retapamulin 95% 7
[Bact: 94%]d n = 345 [Bact: 98%]d
BID: twice daily; FA: fusidic acid; i.m.: intramuscularly.
a
As defined in each study (generally cure or cure/improvement).
b
Mean healing time;
c
Comparator was fusidic acid ointment (table 3b).
d
Bacteriological response rate: generally defined as defined as eradication of the pre-treatment pathogen or no swab being taken at the end of treatment because no pathological material was present. Not
reported in all studies.
e
Fusidic acid + povidone/iodine.
f
Clindamycin, erythromycin, or floxacillin.
g
Comparator was fusidic acid cream (table 3a).
h
Efficacy against Staphylococcus aureus.

EJD, vol. 20, n° 1, January-February 2010

 Table 4. Comparative trials of fusidic acid/corticosteroid combination preparations in infected eczema

Reference Fusidic acid combination Comparator Treatment Resulta

duration
(days)
Poyner 1996 [62] Fusidic acid 2%/ Miconazole 2%/ hydrocortisone 7 Response rates: F 69.5%, M
hydrocortisone 1% cream (F) 1% cream (M) 68.6%
n = 95 n = 102 Faster healing with F (p = 0.04)
Bacteriological efficacy: F
97.9%, M 83.0% (p = 0.04)
Wilkinson 1985 [63] Fusidic acid 2%/ betamethasone Neomycin 0.5%/ 14 Response rates: F 95%, N 90%
0.1% cream (F) betamethasone 0.1% cream (N) Bacteriological efficacy: F
n = 45 n = 46 91%, N 88%
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Javier 1986 [64] Fusidic acid 2%/ betamethasone Neomycin 0.5%/ 7-10 Response rates: F 85%, N 81%
0.1% cream (F) betamethasone 0.1% cream (N) Bacteriological efficacy: F
n = 27 n = 32 78%, N 72%
Strategos 1986 [65] Fusidic acid 2%/ betamethasone Gentamicin 0.1%/ 7-12 Response rates: F 98%, G 90%
valerate 0.1% cream n = 50 betamethasone valerate 0.1% Bacteriological efficacy: F
cream (G), n = 49 86%, G 86%
Hill 1998 [66] Fusidic acid 2%/ betamethasone Clioquinol 3%/ betamethasone Up to 28 Response rates: F 57.9%, C
0.1% cream (F) 0.1% cream (C) 60.4%
n = 58 n = 62 Patients finding cosmetic
acceptability good: F 90.6%, C
29.6%
Bacteriological efficacy: F
92.3%, C 55.2% (p < 0.005)
Schultz Larsen 2007 Fusidic acid 2%/ betamethasone Lipid cream vehicle n = 88 14 Response rate: cream 84.0%,
[67] 0.1% cream, n = 275 and lipid cream, 83.5%, vehicle NR
Fusidic acid 2%/ betamethasone Bacteriological efficacy:
0.1% lipid cream, n = 258 Cream 89.6%, lipid cream
89.7%, vehicle 25.0%
NR: not reported.
a
Rates are given for response as defined in each study (generally good/excellent clinical response, or marked improvement/complete clearance, as
assessed by the investigator). Bacteriological efficacy was generally defined as eradication of the pre-treatment pathogen or post-treatment absence
of any lesions.

incidence of allergic reactions to fusidic acid (0% among (Fucicort®/Fucibet®). A new formulation of fusidic acid
atopic individuals and 1.76% among non-atopic indivi- and betamethasone in a lipid cream (Fucicort®
duals) [54]. More recently, the prevalence of positive reac- Lipid/Fucibet® Lipid) has recently been developed to pro-
tions to patch tests in the general German population was vide an alternative treatment for patients with infected
estimated to be 2.2% for neomycin, 3.2% for gentamicin, eczema in whom the existing combination cream does
and 0.8% for fusidic acid [55]. not provide an adequate moisturizing effect.
Although adverse drug reactions are rare with fusidic acid, The fusidic acid-hydrocortisone combination was more
occasional cases of skin reactions, and in particular appli- effective than fusidic acid alone (n = 68) in achieving a com-
cation site reactions, have been reported [106-110]. bined clinical-bacteriological endpoint, and more effective
According to the authors of these case reports, the aller- than hydrocortisone alone in a subset of patients with
genic potential of sodium fusidate is low, and sensitisation pathogens at baseline (n = 73) [60]. The fusidic acid-
can be favoured by chronic inflammatory states, espe- betamethasone combination was compared with betametha-
cially if associated with stasis dermatitis, as in leg ulcers sone alone by using each therapy on the left or right side of
[106]. A recent case report described the first known case the body in patients with atopic dermatitis, contact dermatitis,
of a generalised urticaria following simultaneous oral and or psoriasis, in a double-blind study [61]. The two treatments
topical fusidic acid [111]. had similar overall efficacy, but investigator assessment of
the efficacy of therapy on each side showed a significant
Use of fusidic acid-steroid combinations in infected atopic preference for combination treatment (p < 0.05).
eczema A number of studies have confirmed the efficacy of these
As atopic eczema is frequently infected with S. aureus, combinations in infected eczema (table 4) [62-67]. In all
combination treatments that include both antibiotic and of these studies, the fusidic acid-steroid combination was
steroid components are useful [56, 57], and are recom- shown to have similar or superior clinical and bacteriolog-
mended as first-line therapy [58]. The ability to address ical efficacy compared to other combination products. In
infection and inflammation with a single preparation one study, significantly more patients rated the cosmetic
rather than separate ones may encourage greater patient acceptability as “good” for fusidic acid-betamethasone
compliance with treatment [59]. than for clioquinol-betamethasone [66].
Fusidic acid is available in some countries in cream for- It is worth mentioning the recent study in which fusidic
mulations that include 1% hydrocortisone acetate acid–betamethasone cream was compared with the new
(Fucidin® H) or 0.1% betamethasone 17-valerate lipid cream formulation [67]. This study had several

EJD, vol. 20, n° 1, January-February 2010 11

 strengths: it was double-blinded, the diagnosis of clini- The prevalence of resistance to fusidic acid was reviewed
cally infected atopic eczema was based on strict criteria, by Turnidge [78]. In general, up to the mid-1980s, studies
and patients were representative of a wide spectrum of on S. aureus bacteraemia showed a low-level resistance of
out-patients with this condition. Finally, the various differ- 0-2.3% to fusidic acid. Later studies showed rates of resis-
ent endpoints that were examined (percentage reduction in tance up to 6.4% in hospital patients [79]. Numerous con-
total severity score, investigators’ assessment of efficacy, tradictory studies can be found in the literature, some with
patients’ assessment of efficacy, bacteriological response) higher rates of resistance for bacterial strains that have
all showed similar high efficacy for the cream and the been isolated from SSTIs. The resistance level to fusidic
lipid cream formulations. acid might have been overestimated in these studies, as
A safety overview of published and unpublished studies the cultures were generally taken from patients who did
and postmarketing surveillance data has shown that, as not respond to therapy [80].
with plain fusidic acid, fusidic acid-steroid combination In Scandinavia, the UK, and Ireland, increased levels of
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products have few and mild side effects [68]. resistance have been observed. This was primarily due the
spread of a clone in impetigo patients, which seems to
have peaked and is now declining [81-83]. The rest of
Resistance Europe has levels of resistance below 10% [84-86]. Resis-
tance of MRSA to topical fusidic acid has remained at a
No cross-resistance with other antibiotics has been low level in Germany (3.4% in 1998, 2.4% in 2002) [87].
observed, probably due to the unique structure of fusidic However, it should also be noted that, in recent years, new
acid [69]. MRSA strains have spread in the community, presumably
A concern amongst microbiologists is the potential devel- arising from several diverse genetic backgrounds in sev-
opment of drug resistance with extensive use of topical eral countries [88]. These MRSA strains, referred to as
fusidic acid. Resistance is due to either chromosomal or community-associated MRSA (CA-MRSA), were isolated
plasmid-mediated resistance. Chromosomal resistance e.g. in North America (ST USA300), Central Europe
appears readily in vitro at a frequency of 10-6 to 10-11, (ST080, ST398), Australia, and New Zealand. CA-
depending on the concentration of fusidic acid used [70]. MRSA are considered to be more virulent than other
The selected variants typically have minimum inhibitory MRSA strains due to their production of Panton-
Valentine leukocidin, and other toxins. Those strains can
concentration (MIC) values ranging from 8 mg/L to more
be resistant to specific antibiotics; for fusidic acid, resis-
than 256 mg/L [71]. This chromosomal resistance is due
tance is due to the far-1 gene [89, 90]. In severe clinical
to modification of elongation factor G (the site of action
infections (deep necrotizing abscesses) S. aureus diagnos-
of fusidic acid) by one or several point mutations. Such
tics should include PCR for the lukF/lukS gene (coding
variants have been detected in clinical settings [71, 72];
for Panton-Valentine leukocidin) and the far-1 gene (cod-
they appear to be defective, because they grow more ing for fusidic acid resistance).
slowly than the parent strain and have a lower pathogenic- Resistance levels to fusidic acid did not change between
ity [71, 73, 74]. Furthermore, those mutants revert to full 1988 and 1994 in Australia [91], and there was no trend to
susceptibility when fusidic acid is absent from the increasing fusidic acid resistance at a Canadian hospital
medium [75]. from 1999 to 2005 [92].
Plasmid-mediated resistance to fusidic acid has been Some reports have suggested that extensive use of topical
called “naturally occurring resistance” as it is detectable antibiotics, including mupirocin and fusidic acid, against
in isolates from patients never exposed to the drug [75]. S. aureus infections, particularly for prolonged periods, is
This resistance may be linked to resistance to heavy linked with increased occurrence of resistance [93, 94].
metals and to other antibiotic resistances, including peni- There is general consensus that short-term therapy, for
cillinase production [76]. These strains are pathogenic and periods of no more than 2 weeks at a time, avoids the
grow normally. However, as the plasmid may be unstable, risk of resistance emerging [59, 95-97]. This suggestion
some resistant colonies revert to fusidic acid susceptibility was reinforced by results from the recent study on the
[75]. efficacy of the new fusidic acid-betamethasone lipid
Recent analyses of clinical isolates have shown that a sin- cream (n = 629), in which a prospective evaluation of
gle gene (fusB) from the plasmid is capable of conferring the emergence of resistance was performed. S. aureus iso-
resistance to fusidic acid in S. aureus and that this gene is lates with resistance or intermediate resistance to fusidic
now inserted into the chromosome of some epidemic acid were seen in 2.3% of the patients who applied fusidic
strains [72]. In addition, chromosomal genes (fusB) acid, and 1.9% of those given the vehicle only [67].
encoding proteins with about 45% similarity to FusB
have been identified [112]. These strains do not have a
modified elongation factor G, nor do they deactivate fusi- Guideline recommendations
dic acid enzymatically. The fusB and fusC genes code for
a protein that binds directly to elongation factor G, The national guidelines of many countries specifically
thereby preventing interference in protein synthesis by recommend topical fusidic acid as the first choice of ther-
fusidic acid [77, 112]. apy in impetigo and/or staphylococcal primary skin infec-
Thus, resistance of S. aureus to fusidic acid may arise tions – including, for example, those of Belgium [98],
from one of at least three different resistance classes: the Canada [99], Denmark [100], France [101], Germany
FusA class (mutation of elongation factor G), FusB class [102], and the Netherlands [103]. Fusidic acid cream or
(plasmid-mediated resistance), and FusC class (chromo- ointment should be applied sparingly two or three times
somal fusC gene) [112]. daily [100, 102] for no longer than 14 days [103]. In

12 EJD, vol. 20, n° 1, January-February 2010

 France, fusidic acid can also be used to eliminate nasal 10. Bogdanovich T, Ednie LM, Shapiro S, Appelbaum PC. Antista-
phylococcal activity of ceftobiprole, a new broad-spectrum cephalo-
carriage of S. aureus in the context of preventing recur- sporin. Antimicrob Agents Chemother 2005; 49: 4210-9.
ring infections, although mupirocin is the first choice for 11. Soriano F, Zapardiel J, Nieto E. Antimicrobial susceptibilities of
this purpose [101]. In the UK, the independent Drugs and Corynebacterium species and other non-spore-forming gram-positive
Therapeutics Bulletin concluded: “On current evidence, bacilli to 18 antimicrobial agents. Antimicrob Agents Chemother
1995; 39: 208-14.
retapamulin should not replace fusidic acid as the first- 12. Hassan H, O’Hare MD, Felmingham D. In vitro activity of teico-
line treatment for impetigo, but may be considered planin, vancomycin, A16686, clindamycin, erythromycin and fusidic
where that treatment has failed” [104]. acid against anaerobic bacteria. Singapore Med J 1990; 31: 56-8.
The joint European/American allergy/immunology guide- 13. Leclercq R, Bismuth R, Casin I, Cavallo JD, Croizé J, Felten A. In
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ized secondary infection in atopic eczema [105]. In order 14. Spelman D. Fusidic acid in skin and soft tissue infections. Int J An-
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restricted to periods of about 2 weeks. 15. Nordin P, Mobacken H. A comparison of fusidic acid and flu-
cloxacillin in the treatment of skin and soft-tissue infection. Eur J Clin
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16. Machet L, Puissant A, Vaillant L. Essai comaratif multicentrique de
Conclusion l’acide fusidique comprimés à deux posologies (500 mg et 1 g/jour)
versus prestinamycine comprimés (2 g/jour) dans le traitement des
infections cutanées. Nouv Dermatol 1994; 13: 520-4 [Treatment of
Fusidic acid is useful in the treatment of SSTIs, particu- skin infections with two dosages of fusidic acid (500 mg/day and
larly those due to S. aureus. The efficacy and tolerability 1 g/day) compared with pristinamycin 2 g/day: a multicenter rando-
of fusidic acid in systemic, plain topical, and combination mised study.].
topical forms have been confirmed over many years of 17. Carr WD, Wall AR, Georgala-Zervogiani S, Stratigos J, Gourio-
tou K. Fusidic acid tablets in patients with skin and soft tissue infec-
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