The document outlines various types of keratitis, including infective, allergic, and trophic forms, detailing their subcategories, causes, and clinical features. It emphasizes the significant role of pathogens in infective keratitis and the stages of corneal ulcer progression, alongside common treatments such as antibiotics and topical steroids. Additional insights cover specific conditions like herpes simplex keratitis and acanthamoeba keratitis, highlighting the need for targeted therapeutic approaches.

1. -SOLANKI RIDDHI
2ND YEAR (B.OPTOM)

2.  INFECTIVE KERATITIS:
I. BACTERIAL CORNEAL ULCERS
i. Hypopyon corneal ulcer
ii. Marginal catarrhal ulcer
iii. Mycotic corneal ulcer
II. VIRAL CORNEAL ULCERS
i. Herpes simplex keratitis
ii. Herpes zoster ophthalmicus
III. PROTOZOAL KERATITIS
i. Acanthamoeba keratitis

3.  ALLERGIC KERATITIS:
I. PHLYCTENULAR KERATITIS
II. VERNAL KERATITIS
III. ATOPIC KERATITIS
 TROPHIC:
I. NEUROPARALYTIC KERATITIS
II. EXPOSURE KERATITIS
 KERATITIS ASSOCIATED WITH DISEASES
OF SKIN & MUCOUS MEMBRANE:
I. ROSACEA KERATITIS

4.  KERATITIS ASSOCIATED WITH SYSTEMIC
COLLAGEN VASCULAR DISEASES
 IDIOPATHIC KERATITIS:
I. MOOREN’S ULCER

5. I. BACTERIAL CORNEAL ULCER:
 Being the most ant. part of eyeball, the
cornea is exposed to atmosphere & hence
prone to get infected easily.
 At the same time cornea is protected from
the defence mechanisms present in tears in
the form of lysozyme, betalysin, & other
protective proteins.
 Infective corneal ulcer may develop when:
 Either the local ocular defence mechanism is
jeopardised, or
 The causative organism is very virulent.

6. ETIOLOGY:
 Following 3 pathogens can invade the intact
corneal epithelium & produce ulceration:
i. Neisseria gonorrhoeae
ii. Corynebacterium diphtheriae
iii. Neisseria meningitidis.
1. Corneal epithelial damage: It may occur in
following conditions:
i. Corneal abrasion
ii. Epithelial drying
iii. Necrosis of epithelium
iv. Desquamation of epithelial cells
v. Epithelial damage due to trophic changes

7. 2. Source of infection include:
i. Exogenous infection
ii. From the ocular tissue
iii. Endogenous infection
3. Causative organism: common bacterias
associated with corneal ulceration are:
i. Staphylococcus aureus
ii. Pseudomonas pyocyanea
iii. Streptococcus pneumoniae
iv. E. coli
v. N. gonorrhoea
vi. N. meningitidis
vii. C. diphtheriae.

9. 1. Stage of progressive infiltration:
 It is characterised by the infiltration of
polymorphonuclear &/or lymphocytes into the
epithelium from the peripheral circulation
supplemented by similar cells from the
underlying stroma if this tissue is also
affected.
 Subsequently necrosis of the involved tissue
may occur.

10. 2. Stage of active ulceration:
 Active ulceration results from necrosis &
sloughing of the epithelium, bowman’s
membrane & the involved stroma.
 During this stage, accumulation of purulent
exudates on the cornea.
 There occurs vascular congestion of the iris &
ciliary body & some degree of iritis due to
absorption of toxins from the ulcer.

11. 3. Stage of regression:
 Regression is induced by the natural host
defence mechanisms.
 A line of demarcation develops around the
ulcer.
 The digestion of necrotic material may result
in initial enlargement of the ulcer.
 This process may be accompanied by
superficial vascularization that increases the
humoral & cellular immune response.
 The ulcer now begins to heal & epithelium
starts growing over the edges.

12. 4. Stage of cicatrization:
 In this stage, healing continues by progressive
epithelization which forms a permanent
covering.
 Beneath the epithelium, fibrous tissue is laid
down partly by the corneal fibroblasts &
partly by the endothelial cells of the new
vessels.
 The degree of scarring from healing varies.
 If the ulcer is very superficial & involves the
epithelium only, it heals without leaving any
opacity behind.
 When ulcer involves bowman’s layer& few
superficial stromal lamellae, the resultant
scar is called a ‘nebula’.

14.  Perforation of corneal ulcer occurs when the
ulcerative process deepens & reaches up to
descemet’s membrane.
 This membrane is tough & bulges out as
Descemetocele.
 At this stage, any exertion on the part of
patient, such as coughing, sneezing, straining for
stool etc. will perforate the corneal ulcer.
 Immediately after perforation, the aqueous
escapes, IOP falls & the iris-lens diaphragm
moves forward.
 When the perforation is small & opp. to iris
tissue, it is usually plugged & healing by
cicatrization proceeds rapidly.

16. i. HYPOPYON CORNEAL ULCER
 Causative Organisms:
i. Staphylococci
ii. Streptococci
iii. Gonococci
iv. Moraxella
v. Pseudomonas pyocyanea
vi. Pneumococcus.
 Source Of Infection: For pneumococcal
infection is usually the chronic dacryocystitis.

17. Clinical features:
 Symptoms:
i. Pain
ii. Foreign body sensation
iii. Watering
iv. Photophobia
v. Blurred vision
vi. Redness of eye.
 Signs:
i. Lids are swollen
ii. Blepharospasm
iii. Conjunctiva is chemosed
iv. Hyperaemia & ciliary congestion.

19.  Complications Of Corneal Ulcer:
1. Toxic iridocyclitis: usually associated with
cases of purulent corneal ulcer.
2. Secondary glaucoma: occurs due to
fibrinous exudates blocking the angle of ant.
chamber (inflammatory glaucoma)
3. Descemetocele: occurs when virulent
organisms extends upto descemet’s memb.
4. Perforation Of Corneal Ulcer: occurs due to
sudden strain due to cough, sneeze or spasm of
orbicularis muscle.
5. Corneal Scarring: It is the usual end result
of healed corneal ulcer.

21. TREATMENT:
i. Topical antibiotics: Ciprofloxacin or
Ofloxacin or Gatifloxacin (0.3%) eye drops,
ii. Cycloplegic drugs
iii. Systemic analgesics
iv. Anti-inflammatory drugs such as
paracetamol & ibuprofen
v. Vitamins ( A, B-complex & C)
vi. Hot fomentation
vii. Removal of any known cause of non-healing
ulcer
viii. Peritomy

22. ii. MARGINAL CATARRHAL ULCER
 These superficial ulcers situated near limbus
are frequently seen especially in old people.
ETIOLOGY:
 Marginal catarrhal ulcer is thought to be
caused by a hypersensitivity rxn to
staphylococcal toxins.
 It occurs in association with chronic
staphylococcal blepharoconjunctivitis.
 Moraxella & Haemophilus are also known to
cause such ulcers.

23. Clinical Features:
i. Patient usually presents with mild ocular
irritation, pain, photophobia & watering.
ii. The ulcer is shallow, slightly infiltrated &
often multiple, usually associated with
staphylococcal conjunctivitis.
iii. Recurrences are very common.
Treatment:
i. Topical corticosteroid
ii. Antibiotic therapy
iii. Treatment of associated blepharitis &
chronic

25. iii. MYCOTIC CORNEAL ULCER
 The incidence of suppurative corneal ulcers
caused by fungi has increased in the recent
years due to injudicious use of antibiotics &
steroids.
ETIOLOGY:
1. Causative fungi:
i. Aspergillus
ii. Fusarium
iii. Alternaria
iv. Penicillium.
v. Candida & Cryptococcus.

26. CLINICAL FEATURES:
Symptoms:
i. Pain
ii. Foreign body sensation
iii. Watering
iv. Photophobia
v. Blurred vision
vi. Redness of eye.
Signs:
i. Dry-looking
ii. Greyish white
iii. Delicate feathery finger-like extensions
iv. A sterile immune ring may be present
v. Multiple, small satellite lesions may be
present

27. TREATMENT:
i. Antifungal drugs
ii. Natamycin, Fluconazol, Nystatin
iii. Therapeutic penetrating keratoplasty

29. i. HERPES SIMPLEX KERATITIS
 Ocular infections with herpes simplex virus
(HSV) are extremely common & constitute
herpetic keratoconjunctivitis & iritis.
ETIOLOGY:
Herpes simplex virus (HSV):
 It is a DNA virus.
 Its only natural host is man.
 According to different clinical & immunological
properties, HSV is of two types: HSV type I
typically causes infection above the waist & HSV
type II below the waist (herpes genitalis).

30. Mode Of Infection:
1. HSV-I infection: It is acquired by kissing or
coming in close contact with a patient
suffering from herpes labialis.
2. HSV-II infection: It is transmitted to eyes of
neonates through infected genitalia of the
mother.
Ocular Lesions Of Herpes Simplex:
[A] Primary herpes:
1. Skin lesions
2. Conjunctiva-acute follicular conjunctivitis
3. Cornea

31. [B] Recurrent herpes:
1. Epithelial keratitis:
i. Punctuate epithelial keratitis
ii. Dendritic ulcer
iii. Geographical ulcer
2. Stromal keratitis
i. Disciform keratitis
ii. Diffuse stromal necrotic keratitis
3. Metaherpetic keratitis

32. [A] Primary Ocular Herpes
 Primary infection (first attack) involves a
nonimmune person.
 It typically occurs in children betn 6 months &
5 yrs & in teenagers.
Clinical Features:
1. Skin lesions: Vesicular lesions may occur
involving skin of lids, periorbital region & the
lid margin.
2. Acute follicular conjunctivitis with regional
lymphadenitis is the usual.
3. Keratitis: Cornea is involved in about 50% of
the cases. The keratitis can occur as a coarse
punctuate or diffuse branching epithelial.

33. [B] Recurrent Ocular Herpes
 The virus which lies dormant in the trigeminal
ganglion, periodically reactivates & causes
recurrent infection.
1. Epithelial keratitis:
i. Punctuate epithelial keratitis:
 The initial epithelial lesions of recurrent
herpes resemble those seen in primary herpes
& may be either in the form of fine or coarse
superficial punctuate lesions.
ii. Dendritic ulcer:
 Dendritic ulcer is a typical lesion of recurrent
epithelial keratitis.
 The ulcer is of an irregular, zigzag linear
branching shape.

34. iii. Geographical ulcer:
 Sometimes, the branches of dendritic ulcer
enlarge & coalesce to form a large epithelial
ulcer with a ‘geographical’ or ‘amoeboid’
configuration, hence the name.
Symptoms
i. Photophobia
ii. Lacrimation
iii. Pain.
Treatment same as of epithelial keratitis.

35. 2. Stromal Keratitis:
i. Disciform keratitis:
 Endothelium damage results in corneal
oedema due to imbibation of aqueous humour.
Signs:
i. Focal disc-shaped patch of stromal oedema
w/o necrosis
ii. Folds in descemet’s memb
iii. Keratic precipitates
iv. Ring of stromal infiltrate
v. Corneal sensations are diminished
vi. IOP may be raised.
Treatment: consists of diluted steroid eye
drops (acyclovir 3%).

36. ii. Diffuse Stromal Necrotic Keratitis:
 It is a type of interstitial keratitis caused by
active viral invasion & tissue destruction.
Symptoms:
i. Pain
ii. Photophobia
iii. Redness
Signs:
i. Necrotic
ii. Blotchy
iii. Cheesy white infiltrates
Treatment: Keratoplasty.

37. 3. Metaherpetic Keratitis:
 It is not an active viral disease, but is a
mechanical healing problem which occurs at
the site of a previous herpetic ulcer.
Clinically it represents as an indolent linear or
ovoid epithelial defect.
Treatment
i. Lubricants (artificial tears)
ii. Bandage soft contact lens
iii. Lid closure (tarsorrhaphy).

39. ii. HERPES ZOSTER OPHTHALMICUS
 Herpes zoster ophthalmicus is an acute
infection of Gasserian ganglion of the Vth
cranial nerve by the varicella-zoster virus
(VZV).
 It constitutes approx 10% of all cases of herpes
zoster.
ETIOLOGY
Varicella-zoster virus:
 It is a DNA virus & produces acidophilic
intranuclear inclusion bodies.
 It is neurotropic in nature.

40. Clinical Features
i. Frontal nerve is more frequently affected
than the lacrimal & nasociliary nerves.
ii. About 50% cases of herpes zoster
ophthalmicus get ocular complications.
iii. The Hutchinson’s rule, which implies that
ocular involvement is frequent if the side or
tip of nose presents vesicles, is useful but
not infallible.
iv. Lesions of herpes zoster are strictly limited
to one side of the midline of head.

41. Clinical Phases of H. zoster ophthalmicus
are:
i. Acute, which may totally resolve.
ii. Chronic, which may persist for years.
iii. Relapsing, where the acute or chronic
lesions reappear sometimes years later.
Treatment:
i. Oral antiviral drugs
ii. Cimetidine
iii. Amitriptyline
iv. Antibiotic-corticosteroid skin ointment or
lotions
v. Keratoplasty

43. i. ACANTHAMOEBA KERATITIS
 Acanthamoeba keratitis has recently gained
importance because of its increasing
incidence, difficulty in diagnosis &
unsatisfactory treatment.
ETIOLOGY
 Acanthamoeba is a free lying amoeba found
in soil, fresh water, well water, sea water,
sewage & air.
 It exists in trophozoite & encysted forms.

44. CLINICAL FEATURES
Symptoms :
i. Very severe pain
ii. Watering
iii. Photophobia
iv. Blepharospasm
v. Blurred vision.
Signs :
i. Initial lesions in the form of Limbitis, Coarse,
Opaque Streaks, Fine Epithelial & Sub-
Epithelial Opacities & Radial Kerato-neuritis.
ii. Advanced cases shows a central or
paracentral ring-shaped lesion with
stromal.Hypopyon may also be present.

45. Treatment :
It is usually unsatisfactory:
i. Non-specific treatment is on the general
lines for corneal ulcer.
ii. Specific medical treatment includes:
propamidine isethionate(0.1%), neomycin
drops, polyhexamethylene biguanide (0.01-
0.02%).
iii. Penetrating keratoplasty is frequently
required in non-responsive cases.

47. I. PHLYCTENULAR KERATITIS
 Corneal involvement may occur secondarily
from extension of conjunctival phlycten; or
rarely as a primary disease.
 It may present in 2 forms:
A. Ulcerative phlyctenular keratitis
B. Diffuse infiltrative keratitis

48. A. Ulcerative Phlyctenular Keratitis
May occur in the following 3 forms:
1. Sacrofulous ulcer:
• Is a shallow marginal ulcer formed due to
breakdown of small limbal phlycten.
• Such an ulcer usually clears up without leaving
any opacity.
2. Fascicular ulcer:
• It has a prominent parallel leash of blood vessels.
• This ulcer usually remains superficial but leaves
behind a band-shaped superficial opacity after
healing.
3. Miliary ulcer:
• In this form multiple small ulcers are scattered
over a portion of or whole of the cornea.

50. B. Diffuse Infiltrative Phlyctenular
Keratitis
 It may appear in the form of central
infiltration of cornea with characteristic rich
vascularization from the periphery, all around
the limbus.
 It may be superficial or deep. Recurrences are
very common.
Treatment
i. Topical steroids
ii. Antibiotic drops & ointments
iii. Atropine (1%) eye ointment.

52. II. VERNAL KERATITIS
 Corneal involvement in VKC may be primary
or secondary due to extension of limbal
lesions.
 Vernal keratitis includes following 5 types of
lesions:
1. Punctuate epithelial keratitis
2. Ulcerative vernal keratitis (shield
ulcertaion)
3. Vernal corneal plaques
4. Subepithelial scarring
5. Pseudogerontoxon

53. 1. Punctuate epithelial keratitis
• Involving upper cornea is usually associated with
palpebral form of disease.
2. Ulcerative vernal keratitis
• Presents as a shallow transverse ulcer in upper part
of cornea.
• The ulceration results due to epithelial
macroerosions.
3. Vernal corneal plaques
• Result due to coating of bare areas of epithelial
macroerosions with a layer of altered exudates.
4. Subepithelial scarring
• Occurs in the form of a ring scar.
5. Pseudogerontoxon
• Is characterised by a classical ‘cupid’s bow’ outline.

54. Treatment
i. Topical steroids
ii. Mast cell stabilizers
iii. Topical antihistaminics
iv. Acetyl cysteine
v. Topical cyclosporine
vi. Supratarsal injection
vii. Cryo application
viii. Surgical excision

56. III. ATOPIC KERATITIS
 It is an adult equivalent of vernal keratitis & is
often associated with atopic dermatitis.
 Most of the patients are young atopic adults, with
male predominance.
Symptoms include:
i. Itching, soreness, dry sensation
ii. Mucoid discharge
iii. Photophobia or blurred vision
Signs
i. Lid margins are chronically inflammed with
rounded posterior borders.
ii. Tarsal conjunctiva has milky appearance.
iii. Cornea may show punctuate epithelial keratitis.

57. Treatment is often frustrating
i. Treat facial eczema & lid margin disease.
ii. Sodium cromoglycate drops, steroids & tear
supplements may be helpful for
conjunctival lesions.

59.  Trophic corneal ulcers develop due to
disturbance in metabolic activity of
epithelial cells.
 This group includes:
I. Neuroparalytic Keratitis
II. Exposure Keratitis

60. I. NEUROPARALYTIC KERATITIS
 Neuroparalytic keratitis occurs due to paralysis
of the sensory nerve supply of the cornea.
Causes
1. Congenital
i. Familial dysautonomia (Riley-Day syndrome)
ii. Congenital insensitivity to pain.
iii. Anhidrotic ectodermal dysplasia.
2. Acquired
i. Following alcohol-block or electrocoagulation
of Gasserian ganglion or section of the
sensory root of trigeminal nerve for
trigeminal neuralgia.

61. ii. A neoplasm pressing on Gasserian ganglion.
iii. Gasserian ganglion destruction due to
acute infection in herpes zoster
ophthalmicus.
iv. Acute infection of Gasserian ganglion by
herpes simplex virus.
v. Syphilitic (luetic) neuropathy.
vi. Involvement of corneal nerves in leprosy.
vii. Injury to Gasserian ganglion.

62. Clinical Features
i. Characteristics features are no pain, no
lacrimation, & complete loss of corneal
sensations.
ii. Ciliary congestion is marked.
iii. Corneal sheen is dull.
iv. Initial corneal changes are in the form of
punctuate epithelial erosions in the inter-
palpebral area followed by ulceration due
to exofoliation of corneal epithelium.
v. Relapses are very common, even the
healed scar quickly breaks down again.

63. Treatment
i. Initial treatment with antibiotic & atropine
eye ointment.
ii. Topical nerve growth factor drops &
amniotic membrane transplantation.
iii. If, however, relapses occur, it is best to
perform lateral tarsorrhaphy which should
be kept for at least one year.
iv. Along with it prolonged use of artificial
tears is also recommended.

65. II. EXPOSURE KERATITIS
 Normally cornea is covered by eyelids during
sleep & is constantly kept moist by blinking
movements during awaking.
 When eyes are covered insufficiently by the
lids & there is loss of protective mechanism
of blinking the condition of exposure
keratopathy develops.
Causes
1. Extreme proptosis due to any cause will
allow inadequate closure of lids.
2. Bell’s palsy or any other cause of facial
palsy.
3. Ectropion of severe degree.
4. Symblepharon causing lagophthalmos.

66. Clinical Features
i. Initial dessication occurs in the
interpalpebral area leading to fine
punctuate epithelial.
ii. Bacterial superinfection may cause deep
suppurative ulceration which may even
perforate.
Treatment
i. Topical antibiotics
ii. Cycloplegic drugs
iii. Systemic analgesics
iv. Vitamins (A,B-complex & C )
v. Hot fomentation.

68. I. ROSACEA KERATITIS
Clinical Features
i. The condition typically occurs in elderly
women in the form of facial eruptions
presenting as butterfly configuration.
ii. Ocular lesions include chronic
blepharoconjunctivitis & keratitis.
iii. Rosacea keratitis occurs as yellowish white
marginal infiltrates & small ulcers.
Treatment
i. Topical steroids
ii. Long course of systemic tetracycline.

70.  Peripheral corneal ulceration &/or melting of
corneal tissue is not infrequent occurrence in
patients suffering from systemic diseases
such as rheumatoid arthritis, systemic lupus
rythematosus, polyarteritis nodosa &
Wegener’s granulomatosis.
 Such corneal ulcers are usually indolent &
difficult to treat.
 Systemic treatment of the primary disease
may be beneficial.

72. I. MOOREN’S ULCER
The Mooren’s ulcer (chronic serpiginous or
rodent ulcer) is a severe inflammatory
peripheral ulcerative keratitis.
ETIOLOGY
Exact etiology is not known. Different views
are:
1. It is an idiopathic degenerative condition.
2. It may be due to an ischaemic necrosis
resulting from vasculitis of limbal vessels.
3. It may be due to the effects of enzyme
collagenase & proteoglyconase from
conjunctiva.

73. Clinical Features
Two clinical varieties of Mooren’ ulcer have
been recognised.
1. Benign form which is usually unilateral,
affects the elderly people & is characterised
by a relative slow progress.
2. Virulent type also called the proressive form
is bilateral, more often occurs in younger
patients. The ulcer is rapidly progressive
with a high incidence of scleral
involvement.

74. Symptoms
i. Severe pain
ii. Photophobia
iii. Lacrimation
iv. Defective vision.
Signs
i. Patches of grey infiltrates which coalesce
to form a shallow furrow over the whole
cornea.
ii. Whitish overhanging edge.
iii. The ulcer rarely perforates & the sclera
remains uninvolved.

75. Treatment
i. Topical corticosteroids
ii. Immunosuppressive therapy
iii. Soft contact lenses
iv. Lamellar or full thickness corneal grafts.