Impetigo and Ecthyma
Impetigo is a superficial skin infection with crusting or bullae caused by streptococci, staphylococci, or both. Ecthyma is an ulcerative form of impetigo.
(See also Overview of Bacterial Skin Infections.)
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 a moist environment, poor hygiene, or chronic nasopharyngeal carriage of staphylococci or streptococci. Impetigo may be bullous or nonbullous. Staphylococcus 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.
Nonbullous impetigo typically manifests 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.
The affected area should be washed gently with soap and water several times a day to remove any crusts. Treatment for localized impetigo is topical mupirocin antibiotic ointment tid for 7 days or retapamulin ointment bid for 5 days. Fusidic acid 2% cream tid to qid until lesions resolve is as effective but is not available in the US. 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; clindamycin 300 mg po q 6 h or erythromycin 250 mg po q 6 h may be used in penicillin-allergic patients, but resistance to both drugs is an increasing problem.
Use of initial empiric therapy against MRSA is not typically advised unless there is compelling clinical evidence (eg, contact with a person who has a documented case, exposure to a documented outbreak, culture-documented local prevalence of > 10% or 15%). Treatment of MRSA should be directed by culture and sensitivity test results; typically, clindamycin, trimethoprim/sulfamethoxazole, and doxycycline are effective against most strains of community-associated 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 or 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 (types 49, 55, 57, 59); nephritis seems to be more common in the southern US than in other regions. It is unlikely that treatment with antibiotics prevents poststreptococcal glomerulonephritis.
S. aureus causes most nonbullous impetigo and all bullous impetigo.
Honey-colored crust is characteristic of bullous and nonbullous impetigo.
For persistent impetigo, culture the wound (to identify MRSA) and the nose (to identify a causative nasal reservoir).
Treat most cases with topical antibiotics.