Common skin infections - cellulitis, and other streptococcal and staphylococcal skin manifestations
Description
- Cellulitis - infection of the dermis and subcutaneous tissue, poorly demarcated, spreading
- Erysipelas - more superficial, sharply demarcated, raised border - classically streptococcal
- Spectrum extends to impetigo (superficial, epidermal) and necrotising fasciitis (deep fascial, surgical emergency) - depth of tissue involvement is the organising axis
Epidemiology
- Cellulitis - among the commonest reasons for hospital admission for a skin condition
- Risk rises with obesity, lymphoedema, chronic venous insufficiency, diabetes, prior cellulitis (recurrence common)
- Impetigo - commonest in children, highly contagious
Aetiopathogenesis
By entity
- Cellulitis: Streptococcus pyogenes (Group A Strep) and Staphylococcus aureus - the two organisms to cover empirically in almost all cases; purulent cellulitis (associated with abscess/discharge) - think S. aureus (including MRSA); non-purulent - think Streptococcus
- Erysipelas: Streptococcus pyogenes almost exclusively
- Impetigo: S. aureus (commonest overall now) and/or Streptococcus pyogenes; bullous impetigo specifically staphylococcal (exfoliative toxin)
- Necrotising fasciitis: Type I (polymicrobial - mixed aerobic/anaerobic, often post-surgical/diabetic) vs Type II (monomicrobial, Group A Streptococcus +/- toxic shock syndrome)
Entry points
- Skin breaks - tinea pedis (classic portal for lower leg cellulitis), wounds, ulcers, IV drug use sites, insect bites
Diagnosis
Clinical - the diagnosis, in almost all cases
- Cellulitis: erythema, warmth, swelling, tenderness, poorly demarcated, +/- lymphangitic streaking, regional lymphadenopathy, fever
- Erysipelas: sharply demarcated, raised, bright red plaque, often facial or lower limb
- Blood cultures/wound swab not routinely needed for typical uncomplicated cellulitis - low yield; reserve for severe disease, immunosuppression, animal/water exposure, or treatment failure
Red flags for necrotising fasciitis - do not miss
- Pain out of proportion to examination findings
- Rapid progression, skin necrosis/bullae/crepitus, systemic toxicity disproportionate to visible skin findings
- Anaesthesia of the affected skin (nerve destruction)
- Surgical exploration is the definitive diagnostic test - do not wait for imaging if clinical suspicion is high; LRINEC score can support but should not delay surgical referral when suspicion is strong
Assess severity
- Systemic toxicity (fever, tachycardia, hypotension) - determines oral vs IV therapy and admission threshold
- Mark the border of erythema to monitor progression
Management
A. Non-purulent cellulitis/erysipelas (Streptococcus-focused)
- Mild, systemically well: oral flucloxacillin (covers both Streptococcus and Staph) or phenoxymethylpenicillin (erysipelas, confidently streptococcal)
- Moderate-severe/systemic toxicity: IV flucloxacillin +/- benzylpenicillin
- Penicillin allergic: clindamycin or a macrolide, per severity and local guidance
B. Purulent cellulitis/abscess (S. aureus-focused, consider MRSA)
- Incision and drainage of any abscess is essential - antibiotics alone are inadequate for a drainable collection
- Empirical MRSA cover (e.g. trimethoprim-sulfamethoxazole, clindamycin, or vancomycin if severe/IV) if local MRSA prevalence or risk factors
C. Impetigo
- Localised, limited: topical mupirocin
- Widespread/bullous: oral flucloxacillin or cefalexin
- Hygiene measures, exclude from school/childcare until 24h after starting treatment or lesions crusted/dry
D. Necrotising fasciitis - surgical emergency
- Urgent surgical debridement - the definitive treatment, source control cannot be substituted by antibiotics
- Broad-spectrum empirical antibiotics immediately: e.g. a broad beta-lactam/beta-lactamase inhibitor or carbapenem + clindamycin (clindamycin's toxin-suppression effect is specifically valuable for Group A Streptococcus) +/- vancomycin for MRSA cover
- ICU-level supportive care, consider IVIG in toxic shock-associated cases
E. Adjuncts and prevention
- Elevate the affected limb - reduces oedema and speeds resolution
- Treat the entry point (e.g. tinea pedis) to reduce recurrence
- Manage predisposing chronic conditions (lymphoedema, venous insufficiency, obesity, diabetes control)
- Recurrent cellulitis - consider prophylactic antibiotics after addressing modifiable risk factors, specialist input if frequent recurrence
Associations
- Chronic venous insufficiency, lymphoedema, obesity
- Diabetes, tinea pedis (entry point)
- Recent surgery/trauma, IV drug use
- Immunosuppression - broader/more severe disease, consider atypical organisms
Natural history & complications
- Uncomplicated cellulitis - responds within 48-72h to appropriate antibiotics; mark the erythema border to objectively track response rather than escalating therapy prematurely
- Recurrence common where predisposing factors (lymphoedema, venous disease, obesity) are unaddressed - each episode can worsen underlying lymphatic damage, perpetuating a cycle
- Necrotising fasciitis - mortality remains high (~20-30%) even with prompt treatment - reflects how much outcome depends on speed to surgical debridement
- Post-streptococcal complications (rare) - glomerulonephritis
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