HERPES ZOSTER OPHTHALMICUS

Herpes zoster ophthalmicus is an acute infection of Gasserian ganglion of the fifth cranial nerve by the varicella-zoster virus (VZV). It constitutes approximately 10 percent of all cases of herpes zoster.

Etiology
Varicella -zoster virus. It is a DNA virus and produces acidophilic intranuclear inclusion bodies. It is neurotropic in nature.

Mode of infection. The infection is contracted in childhood, which manifests as chickenpox and the child develops immunity. The virus then remains
dormant in the sensory ganglion of trigeminal nerve. It is thought that, usually in elderly people (can occur at any age) with depressed
  cellular immunity, the virus reactivates, replicates and travels down along one or
more of the branches of the ophthalmic division of the fifth nerve.

Clinical features
􀁺 In herpes zoster ophthalmicus, frontal nerve is
more frequently affected than the lacrimal and
nasociliary nerves.

• About 50 percent cases of herpes zoster ophthalmicus get ocular complications.
• The Hutchinson's rule, which implies that ocular involvement is frequent if the side or tip of nose presents vesicles (cutaneous involvement of nasociliary nerve), is useful but not infallible.
• Lesions of herpes zoster are strictly limited to one side of the midline of head.

Clinical phases of H. zoster ophthalmicus are :
i. Acute, which may totally resolve.
ii. Chronic, which may persist for years.
iii. Relapsing, where the acute or chronic lesions reappear sometimes years later.

Clinical features of herpes zoster ophthalmicus include general features, cutaneous lesions and ocular lesions. In addition, there may be associated
other neurological complications as described below:
A. General features. The onset of illness is sudden with fever, malaise and severe neuralgic pain along the course of the affected nerve. The distribution of pain is so characteristic of zoster that it usually arouses suspicion of the nature of the disease before appearance of vesicles.

B. Cutaneous lesions. Cutaneous lesions (Fig.1) in the area of distribution of the involved nerve appear usually after 3-4 days of onset of the disease. To
begin with, the skin of lids and other affected areas become red and oedematous (mimicking erysipelas), followed by vesicle formation. In due course of time vesicles are converted into pustules, which subsequently burst to become crusting ulcers. When crusts are shed, permanent pitted scars are left. The active eruptive phase lasts for about 3 weeks. Main symptom is severe neuralgic pain which usually diminishes with the subsidence of eruptive phase; but sometimes it may persist for years with little diminution of intensity. There occurs some anaesthesia of the affected skin which when associated with continued post-herpetic neuralgia is called anaesthesia dolorosa.

Fig. 1. Cutaneous lesions of herpes
zoster ophthalmicus.

C. Ocular lesions. Ocular complications usually appear at the subsidence of skin eruptions and may present as a combination of two or more of the
following lesions:

1. Conjunctivitis is one of the most commoncomplication of herpes zoster. It may occur as mucopurulent conjunctivitis with petechial haemorrhages or acute follicular conjunctivitis with regional lymphadenopathy. Sometimes, severe necrotizing membranous inflammation may be seen.

2. Zoster keratitis occurs in 40 percent of all patients and sometimes may precede the neuralgia or skin lesions. It may occur in several forms, which in order of chronological clinical occurrence are (Fig. 2) :

Fig. 2. Types of zoster keratitis : A, Punctate epithelial
keratitis; B, Microdendritic epithelial ulcer; C, Nummular
keratitis; D, Disciform keratitis.

 

• Fine or coarse punctate epithelial keratitis.
• Microdendritic epithelial ulcers. These unlike dendritic ulcers of herpes simplex are usually peripheral and stellate rather than exactly dendritic in shape. It contrast to Herpes simplex dendrites, they have tapered ends which lack bulbs.
• Nummular keratitis is seen in about one-third number of total cases. It typically occurs as multiple tiny granular deposits surrounded by a halo of stromal haze.
• Disciform keratitis occurs in about 50 percent of cases and is always preceded by nummular keratitis.
• Neuroparalytic ulceration may occur as a sequelae of acute infection and Gasserian ganglion destruction.
• Exposure keratitis may supervene in some cases due to associated facial palsy.
• Mucous plaque keratitis develops in 5% of cases between 3rd and 5th months characterised by sudden development of elevated mucous plaque with stain brilliantly with rose bengal.

3. Episcleritis and scleritis occur in about one-half of the cases. These usually appear at the onset of the rash but are frequently concealed by the overlying
conjunctivitis.
4. Iridocyclitis is of a frequent occurrence and may or may not be associated with keratitis. There may be associated hypopyon and hyphaema (acute
haemorrhagic uveitis).

5. Acute retinal necrosis may occurs in some cases.

6. Anterior segment necrosis and phthisis bulbi. It may also result from zoster vasculitis and ischemia.
7. Secondary glaucoma. It may occur due to trabeculitis in early stages and synechial angle closure in late stages.

D. Associated neurological complications. Herpes zoster ophthalmicus may also be associated with other neurological complications such as :
1. Motor nerve palsies especially third, fourth, sixth and seventh.
2. Optic neuritis occurs in about 1 percent of cases.
3. Encephalitis occurs rarely with severe infection.

HERPES SIMPLEX KERATITIS