keratitis

Keratitis is classified by etiology: infectious (bacterial - Pseudomonas and Staphylococcus common in contact lens wearers; viral - HSV causing dendritic ulcers, VZV in herpes zoster ophthalmicus; fungal - Fusarium, Aspergillus, often post-trauma with plant material; protozoal - Acanthamoeba, strongly associated with contact lens use and exposure to contaminated water) and non-infectious (UV exposure/photokeratitis, exposure keratitis from poor eyelid closure, autoimmune conditions like Sjögren syndrome). Pathophysiology involves epithelial breakdown allowing pathogen invasion, triggering an inflammatory response with stromal infiltration, potential ulceration, and neovascularization if chronic. HSV keratitis classically shows dendritic branching ulcers on fluorescein stain and can recur due to viral latency in the trigeminal ganglion; treatment includes topical/oral antivirals (trifluridine, acyclovir), with corticosteroids contraindicated in active epithelial disease as they worsen HSV replication. Bacterial keratitis requires prompt fluoroquinolone or fortified antibiotic drops; empiric broad coverage is critical given rapid progression risk. Acanthamoeba keratitis presents with severe pain out of proportion to findings and ring-shaped stromal infiltrate; treatment is prolonged topical biguanides. Fungal keratitis often has feathery infiltrates and satellite lesions, treated with natamycin or voriconazole. Complications include corneal scarring, perforation, secondary glaucoma, and endophthalmitis. Diagnosis involves slit-lamp exam with fluorescein staining, corneal scraping for culture/Gram stain/KOH prep. High-yield associations: contact lens wearers (Pseudomonas, Acanthamoeba), dendritic ulcers (HSV), and avoiding steroids in undiagnosed red eye or active viral keratitis.