**4. Pathophysiology**

The process of bacterial keratitis initiates once the epithelial is breached by any *means*. When a critical number of pathogens is exceeded, defense mechanisms fail and the stroma of the cornea is invaded by bacteria. This is facilitated by breaking the continuity of the epithelium. Only a small number of bacteria are able to break the continuous epithelium, these are gonorrhea, *Corynebacterium diphtheria*, *Corynebacterium aegyptian*, *Listeria*, and *Shigella*.

The development of bacterial keratitis progresses through four stages: stage of progressive infiltration, stage of active ulceration, stage of regression, and stage of cicatrization [27].

An important feature that determines pathogenicity is the ability of the bacterium to produce enzymes that facilitate penetration into tissues and their destruction. *Pseudomonas aeruginosa*, which produces protease, trypsin, elastase, and hemolysin, is particularly dangerous. These enzymes lead to rapidly progressing liquefied necrosis of the tissue. This bacterium should always be considered and differential as a cause of acute keratitis in CL users [25, 26, 28]. Another mechanism of tissue damage by the bacteria is the production of toxins in the form of exotoxins and the release of endotoxins after cell death that damage host cells [28]. The final course of bacterial keratitis is dependent on the virulence of the offending bacteria, host defensive mechanisms, and the treatment received.
