This document discusses microbial keratitis, specifically bacterial keratitis. It defines bacterial corneal ulcer as tissue destruction within the corneal layers due to bacterial infection and proliferation. The four main bacterial causes are discussed. Risk factors include trauma, eyelid abnormalities, dry eye, contact lens use, and systemic diseases. Bacterial keratitis progresses through stages including necrosis, line of demarcation, and healing. Diagnosis involves clinical examination, corneal scraping for culture/sensitivity, and treatment involves topical and sometimes systemic antibiotics based on culture results with the goal of preventing complications like perforation and scarring.

1. Dr. Aftab Ahmed Khan

2. Introduction
 Microbial keratitis is a common, potentially sight-
threatening ocular infection caused by bacteria,
viruses, fungi, or parasites .
 Sequelae from microbial keratitis constitute a leading
cause of corneal blindness worldwide.
 The clinical challenge is to distinguish microbial
keratitis from other noninfectious inflammatory
conditions of the cornea.

3.  Today we will discus about the principal bacterial
causative organisms, risk factors, pathogenesis, clinical
features, laboratory diagnostic techniques, and the
medical and surgical therapies for bacterial keratitis.

4. Definition of Bacterial Corneal ulcer
 Tissue destruction within the corneal layers due to
infection and proliferation of bacteria(s).

5. Etiology
Principle Causes
 There are four principal groups of bacteria that are most
frequently responsible .
1)Micrococcaceae – Staphylococcus, Micrococcus
2)Streptococcus species
3)Pseudomonas species- Most common in contact lens wearer.
4)Enterobacteriaceae -Citrobacter, Klebsiella, Enterobacter,
Serratia, Proteus).
 Since the development of a vaccine against Corynebacterium
diphtheriae, isolation of the organism from the eye is rare.

6.  Primary tuberculous keratitis is now extremely rare.
 Nontuberculous mycobacteria, including
Mycobacterium fortuitum , Mycobacterium chelonae ,
Mycobacterium gordonae , and Mycobacterium
avium- intracellulare are all capable of causing an
indolent keratitis, especially after injury with a foreign
body or surgical procedures.
 But any bacteria can potentially cause keratitis under
certain favorable conditions. A classification of the
medically important bacteria.

8. Barriers to microbial infections
 Intact Corneal epithelium – Most of the bacterias
cannot penetrate the intact epithelium but N.
gonorrhoea, N. Meningitidis, H. Influenzae ,
Corynebacterium Diptheriae and Listeria can
penetrate it.
 Eyelid and cillia – Protect the eyes from direct access of
organism.
 Tear film- Provides natural irrigation to remove
organism and it contains immunoglobulins,
complement components and enzymes(Lysozyme,
lectoferrin , betalysin) which are capable to destroy
microrganism.

9.  Normal bacterial flora- To prevent
overgrowth of exogenous organism.
 Conjunctiva contains subepithelial
mucosal associated lymphoid tissue with
collection of T and B cell.

10. Risk factors
 Trauma to the corneal epithelium.
 Eyelid abnormalities- Ectropion, Entropion
with trichiasis , Lagophthalmous.
 Dry eye syndrome- Tear film abnormality
 Dacrocystitis
 Inappropriate uses of topical antibiotics and
corticosteroid.

11.  Contact lenses – Risk of ulcerative keratitis
is more in Extended-wear soft contact lens
wearer than who worn on daily basis.
 Keratorefrective surgery
 Systemic diseases- AIDS, Malnutrition ,
Measles, Malignancies, Diabetes Melitus .
 Occupationals-Farmers, Gardners, Animal
handlers.

15. PATHOGENESIS
STAGE 1
PROGRESSIVESTAGE
•Microbes adhere to epithelium, release
toxins and lytic enzymes and produce
Necrosis.
•Saucer shaped ulcer, with gray zone of
infiltration
•Deeper penetration
•Descemetocele

16. STAGE 2
REGRESSIVE STAGE
•Line of demarcation
•Margin & floor ofulcer become smooth
& transparent
•Superficial vascularization

17. STAGE 3
HEALING STAGE
•Epithelialization starts
(Keratocytes & histiocytes convert
to fibroblasts)
•Vascularization occurs
•Vessels eventuallyregress, may
form ghost vessels
•Degree of scarring depends on
depth of involvement

18. Stage 4
Stage of Cicatrisation
•If only epithelial involvement – No scar
•Upto Bowman’s membrane and Superficial stroma-Nebula
•Upto half of Stroma – Mecula
•More than half of stroma involvement- Leucomatous

19. CLINICAL FEATURES
SYMPTOMS-
 Pain and foreign body sensation
 Redness- Severe in Gonococcal and Haemophilus infection
 Photophobia
 Discharge- Watery, Mucopurulent.
 Dimunition of vision – More in central ulcer.

20. SIGNS
1. Swelling of lid
2. Blepharospasm
3. Conjunctiva – Chemosed, Congested, Hyperaemic
4. Corneal ulcer –
 Yellowish white area of ulcer which may be oval or
irregular in shape.
 Margins are swollen and overhanging.
 Floor is covered by necrotic material
 Stromal oedema present surrounding the ulcer

21. 5. Anterior chamber- May or may not show pus
(hypopyon). In bacterial corneal ulcers, the
hypopyon remains sterile so long as the Descemet's
membrane is intact.
6. Iris – Slighty muddy in color.
7. Pupil – May be small due to toxin induced iritis
8. IOP- May be raised(Inflammatory glucoma)

22. Characteristic features of common
causative bacteria
1. Staphylococcus aureus and Streptococcus pneumoniae
usually produce an oval, yellowish white densely opaque
ulcer which is surrounded by relatively clear cornea.
2. Pseudomonas species usually produce an irregular sharp
ulcer with thick greenish mucopurulent exudate.
 Diffuse liquefactive necrosis and semiopaque (ground
glass) surrounding cornea.
 Such ulcers are usually associated with hypopyon, spread
very rapidly and may even perforate early.

23.  Enterobacteriae (E. coli, Proteus species, and
Klebsiella species) usually produce a shallow ulcer with
greyish white pleomorphic suppuration and diffuse
stromal opalescence. The endotoxins produced by
these Gram-negative bacilli may produce ring-shaped
corneal infiltrate.

24. HYPOPYON CORNEAL ULCER
 Iritis due to bacterial toxins
 Outpouring of leucocytes from vessels
 Leucocytes gravitate to bottom of AC
Hypopyon (Sterile and mobile)

26. COMPLICATIONS
1. Toxic iridocyclitis – Due to absorbtion of toxin into anterior
chamber.
2. Secondary glaucoma -It occurs due to fibrinous exudates
blocking the angle of anterior chamber (inlflammatory
glaucoma)
3. Descemetocele - Some ulcers caused by virulent organisms
extend rapidly up to Descemet's membrane, which gives a
great resistance, but due to the effect of intraocular
pressure, it herniates as a transparent vesicle called the
descemetocele or keratocele . This is a sign of impending
perforation.

27. 4. Perforation of corneal ulcer –
 Sudden strain due to cough, sneeze or spasm of orbicularis
muscle may convert impending perforation into actual
perforation
 Sequelae of corneal perforation include:
i) Prolapse of iris. It occurs immediately following
perforation in a bid to plug it.
ii) Subluxation or anterior dislocation of lens may occur.

28. iii) Anterior capsular cataract - It is formed when the lens
comes in contact with the ulcer following a perforation in
the pupillary area.
iv)Corneal fistula. It is formed when the perforation in the
pupillary area is not plugged by iris and is lined by
epithelium.
v)Purulent uveitis, endophthalmitis and panophthalmilis
may develop due to spread of irntraocular infection.
vi)Intraocular haemorrhage in the form of either vitreous
haemorrhage or expulsive choroidal haemorrhage may
occur in some patients due to sudden lowering of
intraocular pressure.

30. 5. Corneal scaring – It leads to permanent visual impairment
it may be of following types-
 Nebula
 Mecula
 Leucoma
 Ectatic cicatrix
 Anteriorstaphyloma

31. MANAGEMENT
A) Clinical evaluation-
1. History taking – Mode of onset and duration.
2. General physical examination- For built, Nourishment,
anaemia and immunocompromised state.
3. Occular examination-
 Diffuse light examination
 Corneal sensation
 Regurgitation test and syringing to rule out lacrimal sac
infection.

32.  Biomicroscopic examination of corneal ulcer includes
followings-
i) Size, shape, depth, margin, floor and vascularization of
corneal ulcer.
ii) Presence of KPs at back of cornea.
iii) Depth and contents of anterior chamber.
iv) Color and pattern of iris.
v) Condition of crystalline lens.
 Posterior segment examination

33. B. LABORATORY INVESTIGATION
1. Routine lab investigation- CBC, ESR, LFT, KFT, Urine R/M
2. Microbiological investigation –
A)Samples collection for diagnosis of corneal ulcer
 Corneal scraping- Most important
 Eyelid swab
 Conjunctival swab
 Contact lens, contact lens case and solution
 Corneal biopsy with Trephine and Microsurgical blade.
 Suture biopsy
B) Bacterial Growth on culture media- Inoculate bacterial
specimen directly on selective media.

34. CORNEAL SCRAPING
Explain the procedure
to patient
Proparacaine
hydrochloride 0.5%
(minimal inhibitory
effects on organism
recovery
Scrape in one
direction
Scrapingarea
Advancing edge of ulcer ( Streptococcus
pneumoniae)
Base of the ulcer ( Moraxella catarrhalis )
Multiple scraping increase yield
• Wet Dacron/calcium alginate
swab,
• Heat-sterilized platinum
(Kimura) spatula
• No. 15 Bard-Parker blade
• Jeweler'sforceps
• Large-gauge disposable needle
or suture
Cotton swabs should not be used

35. Corneal Scraping
and slide preparation

37. Indications
• Lack of response to treatment
• Repeated negative cultures.
• Infiltrate is located in the mid-deep
stroma with overlying uninvolved tissue
Procedure
• 3mm trephine used
•Both infected and clinically normal 1 mm rim taken
•Biopsy tissue excised with fine toothed forceps
CORNEAL BIOPSY

38. • For deep corneal abscess
• Short 7–0/8–0 vicryl or
silk suture used
• Passed through the
depth of the infiltrate
• Suture cut into two
pieces and sent for
bacterial and fungal C/S
SUTURE BIOPSY

41. ANTIMICROBIAL SUSCEPTIBILITY TESTING
 Effective antimicrobial therapy represents the idea of selec-
tive toxicity and requires that the antimicrobial agent reach
the site of corneal infection in sufficient concentration to
inhibit and preferably kill the causative microorganism,
while causing minimal to no toxicity to the host
 The preferred methods for testing the susceptibility of the
antimicrobial agents are the standard disk diffusion method
and the micro-dilution techniques.

42. TREATMENT
A) General consideration-
 Discontinuation of contact lenses.
 Clear plastic eye shield.
 Hospitalized patient if needed
 Intensive treatment may not be required for small
infiltrates that are clinically sterile and may be
treated by lower-frequency topical antibiotic
 Empirical broad-spectrum treatment is usually
initiated before microscopy results are available

43. B) Local therapy
 Broad spectrum antibiotics
 Initially instillation is at hourly intervals day and night for
24–48 hours and then is tapered according to clinical
progress.
1. Antibiotic monotherapy- It has the major advantage over
duo- therapy to of lower surface toxicity, as well as greater
convenience.
 Fluoroquinolone- Ciprofloxocin, ofloxocin
 8- Methoxy fluoroquinolon- Moxifloxacin, Gatifloxacin

44. 2. Antibiotic duotherapy-
 Combination of two fortified antibiotics includes
cephalosporin and aminoglycoside.
3. Mydriatics – To prevent the formation of posterior
synaechiae and to reduce pain.
4. Steroids - The Steroids for Corneal Ulcers Trial
(SCUT) found no eventual benefit in most cases, but
severe cases (counting fingers vision or large ulcers
involving the central 4 mm of the cornea) tended to do
better.

47.  Systemic antibiotics are not usually given, but may be
appropriate in the following circumstances:
1. Potential for systemic involvement
 N. meningitidis - Treatment is usually with intramuscular
benzylpenicillin, ceftriaxone or cefotaxime, or oral
ciprofloxacin.
 H. influenzae infection should be treated with oral
amoxicillin with clavulanic acid.
 N. gonorrhoeae requires a third-generation cephalosporin
such as ceftriaxone.

48. 2. Severe corneal thinning
 Ciprofloxacin 750 mg BD
 A tetracycline (e.g. doxycycline 100 mg twice daily)

49. Management of apparent
treatment failure
 If no improvement is evident following 48 hours of
intensive treatment, the antibiotic regimen and laboratory
report should be reviewed and rescraping performed.
 If cultures remain negative, it may be necessary to perform a
corneal biopsy for histology and culture.
 There is no need to change the initial therapy if this has
induced a favorable response, even if cultures show a
resistant organism.

50. Treatment of corneal perforation
 A small perforation in which infection is controlled
may be manageable with a bandage contact lens.
 Tissue glue(isobutyl cyanoacrylate) is often adequate
for a slightly larger ulcer.
 A penetrating keratoplasty or corneal patch graft may
be necessary for larger perforations.
 Occlusive surface repair techniques may be
appropriate in some circumstances, such as an eye
with no useful visual potential.

51. Visual rehabilitation
 Keratoplasty (lamellar may be adequate) may be
required for residual dense corneal scarring.•
 Rigid contact lenses may be required for irregular
astigmatism but are generally only introduced at least
3 months after reepithelialization.
 Cataract surgery may be required because of secondary
lens opacities.

52. THANKYOU