**2. Natural history of a corneal infection**

properly cited.

**Colonization:** Colonization is the first step after the arrival of pathogenic bacteria to corneal surface. The ability of bacteria or fungi for its adhesion to corneal epithelial cells defines its pathogenesis. After the adhesion phase, fungus or bacteria start an active replication sup‐ ported by nutritional and temperature conditions of the tissue, reaching a bunch of living microorganism over the corneal epithelial cells.

© 2013 Vanzzini Zago and Perez-Balbuena ; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is © 2013 Vanzzini Zago and Perez-Balbuena, licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**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 to the loss of surface epithelial cells.

**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 phenomenon.

**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 interstitial water between epithelial cells itself and keratocytes.

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

**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 with fibrin small spots named retrokeratic deposit.

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