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Vol 1 January 2009 Clinical Pharmacist 13
By R A Seaton, DTM&H, FRCP(Edin)
S
kin and soft tissue infections (SSTIs) comprise an
important and diverse group of anatomically and
aetiologically distinct infections. In UK hospitals,
34% of patients receive treatment for SSTI. Of these,
47% receive intravenous (IV) therapy, accounting
for 16% of all IV antibiotic-treated patients.
1
Infections of
the skin and subcutaneous tissues account for around 176
admission per 100,000 of the UK population.
2
Since the anatomical site, severity, associated co-
morbidity and aetiology vary, the clinical team managing
patients in hospital is likely to include a variety of
healthcare professionals in both medical and surgical
specialties. This review focuses on important bacterial
SSTIs seen in UK hospital practice.
In terms of clinical features and classification, SSTIs
may be defined by their involvement of deep structures, by
associated risk factors and by their microbiology (see Box
1, p15).
Superficial SSTIs
For people who develop superficial SSTIs, the causative
organisms are usually Staphylococcus aureus and Streptococcus
pyogenes.
Impetigo is a superficial SSTI rarely associated with
systemic upset or extensive skin involvement and more
commonly seen in children and young adults. Discrete,
multiple lesions usually occur on the face or extremities
that are either vesicular-purulent bullous or papular in
appearance. Yellow or brown crusting is characteristic.
Occasionally, secondary cellulitis can occur.
Folliculitis, furuncles and carbuncles comprise a
range of superficial infections involving hair follicles.
Folliculitis consists of superficial epidermal inflammation
around the follicles; furuncles are small abscesses which
may coalesce to form larger carbuncles, usually on the
neck.
Cellulitis and erysipelas are pathologically distinct
dermal infections comprising the most common SSTIs
that require admission to hospital and IV antibiotic
therapy. Both are diffuse, spreading, superficial infections
without underlying suppurative foci in muscle or fascia
and without associated necrosis.
Characterised by heat, erythema, induration and
localised tenderness, there may also be an orange skin
appearance, due to superficial oedema surrounding hair
follicles which remain tethered to underlying dermis.
Blisters or bullae may also occur (Figure 1, p15).
Erysipelas involves the upper dermis and is raised
above surrounding skin with a well demarcated edge
There is a wide range of skin and soft tissue infections with a variety of risk factors and causes. This
article focuses on the diagnosis and treatment of some of these infections
Skin and soft tissue infection
d iagnosis and management
Staphylococcus aureus bacteria (coloured scanning electron micrograph)
Andrew Seaton is consultant in infectious diseases
and general medicine at the Brownlee Centre,
Gartnavel General Hospital, Glasgow.
E: andrew.seaton@ggc.scot.nhs.uk
Skin and soft tissue infections (SSTIs) encompass a broad range of
infections with a variety of risk factors and causes. Careful assessment of
risk factors, severity markers and co-morbidities will inform the most
appropriate therapy.
Key clinical decisions include route of administration of therapy,
switching from IV to oral therapy, adjunctive measures and suitability for
outpatient management. Outpatient parenteral therapy is a viable option
for ambulant patients with moderate SSTI requiring IV therapy and without
risk factors for severe disease or unstable co-morbidities.
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Vol 1 January 2009 Clinical Pharmacist 15
(Figure 2). Cellulitis involves deeper dermis and
subcutaneous fat, is not raised and is without a well
demarcated edge (Figure 3). Each may be accompanied by
a systemic inflammatory response and regional
lymphadenopathy is common. Infection occurs following
a minor skin breach, for example an insect bite (more
common in the summer months). It may also complicate
Tinea pedis or paronychia. Risk of infection is increased in
immunocompromised patients, following trauma or
surgery, in those with diabetes mellitus or lymphoedema,
and in the morbidly obese (Figure 4, p16).
Necrotising SSTIs
Necrotising infection of the skin and soft tissue is severe
and life-threatening, with a systemic inflammatory
response, involvement of deep tissues, including
underlying fascia or muscle, and associated tissue
destruction.
Necrotising infections can be distinguished from more
superficial infections by the presence of a combination of
the following clinical signs: severe, constant pain;
blistering and bruising; oedema beyond the margin of the
erythema; localised skin anaesthesia; gas in the tissues;
systemic inflammatory response and multi-organ failure;
and rapidly evolving and spreading infection.
Necrotising fasciitis involves the tissues deep to the
dermis and superficial to the muscle. Infection moves
along these planes, extending well beyond the superficial
signs of infection, and usually occurs as a direct
consequence of more superficial infection.
Underlying tissues often feel wooden and there may
be a dusky discoloration to the skin (Figures 5a and 5b,
p16).
Myositis involves muscle and two distinct groups are
recognised: anaerobic streptococcal myositis, usually
occurring following surgery or open trauma and involving
muscles and fascial planes; and pyomyositis, which is pus
within an individual muscle group, usually presenting
with localised pain, muscle spasm and fever.
Synergistic necrotising cellulitis is a necrotising soft
tissue infection involving muscle groups, in addition to
superficial skin and fascia (Figure 6, p17).
Fournier gangrene involves the perineum and genitalia,
usually in patients with underlying disease, particularly
diabetes mellitus. Onset is usually sudden but can be
insidious. An initial superficial focus of infection becomes
necrotic and spreads to deep tissues and along fascial
planes.
Clostridial myonecrosis (gas gangrene) is
characterised by severe localised pain, systemic
inflammatory response and rapidly evolving skin changes
within 24 hours of trauma. Affected areas become tense,
fluid-filled blisters develop and gas is visible on plain
radiographs.
Spontaneous gangrene can complicate malignancy and
neutropenia, is usually blood-borne from a colonic focus
and occurs in the absence of trauma.
Microbiology and associated risk factors
Irrespective of site or severity, SSTIs are predominantly
caused by aerobic gram-positive cocci, in particular the
beta-haemolytic streptococci (notably S pyogenes) and S
aureus.
3
Other micro-organisms are variably implicated
Figure 1: Skin blistering in cellulitis. Typically seen
in beta-haemolytic streptococcal infections
Figure 2: Facial erysipelas. Typical of
Streptococcus pyogenes infection
Figure 3: Facial cellulitis with periorbital oedema
Box 1: Microbial causes of SSTI
CLINICAL PRESENTATION CAUSATIVE ORGANISMS
Impetigo, folliculitis, furunculosis, Staphylococcus aureus and Streptococcus
carbuncles, cellulitis and erysipelas pyogenes
Necrotising infections S aureus, S pyogenes, clostridial species, gram-
negative organisms and polymicrobial species
Infections following human or S aureus, aerobic and anaerobic streptococci,
animal bites Fusobacterium and Pasteurella spp;
capnocytophaga (in animals)
Surgical site infections S aureus, beta-haemolytic streptococci; genital
tract or abdominal surgery consider gram-
negatives and anaerobes
Infections in immunocompromised S aureus, S pyogenes, gram-negatives including
patients Pseudomonas aeroginosa, mycobacteria and fungi
Infections in parenteral drug users S aureus, beta-haemolytic streptococci, and
clostridial species
SSTI due to water exposure Vibrio vulnificus, Aeromonas hydrophilia and
Mycobacterium marinum
Travel-related SSTI S aureus, S pyogenes, endemeic mycoses,
Mycobacterium ulcerans, Leishmania spp, and others
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16 Clinical Pharmacist January 2009 Vol 1
depending on the nature of the SSTI and whether it is
healthcare-associated or community-acquired.
Surgical site infection usually occurs more than 48
hours after an incision and is characterised by localised
wound-related erythema, heat, induration and purulent
discharge.
Involvement of deep structures should always be
considered and management depends on the surgical site.
In hospitals, S aureus dominates as a cause of surgical-site
infection
4
(Figure 7, p17), with variable rates of meticillin
resistance (see accompanying article, p23).
Animal or human bites can result in infection, and the
depth and site of the bite is critical. Hand injuries are
common so attention should be paid to potential tendon
involvement and the maintenance of function. Therapy is
often pre-emptive in view of the high risks of loss of
function. Infections are polymicrobial, reflecting oral
flora: S aureus, aerobic and anaerobic streptococci,
clostridial species, fusobacteria and gram-negative
bacteria. With animal bites Pasteurella spp and
capnocytophaga are also important.
Water exposure refers to water-related trauma (eg,
coral or rock laceration) or contamination with water of
an open wound or sore. Both fresh and salinated water
harbour micro-organisms and individuals are at potential
risk of SSTI following such exposure. Vibrio vulnificus and
Aeromonas hydrophilia are frequently responsible.
In hospitals some hydrophilic organisms such as
pseudomonas and stenotrophomonas can also cause
SSTIs, particularly in compromised, post-operative
patients. Mycobacterium marinum infection (or fish tank
granuloma) most frequently occurs following a laceration
incurred when cleaning tropical fish tanks. Systemic
infection is unusual.
Parenteral drug users are an at-risk group for SSTIs.
The full range of infections ranging from simple
injection-site abscesses to necrotising infections can be
seen in inner-city hospitals and clinics. Concomitant
blood-stream infection and venous thromboembolism is
not uncommon (Figure 8, p17).
Individuals are at risk through translocation of
commensal skin organisms into the blood stream directly,
by use of contaminated heroin (usually with heat-resistant
organisms), or via contamination during drug preparation.
Gram-positive organisms, particularly S aureus and beta-
haemolytic streptococci, are usually implicated.
Clostridial species, particularly C perfringens and C novyi,
can cause devastating, rapidly progressive infections
associated with marked leucocytosis and systemic
inflammatory response.
Immunocompromised patients may develop SSTIs,
with S aureus and S pyogenes as the predominant organisms
in this diverse patient group. Gram-negative organisms,
including Pseudomonas aeroginosa, should be considered in
the context of neutropenia and line-related SSTI.
Fungal infections (eg, with Fusarium, Aspergillus or
Sporothrix spp) are less frequently seen, but may occur in
Figure 4: Progressive cellulitis due to group B streptococcus, complicating
lymphoedema and morbid obesity
Figure 5a: Necrotising fasciitis due to Streptococcus
pyogenes showing blistering in lower leg
Figure 5b: Dusky skin discoloration extending over buttock
and flank indicating progressive infection
association with neutropenia, organ transplant or long-
term immunosuppressive therapy. Their presentation is
variable but may consist of papullar, erythematous or
purple eruptions with lymphatic spread or erythema and
skin ulceration. Fungal infections can occur either as a
primary complication or in the context of disseminated
infection with multi-organ involvement.
Mycobacterial infections are uncommon and can be
indistinguishable from fungal infections but should be
considered in the same population.
Travel-related or tropical skin infections are not
uncommon in migrants or people returning from abroad.
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Vol 1 January 2009 Clinical Pharmacist 17
In addition to the usual bacterial species, infection with a
variety of endemic mycoses, mycobacteria (eg, M
tuberculosis and M ulcerans) and parasites (eg, Leishmania
spp) are possible, depending on the source of exposure.
Investigation and management of SSTIs
Severity of SSTI can be determined by several clinical
factors: extent and intensity of inflammation; distribution
and depth of infection; presence of systemic inflammatory
response; and significant co-morbidities. These markers
will help clinicians decide a patients suitability for
treatment in the community or hospital and whether
parenteral or oral therapy is appropriate (Figure 9, p21).
Consideration of these factors will direct the
antimicrobial therapy.
Folliculitis and furuncles are usually treated by GPs
using topical antibiotic treatment, or short-course oral
therapy if the infection fails to respond. Imprudent and
prolonged topical therapy is not advised due to the risk of
promotion of bacterial resistance. More extensive SSTIs
such as localised and limited cellulitis with no systemic
inflammatory response or significant co-morbidities, and
with no compounding microbiological risk factors can
be safely managed with oral antibiotic therapy in the
community and without hospital admission.
If signs of localised inflammation persist or worsen
then parenteral therapy either as an outpatient or
inpatient is indicated. Patients with cellulitis or erysipelas,
with significant heat, erythema and induration, generally
require parenteral therapy. Deep-seated and necrotising
infections always require hospital admission for parenteral
therapy and surgical intervention. Patients with post-
operative wound infections, particularly following joint or
abdominal (or perineal) surgery, should also be admitted
for surgical assessment.
For all patients treated with parenteral therapy or
managed in the hospital environment, attempts should be
made to establish a microbiological diagnosis. In almost all
patients with cellulitis or erysipelas there is no exudate
and therapy is empiric. Swabs in these circumstances may
give misleading results, although evidence of meticillin-
resistant S aureus (MRSA) carriage does influence
empirical choice. Blood cultures are rarely positive.
Nevertheless, they are important prognostically and in
directing route and duration of therapy, and, therefore,
form part of the severity assessment.
Patients with a discharging wound should have a swab
performed. However, results should be interpreted with
some caution as they may reflect commensal flora. Ideal
specimens are obtained aseptically in theatre from the
inflamed tissues. In the case of severe SSTI, it is not
appropriate to delay antibiotics in order to obtain
microbiological specimens and, therefore, specimens are
usually obtained after starting parenteral therapy.
Other useful investigations include full blood count,
renal function and C reactive protein (CRP). The latter is
often normal in patients with cellulitis and erysipelas but
is raised in those with severe infections where there is a
systemic inflammatory response. CRP can also be useful
in the monitoring of more severe infections, particularly
when the microbial cause is uncertain. Plain radiographs
are useful to assess for subcutaneous gas and soft-tissue
oedema. Radiographs are less useful in assessing for acute
bony involvement. Computerised tomography and
ultrasound examination are used to assess for deep-tissue,
bone and joint involvement and for abscess formation. In
rapidly progressive necrotising infections, surgical
management may be both diagnostic and therapeutic
exploring and debriding fascial planes and muscle
compartments to determine the extent and severity of the
infection.
Antibiotic therapy
Antibiotic choices for SSTI vary between specialties and
institutions, reflecting differing patient populations,
anatomical site, resistance patterns, MRSA risk (see
accompanying article, p23) and local policy.
Figure 8: Staphylococcus aureus infection with deep venous
thrombosis in a groin-injecting drug user
IN THE CASE OF
SEVERE SSTI, IT IS
NOT APPROPRIATE
TO DELAY
ANTIBIOTICS IN
ORDER TO OBTAIN
MICROBIOLOGICAL
SPECIMENS
THE MEDIAN
DURATION OF IV
THERAPY IS THREE
TO FIVE DAYS AND IT
IS UNUSUAL FOR
PATIENTS TO
REQUIRE IV
ANTIBIOTICS FOR
MORE THAN 10 DAYS
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Antibiotic prophylaxis should be considered for patients
requiring repeated IV treatment or hospital admission.
Because streptococcal species are the most frequently
recurring organisms, twice-daily phenoxymethylpenicillin
prophylaxis could be considered. Other options include
doxycycline, co-trimoxazole and erythromycin. For patients
with recurrent, rapidly progressive, severe infections it is
the authors practice to give (with counselling) take-home
antibiotics for use at the earliest sign of infection.
ACKNOWLEDGEMENT The author would like to thank Kirsty
Lattka from medical illustration services at Gartnavel General
Hospital, Glasgow, for arranging the photographs published.
References
1 Seaton RA, Nathwani D, Burton P, et al. Point prevalence survey of
antibiotic use in Scottish hospitals utilising the Glasgow Antimicrobial
Audit Tool (GAAT). International Journal of Antimicrobial Agents
2007;29:6939.
2 ISD Scotland. Scottish inpatient, day case and outpatient statistics.
www.isdscotland.org/isd/4334.html (accessed 9 December 2008).
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4 Kirkland KB, Briggs JP, Trivette SL, et al. The impact of surgical site
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