Predisposing factors—such as poor hygiene, anemia, malnutrition, and a warm climate—favor outbreaks of this infection, most of which occur during the late summer and early fall. Impetigo can complicate chickenpox, eczema, and other skin conditions marked by open lesions.
Causes
Coagulase-positive Staphylococcus aureus and group A beta-hemolytic streptococci (or a combination of both) produce epidermal infections.
Signs and symptoms
Common nonbullous impetigo typically begins with a small red macule that turns into a vesicle, becoming pustular with a honey-colored crust within hours. When the vesicle breaks, a thick yellow crust forms from the exudate. Autoinoculation may cause satellite lesions. Other features include pruritus, burning, and regional lymphadenopathy.
A rare but serious complication of streptococcal impetigo is glomerulonephritis.
With bullous impetigo, a thin-walled vesicle opens and a thin, clear crust forms on the subsequent eruption. It commonly appears on exposed areas.
Diagnosis
Characteristic lesions suggest impetigo.
Microscopic visualization of the causative organism in a Gram stain of vesicle fluid usually confirms S. aureus infection and justifies antibiotic therapy.
Culture and sensitivity testing of fluid or denuded skin may indicate the most appropriate antibiotic, but therapy shouldn’t be delayed for laboratory results, which can take 3 days.
Treatment
Treatment generally consists of a systemic antibiotic (usually a penicillinase-resistant penicillin, cephalosporin, or erythromycin) for 10 days. A topical antibiotic, such as mupirocin ointment, may be used for minor infections.
Therapy also includes removal of the exudate by washing the lesions two or three times a day with soap and water or, for stubborn crusts, using warm soaks or compresses of normal saline or a diluted soap solution.
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