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Fig. 1. Cutaneous anatomy, sites of infection, and infecting organisms. (From Feingold DS, Hirschmann JV. Approach to the patient with skin or soft tissue infection. Gorbach SL, Bartlett JG, Blacklow NR, editors. Infectious diseases. 3rd edition. Philadelphia: Lippincott Williams & Wilkins; with permission.)

Fig. 1. Cutaneous anatomy, sites of infection, and infecting organisms. (From Feingold DS, Hirschmann JV. Approach to the patient with skin or soft tissue infection. Gorbach SL, Bartlett JG, Blacklow NR, editors. Infectious diseases. 3rd edition. Philadelphia: Lippincott Williams & Wilkins; with permission.)

hygiene; insect bites; diabetes mellitus; primary varicella infection; preexisting skin disease, such as eczema, atopic dermatitis, and cheilitis; hypogam-maglobulinemia; and HIV infection [1]. Impetigo also can spread among people who are in close contact with each other (ie, children in day care centers and family members of the same household).

Two types of impetigo are described. The nonbullous form is most common and is more likely to be attributable to a mixed staphylococcal and streptococcal infection. Multiple ultimately vesiculopustular lesions cluster together before skin breakdown occurs with the development of a classic thick honey-colored crust. Regional lymphadenopathy without systemic signs often is present [2]. Pruritus and pain are not common. Bullous impetigo is less common than the nonbullous form and is seen primarily in newborns and infants. The microbiology typically consists of phage type II S aureus strains that secrete exfoliative toxin A. Initially vesicular, these lesions ultimately evolve into large yellow fluid-filled flaccid bullae. After rupture, thin light-brown crusts develop. Localized lymphadenopathy is less common than in the nonbullous form, and systemic signs usually are absent.

The differential diagnosis primarily includes herpes simplex virus infections and contact dermatitis. The diagnosis of impetigo usually is based on clinical findings. The identification of the organism from skin lesions or bullae-associated fluid by Gram staining and culture is pursued when the diagnosis is uncertain. Lesions should be de-crusted aseptically before the exudative material beneath is sampled for evaluation. Serologic antibody studies, such as anti-DNase B or antihyaluronidase B, are not considered routinely in this setting except when the diagnosis of acute poststreptococcal glomerulonephritis is entertained [3].

Topical therapy with mupirocin can be used to treat impetigo when there are a limited number of lesions [4]. When disease is more extensive and severe, oral penicillinase-resistant penicillins (ie, dicloxacillin) and first generation cephalosporins (cephalexin) for a total duration of 10 days are recommended because of their antistaphylococcal activity. As in many other skin-associated infections, the practitioner needs to be aware of the increased prevalence of methicillin-resistant S aureus (MRSA) causing infection in the community [5].

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