Bacterial keratitis is a prevalent and serious eye condition caused by various bacteria, primarily affecting individuals with compromised ocular defenses, such as contact lens wearers. It can lead to severe complications, including corneal perforation and scarring, necessitating prompt diagnosis and aggressive treatment to preserve vision. Management involves empirical antibiotic therapy, careful monitoring, and may include surgical interventions if the condition does not respond to medical treatment.

1. BACTERIAL
KERATITIS
SANDEEP
KRISHNAN
PG RESIDENT
OPHTHALMOLO
GY

2. BACTERIAL KERATITIS
• Is a common sight-threatening condition.
• causing cellular infiltration of corneal epithelium or stroma, corneal
inflammation and necrosis.
• If Untreated, leads to progressive tissue destruction with corneal
perforation or extension of infection to adjacent tissue.
Common predisposing factors include
• contact lens wear
• Trauma
• contaminated ocular medications
• impaired defense mechanisms
• altered structure of the corneal surface

3. BACTERIAL KERATITIS
• Bacterial keratitis usually develops only when ocular defences have
been compromised.
• Some bacteria are able to penetrate a healthy corneal epithelium,
includes
– Neisseria gonorrhoeae,
– Neisseria meningitidis,
– Corynebacterium diphtheriae
– Haemophilus influenzae
– Listeria monocytogenes

4. CAUSATIVE ORGANISMS
• gram positive cocci - Streptococcus pneumonia,Staphylococcus
aureus,Staphylococcus epidermidis
• gram negative cocci -Neisseria gonorrhoea,Neisseria meningitidis
• gram positive bacilli - corynebacterium diphtheria, bacillus cereus
• gram negative bacilli-
pseudomonas,Acinetobacter,enterobacteriaceae
• gram positive filamentous bacteria - actinomycetes,nocardia
• Non-tuberculous mycobacterium -Mycobacterium
fortuitum,Mycobacterium chelonae

5. COMMON PATHOGENS
• Pseudomonas aeruginosa is a ubiquitous Gram-
negative bacillus commensal of the GIT. The
infection is typically aggressive and is
responsible for over 60% of contact lens-related
keratitis.
• Staphylococcus aureus is a common Gram-
positive and coagulase-positive commensal of
the nares, skin and conjunctiva.
• S. pyogenes is a common Gram-positive
commensal of the throat and vagina.
• S. pneumoniae (pneumococcus) is a Gram-
positive commensal of the upper respiratory
Contact lens induced
Pseudomonas keratitis

6. RISK FACTORS
• Contact lens wear, is the most important risk factor. Corneal
epithelial compromise secondary to hypoxia and minor trauma is
thought to be important, as is bacterial adherence to the lens
surface. Soft lenses are at higher risk than those of rigid lenses.
• Trauma, including refractive surgery, has been linked to bacterial
infection.
• Ocular surface disease such as herpetic keratitis, bullous
keratopathy, dry eye, chronic blepharitis, trichiasis and entropion,
severe allergic eye disease and corneal anaesthesia.
• Nasolacrimal duct obstruction is another important source of
bacterial infection.
• Corneal foreign body removal without strict sterility precautions is
an important source for devastating bacterial infections

7. SYMPTOMS
• Pain.
• Photophobia.
• Blurred vision.
• Foreign body sensation.
• Mucopurulent or purulent discharge.

8. SIGNS
• An epithelial defect with infiltrate involving a larger area and
significant circumcorneal injection

9. • Blepharospasm may be moderate to
severe cases
• Stromal edema, folds in Descemet
membrane and anterior uveitis,
commonly with a hypopyon and posterior
synechiae in moderate–severe keratitis.
• Plaque like keratic precipitates can form
on the endothelium contiguous with the
affected stroma.
• Chemosis and eyelid swelling in
moderate–severe cases.
• Severe ulceration may lead to
descemetocele formation and

10. • Scleritis can develop, particularly with severe perilimbal infection.
• Endophthalmitis is rare in the absence of perforation.
• Subsequent scarring may be severe, including vascularization. In
addition to opacification, irregular astigmatism may limit vision.
• Reduced corneal sensation may suggest associated neurotrophic
keratopathy, particularly where there is no other major risk factor.
Sensation may also be reduced in chronic surface disease, herpetic
keratitis and long-term contact lens wear.

11. • Corneal ulcer usually starts as an epithelial defect associated with
greyish-white circumscribed infiltrate (seen in early stage).
• The epithelial defect & infiltrate enlarges & stromal edema
develops.
A well established bacterial ulcer is characterized by :
• Yellowish-white area of ulcer which may be oval or irregular in
shape.
• Margins of the ulcer are swollen and over hanging.
• Floor of the ulcer is covered by necrotic material.
• Stromal edema is present surrounding the ulcer area

12. Stage 1: Stage of progressive infiltration:
• Includes adherence and entry of the organism, diffusion of toxins and
enzymes, and resultant tissue destruction.
• Shortly after the bacterial adherence, polymorphonuclear leukocytes
arrive at the site.
• Stromal damage caused by bacterial and neutrophil enzymes facilitates
progressive bacterial invasion.
Stage 2: Stage of active ulceration:
• There is progressive tissue necrosis with subsequent sloughing of the
epithelium and stroma, resulting in a sharply demarcated ulcer with
surrounding neutrophilic infiltration.
PATHOGENISIS

13. Stage 3: Regressive stage:
• Characterized by improvement in clinical signs
and symptoms.
• Natural host defence mechanisms predominate
and humoral and cellular immune defence
mechanisms together with antibacterial therapy
try to retard bacterial replication, promote
phagocytosis of the organism and cellular debris.
• Vascularization may start if the ulceration is of
long duration.
Stage 4: Healing stage:
• Characterized by epithelialization of ulcerated
area, replacement of necrotic stroma with scar
tissue, which is produced by fibroblasts.

14. HYPOPYON CORNEAL ULCER
• Many pyogenic organisms (staphylococci, streptococci, gonococci, Moraxella)
may produce hypopyon
• Most dangerous are pseudomonas pyocyanea and pneumococcus.
• The characteristic hypopyon corneal ulcer caused by pneumococcus is called
ulcus serpens
• Source of infection for pneumococcal infection is usually the chronic
dacryocystitis.
Factors predisposing to development of hypopyon.
• Two main factors which predispose to development of hypopyon in a patient
with corneal ulcer are, the virulence of the infecting organism and the
resistance of the tissues.
• Hence, hypopyon ulcers are MC in old debilitated or alcoholic subjects

15. Mechanism of development of hypopyon
• Corneal ulcer is often associated with some iritis owing to diffusion of
bacterial toxins.
• When the iritis is severe the outpouring of leucocytes from the vessels is
so great that these cells gravitate to the bottom of the anterior chamber
to form a hypopyon.
• Thus, the hypopyon is sterile since the outpouring of polymorphonuclear
cells is due to the toxins and not due to actual invasion by bacteria.
• Once the ulcerative process is controlled, the hypopyon is absorbed

16. Typical features of ulcus serpens:
• a greyish white or yellowish disc shaped ulcer occuring
near the centre of cornea
• The ulcer has a tendency to creep over the cornea in a
serpiginous fashion.
• One edge of the ulcer which the ulcer spreads shows
more infiltration.
• The other side of the ulcer may be undergoing
simultaneous cicatrization and the edges may be
covered with fresh epithelium.
• Violent iridocyclitis is commonly associated with a
definite hypopyon.
• Hypopyon increases in size very rapidly & often results
in secondary glaucoma.

17. 1.Staphylococcal
• Central, oval, opaque
• Distinct margins.
• Mild oedema of remaining cornea.
• Stromal abscess in longstanding
cases.
• Mild to moderate AC reaction.
• Affects compromised corneas e.g.
Bullous keratopathy , dry eyes ,
atopic diseases.
SPECIAL CASES

18. 2. Pseudomonas
• Rapidly spreading.
• Extends periphery & deep within
24 hrs.
• Stromal necrosis with shaggy
surface
• Spreads concentrically and
symmetrically to involve whole
depth of cornea- Ring ulcer.
• Greenish-yellow discharge.
• Hypopyon is present.

19. 3. Streptococcus viridans
• Infectious crystalline
keratopathy type of stromal
keratitis.
• Crystalline arboriform (needle
like) white opacities in stroma ,
not associated with infiltration &
ocular inflammation
• Due to proliferation of bacteria
between the stromal lamellae.
• Seen in following corneal grafts ,
prolonged use of topical steroid.

20. Toxic iridocyclitis
• It is usually associated purulent corneal ulcer due to
absorption of toxins in the anterior chamber.
Secondary glaucoma
• due to fibrinous exudates blocking the angle of anterior
chamber (inflammatory glaucoma).
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 IOP it herniates as
a transparent vesicle called the descemetocele or
keratocele
• This is a sign of impending perforation and is usually
associated with severe pain
COMPLICATIONS OF
CORNEAL ULCER

21. Perforation of corneal ulcer
• Sudden strain due to cough, sneeze or spasm of orbicularis muscle may
convert impending perforation into actual perforation
• Following perforation, immediately pain is decreased and the patient
feels some hot fluid (aqueous) coming out of eyes.
Sequelae of corneal perforation include :
1. Prolapse of iris. It occurs immediately following perforation
2. Subluxation or anterior dislocation of lens may occur due to sudden
stretching and rupture of zonules.
3. Anterior capsular cataract. It is formed when the lens comes in contact
with the ulcer following a perforation in the pupillary area.

22. 4 .Corneal fistula.
• It is formed when the perforation in the pupillary area is not plugged by iris
and is lined by epithelium which gives way repeatedly.
• There occurs continuous leak of aqueous through the fistula.
5 .Purulent uveitis, endophthalmitis or even panophthalmitis may develop
due to spread of intraocular infection.
6 .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.
Corneal scarring.
• It is the usual end result of healed corneal ulcer.
• Corneal scarring leads to permanent visual impairment ranging from slight
blurring to total blindness.

23. MANAGEMENT
Ocular examination should include:
• Diffuse light examination for gross lesions of the lids, conjunctiva and cornea
including testing for sensations.
• Regurgitation test and syringing to rule out lacrimal sac infection.
Biomicroscopic examination
• after staining of corneal ulcer with 2% fluorescein to note site, size, shape,
depth, margin, floor and vascularization of corneal ulcer.
• presence of keratic precipitates at the back of cornea,
• depth and contents of anterior chamber (cells,flares)
• colour and pattern of iris and condition of crystalline lens

24. INVESTIGATIONS
1. Corneal scraping for culture &
sensitivity.
• A non-preserved topical anaesthetic is
instilled.
• Scrapings are taken either with a
disposable scalpel blade or the bent tip
of a 20- or 21-gauge hypodermic needle,
or a sterile spatula (e.g. Kimura).
• Loose mucus and necrotic tissue should
be removed from the surface of the ulcer
prior to scraping.
• The margins and base (except if very
thin) of the lesion are scraped
• A thin smear is placed on one or two

25. INVESTIGATIONS
2. Conjunctival swabs
3. Contact lens cases, as well as bottles of solution and
lenses themselves, should be obtained when possible and
sent to the laboratory for culture.
4. Gram staining - Differentiates bacterial species into
Gram-positive and Gram-negative based on the ability of
the dye (crystal violet) to penetrate the cell wall

26. TREATMENT
• primary goal of therapy is preservation of sight and corneal clarity.
• Bacterial pathogens can produce irreversible corneal scarring over a
period of hours because of their rapid growth, keratolytic enzymes,
and stimulation of destructive host immune responses.
• Therefore, therapy must be initiated before definitive diagnosis is
obtained in order to rapidly reduce the bacterial load and minimize
later visual disability

27. • Initial therapy is empirical with topical broad-spectrum coverage.
Topical Monotherapy :
• Topical FQ initially be given every 30–60 minutes and then tapered in
frequency according to the clinical response.
• In severe cases, administration of antibiotics every 5 min for 30 min as a
loading dose can more rapidly achieve therapeutic concentrations in the
corneal stroma.
• 2nd gen FQ (cipro, ofloxacin) has excellent Pseudomonas coverage but
lack useful gram-positive activity. Ciprofloxacin instillation is associated
with white corneal precipitates that may delay epithelial healing.
• 3rd & 4th gen FQ (eg, moxi, gati, levo, besifloxacin)have improved gram-
positive and atypical mycobacterial coverage but limited activity against
MRSA.

28. Topical combination therapy (DUOTHERAPY)
• One agent active against gram+ve bacteria & another agent active against
gram-ve bacteria
• Empirical duotherapy usually involves a combination of two fortified
antibiotics, typically a cephalosporin and an aminoglycoside.
Indications :
• if monotherapy fails or
• if at initial presentation
– the ulcer is large, vision threatening, or
– atypical in nature
Sub-conjunctival injections of antibiotics are reserved for
non-compliant patients.

29. • Cycloplegics are used to relieve pain due to ciliary spasm, breaks adhesions
and prevent synechia formation.
– Homatropine 1% is preferable,
– since atropine can increase anterior chamber inflammation
– cyclopentolate can be more irritative.
• Systemic analgesics and anti-inflammatory such as paracetamol and ibuprofen
relieve the pain and decrease edema.
• Vitamins (A, B-complex and C) help in early healing
• Physical and general measures
(a) Hot fomentation. Local application of heat (preferably dry) gives
comfort,reduces pain and causes vasodilatation.
(b) Dark goggles may be used to prevent photophobia.
(c) Rest, good diet and fresh air may have a soothing effect.

30. Fortified antibiotics
• compounded at increased concentrations compared to their
commercial formulations in order to achieve therapeutic levels in the
corneal stroma.
• are more difficult to obtain
• have a greater toxic effect on the ocular surface.
• should consider using especially in combination with vancomycin for
gram+ve coverage when MRSA is suspected with large or vision-
threatening ulcers, or with prior antibiotic failure.

31. • Most infectious keratitis is culture Negative after 48–72 hours if treated
effectively
• Treatment should be continued until substantial control of the infection
is seen.
• A prophylactic broad-spectrum antibiotic (not a fortified antibiotic)
may be given at a therapeutic dose until the corneal epithelium is
healed

32. • Systemic antibiotics FQ -have excellent ocular penetration
• Intensive topical antibiotics are indicated in cases with suspected scleral
and/or intraocular extension of infection
• clinical parameters in response to antibiotic therapy:
– blunting of the perimeter of the stromal infiltrate
– decreased density of the stromal infiltrate makes the fuzzy infiltrate
margin to become more defined and demarcated.
– reduction of stromal edema and endothelial inflammatory plaque
– reduction in anterior chamber inflammation
– Re-epithelialization
– cessation of corneal thinning

33. TREATMENT OF NON-HEALING CORNEAL ULCER
Removal of any known cause of non-healing ulcer like
• Local causes: Associated raised IOP, concretions, misdirected cilia, impacted
FB, dacryocystitis, inadequate therapy, wrong diagnosis, lagophthalmos and
excessive vascularization of ulcer.
• Systemic causes: Diabetes mellitus, severe anaemia, malnutrition, chronic
debilitating diseases and patients on systemic steroids.
• Mechanical debridement of ulcer to remove necrosed material by scraping
floor of the ulcer with a spatula under LA may hasten healing.
• Cauterisation with pure carbolic acid or 10-20 % trichloracetic acid.
• Bandage soft contact lens may also help in healing.
• Peritomy, i.e, severing of perilimbal conjunctival vessels may be performed
when excessive corneal vascularization is hindering healing.

34. TREATMENT OF IMPENDING PERFORATION
1. No strain. The patient should be advised to avoid sneezing, coughing and
straining, strict bed rest.
2. Pressure bandage should be applied to give some external support.
3. Lowering of IOP by
– acetazolamide 250 mg QID orally,
– intravenous mannitol (20%) drip stat,
– Oral glycerol twice a day,
– 0.5% timolol eyedrops twice a day, and paracentesis
4. Tissue adhesive glue such as cynoacrylate is helpful in preventing perforation.
5. Conjunctival flap: The cornea may be covered completely or partly by a
conjunctival flap to give support to the weak tissue.
6. Bandage soft contact lens may also be used.
7. Penetrating therapeutic keratoplasty (tectonic graft)

35. ROLE OF CORTICOSTEROID THERAPY FOR BACTERIAL
KERATITIS
• remains controversial.
• Tissue destruction results from a combination of the direct effects of the
bacteria and an exuberant host inflammatory response consisting of
polymorphonuclear leukocytes and proteolytic enzymes, which predominate
even after corneal sterilization.
• Corticosteroids are effective at modifying this response, but they also
inhibit the host response to infection.
• The literature strongly suggests that corticosteroid therapy administered
prior to appropriate antibiotic therapy worsens prognosis.
• The literature is inconclusive about steroid therapy used concomitantly with
antibiotic therapy or after it is initiated

36. PENETRATING KERATOPLASTY
For treatment of bacterial keratitis is indicated
– if the disease progresses despite therapy,
– descemetocele formation or perforation occurs, or
– the keratitis is unresponsive to antimicrobial therapy.
• The involved area should be identified preoperatively, and an attempt
should be made to circumscribe all areas of infection.
• Peripheral iridectomies are indicated, because patients may develop
seclusion of the pupil from inflammatory pupillary membranes.
• Interrupted sutures are recommended.
• The patient should be treated with appropriate antibiotics,cycloplegics, and
intense topical corticosteroids postoperatively.

37. THANK YOU