Lid lesions with edema, follicular conjunctivitis, and corneal epithelial lesions are commonly seen with primary infection while corneal stromal disease is very rare in these instances as is iritis or endothelial disease. The initial ocular symptoms in adult patients usually are the result of recurrence in cases where the primary infection was asymptomatic. Ocular symptoms in children or adolescents may represent primary infection.

Epithelial lesions may be in the form of a dendrite or may be fine punctate lesions which then go on to coalesce into dendrites. (Geographic ulcers are very rare in primary disease.) Dendrite formation follows a very similar course in both primary and recurrent disease.

Clinical symptoms occur 1-2 weeks after contact and are accompanied by fever, malaise, etc. Lid lesions are small, ulcerated vesicles often seen on lid margins. They can be hidden by lashes. Fluorescein staining can help detect/outline them. Conjunctivitis is usually follicular with injection and chemosis. Epithelial dendrites take on the traditional branching pattern with fluorescein staining of the center and rose bengal/lissamine green staining of the edges and terminal end bulbs.

Diagnosis can be confirmed by the presence of corneal hypesthesia. Limbal dendrites are often more refractory to treatment than central dendrites. The disease process is self limiting, but treatment is usually undertaken to improve symptomotology and decrease the likelihood of sight-threatening corneal scarring.

Secondary/Recurrent Infection

Reactivation can lead to several ocular complications. Epithelial disease mimics that seen in primary infection with the exception that geographic or "megaherpetic" lesions are possible. Stromal inflammatory disease is common in secondary cases including disciform keratitis. Stromal disease is an inflammatory reaction to viral replication and is the main cause of scarring-related vision loss.

Mild iritis is often seen. Sectoral iris atrophy accompanied by iritis/trabeculitis and an increase in intraocular pressure (IOP) can be seen even in the absence of corneal disease. Can mimic Possner-Schlossman syndrome. 80% of such cases are caused by Herpes simplex virus; 20%, by VZV.

Tear production is often reduced, pre-disposing the patient to neurotrophic keratitis. The lacrimal and accessory lacrimal glands are not affected, so the damage is from loss of corneal sensitivity and a decreased feedback mechanism. This loss of sensory feedback can lead to neurotrophic corneal lesions. This is the breakdown of the corneal epithelium without trauma, infection, or severe desiccation. Early signs include punctate rose bengal staining. Severe cases lead to persistent, non-healing epithelial defects with ulceration. Endothelial lesions with keratic precipitates (KPs) can also be seen.

Cases of reactivation can include stromal disease alone, epithelial disease alone, or the two in conjunction with one another. The other associated findings can be present with or without corneal involvement.