Skin and Soft Tissue Infections

Skin and soft tissue infections are a broad category of bacterial infections affecting the skin and underlying soft tissue. They range from superficial, self limiting conditions such as impetigo to deep, rapidly progressive, life threatening necrotising infection.

Classification by depth and severity (superficial, purulent, non purulent cellulitis, and necrotising) is the essential framework guiding both investigation and the urgency of intervention.

Classification

• Impetigo is a superficial epidermal infection caused predominantly by Staphylococcus aureus and Streptococcus pyogenes. It presents with honey coloured crusted lesions, typically on the face and extremities, and is particularly common in young children.
• Erysipelas is a more superficial form of cellulitis involving the upper dermis and superficial lymphatics, classically caused by Streptococcus pyogenes. It presents with a sharply demarcated, raised, erythematous, intensely painful plaque, most commonly on the lower limb or face.
• Cellulitis involves the deeper dermis and subcutaneous fat, with less sharply demarcated borders than erysipelas. It is caused by Streptococcus pyogenes or Staphylococcus aureus (including methicillin resistant strains in relevant populations). It typically presents with spreading erythema, warmth, swelling and tenderness.
• Purulent skin and soft tissue infection, including furuncles, carbuncles and cutaneous abscesses, reflects localised collection of pus. It is most commonly caused by Staphylococcus aureus, and drainage is the primary intervention.
• Necrotising soft tissue infection, addressed in greater detail under gas gangrene, represents the most severe end of this spectrum. It shows rapid progression, disproportionate pain, and systemic toxicity requiring emergency surgical intervention.

• Impetigo presents with vesicles or pustules that rupture to form characteristic golden, honey coloured crusted lesions, typically without significant systemic upset.
• Bullous impetigo, specifically caused by exfoliative toxin producing Staphylococcus aureus strains, produces larger, flaccid bullae.
• Erysipelas presents with an abrupt onset of a well demarcated, raised, bright red, warm and tender plaque, often with associated fever, rigors and regional lymphadenopathy. The sharp demarcation between affected and unaffected skin is a useful distinguishing clinical feature from the less well demarcated appearance of typical cellulitis.
• Cellulitis presents with spreading erythema with indistinct borders, warmth, swelling and tenderness. Fever and systemic upset are present in a proportion, particularly with more extensive involvement.
• Lymphangitis (red streaking tracking proximally along lymphatic channels) indicates spread beyond the primary site of cellulitis.
• Purulent infections present with a fluctuant, tender, erythematous swelling, sometimes with a visible or palpable pointing head.
• Features that should prompt urgent concern for necrotising infection rather than simple cellulitis, all detailed further under gas gangrene:
  pain disproportionate to visible examination findings, rapid progression over hours, skin discolouration (dusky or violaceous change, haemorrhagic bullae), crepitus, and significant systemic toxicity.

• Diagnosis of impetigo, erysipelas and typical cellulitis is generally clinical, based on the characteristic appearance and distribution of lesions. Microbiological sampling or imaging is not routinely needed in straightforward presentations.
• Wound or pus swab culture, where an open lesion or drainable collection is present, supports identification of the causative organism.
• Culture guides antibiotic selection where empirical treatment is failing or where risk factors for resistant organisms are present. This is particularly relevant given rising rates of methicillin resistant Staphylococcus aureus in some populations.
• Blood cultures are indicated for patients with significant systemic upset or in the immunocompromised, though yield in uncomplicated cellulitis is generally low.
• Full blood count and inflammatory markers support assessment of severity.
• Imaging is directed by the specific clinical concern rather than performed routinely. Ultrasound identifies an underlying collection.
• Where necrotising infection is suspected, urgent computed tomography is an option, but prompt surgical exploration without awaiting imaging is preferable given the time critical nature of that specific diagnosis.
• A careful assessment for an underlying predisposing or entry point is an important and often revealing component of the assessment, given the relevance to both acute management and prevention of recurrence. Examples are tinea pedis with interdigital fissuring predisposing to recurrent lower limb cellulitis, chronic venous insufficiency, lymphoedema, or a specific wound or bite.

• Impetigo is treated with topical fusidic acid 2 percent applied three times daily for seven days for limited, localised disease.
• Oral flucloxacillin 500 mg four times daily for seven days (or clarithromycin 500 mg twice daily in penicillin allergy) is reserved for more extensive disease or where topical treatment has failed.
• Erysipelas and typical cellulitis (mild to moderate, without evidence of an underlying purulent collection or systemic toxicity) are treated with oral flucloxacillin 500 mg to 1 g four times daily for five to seven days, given its reliable activity against both streptococcal and methicillin sensitive staphylococcal causes.
• Alternatives in penicillin allergy are clarithromycin 500 mg twice daily or clindamycin 300 to 450 mg four times daily.
• More significant cellulitis with systemic upset, or failure to respond to oral therapy, warrants intravenous treatment with flucloxacillin 1 to 2 g intravenously four times daily.
• Where methicillin resistant Staphylococcus aureus is a specific concern, use vancomycin (loaded then dosed to a target trough of 15 to 20 mg per litre) or clindamycin.
• Transition to oral therapy once clinically improving, to complete a total course typically of five to ten days depending on severity and response.
• Purulent infection (abscess, furuncle, carbuncle) is managed primarily with incision and drainage, which is the definitive treatment for a localised collection. Antibiotics are not a substitute for adequate drainage.
• Antibiotics are reserved as an adjunct for significant surrounding cellulitis, systemic upset, immunocompromise, or specific high risk sites (face, particularly the danger triangle given proximity to the cavernous sinus).
• Elevation of the affected limb, marking the border of erythema to monitor progression or resolution, and adequate analgesia form important supportive measures alongside antibiotic therapy for all forms of cellulitis and erysipelas.
• Recurrent cellulitis, particularly affecting the same limb, warrants attention to and treatment of any identified predisposing factor (treatment of interdigital tinea pedis, management of chronic oedema with compression where appropriate, skin care to maintain barrier integrity).
• Prophylactic antibiotics (such as low dose penicillin V or erythromycin) are considered for patients with frequent recurrent episodes despite addressing modifiable risk factors.
• Any suspicion of necrotising soft tissue infection, based on the specific red flag features, mandates immediate surgical referral for emergency exploration and debridement, without delay for confirmatory imaging. Outcome is critically time dependent in this distinct and far more dangerous category of infection, addressed in full under gas gangrene.