In vernal keratoconjunctivitis (VKC), the 'shield ulcer' of the cornea occurs due to:

• A Direct toxic effect of eosinophil major basic protein (MBP) and eosinophil cationic protein (ECP) on the corneal epithelium ✓
• B Mechanical trauma from giant papillae on the superior tarsal conjunctiva abrading the corneal epithelium during blinking
• C Corneal neovascularization from chronic limbal inflammation causing epithelial breakdown
• D IgE-mediated mast cell degranulation directly lysing corneal epithelial tight junctions

Explanation

Shield ulcers (type III plaques) in VKC result from the toxic effects of eosinophil-derived mediators — particularly major basic protein (MBP) and eosinophil cationic protein (ECP) — on corneal epithelial cells. These cationic proteins are directly cytotoxic to epithelium, causing epithelial cell death and ulceration that typically forms a shield-shaped (transverse oval) defect in the superior cornea. While mechanical trauma from giant papillae contributes to triggering epithelial abrasion, the fundamental mechanism preventing re-epithelialization is the sustained toxic environment created by activated eosinophils. Treatment involves topical corticosteroids, mast cell stabilizers (sodium cromoglicate), and superficial keratectomy for plaques.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.