Viral Keratitis

Presenter: Dr Sahil Thakur

Moderator: Professor Sudesh Arya

INTR

OD

UC

TIO

N• Infective keratitis is suppurative infection of cornea

which may be associated with epithelial defects and orsigns of inflammation.

• Worldwide 45 million blind

• 1.5-2.0 million blind due to corneal diseases addedevery year.

• Prevalence of corneal blindness (<6/60 in worse eye) inIndian population is 0.66% i.e (one out of every 150people in India)

• In India ,incidence of corneal ulcer is 113 per 100,000 per year i.e. 8,40,000 corneal ulcers develop annually in India.

BJO 2003;87:133-141

VIR

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Y • Viral keratitis is the commonest cause of keratitis inthe developed world.

• The virus can infect individual layers of the cornea orin more severe form it may involve all the layers ofcornea.

• The various viral infections that can affect the corneacan be broadly grouped under the followingcategories herpes simplex keratitis, varicella zosterinduced keratitis and the adenoviral keratitis.

HSV

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• The global incidence of HSV keratitis is roughly 1.5million, including 40,000 new cases of severemonocular visual impairment or blindness each year.Farooq, A. V., & Shukla, D. (2012). Herpes Simplex Epithelial and Stromal Keratitis: An Epidemiologic Update. Survey of Ophthalmology, 57(5), 448–462.

HSV

KER

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IS• Herpes simplex virus is a large and complex enveloped

virus measuring 150-200 nm.

• It has a double stranded DNA core, which is surrounded by a protein capsid that is made up of 162 subunits called capsomer.

• The capsid is surrounded by the tegument, membrane of the infected cell that has been altered by virus-induced proteins.

• Humans are the only natural reservoirs of herpes.

• The sources of infection are by direct contact with infected lesions, by salivary droplets or fomites from children and adults with active disease and also of asymptomatic virus shedding carriers.

HSV

KER

ATIT

IS• The most common type of herpes simplex virus is HSV-1

which causes cold sore or fever blister in the mouth, face and upper body and may affect the eye.

• HSV-2 causes genital herpes, a sexually transmitted disease. Ocular herpes is caused primarily by HSV-1 and occasionally by HSV type-2 virus.

HSV

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• The main route of HSV spread is viadirect contact.

• Ocular infection can occur as primaryor recurrent episodes.

• HSV epithelial keratitis begins as asuperficial punctate lesion, progressingto a stellate erosion and, finally, adendritic ulcer.

• HSV stromal keratitis is thought tooccur more commonly in recurrences.

• The morbidity in stromal disease isthought to result from CD4+ T-celldestruction in the inflammatoryresponse to the virus, in addition todirect viral effects.

HSV

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•Congenital

•Neonatal

•Primary Ocular HSV

•Recurrent Ocular HSV

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HSV

KER

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IS • HSV-1 and HSV-2 can be acquired in utero,by transplacental or ascending infection,by exposure to genital lesions duringdelivery, or postnatally from relatives orattendants.

• Of all the neonatal HSV, 4 percent isacquired during intrauterine life, 86percent infection occurs at the time ofbirth and remaining 10 percent occurs inthe postnatal period.

• Congenital HSV infection is characterizedby the triad of skin vesicles, eye diseaseand microencephaly.

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• Neonatal HSV infection usually presents as a bilateraldisease at 2 days to 2 weeks of age.

• HSV keratitis in a neonate is invariably associated withconjunctivitis.

• Keratitis may manifest as diffuse microdendritis,serpiginous epithelial defects or a punctate keratitis.

• The diagnosis of ocular HSV must be considered in anyinfant with nonpurulent conjunctivitis or keratitis.

• Treatment of neonatal ocular herpetic disease comprises oftopical antivirals (1% Trifluridine ophthalmic solution or 3%acyclovir ophthalmic ointment) in addition to systemicAcyclovir (2 g/day IV every 8 hourly for 14 days).

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SV• Atypical presentation

• Unilateral blepharoconjuctivitis

-Follicular conjuctivitis

-Skin or eyelid vesicles

• Epithelial keratitis

• Stromal keratitis is rare.

• Primary ocular herpes (1st encounter with virus) should not be confused with First ocular occurrence (1st eye involvement with HSV in a patient who has subclinical infection and is immune)

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HSV

• Reactivation of virus in latently infected sensory ganglion.

• Patients have both cellular and humoral immunity against virus.

• It can present in any one of the combinations:

Blepharoconjuctivitis Episcleritis, Scleritis

Corneal keratitis:

• Epithelial keratitis

• Infectious ulcerative

• Trophic (Metaherpatic) ulceration

Stromal keratitis:

• Necrotizing keratitis

• Non necrotizing keratitis

• Disciform

• Diffuse

• Linear

EndotheliitisIridocyclitis and

Trabeculitis

•Clinical disease develops in less than 1 % of population infected with virus

•Corneal scarring occurs in 18% - 28%.

•Corneal disease is broadly divided into:

oEpithelial

oStromal

oEndothelial

CLI

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• Involved in two- third of cases.

• Earliest lesion- fine or coarse granular spots with epithelialbedewing forming a punctuate epithelial keratopathy.

• Within 12-24 hours cell nuclei become laden withreplicating virus and infected cell swells up prior to releasingthe virus into adjacent areas.

EPIT

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•Clinically manifests first as araised dendritiform lesionthat displaces fluorescein toproduce ‘negative staining’but stains with RoseBengal.• This progress to destruction

of Bowman’s Membrane and forms dendritic ulcer.(base stains with fluorescein)

EPIT

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• Characteristic branching linear shape with large terminal bulbs and swollen epithelial borders.

• Epithelial borders are areas of epitheliolysis that stain negative with fluoresceinbut can be demarcated with Rose Bengal or LissamineGreen.

• Enlargement of ulcer leading to Geographic (amoeboid) ulcer in upto 22% of all cases.

Amoeboid ulcer

EPIT

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• Patients with Marginal or Limbal herpetic ulcers are more symptomatic and less responsive to treatment. Resembles staphylococcal catarrhal ulcer.

• Epithelial disease usually resolves, sequelae may ensue such as a persistent punctate epithelial keratopathy, recurrent corneal erosions orepithelial granularity.

EPIT

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Persistent Punctate Epithelial Keratopathy

Recurrent Corneal Erosion

Persistent Epithelial Defect

• Secondary bacterial infection of ulcer may occur- many features may no longer be recognized

• Impairment of corneal sensation neurotrophic keratopathy with loss of corneal lustre and irregularity of corneal surface

• Punctate epithelial erosions may develop and progress to persistent epithelial or metaherpatic ulcer with shallow smooth borders of grey, elevated, thickened and rolled epithelium. It shows ‘reverse staining’.

• It is not associated with live virus.

EPIT

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• Accounts for 2% of initial presentation and 20-48% of recurrent herpetic disease.

• Viral invasion of stroma, either from reactivation of latent virus from direct invasion from epithelium in the supplying sensory nerves.

• Or from reactivation of latent virus within stroma together with marked immune response produce stromal keratitis.

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•Necrosis, ulceration and dense infiltration of stroma usually with an overlying epithelial defect

•HSV-1 antigens and HSV DNA are present.

•Grayish white homogenous abscesses with edema, KPs, severe iridocyclitis and raised IOP.

• Super added infection may lead to thinning and perforation.

NEC

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• Occurs in 20%.

• There may be no history of previous symptomatic epithelial keratitis and epithelium is usually intact.

• Focal, multifocal or diffuse.

• May have associated anterior uveitis.

• Chronic, recurrent or leading to stromal scarring, thinning, neovascularisation and lipid deposition.

• Occasionally an immune ring is present.

• Marginal keratitis or limbitis is usually accompanied by inflammatory or immune response.

• Stromal neovascularisation may be sectoral or diffuse.

NO

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• Disc-shaped area of stromal edema in the central or par central cornea.

• Usually involving the entire stromal thickness giving a ground glass appearance.

• KPs are present underlying the areas of stromal edema.

• Mild to moderate iritis is usually present.

DIS

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• Diffuse stromal edema with underlying KPs.

• Mild-to-moderate iritis.

• Dense retro corneal plaque of inflammatory cells may follow.

DIF

FUSE

KER

ATIT

ISLI

NEA

R K

ERAT

ITIS • Appears as a serpiginous line of

KPs, that progresses centrally from the limbus.

• Accompanied by peripheral stromal and epithelial oedema.

Schwab et al, Interstitial Linear Keratitis, AJO, 1999.

•Progressive Endotheliitiswith or without uveitis may be associated with dendritic ulceration, disciform edema or marked elevation of IOP

•Pure HSV Endotheliitis is characterized by line of KPs demarcating edematous and non-edematous corneal zones.

END

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• Recurrent non granulomatous HSV iridocyclitis may occur without known prior keratitis or without concomitant keratitis.

• Due to inflammation caused either by reaction to viral antigen in the iris or by irritative effects of keratitis.

• Circumlimbal ciliary flush, KPs, cells and flare in aqueous.

• Multiple recurrence: diffuse iris atrophy, posterior synechiae.

• High intraocular pressure is a common complication of HSV iritis and can serve as a diagnostic hallmark.

• High IOP is due to trabeculitis, as well as inflammatory cells clogging the trabecular meshwork.

• Although antiglaucoma therapy may be required in the acute setting, once the inflammation is controlled, typically the intraocular pressure will normalize and the patient will not require ongoing antiglaucomatreatment.

IRID

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Candy Cane Hypopyon

•Clinically active disease.

•Cutaneous lid or corneal lesions are typical.

•Laboratory tests are aimed at :oCell cytologyoViral antigen detection(Immunoassays)oViral DNA detection(PCR)oVirus isolation(Tissue Culture)

DIA

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Progress in Retinal and Eye Research 25 (2006) 355–380

DIA

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•Fever

•UV light

•Systemic illness, surgery

•Menstruation

•Minor local trauma

•Immunosuppression

•Contact Lens Use

REA

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Arch Ophthal 2000:118:1617-1625

•Prior to HEDS the standard therapy for all forms of HSV keratitis was topical antivirals.

• The HEDS was undertaken to assess the effect of adding steroids and acyclovir to conventional therapy with trifluridine.

• It was a prospective, randomized, double masked, placebo controlled, multicentric study derived into six trials: three therapeutic, two preventive , and 1 cohort.

HED

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• Topical steroids: 1% Prednisolone

•Mannitol/Glycerol/Acetazolamide for acute IOP control

•Non prostamide analog antiglaucoma:Brimonidine or a Beta blocker

•Cycloplegics

•Acyclovir 400mg BD

• Topical antibiotic ointment at bedtime

•Artificial tears

SEC

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•HSV Non Necrotizing stromal keratitis can be treated with topical cyclosporine and acyclovir ointment.

• Treatment of HSV stromal keratitis unresponsive to topical prednisolone 1% with topical cyclosporine 0.05% has also been demonstrated in case series.R

OLE

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Graefe's Arch Clin Exp Ophthalmol, May, 1999.

AJO 2006,141,771-772.

• Topical interferon alpha-2a appears to be an effective treatment adjunct for refractory herpes simplex keratitis.

•Actipol (0.007% paraaminobenzoic acid) is a new interferon inductor. The reparogenic effect on the corneal stroma and antithrombotic, fibrinolytic, and antioxidant activity attributed to PABA.

• Effective drug for the treatment of stromal herpetic keratitis

•No side effects.

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Cornea, May, 2000.

Vestn Oftalmol. 2000 Jan-Feb;116(2):16-8.

• The first antivirals, idoxuridine and vidarabine, seem better than no treatment in healing HSV dendritic keratitis within two weeks.

• Topically applied trifluridine, acyclovir, or brivudine are better and safer than idoxuridine, cure about 90% of treated eyes within two weeks, and have no significant differences in effectiveness. The evidence is conflicting whether ganciclovir is as good as or better than acyclovir.

• Interferon, a natural part of the immune system that can be given as an eye drop, is active against HSV infection of the cornea.

• The integrated use of interferon and an antiviral drug might be slightly better than an antiviral drug by itself.

• Another treatment is to debride, but debridement followed by an antiviral drug is not consistently better than just an antiviral medication.

• Lateral tarsorrhaphy adjunctively with a therapeutic lens

• Lamellar keratoplasty

•Conjunctival flap

•Penetrating keratoplasty

SUR

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Surv Ophthalmol. 2012 Sep; 57(5): 448–462.

•HSV is one of the most important indication for repeat PKP’s after primary graft failure.

•Procedure of choice for visual restoration of significantly scarred or chronically inflamed herpetic eyes

•Higher post op complications:more corneal vascularisation, more epithelial defects, lower corneal sensitivity, more graft rejection episodes, and require larger grafts

Br J Ophthalmol. 2002 Jun;86(6):646-52

•Return of corneal sensitivity negligible

• Incidence of recurrence of keratitisPEN

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•Use of fine, interrupted sutures.

•Use of intensive postoperative topical steroids.

•Oral acyclovir prophylaxis for 12-18 months.

•Administration of full antiviral prophylaxis during intensive topical steroid therapy for graft rejection.

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• Once a visually disabling corneal scar occurs options for improving vision are limited to surgery either in the form of penetrating or lamellar keratoplasty or rarely photo keratectomy.

• Recurrence after PK -12% to 27%

• Incidence of newly acquired HSV keratitis after PK is 14 fold higher than in the general population.

• Antiviral prophylaxis translates to treatment postoperatively.

• Both topical and systemic antivirals have led to a significant reduction in post-transplant recurrence of HSK.

REC

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• It reviews three trials, current up to 2016, involving 126 participants, comparing the use of oral acyclovir to no treatment or placebo.

• People in the studies either took antiviral medication for six months after the corneal graft surgery or they took a placebo (or no treatment).

• The antiviral medication was oral acyclovir in all three studies but the dose varied from 200 to 800 mg/day.

• The review concludes that oral acyclovir may lower the chance of herpetic keratitis (low-certainty evidence). It may also reduce the risk of graft failure (low-certainty evidence).

• Based on data from the included trials, this corresponds to approximately 23 fewer cases of HSK recurrence per 100 corneal graft operations if oral acyclovir is used. This also corresponds to approximately 13 fewer cases of graft failure per 100 corneal graft operations if oral acyclovir is used.

•Amniotic membrane transplantation can be used in severe neurotrophiccorneal ulcers.

•AMT promotes rapid epithelialization and reduces stromal inflammation and ulceration in HSV-1 keratitis.

Br J Ophthalmol. 2000 Aug;84(8):826-33

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• Study to evaluate Quality of Life (QoL) in 33 patients with a unilateral and relapsing herpes simplex keratitis (HSK group) that was quiescent during evaluation (no acute episode in the past 3 months) and compared with 66 patients with no history of HSK.

• Even during a quiescent phase of the disease, unilateral and relapsing HSK significantly impairs the QoL of patients to a similar level as most sight-threatening diseases.

• The decrease of VA has the greatest overall effect, but other factors also significantly affect QoL, such as the frequency of relapses.

Ophthalmology 2017;124:160-169

• The wide use of acyclovir for the treatment of genital, orofacial, and other herpetic diseases, and the over-the-counter availability of the drug in certain countries, has raised concern over the development of resistance, particularly in immunosuppressed patients.

• The mechanism of resistance in the majority of cases appears to be a mutation or deletion of the thymidine kinase gene, which may be difficult to interpret due to gene polymorphisms.

• It appears that antiviral resistance remains low in immunocompetent individuals, likely because the immune system drives the virus into a latent state, whereas resistance is much higher in the immunocompromised.

• However there is no clear indication at this time that long-term prophylactic antivirals in the form of nucleoside analogues should be avoided in the management of ocular herpes.

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Surv Ophthalmol. 2012 Sep; 57(5): 448–462.

• The estimated average overall incidence of HZ is about 3.4–4.82per 1000 person years which increases to more than 11 per 1000person years in those aged at least 80 years.

• Between 20% and 70% of patients with HZO developcomplications that can include blepharitis, keratoconjunctivitis,iritis, scleritis and acute retinal necrosis.

• Neurological complications are less frequent than ocularcomplications and may include ophthalmoplegia, optic neuritisand ptosis.

HER

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Johnson, Robert W. et al. “Herpes Zoster Epidemiology, Management, and Disease and Economic Burden in Europe: A Multidisciplinary Perspective.” Therapeutic Advances in Vaccines 3.4 (2015): 109–120.

• Varicella zoster virus (VZV) belongs to the herpes virus family and cause varicella that is the chickenpox and the herpes zoster that is the shingles.

• The varicella zoster keratitis occurs in two forms:• Primary (varicella)

• Recurrent (herpes zoster)

• The ocular manifestations are uncommon in varicella but common in ophthalmic zoster.

• The various ocular manifestations in ophthalmic VZV include:

Eye lesions which are manifested as pocks on lids and lid margins.

Keratitis occurs rarely in cases of VZV.

Epithelial keratitis with or without pseudodendrites occurs more rarely.

Disciform keratitis with uveitis of varying duration can occur.

VA

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• The rash of chickenpox begins as macules and progresses to papules, vesicles, and then pustules that dry, crust over, and may leave individual scars.

• Ocular involvement may include follicular conjunctivitis, occasionally associated with a vesicular lesion on the bulbar conjunctiva or eyelid margins.

• Punctate or dendritic epithelial keratitis is uncommon. Although subepithelial infiltrates, microdendritic keratitis, stromal keratitis, disciform keratitis, uveitis, and elevated IOP are rare, recurrent varicella keratouveitis may cause significant morbidity in some patients.

CLI

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• Laboratory confirmation of acute or recurrent VZV infection is possible by immunodiagnostic methods, viral culture, and PCR.

• Serologic testing is used primarily to identify varicella-naive adults who might benefit from prophylactic vaccination.

• As with HSV, scrapings from a vesicle base can be tested by cytology, PCR, or culture, or for the presence of VZV antigen.

• Conjunctival scrapings or corneal impression cytology specimens can be similarly analyzed by culture, antigen detection, or PCR.

DIA

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• Because infected individuals shed the virus in respiratory secretions before the onset of the characteristic rash, avoiding infected persons is not always possible.

• Vaccination against varicella is recommended for anyone older than 12 months without a history of chickenpox or with a negative serology.

• The severity of signs and symptoms may be reduced in clinically ill patients by the administration of oral acyclovir.

• Significant keratitis or uveitis can be treated with topical corticosteroids.

MA

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• Following primary infection, VZV establishes latency in sensory neural ganglia. Zoster (shingles) represents endogenous reactivation of latent virus in people with a waning level of immunity to infection.

• Most patients are in their sixth to ninth decades of life, and the majority are healthy, with no specific predisposing factors.

• However, zoster is more common in patients on immunosuppressive therapy; in those with a systemic malignancy, a debilitating disease, or HIV infection; and after major surgery, trauma, or radiation.

• However, herpes zoster in otherwise healthy children has been described in the literature.H

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• Zoster manifests as a painful vesicular dermatitis typically localized to a single dermatome on the thorax or face.

• Patients may complain initially of fever and malaise, and warmth, redness, and increased sensation in the affected dermatome.

• The most commonly affected dermatomes are on the thorax (T3 through L3) and those supplied by CN V.

• The ophthalmic division of the trigeminal nerve is affected more often than the maxillary and mandibular branches, and its involvement is referred to as herpes zoster ophthalmicus (HZO)

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• Ocular involvement occurs in more than 70% ofpatients with zoster.

• Eyelid vesicular eruption can lead to secondarybacterial infection, eyelid scarring, marginal notching,loss of cilia, trichiasis, and cicatricial entropion orectropion.

• Both punctate and dendritic epithelial keratitiscaused by viral replication in corneal epithelium arecommon manifestations.

• Diminished corneal sensation develops in up to 50%of patients.

• Nummular corneal infiltrates are said to becharacteristic of zoster stromal keratitis but theinterstitial keratitis, disciform keratitis, and anterioruveitis with increased IOP in HZO are clinicallyindistinguishable from those caused by HSV infection.

Liesegang TJ. Herpes zoster ophthalmicus: natural history, risk factors, clinical

presentation, and morbidity. Ophthalmology.2008;115(2 Suppl):S3–S12.

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ZO• Focal choroiditis, occlusive retinal vasculitis, and retinal

detachment have been reported.

• Ipsilateral acute retinal necrosis (ARN) temporally associated with HZO is uncommon.

• Orbital or central nervous system (CNS) involvement as a result of an occlusive arteritis may lead to eyelid ptosis, orbital edema, and proptosis.

• Papillitis or retrobulbar optic neuritis may also develop. Cranial nerve palsies, when meticulously investigated, have been reported to occur in up to one-third of cases of HZO, with CN III (oculomotor) most commonly affected.

• Systemic dissemination is unusual in immunocompetentpatients but can occur in up to 25% of those who are immunocompromised.

MA

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• Oral antiviral therapy for HZO reduce viral shedding from vesicular skin lesions, reduce the chance of systemic dissemination of the virus, and decrease the incidence and severity of the most common ocular complications.

• Oral antiviral therapy may reduce the duration if not the incidence of postherpetic neuralgia if begun within 72 hours of the onset of symptoms.

• A varicella-zoster vaccine was approved by the US FDA, after testing in 38,000 patients showed a 50% reduction in incidence of zoster and a 66% reduction in postherpeticneuralgia.

• The vaccine is recommended for immunocompetentindividuals older than 60 years but was recently made available to those aged 50 years and older.

Schmader KE, Levin MJ, Gnann JW Jr, et al. Efficacy, safety, and tolerability of herpes zoster vaccine in persons aged 50–59 years. Clin Infect Dis. 2012;54(7):922–928.

MA

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• The current recommendation for HZO is oral famciclovir 500 mg 3 times per day, valacyclovir 1g 3 times per day, or acyclovir 800 mg 5 times per day for 7–10 days, best if started within 72 hours of the onset of skin lesions.

• Intravenous acyclovir therapy(10 mg/kg every 8 hours) is indicated in patients at risk for disseminated zoster due to immunosuppression.

• Cutaneous lesions may be treated with moist warm compresses and topical antibiotic ointment.

• Topical corticosteroids and cycloplegics are indicated for keratouveitis.

• Oral corticosteroids are recommended by some for treating patients with HZO over age 60 to reduce early zoster pain and facilitate a rapid return to a normal quality of life.

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• Postherpetic neuralgia (PHN) may respond to capsaicin cream applied to the involved skin, but low doses of amitriptyline, desipramine, clomipramine, or carbamazepine may be necessary to control severe symptoms.

• Gabapentin (Neurontin) and pregabalin (Lyrica) have recently been shown to be efficacious in managing PHN.

• Aggressive lubrication with nonpreserved tears, gels, and ointments, combined with punctal occlusion and tarsorrhaphy as necessary, may be indicated for neurotrophic keratopathy.

• In a patient with significant pain, early referral to a pain management specialist should be considered.

• It is causative agent for epidemickeratoconjunctivitis which is predominantlycaused by the serotypes 8, 19, and 37.

• The infection is highly contagious.

• In Stage I corneal vesicles are present which are25 to 30 microns and barely perceptible on slitlamp.

• In Stage II, the lesions coalesce with each other ,become clearly visible on slit lamp. These are theclassical deep epithelial punctuate keratitislesions which may resolve or progress further.

• In Stage III faint subepithelial infiltrates arepresent beside the deep punctate keratitis.

• Stage IV is characterized by nummular opacitieswhich may be present months to weeks after theinitial episode

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• Supportive management of epidemic keratoconjunctivitis includes the following:

Artificial tears

Cold compresses

Cycloplegic agents for severe photophobia

Topical corticosteroids

Topical agents that have antiviral activity

•Depending on the severity of the signs and symptoms, patients should be followed up in several days to weeks.

MA

NA

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• Cytomegalovirus (CMV) is a ubiquitousherpesvirus that infects over 90% of humansby age 80.

• Spread of CMV occurs through the sharing ofsaliva, ingestion of breast milk, or sexualcontact.

• Recently, CMV has been increasinglyidentified as a significant cause of anterioruveitis and corneal endotheliitis.

• The anterior uveitis is characterized by anacute or chronic iritis, with moderate tosevere rises in IOP that are variablyresponsive to topical corticosteroids.

• The addition of keratic precipitates,endothelial cell loss, and diffuse or localcorneal edema suggests CMV endotheliitis.

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• Laboratory confirmation of disease is usually accomplished through PCR testing of aqueous humor for CMV.

• Aqueous humor is obtained by an anterior chamber tap, which must be performed during an episode of active disease.

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T • CMV-associated anterior segment disease is treated with ganciclovir and is not responsive to famciclovir, acyclovir, or its derivatives.

• Resistance of a presumed HSV infection to these agents should raise the suspicion of CMV.

• Recurrence can occur after keratoplasty. The role of corticosteroids is unclear, as there is some suggestion that steroid use may prolong or worsen CMV-associated anterior segment disease.

CO

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•Viral Keratitis is an important cause of considerable ocular morbidity and loss of Quality of Life.

•Viral Keratitis can be managed effectively with good observation, attention to details and good therapeutic regime according to prescribed guidelines.

• Steroids and Antivirals form the mainstay of management for Viral Keratitis if used effectively with newer modalities like interferons, cyclosporine and interferon modulators.