The Journal of Emergency Medicine, Vol 17, No 1, pp 213–220, 1999
Copyright © 1999 Elsevier Science Inc.
PII S0736-4679(98)00148-6
Antimicrobial Wound Management
in the Emergency Department:
An Educational Supplement
OPPORTUNITIES FOR MUPIROCIN CALCIUM CREAM IN THE
EMERGENCY DEPARTMENT
Phillip M. Williford,
Department of Dermatology, Bowman Gray School of Medicine, Winston Salem, North Carolina
Reprint Address: Phillip M. Williford, MD, Department of Dermatology, Bowman Gray School of Medicine, Winston Salem, NC
e Abstract—Mupirocin calcium cream is a newly refor-
mulated topical antibiotic with a bactericidal spectrum spe-
cific for the pathogens that frequently cause secondary
infections in superficial wounds. Both the calcium cream
and ointment formulations have demonstrated efficacy in
the treatment of secondarily infected traumatic lesions and
dermatoses, including eczema, burns, wounds, bites, and
ulcers. Mupirocin has a low risk of systemic and topical
complications. To date, antimicrobial resistance is rare
among target pathogens. The use of mupirocin to treat
secondary wound infection has a profile of high efficacy and
does not impair the normal healing in traumatized skin.
© 1999 Elsevier Science Inc.
e Keywords—mupirocin; mupirocin calcium cream; skin
diseases; infectious; wound infection; secondarily infected
traumatic lesions; Staphylococcus aureus
INTRODUCTION
Secondarily infected traumatic lesions (SITLs) arise
when a preexisting wound or skin lesion becomes in-
fected (1). Antibiotic treatment is often integral to proper
healing. Recently, mupirocin was reformulated into
mupirocin calcium cream to target SITLs. This article
will focus on the treatment of SITLs and dermatoses,
comparing the utility and the safety of the topical anti-
biotic mupirocin calcium cream and mupirocin ointment
with that of oral antibiotics.
Grant Support: SmithKline Beecham.
213
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0736-4679/99 $–see front matter
MD
THE PHYSIOLOGY OF WOUND HEALING
To understand the role of mupirocin in the treatment of
SITLs and dermatoses, one must review the basic phys-
iology of wound repair. Wound healing involves a com-
plex interplay among many cell types, cytokines, and the
extracellular matrix that can be divided into three phases.
These designations are somewhat arbitrary and progress
continuously from one to another. (2,3)
The inflammatory phase, beginning with the injury
and continuing for several days, is characterized by the
influx of platelets, neutrophils, and monocytes and the
release of their cytokines. Chemotactic factors released
as part of the coagulation cascade facilitate diapedesis of
neutrophils through up-regulation of adhesion molecules
on the surface of epithelial cells (4). The interaction of
these blood-borne cells mediates decontamination of the
wound, removal of necrotic debris, and initiation of
angiogenesis (2).
The proliferative phase begins with the formation of
granulation tissue, and the incipient reepithelialization of
the wound. A matrix composed of fibrin, fibronectin, and
type V collagen covers the wound bed and allows kera-
tinocyte migration (2). Keratinocytes progress in sheets
inward from the wound edge within 24 h of injury (2,5).
Growth factors released from macrophages play a role in
the direction and control of keratinocyte migration.
Wound fibroblasts form new connective tissue composed
initially of type III collagen, glycosaminoglycans, and
proteoglycans. The wound subsequently contracts due to
contractile proteins contained within myofibroblasts (2).
The remodeling phase occurs for up to 18 months
after the restoration of a functional epidermal barrier (3).
214
During this phase, type III collagen is replaced by type I
collagen (2). Continued modification of fibronectin and
proteoglycans also occurs. The remodeling phase results
in the near recovery of preinjury tensile strength, which
at its maximum is approximately 80% of preexisting
strength (2,6).
During the process of recreating the functional epi-
dermal barrier after injury, secondary infection may in-
tervene in efficient recovery. Whether this process occurs
is dependent on a number of supervening factors.
DOES WOUND HEALING ALWAYS REQUIRE
AN ANTIBIOTIC?
Most wounds, particularly nonpenetrating wounds, heal
well without the need for antibiotic treatment (7). Al-
though debate continues regarding the timing of wound
closure, choice of suture materials, and utilization of
various scrub solutions and irrigants, it is clear that
management generally revolves around cleaning the
wound, irrigating it, and applying an appropriate dress-
ing. Antiseptic scrub solutions probably should be
avoided, although povidone solution 1% does not appear
to be toxic to tissue and may improve outcome, though
the assertion is open to dispute. Local anesthesia, when
needed, should be administered without epinephrine, as
the use of epinephrine is associated with increased risk of
infection in contaminated wounds because of alterations
in blood flow to injured areas. Avoidance of buried
sutures is likewise recommended.
The impact of topical antibacterial ointments on the
healing of uninfected wounds is somewhat controversial.
Kirsner and Eaglstein maintain that antimicrobial agents
do not convincingly speed healing (2). Some authors
decry the routine use of topical antibiotics in seemingly
clean wounds, citing a low incidence of infection (8).
However, most superficial traumatic wounds are contam-
inated by foreign material, whether iatrogenic (e.g., su-
tures) or otherwise, that alter the probability of infection
and the subsequent usefulness of topical or systemic
antibiotic therapy (9). One study found that topical ap-
plication of neosporin or bacitracin to suture lines de-
creased the risk of infection compared to petrolatum
controls (10). Other evidence suggests that topical anti-
biotics decrease the risk of infection in both animal and
human wounds (11). Watcher and Whelland reported
that mupirocin has no effect on re-epithelialization, but
significantly decreases the rate of wound contraction
(12). Another study found that mupirocin ointment ac-
celerated healing by as much as 8% (13). Several reports
note that topical antibiotics, including mupirocin, are not
toxic to human fibroblasts or keratinocytes (14 –16).
Boyce et al. (17) reported that mupirocin had no toxicity
P. M. Williford
to cultured human skin grafts and was uniformly effec-
tive against S. aureus, including methicillin-resistant S.
aureus.
CLINICAL PHARMACOLOGY OF
MUPIROCIN
Mupirocin (pseudomonic acid A; C26H4409) is a metab-
olite produced by submerged fermentation of Pseudomo-
nas fluorescens (18,19). Its chemical structure and mech-
anism of action are unique among antibiotics in clinical
use; therefore, cross resistance (and shared allergy) be-
tween mupirocin and other antibiotics is not a concern.
Toxicity arising from inhibition of isoleucyl-t-RNA syn-
thetase by mupirocin does not occur in humans because
it has a low affinity for the mammalian enzyme (18).
Mupirocin inhibits bacterial protein synthesis by binding
to the enzyme, isoleucyl-t-RNA synthetase, which pre-
vents the incorporation of isoleucine into proteins (20).
Systemic absorption is minimal with topical adminis-
tration of mupirocin; however, with intravenous admin-
istration, mupirocin is rapidly converted predominantly
to monic acid, an inactive metabolite that is readily
excreted in the urine (20). In one study of mupirocin
ointment, not more than 0.24% of the dose was absorbed
in the 24 h after topical administration (20). Multiple
dosing of mupirocin calcium cream shows marginal per-
cutaneous absorption in adults and children (21). Al-
though one study showed that percutaneous absorption is
more common in children than in adults, pediatric ab-
sorption levels as determined by urinary monic acid
concentrations are within the observed range in the adult
population (21). Radioactivity has been detected in the
stratum corneum 72 h after administration of 14C-labeled
mupirocin, suggesting that mupirocin resides in the skin
for some time (22).
Previously available only as a free acid in a polyeth-
ylene glycol base, the new formation of mupirocin as a
calcium salt in a cream base is nongreasy and therefore
generally better tolerated. The new formulation also
eliminates the potential for allergic contact hypersensi-
tivity that was occasionally caused by the polyethylene
glycol base (23). Accumulation of polyethylene glycol in
patients with poor renal function or hemodynamic insta-
bility also can result in nephrotoxicity and metabolic
abnormalities (24,25).
Mupirocin is bacteriostatic at low concentrations, but
it is bactericidal at the higher local concentrations
achieved with topical administration (26). The bacteri-
cidal activity of mupirocin is enhanced in an acid envi-
ronment such as the skin (26). Mupirocin has a narrow
spectrum of activity encompassing most clinically perti-
nent gram-positive organisms, specifically staphylococci
Muciprocin Cream in the ED
and streptococci. In an in vitro study of 1,000 S. aureus
isolates, 100% of methicillin-sensitive and 95.9% of
methicillin-resistant isolates were susceptible to mupiro-
cin (27). Mupirocin demonstrates significant activity
against Haemophilus influenza, Neisseria gonorrhoeae
and meningitidis, Branhamella catarrhalis, and Pasteu-
rella multocida, but activity against other gram-negative
organisms is suspect (26,28). Interestingly, its in vitro
activity against Candida albicans is comparable to that
of many frequently used antifungals (28). Mupirocin is
inactive against group D streptococci and anaerobes
(26,28). Normal skin flora such as micrococcus, coryne-
bacterium, and propionibacterium are unaffected,
thereby maintaining the body’s natural inhibition of
pathogens through competition from commensals
(26,28).
Resistance to mupirocin among ordinarily sensitive
pathogens, which is an infrequent occurrence, is gener-
ally low level (MIC , 100 mg/mL) (29). The clinical
significance of low-level resistance is unclear because
concentrations of mupirocin applied to wounds reach
20,000 mg/mL, and treatment failures have been only
rarely reported. Nevertheless, high-level resistance
(MIC . 1024 mg/mL) has been reported in some strains
of S. aureus and coagulase-negative staphylococci. The
apparent cause of high-level resistance is plasmid coding
for a modified form of isoleucyl tRNA synthetase (29).
CLINICAL EFFICACY AND SAFETY
OF MUPIROCIN
Treatment of Secondary Infected Traumatic Lesions
and Dermatoses
Because S. aureus and streptococci produce the majority
of secondary skin infections, mupirocin calcium cream is
a reasonable treatment choice compared to oral antibiot-
ics for secondary infections affecting relatively small
areas (#10 cm in length or 100 cm2 in area). Controlled
studies comparing mupirocin with oral antibiotics are
summarized in Table 1 (30 –37). In two randomized,
double-blind trials, mupirocin calcium cream (n 5 357)
applied to SITLs (e.g., lacerations, sutured wounds, abra-
sions) three times daily over 10 days was equally effec-
tive to oral cephalexin (n 5 349) over the same time
period (30). At the end of therapy, the pathogen eradi-
cation rates were 96.9% for mupirocin patients and
98.9% for cephalexin patients. Similar results in another
randomized, double-blind trial showed that mupirocin
calcium cream (n 5 195) and oral cephalexin (n 5
178) were both 100% effective at pathogen eradication,
and their clinical success rates were comparable (96.2%
for mupirocin and 86.5% for cephalexin) (31).
215
As an alternative to systemic antibiotics, mupirocin
calcium cream has demonstrated efficacy in the treat-
ment of secondarily infected dermatoses. Rist et al com-
pared mupirocin calcium cream (n 5 82) to oral cepha-
lexin (n 5 77) in the treatment of secondarily infected
eczema over a 10-day period (33). While both agents
were comparably effective in achieving clinical success
(89% for mupirocin and 82% for cephalexin), mupirocin
was significantly more effective ( p 5 0.004) at patho-
gen eradication.
The groundwork for efficacy of mupirocin calcium
cream in treating secondary infections was first estab-
lished in placebo-controlled trials of mupirocin ointment.
Ward et al evaluated a series of 11 double-blind, ran-
domized clinical trials comparing mupirocin ointment
with its vehicle (free acid in a polyethelene glycol base)
as a placebo for the treatment of secondarily infected
dermatoses including eczema, burns, wounds, bites, and
ulcers (20). With the exception of a single study, bacte-
rial eradication was greater with mupirocin, which was
associated with an overall eradication rate of 90%
(range: 73% to 100%), compared to 53% with its vehicle
(range: 19% to 89%). For S. aureus, the overall eradica-
tion rate was 94% with mupirocin and 40% with its
placebo vehicle. In terms of clinical efficacy, the overall
response rate was 94% with mupirocin (range: 81% to
100%) and 71% with its vehicle (range: 38% to 93%).
The success rates for infected eczema were 97% and
44%, respectively (20).
Breneman evaluated the efficacy of mupirocin oint-
ment vs. its vehicle for secondarily infected dermatoses
in a double-blind, vehicle-controlled study with 92
evaluable patients (38). Patients suffered from atopic
dermatitis, eczema, seborrheic dermatitis, neurodermati-
tis, and contact dermatitis. Mupirocin treatment pro-
duced significantly greater eradication of S. aureus (85%
versus 6%, respectively, p , 0.01) and total pathogens
(69% versus 14%, respectively, p , 0.01. When all
pathogens were considered, there was marked or mod-
erate improvement in global infections in 79% of mupi-
rocin-treated patients and 65% of vehicle-treated pa-
tients. When only S. aureus- or S. pyogenes-associated
infections were considered, marked or moderate im-
provement was observed in 85% of mupirocin-treated
patients compared with 53% of vehicle-treated patients
( p 5 0.007). In addition to infection improvement,
there was also a significantly greater improvement in
dermatoses treated with mupirocin (53% versus 22%,
respectively, p 5 0.01). The extent of beneficial clinical
effect from the placebo treatment (the vehicle) highlights
the difficulty of differentiating significant skin infections
from trivial ones, or from colonization.
216 P. M. Williford

Table 1. Clinical Trials Comparing Mupirocin with Oral Antibiotics for Primary and Secondary Skin Infections* (30 –37)

Primary and
Secondary Clinical Cure or
Reference Dermatoses Number Regimen Improvement (%)

Kraus et al. (30) Secondarily infected open 357 Mupirocin Applied TID for 10 d 233/245 (95.1)
wound (e.g., laceration, 349 Cephalexin PO QID for 10 d 222/233 (95.3)
sutured wound,
abrasion)
Henkel et al. (31) Secondarily infected open 195 Mupirocin Applied TID for 10 d 125/130 (96.2)
wound (e.g., laceration, 178 Cephalexin PO QID for 10 d 110/114 (96.5)
sutured wound,
abrasion)
Bass et al. (32) Impetigo 7 Mupirocin Applied TID for 10 d 7/7 (100)
9 Bacitracin Applied TID for 10 d 3/9 (33)
10 Cephalexin 50 mg/kg/d TID for 10 d 10/10 (100)
Rist et al. (33) Secondarily infected 82 Mupirocin Applied TID for 10 d 39/44 (89)
eczema 77 Cephalexin 250 mg PO QID for 10 d 31/38 (82)
Gratton (34) Impetigo; boils; folliculitis; 30 Mupirocin Applied TID for 7 d 29/30 (97)
furuncles, infected 28 Erythromycin 250 mg PO QID for 7 d 23/28 (82)
lacerations, ulcers,
eczema, herpes or
scabies
Welsh and Impetigo; folliculitis; 27 Mupirocin Applied TID for 5–10 d 26/27 (96)†
Saenz (35) infected eczema, burns, 23 Ampicillin 500 mg PO QID for 5–10 d 18/23 (78)
ulcers; paronychia;
others
Dux et al. (36) Impetigo; folliculitis; 78 Mupirocin Applied TID for 7 d 76/78 (97)
carbuncles; infected 50 Erythromycin 250 mg PO QID for 7 d 47/50 (94)
lacerations, ulcers, 20 Cloxacillin 250 mg PO QID for 7 d 19/20 (95)
eczema; paronychia;
sebaceous cyst; others
Villiger et al. (37) Impetigo; furuncles; 101 Mupirocin Applied TID for 4–10 d 100/101 (99)‡
infected lacerations, 19 Erythromycin Usual PO dose for 4–10 d 14/19 (74)
eczema, ulcers or burns 80 Flucloxacillin Usual PO dose for 4–10 d 79/80 (99)

* Randomized, parallel-group studies.

† Statistically significant difference.
‡ Statistically significant difference for mupirocin vs erythromycin.
Abbreviations: d 5 days; QID 5 four times daily; PO 5 oral; TID 5 three times daily.

Treatment of Impetigo (35). In retrospect, this is to be expected, considering the

Mupirocin is an alternative to systemic antibiotics for the
treatment of impetigo because S. aureus alone or a mixed
flora of S. aureus and S. pyogenes is often recovered
from impetigo lesions (34,35). One small study compar-
ing mupirocin cream (n 5 7) to topical bacitracin (n 5
9) and oral cephalexin (n 5 10) showed no treatment
failures in the mupirocin and cephalexin groups, but six
treatment failures in the bacitracin group ( p , 0.005)
(36). The authors made two conclusions that need to be
confirmed in larger studies: first, that bacitracin can no
longer be recommended to treat impetigo; and second,
that topical mupirocin and oral cephalexin are equally
effective treatment choices.
A number of studies have found mupirocin either
more effective (34,36,37,41) or equivalent (42,43) to oral
erythromycin in eradicating impetigo infection. Mupiro-
cin was significantly more effective than oral ampicillin
in a study comparing mupirocin with oral ampicillin in
the treatment of primary and secondary skin infections
limited staphylococci coverage of ampicillin. For treat-
ing impetigo cases that involve only a small number of
lesions, it is recommended to use mupirocin cream and to
reserve oral antibiotic use for more widespread cases
(32).
The superior performance of mupirocin may be due to
a shift toward erythromycin and ampicillin-resistant S.
aureus as the primary cause of impetigo (40). In a study
in which 93% of impetigo lesion cultures yielded S.
aureus, 28% of evaluable patients were infected with
erythromycin-resistant isolates (44). The clinical failure
rate for erythromycin-treated patients with erythromy-
cin-resistant isolates was 47% compared with failure
rates of 8% for patients infected with susceptible isolates
and 2% for patients treated with mupirocin. A number of
studies comparing mupirocin with oral antibiotics for
impetigo also found it effective for the treatment of
secondarily infected wounds, ulcers, burns, and eczema
(35–37). These studies are summarized in Table 2
(32,46 –56).
Muciprocin Cream in the ED 217

Table 2. Clinical Trials* Comparing Mupirocin Ointment with Its Polyethelene Glycol Vehicle for Secondary Skin Infections
(32,46 –56)

Application Clinical Cure or Bacteriologic

Reference Number Regimen Improvement (%) Cure (%)

Breneman, 1990 (32) 47 Mupirocin TID for 7–9 d 37/47 (79) 52/75 (69)†
43 Vehicle 28/43 (65) 10/69 (14)
Carney and Bickers, 1985 (46) 22 Mupirocin TID for 7–8 d 20/22 (91) 22/30 (73)
22 Vehicle 18/22 (82) 12/31 (39)
D’Alessandri et al., 1985 (47) 16 Mupirocin TID for 8 d 15/16 (94) 18/18 (100)
15 Vehicle 14/15 (93) 16/18 (89)
DeBoer, 1985 (48) 26 Mupirocin TID for #10 d 21/26 (81) 23/29 (79)†
25 Vehicle 21/25 (84) 18/31 (58)
Eaglstein, 1985 (49) 20 Mupirocin TID for #12 d 19/20 (95)† 29/30 (97)†
17 Vehicle 12/17 (71) 11/24 (46)
Golitz and Beehler, 1985 (50) 24 Mupirocin TID for 8 d 22/24 (92) 27/29 (93)†
20 Vehicle 16/20 (80) 5/25 (20)
Leyden, 1985 (51) 26 Mupirocin ND 26/26 (100)† 22/26 (85)†
26 Vehicle 10/26 (38) 5/26 (19)
Orecchio and Mischler, 1986 (52) 76 Mupirocin TID for #10 d 63/76 (83)† ND
78 Vehicle 37/78 (47)
Pekoe and Dobson, 1985 (53) 34 Mupirocin TID for #12 d 32/34 (94) 45/53 (92)†
34 Vehicle 31/34 (91) 38/52 (73)
Rosenberg and Churchwell, 1985 (54) 25 Mupirocin ND 24/25 (96) 32/35 (91)†
23 Vehicle 19/23 (83) 27/41 (66)
Whiting et al., 1985 (55) 17 Mupirocin TID for 5–12 d 17/17 (100) 19/20 (95)†
19 Vehicle 16/19 (84) 10/20 (50)
Zone and Weidner, 1985 (56) 26 Mupirocin ND 25/26 (96) 30/31 (97)†
25 Vehicle 22/25 (88) 18/33 (55)

* Randomized, double-blind, parallel-group studies.

† Statistically significant difference.
Abbreviations: d 5 days; ND 5 no data; TID 5 three times daily.
Adapted, with permission, from Ward (45)

Treatment of Chronic Dermatologic Disorders
Mupirocin has shown a benefit in treating some lesions
of a number of chronic dermatologic disorders that are
exacerbated by S. aureus colonization. In atopic derma-
titis, a decrease in S. aureus colonization with 2 weeks of
mupirocin therapy was associated with a decrease in
clinical severity (57). However, patients quickly became
recolonized after mupirocin was discontinued. Mupiro-
cin has been successfully used to decrease S. aureus
colonization and enhance healing of epidermolysis bul-
losa (58), as well as to prepare wounds for epidermal
autografts (59).
resistant S. aureus was eradicated from all wounds
within 5 days (62). Subsequently, 20 wounds healed
spontaneously, and 39 granulated enough for successful
grafting. In this study, the average burn wound size was
8% of the body surface area (range: 2% to 20%).
Based on these studies, mupirocin has demonstrated
efficacy for the treatment of SITLs. Mupirocin has not
been studied for the treatment of deeper soft tissue in-
fections, such as cellulitis, lymphangitis, or fasciitis. The
inability to reliably predict deep tissue concentrations of
drug, and the rapid metabolism of systemically absorbed
product to an inactive metabolite suggest that systemic
antibiotic therapy is indicated in such cases.

Treatment of Burn Wounds Intranasal Use

In an in vitro burn wound model that mimics penetration
into eschar, 97.8% of S. aureus were killed within 24 h
with mupirocin (60). Another in vitro study demon-
strated diffusion of mupirocin through 1.5 mm of eschar
within 2 h (61). When Rode et al used topical mupirocin
to treat 59 burn wounds infected with methicillin-resis-
tant S. aureus that had not responded to povidone–
iodine, chlorhexidine, or silver sulfadiazine, methicillin-
Nasal carriage of S. aureus can be linked to the transient
contamination of the carrier’s hand, which is the primary
mode of transmission (and subsequent infection) from
the carrier to a patient (63,64). In addition, patients with
S. aureus nasal carriage are susceptible to autoinfection.
The reliable bactericidal activity of mupirocin against
gram-positive organisms routinely implicated in superfi-
cial skin infections has led to its use in clinical settings to
218
modify or prevent disease. In 1996, paraffin-based mupi-
rocin calcium was formulated for intranasal use that
would not irritate the mucous membrane.
Intranasal application of mupirocin calcium is used to
eliminate S. aureus carriage among healthcare workers
and hospitalized patients during outbreaks of methicillin-
resistant S. aureus (65,66). A single course of therapy (a
twice-daily application for 5 days) has been found to
reduce S. aureus nasal carriage in healthcare workers for
up to a year (67). Intranasal administration of mupirocin
has also been used to prevent S. aureus infections in
hemodialysis patients, (68) a patient group at high risk
for colonization and serious staphylococcal infections
(69). The results from a large, controlled clinical trial
conducted at the University of Iowa Hospital and Clinics
investigating the efficacy of intranasal mupirocin use as
surgical prophylaxis are expected to be reported by the
end of this year.
ADVERSE EVENT PROFILE
Mupirocin calcium is exceptionally well tolerated. In
clinical trials of 339 patients, the most commonly re-
ported adverse events were headache (1.7%), rash
(1.1%), and nausea (1.1%). In another study of 82 pa-
tients, the most common adverse events were nausea
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