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Cellulitis & Skin/Soft-Tissue Infection

Last Update 1st September 2026

Cellulitis & Skin/Soft-Tissue Infection

Erysipelas, necrotising fasciitis, folliculitis/boils, impetigo and periorbital cellulitis have their own pages. This one covers the shared assessment, the mimics, and who can be treated at home.

Clinical presentation

Cellulitis extends into the deep dermis and subcutaneous tissue. It commonly involves the lower limbs and in most cases is unilateral. Spreading erythema, warmth, swelling and tenderness are the core findings, often with lymphangitis and regional lymphadenopathy.

Groin pain and tenderness from inguinal lymphadenitis sometimes precedes visible leg cellulitis. Bacteraemia is uncommon, occurring in fewer than five per cent of cases.

Erysipelas is the more superficial form — upper dermis and superficial lymphatics, with a raised, sharply demarcated edge. Classically facial, but the lower limb is common too.

Organisms. Cellulitis is usually Staphylococcus aureus or a beta-haemolytic streptococcus (group A, B, C or G). The clinical pattern gives a hint:

  • Streptococcal — acute onset, rapidly spreading erythema, lymphangitis, lymphadenopathy; typically non-purulent.
  • Staphylococcal — purulent lesions with surrounding erythema; think penetrating trauma or ulceration.

In practice the two often can’t be separated without a positive culture, so empirical cover usually spans both.

Portal of entry

Every cellulitis assessment should look for the breach that let the organism in — treating it is what prevents the next episode.

  • Skin barrier disruption: insect bites, wounds, abrasions
  • Pre-existing skin infection: tinea pedis (check the toe webs every time), impetigo
  • Underlying skin disease: eczema, psoriasis
  • Lymphoedema, or surgical disruption of lymphatic or venous drainage
  • Peripheral vascular disease with impaired arterial supply
  • Chronic venous insufficiency

Differential diagnosis

Bilateral lower-limb cellulitis is exceedingly rare. Bilateral red legs are almost always stasis dermatitis, and do not need antibiotics.

Other non-infectious causes of a hot red leg:

  • Stasis dermatitis
  • Superficial thrombophlebitis
  • Deep vein thrombosis
  • Congestive cardiac failure
  • Drug reactions
  • Insect bites
  • Cutaneous vasculitis
  • Acute gout

Consider these actively in any atypical case, in any case that isn’t responding, and in every bilateral presentation.

Also broaden the differential for unusual exposures — marine or freshwater injury, animal or human bites, immunosuppression, or a remote/tropical setting. Take specimens for culture and susceptibility in these cases, and seek specialist advice for difficult-to-treat or atypical infection.

Red flags

Necrotising soft-tissue infection is the diagnosis not to miss. It is a clinical diagnosis, and when suspected needs urgent surgical referral, not further imaging in the community.

The triad is disproportionate local pain, swelling and erythema or skin change. Pain out of proportion to the visible findings is the earliest and most useful sign.

Other features:

  • Onset after trauma — often minor. Puncture wounds and deep cuts that seed bacteria into deep tissue planes are the highest-risk.
  • Systemic upset out of keeping with the skin: flu-like symptoms, fever, diarrhoea, malaise, dizziness, nausea — progressing to tachycardia, hypotension, altered mental state.
  • Later: dusky or purpuric skin change, haemorrhagic bullae, necrosis, crepitus.

Early NSTI is genuinely hard to diagnose because infection tracks along deep fascia before it is visible on the surface. Have a low threshold for a subcutaneous infection that seems “not quite right”. Risk factors include diabetes (most frequent), immunosuppression, obesity, malnutrition, peripheral vascular disease, injecting drug use, malignancy, older age, Aboriginal and Torres Strait Islander descent, and chronic alcohol use.

Mortality is 20–40%, and surgical debridement is the definitive treatment — refer immediately and give broad-spectrum IV antibiotics without waiting for investigations. See Necrotising Fasciitis.

Investigations

Most uncomplicated cellulitis needs none. Diagnosis is clinical, and blood tests do not confirm or exclude it.

Worth doing when the picture is not straightforward:

  • Swab any wound, blister or purulent focus for culture and susceptibility — particularly if MRSA is a consideration or the patient isn’t improving.
  • Blood cultures if systemically unwell or febrile with rigors.
  • FBE, CRP, UEC in moderate-to-severe disease, and to track response.
  • Doppler ultrasound if DVT is a genuine alternative.
  • Mark the edge of the erythema with a skin pen and date it — the single most useful bedside tool for judging progression at review.

Treatment

For cellulitis or erysipelas without systemic symptoms or extensive erythema:

  • Dicloxacillin 500 mg (child 12.5 mg/kg up to 500 mg) orally, 6-hourly
  • OR flucloxacillin 500 mg (child 12.5 mg/kg up to 500 mg) orally, 6-hourly
  • If S. pyogenes or another beta-haemolytic streptococcus is suspected on clinical grounds, such as non-purulent or recurrent cellulitis: phenoxymethylpenicillin 500 mg (child 12.5 mg/kg up to 500 mg) orally, 6-hourly

In children cefalexin is often preferred, because the liquid formulation is better tolerated: 12.5 mg/kg up to 500 mg orally 6-hourly, or 20 mg/kg up to 750 mg orally 8-hourly where a 6-hourly regimen is unlikely to be followed.

Usual duration is 5 days. Advise patients to return for review after 5 days if symptoms are not improving.

Elevate the limb and treat the predisposing skin condition, tinea in particular.

MRSA. Community-associated MRSA is resistant to beta-lactams — flucloxacillin, dicloxacillin and the cephalosporins. Where it is a consideration, empirical options are clindamycin or trimethoprim+sulfamethoxazole, guided by culture and susceptibility.

Topical antibiotics have almost no role. Mupirocin is for mild impetigo and folliculitis only. Everything else needs incision and drainage, or oral/IV antibiotics. Avoid topical fusidic acid monotherapy — it drives resistance in S. aureus.

Purulent lesions — boils and carbuncles — are drained, not treated with antibiotics. Incision and drainage is the definitive treatment and antibiotics are usually unnecessary. See Folliculitis.

Referral and admission

Patients with no systemic toxicity and no uncontrolled comorbidity can usually be managed with oral antibiotics as outpatients.

Refer for hospital assessment and IV antibiotics if any of:

  • Comorbidity — renal impairment, diabetes, cardiac failure, splenectomy — or immunosuppression
  • Rapidly progressive infection
  • Concern for deep-space infection: bullae, necrosis, or muscle involvement
  • High fevers and rigors
  • Haemodynamic instability
  • Suppurative wound or bite needing surgical drainage, especially face or hand
  • No systemic or local response to oral antibiotics, or a CRP that is rising or static despite adequate therapy
  • Positive blood cultures
  • Unable to tolerate or absorb oral antibiotics

IV therapy does not always mean admission. Outpatient parenteral antibiotic therapy or Hospital in the Home is appropriate for many of these patients and is worth asking about explicitly when referring.

Safety-netting for anyone treated at home: return immediately for pain out of proportion, spreading beyond the marked edge, fever or rigors, vomiting, confusion, or any new dusky/purple discolouration or blistering. Otherwise review at 48 hours, and again at day 5.

Recurrent cellulitis

Each episode damages lymphatics, producing lymphoedema, which makes the limb more prone to the next episode — a self-reinforcing cycle.

Treating the underlying cause is the most important step:

  • Compression bandaging or stockings for chronic lymphoedema and venous stasis, to improve venous return and lymphatic contractility
  • Limb elevation — for leg cellulitis, foot higher than hip
  • Eradicate tinea pedis and treat any chronic skin disease

For recurrent streptococcal cellulitis, long-term suppressive antibiotics offer symptomatic and cost benefit — twice-daily oral penicillin or cephalexin.

For recurrent staphylococcal infection, consider decolonisation: mupirocin nasal ointment for 5 days, plus either chlorhexidine 2% or triclosan 1% wash for 5 days in the shower, or sodium hypochlorite bathwater or triclosan 2% bath oil for 5 days. Don’t share towels; wash linen weekly and towels after each use in hot water. Household contacts are not decolonised unless the index case keeps recurring or a contact also has recurrent infection. Refer to infectious diseases if prophylaxis fails.