HSV-1 and HSV-2 are DNA herpesviruses responsible for primary and recurrent mucocutaneous herpetic infections.14,15 HSV-1 is predominately associated with orolabial infections and HSV-2 is predominately associated with genital disease. The viruses are spread through direct contact with a lesion or infected body fluids, e.g., vesicular exudates, saliva, and genital fluids; less frequently by touching freshly contaminated articles and environmental surfaces.
The most common initial presentation of HSV-1 infection is primary herpetic gingivostomatitis (PHGS). The overwhelming majority of primary infections is asymptomatic or is so mild that it goes unnoticed. In symptomatic patients, following an incubation period of 2-20 days, prodromal signs and symptoms include fever, chills, malaise, irritability, headache, and anorexia. The onset of the acute phase is abrupt and is usually characterized by pain, salivation, fetor oris, and sub-mandibular and cervical lymphadenopathy.
Examination reveals inflammation of the marginal and attached gingivae characterized by erythema, edema, capillary proliferation, and widespread vesicular eruptions affecting all oral tissues. New vesicles continue to erupt for 3 to 5 days, coalesce, rupture within 24 to 48 hours, and produce shallow, painful, irregular erosions. Gradual healing, without scaring, occurs within 7 to 14 days. PHGS in immunocompromised patients tends to be more severe, last longer, and may lead to systemic viremia.
The most common presentation of a recurrent herpetic infection in the head and neck area is recurrent herpes labialis (RHL). While the frequency of recurrence varies greatly among patients, the lesions tend to recur in a similar site in any given individual. Constitutional symptoms are absent, but patients often experience a prodrome of paresthesia, tenderness, pain, burning sensation, tingling or itching at the site of recurrence, i.e., the lip vermilion or some other perioral site such as the skin or ala of the nose.
The onset of the acute phase is characterized by multiple small erythematous papules that rapidly become vesicular. The vesicles coalesce and rupture within 2 days to form characteristic crusting lesions. RHL in an otherwise healthy patient typically heals within 7 to 14 days. In immunocompromised patients RHL tends to be more severe, last longer, may mimic primary infections, and may lead to systemic viremia.
Outbreaks of recurrent herpetic stomatitis (RHS), in otherwise healthy individuals, have been attributed to traumatic triggers such as dental injections or thermal burns. The lesions occur on keratinized oral mucosa, i.e., the hard palate or gingivae. Typical features include a cluster of small vesicles, which rapidly break down into shallow, mildly painful erosions that persist for several days. RHS in immunocompromised patients tends to be more severe, last longer, may mimic primary HSV infection, and may lead to systemic viremia.
There are no vaccines available for the prevention of HSV infections and there is no recommendation for passive immunization, i.e., for the administration of post-exposure immunoglobulin preparations.
Topical (acyclovir, penciclovir, and docosanol), oral (acyclovir, valacyclovir, and famciclovir) and IV (acyclovir and foscarnet) formulations of antiviral agents are available to treat first episodes, recurrences, and suppression of HSV-1 infections. Medical care is supportive to help relieve symptoms and to address complications such as bacterial infections.