*4.2.3 Risk factors*

*Visual Impairment and Blindness - What We Know and What We Have to Know*

matrix metalloproteinases [71].

**4.2 Fungal keratitis**

*4.2.1 Epidemiology*

[18, 24, 45, 61, 72]:

epithelium [56].

*4.2.2 Manifestations*

*Scedosporium* spp. are frequent causes.

and/or needing therapeutic keratoplasty [73].

and 40–50% of these patients recover useful vision [24].

to fluoroquinolones [70]. In terms of patients' tolerance to medications, fluoroquinolones are more favorable than combined fortified antibiotics [69]. The initial empirical therapy should be prescribed until definite microbial identity and sensitivity are disclosed [11]. For central or severe keratitis, a loading dose every 5–15 minutes followed by frequent applications such as every hour is recommended [24, 44]. Subconjunctival antibiotics may be useful in impending scleral spreading and questionable adherence to topical treatment. In cases of scleral or intraocular extension of infection, perforation, or systemic infection, systemic therapy may be helpful [24, 44]. Oral tetracycline class antibiotics (including doxycycline) could be used to inhibit corneal stromal thinning by

Reevaluation depends on the extent and severity of disease. The initial treatment should be modified when the eye shows a lack of improvement or stabilization within 48 hours [44]. Coexisting conditions and/or complications, such as glaucoma, corneal perforation, endophthalmitis, and eye lid abnormalities, should be treated promptly. The progressive corneal stromal thinning should be managed by application of tissue adhesive, penetrating keratoplasty, or lamellar keratoplasty [44]. Therapeutic keratoplasty may be indicated in cases of large corneal perforation or uncontrolled infection [24, 44]. Corneal transplantation in active infection has high failure rate [34]. However, the result is usually better than fungal keratitis,

Fungal keratitis, potentially blinding condition, is an important cause of infectious keratitis [72]. Fungal keratitis is very common, accounts for 30–62% of infectious keratitis, in tropical region, but is uncommon in temperate climates [72]. The important pathogens of fungal keratitis can be classified as follows

Filamentous fungi such as *Aspergillus* spp., *Fusarium* spp., *Curvularia* spp., and

Yeasts such as *Candida albicans*, *Candida* spp., and *Cryptococcus* spp., are less common [18]. The fungi invade the ocular surface only when it is compromised or has a defect in the epithelial barrier and access into the corneal stroma [72]. However, the keratitis may present as chronic infiltration or even with an intact

Symptoms of fungal keratitis typically are not as acute as other microbial keratitis [72]. The pain, redness, and lid edema are similar with bacterial keratitis. Early fungal keratitis may appear like a dendritic ulcer of herpes simplex virus. The feathery edge is a pathognomonic clinical feature [24]. Satellite lesions, immune ring, and unlevelled hypopyon may support the diagnosis but not specific clinical figures [24]. The surface is raised with grayish-white creamy infiltrates, which may or may not appear dry [24]. The keratitis due to pigmented fungi such as Curvularia spp., Bipolaris, and Exserohilum spp. will appear as brown or dark, raised, dry, rough, leathery plaque on the corneal surface [24, 46]. A recent report from the Mycotic Ulcer Treatment Trial II (MUTT II) stated that the presence of hypopyon at baseline indicated 2.28 times the odds of the patient developing corneal perforation

**12**

Fungal keratitis must be suspected if the patient is in agricultural work [24]. For filamentous fungi, trauma with subsequent exposure to plant or vegetable material is usually the only predisposing factor, although previous use of corticosteroids, native medicine, and contact lens wear are increasing in importance as risk factors [24, 45, 61]. For yeast, there is usually some systemic or ocular surface compromise [61].
