Herpes Simplex

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INTRODUCTION Herpes simplex is caused by a DNA virus that is estimated to infect 60% to 90% of individuals at sometime during their life. Clinically evident infections however are much less common. Involvement of the facial region is predominantly due to type I herpes virus, with the exception of newborns, in whom overwhelming exposure to the type II variety during birth can result in development of typical skin lesions during the first few days of life, often associated with devastating CNS and systemic involvement. Primary herpes occurs in previously uninfected individuals. The chief mode of transmission is by kissing or other forms of intimate contact with an individual who has an active, usually recurrent, herpetic lesion.

CLINICAL PRESENTATION Following a 2 to 14 day incubation period there develops a mild fever with moderately painful, usually unilateral, edema and erythema of the eyelid region. This is soon followed by the development of multiple discrete 2 to 3 mm vesicles that generally have a central umblilication. These break, crust over, and most often resolve without bacterial infection or scarring over the ensuing few weeks. There is a mildly tender preauricular lymphadenopa-thy, and often vesicular lesions are found elsewhere on the face or mucous membranes. Atypical dermal manifestations include the development of a black eschar early on, or edema without obvious vesicles. A careful search often reveals a few minute vesicles sometimes hidden at the base of the lashes. Following resolution the herpes virus retreats to the trigeminal ganglion where it can later reactivate and incite recurrent infections. Recurrent herpetic infections frequently follow a fever, head cold, sun exposure, or some other trivial physical or emotional insult. Onset is often preceded by a 24-hour prodrome with focal dysethesia, numbness, and tingling. The recurrent eruption is usually less severe than the primary and is more limited. Associated ocular involvement may include a follicular conjunctivitis, dendritic keratitis, disciform keratitis, acute anterior uveitis, and rarely a necrotizing retinitis or optic neuritis.

Hsv Blepharoconjunctivitis
(Courtesy of Kenneth Cohen, M.D.) (Courtesy of Robert A. Goldberg, M.D.)

HISTOPATHOLOGY The histological features of herpes simplex virus (HSV), varicella, and herpes zoster virus skin infections are similar. In HSV, the earliest changes are seen in the epidermal cell nuclei, which enlarge, develop a homogenous "ground glass" appearance, and have peripherally clumped chromatin. Changes begin along the basal epidermal layer and progress to involve all layers. Intraepidermal vesicles soon form secondary to ballooning and acantholysis of keratinocytes. Subepidermal vesicles may result from destruction of the basal layer of epidermis. Multinucleated keratinocytes are more conspicuous in lesions that have been present for several days. The histopathological clue to diagnosis is eosinophilic nuclear inclusions, which are more common in the multinucleated cells. Diagnosis is confirmed using immunohistochemistry.

Herpes Zoster Lamina Histologica

DIFFERENTIAL DIAGNOSIS The differential diagnosis includes acute stye, insect bite, chickenpox, herpes zoster, contact dermatitis, and ulcerative blepharitis.

TREATMENT The diagnosis can usually be made clinically; however, confirmation can be accomplished by finding multinucleated giant cells on a Giemsa-stained smear. Viral cultures can be obtained and would be needed to exclude herpes zoster, which will look the same on smear. An enzyme-linked immunosorbent assay (ELISA) is also available. Because of the high risk of secondary corneal involvement in cases involving the eyelids, prophylactic treatment with idoxuridine or vidara-bine ointment to the eye four times a day until the skin lesions have dried and crusted, and then twice a day for an additional two weeks, reduces the incidence and severity of ocular infection. Use of antiviral medications on the skin lesions is also recommended in the hope of suppressing the shed of viral particles. For recurrent attacks prophylactic use of topical antiviral agents in the prodromal phase will often abort the attack. Bacterial infection occurs only occasionally, so antibiotics are not generally employed until or unless secondary infection becomes manifest. Steroids should not be used because they exacerbate ocular infections. In younger children without corneal involvement the disease can be self-limited with spontaneous resolution.


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