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HIGH-YIELD FACTS

  • Staphylococcus and Streptococcus are by far the most common bacteriological etiologic agents of most superficial skin infections.

  • The marked increase in prevalence of community-acquired methicillin-resistant S. aureus (CA-MRSA) has made it necessary to consider using an antibiotic that targets this resistant organism (clindamycin or trimethoprim/sulfamethoxazole) when using an oral agent to treat severe, recurrent, or disseminated infections.

  • Poststreptococcal glomerulonephritis is caused by nephritogenic strains of streptococci which can cause skin infections and pharyngitis. It presents about 2 weeks after the primary infection.

  • Tinea corporis can be treated effectively with topical antifungals, but tinea capitis requires long courses (4–8 weeks) of systemic antifungal therapy.

IMPETIGO

ETIOLOGY

Impetigo is a common childhood superficial skin infection seen in preschool and school-aged children that is classically caused by Staphylococcus aureus bacteria but can also be caused by Group A streptococcus species (Streptococcus pyogenes). It usually peaks in incidence during the summer and fall seasons.1 Given the steady increase in the prevalence of community-acquired methicillin-resistant S. aureus (CA-MRSA) over the past two decades, up to 70% prevalence in some areas, antibiotic selection must take into account this prevailing resistance pattern within the community.2–4

PATHOPHYSIOLOGY

Impetigo infections occur when bacteria that is usually present on the surface of the skin enters into the epidermal layer through areas of skin breaks, microabrasions, or at sites of skin trauma. The bacteria then replicate beneath the skin, causing the characteristic crusted “honey-colored” gold lesions. Transmission of infection occurs through direct contact or fomites.1

RECOGNITION

The classic impetigo rash begins with erythematous macular or papular lesions that then progress to superficial vesicles or bullae, which then rupture leaving crusted “honey-colored” gold lesions. Lesions can be solitary, arranged in clusters, or confluent. Typical distribution includes the face, extremities, and/or distal fingers or toes for nonbullous impetigo, and intertriginous areas of the neck, diaper area, or axillae for bullous impetigo (Fig. 91-1).1,4

FIGURE 91-1.

Impetigo of face of an adolescent.

MANAGEMENT

Impetigo is often a benign self-limited disease lasting 2 to 3 weeks. However, it is easily transmitted to others and some studies report a 5% chance of Group A strep impetigo leading to acute glomerulonephritis.1,4 Maintaining good skin hygiene, using antibacterial soaps, and/or dilute bleach baths have shown varying degrees of success in eradicating colonization. Over-the-counter topical agents such as bacitracin or neomycin tend to be ineffective due to the emergence of MRSA. Mupirocin or fusidic acid (not approved in the United States) ointments have been the mainstay of topical treatment for impetigo, and in a recent Cochrane review, shows evidence of being the most effective treatment.5 Due to reported resistance ...

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