1. Herpes simplex virus (HSV) and varicella zoster virus (VZV) can cause ocular infections and disease. HSV commonly causes blepharoconjunctivitis but can also lead to recurrent epithelial, stromal, or endothelial keratitis. VZV reactivation causes herpes zoster ophthalmicus (HZO), presenting with rash in the V1 dermatome and potentially causing keratitis. 2. HSV keratitis presentations include punctate epithelial erosions, dendritic ulcers, or stromal infiltrates and opacities. Treatment involves topical antivirals like acyclovir and topical steroids. Recurrent disease may

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Compiled by: Dr. Iddi Ndyabawe
HERPETIC KERATITIS:
Herpes simplex keratitis
HSV is a dsDNA virus with two serotypes.
HSV1 shows airborne transmission and classically causes infection of the eyes, face, and trunk;
HSV2 infection is sexually transmitted and usually causes genital herpes with rare ophthalmic
involvement.
Primary infection is usually with a blepharoconjunctivitis, occasionally with corneal
involvement.
Following this, the virus ascends the sensory nerve axon to reside in latency in the trigeminal
ganglion.
Viral reactivation, replication, and retrograde migration to the cornea results in recurrent
keratitis, which may be epithelial, stromal, endothelial (discoid), or neurotrophic.
Potential intraocular involvement includes anterior uveitis and retinitis.
Additionally, the resultant neurotrophic cornea is vulnerable to bacterial and fungal keratitis.
Blepharoconjunctivitis
HSV infection is common (90% of the population are seropositive).
Primary infection occurs in childhood with generalized viral malaise and is usually
ophthalmically silent.
The most common ocular manifestation is a self-limiting blepharoconjunctivitis, characterized
by:
-periorbital vesicular rash,
-follicular conjunctivitis, and
-preauricular lymphadenopathy.

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HSV keratitis in primary infection is rare; however, prophylactic topical (Oc) aciclovir 3% 5×/d
or oral aciclovir prophylaxis may be considered. The skin is treated with topical aciclovir 5%
cream 3×/d.
Epithelial keratitis
Clinical features
• FB sensation, pain, blurred vision, lacrimation.
• Superficial punctate keratitis l stellate erosion l dendritic ulcer (branching morphology with
terminal bulbs, cf. pseudodendrites) causes geographic ulcer (large amoeboid ulcer with
dendritic advancing edges; more common if immunosuppressed/topical steroids). Ulcer base
stains with fluorescein (de-epithelialized); ulcer margins stain with Rose Bengal (devitalized
viral-infected epithelial cells); decreased corneal sensation.
• Systemic: may have associated orofacial or genital ulceration.
Investigation
• This is usually a clinical diagnosis, but, where diagnostic uncertainty, investigate both for viral
and other microbial causes
• Conjunctival and corneal swabs for molecular diagnosis (PCR and ELISA).
• Corneal scrapings: giemsa stain (multinuclear giant cells).
Treatment
• Topical antiviral: aciclovir 3% Oc initially 5×/d for 10–14 days and continued for at least 3d
after complete healing; if resistant, consider trifluorothymidine 1% initially 9×/d, but beware
epithelial toxicity.
• Consider cycloplegia (e.g. cyclopentolate 1% 2×/d) for comfort/AC inflammation.
• If patient is on topical steroids for coexistent ocular disease, reduce steroid dose (potency and
frequency) where possible. Where HSV keratitis is occurring in a corneal graft, reduction of
topical steroids may increase the risk of graft rejection.
• If recurrent attacks, consider oral antivirals (e.g. aciclovir 400mg PO 2×/d, with an aim of
providing a prolonged remission period) as prophylaxis.
Stromal keratitis
Stromal keratitis may occur with or without epithelial ulceration.
Clinical features
• Multiple or diffuse opacities cause corneal vascularization, lipid exudation, and scarring; or
may cause thinning; AC activity.
• Complications: increased IOP; rarely perforation.

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Treatment
• Topical steroid: defer (where possible) until epithelium intact; aim for minimum effective dose
(e.g. prednisolone 0.1–1%, 1–4×/d, titrating down in frequency and strength).
• Antiviral: systemic aciclovir (initially 400mg 5×/d, then reduce; prophylactic dose is 400mg
2×/d). There is clear evidence that systemic aciclovir is beneficial and useful in prevention of
recurrence. Consider in all patients with atopic keratoconjunctivitis, ocular surface disease, or
frequent recurrences. Use of topical aciclovir (3% Oc 5×/d) is controversial but may be of benefit
if stromal keratitis is associated with epithelial breakdown. Valaciclovir or famciclovir may be
considered in cases intolerant to aciclovir.
• Monitor IOP and treat, as necessary.
• Surgery: may be indicated acutely for perforation (tectonic graft) or in the long term for
scarring (deep anterior lamellar keratoplasty preferred to PK where possible).
NB: If facilities available, quantify and delineate corneal neovascularization, using fluorescein
and ICg angiography, to monitor treatment.
Disciform keratitis (endotheliitis)
Disciform keratitis probably results from viral antigen hypersensitivity, rather than reactivation.
Clinical features
• Painless, decreased VA, haloes.
• Central/paracentral disc of corneal oedema, Descemet’s folds, mild AC activity, fine KPs;
Wessely ring (stromal halo of precipitated viral antigen/host antibody).
• Complications:
-IOP,
-chronic anterior uveitis.
Investigation
• If presentation is atypical and there is no previous history of herpetic keratitis, AC paracentesis
and PCR of aqueous are of diagnostic benefit.
Beware false negatives, as long-term aciclovir will reduce HSV DNA copy number.
Treatment
• Topical steroid: defer (where possible) until epithelium intact; aim for minimum effective dose
(e.g. dexamethasone 0.5% or prednisolone 0.5% 1–4×/d, titrating down in frequency and

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strength); some patients may require low dose (e.g. prednisolone 0.1% alt—1×/d) for months or
even maintenance. Use preservative-free treatment if coexistent ocular surface disease.
• Antiviral: aciclovir, systemic (initially 400mg 5x /d, then reduce; prophylactic dose is 400mg
2x/d); continue as prophylaxis (can decease frequency) until on low-frequency/low-strength
topical steroid.
• Monitor IOP and treat, as necessary

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Herpes zoster ophthalmicus
in chickenpox
(varicella). Reactivation of virus dormant in the sensory ganglion results in shingles (herpes
zoster) of the innervated dermatome.
Involvement of the ophthalmic branch of the trigeminal nerve occurs in
15% of shingles cases and results in HZO.
Transmission is by direct contact or droplet spread.
Those never previously infected with VZV may contract chickenpox from contact with shingles.
VZV infection may be more severe in the immunosuppressed, the elderly, pregnant women, and
neonates. Maternal infection may also cause fetal malformations (3% risk in first trimester).
Systemic and cutaneous disease
Clinical features
-Viral prodrome,
-preherpetic neuralgia (mild intermittent tingling to severe constant electric pain),
-rash (papules l vesicles l pustules l scabs) predominantly within the one dermatome (Va);
-Hutchinson’s sign (cutaneous involvement of the tip of the nose, indicating nasociliary nerve
involvement and likelihood of ocular complications);
-may be disseminated in the immunocompromised.
-Additionally, the resultant neurotrophic cornea is vulnerable to bacterial and fungal keratitis.
Treatment
• Systemic antiviral: start as soon as rash appears,
either aciclovir PO 800mg 5×/d for 5d, valaciclovir PO 1g 3×/d for 7d, or famciclovir PO
750mg 1×/d for 7d; if immunosuppressed, then aciclovir IV 10mg/kg 3×/d.
• Post-herpetic neuralgia may cause depression (even suicide); treatments include amitriptyline,
gabapentin, and topical capsaicin cream.
Keratitis
Clinical features
• Epithelial: superficial punctate keratitis + pseudodendrites, often with anterior stromal
infiltrates; acute (onset 2–3d after rash; resolve in few week); common.
• Stromal: nummular keratitis with anterior stromal granular deposits is uncommon and occurs
early (10d); necrotizing interstitial keratitis with stromal infiltrates, thinning, and even

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perforation (cf. HSV) is rare and occurs late (3mo–years).
• Disciform: endotheliitis with disc of corneal oedema, Descemet’s folds, mild AC activity, fine
KPs (cf. HSV); late onset (3mo–years); chronic; uncommon.
• Neurotrophic: corneal nerve damage causes persistent epithelial defect, thinning, and even
perforation; late onset; chronic; uncommon.
• Mucus plaques: linear grey elevations, loosely adherent to underlying diseased
epithelium/stroma; late onset (3mo–years); chronic.
Treatment
• Ensure adequate systemic antiviral treatment.
Additionally:
• Epithelial: topical lubricants, usually preservative-free (e.g. Celluvisc® 0.5–1% 8×/d).
• Stromal and disciform: topical steroid treatment (e.g. prednisolone
0.1–1% 1–4×/d, titrating down in frequency and strength); some patients may require low dose
(e.g. prednisolone 0.1% alt—12×/d) for months or even maintenance; threatened perforation may
require gluing, BCL, or tectonic grafting.
• Neurotrophic: preservative-free topical lubricants (e.g. Celluvisc® 0.5–1% 8×/d + Lacri-
Lube® nocte), and consider tarsorrhaphy (surgical or medical with botulinum toxin-induced
ptosis), AMg, or conjunctival flap.
• Mucus plaques: require mucolytics (e.g. acetylcysteine 5– non-preserved 3×/d) or surgical
debridement.
• Anterior uveitis: topical steroid treatment (e.g. dexamethasone 0.1%) and cycloplegia (e.g.
• Monitor IOP: assess whether due to inflammation or steroids, and treat accordingly.
• Corneal scarring: axial scarring may require PK.
Other complications associated with HZO
• Ocular:
conjunctivitis,
2° microbial keratitis,
glaucoma,
anterior uveitis,
necrotizing retinitis (acute retinal necrosis (ARN),

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progressive outer retinal necrosis (PORN)), episcleritis, scleritis, optic neuritis, cranial nerve
palsies.
• Systemic: strokes (cerebral vasculitis), neuralgia