Cornea · Bacterial keratitis

Corneal ulcer with hypopon

The development of bacterial keratitis progresses through multiple stages Stages of corneal ulcer formation 1. Progressive infiltration – Once the epithelium is breached, polymorphonuclear cells and lymphocytes infiltrate the epithelium, joined by similar cells migrating in from the adjacent stroma. Depending on the host's defenses versus the bacteria's virulence, this can progress to tissue necrosis. 2. Active ulceration – The epithelium, Bowman's membrane, and stroma undergo necrosis and slough off, forming the ulcer. The ulcer walls swell from fluid imbibition and leucocyte infiltration. Vascular congestion (from hyperemia) and purulent exudate accumulate in the cornea. Toxins can also trigger iritis, causing congestion of the iris and ciliary body. 3. Hypopyon formation – This happens when inflammatory exudate from the congested iris and ciliary body migrates into the anterior chamber, settling as a layer of pus (hypopyon) at the bottom. 4. Regression – Antibody production and cellular defenses take over. A demarcation line forms at the ulcer's edge, rich in leucocytes that neutralize and phagocytose bacteria and necrotic debris. Interestingly, this debris clearance can initially enlarge the ulcer before superficial vascularization kicks in to boost the immune response further. 5. Cicatrization (healing) – Progressive epithelization occurs, with fibroblasts and endothelial cells laying down fibrous tissue beneath the epithelium. Stromal thickening then pushes the epithelium forward. The resulting scar is classified by depth: Nebular opacity – superficial, limited to epithelium/subepithelium and superficial stroma Macular/leucomatous opacity – involves more than one-third of stromal thickness, distinguished by whether underlying structures (iris, pupil) remain visible

Contributed byDr. Mohammed Arif KaderiResident, JNMC, Wardha

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