The cellular migration into the anterior chamber may plaster in the endothelial surface and later may invade the corneal tissue (Fig. 28.2). Disorganization and edematous stoma may be visible if associated with raised intraocular pressure. A marked polymorphonuclear migration into cornea with corneal ring abscess formation in response to the bacterial invasion or locally produced inflammatory mediators is hallmark of Bacillus cereus [9]. Besides, hyphae of fungus may also be observed within the corneal stroma in case of fungal endophthalmitis.

Exudation of polymorphonuclear leukocytes with or without macrophage is seen in aqueous humor. The rupture of anterior vitreous face with disruption of blood–aqueous barrier is the cause of exudates in anterior chamber (Fig. 28.2). Sometimes, there can be necrotic leukocytes admixed with a large amount of uveal pigment leading to brown hypopyon due to Streptococcus bovis endogenous endophthalmitis [10].

Clustering of microorganisms like Pseudomonas aeruginosa and Paecilomyces lilacinus may occur within the lens capsule following accidental trauma causing the rupture of capsule or after the cataract surgery creating a localized infection within the lens capsular sac [9]. Sometimes, residual lens cortex, phacotoxic reaction, and phacoanaphylaxis reaction can lead to sterile granulomatous endophthalmitis [11]. It is characterized histologically by a zonal granulomatous inflammatory reaction to the lens capsular remnants with central polymorphonuclear reaction.