Contributor: Gordon K. Klintworth
Fungal keratitis (mycotic keratitis, keratomycosis) is a fungal infection of the cornea. Keratitis is common and more than 35 genera of fungi (including Aspergillus [aspergillosis, aspergillus keratitis [keratitis - aspergillus], Blastomyces dermatitidis [blastomycosis], Candida [candidiasis], Cephalosporium, Cryptococcus neoformans[cryptococcosis] Fusarium [fusariosis], Curvularia, and Phoma) have been implicated in fungal keratitis. The causative agents vary with the geographic locale. Fungal keratitis is usually caused by saprophytic fungi in the setting of corneal trauma and an altered host resistance. Many cases follow prior treatment with antibiotics and topical corticosteroids. The clinical presentation of fungal keratitis is often identical to that of bacterial keratitis [keratitis - bacterial]. A red painful eye is associated with photophobia, tearing, a mucopurent discharge, a foreign body sensation and decreased vision. A dense stromal infiltrate is present on examination. In contrast to bacteria fungi can not only infiltrate through the corneal stroma, but even penetrate Descemet membrane to reach the anterior chamber. When this happens iritis, hypopyon and an endothelial plaque can become evident and corneal perforation may occur. Because fungal keratitis is less common than bacterial keratitis, ophthalmologists usually treat corneal ulcers initially on the assumption that they are due to bacteria. Hospitalization and aggressive hourly treatment with antifungal agents is necessary for the treatment of fungal keratitis and the response to therapy tends to be slower than with bacterial keratitis. The recommended antifungal agent depends on the fungus. Amphotericin is useful for Aspergillus and Candida. Natamycin is effective with Fusarium and Curvalaria. Fusarium is the major cause of fungal keratitis in the southern USA and Fusarium solani is responsible for more than half of the cases. Certain stains of Fusarium synthesize complex toxins and potent proteolytic enzymes, which are responsible for producing extensive necrosis and a rapidly destructive severe, suppurative keratitis. The large hyphae escape phagocytic ingestion by neutrophils and may penetrate the stromal lamellae, as well as extend through Descemet membrane into the anterior chamber. The ability of hyphal elements to penetrate deeper layers of the corneal stroma explains the common failure of lamellar keratectomy in the treatment of fungal keratitis.