Bacterial skin infections

Acknowledgements

Developed in collaboration with the University of Auckland Goodfellow Unit in 2007.

Author: Hon A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand, 2008.  

Images have been sourced from the following:

  • Hon Assoc Prof Amanda Oakley
  • The Department of Dermatology, Health Waikato
  • Prof Raimo Suhonen (Finland)
  • Arthur Ellis (medical artist)

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Cellulitis

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Learning objectives

  • Identify and manage erysipelas and cellulitis

Introduction

Erysipelas, cellulitis and many cases of necrotising fasciitis are most frequently caused by Streptococcus pyogenes, less often by Staphylococcus aureus, enterobacteriae and anaerobes. Identification and early treatment is essential to prevent septicaemia, skin necrosis and permanent tissue damage.

Clinical features

Invasive streptococci result in erysipelas (superficial lymphatic invasion) and cellulitis (involvement of subcutis). Erysipelas has elevated sharply demarcated borders. Cellulitis is less well defined and is sometimes due to other organisms, but the distinction is somewhat arbitrary.

Early infection is characterised by fever, rigors and malaise. There may or may not be a history of initial skin injury. Although any site may be affected, the face, hands and lower legs are the most common. The affected skin becomes red, hot, swollen and painful. In severe cases, there may be bullae, ulceration and necrosis. There may be associated lymphangitis and lymphadenopathy.

Differential diagnosis

The differential diagnosis includes:

Contact dermatitis
Contact allergy, especially to plants, may cause considerable oedema. Characteristically, plant allergy results in an asymmetrical and bizarre eruption with surface blistering. Affected patients (often children) are systemically well and the face is a common site
Gravitational dermatitis
Also known as venous or stasis eczema, this has a slower onset than cellulitis, does not cause systemic upset and is frequently bilateral. Surface skin may be blistered, but is often dry and intensely itchy. Look for other signs of venous disease (varicose veins, pigmentation, brawny induration).
Vasculitis
Look for purpuric papules, plaques, bullae and erosions.
Thrombophlebitis
Evaluate superficial vasculature; thrombophlebitis results in a tender red or purple subcutaneous 'cord' and associated swelling.
Deep venous thrombosis
Pain and swelling without redness or blistering. Positive Homan's sign.

Cellulitis may coexist with these disorders. If in doubt, treat for infection. It is quite safe to prescribe additional potent topical steroid for a few days. Arrange vascular studies if clinically indicated.

Investigations

Surface swabs are generally negative

  • The organism can be cultured in 30% by needle aspiration of the advancing edge
  • Blood cultures are positive in only 2%

Treatment

Streptococcal infections must be treated aggressively as they are potentially fatal. Group A streptococci are uniformly sensitive to penicillin and improvement is usually seen within hours of treatment.

  • Mild cases may received oral antibiotics as outpatient
  • More severe cases require intravenous antibiotics according to hospital policy
  • Immobilise and elevate the affected limb
  • Incision and drainage of suppurating abscesses may be required
  • May be complicated by thrombophlebitis, deep venous thrombosis, septicaemia, shock and endocarditis. Consider anticoagulants.

Follow up carefully. If there is no improvement within 24 hours of oral treatment, consider intravenous antibiotics and if necessary, admission.

Erysipelas and cellulitis may recur in the same site and prolonged courses of penicillin are sometimes prescribed prophylactically. Treat tinea pedis actively, as fissured toe clefts appear to predispose to recurrence. Prophylactic compression stockings may be helpful for persistent lymphoedema.

Activity

Outline the criteria for hospital admission of a patient with cellulitis.

Related information

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