GOOD MORNING &
CONGRATULATION
M.R.SHOJA
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M.R. SHOJA
Professor Of
Ophthalmology
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BACTERIAL KERATITIS
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An ocular emergency
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Prompt diagnosis
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Initiation of approtiate antibiotic
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Limit amount of tissue destruction
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Improve patient,s visual prognosis
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Most important defense barrier
for cornea is intact epithelial layer
Major risk factors for infectious
keratitis is compromised
epithelium protective layer .
Precipitating event is epithelial
defect produced by trauma,
contact lens wear or a chronic
corneal disorders
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Ocular
Defense
Mechanism
Chemical
Mechanical
Abnormality of tear film
• Intact corneal epitheliuma
Lysozym
(first line of defence)
Lactoferin
• Blinking reflex
immunoglubulinA
• (reduced bacterial colonization)
Mucin deficiency
Pathogenesis
Proliferation of Bacteria
Adherence to ulcerated epithelium
invasion into stroma
Migration of neutrophile
Production of proteinase
Inflammatory
necrosis
Neovascular scar formation
Corneal perforation
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Risk factors (Corneal)
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Trauma
Contact lens wear
Previous ocular surgery
Ocular adnexal disorders
Chronic surface disease of cornea
Decreased corneal sensation
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Risk
Factors
Systemic
condition
• Diabetes
• Systemic infections
• Collagen vascular diseases
• Immuno suppressive drug
• Pregnancy
• Chronic alcholism
• Extensive body burns
• Drug addiction
• AIDS
Local
Topical: Steroid
Antiviral
Antibiotic
Anesthestics
Chronic Corneal Surface
Disease

Bullous keratitis
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Exposure keratopathy
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Keratoconjunctivitis sicca
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Neurotrophic keratopathy
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Previous ocular surgery
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Cataract extraction
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Keratoplasty
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Pterygium excision
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Loose corneal sutures
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Refractive surgery
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Ocular Adnexal Conditions
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Entropion
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Ectropion
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Trichiasis
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Blepharitis /
Rosacea
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Normal flora of ocular surface
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GRAM POSITIVE:
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Staphylococcus Aureus (more common)
Staphylococcus Epidermidis (more common)
Propionibacterium acnes.
Streptococcus Viridans
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GRAM NEGATIVE
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(less common)
Escheria Coli
Klebsiella
Proteus
Moraxella
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Causes of Bacterial keratitis
(87%)
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus pneumoniea
Pseudomonas aeruginosa
Most common organism in soft contact lens
Enterobacteriaceae (proteus, enterobacter)
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ETIOLOGY
Now york
London
S.aureus
S.aureus
Pseudomonas
S.pneumonia
Moraxella
Pseudomonas
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Organisms penetrate intact epithelium
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Neisseria gonorroae
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Haemophilus agegyptius
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Corynebacterium diphteria
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Listeria
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Clinical presentation
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Rapid onset of pain
Conjunctival injection (Redness)
Photophobia
Decreased vision
Discharge and lid edema
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Clinical features of G+ & G- keratitis
Feature
Gram positive
Gram negative
Appearance
Mild to dense infiltrate Dense infiltrate
necrosis
Borders
Distinct infiltrate
borders
Indistinct borders
Surrounding cornea
hypopyon
Generally clear less
common M.R.SHOJA
Often hazy more
common
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CORNEAL PERFORATION
IN PSEUDOMONAS & GONOCOCCAL KERATITIS.
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SYMPTOMS:
SUDDEN LOSS OF HYPOPYON
RADIAL FOLD IN DESCEMET MEMBRANE
PROTRUSION OF CORNEA AND
DESMATOCELE FORMATION.
TREATMENT:
PATCH GRAFT OR
PENETRATING K.
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Pseudomonas
Keratitis (G -)
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Most common in Scls wear,burn ,comatose ,
mechanical respiratory patients.
Yellowish green hue with resistant to treatment.
Most common in children < 3 years Contaminant
in hospital, fluoresnce solutions.
Rapidly progressive,destructive keratitis.
May cause infectious Scleritis.
Within 24-48 h perforation may occur.
Systemic antibiotic is necessary.
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Gonococci Keratitis
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Hyperacute conjunctivitis , preauricular
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Penetrate intact epithelium ,produce rapid
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adenopathy
corneal ulceration and perforation as 24 to 48
hours after infection.
Choice of treatment is 1 g ceftriaxone IM or IV
for 3 to 5 days for keratitis.
Frequent irrigation is necessary.
Sexual partners should be evaluated.
In all hyperacute conjunctivitis the entire cornea
must be evaluated for ulceration
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Gonococci Conjunctivitis &
Keratitis
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Clinical signs of
resolution
Improved patient comfort
Progressive re-epithelialization over infiltrate
Decreasing size and density of infiltration.
Loss of adherent mucopurulent discharge
Reduction in hypopyon
Reduction of stromal edema surrounding infiltrate
Development of well-defined infiltrate borders
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Stain or culture media
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Stains
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Gram stain
Giemsa stain
Calcofluor white stain
Acid fast stain
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Culture media
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Blood agar
Sabourauds agar
Chocolate agar
Thioglycolate broth
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Goals of therapy
Rapid elimination of bacteria
 Reduction of inflammatory response
 Prevent of structural damage
 Promotion healing of epithelial
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Hospitalization
Monotherapy
Fluroquinolone
Treatment
Systemic Antibiotic
Fortified
combined drops
Corneal Graft
Drug penetartion in to cornea increased with
higher concentration and frequent application
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Treatment (Imprical)
Loading dose : 5 application every 2 Min
Frequent instillation every 30 Min
Fortified cephalosporin (50mg/dl) +
gentamycin or tobramycin (15mg/ml)
Modification of initial AB is based on culture
results and clinical response
For (G +) Vancomycin is alternative
For (G-) Ceftazidime or Amikacine
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Initial therapy for bacterial keratitis
Organism
Antibiotic
Topical dose
Gram- positive cocci
Cefazolin
Vancomycin *
50 mg/ml
50 mg/ml
Gram- negative rods
Tobramycin
Ceftazidime
Gentamycin
9-14 mg/ml
50 mg/ml
14 mg/ml
No organism or
multiple types of organisms
Cefazolin With
Tobramycin or
Fluoroquinolones
50 mg/ml
Ceftriaxone
ceftazidime
50 mg/ml
50 mg/ml
Gram-negative cocci
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3 mg/ml
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Antibiotics
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The choice of antibiotics is standard topical,
commercially unavailable, fortified
aminoglycoside and fortified cephalosporin
drops (ie gentamicin 1.5% and cefuroxime
5%) or the new regime of fluoroquinolone
monotherapy with commercially available
ciprofloxacin or ofloxacin 0.3%.
Currently both the standard and
fluoroquinolone regimen encounter bacterial
resistance in about 5% of cases
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Treatment
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Subconjunctival injection for impending
corneal perforation
Hydrophilic soft contact lens
Parenteral
1-Impending perforation
2-Perforated infection
3-Scleral involvement
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Topical
Corticosteroid
Inhibit chemotaxis &
phagocytosis
Reduced stromal
inflammatory reaction
Recurrent
of
infection
Limit tissue destruction by PMN
and neovascuarization with scar
•Not to be use in initial phase
•Favourable response to antibiotic is advised.
•Prednisolone acetate 1% QID
•Patient must have frequent follow-up
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Corneal Exposure
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Corneal Melt
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Corneal Ulcer
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Hypopion Ulcer
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Fungal Keratitis
Fungal keratitis is challenging corneal
disease and presents as very difficult form
bacterial keratitis. Difficulty arise in making
correct clinical and laboratory diagnosis. The
treatment of fungal keratitis is also difficult
due to poor availability of antifungal drugs
and delay in starting treatment.
Treatment is required on long term basis,
intensively and often cases require
therapeutic keratoplasty.
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Fungal Keratitis
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Fungi enter into corneal stroma through
epithelial defect, which may be due to
trauma, contact lens wear, bad ocular
surface or previous corneal surgery.
In stroma fungi multiply and causes tissue
necrosis and inflammatory reaction.
Organisms enter deep into the stroma and
through an intact Descemets membrane
into the anterior chamber and iris. They can
also involve Sclera.
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Risk Factors
1.
2.
3.
4.
5.
Trauma outdoor/ or the one which involves
plant matter (including contact lenses)
Topical medications:
corticosteroids,
anaesthetic drug abuse
topical broad spectrum antibiotics use for
long time
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Risk Factors
6. Systemic use of steroids
7. Corneal surgeries (Penetrating keratoplasty,
refractive surgery)
8. Chronic keratitis (herpes simplex, herpes
zoster, Vernal or allergic keratoconjunctivitis,
and neurotrophic ulcer)
9. Diabetes , Chronically ill / hospitalised
patients, AIDS and leprosy
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Causative fungi
I.
II.
Yeast: Candida species (albicans),
Cryptococcus
Filamentous septated
A. Non-pigmented hyphae: Fusarium
species (solani), Aspergillus species
(fumigatus, flavus, niger)
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Causative fungi
III. Filamentous non-septated : Mucor
and Rhizopus species
IV. Diphasic forms: Histoplasma,
Coccidiodes, Blastomyces
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Symptoms
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Onset is slow
Symptoms are less compared to signs
Diminution of vision, pain, foreign
body sensation
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Signs
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Diminution of vision, depending on
location of ulcer
Conjunctival and ciliary congestion
Epithelial defect
Stromal infiltrates
Elevated areas, hypate (branching)
ulcers, irregular feathery margins
Dry and rough texture
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Fungal Keratitis with
Hypopyon
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Signs
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Satellite lesions
Brown pigmentation due to
dematiaceous fungus (Curvularia
lunata)
Intact epithelium with stromal
infiltrates
Anterior chamber reaction
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Fungal Keratitis
Fungal Keratitis – Pigmented Lesion
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Case of Fungal+ Bacterial
Keratitis
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Laboratory Diagnosis
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The Gram and Giemsa stains are used as
initial stains
Potassium Hydroxide (10-20 %) wet mounts
Culture Media: Sheep blood agar, Chocolate
agar, Sabouraud dextrose agar,
Thioglycollate broth
Anterior chamber tap under aseptic
conditions to aspirate hypopyon and or
endothelial plaque
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Treatment
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Natamycin 5% suspension: Candida
species respond better to Amphotericin
B 0.15%
Fluconazole 2%
Miconazole 1%
Scrapping every 24 to 48 hours
Treatment is required for 4 – 6 weeks
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Treatment
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Sub-conjunctival injection of Miconazole 5 –
10 mgm of 10 mgm/ml suspension
(indicated in severe form of keratitis,
scleritis and endophthalmitis)
Systemic:
Fluconazole or Ketoconazole is indicated in
severe form of keratitis, scleritis and
endophthalmitis
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Surgical Treatment
1.
2.
3.
Daily debridement with spatula/ blade every 24 –
48 hours
Surgical treatment is required in approximately 1/3rd
cases of fungal keratitis due to failure of medical
treatment or perforation
Surgical treatment in the form of :
therapeutic keratoplasty, conjunctival flap or
lamellar keratoplasty
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Surgical Treatment
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Surgery is usually indicated within 4 weeks
due to failure of medical treatment or
recurrence of infection
Unfavorable outcome is due to scleritis,
endophthalmitis and recurrence
Cryotherapy with topical antifungal
treatment or corneoscleral graft in cases of
fungal scleritis and keratoscleritis
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Viral Keratitis
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Herpes Simplex
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Large dendrites with central ulceration and
terminal bulbs
Herpes Zoster
Small, medusa-like dendrites WITHOUT
central ulceration or terminal bulbs
Herpes Simplex Keratitis:
Pathogenesis

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HSV is a DNA virus that commonly infects
humans
Two distinct strains exist
– HSV-1: orofacial and ocular
– HSV-2: orogenital STD, neonatal

Recurrent HSV keratitis is one of the most
frequent causes of infective corneal blindness
in the US
Herpes Simplex Keratitis:
Primary Ocular Infection
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Most commonly occurs on the mucocutaneous
areas of the head innervated by CN V
Manifests as a nonspecific URI
May travel to the sensory ganglion and remain
in a latent nonpathogenic state
HSV:Primary Ocular Infection:
Clinical Presentation
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Unilateral vesicular
blepharokeratoconjunctivitis
Follicular conjuntivitis with
occasional membrane
formation
Cutaneous vesicles on eyelid
skin or margin
Preauricular nodes
2/3 develop epithelial
keratitis
HSV: Primary Ocular Infection
Treatment
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Self-limited condition
Topical antiviral therapy
– Trifluridine (Viroptic)
– Vidarabine
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Oral antiviral therapy (one week)*
– Acyclovir 400mg 5x/day
– Famcyclovir 500mg 3x/day
*may reduce recurrence rate