Keratomycosis:Clinical diagnosis, Medical and Surgical Treatment

Keratomycosis is a major cause ofvisual disability in developing countries(1). It is common in our country because of the tropical climate and a large agrarian population at risk. Since the first report ofkeratomycosis. by Professor Theodor Leber, fungi have been increasingly implicated in the cause ofcorneal ulcer (2,3), there has been a dramatic rise in frequency of these infections in the last two decades possibly because of the indiscriminate use of antibiotics and corticosteroids in ophthalmology practice (3, 4). An increased clinical awareness has also partially contributed to its frequent reporting (4). In northern India, fungal keratitis has a prevalence of 8.4% (5) while it has been reported as high as 46.3% from southern India (6). Keratomycosis can be caused by as many as 60 species of fungi. The predominant etiological agents VaJy in different geographical areas. However, Aspergillus spp. is the commonest isolate in India (5,6). Risk factors for keratomycosis Fungi are opportunistic agents ofinfection and become pathogenic under conditions of impaired inununodefense. Fungal infection in the absence of precipitating event is unusual Trauma is the most common precipitating factor in most of the cases(7). The nature of injury often is vegetative in origin, which may consist of trauma with plant twigs, rice-husk, cotton plant etc. Trauma leads to destruction ofthe epithelium and Bowman's membrane, impairing barrier to infection. The underlying stroma becomes, excessively hydrated and possibly altered in such a way to constitute a more Cavorable site for fungus to grow. Keratomycosis caused by filamentous fungi is an occupational hazard of farmers and agricultural workers(8). The seasonal variation noted in most series most likely represent occupational injuries associated with harvesting. Alternately. mycotic infection especially Candidal spp.may develop in pre existing lesions like herpetic scars, neurotrophic keratitis which alters local ocular inununo defense (9). The time interval from trauma to clinical lCatures can be 24-48 hours but often is as long as 10 to 21 days, depending 011 the organism, the size of inoculum and host resistance (10). The topical corticosteroids therapy has been associated with increased incidence and worsening of fungal keratitis (11-13). The increased incidence is probably due to altered local immune response and increased rates of conjunctival colonization by fungi. Additionally, it indirectly promotes fungal replication and corneal invasion by interfering with host's inflammatory response. The systemic use of corticosteroids may predispose to fungal keratitis by causing immunosuppression (12). Candida spp. commonly colonize conjunctive and eye lid margins ofnonnal individuals(l4). However. it may produce keratitis in patients with impaired immune response. The local ocular resistance may be lowered by atopic disease, eye-lid malposition. dry-eye conditions, neurotrophic or herpetic keratitis predisposing to ftmgal keratitis(l5).