Impetigo
Presentation
Impetigo is the most common bacterial skin infection in children caused by S aureus or Streptococcus pyogenes.7-9 It begins as erythematous papules transitioning to thin-walled vesicles that rapidly rupture and result in honey-crusted papules.7,9,10 Individuals of any age can be affected by nonbullous impetigo, but it is the most common skin infection in children aged 2 to 5 years.7
Bullous impetigo primarily is seen in children, especially infants, and rarely can occur in teenagers or adults.7 It most commonly is caused by the exfoliative toxins of S aureus. Bullous impetigo presents as small vesicles that may converge into larger flaccid bullae or pustules.7-10 Once the bullae rupture, an erythematous base with a collarette of scale remains without the formation of a honey-colored crust.8 Bullous impetigo usually affects moist intertriginous areas such as the axillae, neck, and diaper area8,10 (Figure 3). Complications may result in cellulitis, septicemia, osteomyelitis, poststreptococcal glomerulonephritis associated with S pyogenes, and S aureus–induced SSSS.7-9
Figure 3. Bullous impetigo. A burst bulla on the anterior aspect of the left thigh.
Diagnosis
Nonbullous and bullous impetigo are largely clinical diagnoses that can be confirmed by culture of a vesicle or pustular fluid.10 Treatment of impetigo includes topical or systemic antibiotics.7,10 Patients should be advised to keep lesions covered and avoid contact with others until all lesions resolve, as lesions are contagious.9
Eczema Herpeticum
Presentation
Eczema herpeticum (EH), also known as Kaposi varicelliform eruption, is a disseminated herpes simplex virus infection of impaired skin, most commonly in patients with atopic dermatitis (AD).11 Eczema herpeticum presents as a widespread eruption of erythematous monomorphic vesicles that progress to punched-out erosions with hemorrhagic crusting (Figure 4). Patients may have associated fever or lymphadenopathy.12,13
Figure 4. Eczema herpeticum. Diffuse and confluent punched-out and crusted erosions on the neck.
Causes
The number of children hospitalized annually for EH in the United States is approximately 4 to 7 cases per million children. Less than 3% of pediatric AD patients are affected, with a particularly increased risk in patients with severe and earlier-onset AD.12-15 Patients with AD have skin barrier defects, and decreased IFN-γ expression and cathelicidins predispose patients with AD to developing EH.12,16,17
Diagnosis
Viral polymerase chain reaction for herpes simplex virus types 1 and 2 is the standard for confirmatory diagnosis. Herpes simplex virus cultures from cutaneous scrapings, direct fluorescent antibody testing, or Tzanck test revealing multinucleated giant cells also may help establish the diagnosis.11,12,17
Management
Individuals with severe AD and other dermatologic conditions with cutaneous barrier compromise are at risk for developing EH, which is a medical emergency requiring hospitalization and prompt treatment with antiviral therapy such as acyclovir, often intravenously, as death can result if left untreated.11,17 Topical or systemic antibiotic therapy should be initiated if there is suspicion for secondary bacterial superinfection. Patients should be evaluated for multiorgan involvement such as keratoconjunctivitis, meningitis, encephalitis, and systemic viremia due to increased mortality, especially in infants.12,15,16
Langerhans Cell Histiocytosis
Presentation
Langerhans cell histiocytosis (LCH) has a variable clinical presentation and can involve a single or multiple organ systems, including the bones and skin. Cutaneous LCH can present as violaceous papules, nodules, or ulcerations and crusted erosions (Figure 5). The lymph nodes, liver, spleen, oral mucosa, and respiratory and central nervous systems also may be involved.
Figure 5. Langerhans cell histiocytosis. Congenital red to slightly violaceous nodule with an overlying pustule on the right cheek.