Herpes simplex virus type 1 (HSV-1) infection occurs worldwide. Infection occurs equally between the sexes and without seasonal variation. The prevalence is highest in low- and middle-income countries, whereas the prevalence rate in high-income countries has been declining.
Transmission of HSV-1 occurs when someone with no prior infection with HSV-1 comes in contact with herpetic lesions or oral secretions that contain HSV-1.
HSV-1 transmission typically occurs via oral-oral, oral-genital, or genital-genital contact. It can also occur via contamination of skin abrasions with infected oral secretions.
Transmission via oral-genital or genital-genital contact has resulted in an increasing number of cases of HSV-1 genital herpes infection, especially among young women and men who have sex with men.
The clinical manifestations of HSV-1 infection depend upon the anatomic site involved and whether the clinical episode is due to primary infection or reactivation disease. While infection is lifelong, it is rarely fatal in the immunocompetent host.
•Gingivostomatitis and pharyngitis are the most frequent clinical manifestations of primary HSV-1 infection, whereas herpes labialis is the most frequent sign of reactivation disease.
•Patients with primary genital HSV-1 typically present with bilateral genital ulcerations and tender lymphadenopathy. Genital HSV-1 lesions may recur, particularly during the first year after infection; however, multiple recurrences are rare.
•There are a variety of cutaneous manifestations associated with HSV-1 infection of the skin. These include herpetic whitlow, herpes gladiatorum, erythema multiforme, and eczema herpeticum.
•Ocular HSV infections occur in less than 5 percent of patients but can cause significant morbidity, leading to vision loss and blindness. The most common ophthalmologic complications of HSV-1 are keratitis and acute retinal necrosis.
•HSV-1 can be associated with severe disease (eg, encephalitis, meningitis, hepatitis, respiratory tract infections, esophagitis). Risk factors for severe disease include HIV infection, malignancy, organ transplantation, malnutrition, burn and skin disorders, and pregnancy.
The approach to diagnosis depends upon the site of disease (eg, mucocutaneous, ocular, neurologic or visceral). Polymerase chain reaction assays have emerged as the most sensitive method to confirm the diagnosis.
Type-specific antibodies to HSV develop during the first several weeks after primary infection and persist indefinitely. However, serologic testing has a limited role in the diagnosis of HSV-1 infection, since patients with acute infection who are HSV antibody negative may have virologic evidence of acute infection. Serologies may be most helpful in determining prognosis and the need for prevention.
Varicella-zoster virus (VZV) infection causes two distinct diseases. Primary infection with VZV results in varicella (chickenpox), characterized by vesicular lesions in different stages of development on the face, trunk, and extremities. Herpes zoster, also known as shingles, results from reactivation of latent VZV infection within the sensory ganglia.
The incidence of herpes zoster is influenced by the immune status of the host, age-related immunosenescence, disease-related immunocompromise, or iatrogenic immunosuppression, with age being the major risk factor for 90 percent of cases of herpes zoster in adults.
People with herpes zoster can spread VZV to those who have not had varicella and have never received the varicella vaccine. The virus can spread through direct contact with herpes zoster lesions (the lesions are considered infectious until they dry and crust over). Airborne transmission of VZV from individuals with localized herpes zoster also occurs.
The presenting clinical manifestations of herpes zoster are usually characterized by rash and acute neuritis. The thoracic and lumbar dermatomes are the most commonly involved sites of herpes zoster, although any dermatome can be affected. (See ‘Common findings’ above.)
Immunocompromised hosts are at risk for cutaneous and visceral dissemination.
The most common complication of herpes zoster is postherpetic neuralgia. Other complications include herpes zoster ophthalmicus or oticus, and less commonly acute retinal necrosis, aseptic meningitis, and encephalitis.
In immunocompetent individuals, the diagnosis of herpes zoster is usually based on the clinical presentation (ie, unilateral, usually painful, vesicular eruption with a well-defined dermatomal distribution). However, when the diagnosis is uncertain, laboratory confirmation is indicated. Diagnostic techniques include the polymerase chain reaction (PCR) assay (which is the most sensitive test), direct fluorescent antibody testing, and viral culture.