HERPES SIMPLEX KERATITIS

Ocular infections with herpes simplex virus (HSV) are
extremely common and constitute herpetic
keratoconjunctivitis and iritis.
Etiology
Herpes simplex virus (HSV). It is a DNA virus. Its
only natural host is man. Basically HSV is
epitheliotropic but may become neurotropic.
According to different clinical and immunological
properties, HSV is of two types: HSV type I typically
causes infection above the waist and HSV type II
below the waist (herpes genitalis). HSV-II has also
been reported to cause ocular lesions.
Mode of Infection
HSV-1 infection. It is acquired by kissing or
coming in close contact with a patient suffering
from herpes labialis.
HSV-II infection. It is transmitted to eyes of
neonates through infected genitalia of the mother.
Ocular lesions of herpes simplex
Ocular involvement by HSV occurs in two forms,
primary and recurrent; with following lesions:
[A] Primary herpes
1. Skin lesions
2. Conjunctiva-acute follicular conjunctivitis
3. Cornea
i. Fine epithelial punctate keratitis
ii. Coarse epithelial punctate keratitis
iii. Dendritic ulcer
[B] Recurrent herpes
1. Active epithelial keratitis
i. Punctate epthelial keratitis
ii. Dendritic ulcer
iii. Geographical ulcer
2. Stromal keratitis
i. Disciform keratitis
ii. Diffuse stromal necrotic keratitis
3. Trophic keratitis (meta-herpetic)
4. Herpetic iridocyclitis

[A] Primary ocular herpes
Primary infection (first attack) involves a nonimmune
person. It typically occurs in children between 6
months and 5 years of age and in teenagers.
Clinical features
1. Skin lesions. Vesicular lesions may occur
involving skin of lids, periorbital region and the
lid margin (vesicular blepharitis).
2. Acute follicular conjunctivitis with regional
lymphadenitis is the usual and sometimes the
only manifestation of the primary infection.
3. Keratitis. Cornea is involved in about 50 percent
of the cases. The keratitis can occur as a coarse
punctate or diffuse branching epithelial keratitis
that does not usually involve the stroma.
Primary infection is usually self-limiting but the
virus travels up to the trigeminal ganglion and
establishes the latent infection.
[B] Recurrent ocular herpes
The virus which lies dormant in the trigeminal
ganglion, periodically reactivates and causes
recurrent infection.
Predisposing stress stimuli which trigger an attack
of herpetic keratitis include: fever such as malaria,
flu, exposure to ultraviolet rays, general ill- health,
emotional or physical exhaustion, mild trauma,
menstrual stress, following administration of topical
or systemic steroids and immunosuppressive agents.
1. Epithelial keratitis
i. Punctate epithelial keratitis (Fig. 5.9A). The
initial epithelial lesions of recurrent herpes resemble
those seen in primary herpes and may be either in
the form of fine or coarse superficial punctate
lesions.
ii. Dendritic ulcer (Figs. 5.9B and C). Dendritic ulcer
is a typical lesion of recurrent epithelial keratitis.
The ulcer is of an irregular, zigzag linear branching
shape. The branches are generally knobbed at the
ends. Floor of the ulcer stains with fluorescein and
the virus-laden cells at the margin take up rose
bengal. There is an associated marked diminution of
corneal sensations.
iii. Geographical ulcer (Fig. 5.9D). Sometimes, the
branches of dendritic ulcer enlarge and coalesce to
form a large epithelial ulcer with a 'geographical' or
'amoeboid' configuration, hence the name. The use
of steroids in dendritic ulcer hastens the formation
of geographical ulcer.
Symptoms of epithelial keratitis are: photophobia
lacrimation, pain.
Treatment of epithelial keratitis
I. Specific treatment
1. Antiviral drugs are the first choice presently.
Always start with one drug first and see the response.
Usually after 4 days the lesion starts healing which is
completed by 10 days. After healing, taper the drug
and withdraw in 5 days. If after 7 days of initial therapy,
there is no response, it means the virus is resistant to
this drug. So change the drug and/or do mechanical
debridement. Commonly used antiviral drugs with
their dose regime is given below (for details see page
420).
i. Acycloguanosine (Aciclovir) 3 percent ointment:
5 times a day until ulcer heals and then 3 times
a day for 5 days. It is least toxic and most
commonly used antiviral drug. It penetrates intact
corneal epithelium and stroma, achieving
therapeutic levels in aqueous humour, and can
therefore be used to treat herpetic keratitis.

ii. Ganciclovir (0.15% gel), 5 times a day until ulcer
heals and then 3 times a day for 5 days. It is more
toxic than aciclovir.
iii. Triflurothymidine 1 percent drops : Two hourly
until ulcer heals and then 4 times a day for 5
days.
iv. Adenine arabinoside (Vidarabine) 3 percent
ointment: 5 times a day until ulcer heals and then
3 times a day for 5 days.
2. Mechanical debridement of the involved area along
with a rim of surrounding healthy epithelium with the
help of sterile cotton applicator under magnification
helps by removing the virus-laden cells.
Before the advent of antiviral drugs, it used to be
the treatment of choice. Now it is reserved for:
resistant cases, cases with non-compliance and those
allergic to antiviral drugs.
II. Non-specific supportive therapy and physical and
general measures are same as for bacterial corneal
ulcer (see page 98).
2. Stromal keratitis
(a) Disciform keratitis
Pathogenesis. It is due to delayed hypersensitivity
reaction to the HSV antigen. There occurs low grade
stromal inflammation and damage to the underlying
endothelium. Endothelial damage results in corneal
oedema due to imbibation of aqueous humour.
Signs. Disciform keratitis is characterized by (Fig.
5.9E):
Focal disc-shaped patch of stromal oedema
without necrosis,
Folds in Descemet's membrane,
Keratic precipitates,
Ring of stromal infilterate (Wessley immune ring)
may be present surrounding the stromal oedema.
It signifies the junction between viral antigen and
host antibody.
Corneal sensations are diminished.
Intraocular pressure (IOP) may be raised despite
only mild anterior uveitis. In severe cases, anterior
uveitis may be marked.
Sometimes epithelial lesions may be associated
with disciform keratitis.
Important note. During active stage diminished
corneal sensations and keratic precipitates are the
differentiating points from other causes of stromal
oedema.
Treatment consists of diluted steroid eye drops
instilled 4-5 times a day with an antiviral cover
(aciclovir 3%) twice a day. Steroids should be tapered
over a period of several weeks. When disciform
keratitis is present with an infected epithelial ulcer,
antiviral drugs should be started 5-7 days before the
steroids.
(b) Diffuse stromal necrotic keratitis. It is a type of
interstitial keratitis caused by active viral invasion
and tissue destruction.
Symptoms : Pain, photophobia and redness are
common symptom.
Signs. It presents as necrotic, blotchy, cheesy white
infiltrates that may lie under the epithelial ulcer or
may present independently under the intact
epithelium. It may be associated with mild iritis and
keratic precipitates. After several weeks of
smouldering inflammation, stromal vascularization
may occur.
Treatment is similar to disciform keratitis but
frequently the results are unsatisfactory.
Keratoplasty should be deferred until the eye has
been quiet with little or no steroidal treatment for
several months; because viral interstitial keratitis is
the form of herpes which is most likely to recur in a
new graft.
3. Metaherpetic keratitis
Metaherpetic keratitis (Epithelial sterile trophic
ulceration) is not an active viral disease, but is a
mechanical healing problem (similar to recurrent
traumatic erosions) which occurs at the site of a
previous herpetic ulcer.
Clinically it presents as an indolent linear or
ovoid epithelial defect.
Treatment is aimed at promoting healing by use
of lubricants (artificial tears), bandage soft