Approach To Microbial Keratitis - 1

Moderator – Dr. Radhika Torgal

*Approach To Microbial Keratitis - I

*Keratitis is a descriptive term for any type of corneal inflammation

*Characterized by corneal edema, cellular infiltration and ciliary congestion

*Microbial Corneal ulcer is corneal epithelial defect caused by microorganisms with underlying stromal infiltrate

*Microbial Keratitis is one of the leading causes of preventable blindness

*INTRODUCTION

*CLASSIFICATION

MORPHOLOGICAL

ETIOLOGICAL

*MORPHOLOGICAL CLASSIFICATION

A) Ulcerative Keratitis ( Corneal Ulcer)1. Depending Upon Location

2. Depending Upon Purulence

3. Depending Upon Association Of Hypopyon

4. Depending Upon Depth Of Ulcer

5. Depending Upon Slough Formation

B) Non - Ulcerative Keratitis 1. Superficial Keratitis

2. Deep Keratitis

*ETIOLOGICAL CLASSIFICATION

A)Infective or Microbial Keratitis

B)Allergic

C)Trophic

D)Associated with skin and mucous membrane diseases

E)Associated with systemic collagen vascular diseases

F)Traumatic

G)Idiopathic

*Defensive mechanisms

*Eyelids

*Smooth corneal surface

*Precorneal tear film(Ig & enzymes)

*Normal ocular flora

*Predisposing factors

*Trauma / foreign body

*Contact lens wear

*Previous surgery

*Eyelid disorders

*Conj. disorders

*Systemic illness- DM, Arthritis, CVD, leprosy , malnutrition, HIV, Hep B, etc

*Ocular Examination

*A complete ocular examination is mandatory

*Careful examination of the other eye

*The lacrimal sac, conjunctiva & sclera

*Ocular Examination

*Eyelids:

- Position

- Lid margin regularity

*Ocular surface:

- Signs of dry eye

*Careful examination of the eyelids

Lagophthalmos

*Examination of Corneal Ulcer

*Location

*Size

*Depth

*Margins

*Ulcer bed

*Satellite lesions

*Height of hypopyon

* Size

*Size of epithelial defect

*Size of infiltrate

* Note the size, nature & depth of infiltrate

*Note the surrounding stromal edema

*Corneal endothelium

*AC reaction

*Limbus / scleral involvement

*Fundus exam – for any vitreous reaction

*B scan

Examination

*Bacterial keratitis

Gram positive GPC

*Staphylococci

*Streptococci

GPB

*Nocardia

*Corynebacterium

*Bacillus

*Actinomyces

Gram negativeGNC

*Neisseria

GNB

*Pseudomonas

*Proteus

*Moraxella

*Hemophilus

1] EXOGENOUS INFECTION:- Lacrimal sac, infected foriegn bodies, water or air borne infections

2] FROM THE OCULAR TISSUE: Owing to the direct anatomical continuity diseases spread from...•Conjuctiva to the corneal epithelium•Sclera to stroma•Uveal tract to endothelium of cornea

3] ENDOGENOUS INFECTION: Rare

*Source of infection

THERE ARE 2 MAJOR FACTORS IN THE PRODUCTION OF A ULCER:-

A]CORNEAL

EPITHELIAL DAMAGE

B]INFECTION OF THE

ERODED AREA

HOWEVER, THE FOLLOWING ORGANISMS CAN INVADE AN INTACT CORNEAL EPITHELIUM AND PRODUCE ULCERATION....

Neisseria gonorrhoeaN.meingitidisCorynebacterium diptheriaeH influenzae

*Pathogenesis

*Pathogenesis

4)STAGE OF CICATRIZATION.

3)STAGE OF REGRESSION.

2)STAGE OF ACTIVE ULCERATION.

1)STAGE OF PROGRESSIVE INFILTRATION.

*Pathogenesis Of Bacterial Corneal Ulcer

Infiltration of lymphocytes into the epithelium & the underlying stroma from the peripheral circulation

Subsequently, necrosis of the involved tissue may occur

1.Stage Of Progessive Infiltration

Necrosis & sloughing of the epithelium, bowman’s membrane & the involved stroma

The walls of the ulcer project owing to swelling of the lamellae by imbibition of fluid & packing of masses of leucocytes between them

Hyperemia of circumcorneal vessels resulting in accumulation of purulent exudates of the cornea

Exudation into the anterior chamber from vessels of iris & ciliary body lead to hypopyon formation

2.Stage Of Active Ulceration

Induced by natural host defence mechanisms & treatment that augments the normal host response

A line of demarcation develops around the ulcer which consists of leucocytes that phagocytose the offending agents

Digestion of necrotic debri may result in initial enlargement of the ulcer

Accompanied by vascularization that increases the immune response

The ulcer now begins to heal & epithelium begins to grow over the edges

3.Stage of Regression

Healing continues by progressive epithelization which forms a permanent covering

Beneath the epithelium, fibrous tissue is laid down, partly by the corneal fibroblasts & partly by the endothelium of new vessels

Stroma thus thickens, pushing the epithelial surface anteriorly

The degree of scarring from healing varies

Nebular / macular / leucomatous opacities

4.Stage Of Cicatrization

LEUKOMATOUS CORNEAL ULCERATION WITH FATTY INFILTRATION

*Clinical features

Clinical signs and symptoms are variable depends on the

*Virulence of the organism

*Duration of infection,

*Pre-existing corneal conditions

*Immune status of host

*Previous use of local steroids

*Presentation

1. Photophobia

2. Diminution of vision

3. Watering

4. Pain due to exposed nerve endings

5. Mucopurulent / purulent discharge

6. Redness

*Clinical Signs*Infiltration within stroma and epithelium

*Overlying epithelial defect

*Lid Erythema and edema

*Conjuctival injection and chemosis

*Discharge

*Conjuctival papillary response

*Anterior chamber inflammation

*Special features1.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

2.Pneumococcal* Ulcer serpens

*Tendency to creep over the cornea in serpiginous fashion

*After trauma

*Starts at periphery & spreads towards centre

*Violent iridocyclitis is often associated with it

*Hypopyon – always present

*It has great tendency for PERFORATION

*After corneal trauma, dacrocystitis, bleb infection

BACTERIAL ULCER WITH HYPOPYON

HYPOPYON.

3. 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.

*Untreated corneal melting.

*Infectious Crystalline Keratopathy

*Type of stromal keratitis

*Crystalline 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

*Most common organism Strep. Viridans

*Fungal keratitis

*Ubiquitous organisms

*Classification : Filamentous, Yeasts & Diphasic forms

*Filamentous - Multicellular with branched hyphae, can be septate or aseptate e.g. aspergillus, fusarium

*Yeast – Unicellular, reproduces by budding, pseudohyphae in tissues e.g. candida, cryptococcus

*Aspergillus is most common followed by fusarium and candida

Gram's stain of scraping from Fusarium corneal ulcer demonstrating branching fungal hyphae

*Predisposing Factors

* Trauma by vegetative matter

*Long term steroid use

*Immuno-compromised states

*Contact lens users

*Post surgery

*Chronic keratitis

*Clinical Features

*Symptoms are much milder than signs would suggest

*Dry looking infiltrate

*Hyphate or feathery edges

*Satellite lesions

*Endothelial plaque

*Brown pigmentation in fungal keratitis may be due to the presence of dematiaceous fungi

* Fungal keratitis. (A) Candida keratitis; (B) filamentous keratitis with satellite lesions and a small hypopyon; (C) Gram-stained Candida spp shows pseudohyphae; (D) corneal smear stained with Grocott hexamine silver shows Aspergillus spp

Filamentous fungi Yeasts

Occurs more frequently in young people

(occupational and outdoor activity),

usually no predisposing factor.

Usually occurs in an

immunocompromized host, preexisting

corneal disease or steroid treatment.

Involved area can be localized and is

often elevated; epithelial defect may or

may not be present;

Usually more focal, elevated and

suppurative, resembling bacterial keratitis

Often has feathery edges and satellite

lesions.

Edges not feathery and satellitism not

usually seen.

*

Thank You