Important Information to Know During Our Campus Transformation — Read More

Rady Children's Specialists


Eczema compromises the skin barrier, which puts patients at an increased risk for developing infections. Skin infections with bacteria, fungi and viruses, can then trigger or aggravate the eczema by stimulating the immune system to cause inflammation.

Bacterial Infection

Staphylococcus aureus is the major pathogen in eczema, found on the skin of most patients (up to 90 percent). In contrast, less than 5 percent of patients without eczema have S. aureus on their skin. Honey-colored crusting, extensive serous weeping, folliculitis and pyoderma indicate bacterial infection usually secondary to S. aureus in patients with atopic dermatitis.

In patients with an acute exacerbation of atopic dermatitis due to S. aureus infection, antistaphylococcal antibiotics are helpful in regaining control of the skin disease. Topical mupirocin or fusidic acid offers some utility in the treatment of localized impetiginized lesions.

In patients with extensive superinfection with sensitive S. aureus strains, a course of systemic antibiotics such as erythromycin and the newer macrolide antibiotics (azithromycin and clarithromycin) is usually beneficial. However, for macrolide-resistant S. aureus, a penicillinase-resistant penicillin (dicloxacillin, oxacillin, or cloxacillin) or first-generation cephalosporins are preferred.

Due to the increased risk of bacterial antibiotic resistance accompanying frequent use of antibiotics, it is important to combine antimicrobial therapy with effective anti-inflammatory therapy. In selected patients, phototherapy may be useful in reducing bacterial load and gaining control of skin inflammation.

Bleach baths can reduce staph infections on the skin. Read these instructions on how to make oneAlternative treatments may include certain types of body washes that are better-suited for adolescents.

Viral Infections

Individuals with eczema have an increased propensity toward severe viral skin infections, especially with Herpes simplex virus, which can result in eczema herpeticum, also known as Kaposi’s varicelliform eruption. After an incubation period of 5 to 12 days, a crop of itchy, vesiculopustular lesions erupts in a disseminated pattern. The lesions later umbilicate, may form punched-out erosions, and often become hemorrhagic and crusted. Skin lesions that match this description and fail to respond to oral antibiotics should initiate a search for herpes simplex. Antiviral treatment for cutaneous herpes simplex infections is of critical importance in the patient with widespread eczema, as it may become life-threatening.

Molluscum contagiosum, a poxvirus infection, and warts can cause significant problems. The viral manifestations of atopic dermatitis recently attracted much worldwide attention because smallpox vaccination of these patients or even exposure to vaccinated individuals may cause a severe widespread skin rash called eczema vaccinatum, similar in appearance to eczema herpeticum. The mechanisms underlying this propensity for viral infections in patients with atopic dermatitis likely relates to defects in innate and adaptive immune responses.

Fungal Infections

Patients with eczema have an increased prevalence of fungal infections. Malassezia furfur (Pityrosporum ovale), a lipophilic yeast commonly present in the seborrheic areas of the skin such as the scalp, face and neck may play a role.

M. furfur is most frequently found in patients with head and neck dermatitis. Reports indicate that M. furfur as well as other fungal skin infections improve following treatment with anti-fungal agents. Other fungi, including Candida albicans, have been implicated in atopic dermatitis, but the data supporting their role is unproven.