1. GOOD MORNING & CONGRATULATION
M.R.SHOJA

2. M.R. SHOJA Professor Of Ophthalmology
Bacterial
keratitis
M.R. SHOJA
Professor Of
Ophthalmology
M.R.SHOJA

3. BACTERIAL KERATITIS An ocular emergency Prompt diagnosis
Initiation of approtiate antibiotic
Limit amount of tissue destruction
Improve patient,s visual prognosis
M.R.SHOJA

4. 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
M.R.SHOJA

5. Abnormality of tear film
Ocular
Defense
Mechanism
Chemical
Mechanical
Abnormality of tear film
Lysozym
Lactoferin
immunoglubulinA
Mucin deficiency
Intact corneal epitheliuma
(first line of defence)
Blinking reflex
(reduced bacterial colonization)

6. Pathogenesis
M.R.SHOJA

7. Risk factors (Corneal)
Trauma
Contact lens wear
Previous ocular surgery
Ocular adnexal disorders
Chronic surface disease of cornea
Decreased corneal sensation
M.R.SHOJA

8. Antiviral Antibiotic Anesthestics Risk Factors Systemic condition
Local
Diabetes
Systemic infections
Collagen vascular diseases
Immuno suppressive drug
Pregnancy
Chronic alcholism
Extensive body burns
Drug addiction
AIDS
Topical: Steroid
Antiviral
Antibiotic
Anesthestics

9. Chronic Corneal Surface Disease
Bullous keratitis
Exposure keratopathy
Keratoconjunctivitis sicca
Neurotrophic keratopathy
M.R.SHOJA

10. Previous ocular surgery
Cataract extraction
Keratoplasty
Pterygium excision
Loose corneal sutures
Refractive surgery
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11. Ocular Adnexal Conditions
Entropion
Ectropion
Trichiasis
Blepharitis / Rosacea
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12. Normal flora of ocular surface
GRAM POSITIVE:
Staphylococcus Aureus (more common)
Staphylococcus Epidermidis (more common)
Propionibacterium acnes.
Streptococcus Viridans
GRAM NEGATIVE (less common)
Escheria Coli
Klebsiella
Proteus
Moraxella
M.R.SHOJA

13. 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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14. ETIOLOGY
Now york London S.aureus S.aureus Pseudomonas Moraxella S.pneumonia Pseudomonas
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15. Organisms penetrate intact epithelium
Neisseria gonorroae
Haemophilus agegyptius
Corynebacterium diphteria
Listeria
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16. Clinical presentation
Rapid onset of pain
Conjunctival injection (Redness)
Photophobia
Decreased vision
Discharge and lid edema
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17. Clinical features of G+ & G- keratitis
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
Often hazy more common
M.R.SHOJA

18. CORNEAL PERFORATION IN PSEUDOMONAS & GONOCOCCAL KERATITIS. SYMPTOMS:
SUDDEN LOSS OF HYPOPYON
RADIAL FOLD IN DESCEMET MEMBRANE
PROTRUSION OF CORNEA AND
DESMATOCELE FORMATION.
TREATMENT:
PATCH GRAFT OR
PENETRATING K.
M.R.SHOJA

19. Pseudomonas Keratitis (G -)
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 h perforation may occur.
Systemic antibiotic is necessary.
M.R.SHOJA

20. Gonococci Keratitis
Hyperacute conjunctivitis , preauricular adenopathy
Penetrate intact epithelium ,produce rapid 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
M.R.SHOJA

21. Gonococci Conjunctivitis & Keratitis
M.R.SHOJA

22. 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
M.R.SHOJA

23. Stain or culture media Stains Culture media Gram stain Giemsa stain
Calcofluor white stain
Acid fast stain
Culture media
Blood agar
Sabourauds agar
Chocolate agar
Thioglycolate broth
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24. Goals of therapy Reduction of inflammatory response
Rapid elimination of bacteria
Reduction of inflammatory response
Prevent of structural damage
Promotion healing of epithelial
M.R.SHOJA

25. Monotherapy Fluroquinolone Fortified combined drops
Hospitalization
Monotherapy Fluroquinolone
Treatment
Fortified combined drops
Systemic Antibiotic
Corneal Graft
Drug penetartion in to cornea increased with higher concentration and frequent application
M.R.SHOJA

26. Loading dose : 5 application every 2 Min
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
M.R.SHOJA

27. Initial therapy for bacterial keratitis
Organism
Antibiotic
Topical dose
Gram- positive cocci
Cefazolin
Vancomycin *
50 mg/ml
Gram- negative rods
Tobramycin
Ceftazidime
Gentamycin
9-14 mg/ml
14 mg/ml
No organism or
multiple types of organisms
Cefazolin With
Tobramycin or
Fluoroquinolones
3 mg/ml
Gram-negative cocci
Ceftriaxone
ceftazidime
M.R.SHOJA

28. Antibiotics
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
M.R.SHOJA

29. Treatment Subconjunctival injection for impending corneal perforation
Hydrophilic soft contact lens
Parenteral
1-Impending perforation
2-Perforated infection
3-Scleral involvement
M.R.SHOJA

30. Topical Corticosteroid
Recurrent of
infection
Inhibit chemotaxis &
phagocytosis
Reduced stromal
inflammatory reaction
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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31. Corneal Exposure
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32. Corneal Melt
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33. Corneal Ulcer
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34. Hypopion Ulcer
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35. 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.
M.R.SHOJA

36. Fungal Keratitis
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.
M.R.SHOJA

37. Risk Factors
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
M.R.SHOJA

38. 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
M.R.SHOJA

39. Causative fungi Yeast: Candida species (albicans), Cryptococcus
Filamentous septated
A. Non-pigmented hyphae: Fusarium species (solani), Aspergillus species (fumigatus, flavus, niger)
M.R.SHOJA

40. Causative fungi
III. Filamentous non-septated : Mucor and Rhizopus species
IV. Diphasic forms: Histoplasma, Coccidiodes, Blastomyces
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41. Symptoms Onset is slow Symptoms are less compared to signs
Diminution of vision, pain, foreign body sensation
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42. Signs 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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43. Fungal Keratitis with Hypopyon
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44. Signs Satellite lesions
Brown pigmentation due to dematiaceous fungus (Curvularia lunata)
Intact epithelium with stromal infiltrates
Anterior chamber reaction
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45. Fungal Keratitis
Fungal Keratitis – Pigmented Lesion
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46. Case of Fungal+ Bacterial Keratitis
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47. Laboratory Diagnosis
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
M.R.SHOJA

48. Treatment
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
M.R.SHOJA

49. Treatment
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
M.R.SHOJA

50. Surgical Treatment
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
M.R.SHOJA

51. Surgical Treatment
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
M.R.SHOJA

52. Viral Keratitis Herpes Simplex Herpes Zoster
Small, medusa-like dendrites WITHOUT central ulceration or terminal bulbs
Large dendrites with central ulceration and terminal bulbs

53. Herpes Simplex Keratitis: Pathogenesis
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

54. Herpes Simplex Keratitis: Primary Ocular Infection
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

55. HSV:Primary Ocular Infection: Clinical Presentation
Unilateral vesicular blepharokeratoconjunctivitis
Follicular conjuntivitis with occasional membrane formation
Cutaneous vesicles on eyelid skin or margin
Preauricular nodes
2/3 develop epithelial keratitis

56. HSV: Primary Ocular Infection Treatment
Self-limited condition
Topical antiviral therapy
Trifluridine (Viroptic)
Vidarabine
Oral antiviral therapy (one week)*
Acyclovir 400mg 5x/day
Famcyclovir 500mg 3x/day
*may reduce recurrence rate