Seminar presented by

DR PRITI GUPTA

Bacterial keratitis
Keratitis - Inflammation of the cornea.
Microbial keratitis or infectious corneal ulcer
is due to the proliferation of microorganisms
(including bacteria, fungi, viruses, and
parasites) and associated inflammation and
tissue destruction within the corneal tissue .
Bacterialkeratitis- most common cause of
suppurative corneal ulceration.

Corneal ulcer- Disruption of the epithelial layer

with involvement of the corneal stroma.
Human cornea's natural resistance to infection.

BACTERIAL KERATITIS
Needs urgent medical attention
Prompt diagnosis
Initiation of appropriate antibiotic
Limit amount of tissue destruction
Improve patients visual prognosis

Ocular
Defense
Mechanism

Chemical

Mechanical

Lysozyme

Intact corneal epithelium

Lactoferrin

(first line of defence)

Immunoglobulin A

Blinking reflex
(reduced bacterial colonization)
Cilia

1.Most important
defense barrier- Intact
epithelial layer
2.Major risk factors
-Compromised
epithelium
3.Precipitating event is
epithelial defect
produced by trauma,
contact lens wear or a
chronic corneal
disorders.

PATHOGENESIS
Proliferation of bacteria

Adherence to ulcerated epithelium

Invasion into stroma

Production of proteniase

Migration of neutrophiles

Inflamatory necrosis
Desmatocele
Neovascular scar formation

Corneal perforation

Risk
Factors for
Bacterial keratits
EXTRINSIC FACTORS

CORNEAL SURFACE
DISEASE

SYSTEMIC
CONDITIONS

CORNEAL EPITHELIAL
ABNORMALITIES

EXTRINSIC FACTORS
Contact lens wear
Trauma
Previous ocular and eyelid surgery
Loose corneal sutures
Medication-related factors
Immunosuppression

Corneal surface disease

Tear-film deficiencies
Abnormalities of the eyelid anatomy and
function
Misdirection of eyelashes
Adjacent infection/inflammationBlepharitis

Corneal epithelial abnormalities

Neurotrophic keratopathy
Recurrent corneal erosion
Corneal abrasion or epithelial defect
Viral keratitis
Corneal epithelial edema

Systemic conditions
Diabetes
Systemic infections
Collagen vascular diseases
Immuno suppressive drug
Chronic alcholism
Extensive body burns
Drug addiction
AIDS

Bacterial pathogens that cause keratitis

Bacterium

Typical characteristics of infection

Staphylococcus aureus(most common)

Infection progresses slowly with little pain

Staphylococcus
epidermidis
Streptococcus
pneumoniae

Typical serpiginous corneal ulcer: cornea is

Pseudomonas aeruginosa ( most common organism

in soft contact lens wearers)

Bluish green mucoid exudate,occasionally with

Uncommon Organisms
Neisseria spp
Moraxella spp
Mycobacterium spp
Nocardia spp
Corynebacterium spp

rapidly
Perforated with early intraocular involvement;very
painful.
a ring shaped corneal abscess.Progressionis rapid with
a tendency to ward melting of the cornea over a wide
area;painful.

Organisms penetrate intact epithelium

Neisseria gonorroae

Haemophilus agegyptius

Corynebacterium diphteria

Listeria

Clinical presentation
(SYMPTOMS)
Rapid onset of pain
Conjunctival injection (Redness)
Photophobia
Decreased vision
Discharge and lid edema

Clinical features of Gram positive and Gram negative

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

Often hazy
More common

SIGNS
White stromal infiltrate associated with an
overlying epithelial defect and secondary anterior
uveitis .
1.

Enlargement of stromal infiltration associated

with stromal oedema
2.

3.Severe infiltration and hypopyon

formation

4.Progressive ulceration and

enlargement of hypopyon

5.Corneal perforation and

endophthalmitis in neglected cases

Bacterial corneal ulcers :It is a localized suppuration and necrosis of the

corneal epithelium and underlying stroma due to
invasion by bacteria.

Stages:
1. Progressive stage:
-Organism
adherent to the damaged epithelium
Collection of PNL Proteolytic enzymes

toxins

-Grey unclean appearance with necrotic walland PNL

infiltration around the ulcer
-Bulges as a small sac called "Descematocele". Finally
perforation occurs
- Irritation the iris toxic iridocyclitis.

2. Regressive ulcer stage :

- Necrotic material is shed off ulcer will be larger and more
demarcated with regular transparent sloping edges.
3. Stage of healing:
-The epithelium heals by migration to cover the ulcer then
regenerates by mitosis.
The stroma and Bowmans membrane heal by irregular
fibrous scar. So that, once Bowman's membrane is injured, a
permanent scar will result. This scar may be dense
(leukoma) or faint (nebula). The scar may be vascularized.

Specific forms of keratitis:

1. Staphylococci bacterial keratitis

staphylococcus
keratitis occurs more frequently in compromised cornea
cases such as bullous keratopathy,chronic herpetic
keratitis,keratoconjuctivitis sicca,atopic keratoconjuctivitis.
Bacteria grow easily on routine culture media as pearly white
colonies.

pearly white colonies

2.Streptococcus pneumoniae keratitis

:usually
occurs after corneal trauma, dacryocystitis, or filtering bleb
infection. The ulcer tends to be acute, purulent, and rapidly
progressive with a deep stromal abscess The anterior
chamber reaction is usually severe with marked hypopyon
and retrocorneal fibrin coagulation. A culture appears
nonhemolytic on a blood or chocolate agar plate . Perforation
secondary to ulcer is common.

3. Infectious crystalline keratitis

Very rare, indolent infection (Strep. viridans)
Usually associated with long-term topical steroid use
Particularly following penetrating keratoplasty

White, branching, anterior stromal crystalline deposits

Treatment:Topical antibiotics

4. Pseudomonas Keratitis

Most common in contact lens 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.

5.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.
In all hyperacute conjunctivitis the entire cornea must be
evaluated for ulceration .

6.Mycobaacterium keratitis

These infections usually arise after

trauma or surgical intervention. The periphery of the infiltrate has a
characteristic "frosted

glass" appearance.

Differential diagnosis

Non bacterial infectious

causes of corneal
infiltrates

Non-infectious causes
of corneal infiltrates

Non bacterial corneal pathogens

Include fungi (both yeast and mold), parasites (including

protozoa such as Acanthamoeba), nematodes (such
as Onchocerca), and viral infection.

Systemic diseases

Collagen vascular disorders (e.g. rheumatoid arthritis, systemic

lupus erythematosus), vasculitic disorders (e.g. polyarteritisnodosa,
Wegener's granulomatosis), and other inflammatory disorders such
as sarcoidosis may produce infiltrative keratitis.

Other causes include dermatologic disorders (e.g.

severe ocular rosacea) and allergic conditions (e.g.
vernal keratoconjunctivitis).

Sequelae and Complications

Irregular astigmatism -Uneven healing of the stroma
Irregular astigmatism.

Non healing corneal ulcer:A non-healing ulcer is a corneal

ulceration that is not responding to anti-microbial treatment for a
period of three to four weeks.

or When the ulcer does not show any signs of

improvement or shows worsening despite appropriate and
adequate therapy.

Corneal perforation: Most feared complication may result in

secondary endophthalmitis and possible loss of the eye.

Corneal Perforation
Pseudomonas and gonococcal keratitis

Clinical presentaion:
Sudden relieve of pain
Radial folds in descements membrane
Perforation of cornea and
desmatocele formation

Treatment :
Tectonic keratoplasty

Prevention and Early Detection

Screening of patient with high risk factors
Education on use of extended wear contact
lens
Protective eye wear for work and sports
Treatment of ocular surface disease

Initial Assessment
History
Ocular symptoms
Review of prior ocular surgery
Review of other medical problems
Current ocular medications
Drug allergies

Initial Assessment
Examination
General appearance of the patient
including skin conditions
Facial examination
Eyelids and eyelid closure
Conjunctiva
Nasolacrimal apparatus
Corneal sensation

Initial Assessment
Slit Lamp Biomicroscopy
Eyelid margins
Conjunctiva
Sclera
Cornea
Anterior Chamber
Anterior Vitreous

Diagnostic Tests
Include corneal scraping to obtain specimens for microbiological
stainings and cultures to isolate the causative organism and
determine sensitivity to antibiotics.
The majority of community-acquired cases of bacterial keratitis
resolve with empirical therapy and are managed without smears or
cultures.
Prior to initiating antimicrobial therapy, smears and cultures are
indicated in cases where the corneal infiltrate is central, large, deep,
is chronic in nature, or has atypical clinical features suggestive of
fungal, amoebic, or mycobacterial keratitis.
In addition, cultures are helpful to guide modification of therapy in
patients with a poor clinical response to empirical treatmentand to
decrease toxicity by eliminating unnecessary drugs.

Stains
Microbial pathogens may be categorized by examining
stained smears of corneal scrapings
Stain

Organisms visualized

Gram stain

Best for bacteria; can also visualize

fungi, Acanthamoeba

Giemsa stain

Bacteria,
fungi,Chlamydia, Acanthamoeba

Acid fast

Mycobacterium, Nocardia

Calcofluor white

Fungi, Acanthamoeba

Cultures
Corneal material is obtained
by scraping corneal tissues
from the advancing borders
of the infected area.
Obtaining only purulent
material usually results in
inadequate yield.
Cultures of contact lenses,
lens case, and contact lens
solution may provide
additional information to
guide therapy

CULTURE MEDIA FOR BACTERIAL

KERATITIS
Standard Media

Common Isolates

Blood agar

Aerobic and facultatively anaerobic bacteria, including P.

aeruginosa, S. aureus, S. epidermidis, S. pneumoniae

Chocolate agar

Aerobic and facultatively anaerobic bacteria, including H.

influenzae, N. gonorrhea, and Bartonella species

Thioglycollate broth

Aerobic and facultatively anaerobic bacteria

Supplemental Media
Anaerobic blood agar (CDC,
Schaedler, Brucella)

P. acnes, Peptostreptococcus

Lwenstein-Jensen medium

Mycobacteria species, Nocardia species

Middlebrook agar

Mycobacteria species

Thayer-Martin agar

Pathogenic Neisseria species

Corneal Biopsy
Lack of response
More that 1 negative
culture result
Deep stromal infiltrate
with normal overlying
tissue

Goals of therapy

Rapid elimination of bacteria

Reduction of inflammatory response
Prevent of structural damage
Promotion healing of epithelial

Treatment
Initial
Topical antibiotic eye drops are able to achieve high
tissue levels and is the preferred choice of treatment in
most cases.

Topical antibiotic ointment at bedtime may be useful in

less severe cases as an adjunctive treatment.

Sub-conjunctival antibiotics maybe helpful in cases of

imminent scleral spread or perforation .

Systemic therapy maybe useful in cases where there is

scleral or intraocular involvement or systemic infection
(gonorrhea)

Singledrug therapy

Using fluoroquinolones shown to be as effective as

combination fortified antibiotics.

Rule of 2: <2mm diameter, <2+AC cells & >2mm from

visual axis.

Combination Fortified-Antibiotic/ Systemic Therapy

Severe infections
Previously unresponsive to single-drug therapy

Systemic
Infection extending to sclera
Impending or frank perforation
Gonococcal keratitis

Fortified 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

3 mg/ml

Treatment

Severe keratitis may require a loading dose

(Every 5-15 mins for the 1st hour, followed by
every 15mins-1hour around the clock).

Cycloplegics to relief pain from cilary spasm and

reduce synechial formation.

Modification of Therapy

Efficacy of treatment is judged primarily on the clinical

response towards the current treatment.

Culture results may have an impact on modification of

therapy especially when the response to treatment is poor

Modification should be done if the eye show lack of

improvement or stabilisation after 48-72hrs after treatment .

Features suggestive of positive response to treatment

Reduction in pain
Reduced amount of discharge
Lessened eyelid edema or conjunctival injection
Decreased density of the stromal infiltrate in the absence
of progressive stromal loss
Reduced stromal edema and endothelial inflammatory
plaque
Consolidation and sharper demarcation of the perimeter
of the stromal infiltrate
Reduced anterior chamber cell, fibrin, or hypopyon
Initial re-epithelialisation
Cessation of progressive corneal thinning .

Topical
Corticosteroid undercoverage
of antibiotics

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

Prednisolone acetate 1% QID
Patient must have frequent follow-up

Cyanoacrylate tissue adhesive

Cyanoacrylate tissue adhesive (N-butyl-2cyanoacrylate) has been used to treat

progressive corneal thinning, descemetocele,
and corneal perforation with satisfactory
results.
In addition to its tectonic support and
bacteriostatic effects, the tissue glue can
arrest keratolysis by blocking leukocytic
proteases from the corneal wound.
Perforations up to 23 mm in diameter can be
sealed by the tissue adhesive.
Necrotic tissue and debris should be removed
from the ulcer bed prior to application of the
glue.
Due to potential corneal toxicity, only the
minimum amount of glue required to cover the
defect should be used.
The adhesive is usually left in place until it
dislodges spontaneously or a keratoplasty is
performed.

Collagen Cross linking

Collagen cross linking (CXL) of the cornea has been developed

recently as a new treatment for multidrug-resistant infectious
keratitis.

This technique has showed promising results specially in patients

with corneal melting and impending perforation.

Corneal melting has been arrested and complete epithelialization

achieved in several cases.

The success rate was higher for bacterial infections than fungal
infections.

Cauterization
Performed by - Pure carbolic acid (100%)
Tricloacetic acid(10-20%)
Parts touched immediately turns white,normal
epithelium rapidly recovers.
Contraindications ulcers with excessive thinning or
perforated crneal ulcers

Surgical Management

1.Conjunctival flap:
Conjunctival flap has been
used to treat recalcitrant
microbial keratitis.
The flap can bring blood
vessels to the infected area,
promote healing, and provides
a stable surface covering.
A conjunctival flap is
particularly useful in cases of
nonhealing peripheral corneal
ulcer, where the flap can be
placed without compromising
vision.
2.Keratoplasty
3.Amniotic membrane
transplantation (AMT) can stabilise
the cornea in
cases of corneal melt and
descemetocele.

Thank You