ophthalmology

2. It is sight-threateningsight-threatening condition and
frequently presents as an ocularocular
emergency.emergency.
Bacterial keratitis rarely occurs in therarely 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 ofproliferation of bacteria, fungi, viruses, and parasites and
associated inflammation and tissue destructiontissue destruction within the
cornea

3. Bacterial Keratitis is most common causemost 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 factorsrisk factors and assessment of
corneal findings will help in determination of
potential etiologiespotential etiologies.

4. Defense of Ocular
Surface
Eyelids
Tear film proteins
Corneal epithelium
Normal ocular flora
Conjunctival mucosal associated lymphoid tissue

5. Risk Factors
Chronic infection of the eyelid margin can
reducing concentrationreducing concentration of certain antibacterial
substances.
Dry eyeDry eye
Presence of N Gonorrhoeae, C Diphtheriae,
Hemophilus Aegyptius and Listeria
Monocytogenes – they can penetrate intactpenetrate intact
epithelium.epithelium.

6. 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 topicaltopical
corticosteroidscorticosteroids
Previous viral infectionviral infection
Drugs used in viral keratitis

7. External Risk
Factors
1. Trauma
2. Exposure to contaminated water or
solutions
3. Smoking (disrupting corneal epithelium
via associated cellular and neuronal
toxicity.

8. Predisposing Systemic
Conditions
1. Malnutrition
2. Diabetes
3. Collagen vascular diseases
4. Chronic alcoholism

9. 9
Causative organisms
GRAM POSITIVE:
 Staphylococcus Aureus (more common)
 Staphylococcus Epidermidis (more common)
 Propionibacterium acnes.
 Streptococcus Viridans
GRAM NEGATIVE (less common)
 Escheria Coli
 Klebsiella
 Proteus
 Moraxella

10. •Gram stain: positive
•Morphology: cocci in clusters
•Facultative anaerobe
Staphylococcus aureusStaphylococcus aureus

11. Staphylococcus epidermidisStaphylococcus epidermidis
•Sphere-shaped bacteria that forms clumps.
•Gram positive bacteria

12. Streptococcus pneumoniaeStreptococcus pneumoniae
•Gram-positive cocci.
•Found in pairs (diplococci)
•Alpha hemolytic

13. Pseudomonas aeruginosaPseudomonas aeruginosa
•Gram-negative, rod-shaped monoflagellated
bacterium

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

15. OrOrgganismsanisms penetrate intact epitheliumpenetrate intact epithelium
 NNeisseria gonorroae
 HHaemophilus agegyptius
 Corynebacterium ddiphteria
 LListeria
M.R.SHOJA 15

16. PathogenesisPathogenesis
Steps
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

17. Epithelial regenerationregeneration, at times it covers the edges
and floor area
A saucer shaped defect with projecting wallsdefect 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 progressive stageThis is progressive stage..

18. 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 regressive stageThis is regressive stage..
VascularizationVascularization develops from limus to corneal ulcer
to restore lost tissue and to supply antibodies.

19. 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

20. 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.

21. Diffusion toxinsDiffusion 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.

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

24. 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

25. Oval, yellow-white, densely
opaque stromal suppuration
clear cornea

28. Examination
Visual acuity
An external ocular examination
Conjunctiva, Nasolacrimal apparatus, corneal
Sensation
Slit Lamp Biomicroscopy: For Eyelid margin
Conjunctiva Sclera
Cornea (epithelial defects, punctate keratopathy,
edem

29. 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

30. 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.

31. Laboratory InvestigationLaboratory Investigation
corneal 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 .

32. Culture media
Media 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 agarSabouraud's dextrose agar Fungi

33. Stains
.
Stain Organisms visualized
Gram stain Best for bacteria; can also visualize
fungi, Acanthamoeba
Giemsa stain Bacteria, fungi,
Chlamydia, Acanthamoeba
Acid fast Mycobacterium, Nocardia

34. Complications of Corneal UlcerComplications of Corneal Ulcer
1. 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

35. 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:

37. 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

38. 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.

39. 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

40. D. Intra-ocular infectionD. Intra-ocular infection: due to perforation
bacteria enter in the eye and causes
endophthalmitis and panophthalmitis

41. Treatment of uncomplicated corneal ulcerTreatment of uncomplicated corneal ulcer
LOCAL TREATMENTLOCAL 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.

42. ManagementManagement
MonotherapyMonotherapy;
Fluoroquinolone (Ciprofloxacin 0.3% or ofloxacin
0.3%
But may be corneal toxicity (white corneal
precipitates)
Topical antibioticsTopical antibiotics
Initial instilation hourly intervals.
If response favourable => reduced 2hourly during
waking hours.
If progress => fortified drops

43. ManagementManagement
Oral ciprofloxacinOral ciprofloxacin, 750mg b.id, when
juxtalimbal ulcer, to prevent spread to sclera.
SteroidSteroid is controversial
Benefits of steroid topical reducing stromal
necrosis vs scarring, but decreased fibroblast
activity vs wound healing  incraesed risk of
perforation.

44. 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

45. 3. CleanlinessCleanliness: 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 glassesdark glasses

46. 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

47. 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

48. Treatment of perforated corneal ulcerTreatment of perforated corneal ulcer
Rest
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

49. Cyanoacrylate tissue adhesiveCyanoacrylate tissue adhesive
 treat progressive corneal thinning,
descemetocele, and corneal perforation .
In addition to its tectonic supporttectonic 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.

51. Collagen Cross linkingCollagen Cross linking
new 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.

52. 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 worldwide
Candida Penicillium Cladosporium

53. Diagnostic/Laboratory GroupsDiagnostic/Laboratory Groups
 Filamentous Non Pigmented:
Fusarium, Aspergillus
 Filamentous Pigmented:
Alternaria
 Filamentous Non Septate:
Mucor
 Yeasts: Candida

54. 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 ofwhy conjunctival flap help in control of
fungal infection.fungal infection.

55. Risk FactorsRisk Factors
Trauma
Contact lens use.
Topical Medications- Corticosteroids
Anaesthetic Abuse Broad Spectrum Antibiotics
Penetrating Keratoplasty, LASIK.
Chronic Keratitis.
Immunocompromised State- HIV, Leprosy

56. Clinical Features
Symptoms:
Foreign body Sensation Slow onset increasing Pain
Clinical signs are more severe than symptoms.Clinical signs are more severe than symptoms.
Signs:
NonspecificNonspecific:
Conjunctival injection Epithelial defect A C reaction
SpecificSpecific:
Infiltrate Feathery MarginsFeathery Margins Elevated edges
Rough Textured Satellite lesionsSatellite lesions Endothelial Plaque
HypopyonHypopyon ( Non Sterile, thick & immobile)
Yellow line of demarcationYellow line of demarcation

57. An early fungal ulcer presenting with very mil
d congestion and few symptoms.

58. Typical feathery margins at the 7’O clock position.

59. 10 days old fungal corneal ulcer showing central
(→) and two peripheral satellite lesion

60. Fusarium keratitis with hypopyo
n

61. Laboratory DiagnosisLaboratory Diagnosis
StainsStains: Gram Stain
Giemsa Stain
PAS Stain
Fluoroscent MicroscopyFluoroscent Microscopy
Acridine Orange
Calcoflour white
SmearSmear: Potassium Hydroxide Wet Mount
(10-20%)

62. Sabouraud's agarSabouraud's agar is the principalis the principal
mediummedium
 CulturesCultures
 CornealCorneal biopsybiopsy
 It is more sensitive than histopathological examination.It is more sensitive than histopathological examination.
 It is a micro-trephineIt is a micro-trephine

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

64.  By measuringBy measuring (l,3)-beta-D-glucan(l,3)-beta-D-glucan,,
one of the major components of fungalone of the major components of fungal
cell wall in tears it is a reliable noncell wall in tears it is a reliable non
invasive methodinvasive method
 polymerase chain reactionpolymerase chain reaction (PCR)(PCR)

65. Management
ANTIFUNGALS
POLYENES:
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

67. Indication for SystemicIndication for Systemic
antifungalsantifungals:
( voriconazole 1st
choice)
 Severe deep keratitis
 Scleritis
 Endophthalmitis
 Prophylactic after Penetrating
Keratoplasty

68. Surgical management
1. Debridement
2. Therapeutic Penetrating Keratoplasty
3. Conjunctival Flap
4. Flap + Penetrating Graft
5. Lamellar Graft
6. Cryotherapy ( In Keratoscleritis)
7. Excimer LASER:
PTK to eradicate the infiltrates and facilitate
antifungal therapy.

69. HSV-1 (Herpes simplex)
Cold sores, keratitis
HSV-2
Genital herpes
VZV (Varicella zoster)
Chicken pox, shingles,
HZO
All neurotrophic 
sensory nerve ganglia
Trigeminal

70. Herpes Simplex KeratitisHerpes Simplex Keratitis
Primary HSV infection by direct
contact
May get a
blepharoconjunctivitis
(follicular)
Latency
Utilises cellular enzymes for
replication  host cell death
Loss of ganglion cells  reduced
corneal sensation
Basic forms:
Epithelial
Stromal
Endothelial

71. Epithelial KeratitisEpithelial Keratitis
 SymptomsSymptoms
FB sensationFB sensation
photophobiaphotophobia
RednessRedness
Blurred visionBlurred vision
Clinical featuresClinical features
Punctate epithelial keratitisPunctate epithelial keratitis
Classic dendritic ulcers with terminal bulbsClassic dendritic ulcers with terminal bulbs
Geographic ulcerGeographic ulcer
Marginal keratitisMarginal keratitis
Metaherpetic ulcerMetaherpetic ulcer

72. Dendritic ulcerDendritic ulcer
Classic herpetic lesionClassic herpetic lesion
The borders are slightly raised,grayish.The borders are slightly raised,grayish.
On resolution, a dendrite-shaped scar, calledOn resolution, a dendrite-shaped scar, called
aa ghost dendriteghost dendrite, may remain in the, may remain in the
superficial stromasuperficial stroma

73. Geographic ulcerGeographic ulcer
Immunocompromised, on topical steroids, orImmunocompromised, on topical steroids, or
have longstanding, untreated ulcers terminalhave longstanding, untreated ulcers terminal
bulbs are seen at the peripherybulbs are seen at the periphery

74. Marginal keratitisMarginal keratitis
Located near the limbusLocated near the limbus
The presence of an epithelial defect and lack ofThe presence of an epithelial defect and lack of
corneal sensation can aid in diagnosiscorneal sensation can aid in diagnosis
They are more resistant to treatment and frequentlyThey are more resistant to treatment and frequently
become trophic ulcersbecome trophic ulcers

75. Metaherpetic (trophic) ulcerMetaherpetic (trophic) ulcer
Causes-Causes-
Toxicity from antiviral medicationsToxicity from antiviral medications
Lack of neural-derived growth factorsLack of neural-derived growth factors
Poor tear surface.Poor tear surface.
Neurotrophic ulcers start as roughenedNeurotrophic ulcers start as roughened
epithelium, then breaks down to produce anepithelium, then breaks down to produce an
epithelial defect with smooth marginsepithelial defect with smooth margins

76. TreatmentTreatment
Stop toxic medicationsStop toxic medications
Tear film supplementationTear film supplementation
Bandage contact lensesBandage contact lenses
Amniotic membraneAmniotic membrane
The cautious use of topical steroids may beThe cautious use of topical steroids may be
necessary if there is significant underlyingnecessary if there is significant underlying
inflammationinflammation

77. Stromal and endothelial keratitisStromal and endothelial keratitis
Immune-mediated response.
Focal, multifocal or diffuse stromal
opacities
With new vessels  “interstitial
keratitis”
Necrotising keratitis
Localised endothelial dysfunction
 “disciform keratitis”
Keratouveitis

78. Triggers for recurrence of HSKTriggers for recurrence of HSK
OphthalmicOphthalmic SystemicSystemic
Contact lens wear
Eye injury
Corneal grafting
Laser eye surgery
Cataract surgery
Intravitreal injections
Topical prostaglandin
analogs
Stress
Systemic infection/fever
Sunlight exposure
Menstruation
Genetic factors

79. TreatmentTreatment
Debridement (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 weeks
If not  think toxicity, resistance or wrong
diagnosis!

80. Treatment
Stromal disease
Mainstay is topical steroids
Always under antiviral coverAlways under antiviral cover
Systemic aciclovir reduces
recurrence of stromal keratitis by
50%
Aciclovir 400 mg bdAciclovir 400 mg bd

81. Herpes Zoster OphthalmicusHerpes Zoster Ophthalmicus
Involvement of first Division (Ophthalmic) of
Trigeminal nerve

82. PathogenesisPathogenesis
primary infection occurs before the age of 10,
manifests as chickenpox (varicella)
The virus then establishes a latent state in the
sensory ganglia
When there is diminished virus-specific and cell-
mediated immunity, the virus may reactivate and
spread to the corresponding dermatome .

83. Clinical manifestationsClinical manifestations
Eyelids
Periorbital edema, pain, and hyperesthesia of the
eyelid skin
Secondary bacterial infection.
Complications- scarring, cicatricial ectropion or
entropion, trichiasis, madarosis.

84. Clinical manifestationsClinical manifestations
Conjunctiva
papillary,
pseudomembranous,
membranous, or follicular
reaction
Episclera/Sclera
HZV episcleritis and scleritis
may be either localized or
diffuse

85. CorneaCornea
Five basic clinical forms:
Epithelial keratitis
(acute or chronic)
Stromal keratitis
Disciform keratitis
Limbal vascular keratitis
Neurotrophic keratitis.

86. UveitisUveitis
 Nongranulomatous or granulomatous
iridocyclitis
LensLens Posterior subcapsular cataracts
Anterior Chamber Angle and GlaucomaAnterior Chamber Angle and Glaucoma
Plugging of the trabecular meshwork
Pupillary-block glaucoma secondary to
posterior synechiae.
Peripheral anterior synechiae
Chronic open-angle glaucoma-due to
damage to the trabecular meshwork

87. Pupil
Horner’s syndrome
A tonic pupil secondary to herpes zoster
ciliary ganglionitis
Optic Nerve
Neuroretinitis, retrobulbar neuritis, or an
ischemic optic neuropathy.

88. VitreousVitreous
Vitreous opacities, vitritis, and vitreous hemorrhage
RetinaRetina
Retinal hemorrhages
Retinal thrombophlebitis
Branch or central retinal artery occlusion
Retinal arteritis
Necrotizing retinopathy, necrotizing retinitis
Exudative or rhegmatogenous retinal detachment
 Ischemic perivasculitis

89. Extraocular MusclesExtraocular Muscles
Ophthalmoplegia
Affect cranial nerves three, four,
and six
Can also manifest as a myositis
that may also lead to
ophthalmoplegia

90. Postherpetic NeuralgiaPostherpetic 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

91. 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 preparationTzanck preparation)
Electron microscopy
PCR

92. ManagementManagement
Systemic medication-
Oral acyclovir (800 mg, five times daily) for 7–10
days
Famciclovir (500 mg three times daily for 7 days)
Valacyclovir (1000 mg three times daily)

93. Palliative therapy including cool
compresses, mechanical cleansing of the
involved skin, and topical antibiotic
ointment without steroid.
Débridement may also be helpful
Neurotrophic keratitis or the epithelial
defects -nonpreserved artificial tears, eye
ointments, therapeutic soft contact lenses

94. Tarsorrhaphy, conjunctival flap.
Steroids should not be used in cases of
exposure or neurotrophic keratitis because
of the possibility of keratolysis.
Topical cycloplegics
Aqueous suppressants and topical
corticosteroids should be used to treat HZO
glaucoma

95. 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

96. Postherpetic Neuralgia treatmentPostherpetic Neuralgia treatment
Analgesics
Antidepressants as carbamazepine, and
phenytoin
Famciclovir significantly reduce the
duration but not incidence
Steroids have no effect on PHN
Amitriptyline for 90 days reduced the
incidence of pain at 6 months.
Trial of percutaneous electrical nerve
stimulation (PENS)

97. FUTURE DIRECTIONSFUTURE DIRECTIONS
Heat 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

98. •First recognized in 1973, is a rare, vision
threatening, parasitic infection seen most
often in contact lens wearerscontact lens wearers.
•It is often characterized by pain out ofpain out of
proportion to findingsproportion to findings and the late
clinical appearance of a stromal ring
shaped infiltrate.

99. EtiologyEtiology
Two of the eight known species of Acanthamoeba, A.
castellanii and A polyphaga,. Acanthamoeba are commonly
found shower water, and contact lens solution.

100. 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.

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

102. 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, radialradial
keratoneuritiskeratoneuritis, scleritis, and anterior uveitis (with
possible hypopyon). Advanced signs include
stromal thinning and corneal perforation.

103. Early epithelial stage of infection. Linear
configuration resembles the epithelial form
(dendritic) of herpes simplex keratitis.

105. Perineuritis. Inflammatory cell
around corneal nerves.

106. Medical therapyMedical therapy
Different regimens include topical
preparations of BroleneBrolene, Neomycin-
Polymyxin, polyhexamethylene
biguanide (PHMB), chlorhexadine,
and voriconazole. Some
practitioners recommend oral
ketoconazole.

107. 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 controversialare controversial and may worsen the
condition by inhibiting the host immune
response.