Topic: Cornea Course: BSc. Optometry Subject: Pathology Faculty: Medical Subtopics: - Anatomy of Cornea - Corneal degeneration and dystrophies - Keratitis - Healing in corneal ulcer - Previous Rajiv Gandhi University exam questions

1. CORNEA
Dr. Salman Ahmad Ansari
Dept. of Pathology
Kanachur Institute of Medical Sciences

2. Contents
● Anatomy of cornea
● Corneal degenerations
● Corneal dystrophies
● Keratitis
○ Acanthamoeba keratitis
○ Mycotic keratitis
○ Epidemic keratoconjunctivitis
○ Bacterial keratitis
○ Herpetic keratitis
● Healing in corneal ulcer
● Past university exam questions

3. Anatomy
Globe of eye consists of 3 layers:
1. Cornea-sclera
2. Choroid-iris
3. Retina

5. Cornea-sclera
- Transparent structure, continuation of the conjunctiva over the
cornea present in the anterior part of the eyeball
- Sclera is the outermost layer of the eyeball

7. Anatomy of the Cornea
The cornea is the transparent, avascular outermost layer of the
eye, playing a key role in focusing light. It consists of six layers:
1. Epithelium:
○ Outermost layer, provides barrier and smooth refractive
surface.
○ Regenerates rapidly after minor injuries.
2. Bowman’s Layer:
○ Acellular, collagen-rich layer beneath the epithelium.

8. 3. Stroma:
○ Makes up ~90% of corneal thickness.
○ Contains collagen fibrils and keratocytes.
○ Maintains corneal transparency through regular fibril
arrangement and dehydration.
4. Pre-Descemet’s membrane(Dua’s layer)
5. Descemet’s Membrane:
○ Basement membrane of the endothelium.
○ Thickens with age and can regenerate.

9. 6. Endothelium:
○ Single layer of cells on the inner surface.
○ Maintains corneal dehydration via active ion transport
(Na /K ATPase).
⁺ ⁺
○ Non-regenerative; damage leads to corneal edema.

12. Blood supply:
- It is an avascular structure
Nerve supply:
- Supplied by long ciliary nerves which are branches
of nasociliary nerve from ophthalmic division of
trigeminal nerve
- 3 plexuses: stromal, subepithelial and intraepithelial

13. Functions
- Acts as a major refracting medium
- Protects intraocular contents

14. Corneal disorders
● Degenerations
● Dystrophies

15. Corneal degeneration

16. Corneal degenerations
- Conditions in which normal cells undergo some degenerative
changes under the influence of age or other pathological
conditions
- They can be either unilateral or bilateral
- Non-familial

17. Classification
Depending upon location:
- Axial corneal degeneration: e.g: calcific degeneration(band
keratopathy)
- Peripheral degeneration: e.g: arcus senilis
Depending upon upon etiology:
- Age-related degeneration: e.g: arcus senilis, mosaic
degeneration
- Pathological degeneration: e.g: fatty degeneration, amyloidosis

18. Types of Corneal Degeneration:
1. Arcus Senilis (Gerontoxon)
● Site: Peripheral corneal stroma.
● Features: Grayish-white arc (lipid deposits), usually bilateral.
● Cause: Age-related lipid metabolism changes.
● Effect on vision: Usually none.

20. 2. Band Keratopathy
● Site: Bowman's layer and superficial stroma.
● Features: Calcium deposition appearing as a horizontal band
across the cornea.
● Associated with: Chronic uveitis, hypercalcemia, renal failure.
● Effect: May impair vision if it involves the visual axis.

21. Band Keratopathy

23. 3. Spheroidal Degeneration (Climatic Droplet Keratopathy)
● Site: Superficial stroma and epithelium.
● Features: Amber-colored, oily-appearing spherules.
● Cause: UV exposure, environmental stress (common in
outdoor workers).
● Effect: Progressive vision loss if central.

24. 4. Salzmann's Nodular Degeneration
● Site: Between epithelium and Bowman’s layer.
● Features: Blue-gray elevated nodules.
● Associated with: Chronic keratitis, trachoma.
● Effect: May cause astigmatism and visual disturbance.

26. 5. Terrien’s Marginal Degeneration
● Site: Peripheral cornea.
● Features: Painless, progressive thinning starting superiorly.
● Effect: Irregular astigmatism, risk of perforation.

27. 6. Lipid Keratopathy
● Site: Corneal stroma.
● Features: Yellow-white lipid deposits.
● Primary or secondary: Often follows neovascularization.
● Effect: Vision loss depending on extent.

28. Corneal dystrophy

29. Corneal dystrophy
- Group of disorders characterised by non-inflammatory,
inherited, bilateral opacity of cornea with no vascularisation
- Inborn defect
- Bilateral dystrophy
- No associated systemic disease
- Manifests usually by 1st to 2nd decade of life

30. Classification of corneal dystrophies:
- Epithelial and subepithelial dystrophies
- Bowman layer dystrophies
- Stromal dystrophies
- Descemet membrane and endothelial dystrophies

35. Keratitis

36. Keratitis
Keratitis: inflammation of cornea
Causes:
Due to various pathogens
- Bacterial
- Fungal
- viral(herpes simplex, herpes zoster)
- protozoal(acanthamoeba)

37. Due to various pathogens
● BacterialQ:
- Gram-positive bacteria:
○ Staphylococcus aureus
○ Staphylococcus epidermidis
- Gram-negative bacteria:
○ Klebsiella
○ Moraxella
○ Haemophilus

38. ● FungalQ
:
- Filamentous fungi:
○ Fusarium
○ Aspergillus
○ Curvularia
- Yeasts:
○ Candida albicans
○ Cryptococcus
○ Malassezia

39. ● Viral:
○ Adenovirus: causes epidemic keratoconjunctivitis
○ herpes simplex virus(HSV): causes herpetic keratitis
○ Varicella zoster virus: causes herpes zoster ophthalmicus
○ Cytomegalovirus
● protozoal(acanthamoeba)

41. Corneal ulcer
- It is a discontinuation in normal epithelial surface of
cornea
- demonstrated by staining with 1% sodium fluorescein dye
and viewed with cobalt blue filter light .
Corneal Abrasion or Erosion: the epithelial defect, if
superficial without inflammation
Corneal Ulcer: epithelial defect with inflammation in the
surrounding area. May be infective or sterile .

42. Corneal ulcer

43. Hypopyon
Definition: hypopyon is the accumulation of pus resulting from
suppurative infection inferiorly in the anterior chamber
● Consists of neutrophils which accumulate in the lower angle of
anterior chamber and eventually become enmeshed in a
network of fibrin .
● It is seen in severe corneal ulcers as a collection of pus in the
anterior chamber

44. Hypopyon

45. Acanthamoeba Keratitis

46. Acanthamoeba Keratitis
- Infection of the cornea, caused by Acanthamoeba, a free-
living protozoan found widely in in water and soil

47. Causative Agent
Acanthamoeba species
Exists in two forms:
● Trophozoite: Active, feeding, replicating form that causes
tissue damage.
● Cyst: Dormant, highly resistant form

49. Risk Factors
Contact Lens Use (most common)
● Poor hygiene (e.g., rinsing with tap water)
● Wearing lenses while swimming, showering, or using hot tubs
● Improper disinfection/storage
Corneal Trauma: Especially with exposure to contaminated water
or soil

50. Exposure to Contaminated Water
Use of Homemade Saline Solutions
Immunocompromised State

51. Pathophysiology
● Entry: Through microtrauma (e.g. contact lens use,
contaminated water).
● Adherence: Trophozoites attach to corneal epithelium via
mannose receptors.
● Invasion: Penetrate stroma and release proteases → tissue
destruction.

52. ● Nerve Involvement: Invade corneal nerves → severe pain
(radial keratoneuritis).
● Cyst Formation: Converts to resistant cysts →
chronic/recurrent infection.
● Sequelae: Inflammation, scarring, vision loss.

53. Symptoms
● Severe eye pain (often disproportionate to clinical findings)
● Eye redness
● Blurred vision
● Photophobia (light sensitivity)
● Excessive tearing
● Sensation of something in the eye (foreign body sensation)
● Ring infiltrate in the cornea (late-stage, pathognomonic)
● Ulceration and stromal inflammation

54. Diagnosis
Clinical Evaluation
● History taking, especially contact lens usage and water
exposure
● Slit-lamp examination
Laboratory Tests
1. Corneal scraping
○ Microscopic examination with stains (e.g., calcofluor white,
Giemsa)
○ Culture on non-nutrient agar with E. coli overlay

55. 2. Confocal microscopy
○ shows cysts and trophozoites in the cornea
3. PCR (Polymerase Chain Reaction)
4. Immunofluorescence assays

56. Treatment
Medical Therapy
● Topical agents:
○ Biguanides (e.g. PHMB 0.02%, chlorhexidine 0.02%)
○ Diamidines (e.g. hexamidine)
● Combination therapy of biguanide + diamidine is preferred
● Dosing initially every hour for several days to weeks

57. ● Cycloplegics for pain control
● Oral antifungals (e.g., itraconazole, voriconazole) in severe
cases
Surgical Options
● Penetrating keratoplasty (corneal transplant) in refractory or
advanced cases with corneal perforation or scarring

58. Mycotic keratitis

59. Mycotic Keratitis
Mycotic keratitis, also known as fungal keratitis
Infection of the cornea caused by fungal organisms
Significant cause of corneal blindness

60. Causative Agents
Fungal keratitis can be caused by filamentous fungi and yeasts.
a) Filamentous fungi:
● Fusarium
● Aspergillus
● Curvularia
b) Yeasts:
● Candida albicans and other Candida species

61. Pathogenesis
Corneal Injury or Predisposing Factor
● Entry often follows trauma with vegetative matter, contact
lens use, ocular surgery, or prolonged steroid use.
Adherence and Penetration
● Fungal spores adhere to damaged epithelium.
● Filamentous fungi penetrate the corneal stroma by extending
hyphae, causing mechanical and enzymatic damage.

62. Immune Response
● Host mounts an inflammatory response involving neutrophils
and macrophages.
● This results in corneal ulceration, stromal necrosis, and
possible hypopyon.
Progression
● The infection can progress to deep stromal involvement and
corneal perforation if not treated promptly.

63. Symptoms
Gradual onset of symptoms:
● Eye pain
● Redness
● Foreign body sensation
● Photophobia
● Blurry vision
● Watery or mucopurulent discharge
● White or grayish corneal ulcer with feathery borders
● Satellite lesions may be present
● Hypopyon (pus in the anterior chamber) in advanced cases

64. Diagnosis
a) Clinical Examination
● Slit-lamp findings: Dry-looking ulcer with feathery margins,
satellite lesions, endothelial plaque, and possible hypopyon.
b) Laboratory Tests
● Corneal scraping:
○ KOH wet mount – reveals branching hyphae (filamentous
fungi)

65. ○ Gram stain – useful for Candida
○ Culture on Sabouraud Dextrose Agar (SDA)
● Confocal microscopy – can visualize fungal filaments in vivo
● PCR – for species identification (advanced centers)

66. Treatment
a) Topical Antifungal Therapy
● Natamycin 5% – first-line treatment for filamentous fungi
(Fusarium, Aspergillus)
● Amphotericin B 0.15% – effective for yeasts (Candida) and
some filamentous fungi
● Voriconazole 1% – broad-spectrum, especially useful in
resistant or deep infections

67. b) Oral Antifungal Therapy
● Used in severe or deep stromal infections:
○ Voriconazole, Itraconazole, Fluconazole (especially for
Candida)
c) Adjunctive Therapy
● Cycloplegics to relieve ciliary spasm and pain
● Avoid corticosteroids
d) Surgical Intervention
● Therapeutic penetrating keratoplasty

68. Epidemic keratoconjunctivitis

69. Epidemic Keratoconjunctivitis
Epidemic keratoconjunctivitis (EKC) is a highly contagious viral
infection of the conjunctiva and cornea, primarily caused by
adenovirus characterized by outbreaks in community or
healthcare settings.

70. Causative Agent
Adenovirus – serotypes 8, 19, and 37
Part of the adenovirus group D
Spread through:
● Direct contact with eye secretions
● Contaminated hands, towels, instruments (e.g., tonometers)
● Swimming pools and ophthalmic clinics

71. Incubation and Transmission
Incubation period: 5–12 days
Highly contagious, even before symptoms begin
Can spread rapidly in hospitals, schools, or offices

72. Symptoms
● Redness (conjunctival injection)
● Watery discharge
● Gritty or foreign body sensation
● Photophobia
● Lid swelling
● Blurred vision (if cornea is involved)
● Often starts in one eye, spreads to the other within a few days

73. Signs
● Conjunctival hyperemia
● Chemosis (conjunctival swelling)
● Follicular conjunctivitis
● Preauricular lymphadenopathy (tender lymph node in front of
the ear)
● Pseudomembrane formation
● Subepithelial infiltrates in the cornea (after 7–10 days)

74. Diagnosis
● Usually clinical
● Laboratory confirmation:
○ Adenovirus antigen detection via immunoassay
○ PCR for viral DNA
○ Conjunctival swab and culture

75. Complications
● Subepithelial corneal infiltrates → may cause blurred vision
for weeks or months
● Pseudomembrane scarring
● Secondary bacterial infection

76. Treatment
No specific antiviral treatment; supportive care is the mainstay.
a) Supportive Care
● Cold compresses for comfort
● Lubricant eye drops (artificial tears)
● Topical antihistamines or vasoconstrictors for
itching/redness

77. b) Topical corticosteroids (with caution)
● May be used in severe inflammation or subepithelial
infiltrates
● Only under ophthalmologist supervision
c) Preventive Measures
● Strict hand hygiene
● Avoid sharing towels, cosmetics
● Disinfect instruments in eye clinics
● Isolation of affected individuals if possible

78. Bacterial keratitis

79. Bacterial Keratitis
Bacterial keratitis is a corneal infection caused by bacteria,
resulting in inflammation, ulceration, and potential loss of vision
if not treated promptly.
It is one of the most common and sight-threatening ocular
emergencies.

80. Causes of Bacterial Keratitis
Bacterial keratitis is most commonly caused by the following
organisms:
1. Gram-positive bacteria
● Staphylococcus aureus
● Staphylococcus epidermidis
● Streptococcus pneumoniae

81. 2. Gram-negative bacteria
● Pseudomonas aeruginosa
● Moraxella spp.
● Klebsiella spp.
● Haemophilus influenzae
● Neisseria gonorrhoeae

82. Predisposing Factors
● Contact lens wear (most common modern risk)
● Corneal trauma (especially with vegetative matter)
● Dry eye, blepharitis
● Topical corticosteroid use
● Ocular surgery

83. Clinical Features
● Sudden onset eye pain
● Redness
● Photophobia
● Tearing or discharge
● Decreased vision
● On examination: corneal ulcer, stromal infiltration, hypopyon
(pus in anterior chamber)

84. Diagnosis
Clinical suspicion based on symptoms and slit-lamp exam
Corneal scrapings for:
● Gram stain
● Culture and sensitivity (e.g., blood agar, chocolate agar)

85. Treatment
Topical broad-spectrum antibiotics (e.g., fluoroquinolones like
moxifloxacin)
In severe cases: fortified antibiotics (e.g., fortified vancomycin +
tobramycin)
Cycloplegics for pain
Avoid steroids initially

86. Complications
● Corneal perforation
● Scarring and permanent vision loss
● Endophthalmitis (rare but serious)

87. Q: Describe the lab diagnosis of bacterial keratitis

88. Lab diagnosis of bacterial keratitis
1. Sample Collection
● Corneal scrapings are obtained from the base and edges of
the ulcer using:
○ Sterile spatula or blade
○ Under aseptic conditions, often with topical anesthesia
● Multiple scrapings are taken for:
○ Direct microscopy
○ Culture

89. 2. Direct Microscopy
a) Gram Stain
● Detects Gram-positive or Gram-negative bacteria
● Helps guide initial antibiotic choice
● Shows bacteria and polymorphonuclear leukocytes (PMNs)
b) Giemsa Stain
● Helps visualize inflammatory cells and intracellular organisms
c) KOH wet mount
● Mainly to rule out fungal elements if fungal keratitis is
suspected

90. 3. Culture and Sensitivity
● Culture media used:
○ Blood agar (for most bacteria)
○ Chocolate agar (for Haemophilus, Neisseria)
MacConkey agar (for Gram-negative bacilli)
○ Thioglycolate broth (for enrichment)
● Plates are incubated at 35–37°C for 24–48 hours
● Antibiotic sensitivity testing is done using:
○ Kirby-Bauer disk diffusion method

91. 4. Additional Tests
● PCR (Polymerase Chain Reaction) – for rapid and specific
bacterial DNA detection (used in advanced settings)
● Confocal microscopy

92. Herpetic keratitis

93. Herpetic Keratitis
Herpetic keratitis is a corneal infection caused by the herpes
simplex virus (HSV), most commonly HSV-1

94. Etiology
Primary infection: Often asymptomatic or presents as mild conjunctivitis.
Reactivation: Virus remains latent in the trigeminal ganglion and can
reactivate due to:
● Stress
● Fever
● UV exposure
● Trauma
● Immunosuppression

95. Types
Epithelial Keratitis (most common)
● Site: Corneal epithelium
● Features:
○ Dendritic ulcers (branching pattern with terminal bulbs)
○ Stains with fluorescein and rose bengal
● Symptoms: Pain, photophobia, tearing, foreign body sensation

96. Stromal Keratitis (Disciform keratitis)
● Site: Corneal stroma (immune-mediated)
● Features:
○ Stromal edema, central disc-shaped opacity, Descemet’s
folds
○ No active viral replication
● Risk: Scarring and vision loss

97. Endotheliitis
● Site: Corneal endothelium
● Features:
○ Keratic precipitates (KPs), corneal edema, mild anterior
chamber reaction
Neurotrophic Keratopathy
● Cause: Chronic HSV leads to decreased corneal sensation
● Features:
○ Non-healing epithelial defect
○ Risk of corneal ulceration and perforation

98. Diagnosis
Clinical examination (dendrites, decreased corneal sensation)
Slit-lamp exam
Staining (fluorescein, rose bengal)
PCR or viral culture (rarely needed)

99. Treatment
Epithelial Herpetic Keratitis:
● Topical antivirals:
○ Acyclovir 3% ointment 5x/day
○ Ganciclovir gel 0.15%
● Oral Acyclovir: 400 mg 5x/day (preferred in some cases)
● Avoid corticosteroids

100. Stromal Keratitis or Endotheliitis:
● Oral antivirals + topical corticosteroids (e.g., prednisolone
acetate)
○ Steroids only under antiviral cover
Neurotrophic Keratopathy:
● Lubricants, autologous serum drops, or amniotic membrane
grafts

101. Complications
● Corneal scarring
● Thinning and perforation
● Secondary bacterial infection
● Vision loss

102. Short answers

103. Causes of Fungal Keratitis
A. Filamentous Fungi
● Fusarium species
● Aspergillus species
● Curvularia
● Penicillium
● Alternaria
B. Yeast-like Fungi
● Candida albicans
● Cryptococcus
● Malassezia

104. Causes of bacterial keratitis
Keratitis (Corneal Infection)
● Pseudomonas aeruginosa
● Staphylococcus aureus
● Streptococcus pneumoniae
● Moraxella spp.
● Nocardia spp.

105. Healing in corneal ulcer

106. Healing of a Corneal Ulcer
A corneal ulcer is an open epithelial defect of the cornea
associated with stromal inflammation, typically due to infection
(bacterial, fungal, viral, or parasitic).

107. Phases of Healing
1. Initial inflammatory phase
2. Epithelial Regeneration
3. Stromal Repair
4. Endothelial Response
5. Remodeling and Maturation
6. Vascularization (in severe/prolonged ulcers)

108. 1.Inflammatory phase:
First few hours to 1–2 days
● Events:
- Upon injury or infection, epithelial cells at the ulcer site are lost.
- Inflammatory cells (neutrophils, macrophages) are recruited to
fight infection and remove dead tissue.
- Tear film becomes rich in inflammatory cytokines
- Blood vessels from the limbus may start to invade the cornea if
damage is deep—this is corneal neovascularization.

109. 2. Epithelial Regeneration
Starts within 24–48 hours
● Migration and proliferation of adjacent healthy epithelial cells.
● Reepithelialization begins within 24–48 hours if the basement
membrane is intact.
● Growth factors (e.g., EGF, TGF-β) assist in healing.
● Limbal stem cells (at the corneal edge) proliferate to replenish
epithelial layers.
● Mitosis increases in nearby healthy epithelial cells.
● As the infection resolves, inflammatory signals reduce.

110. 3.Stromal Repair
Days to weeks depending on ulcer depth
● Keratocytes in the stroma proliferate and synthesize collagen and
proteoglycans.
● May result in scar formation(leucoma) due to disorganized
collagen.
● In deeper ulcers, tissue remodeling can take several weeks or
months
3.Endothelial Response
● The corneal endothelium does not regenerate.
● Remaining cells enlarge and spread to maintain function.
● Damage here may result in corneal edema.

111. 5.Remodeling and Maturation
Weeks to months
● Gradual reorganization of new collagen and ECM.
● Reduction of blood vessels and inflammation.
● Transparency may be partially or fully restored, depending on the
depth and severity of the ulcer.
● Scarring may persist, affecting visual acuity.
5.Vascularization
● in severe/prolonged ulcers
● neovascularization may occur from the limbus to aid healing.
● Can interfere with corneal transparency.

112. Sequelae/complications of a Corneal Ulcer
● Corneal Scarring (Leucoma)
● Corneal Thinning / Ectasia
● Neovascularization
● Secondary Glaucoma
● Irregular Astigmatism from scarring
● Anterior Synechiae / Posterior Synechiae: Adhesions to the iris
or lens
● Vision Loss

113. Past university questions

114. Past questions:
Long essays:
● Enumerate the viruses causing eye infection. Add a note on herpetic
keratitis(2023)
● Give an account on causative agents, pathogenesis and treatment of Mycotic
keratitis(2022)
● Write anatomy and pathology in degeneration of cornea(2022)
● Write in detail about Acanthamoeba Keratitis(2022, 2015)
● Enumerate the causes of eye infection. Add a note on Herpetic keratitis(2021)
● List the fungal agents encountered in fungal keratitis. Discuss the steps in
laboratory diagnosis of any one of them.(2016)
● Enumerate the viruses causing eye infections. Add a note on herpes simplex
virus(2016)(refer to micro notes for this, not covered adequately in
patho)
● Describe the healing of a corneal ulcer and the sequelae.(2015)

115. Short essays:
● Acanthamoeba keratitis(2024, 2022, 2023, 2018, 2016)
● Name the causes of bacterial keratitis. Describe the laboratory diagnosis of bacterial
keratitis(2024, 2017)
● Common bacterial infections of cornea and conjunctiva(2023)
● Epidemic keratoconjunctivitis(2022, 2019)
Short answers:
● Name any two Virus causing Eye infections.(2023)
● Name any two fungi causing eye infection(2023, 2022, 2021, 2019)
● What is Acanthamoeba keratitis?(2019)
● Name two bacterial infections of the eye.(2016)

116. For print-friendly version of
notes, click here or scan:
References:
- Ramadas Nayak - Textbook of Pathology
for Allied Health Sciences
- A.K Khurana - Comprehensive
Ophthalmology - 7th Ed.
Questions:
salman.s.ansari92@gmail.com
For updated PPT,
click here or scan: