**1. Introduction**

Bacterial keratitis (BK) is an acute condition perverting the vision to cause blindness if untreated acutely. Currently, microbial keratitis may be epidemic and may exceed 2 million cases per year worldwide [1]. In the US among one million infectious keratitis around 58,000 cases of BK were reported [2]. Bacterial infection was predominant in developed countries whereas developing countries face challenges in corneal infections due to fungal, bacterial, and other origins. One of the reports from the south Indian cities claimed 113 MK in 100,000 individuals [3].

Generally, the bacterial keratitis in its acute condition, the treatment was initiated with a time lag due to delayed presentations in developing countries. In addition, Gram staining and culture sensitivity with antibiogram are time-consuming procedures with challenging availability at all primary or secondary eye care setups.

Hence, while initiating the therapy the size of the ulcer or the intensity of the severity would have progressed to another grade. An intensive approach would impact early recovery and prevent the incidence of smaller ulcers becoming larger corneal ulcers.

Surgical modalities of therapeutic Deep Anterior Lamellar Keratoplasty (DALK), and therapeutic penetrating keratoplasty in cases of fulminating bacterial keratitis, impending perforation, or actual perforation are not discussed in this chapter. Other alternate modalities of treatment of BK are given importance and are discussed here.

## **2. Bacterial keratitis management**

#### **2.1 Standard medical treatment**

Bacterial keratitis is generally treated instantaneously upon its diagnosis by clinicians. After confirming bacterial etiology, the patient should be started on broad-spectrum antibiotic therapy, covering both gram-positive and negative bacteria. Once the culture results are available after 48 to 72 hours, the treatment may be switched to targeted antibacterial therapy if an empirical therapy is not responsive. To treat peripheral ulcers without visual axis involvement (<3 mm), monotherapy with fourth generations of quinolones is initiated. In the case of larger and deep stromal ulcers, it is better to start two antibacterials to prevent irreversible visionthreatening sequelae [4].

#### *2.1.1 Topical antibiotics*

The topical fluoroquinolones are available as 0.3% ciprofloxacin, 0.3% ofloxacin, 0.5% moxifloxacin, and 0.3% gatifloxacin. They are primarily instilled as monotherapy. Recently, growing resistance has been noted for ciprofloxacin and ofloxacin; hence, moxifloxacin and gatifloxacin are being used with more efficacy in managing bacterial keratitis [5].

The most common cephalosporins implicated is bacterial keratitis with topical cefazolin 5% (fortified). It is best suitable for non-penicillinase-producing grampositive bacteria.

Aminoglycosides including fortified topical tobramycin 0.3% or gentamicin 0.3%, or amikacin 1 g/ml injection are very effective against gram-negative bacteria, streptococci, and staphylococci but have a very limited response against pneumococci. Fortified cefazolin and tobramycin as combination therapy are most commonly employed as an alternative to monotherapy with fourth-generation quinolones in bacterial keratitis. Fortified vancomycin 5% is very active against methicillin-resistant *staphylococcus aureus* (MRSA).

Poor drug availability due to pre-corneal factors and deeper penetration into corneal layers remains a challenge with topical therapy and hence alternative treatment options are needed to be explored.

The role of systemic antibiotics in the management of bacterial keratitis is limited. It was used only in endophthalmitis, scleritis, or non-resolving progressive bacterial ulcers. The drugs implicated are ciprofloxacin 750 mg BD or an aminoglycoside with cephalosporin [6].

#### *2.1.2 Steroids*

The main treatment is the topical antibiotic for the management of bacterial keratitis and the clinical benefits are appreciable when corticosteroids were used along with topical antibiotics. The topical steroids in the case of microbial keratitis are controversial. Steroids minimize tissue damage by reducing neovascularization, stromal melting, and scarring [7, 8]. Overall pain control and comfort are obvious in steroids that also improve patient compliance [8]. Conversely, steroid therapy may delay epithelial healing and potentiate bacterial keratitis, leading to stromal thinning and melting.

Four clinical trials, including one randomized, placebo-controlled, double-masked trial known as the Steroid for Corneal Ulcer Trial (SCUT), have compared clinical outcomes in bacterial keratitis treated with antibiotics and steroids vs. antibiotics alone [8, 9].

Earlier trials with topical steroids yielded an ambiguous result; however, it gave insight into the subgroup analysis within SCUT patients with low vision patients conveying an appreciable visual improvement at 3 months when compared with placebo, as did patients with invasive Pseudomonas strains. No significant difference in adverse effects was noted between steroid and placebo arms [9].
