Abstract
While eczema herpeticum, also known as Kaposi varioliform eruption, is not a common complication of atopic dermatitis, it is a classic example of how a defective skin barrier can allow for widespread, exaggerated infection. Herpes simplex virus (HSV) with primary or recurrent infection can disseminate over eczematous skin instead of remaining localized as is typically seen. Persons with other skin diseases that damage the epidermal barrier, such as Darier disease, Hailey-Hailey disease, bullous pemphigus, pemphigus foliaceus, ichthyosis vulgaris, and burns, can also experience eczema herpeticum. Defects in the innate immunity, evidenced by low cathelicidin and β-defensin levels, and specific defects in the gene encoding filaggrin, an important structural protein in the skin, explain why the virus is not held in check by the body’s immune system. Clinically, risk factors for eczema herpeticum include head and neck involvement of atopic dermatitis and having more severe and generalized disease. While HSV1 is more common, HSV2 can also cause eczema herpeticum. Children with atopic dermatitis have altered skin immunity with lowered innate immunity thus leading to an increased risk of infection. Children who have a history of eczema herpeticum are even more likely to experience secondary bacterial infections and infection with molluscum.
Original language | English (US) |
---|---|
Title of host publication | Curbside Consultation in Pediatric Dermatology |
Subtitle of host publication | 49 Clinical Questions |
Publisher | CRC Press |
Pages | 153-156 |
Number of pages | 4 |
ISBN (Electronic) | 9781040141526 |
ISBN (Print) | 9781617110030 |
DOIs | |
State | Published - Jan 1 2024 |
All Science Journal Classification (ASJC) codes
- General Medicine