|
Impetigo is
a superficial skin infection with crusting or bullae caused by streptococci,
staphylococci, or both. Ecthyma is an ulcerative form of impetigo.
No predisposing lesion is identified in most patients, but impetigo may follow any type of break in the skin. General risk factors seem to be moist environment, poor hygiene, and chronic nasal carriage of staphylococci. Impetigo may be bullous or nonbullous. S. aureus is the predominant cause of nonbullous impetigo and the cause of all bullous impetigo. Bullae are caused by exfoliative toxin produced by staphylococci. Methicillin-resistant S. aureus (MRSA) has been isolated in about 20% of recent cases of impetigo.
Symptoms and Signs
Nonbullous impetigo typically presents as clusters of vesicles or pustules that rupture and develop a honey-colored crust (exudate from the lesion base) over the lesions. Bullous impetigo is similar except that vesicles typically enlarge rapidly to form bullae. The bullae burst and expose larger bases, which become covered with honey-colored varnish or crust. Ecthyma is characterized by small, purulent, shallow, punched-out ulcers with thick, brown-black crusts and surrounding erythema.
Impetigo and ecthyma cause mild pain or discomfort. Pruritus is common; scratching may spread infection, inoculating adjacent and nonadjacent skin.
Diagnosis
Diagnosis is by characteristic appearance. Cultures of lesions are indicated only when the patient does not respond to empiric therapy. Patients with recurrent impetigo should have nasal culture. Persistent infections should be cultured to identify MRSA.
Treatment
The affected area should be washed gently with soap and water several times a day to remove any crusts. Treatment for localized disease is topical mupirocin antibiotic ointment tid for 7 days or retapamulin ointment bid for 5 days. Oral antibiotics (eg, dicloxacillin or cephalexin 250 to 500 mg qid, 12.5 mg/kg qid for children, for 10 days) may be needed in patients with extensive or resistant lesions. Use of initial empiric therapy against MRSA is not typically advised unless there is compelling clinical evidence (eg, contact with a documented case or outbreak; high culture-documented prevalence in a practice area). Treatment of MRSA should be directed by culture and sensitivity test results; typically, clindamycin , rifampin , and trimethoprim-sulfamethoxazole are effective against most strains of community-acquired MRSA.
Other therapy includes restoring a normal cutaneous barrier in patients with underlying atopic dermatitis or extensive xerosis using topical emollients and corticosteroids if warranted. Chronic staphylococcal nasal carriers are given topical antibiotics ( mupirocin ) for 1 wk each of 3 consecutive months.
Prompt recovery usually follows timely treatment. Delay can cause cellulitis, lymphangitis, furunculosis, and hyperpigmentation and hypopigmentation with or without scarring. Children aged 2 to 4 yr are at risk of acute glomerulonephritis if nephritogenic strains of group A streptococci are involved; nephritis seems to be more common in the southern US than in other regions.
Last full review/revision October 2007 by A. Damian Dhar, MD
Content last modified October 2007
| 
