*4.3.4 Treatment*

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

Surgical debridement of the epithelium and base of the fungal keratitis is crucial in the management because it debulks the organisms and enhances drug penetration into cornea [79]. Surgery for fungal keratitis, ranging from lamellar or penetrating keratoplasty to evisceration or enucleation, plays a role as an adjunct to medical therapy for initial management and when medical therapy fails or impending corneal perforation [51, 61, 79]. The prognosis of fungal keratitis is worse than bacterial keratitis [80]. The course is favorable with medical treatment in 50—70% of cases. A surgery is required in 30 to 54% of cases [80]. These infections may lead to loss of the globe in 10 to 25% of cases [80]. High risk of developing corneal perforation and the need to undergo therapeutic penetrating keratoplasty (TPK) are due to infiltrate size of more than 6.6 mm, an infiltrate involving the posterior one-third of the stroma, and the presence of a hypopyon [73]. Unfortunately, recurrence keratitis can occur approximately 6–7% after therapeutic keratoplasty [81]. Hypopyon, corneal perforation, and corneal infection expanding to limbus and lens infection are predominant risk factors for the recurrence of fungal keratitis after corneal transplantation [81]. After therapeutic keratoplasty, systemic and topical antifungal treatments should be used for 2 weeks routinely and possibly for 6 to 8 weeks in high-risk cases [81]. Generally, if no typical signs of recurrence were present 2 weeks after surgery, low-concentration topical steroids may be adminis-

Herpes simplex virus (HSV) is a common cause of viral keratitis and the most common cause of unilateral infectious corneal blindness in the world [5, 9]. Varicellazoster and cytomegalovirus can also cause viral keratitis but are much less common [9]. The prevalence of viral keratitis was 0.11% in a recent population-based study [5]. The majority of corneal HSV-1 infection is not the outcome of primary ocular infection, but in response to reactivation of latent virus from the trigeminal ganglion [82]. However, recurrent corneal epithelial infection with HSV-1 can have stromal involvement known as herpes stromal keratitis (HSK), which can be necrotizing, nonnecrotizing, or a mix of both [82, 83]. One study with HSV stromal keratitis reported that disease was of the necrotizing type in 7%, nonnecrotizing in 88%, and a mix of the two in 5% [84]. In this review, we address only the herpes necrotizing stromal keratitis that may mimic infectious keratitis from other organisms.

Viral keratitis differs from bacterial and fungal keratitis in that it can become recurrent and chronic [9]. In necrotizing HSV stromal keratitis, necrosis, ulceration, and dense leukocytic infiltration of the stroma are present and often associated with an overlying epithelial defect and neovascularization [18, 83, 85]. The viral keratitis diagnosis is usually based on clinical findings [43] and diagnosis by exclusion. However, in atypical cases, the investigations such as tissue culture,

The risk of HSV reactivation can occur after excimer laser refractive surgery such as LASIK or PRK. The exposure to ultraviolet light during corneal collagen cross-linking

ELISA, and PCR may aid in the diagnostic confirmation [43].

**14**

tered with caution [81].

**4.3 Viral keratitis**

*4.3.1 Epidemiology*

*4.3.2 Manifestations*

*4.3.3 Risk factors*

Both immune and active viral replications are responsible for the disease pathogenesis [83]. In contrast to nonnecrotizing stromal keratitis where topical corticosteroid is the mainstay treatment, oral acyclovir is used to control the viral invasion and replication in cornea, while low-dose topical corticosteroids are given to control inflammation in necrotizing stromal keratitis [18]. Topical CsA administration can resolve stromal inflammation and neovascularization in 50 and 64% of cases, respectively [83]. Without timely and effective treatment, necrotizing HSV stromal keratitis can rapidly lead to corneal perforation [83]. Amniotic membrane transplantation onto the ocular surface promotes corneal epithelial healing and reduces stromal inflammation, angiogenesis, and scarring [83]. Various oral antiviral agents to treat active viral replication and prevent recurrences are available as mentioned below [86]:

1.Acyclovir: 800 mg, 3–5 times/day, 7–10 days

2.Valacyclovir: 1 g, 3 times per day, 7–10 days

3.Famciclovir: 500 mg, 2 times/day, 7–10 days

Data from the Herpetic Eye Disease (HEDS) study concluded that the HSV stromal keratitis patients who received 400 mg oral acyclovir twice per day for 12 months had reduced rate of recurrent HSV stromal keratitis by about 50%. The research about HSV vaccination is underway, and no vaccine is currently available [83, 86, 88].
