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Microbial
Keratitis
By
Haseeb Ahmed Bhatti
Ziauddin Medical College
CORNEA
The cornea is a round, convex, transparent,
avascular structure that forms the anterior one-
sixth of the outer coat of eyeball
•Vertical diameter is 10.6mm
•Horizontal diameter is11.7mm
•Cornea is thinnest at its center and
thicker at periphery
•Is avascular and devoid of lymphatic
drainage
•Nerve supply is from long ciliary
nerves, a branch of the ophthalmic
division of trigeminal nerve.
•Refractory power = +43diopter
Histologically
consists of five
layers
• The epithelium
• The bowman’s
membrane
• The stroma
• The
descement’s
membrane
• The
endothelium
Microbial/Infective Keratitis
Inflammation of the cornea,
resulting from the menace of
micro-organisms.
The keratitis may be :
1. Bacterial
2. Fungal
3. Viral
4. Protozoal
Bacterial Keratitis
Most common-Suppurative corneal ulceration
Etiology
 Staphylococcus aureus
 Streptococcus pneumoniae
 Niesseria gonorrhea
 Hemophilus influenza
 Pseudomonas aerogenosa
 Moraxella
 Other gram –ve bacilli
Predisposing Factors
1. Corneal epithelial trauma
2. Contact lens Wearers
3. Aqueous tear deficiency
4. Chronic use of Steroids
5. Hypovitaminosis A
Pathogenesis of Corneal ulcer
Occurs through four stages:
1) Infiltrative stage: Injury to epithelium causes
inflammation, with PMN cell infiltrates and
edema, giving rise to a yellow/white corneal
opacity
2) Active stage: Necrosis and sloughing off of
epithelium causing ulcer formation.
3) Regressive stage: A line of demarcation
develops around the ulcer consisting of
leucocytes while the surrounding cornea
becomes clear. This is induced by treatment or
natural host mechanisms.
4) Cicatrization stage: Healing by
Symptoms
 Sudden/Rapid onset
 Pain
 Foreign body sensation
 Photophobia
 Blurred vision
 Redness of eye
 Muco-purulent Discharge
Bacterial
corneal
Ulceration
with
Accumulation
of
Pus inside
the
Eye –Anterior
chamber
(hypopyon).
Signs
 Upper eyelid Edema and discharge
 Cunjuctival hyperemia
 Surrounding corneal inflammation (focal
or difffuse) - Haziness
 Ulceration of epithelium
 Corneal Stain positive
 Hypopyon/Sterile pus
 Raised IOP
Acute
painful red
eye with
White spot
on Corneal
surface.
 Strep-
pneumonia
Corneal ulcer
Management
 Admission if Necessary
 Proper History & Examination
 Investigations
Baseline
Microbiological - C/S
 Treatment
Treatment
1. Infection Control – Antibiotics
 Dual therapy (Aminoglycoside+cephalosporin)
 Mono therapy (Flouroquinolones)
 Systemic (Ciprofloxacin 750mg bd)
2. Atropine 1%
 Pain relief
 Prevent posterior synechie formation
 Decrease exudation by decreasing capillary
permeability
3. Antigluacoma drugs
 Decrease IOP
4. Prevention of perforation
 Pressure bandage
 Conjuctival flap
 Therapeutic corneal graft
Treatment
Complications
 Toxic Iridocyclitis
 Secondary Glaucoma
 Descemetocele
 Perforation of corneal ulcer
 Corneal scarring
Fungal keratitis
 Aspergillus
 Fusarium
Filamentous
Most common in Tropical climates
 Candida
Non-filamentous/Yeast
Most common in temperate climate
Predisposing Factors
 Trauma-organic matter (wood+plants)
 Chronic use of topical steroids
 Ocular surface disease
 Compromised immune system
Symptoms
 Gradual onset - slow progress
 Foreign body sensation
 Photophobia
 Blurred vision
 Discharge - Purulent
Signs
 Greyish white ulcer that has delicate fine
feathery edges
 Elevated surface & irregular contour
 Endothelial plaque may be present
 Progressive infiltration, may be
surrounded by stellate lesions
 Immune ring
 Ciliary congestion
 Yeast: Yellow white ulcer with dense
suupuration
Management
 History & Examination
 Investigation
Baseline
Giemsa , KOH and methamine silver stain
Culture
 Treatment
Treatment
 Topical Antifungal therapy
Natamycin 5% suspension
Fluconazole 2% suspension
Amphotericin B 0.15% solution
 Systemic Antifungal therapy
Ketoconazole 200-600mg od
Fluconazloe 200-400mg od
 Mechanical debridement
 Therapeutic keratoplasty
Protozoal keratitis
 Acanthamoeba spp.
 Microsporidea
o Acanthamoeba is free living ubiquitous
protozoa found in fresh water and soil
o Active trophozoite or dormant cyst
Risk factors
Contact lens
Ocular trauma – Corneal
abrasion
Herpetic keratitis
Clinical features
Symptoms: Blurred vision, Severe pain &
Photophobia
Signs:
 Diffuse punctate Epitheliopathy
 Epithelial pseudodentrites
 Limbitis-diffuse or focal anterior stromal
infiltrates
 Ring Abcess
 Perineural infiltrates (radial keratoneuritis)
– enlargement of corneal nerves
Diagnosis
 Soft contact leans wear
 Severe persistant pain
 Radial keratoneuritis
 Identification of Amoebis cyst in
smear & culture
 Calcoflour white (flourescent dye)
 Laminar corneal biopsy
Treatment
 Debridement – infected epithelium
 Topical Amoebicides as dual therapy
a. Propamidine isethionate 0.1% (broline) +
Polyhexamethyl biguanide 0.02%
b. Neomycin + Broline + Chlorhexadine 0.02%
 Therapeutic keratoplasty
Avoid in Inflammed eyes
Viral Keratitis
 Herpes simplex
 Herpes zoster
 Adenovirus
 Measles
 Paramyxovirus parotitis
 CMV
 EBV
Herpes Simplex keratitis
 DNA virus of he Herpesviridae Family
 Infection is extremely common
 Major cause ofunilateral corneal scarring
worldwide
 TYPE 1
 Predominantly causes infection above the waist.
 Droplet infection or close contact with infected
individual
 TYPE 2
 Below the Waist (genital herpes)
 STD
 Genital secretions - Birth
Primary infection
 Infection in early life
 Uncommon during first six months
 Subclinical causing mild fever and malaise
 Virus eventually travels up the axon of sensory
nerves into its ganglions.
 Type 1 remains dormant in trigeminal ganglion
 Type 2 in spinal ganglia.
Ocular involvement
 Blepharitis
 Acute Follicular Conjunctivitis
 Epithelial Punctuate Keratitis
Pathogenesis
Recurrent keratitis
 Poor health
 Exposure to ultraviolet rays
 Fever
 Psychatric disturbance
 Use of steroids.
 Lesions
 Acute/Active Epithelieal Keratitis
 Stromal Keratitis
 Kerato uveitis.
Clinical Features of HSV keratitis
Symptoms
 Foreign Body Sensation
 Lacrimation – Watery discharge
 Photophobia
 Pain (mild to moderate)
 Reduced Vision
Signs
 Ciliary congestion
 Diminished corneal Sensitivity
Active epithelial keratitis: Dendritic ulcer
 Most characteristic lesion, occurs in corneal
epithelium
 Typical branching, linear pattern with
feathery edges and terminal bulbs at ends.
 Visualized by fluorescein staining
HSV dendritic ulcer stained
with fluorescein
Geographic/Amoeboid ulceration
Delicate dendritic lesions take
a broader form.
Diagnosis
 Morphological appearance of corneal ulcer
 Diminished corneal Sensitivity
Differential diagnosis
 Herpes zoster Keratitis
 Acanthomebia Keratitis
 Healing Corneal ulcer
 Toxic drug Keratopathy
Treatment
 Topical Anti-viral drugs
I. Acycloguanosine - Acyclovir
II. Trifluorothymidine
III.Adenine Arabinoside
IV.Idoxuridine
 Debridement
 Topical antibiotics
 Cycloplegics
o Active viral invasion and destruction of Endothelium
of cornea
Signs
 Stroma appears cheesy and necrotic.
 Keratic precipitates or KP bodies (Anterior Uveitis)
 Features of AEK may be present.
Stomal Necrotic Keratitis
Treatment
Topical Antivirals
Topical Antibiotics
Topical Cycloplegics
Lubricants/Pressure patching Bandage contact lens
Disiform Keratits
 Definition: It is viral endothelitis in
which there is disc shaped grey area
of stromal edema with localised
keratic precipitates
o Reactivated viral infection of
keratocytesand Endothelium
o Hypersensitivity reaction to viral
antigen
Clinical Features
 Central zone of epithelial
edema
 Stromal thickening - edema
 Folds in descemet;s
membrane
 Mild to moderate anterior
uveitis
 Keratic precipitates
 Reduced corneal sensitivity
Treatment
 Topical Antiviral
 Topical antibiotics
 Topical weak steroids
 Cycloplegics
• Caused by HHV3 (VZV)
• Primary infection as Chicken pox
• Virus may travel into sensory ganglia of dorsal
root ganglion and trigeminal nerve ganglion
• Reactivation of virus causes Herpes Zoster or
Herpes Zoster opthalmicus
Mechanism of damage.
Cellular infiltration
Ischemic vasculitis
Inflamatory granulomatous reaction
Herpes Zoster Ophthalmicus (HZO)
Pain
Rashes
Edema
Post Herpetic Neuralgia
Corneal lesions
 Acute epithelial keratitis
 Microdendritic ulcer
 Nummular keratitis
 Diciform keratitis
 Reduced corneal sensation
Other Ocular Features
 Conjunctivitis
 Episcleritis
 Secondary glaucoma
 Anterior Uveitis
Clinical Features
Neurologic complications
o Cranial nerve palsy
Mostly 3rd nerve
o Optic neuritis
1:400
Treatment
Systemic
 Acyclovir – 800mg 5/day
 Analgesics
 Antibiotics
 Systemic steroids - prednisolone 40-
60mg
References
 Jack J. Kanski's Clinical
Ophthalmoscopy a Systemic
Approach fifth edition
 Infective keratitis lecture by Dr.
Shabbir Hussain, Department of
Ophthalmology
Edward S. Harkness institute,
columbia university college of
physicians and surgeons
 Clinical Opthalmology; Shafi M.
Jatoi
EnjoIX

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Microbial keratitis

  • 2. CORNEA The cornea is a round, convex, transparent, avascular structure that forms the anterior one- sixth of the outer coat of eyeball
  • 3. •Vertical diameter is 10.6mm •Horizontal diameter is11.7mm •Cornea is thinnest at its center and thicker at periphery •Is avascular and devoid of lymphatic drainage •Nerve supply is from long ciliary nerves, a branch of the ophthalmic division of trigeminal nerve. •Refractory power = +43diopter
  • 4. Histologically consists of five layers • The epithelium • The bowman’s membrane • The stroma • The descement’s membrane • The endothelium
  • 5. Microbial/Infective Keratitis Inflammation of the cornea, resulting from the menace of micro-organisms. The keratitis may be : 1. Bacterial 2. Fungal 3. Viral 4. Protozoal
  • 6. Bacterial Keratitis Most common-Suppurative corneal ulceration Etiology  Staphylococcus aureus  Streptococcus pneumoniae  Niesseria gonorrhea  Hemophilus influenza  Pseudomonas aerogenosa  Moraxella  Other gram –ve bacilli
  • 7. Predisposing Factors 1. Corneal epithelial trauma 2. Contact lens Wearers 3. Aqueous tear deficiency 4. Chronic use of Steroids 5. Hypovitaminosis A
  • 8. Pathogenesis of Corneal ulcer Occurs through four stages: 1) Infiltrative stage: Injury to epithelium causes inflammation, with PMN cell infiltrates and edema, giving rise to a yellow/white corneal opacity 2) Active stage: Necrosis and sloughing off of epithelium causing ulcer formation. 3) Regressive stage: A line of demarcation develops around the ulcer consisting of leucocytes while the surrounding cornea becomes clear. This is induced by treatment or natural host mechanisms. 4) Cicatrization stage: Healing by
  • 9. Symptoms  Sudden/Rapid onset  Pain  Foreign body sensation  Photophobia  Blurred vision  Redness of eye  Muco-purulent Discharge
  • 11. Signs  Upper eyelid Edema and discharge  Cunjuctival hyperemia  Surrounding corneal inflammation (focal or difffuse) - Haziness  Ulceration of epithelium  Corneal Stain positive  Hypopyon/Sterile pus  Raised IOP
  • 12. Acute painful red eye with White spot on Corneal surface.
  • 14. Management  Admission if Necessary  Proper History & Examination  Investigations Baseline Microbiological - C/S  Treatment
  • 15. Treatment 1. Infection Control – Antibiotics  Dual therapy (Aminoglycoside+cephalosporin)  Mono therapy (Flouroquinolones)  Systemic (Ciprofloxacin 750mg bd) 2. Atropine 1%  Pain relief  Prevent posterior synechie formation  Decrease exudation by decreasing capillary permeability
  • 16. 3. Antigluacoma drugs  Decrease IOP 4. Prevention of perforation  Pressure bandage  Conjuctival flap  Therapeutic corneal graft Treatment
  • 17. Complications  Toxic Iridocyclitis  Secondary Glaucoma  Descemetocele  Perforation of corneal ulcer  Corneal scarring
  • 18. Fungal keratitis  Aspergillus  Fusarium Filamentous Most common in Tropical climates  Candida Non-filamentous/Yeast Most common in temperate climate
  • 19. Predisposing Factors  Trauma-organic matter (wood+plants)  Chronic use of topical steroids  Ocular surface disease  Compromised immune system
  • 20. Symptoms  Gradual onset - slow progress  Foreign body sensation  Photophobia  Blurred vision  Discharge - Purulent
  • 21. Signs  Greyish white ulcer that has delicate fine feathery edges  Elevated surface & irregular contour  Endothelial plaque may be present  Progressive infiltration, may be surrounded by stellate lesions  Immune ring  Ciliary congestion  Yeast: Yellow white ulcer with dense suupuration
  • 22.
  • 23. Management  History & Examination  Investigation Baseline Giemsa , KOH and methamine silver stain Culture  Treatment
  • 24. Treatment  Topical Antifungal therapy Natamycin 5% suspension Fluconazole 2% suspension Amphotericin B 0.15% solution  Systemic Antifungal therapy Ketoconazole 200-600mg od Fluconazloe 200-400mg od  Mechanical debridement  Therapeutic keratoplasty
  • 25. Protozoal keratitis  Acanthamoeba spp.  Microsporidea o Acanthamoeba is free living ubiquitous protozoa found in fresh water and soil o Active trophozoite or dormant cyst
  • 26. Risk factors Contact lens Ocular trauma – Corneal abrasion Herpetic keratitis
  • 27. Clinical features Symptoms: Blurred vision, Severe pain & Photophobia Signs:  Diffuse punctate Epitheliopathy  Epithelial pseudodentrites  Limbitis-diffuse or focal anterior stromal infiltrates  Ring Abcess  Perineural infiltrates (radial keratoneuritis) – enlargement of corneal nerves
  • 28.
  • 29. Diagnosis  Soft contact leans wear  Severe persistant pain  Radial keratoneuritis  Identification of Amoebis cyst in smear & culture  Calcoflour white (flourescent dye)  Laminar corneal biopsy
  • 30. Treatment  Debridement – infected epithelium  Topical Amoebicides as dual therapy a. Propamidine isethionate 0.1% (broline) + Polyhexamethyl biguanide 0.02% b. Neomycin + Broline + Chlorhexadine 0.02%  Therapeutic keratoplasty Avoid in Inflammed eyes
  • 31. Viral Keratitis  Herpes simplex  Herpes zoster  Adenovirus  Measles  Paramyxovirus parotitis  CMV  EBV
  • 32. Herpes Simplex keratitis  DNA virus of he Herpesviridae Family  Infection is extremely common  Major cause ofunilateral corneal scarring worldwide  TYPE 1  Predominantly causes infection above the waist.  Droplet infection or close contact with infected individual  TYPE 2  Below the Waist (genital herpes)  STD  Genital secretions - Birth
  • 33. Primary infection  Infection in early life  Uncommon during first six months  Subclinical causing mild fever and malaise  Virus eventually travels up the axon of sensory nerves into its ganglions.  Type 1 remains dormant in trigeminal ganglion  Type 2 in spinal ganglia. Ocular involvement  Blepharitis  Acute Follicular Conjunctivitis  Epithelial Punctuate Keratitis Pathogenesis
  • 34. Recurrent keratitis  Poor health  Exposure to ultraviolet rays  Fever  Psychatric disturbance  Use of steroids.  Lesions  Acute/Active Epithelieal Keratitis  Stromal Keratitis  Kerato uveitis.
  • 35. Clinical Features of HSV keratitis Symptoms  Foreign Body Sensation  Lacrimation – Watery discharge  Photophobia  Pain (mild to moderate)  Reduced Vision Signs  Ciliary congestion  Diminished corneal Sensitivity
  • 36. Active epithelial keratitis: Dendritic ulcer  Most characteristic lesion, occurs in corneal epithelium  Typical branching, linear pattern with feathery edges and terminal bulbs at ends.  Visualized by fluorescein staining HSV dendritic ulcer stained with fluorescein
  • 37.
  • 39. Diagnosis  Morphological appearance of corneal ulcer  Diminished corneal Sensitivity Differential diagnosis  Herpes zoster Keratitis  Acanthomebia Keratitis  Healing Corneal ulcer  Toxic drug Keratopathy
  • 40. Treatment  Topical Anti-viral drugs I. Acycloguanosine - Acyclovir II. Trifluorothymidine III.Adenine Arabinoside IV.Idoxuridine  Debridement  Topical antibiotics  Cycloplegics
  • 41. o Active viral invasion and destruction of Endothelium of cornea Signs  Stroma appears cheesy and necrotic.  Keratic precipitates or KP bodies (Anterior Uveitis)  Features of AEK may be present. Stomal Necrotic Keratitis Treatment Topical Antivirals Topical Antibiotics Topical Cycloplegics Lubricants/Pressure patching Bandage contact lens
  • 42.
  • 43.
  • 44. Disiform Keratits  Definition: It is viral endothelitis in which there is disc shaped grey area of stromal edema with localised keratic precipitates o Reactivated viral infection of keratocytesand Endothelium o Hypersensitivity reaction to viral antigen
  • 45. Clinical Features  Central zone of epithelial edema  Stromal thickening - edema  Folds in descemet;s membrane  Mild to moderate anterior uveitis  Keratic precipitates  Reduced corneal sensitivity
  • 46.
  • 47.
  • 48. Treatment  Topical Antiviral  Topical antibiotics  Topical weak steroids  Cycloplegics
  • 49. • Caused by HHV3 (VZV) • Primary infection as Chicken pox • Virus may travel into sensory ganglia of dorsal root ganglion and trigeminal nerve ganglion • Reactivation of virus causes Herpes Zoster or Herpes Zoster opthalmicus Mechanism of damage. Cellular infiltration Ischemic vasculitis Inflamatory granulomatous reaction Herpes Zoster Ophthalmicus (HZO)
  • 50.
  • 51. Pain Rashes Edema Post Herpetic Neuralgia Corneal lesions  Acute epithelial keratitis  Microdendritic ulcer  Nummular keratitis  Diciform keratitis  Reduced corneal sensation Other Ocular Features  Conjunctivitis  Episcleritis  Secondary glaucoma  Anterior Uveitis Clinical Features
  • 52.
  • 53. Neurologic complications o Cranial nerve palsy Mostly 3rd nerve o Optic neuritis 1:400
  • 54. Treatment Systemic  Acyclovir – 800mg 5/day  Analgesics  Antibiotics  Systemic steroids - prednisolone 40- 60mg
  • 55. References  Jack J. Kanski's Clinical Ophthalmoscopy a Systemic Approach fifth edition  Infective keratitis lecture by Dr. Shabbir Hussain, Department of Ophthalmology Edward S. Harkness institute, columbia university college of physicians and surgeons  Clinical Opthalmology; Shafi M. Jatoi