Advice that equates all corneal infections is convenient. It is also risky. Viral keratitis behaves differently from bacterial disease, and the response strategy must reflect that difference. I set out what actually matters for diagnosis, timely escalation, and safe recovery. The focus is practical. How to recognise patterns early, how to select therapy, and how to protect future vision.

Types of Viral Keratitis and Their Causes

Herpes Simplex Keratitis

In clinical practice, herpes simplex keratitis is the archetype. I see dendritic epithelial ulcers with terminal bulbs, reduced corneal sensitivity, and recurrent flares that follow stress or fever. The causative agent is herpes simplex virus type 1 in most adults. Type 2 can affect neonates and some adults, though less often.

Pathology typically starts in the epithelium. A dendrite appears, stains brightly with fluorescein, and respects the corneal nerves. Deeper involvement manifests as stromal keratitis. That phase brings haze, oedema, and possibly uveitis. It can threaten vision to a greater extent than the epithelial stage.

• Triggers: intercurrent illness, ultraviolet exposure, ocular trauma, or steroid use without antiviral cover.

• Clinical clues: dendritic or geographic ulcers, reduced sensation, sectoral anterior uveitis, and keratic precipitates in severe cases.

• Complications: scarring, thinning, and irregular astigmatism. In recurrences, neurotrophic keratopathy may develop.

Diagnosis is largely clinical. Polymerase chain reaction (PCR) helps when the picture is atypical. Serology is less useful for immediate decisions. I treat based on pattern recognition supported by targeted tests when uncertainty persists.

Varicella-Zoster Keratitis

Varicella-zoster keratitis follows herpes zoster ophthalmicus. The skin rash respects the ophthalmic branch of the trigeminal nerve. The cornea may show pseudodendrites that lack terminal bulbs and stain irregularly. Corneal anaesthesia can be profound. That increases the risk of epithelial breakdown.

Reactivation risk grows with age or immunosuppression. The disease spectrum is broad. From mild punctate keratitis to stromal keratitis with disciform oedema and endotheliitis. Elevated intraocular pressure may accompany inflammation.

• Hallmarks: dermatomal rash, pseudodendrites, and reduced corneal sensation.

• Late issues: neurotrophic ulcers, lipid keratopathy, and scarring that impairs best corrected visual acuity (BCVA).

• Adjunctive care: pain control and skin care are often decisive for recovery speed.

Early systemic antivirals shorten the acute course. They likely reduce the intensity of later ocular inflammation, though not all cases follow the textbook. Pain management requires equal focus.

Adenoviral Keratitis

Adenoviral keratitis emerges during or after a conjunctivitis outbreak. Follicles, preauricular lymphadenopathy, and watery discharge are typical. The cornea may show superficial punctate lesions early. Later, subepithelial infiltrates arise. Those can persist for months and fluctuate.

The infection spreads easily in households and clinics. Hygiene measures are therefore essential. I advise strict hand washing, towel separation, and surface cleaning. Steroids can ease symptoms when subepithelial infiltrates degrade vision. They must be used judiciously to avoid prolonged viral shedding.

• Common setting: community outbreaks or exposure in healthcare settings.

• Corneal impact: subepithelial infiltrates that cause glare and reduced contrast sensitivity.

• Recovery pattern: slow resolution with temporary fluctuations. Visual quality may lag behind clinical appearance.

Nummular Keratitis Features

Nummular keratitis describes small round anterior stromal infiltrates that follow viral keratoconjunctivitis. As Nummular keratitis notes, multiple tiny granular deposits can be seen on examination, and some residual scarring may remain after healing. I look for well defined subepithelial opacities under intact epithelium. The distribution can be central or paracentral.

Diagnosis can be tricky because similar patterns occur in other inflammatory keratitides. A careful history helps. Recent adenoviral conjunctivitis is a common clue. Photophobia and glare are frequent complaints.

• Key features: round subepithelial opacities, preserved epithelium, and variable impact on acuity.

• Course: recurrent or fluctuating activity over weeks to months.

• Management: topical anti inflammatory therapy balanced with the risk of delayed virus clearance.

Risk Factors for Viral Keratitis

Risk accumulates from several directions. Prior ocular herpes infection, atopy, or systemic immunosuppression raise the risk. Contact lens wear complicates the picture, mainly by masking symptoms or adding surface injury. Ocular surface disease and dry eye increase epithelial vulnerability.

Exogenous steroids without antiviral cover can reactivate latent herpes simplex keratitis. That single misstep can convert a benign case into weeks of morbidity. I monitor steroid use closely in anyone with previous viral keratitis.

• Systemic: immunosuppressive therapy, diabetes, malnutrition.

• Local: neurotrophic cornea, chronic blepharitis, previous corneal surgery.

• Environmental: ultraviolet exposure and crowded settings during adenoviral outbreaks.

Risk is cumulative. Small individual factors combine and shift the threshold for reactivation or severe disease.

Recognising Keratitis Symptoms

Early Warning Signs

The earliest signals are usually simple. Eye pain, redness, photophobia, and blurred vision are common. As Cleveland Clinic describes, these early signs cluster and should prompt swift review. I add a gritty sensation and tearing to the list. Those often bring patients in early.

• Pain or irritation that worsens with light exposure.

• Redness localised near the limbus, not just general conjunctival injection.

• Smearing or blur unresponsive to blinking or artificial tears.

These features are non specific. The pattern and tempo guide the next steps. A unilateral, light sensitive, painful eye with reduced corneal sensitivity raises suspicion for viral keratitis.

Progressive Symptoms

If untreated, the picture escalates. Stromal haze develops. Vision declines. The eye may become more sensitive to light and touch. In herpes zoster, pain can intensify even as the surface appears quiet. In adenoviral disease, subepithelial infiltrates create disabling glare.

• Corneal haze and oedema with loss of crispness in detail.

• Foreign body sensation that does not settle with lubrication.

• Reduced contrast sensitivity, especially at dusk or under glare.

Progression speed varies. Some cases worsen over days. Others over hours. That variability informs the urgency of review and possible escalation.

Differences Between Viral and Bacterial Keratitis

Feature	Viral Keratitis
Onset	Often subacute with recent systemic or ocular viral symptoms.
Pain	Variable, sometimes less than expected when corneal sensitivity drops.
Discharge	Watery or minimal mucus. Rarely purulent.
Lesion shape	Dendritic or pseudodendritic patterns, or subepithelial infiltrates.
Response to antibiotics	No meaningful improvement without antivirals or anti inflammatory treatment.

Bacterial keratitis tends to produce more purulent discharge and a focal stromal infiltrate with an overlying epithelial defect. Viral keratitis produces patterns that reflect the specific virus. The distinction directs therapy promptly.

When to Seek Emergency Care

Urgent assessment is mandatory in several situations. Rapidly declining vision, severe photophobia, or a large epithelial defect must not be watched at home. Intense pain after steroid use is another warning sign.

• Immediate review for unilateral red eye with reduced vision and photophobia.

• Emergency care for contact lens wearers with corneal opacity or severe pain.

• Same day review for any suspected dendrite or geographic ulcer.

Time matters. Each hour without appropriate therapy can deepen scarring or trigger complications. Safe care prioritises early diagnosis over reassurance.

Keratitis Treatment Options

Antiviral Medications

Antivirals are the core of keratitis treatment when the aetiology is viral. In epithelial herpes simplex keratitis, I prescribe topical or systemic antivirals depending on severity and adherence considerations. Oral aciclovir or valaciclovir are common choices. Topical ganciclovir gel is useful for local disease.

• Herpes simplex epithelial disease: topical antiviral or oral therapy for 7 to 14 days.

• Stromal disease: systemic antiviral cover alongside anti inflammatory control.

• Varicella zoster: early systemic antivirals, ideally within 72 hours of rash onset.

Dosing must be precise. Under dosing encourages persistence. Overuse invites toxicity. I adjust by renal function and clinical response. It is basically pharmacology and close follow up.

Topical Corticosteroids

Topical corticosteroids reduce inflammation in stromal keratitis and endotheliitis. They improve haze and oedema. Steroids are contraindicated in active epithelial herpes simplex keratitis without antiviral cover. That rule is strict.

• Indication: stromal inflammation with intact epithelium and sufficient antiviral cover.

• Taper: slow and deliberate to prevent rebound inflammation.

• Monitoring: intraocular pressure and signs of reactivation.

Where adenoviral subepithelial infiltrates limit function, a cautious steroid course may help. I use the lowest effective dose. Then taper with close review. Balance is everything.

Supportive Care Measures

Supportive care protects the surface and comfort. Lubrication, cycloplegia, and lid hygiene matter. Pain control requires attention, especially in zoster. Cold compresses help photophobia briefly. I avoid contact lenses until full epithelial recovery.

• Frequent preservative free lubricants during the acute phase.

• Cycloplegics when ciliary spasm drives pain.

• Antibiotic prophylaxis when epithelial defects increase infection risk.

In neurotrophic cases, I consider autologous serum tears or amniotic membrane. Those support epithelial integrity. Small measures prevent big complications.

Treatment for Herpes Simplex Keratitis

I tailor herpes simplex keratitis therapy to the anatomical layer involved. Epithelial disease receives antiviral therapy without steroids. Stromal disease requires steroids with antiviral cover. In endotheliitis, I add stronger anti inflammatory therapy and monitor pressure.

1. Confirm the pattern: dendritic ulcer, geographic ulcer, stromal haze, or endotheliitis.

2. Initiate antiviral therapy: topical or oral, adjusted to severity and adherence.

3. Add steroid for stromal or endothelial involvement with strict tapering.

4. Protect the surface: lubricants, punctal occlusion if dryness is evident.

5. Schedule close follow up to confirm re epithelialisation and resolution of haze.

PCR is reserved for atypical or unresponsive cases. It clarifies the pathogen and guides escalation. Most cases respond to first line therapy when applied early.

Managing Recurrent Episodes

Recurrent viral keratitis is common. Prophylaxis reduces flare frequency. In herpes simplex, oral antiviral prophylaxis over months lowers recurrence risk. The decision is individual. I weigh flare frequency, scarring risk, and patient preference.

• Trigger control: manage dry eye, sleep deprivation, and ultraviolet exposure.

• Medication plan: long term antiviral prophylaxis in high risk recurrent disease.

• Education: early presentation if a new dendrite or photophobia appears.

For adenoviral sequelae like nummular keratitis, periodic low dose anti inflammatory therapy may help. I taper cautiously to prevent dependence. Some residual glare may persist for a period.

Surgical Interventions

Surgery is rare but sometimes necessary. Non healing epithelial defects may need amniotic membrane grafts or tarsorrhaphy. Deep scarring after multiple flares may require keratoplasty. Timing is critical.

• Amniotic membrane for persistent epithelial defects with neurotrophic changes.

• Anterior stromal puncture for recurrent erosions in selected cases.

• Keratoplasty for visually significant scarring after disease quiescence.

I wait for disease inactivity before elective grafting. Otherwise the graft risks reactivation and rejection. Patience preserves outcomes.

Living with Viral Keratitis

Life after viral keratitis demands routine and vigilance. I recommend protective habits that are simple and sustainable. Consistency keeps recurrences in check and reduces anxiety.

• Hygiene: wash hands, avoid eye rubbing, and clean pillowcases during active episodes.

• Optics: update spectacles after scarring shifts refraction. Consider rigid lenses if irregular astigmatism persists.

• Surface care: treat blepharitis, control dry eye, and maintain lid hygiene daily.

• Work and screens: schedule regular breaks to reduce surface stress and glare.

• Travel kit: lubricants, sunglasses, and a written treatment plan for emergencies.

Psychological load is real. Recurrent disease undermines confidence. A clear action plan helps. Who to call, how fast to attend, and what first steps to take. Clarity reduces fear and delays.

Two brief examples illustrate this. A photographer with recurrent herpes simplex keratitis used daily lid hygiene and seasonal antiviral prophylaxis. Flares reduced from four per year to one. A teacher with adenoviral nummular keratitis managed glare with anti reflective lenses and controlled steroids. Classroom performance and comfort improved markedly.

Good routine becomes quiet insurance. It protects the cornea and restores control.

Frequently Asked Questions

Can viral keratitis spread to both eyes?

Yes, though patterns differ by virus. Adenoviral disease can involve both eyes, often sequentially. Herpes simplex keratitis is usually unilateral. Bilateral involvement occurs, but less often, and usually in severe or immunocompromised cases.

• Hygiene reduces the risk of self inoculation.

• Avoid contact lenses and eye rubbing during active episodes.

• Follow the antiviral plan precisely to shorten the infectious phase.

In practice, careful hygiene and early review limit bilateral spread. That is the target.

How long does viral keratitis take to heal?

Timeframes vary. Epithelial herpes simplex keratitis often heals in 1 to 2 weeks on therapy. Stromal disease takes longer. Adenoviral subepithelial infiltrates may linger for months, though symptoms ease earlier.

• Epithelial healing: days to a fortnight, depending on lesion size.

• Stromal clarity: several weeks to months for haze to settle fully.

• Residual symptoms: glare and contrast loss may outlast clinical signs.

Roughly speaking, the surface recovers before visual quality fully returns. Patience and tapering prevent rebound.

Is viral keratitis contagious to others?

Adenoviral keratitis is contagious to others, especially early. Herpes simplex keratitis is not easily passed by casual contact, though shared towels or direct contact pose a risk. Varicella zoster is transmissible to non immune individuals as chickenpox.

• Do not share towels, cosmetics, or pillowcases during the acute phase.

• Clean hands and surfaces thoroughly after eye care.

• Discuss isolation measures if working in a clinical or childcare environment.

The aim is sensible precautions. Not alarm. Targeted hygiene is effective.

Can children get viral keratitis?

Children can develop viral keratitis from adenovirus, varicella zoster, and less often herpes simplex. Presentation may be less specific. Photophobia and irritability may be prominent. Examination can require patience and, rarely, sedation for procedures.

• Paediatric dosing of antivirals must be weight based.

• Hydration and pain control are priorities in recovery.

• Household hygiene reduces family spread during adenoviral outbreaks.

Parents benefit from a written plan. That reduces repeat visits and improves adherence.

What happens if viral keratitis is left untreated?

Untreated viral keratitis can progress to scarring, thinning, and compromised vision. Stromal disease may cause long term irregular astigmatism. Neurotrophic ulcers can form. Secondary infection remains a risk where the epithelium is absent.

• Vision loss may become permanent if scarring is central and dense.

• Chronic discomfort and photophobia can impair daily function.

• Surgery may be required, with variable outcomes and additional risk.

Prompt assessment averts most of these outcomes. Early action protects the cornea and preserves options.