**4. Bacterial pathogenesis**

**Invasion:** By means of proteases, lipopolysaccharides, streptolisines, dermonecrotic staphy‐ lolisines, the microorganism can breakdown the epithelium layer cells and originate a cor‐ neal epithelial ulcer or crossing Bauman layer, in some cases reaching corneal stroma. This tissue invasion can be observed in the slit lamp and itis described as desepithelization due

**Multiplication:** In the surface of epithelial layers, or because a traumatism some microor‐ ganism reach corneal stroma, finding good conditions in nutrients and temperature for an active multiplication and liberation of harmful substances that initiate the inflammatory

**Inflammatory response:** As a response of the invasion of pathogenic microorganism, the corneal tissue elaborates some potent mediators substances for inflammatory and immune response named cytokines, synthesized mainly by lymphocyte cells, chemo tactic,and tumor necrotic factors (TNF). The first sign of inflammatory response is edema by accumulation of

**Migration of leukocytes.** By diapedesis phenomenon, the migrating leukocytes arrive to in‐ flicted corneal tissue, from new vessels formed on clear cornea or from limbus, after this fi‐ brin and collagen IV accumulation into deep corneal stroma form an evident infiltrate. The role of polymorphonuclear leukocytesis part of innate immune defense, mainly is based on his ability of ingest bacteria and digest it, by the oxygen dependent killing pathway or by potent oxidants like hydrogen-peroxide, hydroxyl radicals, chloramines and hipoclorous acid. In fungal keratitis, extensive migration of polymorphonuclear neutrophils (PN), around fungal hyphae in order to destroy it, plasma cell and in some cases eosinophils are observed. The dead of inflammatory cells (PN) contribute to the destruction of surrounding

**Anterior chamber inflammatory reaction:** The arrival of leucocytes and fibrin to anterior chamber is called flare and the accumulation of inflammatory cells (PN)is visualized like hy‐ popyon, this phenomenon can be accompanied by inflammation of the endothelial tissue

**Scar:** The last step of an infectious keratitis is the accumulation of fibrin in the site of corneal wound or where invasive infectious process has begun, and form a permanent scar that, de‐

**a. Local corneal and systemic factor.** The risk factors that predispose to corneal infection involve a breakdown of normal defense mechanism like in diabetes, Sjögren or any kind of systemic immunosuppressant that helps the invasion of pathogenic microorgan‐

**b. Corneal trauma.** It is one of the most frequent predisposing factors for bacterial and fungal keratitis. Ocular surface disorders like, dysfunctional tear film and dry eye syn‐

corneal tissue because the release of lysosomal enzymes and oxygen metabolites.

pending on its size and localization, can permanently low the visual acuity. [3]

**3. Corneal predisposing factors in corneal infections**

interstitial water between epithelial cells itself and keratocytes.

with fibrin small spots named retrokeratic deposit.

to the loss of surface epithelial cells.

phenomenon.

62 Common Eye Infections

ism.

