Eye Diseases > Cornea

Herpes Simplex Keratitis

Evidence-based assessment and management of herpes simplex virus keratitis. Comprehensive guide covering etiology, pathogenesis, classification, diagnosis, and treatment protocols for optometry practice.

Herpes Simplex Keratitis: Dendritic epithelial ulcer (red) with characteristic terminal bulbs — the hallmark fluorescein staining pattern of HSV epithelial keratitis

Herpes simplex keratitis (HSK) is a corneal infection caused by herpes simplex virus (HSV), most commonly HSV-1. It is the leading infectious cause of corneal blindness in the developed world. The virus establishes lifelong latency in the trigeminal ganglion following primary infection, with subsequent reactivation episodes producing a spectrum of ocular disease ranging from self-limited epithelial ulceration to vision-threatening stromal inflammation. Recurrent episodes are responsible for progressive corneal scarring, neovascularisation, and ultimately, reduced visual acuity.

Causative Virus

HSV-1 (Herpes Simplex Virus type 1): Responsible for >90% of ocular HSV infections; typically acquired in childhood via oral or respiratory secretions
HSV-2 (Herpes Simplex Virus type 2): Less common cause; more often associated with neonatal and genital disease; may cause keratitis particularly in immunocompromised individuals

Primary vs. Recurrent Disease

Primary infection: Usually asymptomatic or mild; may present as unilateral follicular conjunctivitis, vesicular lid lesions, or rarely corneal involvement; typically occurs in children
Recurrent disease: Results from reactivation of latent virus in the trigeminal ganglion; responsible for the majority of clinically significant HSK and progressive corneal damage

Triggers of Reactivation

Ultraviolet light exposure: A well-established precipitant
Physical or psychological stress: Systemic illness, febrile episodes, emotional stress
Trauma: Corneal surgery, contact lens wear, ocular trauma
Immunosuppression: Systemic corticosteroids, HIV/AIDS, post-transplant immunosuppression
Hormonal changes: Menstruation in some individuals
Topical steroids: Can provoke or worsen epithelial disease if used without antiviral cover

Mechanism of Disease

Primary infection and latency: HSV-1 enters via mucous membranes or skin abrasions; replicates locally; travels retrograde along sensory axons of the trigeminal nerve to establish lifelong latency in the trigeminal (Gasserian) ganglion
Reactivation: Upon trigger stimulation, the virus replicates within the ganglion and travels anterograde along the ophthalmic division (V1) to reach the cornea and periocular tissues
Epithelial disease (direct viral cytopathic effect): Active viral replication in corneal epithelial cells causes cell lysis and the formation of the characteristic dendritic ulcer with terminal bulbs; no significant immune infiltration in early stages
Stromal disease (immune-mediated): Viral antigens in the stroma trigger a Type IV (delayed-type) hypersensitivity response; stromal infiltration by T-lymphocytes and macrophages leads to oedema, neovascularisation, and scarring
Endotheliitis: Direct viral invasion of endothelial cells combined with immune-mediated inflammatory response results in keratic precipitates (KPs), corneal oedema, and raised intraocular pressure
Neurotrophic sequelae: Repeated inflammatory episodes and viral damage to corneal nerves reduce corneal sensation (hypoesthesia), impairing the normal trophic support of the epithelium and predisposing to persistent epithelial defects and neurotrophic keratopathy

Based on the Holland & Schwartz classification and the Liesegang scheme, HSK is categorised by the anatomical layer involved and the underlying mechanism (infectious vs. immune-mediated).

1. Epithelial Keratitis (Infectious)

Dendritic keratitis: The most common and pathognomonic form. A branching (dendritic) epithelial ulcer with characteristic terminal end bulbs; stains with fluorescein (ulcer base) and rose bengal/lissamine green (devitalised margins)
Geographic keratitis: An enlarged, amoeboid ulcer resulting from coalescence of dendritic lesions; occurs with prolonged or inadequately treated disease; may be exacerbated by topical steroids

2. Stromal Keratitis (Inflammatory)

Immune (non-necrotising) stromal keratitis / Disciform keratitis: The most common form of stromal disease. Disc-shaped area of stromal oedema, typically without active epithelial ulceration; caused by immune-mediated hypersensitivity to viral antigens; Wessely immune ring may be present
Necrotising stromal keratitis: A rare but severe form with active viral replication in the stroma; characterised by stromal infiltration, necrosis, thinning, and high risk of perforation; requires combined antiviral and careful steroid management

3. Endotheliitis

Disciform endotheliitis: Localised corneal oedema with a disc of KPs; the most common subtype
Diffuse endotheliitis: Diffuse corneal oedema with scattered KPs and raised IOP; may mimic acute angle-closure glaucoma
Linear endotheliitis: KPs in a linear pattern progressing across the endothelium; rare

4. Neurotrophic Keratopathy

Consequence of reduced corneal sensation from recurrent HSV damage to corneal nerves; results in persistent epithelial defects, corneal thinning, and ulceration unrelated to active viral replication

5. Mixed Pattern

Combined epithelial and stromal involvement occurring concurrently; requires careful individualised management

Host-Related Factors

Prior HSV infection: Essential prerequisite for recurrent ocular disease; a history of herpes labialis increases risk
Immunocompromise: HIV/AIDS, organ transplantation, haematological malignancies, systemic corticosteroid therapy — associated with increased severity, atypical presentation, and resistance to antivirals
Atopic disease: Atopic dermatitis is associated with increased susceptibility to herpetic infections including eczema herpeticum
Age: Bimodal distribution; children (primary) and middle-aged to older adults (recurrent); no significant sex predilection

Ocular and Iatrogenic Factors

Contact lens wear: May induce reactivation through mechanical trauma and hypoxia
Ocular surgery: Corneal transplantation, refractive surgery (LASIK/PRK), and cataract surgery can precipitate recurrence
Ocular trauma: Corneal abrasion or injury may trigger reactivation
Topical steroids without antiviral cover: Significant risk of exacerbating epithelial disease and converting to geographic ulceration

Environmental and Systemic Factors

UV exposure: Sunlight and UV radiation are recognised reactivation triggers
Febrile illness: Systemic infections with high fever may precipitate recurrence
Psychological stress: Emotional and physical stress are consistently reported triggers

Epithelial Signs

Dendritic ulcer: Branching epithelial ulcer with terminal end bulbs — pathognomonic of HSV epithelial keratitis; positive fluorescein staining of ulcer base and rose bengal staining of margins
Geographic ulcer: Large, amoeboid-shaped epithelial defect arising from coalescent dendritic lesions; may have scalloped edges
Conjunctival injection: Unilateral; often mild to moderate in recurrent disease
Vesicular lid lesions: More characteristic of primary HSV infection; periorbital vesicles on an erythematous base

Stromal Signs

Disciform stromal oedema: Central or paracentral disc of stromal thickening with overlying epithelial oedema; hallmark of immune stromal (disciform) keratitis
Stromal infiltrates: White/grey opacities within the stroma; may be focal, multifocal, or diffuse
Wessely immune ring: A ring-shaped stromal precipitate around a central clearing; represents antigen-antibody complex deposition
Stromal neovascularisation: Deep stromal vessel ingrowth; a sign of chronic or recurrent disease
Stromal thinning: Indicates necrotising stromal involvement; risk of perforation in severe cases

Endothelial and Anterior Chamber Signs

Keratic precipitates (KPs): Fine or medium-sized KPs in a disc distribution (endotheliitis); may be mutton-fat KPs if associated with granulomatous inflammation
Corneal oedema: Endothelial decompensation leading to epithelial and stromal oedema
Anterior uveitis: Flare and cells in the anterior chamber; often associated with stromal and endothelial disease
Elevated intraocular pressure: Trabeculitis from viral antigen deposition; can mimic acute glaucoma

Other Signs

Reduced corneal sensation (hypoesthesia): A hallmark of HSK; tested with a cotton-wool wisp or Cochet-Bonnet aesthesiometer; may be the only finding in early or recurrent disease
Corneal scarring: Subepithelial or stromal opacities indicating prior episodes; may progress with each recurrence
Follicular conjunctivitis: More commonly seen in primary herpetic disease

Common Symptoms

Ocular pain or discomfort: Typically unilateral; may be mild to moderate in epithelial disease; more severe with stromal or endothelial involvement
Foreign body sensation: Gritty or scratchy feeling due to epithelial disruption
Photophobia: Particularly prominent with associated anterior uveitis or significant epithelial involvement
Epiphora (tearing): Reflex lacrimation in response to corneal irritation
Blurred vision: Present when the lesion involves the visual axis or with significant stromal oedema
Redness: Unilateral conjunctival and ciliary injection

Symptoms in Primary vs. Recurrent Disease

Primary infection: May include periorbital vesicular rash, eyelid oedema, preauricular lymphadenopathy, and systemic symptoms (low-grade fever, malaise)
Recurrent disease: Typically lacks systemic features; may present with a prodromal tingling or itch around the eye; often a history of prior episodes; may have paradoxically reduced pain due to corneal hypoesthesia

Clinical note: Patients with significant corneal hypoesthesia from recurrent HSK may present with minimal pain despite extensive corneal pathology. A low threshold for examination is warranted in patients with a history of HSK, even if symptoms appear mild.

Corneal Complications

Corneal scarring: Progressive with each episode of stromal keratitis; the primary cause of visual loss in HSK
Stromal neovascularisation: Deep corneal vessel ingrowth secondary to chronic inflammation; increases risk of rejection after corneal transplantation
Persistent epithelial defect: Failure of epithelial healing, often related to neurotrophic keratopathy
Neurotrophic keratopathy: Impaired corneal sensation leading to poor epithelial healing and recurrent breakdown
Corneal perforation: A rare but vision-threatening complication of severe necrotising stromal keratitis; requires emergency ophthalmology management
Corneal thinning (ectasia): Structural weakening in the setting of necrotising disease or prolonged inflammation

Intraocular Complications

Anterior uveitis (iridocyclitis): May occur independently of or alongside keratitis; risk of posterior synechiae and cataract
Elevated intraocular pressure / trabeculitis: Viral antigen deposition in the trabecular meshwork; risk of secondary glaucoma with repeated episodes
Cataract: Secondary to recurrent uveitis or prolonged topical steroid use
Secondary bacterial or fungal superinfection: Compromised epithelial barrier predisposes to opportunistic infection

Developmental Complications

Amblyopia: In children with central corneal scarring or prolonged monocular patching; requires prompt management to prevent permanent visual deprivation

Associated Systemic Conditions

Herpes labialis (oral HSV-1): A history of cold sores is present in many patients with recurrent HSK; both share the same trigeminal ganglion reservoir
HIV/AIDS and immunodeficiency: Associated with increased frequency of recurrence, bilateral disease, atypical clinical presentation (giant geographic ulcers, treatment-resistant disease), and acyclovir-resistant strains
Atopic dermatitis: Increased susceptibility to herpetic infections; risk of eczema herpeticum (Kaposi varicelliform eruption), a widespread cutaneous HSV infection on eczematous skin
Organ transplantation and immunosuppressive therapy: Systemic immunosuppression markedly increases risk of severe, bilateral, and treatment-resistant HSK
Malignancy and haematological conditions: Chemotherapy-related immunosuppression; HSK may indicate underlying immune dysfunction

Systemic Complications of HSV

Herpetic encephalitis: A rare but life-threatening complication of HSV-1 dissemination; should be considered in immunocompromised patients presenting with neurological symptoms alongside HSK
Neonatal HSV (HSV-2): Neonatal exposure during vaginal delivery from a mother with active genital HSV-2 infection; can cause disseminated neonatal herpes with ocular involvement; an ophthalmology emergency
Recurrent HSV and psychological impact: The chronic recurrent nature of HSK can have significant impact on quality of life, driving long-term antiviral prophylaxis decisions

Systemic workup consideration: In patients presenting with severe, bilateral, or treatment-resistant HSK, consider screening for underlying immunodeficiency (HIV, haematological malignancy, organ transplant history) and refer to the relevant specialist where indicated.

Clinical Diagnosis

HSK is primarily a clinical diagnosis based on history and slit-lamp findings. Laboratory investigations are reserved for atypical or refractory cases.

History: Prior episodes of HSK or herpes labialis; relevant triggers; immunosuppressive medications; contact lens wear; recent surgery or trauma
Slit-lamp examination: The cornerstone of diagnosis; assess for dendritic/geographic ulceration, stromal oedema, KPs, AC reaction, and corneal sensation

Staining Techniques

Fluorescein sodium: Stains the ulcer base (epithelial defect) green under cobalt blue light; outlines the dendritic pattern; also highlights corneal oedema (pooling pattern in stromal disease)
Rose bengal or lissamine green: Stains devitalised and damaged epithelial cells at the margins of the dendrite; particularly useful for defining the extent of the lesion and identifying early or subtle disease

Corneal Sensation Testing

Cotton-wool wisp test: A simple bedside test; compare sensitivity between the two eyes and across different corneal quadrants
Cochet-Bonnet aesthesiometer: Quantitative assessment of corneal sensation; the gold standard for documenting hypoesthesia; useful for monitoring disease progression

Laboratory and Ancillary Investigations

Reserved for atypical presentations, immunocompromised patients, or cases not responding to standard antiviral treatment:

Polymerase chain reaction (PCR): The gold standard confirmatory test; performed on corneal scraping, conjunctival swab, or tear film; highly sensitive and specific; useful for distinguishing HSV from VZV, Acanthamoeba, and other causes
Viral culture: Low sensitivity (<50%); rarely performed in routine clinical practice but may identify acyclovir-resistant strains
Impression cytology: Identifies viral inclusions and multinucleated giant cells (Tzanck cells) in epithelial scrapings; not widely used
Anterior segment OCT (AS-OCT): Useful for quantifying stromal oedema, thinning, and detecting subtle endothelial pathology
Intraocular pressure measurement: Essential when endotheliitis or trabeculitis is suspected; elevated IOP without other obvious cause warrants consideration of herpetic aetiology

1. Epithelial Keratitis

Topical antiviral (first-line):
- Acyclovir 3% ophthalmic ointment — 5 times daily for 10 days
- Ganciclovir 0.15% ophthalmic gel — 5 times daily for 7 days (until healed), then 3 times daily for 7 days
- Both are equivalent in efficacy; ganciclovir gel has improved patient tolerability
Avoid topical steroids: Contraindicated in active epithelial disease; may enlarge ulcer and convert dendritic to geographic pattern
Lubricants: Preservative-free artificial tears for symptomatic relief
Cycloplegia: Consider cyclopentolate 1% or homatropine 2% if associated anterior uveitis is present
Débridement: Gentle removal of infected epithelial cells; adjunct to topical antivirals; not routinely required
Discontinue contact lens wear until resolution and review

2. Immune (Non-Necrotising) Stromal Keratitis

Topical corticosteroid (under antiviral cover): Prednisolone acetate 1% eye drops; starting dose varies by severity (e.g., 4–8 times daily); gradual taper over weeks to months based on clinical response
Mandatory topical antiviral prophylaxis while on steroid: Acyclovir 3% ointment 3–5 times daily throughout the course of steroid treatment
Monitor IOP: Steroid-induced IOP rise; monitor regularly during treatment
Cycloplegia: If associated uveitis present

3. Necrotising Stromal Keratitis

Oral antiviral: Acyclovir 400 mg five times daily or valacyclovir 500–1000 mg twice daily; systemic antivirals provide better tissue penetration for stromal disease
Topical antiviral: Acyclovir 3% ointment as adjunct
Cautious use of topical steroids: May be required for immune-mediated component but must be used judiciously given active viral replication; requires close ophthalmology supervision
Urgent ophthalmology referral: For monitoring of thinning, risk of perforation, and consideration of tissue adhesive or tectonic keratoplasty if needed

4. Endotheliitis

Combined topical steroid and antiviral: Prednisolone acetate 1% with topical acyclovir 3% ointment simultaneously
Oral antiviral: Consider oral acyclovir or valacyclovir for moderate-to-severe endotheliitis
IOP management: Topical IOP-lowering agents (beta-blockers, carbonic anhydrase inhibitors) if trabeculitis-associated IOP elevation is present; avoid prostaglandins in active disease

5. Recurrence Prophylaxis (HEDS Trial)

HEDS Trial Evidence: The Herpetic Eye Disease Study demonstrated that long-term oral acyclovir 400 mg twice daily reduces the rate of recurrent HSV stromal keratitis by approximately 50% over 12 months. This is the evidence base for long-term antiviral prophylaxis in patients with frequent recurrences.

Oral acyclovir 400 mg twice daily: Standard prophylactic regimen; generally well-tolerated; indicated after 2 or more episodes of epithelial keratitis or one episode of stromal disease within 12 months
Oral valacyclovir 500 mg once daily: An alternative with improved bioavailability and once-daily dosing; increasing clinical preference
Duration: Typically 12 months minimum; long-term prophylaxis may be considered in patients with frequent recurrences or significant prior corneal damage

Treatment Summary Table

Disease Type	First-Line Treatment	Key Caution
Dendritic/Geographic keratitis	Topical acyclovir 3% or ganciclovir 0.15%	Avoid topical steroids
Immune stromal keratitis	Topical steroid + topical antiviral cover	Never use steroid without antiviral cover
Necrotising stromal keratitis	Oral antiviral + cautious topical steroid	Urgent ophthalmology; risk of perforation
Endotheliitis	Topical steroid + antiviral ± oral antiviral	Monitor IOP; avoid prostaglandins
Recurrence prophylaxis	Oral acyclovir 400 mg BD or valacyclovir 500 mg OD	Minimum 12 months; reduces recurrence by ~50%

Refer to Ophthalmology for:

Urgent referral:

Necrotising stromal keratitis with thinning or risk of perforation
No improvement after 7–10 days of appropriate antiviral therapy
Suspected secondary bacterial or fungal superinfection
Immunocompromised patient with progressive or atypical disease
Acute IOP elevation with corneal oedema

Routine referral:

First episode of stromal or endothelial disease (for co-management)
Recurrent HSK causing progressive corneal scarring
Consideration of long-term antiviral prophylaxis in recurrent disease
Corneal transplantation assessment

Singapore Optometry Scope Note: Optometrists in Singapore may clinically diagnose herpes simplex keratitis and initiate emergency ophthalmology referral. Therapeutic-endorsed optometrists (holding Schedule 1 or Schedule 2 authorisation under the Optometrists and Opticians Act) may prescribe topical antivirals (acyclovir 3% ointment, ganciclovir 0.15% gel) for epithelial disease. Management of stromal keratitis, endotheliitis, and neurotrophic keratopathy — including steroid prescription, dose titration, and corneal scraping — requires ophthalmology co-management or referral.

Visual Prognosis by Disease Type

Epithelial keratitis: Excellent with prompt antiviral treatment; heals within 1–2 weeks; minimal or no corneal scarring with appropriate management
Immune stromal keratitis: Good if treated early and adequately; risk of cumulative stromal scarring and neovascularisation with each recurrence; vision may deteriorate over time in patients with multiple episodes
Necrotising stromal keratitis: Guarded; significant risk of permanent stromal scarring, irregular astigmatism, and visual loss; may require corneal transplantation
Endotheliitis: Generally good with treatment; however, repeated episodes can result in endothelial cell loss and corneal decompensation
Neurotrophic keratopathy: Variable; depends on the severity of corneal sensation loss and compliance with intensive lubrication and protective measures

Impact of Recurrence

Each episode of stromal keratitis increases the risk of cumulative corneal scarring and neovascularisation
Approximately 5% of patients with recurrent HSK develop vision-threatening complications requiring surgical intervention (corneal transplantation)
Long-term oral antiviral prophylaxis (HEDS trial) reduces stromal keratitis recurrence by ~50% and is associated with improved long-term visual outcomes
High-risk corneal grafts (those with pre-existing vascularisation from HSK) have lower success rates; antiviral prophylaxis is essential perioperatively

Factors Affecting Prognosis

Favourable factors:

Early diagnosis and treatment
Epithelial disease only (no stromal involvement)
Peripheral lesion (not involving visual axis)
Good patient compliance with antiviral therapy
Prophylaxis initiated after first stromal episode
Immunocompetent host

Poor prognostic factors:

Recurrent or bilateral disease
Central corneal involvement
Significant pre-existing corneal scarring or vascularisation
Immunocompromised status
Acyclovir-resistant HSV strains
Delayed or inadequate treatment
History of necrotising stromal keratitis

Condition	Key Differentiating Features	Distinguishing Point from HSK
Herpes Zoster Ophthalmicus (HZO)	Pseudodendrites (elevated mucous plaques, not true ulcers); dermatomal vesicular rash (V1 distribution); older patient; post-herpetic neuralgia	No terminal end bulbs; rash does not cross midline; associated VZV serology; positive PCR for VZV (not HSV)
Acanthamoeba Keratitis	Contact lens wear (often in tap water exposure); ring-shaped stromal infiltrate; severe, disproportionate pain; radial perineuritis; resistant to standard antibiotics	No dendritic pattern; extreme pain; ring infiltrate; CL history; confocal microscopy or culture confirms diagnosis
Bacterial Keratitis	Suppurative stromal infiltrate with mucopurulent discharge; dense grey-white opacity; significant anterior chamber reaction; may have hypopyon	No dendritic pattern; purulent discharge; no hypoesthesia; corneal culture positive for bacteria
Fungal Keratitis	History of vegetative or soil trauma; feathery lesion borders with satellite infiltrates; slowly progressive; may have endothelial plaque; often in agricultural workers	Feathery not dendritic; satellite lesions; endothelial plaque; positive KOH prep or culture; tropical climate association
Recurrent Corneal Erosion Syndrome	History of previous corneal trauma; map-dot-fingerprint dystrophy; spontaneous onset (often on waking); no terminal bulbs on any dendritiform lesion	No terminal bulbs; no viral staining pattern; history of trauma or ABMD; responds to lubricants not antivirals
Thyrosinaemia / Drug-Induced Keratopathy	Dendritiform pseudodendrites (e.g., from contact lens overwear, topical anaesthetic abuse, amiodarone); bilateral; no terminal bulbs; no ulceration	Often bilateral; no true terminal bulbs; no fluorescein ulcer staining; medication or CL history; no HSV on PCR
Neurotrophic Keratopathy (non-herpetic)	Persistent epithelial defect; absent or reduced corneal sensation; no active virus; may follow other causes (e.g., acoustic neuroma, trigeminal surgery, chemical burns)	No active viral replication; no dendrites; PCR negative; known underlying cause of CN V damage; antivirals not effective

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Clinical Illustration

Overview

Etiology