Defective cell-mediated immunity leads to increased susceptibility to many bacterial, viral, and fungal infections of the skin. More than 90% of patients with atopic dermatitis have colonization of lesional skin with Staphylococcus aureus, and more than 75% of patients have colonization of uninvolved skin. Colonization and infection by S. aureus are associated with disease severity. S. aureus secretes exotoxins that act as a superantigen, stimulating T cells and increasing IgE production. Secondarily infected atopic dermatitis often presents as impetiginous, pustular lesions with crusting and honey-colored exudate. Topical antibiotics, such as mupirocin or retapamulin, can be used to treat local areas of infection, or oral antibiotics (such as cephalexin, dicloxacillin, or amoxicillin-clavulanate) can be used for multifocal disease or for infection around the eyes and mouth that is difficult to treat topically. Bacterial cultures may be helpful in patients who do not respond to oral antibiotics or who have infection after multiple antibiotic courses. The incidence of community-acquired methicillin-resistant S. aureus is increasing.
Herpes simplex superinfection of affected skin, or Kaposi varicelliform eruption or eczema herpeticum, results in vesiculopustular lesions that appear in clusters and can become hemorrhagic. Herpes simplex virus infection can be misdiagnosed as bacterial infection and should be considered if skin lesions fail to respond to antibiotics.
In individuals with atopic dermatitis, smallpox vaccination or exposure to a vaccinated individual may lead to eczema vaccinatum, a localized vaccinial superinfection of affected skin. Eczema vaccinatum may progress to generalized vaccinia with vaccinial lesions appearing at sites distant from the inoculation. In patients with underlying immunodeficiencies, it may be life threatening.
Widespread infections with human papillomavirus (warts) and molluscum contagiosum are also common in children with atopic dermatitis.
Atopic dermatitis is a chronic, relapsing skin disorder that tends to be more severe and prominent in young children. Symptoms become less severe in two thirds of children, with complete remission for approximately 20%. Early onset disease that is more widespread, concomitant asthma and allergic rhinitis, family history of atopic dermatitis, and elevated serum IgE levels may predict a more persistent course. Patients and families should be taught that a single cause and cure for atopic dermatitis is unlikely but that good control is possible for the majority of affected patients.
An important step in the management of atopic dermatitis is to identify and avoid allergens and irritants. Common irritants include soaps, detergents, fragrances, chemicals, smoke, and extremes of temperature and humidity. Wool and synthetic fabrics can be irritating to the skin; 100% cotton fabric is preferred. Sweating is a recognized trigger. Fingernails should be trimmed frequently to minimize excoriations from scratching.
In infants and younger children who do not respond to the usual therapies, identifying and removing a food allergen from the diet may lead to clinical improvement. Food allergy is not a common trigger for older patients. Other environmental exposures, such as dust mites, pet dander, or pollens, can also contribute to the disease state.
URTICARIA, ANGIOEDEMA, AND ANAPHYLAXIS