SKIN AND SOFT TISSUE INFECTIONS
Skin and soft tissue
infections
ID Ramsay
€ ro
ME To €k
Abstract
Skin and soft tissue infections (SSTIs) range from common superficial
skin infections to rare but life-threatening infections such as necro-
tizing fasciitis. They affect all ages. Predisposing factors include
trauma, pre-existing dermatoses, diabetes mellitus and immunosup-
pression. SSTIs are often caused by organisms that colonize the
skin, such as Staphylococcus aureus or group A streptococci,
because of a breach in the skin’s integrity. Community-acquired
meticillin-resistant S. aureus is increasingly recognized as a cause of
SSTI. Treatment is usually with topical or systemic antimicrobials,
directed against the suspected organism. Outpatient intravenous anti-
biotics are increasingly used, and new antimicrobials are emerging for
use in these infections. Urgent surgical debridement is sometimes
required.
Keywords Cellulitis; ecthyma; erysipelas; folliculitis; gas gangrene;
group A streptococci; impetigo; MRCP; necrotizing fasciitis; skin and
soft tissue infection; Staphylococcus aureus
Introduction
Skin and soft tissue infections (SSTIs) make up a large proportion
of infectious disease presentations to primary and secondary
care. Infectious Diseases Society of America guidance1 suggests
classification based on three clinical criteria:
 skin extension (uncomplicated or complicated)
 rate of progression (acute or chronic)
 tissue necrosis (necrotizing or non-necrotizing).
The US Food and Drug Administration (FDA) has introduced
the term ‘acute bacterial skin and soft tissue infection’ to cover
lesions >75 cm2. Most SSTIs are caused by Gram-positive or-
ganisms, particularly Staphylococcus aureus and b-haemolytic
group A streptococci. However, Gram-negative or anaerobic
bacteria, viruses, fungi and parasites can be involved.
Host factors
SSTIs can affect any age group, with elderly individuals being at
higher risk of severe disease. Conditions predisposing to SSTIs
include trauma, pre-existing skin conditions, diabetes mellitus,
ID Ramsay MA BM BCh MRCP is a Specialist Registrar in Infectious
Diseases and Microbiology, Addenbrooke’s Hospital, Cambridge,
UK. Competing interests: none declared.
€ ro
€ k MA PhD FRCP FRCPath is an Honorary Consultant in
ME To
Infectious Diseases and Microbiology, Department of Medicine,
Addenbrooke’s Hospital, Cambridge, UK. Competing interests: none
declared.
MEDICINE 45:11
Key points
C The incidence of severe infections, such as necrotizing fascii-
tis, appears to be increasing
C Outpatient parenteral antibiotic treatment services are
increasingly providing a route for avoiding admission with skin
and soft tissue infections (SSTIs)
C New antimicrobials are emerging for use in SSTI
C Antibiotic resistance is an increasing concern in both Gram-
positive, particularly community-acquired meticillin-resistant
Staphylococcus aureus, and Gram-negative organisms
alcoholism, intravenous drug use, peripheral arterial or venous
disease, malignancy and immunosuppression. SSTIs can be mild
and self-limiting or severe and progressive, leading to tissue
necrosis. Clues to potentially severe deep soft tissue infection
include pain disproportionate to the physical findings, violaceous
bullae, cutaneous haemorrhage, skin sloughing, skin anaes-
thesia, rapid progression and gas in the tissue.
A detailed history is essential to establish a specific diagnosis
and should include:
 onset, duration and progression of symptoms
 appearance and anatomical distribution of the lesion
 history of trauma or surgery
 contact with insects or other animals
 infectious contacts
 recent foreign travel
 pre-existing medical conditions
 previous antibiotic therapy and allergies.
Systemically unwell patients should be admitted to hospital,
with blood sampling for full blood count, biochemical profile,
inflammatory markers and blood cultures. If the diagnosis of
SSTI cannot be made on clinical grounds, investigations such as
needle aspiration, punch biopsy or surgical debridement may be
necessary.
Antibiotic therapy and antimicrobial resistance
Empirical antimicrobial therapy should be directed towards the
likely organism(s) and subsequently tailored in the light of
microbiological data.2 Worldwide, antimicrobial resistance is of
increasing concern, but the prevalence of resistant organisms
varies widely, and a knowledge of local epidemiology is vital to
inform optimal treatment.
Community-acquired meticillin-resistant S. aureus (CA-
MRSA) is a common cause of SSTI in the USA, and is variably
seen across Europe, with a relatively low prevalence in the UK.
Vancomycin-intermediate and vancomycin-resistant S. aureus
have been sporadically described, particularly in the USA.
Multidrug-resistant Gram-negative organisms are increasingly
prevalent, particularly in hospital-acquired infections, for
example surgical site infections (SSIs).
Several new antibiotic agents have emerged.3 These include
second-generation lipoglycopeptide antibiotics, for example
699 Ó 2017 Published by Elsevier Ltd.
 SKIN AND SOFT TISSUE INFECTIONS
dalbavancin, which has broad Gram-positive cover including
MRSA and, in vitro, has activity against organisms with reduced
susceptibility to vancomycin. Dalbavancin is amenable for
outpatient settings as it is dosed once weekly. Tedizolid is a
second-generation oxazolidinone with enhanced activity against
staphylococci and enterococci compared with linezolid. The new
topical agent retapamulin has activity against both staphylococci
(including MRSA) and streptococci, and has been approved by
the FDA for treatment of impetigo.
In patients who are well enough not to be in hospital with
SSTIs but require intravenous antibiotics, outpatient parenteral
antibiotic treatment4 services are being used to facilitate earlier
discharge or avoid hospital admission. Antibiotics are adminis-
tered in an outpatient setting, in the patient’s own home or, in
some cases, by the patients themselves, after appropriate
training.
Impetigo
Impetigo is a highly contagious superficial pyogenic infection of
the epidermis, typically affecting young children. It is commonly
caused by S. aureus or group A streptococci. Two forms are
recognized: bullous and non-bullous. Non-bullous impetigo is
characterized by coalescing intraepidermal vesicles, often on the
face or hands, which rupture to form a golden crust. In bullous
impetigo, larger bullae form and rupture, leaving a brown, scaly
appearance. Constitutional symptoms are usually absent. Pa-
tients often report a history of minor skin trauma, insect bites or
pre-existing dermatoses.
Impetigo is treated by removing the crusts and applying
topical antibiotics, such as mupirocin. Widespread infection re-
sponds better to oral or intravenous antibiotics (e.g. fluclox-
acillin, clindamycin). It can cause outbreaks in households,
institutions and sports teams. Affected children should be
excluded from school until the lesions have crusted and healed,
or for 48 hours after starting antibiotic treatment.
Ecthyma
Ecthyma is a form of impetigo that penetrates deeper into the
dermis and can scar. It starts as a vesicle and progresses to form a
punched-out ulcer surrounded by a violaceous border (Figure 1).
Regional lymphadenopathy can be present. Ecthyma often occurs
on the legs and is associated with minor trauma, insect bites,
eczema, pediculosis, diabetes mellitus and immunodeficiency.
Most cases are caused by group A streptococci. A similar lesion
called ecthyma gangrenosum is sometimes seen in immunocom-
promised patients and is usually associated with Pseudomonas
aeruginosa bacteraemia, but has been reported rarely with other
organisms (e.g. MRSA, Stenotrophomonas maltophilia).
Mild cases can be treated with topical mupirocin, and more
severe cases with oral penicillin or clindamycin. Debridement of
the crusts may be required. Ecthyma gangrenosum should be
treated with appropriate parenteral antibiotics, depending on the
causative organism.
Folliculitis
Folliculitis is an inflammation of the hair follicles characterized
by clusters of small, erythematous papules or pustules. Any hair-
MEDICINE 45:11
bearing site can be affected, but the sites most often involved are
the face, scalp, thighs, axillas and inguinal area. Predisposing
factors include frequent shaving, pre-existing skin conditions,
occlusive clothing/dressings, exposure to hot humid tempera-
tures, diabetes mellitus, obesity, long-term antibiotic or cortico-
steroid use, and immunosuppression.
The most common form of folliculitis is sycosis barbae (bar-
ber’s itch), which is caused by S. aureus. Tinea barbae is a fungal
folliculitis, caused by dermatophytes, that resembles its bacterial
counterpart. Other infectious causes include Enterobacteriaceae
(often associated with prolonged antibiotic therapy), P. aerugi-
nosa (associated with hot tubs and wet suits),5 Malassezia furfur,
herpes simplex virus, varicella-zoster virus and Demodex mites.
Non-infectious causes include eosinophilic folliculitis seen in
advanced HIV and malignancy and a self-limiting papulo-pustu-
lar follicular eruption that occurs after treatment with epidermal
growth factor receptor inhibitors.
Antibacterial soaps and good hygiene may be all that is required
for recurrent uncomplicated superficial folliculitis. Systemic anti-
biotics can be required in more severe infection (e.g. oral fluclox-
acillin for staphylococcal folliculitis; treatment may need to cover
MRSA if the patient is colonized). P. folliculitis is usually self-
limiting, but oral ciprofloxacin can be given if lesions are persis-
tent or the patient is immunocompromised. Malassezia folliculitis
usually responds to topical antifungals (e.g. ketoconazole cream).
Herpetic folliculitis responds to oral antivirals (e.g. valaciclovir).
Eosinophilic folliculitis may respond to the introduction of antire-
troviral therapy in HIV patients or to metronidazole, ultraviolet B
phototherapy or itraconazole.
Furuncles and carbuncles
Furuncles are subcutaneous boils or abscesses. The usual cause
is S. aureus. If several furuncles coalesce, a ‘carbuncle’ is formed
(Figure 2). Carbuncles are characterized by inflamed skin with
pus draining from several hair follicles and are commonly found
on areas of thickened skin such as the nape of the neck, the back
and the thighs. Fever and malaise are common. Rarely, recurrent
furuncles become a problem. Diabetes mellitus and rare causes
of immunodeficiency, such as hyperimmunoglobulin E syn-
drome (Job’s syndrome) and chronic granulomatous disease,
should be considered.
Small furuncles can burst and heal spontaneously; larger ones
can require incision and drainage. Carbuncles usually require
incision and drainage along with systemic antimicrobials (e.g.
oral or intravenous flucloxacillin). Patients with recurrent fu-
runcles who do not have underlying immunodeficiency should
be considered for staphylococcal decolonization using mupirocin
2% nasal ointment and chlorhexidine gluconate 4% shampoo/
body wash.
PantoneValentine leucocidin (PVL)
In individuals with recurrent abscesses or furuncles, or where
there is a cluster of cases within a household, consideration
should be given to detection of PVL-producing S. aureus. The
clinical significance of PVL is debated, but current guidelines
recommend using two or three agents, for example oral rifam-
picin, linezolid and intravenous clindamycin, for severe SSTIs
caused by PVL-positive strains.
700 Ó 2017 Published by Elsevier Ltd.
 SKIN AND SOFT TISSUE INFECTIONS
Figure 1 Ecthyma in an immunocompromised patient.
Figure 2 Carbuncle on the dorsum of the foot.
Erysipelas
Erysipelas is a superficial bacterial infection of the dermis,
involving the cutaneous lymphatics. It is characterized by abrupt
onset of a painful, erythematous, spreading rash with well-
demarcated edges (Figure 3). There are often systemic features
(e.g. fever, malaise, chills).
Most erysipelas infections occur on the lower extremities,
with non-group A streptococci being the most common cause.
Facial erysipelas is more commonly caused by group A strepto-
cocci. Atypical forms, caused by Streptococcus pneumoniae,
Klebsiella pneumoniae, Haemophilus influenzae, Yersinia enter-
ocolitica, and Moraxella spp., have been described. Predisposing
factors include skin conditions (e.g. eczema, dermatophyte in-
fections), venous stasis, paraparesis, diabetes mellitus, nephrotic
MEDICINE 45:11
syndrome, alcohol abuse and immunodeficiency. Erysipelas
tends to occur in areas of lymphatic obstruction and, because it
also causes lymphatic damage, to recur.
Treatment is with intravenous benzylpenicillin; clindamycin
can be used in penicillin-allergic patients. Staphylococci are not
usually implicated in erysipelas, so anti-staphylococcal therapy
(flucloxacillin, vancomycin) is not usually considered necessary
unless there are features suggestive of staphylococcal infection
(e.g. bullous erysipelas).
Cellulitis
Cellulitis is rapidly spreading inflammation of the deep dermis
and subcutaneous fat (Figure 4),5 commonly caused by group A
streptococci or S. aureus. Soft tissue infection caused by CA-
MRSA is becoming increasingly common and usually results in
skin abscesses. Rarer causes of cellulitis include groups B, C and
G streptococci (particularly in lymphatic obstruction), Strep.
pneumoniae, Enterobacteriaceae, Pseudomonas spp., Pasteurella
multocida (associated with animal contact), Aeromonas hydro-
phila and Vibrio vulnificus (associated with freshwater and salt
water contact, respectively) Brucella spp., Legionella spp. and
Neisseria meningitidis.
There is often a clear causative injury or breach of the skin
(e.g. eczema, tinea infections). Patients with diabetes mellitus
are at increased risk of complications, as are those with leg ul-
cers, lymphoedema, varicose veins or peripheral vascular dis-
ease. Cellulitis usually affects the legs and is almost always
unilateral. It presents as a red, hot, swollen, tender area that is
not as well demarcated or elevated as in erysipelas. Thrombo-
phlebitis, lymphangitis, regional lymphadenopathy and fever are
common. Local abscesses can develop, and the overlying skin
can become necrotic.
The diagnosis of cellulitis is almost entirely clinical; skin
swabs are unhelpful and blood cultures, skin biopsies and tissue
aspirates are seldom positive. Imaging cannot diagnose cellulitis
but can be useful in identifying abscesses or underlying
osteomyelitis.
Patients with mild cellulitis and no systemic symptoms can be
treated with oral flucloxacillin; clindamycin is an alternative in
penicillin-allergic patients. In patients with more severe infection
or facial or peri-orbital cellulitis, treatment with intravenous
antibiotics is usually warranted. If the patient has diabetes mel-
litus or leg ulcers, Gram-negative organisms and anaerobes are
more likely, so intravenous co-amoxiclav can be used instead. In
patients who are MRSA-colonized, a glycopeptide should be
considered; linezolid and daptomycin are suitable although more
expensive alternatives. There is little evidence that MRSA needs
to be covered if the cellulitis is community acquired, even in the
USA, unless an abscess is present. Analgesia, elevation of the
limb and subcutaneous heparin are useful adjunctive measures.
A surgical opinion should be sought if there is circumferential
cellulitis or necrotic skin.
Prophylactic antibiotics (usually penicillin) remain contro-
versial; however, they can be considered in patients with three or
four episodes per year. Important non-pharmacological measures
include foot care, including treatment of tinea pedis, lymphoe-
dema management and wound care for ulceration.
701 Ó 2017 Published by Elsevier Ltd.
 SKIN AND SOFT TISSUE INFECTIONS
Figure 3 Erysipelas caused by group A Streptococcus.
Figure 4 Cellulitis of the lower limb.
Bursitis
Bursitis is an inflammation of a bursa that can be caused by re-
petitive use, trauma, gout, rheumatoid arthritis or infection
(septic bursitis). Septic bursitis occurs from direct inoculation of
microorganisms through the skin or spread from adjacent cellu-
litis; it rarely occurs as a result of haematogenous spread. The
predominant cause is S. aureus, followed by streptococci and,
rarely, mycobacteria or fungi. Predisposing factors include
trauma, skin diseases, diabetes mellitus, alcoholism and corti-
costeroid therapy. The diagnosis is clinical and based on fever
plus swelling, erythema and tenderness over the affected bursa.
MEDICINE 45:11
The most common sites are the olecranon and pre-patellar
bursae.
Treatment is with intravenous flucloxacillin, elevation of the
limb and, if necessary, aspiration of pus from the affected bursa.
In penicillin-allergic or MRSA-colonized patients, a glycopeptide
is appropriate. Surgical drainage is rarely required.
Surgical site infections
Despite the use of antibiotic prophylaxis, SSIs develop in at least
5% of patients undergoing a surgical procedure, causing signif-
icant morbidity. Factors known to contribute to the risk include:
 host (age, obesity, nutritional status, immune status,
perioperative variables such as blood glucose, body tem-
perature and oxygenation)
 surgical (type of procedure, surgical technique, use of
foreign material)
 microbial (concentration and virulence of organisms,
resistance to antimicrobial prophylaxis).
SSIs are defined by the US Centers for Disease Control and
Prevention as occurring at or near the surgical site within 30 days
of operation, or within 1 year if prosthetic material is present.
They can be divided into three types: superficial incisional
(involving skin or subcutaneous tissues), deep incisional
(involving fascia or muscle) and organ/space infection.
The infecting organisms are usually the patient’s endogenous
flora. S. aureus (including MRSA), coagulase-negative staphylo-
cocci and enterococci are the most common organisms. SSIs
caused by enterobacteriaceae are becoming increasingly preva-
lent, particularly after gastrointestinal surgery. Anaerobes and
Candida spp. can also be implicated. Polymicrobial infections are
more likely in surgery involving a viscus. Early SSIs (in the first
48 hours after surgery) are often caused by Clostridia spp. or
streptococci.
Most superficial incisional SSIs present within days after
surgery, although rarely in the first 48 hours, with fever and local
pain, swelling, erythema, tenderness, a purulent discharge or
wound dehiscence. These symptoms and signs can be delayed in
individuals who are morbidly obese or have multilayer wounds.
Ultrasonography or computed tomography (CT) can be required
to identify deep incisional infections in patients with clinical
evidence of systemic infection but no local signs.
Initial management of SSI involves incision and drainage,
debridement of necrotic tissue, removal of foreign material and
local wound care. Superficial swabs have limited use and can
reflect colonizing flora only; therefore deep pus or tissue samples
should be sent for microbiological examination.
Most superficial SSIs do not require any further therapy. The
need for antimicrobial therapy should be guided by clinical
findings (e.g. spreading cellulitis, systemic symptoms). The
initial choice of antimicrobial agent should be directed towards
the most likely organisms, according to the type of operation
performed. Treatment can then be tailored in light of microbio-
logical findings. Most incisional SSIs are left open and allowed to
heal by secondary intention.
Bite infections
Bite wounds are usually caused by domestic pets, such as dogs
(most common), cats, rabbits, reptiles and, occasionally,
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 SKIN AND SOFT TISSUE INFECTIONS
monkeys. It is estimated that 3e18% of dog-bite wounds and 28
e80% of cat-bite wounds become infected, most frequently on
the hand. The organisms implicated are usually the oral flora of
the biting animal. P. multocida and Pasteurella canis are com-
mon, but a wide spectrum of organisms has been isolated from
bite wounds (e.g. staphylococci, streptococci, enterococci, Neis-
seria spp., Haemophilus spp., Eikenella spp., Enterobacteriaceae,
Capnocytophaga canimorsus, anaerobes). Bites from marine an-
imals can lead to infection with Vibrio spp. Human bites are the
third most common after dogs and cats; around 10e15% become
infected, usually with oral flora.
Treatment involves wound irrigation, debridement, eleva-
tion of the affected part and, if appropriate, tetanus and rabies
immunization. Primary wound closure is usually undertaken
only for facial wounds. Human and animal bites should be
managed with prophylactic antibiotics (e.g. co-amoxiclav), but
the risk of blood-borne viral infections should be considered.
Recipients of monkey bites should be given prophylactic vala-
ciclovir or aciclovir because of the risk of simian herpes-
virus B.
Infections in injection drug-users (IDUs)
SSTIs are common in (IDUs) as they often introduce bacteria into
normally sterile sites. Because of delays in accessing healthcare,
this patient group often presents late and can be poorly adherent
to treatment. The most common organism is S. aureus (including
MRSA), but oral flora (e.g. a-haemolytic streptococci, Neisseria
spp., Haemophilus spp., Eikenella corrodens) can be found in
those who lick their needles. Other causes include Strep. pneu-
moniae, Gram-negative bacteria, Clostridia spp. and fungi. In
2000, a high-fatality outbreak of SSTI occurred in the UK from
heroin contaminated with Clostridium novyi. In 2009e2010,
>100 cases of cutaneous anthrax, related to contaminated her-
oin, were reported in IDUs in Scotland.
Cellulitis or abscesses can occur at the site of injection and
cause considerable soft tissue damage. Injections can also cause
intramuscular abscesses (pyomyositis) or necrotizing fasciitis.
Complications include bacteraemia, septic arthritis, osteomyelitis
and infectious endocarditis.
Treatment is with intravenous antibiotics and, usually, sur-
gical drainage or debridement. These patients should be
routinely screened for blood-borne virus infections.
Necrotizing fasciitis
Necrotizing fasciitis is an uncommon, severe infection that re-
sults in destruction of subcutaneous tissue and fascia. Predis-
posing factors include diabetes mellitus, alcoholism and injecting
drug use. There are two clinical types:
 Type I necrotizing fasciitis is a mixed infection caused by
streptococci, Enterobacteriaceae, Bacteroides spp. and
Peptostreptococcus spp. It occurs in middle-aged and
elderly individuals, most commonly after surgical proced-
ures, and in patients with diabetes or peripheral vascular
disease. Infection usually starts in the feet and progresses
rapidly along the fascia into the leg. Clinical presentation is
with cellulitis and systemic signs of severe infection. Type I
necrotizing fasciitis can also develop in the head and neck
MEDICINE 45:11
following a breach of the mucous membranes by surgery
or instrumentation.
 Type II necrotizing fasciitis is typically monomicrobial,
and caused by group A streptococci. It can occur in any age
group. The cardinal symptom is excruciating pain with
minimal cutaneous findings. Initially, there may also be
fever, malaise, myalgia and diarrhoea. After 24e48 hours,
erythema can develop, the skin can darken to a reddish-
purple colour, and bullae can develop. Patients are sys-
temically unwell and can develop streptococcal toxic shock
syndrome. CA-MRSA is increasingly recognized as a cause
of necrotizing fasciitis in the USA, particularly in IDUs.
Other causative agents include V. vulnificus (seawater
exposure) and Aeromonas spp (freshwater exposure).
Necrotizing fasciitis is a surgical emergency and requires
prompt surgical debridement. Intravenous broad-spectrum anti-
biotics (e.g. piperacillin/tazobactam clindamycin) should be
given until microbiological data are available. Clindamycin has a
theoretical advantage in that it can interrupt toxin production
and reduce systemic toxic effects.
Patients often require intensive care. Imaging studies can be
helpful for monitoring progress and assessing the need for
further surgery, but should not delay initial debridement.
Adjunctive therapies such as intravenous immunoglobulin and
hyperbaric oxygen have been advocated but lack convincing
evidence.
Fournier’s gangrene
Fournier’s gangrene is a form of necrotizing fasciitis that affects
the genital, perineal and perianal regions. Most cases occur in
patients aged 30e60 years, and there is a 10:1 male-to-female
ratio. Risk factors include advanced age, diabetes mellitus,
alcohol abuse, colorectal disease/surgery, malignancy, malnu-
trition and immunosuppression.
Fournier’s gangrene is a polymicrobial infection caused by a
mixture of aerobic (e.g. Enterobacteriaceae, streptococci,
enterococci, Pseudomonas spp.), and anaerobic (e.g. Bacteroides
spp., Clostridium spp.) bacteria. The incidence of MRSA in-
fections appears to be increasing. Rarely, Candida albicans has
been implicated.
Symptoms usually begin with the insidious onset of pruritus
and discomfort in the external genitalia. This is followed by
swelling and erythema of the genital/perineal region associated
with severe pain and systemic symptoms.
Fournier’s gangrene is a surgical emergency that requires
prompt surgical debridement and broad-spectrum intravenous
antibiotic therapy (e.g. co-amoxiclav, metronidazole, genta-
micin). A glycopeptide or other suitable antibiotic should be
included if the patient is known or likely to be colonized with
MRSA. Consider a tetanus booster if immunization status is un-
known e cases of fatal tetanus have been associated with
Fournier’s gangrene.
Gas gangrene
Gas gangrene and clostridial myonecrosis are terms used to
describe a rare infection caused by toxin-producing clostridia.
Clostridium perfringens is the main cause of trauma-related gas
703 Ó 2017 Published by Elsevier Ltd.
 SKIN AND SOFT TISSUE INFECTIONS
gangrene. In spontaneous cases, Clostridium septicum is more
commonly implicated. Typically, wounds are contaminated with
clostridia, which multiply in anaerobic conditions and produce
exotoxins that cause tissue damage. Spontaneous cases result
from haematogenous spread of clostridia from the gastrointes-
tinal tract, often in the setting of bowel cancer.
Clinical features include the sudden onset of pain 6e8 hours
after injury. This is followed by increasing pain and tenderness,
darkening of the skin to a purplish-red colour, formation of bullae,
crepitus, fever, shock, haemolytic anaemia, liver and renal failure.
Gas in the soft tissues can be confirmed by plain radiography, CT
or magnetic resonance imaging. The diagnosis is confirmed by
demonstrating Gram-positive rods in the affected tissue.
Management is with aggressive surgical debridement com-
bined with intravenous antibiotics (e.g. piperacillin/tazobactam,
clindamycin). Intensive care support and multiple debridements
may be required. The use of adjuvant therapies (e.g. hyperbaric
oxygen) is controversial.
Uncommon infections
Bacterial
Anthrax: is caused by Bacillus anthracis and most commonly
affects the skin, resulting in a ‘malignant pustule’. Infections
occur in abattoir workers and result from inoculation of bacterial
spores into skin abrasions caused by handling the hides of
infected animals. Recent outbreaks have also been seen in IDUs.
After a few days, a papule forms at the site of infection; this
develops into a vesicle and ulcerates to form a necrotic centre or
eschar. Local oedema, painful regional lymphadenopathy and
systemic features are often present. The diagnosis is confirmed
by demonstrating Gram-positive bacilli in the ulcer fluid or tis-
sues and by culturing the organism. Penicillin therapy is
adequate, although quinolones and tetracyclines are also effec-
tive. In some settings, surgical debridement is appropriate.
Cat-scratch disease: is usually caused by Bartonella henselae.
Clinical features include regional lymphadenopathy, fever and a
red papule at the inoculation site. Atypical presentations include
Parinaud’s ocular glandular syndrome, maculopapular rash, er-
ythema multiforme, erythema nodosum and leukocytoclastic
vasculitis. The diagnosis is confirmed serologically and by po-
lymerase chain reaction analysis. Treatment is with azithromycin
or doxycycline.
Erysipeloid: is a rare condition is caused by Erysipelothrix rhu-
siopathiae. It is usually acquired from infected animals and af-
fects veterinary surgeons, farmers and butchers. The organism is
inoculated into the skin and causes characteristic dark, purplish
lesions with swelling of the digits. Rarely, septicaemia occurs and
can be complicated by endocarditis. The condition is treated with
penicillin.
Erythema chronicum migrans: is the cutaneous manifestation
of Lyme disease, which is caused by Borrelia burgdorferi. It is
acquired by inoculation from a tick bite. A red, circular lesion
develops and spreads from the site of the bite. Other features
include fever, malaise and arthralgia. Diagnosis is serological.
Treatment is with doxycycline.
MEDICINE 45:11
Tick typhus: is of several types. African tick typhus, caused by
Rickettsia conorii and Rickettsia africae, is commonly seen in
patients returning from safari in southern Africa. Endemic typhus
is caused by Rickettsia typhi and transmitted by the rat flea.
Epidemic typhus is caused by Rickettsia prowazekii and trans-
mitted by the human louse. Clinical features include fever,
headache, malaise, myalgia, lymphadenopathy and splenomeg-
aly. There may be an eschar at the site of inoculation and a
maculopapular rash, although some spotted fevers produce few
if any spots. Diagnosis is confirmed serologically. Treatment is
with doxycycline.
Mycobacterial
Leprosy: is caused by infection with Mycobacterium leprae. The
spectrum of clinical disease ranges from tuberculoid to lepro-
matous leprosy. In tuberculoid leprosy, anaesthetic macules or
plaques, pigmentary change and thickened peripheral nerves
develop. In lepromatous leprosy, macules, papules, nodules and
ulceration occur, resulting in collapse of the nasal bones and
coarsening of the facial tissues, producing the characteristic
‘leonine’ facies. The diagnosis is confirmed by biopsy and split-
skin smears. Treatment is with dapsone, clofazimine and
rifampicin.
Lupus vulgaris: is a cutaneous infection caused by Mycobacte-
rium tuberculosis. It usually affects the face and neck, and ap-
pears as firm, translucent, yellowish-brown ‘apple jelly’ nodules.
Untreated lesions spread, leading to disfiguring scarring and
contractures. Diagnosis is confirmed by biopsy, which shows
tuberculoid granulomas in the mid-dermis. Treatment is with
antituberculous chemotherapy.
Non-tuberculous mycobacteria: can cause soft tissue infections.
Mycobacterium marinum is associated with granulomas, partic-
ularly on the hands, in people who handle certain tropical fish.
Mycobacterium chelonae infections have been associated with
tattoos and with nosocomial infections related to intravenous
devices.
Fungal
Eumycetoma (Madura foot): is a chronic subcutaneous fungal
infection typically of the foot characterized by lesions, sinus
tracts and macroscopic grains. It is caused by a variety of molds
and is typically seen in labourers and farmers in subtropical and
tropical areas. Filamentous bacteria can cause a similar disease
(actinomycetoma). Treatment is with prolonged antifungal
therapy. Surgical intervention is sometimes required.
Sporotrichosis: is a subacute fungal infection caused by Sporo-
thrix schenkii that is related to soil inoculation into the skin. It is
typically seen in gardeners and is treated with antifungals.
Parasitic
Cutaneous larva migrans: this occurs in returning travellers,
particularly those who have visited tropical beaches. It is caused
by infection with animal hookworm larvae such as Ancylostoma
braziliense, Ancylostoma caninum and Uncinaria stenocephala,
and presents as an itchy cluster of lesions or a sinuous track on
exposed areas. Treatment is with albendazole.
704 Ó 2017 Published by Elsevier Ltd.
 SKIN AND SOFT TISSUE INFECTIONS

Leishmaniasis: cutaneous leishmaniasis is acquired from a
sandfly bite. ‘Old world’ leishmaniasis, caused by Leishmania
major, Leishmania tropica and Leishmania aethiopica, is
endemic in Africa, Asia, India, the Middle East and the Medi-
terranean. ‘New world’ leishmaniasis, caused by Leishmania
brasiliensis, Leishmania mexicana and Leishmania panamensis,
is endemic in Latin America. Clinical presentation is with a
crusted sore on the face, hand or leg 6e8 weeks after returning
from an endemic area. Diagnosis is clinical and confirmed his-
tologically. Lesions often resolve spontaneously, but some
require cryotherapy or treatment with amphotericin or pentam-
idine. Patients with L. brasiliensis should be given systemic
treatment to avoid the possibility of espundia (mucocutaneous
disease).
Viral
Herpes zoster (shingles): is caused by reactivation of
varicella-zoster virus infection and characterized by a painful,
vesicular eruption in a dermatomal distribution. Risk factors
include increasing age, immunosuppression and autoimmune
disease. Complications include post-herpetic neuralgia, sec-
ondary bacterial skin infection, herpes zoster ophthalmicus,
Ramsay Hunt syndrome (herpes zoster oticus) and meningitis.
Treatment is with oral valaciclovir (for uncomplicated zoster)
or intravenous aciclovir for immunocompromised patients or
those with ocular involvement. A vaccine to prevent shingles
is available.
Herpetic whitlow: (herpes simplex infection of the skin)
occurs as a complication of oral or genital herpes simplex
virus infection. It is characterized by a painful, erythematous
vesicular or pustular skin lesion. There may be associated
fever and lymphadenopathy. The diagnosis is based on
exposure history. Herpetic whitlow usually resolves sponta-
neously in 2e3 weeks, but some recommend treatment with
oral aciclovir.
Molluscum contagiosum: is a benign condition caused by a pox
virus. It usually affects children or immunocompromised in-
dividuals. The lesions are most commonly seen on the face and
trunk, and are papular with a central punctum.
Orf: is an infectious cutaneous lesion caused by a pox virus ac-
quired from sheep. It commonly affects farmers (particularly
those who bottle-feed lambs) and veterinary surgeons. A red
papule develops, commonly on the sides of the fingers, and
grows rapidly, often becoming vesicular, before developing a
central necrotic area. Lymphangitis, regional lymphadenopathy
and fever are common. Recovery is spontaneous.
Ectoparasites
Scabies: is a pruritic skin lesion caused by infestation with
Sarcoptes scabiei. It is associated with poor socioeconomic
conditions and overcrowding. The female mite lays her eggs in
a burrow in the stratum corneum, generating a local hyper-
sensitivity reaction; when the eggs hatch, the cycle is repeated.
Diagnosis is confirmed by extracting the mite from a burrow.
Treatment comprises topical acaricides (e.g. permethrin) and
washing of all clothing and linen. All members of the house-
hold should be treated at the same time. So-called Norwegian
scabies is a severe form with extensive crusting, most
commonly seen in HIV infection and best treated with
ivermectin. A
KEY REFERENCES
1 Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for
the diagnosis and management of skin and soft tissue infections:
2014 update by the infectious diseases society of America. Clin
Infect Dis 2014; 59: 147e59.
2 Esposito S, Noviello S, Leone S. Epidemiology and microbiology of
skin and soft tissue infections. Curr Opin Infect Dis 2016; 29:
109e15.
3 McClain SL, Bohan JG, Stevens DL. Advances in the medical
management of skin and soft tissue infections. Br Med J 2016; 355:
i6004.
4 Chapman ALN. Outpatient parenteral antimicrobial therapy. Br Med
J 2013; 346: f1585.
5 Raff AB, Kroshinsky D. Cellulitis: a review. J Am Med Assoc 2016;
316: 325e37.

TEST YOURSELF
To test your knowledge based on the article you have just read, please complete the questions below. The answers can be found at the
end of the issue or online here.

Question 1 Which of the following organisms would be of particular

concern in this patient?
A 25-year-old man presented with a 2-day history of a swollen
A. Capnocytophaga canimorsus
erythematous hand after being bitten by his dog. He had a past
B. Pasteurella canis
medical history of splenectomy following traumatic injury. He
C. Rabies virus
had no recent travel outside the UK. On clinical examination,
D. Staphylococcus aureus
there was a 5 cm, erythematous, swollen area on the back of the
E. Streptococcus pyogenes
right hand.

MEDICINE 45:11 705 Ó 2017 Published by Elsevier Ltd.

 SKIN AND SOFT TISSUE INFECTIONS
Question 2
A 30-year-old woman presented with a 3-day history of pain and
swelling on the left leg. She was an active intravenous drug user
with a history of meticillin-resistant S. aureus colonization. On
clinical examination, her temperature was 37.0 C, heart rate 88
beats/minute and blood pressure 115/68 mmHg. There was
extensive cellulitis of the left leg.
Which of the following is the most appropriate initial anti-
biotic management?
A. Give intravenous flucloxacillin as an inpatient
B. Give intravenous vancomycin as an inpatient
C. Give intravenous teicoplanin via an outpatient parenteral
antibiotic treatment (OPAT) service
D. Give intravenous ceftriaxone via an OPAT service
E. Give oral doxycycline as an outpatient
MEDICINE 45:11
Question 3
A 55-year-old man became febrile and his laparotomy wound
dehisced 4 days after an emergency laparotomy for bowel
perforation. He had no known allergies. On clinical examination,
his temperature was 38.4 C, heart rate 120 beats/minute, blood
pressure 85/55 mmHg and respiratory rate 20/minute. Oxygen
saturation on air was 92%.
Which of the following empirical antibiotic regimes would be
most appropriate?
A. Ceftriaxone 2 g once daily i.v.
B. Flucloxacillin 1 g four times daily i.v.
C. Gentamicin 5 mg/kg once daily i.v.
D. Piperacillin/tazobactam 4.5 g 8-hourly i.v.
E. Metronidazole 500 mg 8-hourly i.v.
706 Ó 2017 Published by Elsevier Ltd.