The herpesviridae are all dsDNA viruses which can cause a variety of cutaneous and disseminated infections depending on the clinical context. Herpes simples is characterized by grouped vesicles or pustules on an edematous and erythematous based and is caused by HSV-1 (usually orofacial type or HSV-2 (usually genital type). Primary HSV infections are most commonly subclinical, but children more commonly than adults may present with acute gingivostomatitis or less commonly as keratoconjuctivitis. Other variants of cutaneous herpes simplex include eczema herpeticum, herpes gladiatorum, herpes folliculitis, and herpetic whitlow.

Histologically, herpes first causes change to the basilar layer of the epidermis in the form of nuclear swelling and Cowdry B-bodies (margination of chromatin to nuclear membrane that appears as basophilic granules). These nuclear changes can progress to involve the entire epidermis and adnexal structures (especially sebaceous glands). These cnages are followed by keratinocyte ballooning degeneration, acantholysis and formation of multi-nucleated giant cells. At this point, nuclei lose their basophilia and eosinophilic inclusions are seen (Cowdry A-bodies). The associated inflammatory infiltrate is mixed (lymphocytes, neutrophils and scattered eosinophils).

Immunophenotyping is possible with antibodies to HSV1/2, but PCR or culture is required to distinguish the two.