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Impetigo is a highly contagious infection of the superficial epidermis that can occur at any age, but predominantly occurs in infants and preschool-age children during summer months. Exposed areas such as the face, neck, arms, and legs are most commonly affected. Children in daycare and athletes are some of the persons at higher risk, but most patients are young, healthy, and immunocompetent. In general, intact skin is resistant to impetiginization, and some form of compromise of the epidermal surface is necessary to permit infection. Predisposing factors include minor abrasions and lacerations, arthropod bites, burns, varicella, herpes simplex, pediculosis capitis, and several types of dermatitis, especially atopic dermatitis.

Impetigo usually presents in 1 of 2 clinical forms: nonbullous and bullous. Nonbullous (crusted) impetigo, which accounts for more than 70% of cases, is caused by group A β-hemolytic streptococci (GABHS), Staphylococcus aureus, both methicillin-sensitive S aureus (MSSA) and methicillin-resistant S aureus (MRSA), and less commonly anaerobic bacteria. Nonbullous impetigo begins with small vesicles or vesiculopustules that rupture rapidly, leaving behind a honey-colored crust superimposed on a moist red base. Accumulation of exudate can rapidly reaccumulate, lending itself to spread of the lesions via autoinoculation of the infection from scratching, digital manipulation, towels, and clothing. A gyrate or circinate morphology can be noted as lesions clear centrally and spread peripherally. Lesions are minimally symptomatic, although mild pain or pruritus may be present. Associated findings include lymphadenopathy in 90% of patients and leukocytosis in up to 50% of cases. Impetigo caused by GABHS can sometimes be followed by acute glomerulonephritis. Type 49, 55, 57, 60, and M-type 2 strains are related to nephritis. The incidence is thought to be around 2% to 5%. The prognosis in children is generally very good, but the risk of acute glomerulonephritis is not prevented with early and appropriate treatment.

Bullous impetigo is caused by infection with a toxin-producing strain of S aureus, primarily by phage group 2 or type 71, and less commonly types 3A, 3B, 3C, and 55. The same S aureus toxin of bullous impetigo also causes staphylococcal scalded skin syndrome (SSSS). The initial lesions consist of flaccid bullae that rupture easily given the superficial, subcorneal location of lysis caused by the action of the toxin on the epidermis. Patients usually present with shallow, moist, erythematous erosions with a surrounding collarette of residual blister roof (Fig. 362-1). Even in the absence of intact bullae, the clinical lesions are usually quite diagnostic. Lesions of bullous impetigo may have a propensity for moist, intertriginous areas such as the diaper region, axillae, and neck folds.

Figure 362-1

Bullous impetigo. Note ruptured lesions with a collarette of scale.

Treatment of impetigo can be solely topical when lesions are mild, localized, and due to S aureus, but ...

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