Patients with bacterial keratitis present with hyperemia of the conjunctiva, ciliary injection, and purulent discharge. Biomicroscopy of the cornea reveals an epithelial defect with creamy-white infiltration surrounded by ground-glass appearance. The ulcer may be small or large. The cornea may show folds in Descemet’s membrane with edema and keratic precipitates found on the endothelium. The anterior chamber demonstrates varying degrees of cells and flare. Fibrin or hypopyon may be present. It is important to examine the stroma carefully to assess the amount of necrosis that may lead to thinning of the cornea. This is true in patients with Pseudomonas infection where thinning of the stroma may be marked and sometimes a descemetocele may form which carries a poor prognosis. The descemetocele may lead to corneal perforation and iris adhesion to the cornea. Central corneal ulcers are usually infectious in nature, while noninfectious infiltrates may appear as single or multiple peripheral corneal infiltration ulcer secondary to immune-mediated reactions. Marginal ulcers that extent to the center may be infectious in nature. Staphylococcus corneal ulcers are usually round, well circumscribed with an epithelial defect and corneal infiltration. In some patients with Staphylococcus ulcer, multiple deep stromal infiltrates may be seen together with small infiltrates adjacent to the corneal ulcer. The surrounding cornea may show minimal edema. Streptococcus pneumoniae may appear as serpiginous ulceration that moves across the cornea with infiltration. On the other hand, Pseudomonas aeruginosa causes an aggressive and fulminant corneal ulcer which is rapidly progressing and may lead to corneal perforation if not treated early. The corneal ulcer is usually extensive with necrosis and yellow-green purulent discharge adherent to the surface. The corneal surrounding of the ulcer shows edema with ground-glass appearance and loss of its transparency. A hypopyon is usually present. Certain bacterial ulcers are indolent and insidious in nature such as Moraxella, Nocardia, and nontuberculous Mycobacteria. The corneal ulcers show a localized epithelial defect with infiltration. The ulcer tends to be round or oval, and the cornea surrounding the ulcer appears to be relatively clear unlike cases with Pseudomonas corneal ulcer. In cases of traumatic penetrating corneal laceration, the patient may be infected with Bacillus species or Clostridium species which may produce gas in the anterior chamber or corneal stroma. On the other hand, Serratia marcescens corneal ulcer may produce red pigment that appears in the stroma.

Simple corneal ulcers should always be scraped for cytological evaluation with Gram and Giemsa stains and for cultures. The corneal scrapings should be performed at the area of corneal infiltration obtaining adequate specimens. Part of the scraping specimen is placed on two slides for Gram and Giemsa staining, and another specimen should be placed onto culture plates, blood agar, and chocolate agar. Other media may be used, as indicated, such as Löwestein-Jensen medium, cooked meat, or brain-heart infusion medium. Corneal cultures are obtained in the office utilizing topical anesthetic such as proparacaine 0.5 %, tetracaine 0.1 %, or benoxinate 0.4 %. The corneal scrapings are obtained with the slit-lamp magnification using either Kimura spatula or a 25 g needle. The scrapings should be done aggressively in the bed of the ulcer as well as the leading edge of the infiltrate. Mucopurulent discharge should be avoided. A wire lid speculum may be used to prevent blinking during the procedure. Thioglycolate medium is use for anaerobic cultures. If fungi are suspected, Sabouraud’s dextrose agar should be used. An additional slide may be prepared for periodic acid-Schiff (PAS) or Grocott-Gomori methenamine-silver nitrate stain. The corneal specimen should be cultured even in patients who are on antibiotics. Media with antibiotic removal device may be used. Molecular diagnostic techniques are available such as polymerase chain reaction (PCR). Molecular diagnostic tests may not be readily available in every institution but may prove to be helpful.

Clinical severity of corneal ulcers is divided into three grades: mild, moderate, and severe. Mild corneal ulcers are those that are less than 2 mm in size, and the depth of the ulcer is less than 20 % or 100 μm of the corneal thickness. The infiltrates may be superficial next to the base of the ulcer. In cases with moderate corneal ulcers, the size of the ulcer is 2–5 mm, the depth of the ulcer is 20–50 % (100–275 μm) of the cornea, and the infiltrate is dense extending to the midstroma. In severe corneal ulcers, the ulcer size is more than 5 mm in size, the depth of the ulcer is more than 50 % (>275 μm) of corneal thickness, and the infiltration is dense reaching the deep layers of the corneal stroma. The sclera may be involved in patients with severe peripheral bacterial keratitis. After obtaining the corneal scrapings for culture and cytology, the patient should be started on combination of topical antibiotics to cover the most commonly encountered organisms while the patient is still in the office. The mainstay of treatment includes frequent aggressive administration of topical antibiotics. Certain antibiotics may have to be compounded and made available for the patient. Mild and moderate bacterial keratitis may be treated on an out-patient basis whereas patients with severe bacterial keratitis may have to be admitted to the hospital for the intensive in-patient management.

The patient should be treated with topical antibiotics every hour in addition to the pulse therapy which should be given three times a day and consists of one drop every minute for 5 min.

In moderate and severe corneal ulcers, treatment should be aggressive, and antibiotic eye drops should be administered every 15 min around the clock with an initial pulse therapy. It is of great importance to monitor the corneal thinning and stromal necrosis in cases of imminent perforations, shallowing of the anterior chamber, or sudden appearance of the hypopyon.

In patients with small perforations, tissue adhesive may be applied. In patients where there is rapid reepithelialization, it is recommended to re-scrape the cornea in order to increase the corneal penetration of the antimicrobial agents where the infiltration is persistent. Antibiotic therapy is modified when the culture is available. When the infiltration subsides and the epithelial defect heals, frequency of the antibiotics may be tapered. The size of the infiltration and the ulcer should be measured by slit beam. Optical coherence tomography (OCT) and external photography are helpful. The size of the infiltration and the epithelial defect are recorded and followed up closely. The size of the epithelial defect is usually smaller than the infiltration. Cycloplegic agents such as cyclopentolate 0.1 % eye drops may be given twice daily to minimize pain and blepharospasm. Oral analgesics may be required in patients with severe ocular pain. It is always recommended not to patch the infected eye, but a plastic clear shield may be applied.

Patients may be started on empirical therapy consisting of tobramycin 14 mg/ml and vancomycin 50 mg/ml eye drops. These can be given 5 min apart initially in the first hour followed by every hour. A pulse topical therapy may be given every 1 min for 5 times 3 times daily. Commercially available fluoroquinolones such as gatifloxacin, moxifloxacin, and besifloxacin may be used as initial empiric therapy in mild cases. Ciprofloxacin is approved for use in bacterial keratitis and has demonstrated clinical efficacy and safety in a large clinical trial [2]. Ciprofloxacin is potent against Gram-negative organisms such as Pseudomonas but has limited efficacy against staphylococci and streptococci.

The treatment for bacterial keratitis is the topical administration of commercially available antibiotics or fortified compounded antibiotics. Increasing the concentration of antibiotic solutions creates a larger diffusion grading across the cornea, and this serves to increase the corneal penetration of the antibiotic. Subconjunctival or subtenon injection of antibiotics is occasionally used in patients with moderate to severe corneal ulcers, ulcers with imminent perforation, patients with scleral extension of the corneal ulcers, and patients with associated endophthalmitis. Subconjunctival injection may also be indicated in patients who are not compliant. Repeated injections must be administered to maintain appropriate drug loads.

Intravenous administration of antibiotics is rarely indicated in patients with bacterial keratitis. Neisseria species and Haemophilus species are treated with systemic as well as topical antibiotics because of the possibility of systemic infection, particularly, in the pediatric age group.

The severe inflammation associated with bacterial keratitis may lead to damage to the corneal tissue, and this inflammatory reaction should be taken into consideration. Topical corticosteroids are contraindicated in the initial therapy of bacterial keratitis but once the infection is under control and the epithelium has healed, corticosteroids may be used with care. Clinical trials have shown that topical corticosteroids given 2 days after initiation of topical antibiotic therapy did not worsen the course of the disease. Topical corticosteroids, however, may inhibit the immune mechanisms of the ocular surface leading to persistence of the infection. The risks and benefits of topical corticosteroids should be weighed carefully.

Corneal scrapings in corneal herpetic epithelial disease may be subjected to cytologic examination, PCR, culture, and electron microscopy. Giemsa-stained corneal scrapings may show multinucleated epithelial cells. Giemsa stain obscures nuclear details, and therefore, intranuclear inclusions typical of HSV infection cannot be seen. Specimens fixed with 95 % ethanol and stained with Papanicolaou (PA) method may demonstrate intranuclear inclusion bodies. Fluorescent antibody staining of the corneal scrapings can be done and may demonstrate the presence of herpetic antigens. Cultures taken from epithelial disease are usually positive, while cultures from geographic stromal or disciform lesions are much less likely to be positive. This denotes that the number of virus particles is low in such lesions. Cultures for bacteria and fungi should be obtained from patients with stromal infiltration where secondary infection is suspected.

The treatment epithelial dendrites or geographic corneal ulcers consists of applying topical anesthesia in the form of tetracaine 1 % or benoxinate 0.4 % and sweeping the epithelium with a sterile cotton applicator followed by topical application of acyclovir 3 % ophthalmic ointment 5 times daily or ganciclovir 0.15 % gel 5 times daily [9]. Antiviral therapy should be continued for a period of 7–10 days after. Antiviral agents such as idoxuridine, adenine arabinoside, and trifluridine are all toxic to the corneal epithelium and should be avoided [10]. An alternate therapy is trifluridine 1 % solution administered every 2 h. This dosage is used in the initial treatment period for 2–4 days and later decreased to 5 times daily. If there is lack of response or increase in the size of the ulcer, the therapy should be discontinued. Topical trifluridine may cause toxicity to the corneal epithelium.

It is estimated that 20 % of unvaccinated adults develop disease at one time or another. Herpes zoster ophthalmicus (HZO) is much less common than varicella. It is postulated that with age there is decrease in the immunity to the varicella-zoster virus and this may lead to reactivation of the latent virus [19]. Other triggers to reactivation of latent varicella zoster are trauma, stress, systemic disease, surgery, immunosuppression, or disease such as leukemia and lymphoma.

Herpes zoster begins with a localized pain, tingling sensation, dysesthesia in the affected dermatome associated with fever and malaise. A cutaneous eruption occurs 3–4 days after with edematous and maculopapular eruption which becomes vesicular followed by ulceration and scarring [20]. The ophthalmic branch of the trigeminal nerve is involved and lead to swelling of the lids, conjunctival hyperemia. Involvement of the tip of the nose also known as, Hutchinson’s sign, is evidence of nasociliary nerve distribution, and the ocular structures may be involved in 85 % of the cases. The cutaneous eruptions in Hutchinson’s sign are on the tip of the nose [21]. The side of the midportion of the nose may also be involved. It should be kept in mind that herpes simplex dermatitis may have a dermatomal distribution and should be in the differential diagnosis of HZO. Recurrences of HZO is extremely rare but has been reported. The possible ocular manifestations of HZO are numerous. Herpes zoster can cause blepharitis, canaliculitis, episcleritis, conjunctivitis, keratitis, iridocyclitis, uveitis, retinal vasculitis, retinal necrosis, choroiditis, papillitis, and optic neuritis.

Herpes zoster keratitis may have variable ocular manifestations. The corneal epithelium shows punctate keratitis and fine with no terminal bulbs dendritic epithelial lesions and sometimes progress to geographic or neurotrophic corneal ulcerations. The corneal stroma may be involved showing disciform keratitis or nummular opacities. The nummular opacities are more frequently seen at the periphery. The lesions may cause corneal necrosis and melting, and corneal perforation may occur [22]. Lid corneal scarring and vascularization with lipid deposition in the cornea are seen. Zoster dendrites do not have terminal bulbs and are usually small, linear, and less ulcerative than herpetic keratitis caused by herpes simplex. The dendrites are softer and less branching than the herpes simplex dendrites. They tend to be small and in starfish configuration. Corneal sensation is diminished. Herpes zoster may cause disciform keratitis and sometimes keratouveitis [23]. The anterior uveitis may be associated with sector iris atrophy.