It is sight-threateningsight-threatening condition and

frequently presents as an ocular ocular

emergency. emergency.

Bacterial keratitis rarely occurs in the rarely occurs in the

normal eyenormal eye because of the human

cornea's natural resistance to infection.

Microbial keratitisMicrobial keratitis or infectious corneal ulcer is due

to the proliferation of proliferation of bacteria, fungi, viruses, and

parasites and associated inflammation and tissue tissue

destruction destruction within the cornea

Bacterial Keratitis is most common cause most common cause of

suppurative c u.

There are no specific clinical signsno specific clinical signs to help

confirm a definite bacterial cause in Bacterial

Keratitis.

Identification of risk factors risk factors and assessment

of corneal findings will help in determination

of potential etiologiespotential etiologies.

Defense of Ocular Surface

Eyelids

Tear film proteins

Corneal epithelium

Normal ocular flora

Conjunctival mucosal associated lymphoid tissue

Risk FactorsChronic infection of the eyelid margin can

reducing concentration reducing concentration of certain

antibacterial substances.

Dry eyeDry eye

Presence of N Gonorrhoeae, C

Diphtheriae, Hemophilus Aegyptius and

Listeria Monocytogenes – they can

penetrate intact epithelium. penetrate intact epithelium.

Corneal anaesthesia

AbuseAbuse of topical anaesthetic solution

Compromised c epithelium as contact

lenses,bullous keratopathybullous keratopathy.

Absence of normal conjunctival flora.

Local immune suppression as topical topical

corticosteroidscorticosteroids

Previous viral infectionviral infection

Drugs used in viral keratitis

External Risk Factors

1. Trauma

2. Exposure to contaminated water or

solutions

3. Smoking (disrupting corneal

epithelium via associated cellular

and neuronal toxicity.

Predisposing Systemic Conditions

1. Malnutrition

2. Diabetes

3. Collagen vascular

diseases

4. Chronic alcoholism

9

Causative organismsGRAM POSITIVE:

Staphylococcus Aureus (more common)

Staphylococcus Epidermidis (more common)

Propionibacterium acnes.

Streptococcus Viridans

GRAM NEGATIVE (less common)

Escheria Coli

Klebsiella

Proteus

Moraxella

•Gram stain: positive•Morphology: cocci in clusters•Facultative anaerobe

Staphylococcus Staphylococcus aureusaureus

Staphylococcus epidermidisStaphylococcus epidermidis

•Sphere-shaped bacteria that forms clumps.•Gram positive bacteria

Streptococcus pneumoniaeStreptococcus pneumoniae

•Gram-positive cocci. •Found in pairs (diplococci)•Alpha hemolytic

Pseudomonas aeruginosaPseudomonas aeruginosa

•Gram-negative, rod-shaped monoflagellated bacterium

ProteusProteus  

•Gram-negative•facultatively anaerobic, rod-shaped bacterium.

OrOrgganismsanisms penetrate intact epitheliumpenetrate intact epithelium

NNeisseria gonorroae

HHaemophilus agegyptius

Corynebacterium ddiphteria

LListeria

M.R.SHOJA 15

PathogenesisPathogenesisSteps

1. Corneal abrasionabrasion

2.2. InfectionInfection by microorganism in presence of

predisposing factor(s).

3. Localized necrosisnecrosis of superficial layers of cornea

4. Formation of sequestrumsequestrum It cast off in

conjunctival sac

5.5. DesquamationDesquamation of corneal epithelium and damage

to Bowman’s membrane

Epithelial regenerationregeneration, at times it covers the

edges and floor area

A saucer shaped defect with projecting walls defect with projecting walls

above the normal surface due to swelling of

tissue resulting from fluid imbibition by

corneal stroma

Surrounding area is packed by leucocytes,

seen as gray zone of infiltration. This is This is

progressive stageprogressive stage. .

Necrotic material fall off- Necrotic material fall off- ulcer becomes larger

-> infiltration and swelling reduce and

disappears -> margin becomes smooth, floor

also looks smooth and transparent. This is This is

regressive stageregressive stage..

VascularizationVascularization develops from limus to corneal

ulcer to restore lost tissue and to supply

antibodies.

Vascularisation is followed by cicatrizationcicatrization due

to regeneration of collagen and formation of

fibrous tissue

Newly formed fibres are laid down irregularlyirregularly,

not conforming to normal pattern of stromal

fibres. Therefore this fibrous tissue reflects

light irregularly. The scar tissue is more or less

opaque. Some vessels may persist in large

scar

Bowman’s membrane never regenerates

and whenever it is destroyed some degree

of corneal opacity remains.

Corneal opacity may clear with time

especially if it is not dense. The

vascularization plays part in clearing

corneal opacity.

Diffusion toxins Diffusion toxins into the

anterior chamber leads to

hyperaemiahyperaemia and

inflammation of the iris and

ciliary body (Keratouveitis).

Polymorphonuclear cells

coming out from the uveal

tissue may gravitate to

bottom of anterior chamber

to form hypopyonhypopyon.

SymptomsSymptoms are usually

markedmarked, they are:1. Diminution of visionDiminution of vision,2. WateringWatering (lacrimation)3. photophobia and blepharospasm 4. PainPain and foreign body/ gritty sensation5. There may be dischargedischarge (Mucopurulent / purulent)

Signs 1. Visual acuity may be affected, depending on

location of corneal ulcer

2. Edema of lids of affected eye, in severe cases

3. Blepharospasm

4. Ciliary and conjunctival congestion

5. Hazyness / pus may be present in anterior

chamber

Oval, yellow-white,

densely opaque stromal

suppuration

clear cornea

ExaminationVisual acuity

An external ocular examination

Conjunctiva, Nasolacrimal apparatus, cornealSensation

Slit Lamp Biomicroscopy: For Eyelid margin

Conjunctiva Sclera

Cornea (epithelial defects, punctate

keratopathy, edem

Location of lesion

Density, Size , shape , depth, colour

Endothelium Anterior chamber

Loose or Broken sutures Signs of corneal

dystrophy

Anterior Vitreous

Fluorescein

Rose Bengal staining

Rose BengalRose Bengal•Derivative of sodium fluorescein (NaFL)•Stain dead or degenerated cells and mucous strands• Best used to examine the conjunctiva

FluoresceinFluorescein•Synthetic organic compound•Stains epithelial lesions,•Fluorescein does not stain normal corneae or bulbar

conjunctivae.

Laboratory InvestigationLaboratory Investigationcorneal scraping for stainings and cultures .

The majority of cases resolve with empirical

therapy and without smears or cultures.

cultures are indicated in cases where the

corneal infiltrate is central, large, deep, is

chronic in nature, or has atypical clinical

features .

poor clinical response to empirical treatment .

Culture mediaMedia Common isolates

Blood AgarBlood Agar Aerobic and facultative, anaerobic bacteria, including P. aeruginosa, S. aureus, S. epidermidis, S. pneumoniae

Chocolate AgarChocolate Agar Aerobic and facultative, anaerobic bacteria, including H. influenzae, N. gonorrhoeae, and Bartonella species

Thyoglicollate broth Aerobic and facultative, anaerobic bacteria

Lowenstein-Jensen medium

Mycobacterium species

Thayer-Martin agar Pathologic Neisseria

Sabouraud's dextrose Sabouraud's dextrose agaragar

Fungi

Stains.

Stain Organisms visualized

Gram stain Best for bacteria; can also visualize fungi, Acanthamoeba

Giemsa stain Bacteria, fungi,

Chlamydia, Acanthamoeba

Acid fast Mycobacterium, Nocardia

Complications of Corneal UlcerComplications of Corneal Ulcer1. Spread of ulcer horizontally

and depth-wise, leading to

thinningthinning of cornea

2. Bulging of descemet’s

membrane (Keratocele or

DescemetoceleDescemetocele represents

condition of impending

perforation of cornea

3. PerforationPerforation of by sudden exertion such

as coughing,

Complications of perforation may be

serious and sight threatening

A.A.Peripheral perforationPeripheral perforation: Iris is thrown

forward -> opening is occluded ->

anterior chamber is formed , scarring

takes place:

B.Central perforationB.Central perforation: small central

perforation -> anterior chamber collapse

-> lens comes in contact with corneal

endothelial surface -> anterior capsular

cataract -> repeated healing and

perforation leading to corneal fistula

formation

C. Sloughing of whole corneaC. Sloughing of whole cornea: prolapse of iris

-> pupillary block and exudation on iris ->

pseudocorneapseudocornea formation (iris covered with

exudates , formation of fibrous tissue and

formation of scar tissue) -> anterior chamber

anatomy is lost.

In case of sudden large perforation lens may

subluxate

Lens and vitreous may prolapse through

perforation.

This may lead to vitreous haemorrhage ,

choroidal , sub-retinal or sub-choroidal

haemorrhage. In elderly patients there

may be expulsive haemorrhage

D. Intra-ocular infectionD. Intra-ocular infection: due to perforation

bacteria enter in the eye and causes

endophthalmitis and panophthalmitis

Treatment of uncomplicated corneal ulcerTreatment of uncomplicated corneal ulcer

LOCAL TREATMENT LOCAL TREATMENT

1. Control of infection with antibiotic(s).

Sub-conjunctival antibiotics may be

helpful where there is scleral spread or

perforation or in cases where compliance

with the treatment regimen is

questionable.

ManagementManagementMonotherapyMonotherapy;

Fluoroquinolone (Ciprofloxacin 0.3% or ofloxacin 0.3%

But may be corneal toxicity (white corneal precipitates)

Topical antibioticsTopical antibioticsInitial instilation hourly intervals.If response favourable => reduced 2hourly

during waking hours. If progress => fortified drops

ManagementManagementOral ciprofloxacinOral ciprofloxacin, 750mg b.id, when

juxtalimbal ulcer, to prevent spread to sclera.

SteroidSteroid is controversialBenefits of steroid topical reducing stromal necrosis vs scarring, but decreased fibroblast activity vs wound healing incraesed risk of perforation.

Cycloplegic and mydriatic drug:

atropine 1% or cyclopentolate 1% or

Homatropine 2%. These drugs prevents

ciliary spasm, relieves pain, prevent

dangerous results of iridocyclitis, breaks

adhesions and prevent synechia

formation

3. Cleanliness Cleanliness: Irrigation with normal

salin to remove conjunctival

discharge and necrotic material

4. Application of heatApplication of heat: provides

comfort and causes vasodilatation

5. Protection of eye from external

environment with dark glasses dark glasses

In cases of progressive corneal ulcer

Scraping of ulcer may be used.

Analgesic anti-inflammatory.

Acetazolamide Tab is added in cases of

impending perforation or perforated

corneal ulcer in dosage of 250 mgm

upto four times a day

Non-responsive / Progressive Corneal UlcerNon-responsive / Progressive Corneal Ulcer

Re-evaluate for

Drug toxicity

Non-infectious causes or Unusual organisms.

Modification of anti-microbial therapy

Therapeutic keratoplasty may be

undertaken

Treatment of perforated corneal ulcerTreatment of perforated corneal ulcerRest Continue treatment of corneal ulcer with

modification, i.e. firm bandage or bandage contact lens

All forced expiration like coughing, sneezing, blowing of nose etc must be avoided

Use of tissue adhesive (Glue): N-butyl 2-ethyl cyanoacrylate

Therapeutic penetrating keratoplasty or conjunctival flap

Cyanoacrylate tissue adhesiveCyanoacrylate tissue adhesive treat progressive corneal thinning,

descemetocele, and corneal perforation . In addition to its tectonic support tectonic support and

bacteriostatic effectsbacteriostatic effects. Perforations up to 2–3 mm in diameter

can be sealed by the tissue adhesive. Necrotic tissue and debris should be

removed prior to application of the glue.The adhesive is usually left in place until

it dislodges spontaneously or a keratoplasty is performed.

Collagen Cross linkingCollagen Cross linkingnew treatment for multidrug-

resistant infectious keratitis.This technique has showed promising

results specially in patients with corneal melting and impending perforation.

Corneal melting has been arrested and complete epithelialization achieved in several cases.

is one of the most difficultdifficult forms of microbial keratitis to diagnose & to treat successfully.

Fugus may be a part of normal external ocular flora. ( 3-28% of normal eyes)

Most commonly seen are:Most commonly seen are:Aspergillus most common organism worldwideCandida Penicillium Cladosporium

Diagnostic/Laboratory GroupsDiagnostic/Laboratory Groups

Filamentous Non Pigmented: Fusarium, Aspergillus Filamentous Pigmented: Alternaria Filamentous Non Septate: Mucor Yeasts: Candida

PathogenesisPathogenesis Fungi gain entry into stroma through a defect in epithelial

barrier.

In stroma, cause tissue necrosis & host inflammatory

reaction.

Fungus can penetrate deep into stroma & through intact

descemet’s membrane.

Blood borne growth inhibiting factors may not reach

avascular structures of eye like cornea so fungi continues to

grow & persists i.e. why conjunctival flap help in control of why conjunctival flap help in control of

fungal infection.fungal infection.

Risk FactorsRisk FactorsTrauma

Contact lens use.

Topical Medications- Corticosteroids Anaesthetic

Abuse Broad Spectrum Antibiotics

Penetrating Keratoplasty, LASIK.

Chronic Keratitis.

Immunocompromised State- HIV, Leprosy

Clinical FeaturesSymptoms:Foreign body Sensation Slow onset increasing PainClinical signs are more severe than symptoms.Clinical signs are more severe than symptoms.Signs:NonspecificNonspecific:Conjunctival injection Epithelial defect A C reactionSpecificSpecific: Infiltrate Feathery Margins Feathery Margins Elevated edgesRough Textured Satellite lesions Satellite lesions Endothelial PlaqueHypopyonHypopyon ( Non Sterile, thick & immobile)Yellow line of demarcationYellow line of demarcation

 An early fungal ulcer presenting with very mild congestion and few symptoms.

Typical feathery margins at the 7’O clock position  .

 10 days old fungal corneal ulcer showing central (→) and two peripheral satellite lesion

Fusarium keratitis with  hypopyon

Laboratory DiagnosisLaboratory DiagnosisStainsStains: Gram Stain Giemsa Stain PAS StainFluoroscent MicroscopyFluoroscent Microscopy Acridine Orange Calcoflour whiteSmearSmear: Potassium Hydroxide Wet Mount

(10-20%)

Sabouraud's agar Sabouraud's agar is the principal is the principal medium medium

CulturesCultures

CornealCorneal biopsybiopsy It is more sensitive than histopathological It is more sensitive than histopathological

examination. examination. It is a micro-trephine It is a micro-trephine

Confocal Microscopy allows in vivo visualization of the organisms allows in vivo visualization of the organisms at various levels in cornea.at various levels in cornea. It offers magnifications of up to It offers magnifications of up to 32003200 to to 35003500 with increased image contrast. with increased image contrast.

By measuring By measuring (l,3)-beta-D-(l,3)-beta-D-glucanglucan, one of the major , one of the major components of fungal cell wall components of fungal cell wall in tears it is a reliable non in tears it is a reliable non invasive method invasive method polymerase chain reaction polymerase chain reaction (PCR) (PCR)

ManagementANTIFUNGALSPOLYENES:

Amphotericin "fungizone":

1.vial "50mg" + 10ml sterile water=5mg/ml.

2.take 3ml"15mg" + 7ml artificial tears drops=1.5mg/ml.

Topical Natamycin 5% is Initial drug of choice

• AZOLES: Ketoconazole, Fluconazole, Voriconazole

Indication for Systemic antifungalsIndication for Systemic antifungals: ( voriconazole 1st choice) Severe deep keratitis Scleritis Endophthalmitis Prophylactic after Penetrating Keratoplasty

Surgical management1. Debridement2. Therapeutic Penetrating Keratoplasty3. Conjunctival Flap4. Flap + Penetrating Graft5. Lamellar Graft6. Cryotherapy ( In Keratoscleritis)

7. Excimer LASER:PTK to eradicate the infiltrates and

facilitate antifungal therapy.

HSV-1 (Herpes simplex)Cold sores, keratitis

HSV-2Genital herpes

VZV (Varicella zoster)Chicken pox, shingles,

HZO

All neurotrophic sensory nerve gangliaTrigeminal

Herpes Simplex KeratitisHerpes Simplex KeratitisPrimary HSV infection by

direct contactMay get a

blepharoconjunctivitis (follicular)

LatencyUtilises cellular enzymes for

replication host cell deathLoss of ganglion cells

reduced corneal sensationBasic forms:

EpithelialStromalEndothelial

Epithelial KeratitisEpithelial Keratitis

SymptomsSymptomsFB sensationFB sensationphotophobiaphotophobiaRednessRednessBlurred visionBlurred vision

Clinical featuresClinical featuresPunctate epithelial keratitisPunctate epithelial keratitisClassic dendritic ulcers with terminal bulbsClassic dendritic ulcers with terminal bulbsGeographic ulcerGeographic ulcerMarginal keratitisMarginal keratitisMetaherpetic ulcerMetaherpetic ulcer

Dendritic ulcerDendritic ulcer

Classic herpetic lesionClassic herpetic lesionThe borders are slightly The borders are slightly

raised,grayish.raised,grayish.On resolution, a dendrite-shaped scar, On resolution, a dendrite-shaped scar,

called a called a ghost dendriteghost dendrite, may remain in , may remain in the superficial stromathe superficial stroma

Geographic ulcerGeographic ulcerImmunocompromised, on topical Immunocompromised, on topical

steroids, or have longstanding, steroids, or have longstanding, untreated ulcers terminal bulbs are untreated ulcers terminal bulbs are seen at the peripheryseen at the periphery

Marginal keratitisMarginal keratitisLocated near the limbus Located near the limbus The presence of an epithelial defect and lack The presence of an epithelial defect and lack

of corneal sensation can aid in diagnosisof corneal sensation can aid in diagnosisThey are more resistant to treatment and They are more resistant to treatment and

frequently become trophic ulcersfrequently become trophic ulcers

Metaherpetic (trophic) ulcerMetaherpetic (trophic) ulcerCauses-Causes-

Toxicity from antiviral medicationsToxicity from antiviral medicationsLack of neural-derived growth factorsLack of neural-derived growth factorsPoor tear surface.Poor tear surface.

Neurotrophic ulcers start as roughened Neurotrophic ulcers start as roughened epithelium, then breaks down to produce epithelium, then breaks down to produce an epithelial defect with smooth margins an epithelial defect with smooth margins

TreatmentTreatment

Stop toxic medicationsStop toxic medicationsTear film supplementationTear film supplementationBandage contact lenses Bandage contact lenses Amniotic membraneAmniotic membraneThe cautious use of topical steroids The cautious use of topical steroids

may be necessary if there is significant may be necessary if there is significant underlying inflammationunderlying inflammation

Stromal and endothelial Stromal and endothelial keratitiskeratitis

Immune-mediated response.Focal, multifocal or diffuse

stromal opacitiesWith new vessels

“interstitial keratitis”Necrotising keratitisLocalised endothelial

dysfunction “disciform keratitis”

Keratouveitis

Triggers for recurrence of HSKTriggers for recurrence of HSK

OphthalmicOphthalmic SystemicSystemic

Contact lens wearEye injuryCorneal graftingLaser eye surgeryCataract surgeryIntravitreal injectionsTopical prostaglandin

analogs

StressSystemic

infection/feverSunlight exposureMenstruationGenetic factors

TreatmentTreatmentDebridement (also use for PCR or culture)

Monotherapy with topical antiviral (Aciclovir, Ganciclovir, Trifluridine)

No added benefit of oral antiviral but may be useful in kids or allergic patients

Normal dendrites heal in 1-3 weeksIf not think toxicity, resistance or wrong diagnosis!

TreatmentStromal disease

Mainstay is topical steroidsAlways under antiviral coverAlways under antiviral cover

Systemic aciclovir reduces recurrence of stromal keratitis by 50% Aciclovir 400 mg bdAciclovir 400 mg bd

Herpes Zoster OphthalmicusHerpes Zoster OphthalmicusInvolvement of first Division

(Ophthalmic) of Trigeminal nerve

PathogenesisPathogenesis primary infection occurs before the age of

10, manifests as chickenpox (varicella)The virus then establishes a latent state in

the sensory gangliaWhen there is diminished virus-specific and

cell-mediated immunity, the virus may reactivate and spread to the corresponding dermatome .

Clinical manifestationsClinical manifestations

Eyelids Periorbital edema, pain, and

hyperesthesia of the eyelid skinSecondary bacterial infection.Complications- scarring, cicatricial

ectropion or entropion, trichiasis, madarosis.

Clinical manifestationsClinical manifestationsConjunctiva

papillary, pseudomembranous,

membranous, or follicular reaction

Episclera/Sclera HZV episcleritis and

scleritis may be either localized or diffuse

CorneaCornea Five basic clinical forms:

Epithelial keratitis (acute or chronic)

Stromal keratitisDisciform keratitisLimbal vascular keratitis

Neurotrophic keratitis.

UveitisUveitis Nongranulomatous or granulomatous iridocyclitis

LensLens Posterior subcapsular cataractsAnterior Chamber Angle and Glaucoma Anterior Chamber Angle and Glaucoma

Plugging of the trabecular meshwork Pupillary-block glaucoma secondary to posterior synechiae.

Peripheral anterior synechiaeChronic open-angle glaucoma-due to damage to the trabecular meshwork

Pupil Horner’s syndrome A tonic pupil secondary to herpes zoster ciliary ganglionitis

Optic Nerve Neuroretinitis, retrobulbar neuritis, or an ischemic optic neuropathy.

VitreousVitreousVitreous opacities, vitritis, and vitreous

hemorrhage

RetinaRetina Retinal hemorrhagesRetinal thrombophlebitisBranch or central retinal artery occlusionRetinal arteritisNecrotizing retinopathy, necrotizing retinitisExudative or rhegmatogenous retinal

detachment Ischemic perivasculitis

Extraocular Muscles Extraocular Muscles Ophthalmoplegia Affect cranial nerves three, four, and six

Can also manifest as a myositis that may also lead to ophthalmoplegia

Postherpetic Neuralgia Postherpetic Neuralgia Pain that continues following rash healing

Pain has three phases:Acute pain occurring within 30 days after rash onset

Subacute herpetic neuralgia that persists beyond the acute phase but resolves before 120 days

Chronic PHN that persists 120 days or more after rash onset

DiagnosisDiagnosis

The diagnosis of herpes zoster disease is based on clinical findings

Cytologic examination reveals multiple eosinophilic intranuclear inclusions (Lipschutz bodiesLipschutz bodies) and multinucleated giant cells (Tzanck Tzanck preparationpreparation)

Electron microscopy PCR

ManagementManagement

Systemic medication-Oral acyclovir (800 mg, five times daily)

for 7–10 daysFamciclovir (500 mg three times daily for

7 days)Valacyclovir (1000 mg three times daily)

Palliative therapy including cool compresses, mechanical cleansing of the involved skin, and topical antibiotic ointment without steroid.

Débridement may also be helpfulNeurotrophic keratitis or the

epithelial defects -nonpreserved artificial tears, eye ointments, therapeutic soft contact lenses

Tarsorrhaphy, conjunctival flap.Steroids should not be used in cases

of exposure or neurotrophic keratitis because of the possibility of keratolysis.

Topical cycloplegicsAqueous suppressants and topical

corticosteroids should be used to treat HZO glaucoma

Herpes zoster retinitis, optic neuritis, chorioretinitis, acute retinal necrosis syndrome, and progressive outer retinal necrosis are best treated with a combination of systemic steroids and acyclovir i.v

Postherpetic Neuralgia treatmentPostherpetic Neuralgia treatmentAnalgesicsAntidepressants as carbamazepine,

and phenytoinFamciclovir significantly reduce the

duration but not incidenceSteroids have no effect on PHNAmitriptyline for 90 days reduced

the incidence of pain at 6 months.Trial of percutaneous electrical

nerve stimulation (PENS)

FUTURE DIRECTIONSFUTURE DIRECTIONSHeat shock and glycoprotein subunit

vaccines have shown some promise in

clinical trials in decreasing the number and

severity of recurrences

Although monotherapy with interferon has

not been found to be effective, it increases

the efficacy of acyclovir and ganciclovir

when given in combination

•First recognized in 1973, is a rare,

vision threatening, parasitic infection

seen most often in contact lens contact lens

wearerswearers.

•It is often characterized by pain out pain out

of proportion to findingsof proportion to findings and the late

clinical appearance of a stromal ring

shaped infiltrate.

EtiologyEtiology

Two of the eight known species of

Acanthamoeba, A. castellanii and A polyphaga,.

Acanthamoeba are commonly found shower

water, and contact lens solution.

Risk FactorsRisk Factors•contact lens wear, 80% of A keratitis appears in contact lens wearers.•exposure to organism (often through contaminated water)•corneal trauma.  •Low levels of anti-Acanthamoeba IgA in tears.  

Diagnosis of AcanthamoebaDiagnosis of Acanthamoeba

HistoryHistoryPatients should be asked about contact lens wear and hygiene, contact lens solutions, recent corneal trauma, and recent exposure to water sources.SymptomsSymptomspain out of proportion to findings. Patients may also complain of decreased vision, redness, foreign body sensation, photophobia, tearing, and discharge.

Signs•Early signs may be mild and non-specific. •Possible findings include epithelial irregularities, epithelial or subepithelial infiltrates, and pseudodendritespseudodendrites. •Later signs include stromal infiltrates (ring-ring-shaped, disciformshaped, disciform), epithelial defects, radial keratoneuritisradial keratoneuritis, scleritis, and anterior uveitis (with possible hypopyon).  Advanced signs include stromal thinning and corneal perforation.

Early epithelial stage of infection. Linear

configuration resembles the epithelial form

(dendritic) of herpes simplex keratitis.

Perineuritis. Inflammatory cell around corneal nerves.

Medical therapyMedical therapy

Different regimens include

topical preparations of BroleneBrolene,

Neomycin-Polymyxin,

polyhexamethylene biguanide

(PHMB), chlorhexadine, and

voriconazole.  Some

practitioners recommend oral

ketoconazole.

Medical follow upMedical follow up•Patients should be followed very closely (daily or almost daily).  •Acanthamoeba cysts are so resistant to treatment, medical treatments should be tapered very slowly and, if necessary, continued for many months.  •SteroidsSteroids are controversial are controversial and may worsen the condition by inhibiting the host immune response.