**4. Corneal infections**

transmitted disease and both mates should be treated. Gonorrhea conjunctivitis is character‐ ized by copious purulent discharge while other agents cause mucopurulent, mucoid or serous discharge. A form of viral conjunctivitis is hemorrhagic conjunctivitis in which conjunctival

**Figure 2.** Viral conjunctivitis. Note the conjunctival congestion without corneal or intraocular involvement.

migrate into the lacrimal drainage system and cause obstruction.

qid for 3 weeks is effective for prevention and treatment.

*Haemophilus aegyptius* and Listeria.

Conjunctival myiasis is conjunctival infestation by larvae of different types of flies depending on the habitat [9]. The larvae are tiny white and move quickly. They cause conjunctival hyperemia and the patient complains of unilateral ocular irritation. Rarely, the larva may

Infectious agents include bacteria, virus and chlamydia. Most microorganisms cannot invade intact epithelium. The only exceptions are *Neisseria gonorrhoeae*, *Corynebacterium diphtheria*,

Infectious conjunctivitis should be differentiated from noninfectious agents such as allergic conjunctivitis and dry eyes. In neonates occurring in the first month of life, ophthalmia neonatorum is an entity that may be caused by various microorganisms such as chlamydia and less commonly by *Neisseria gonorrhoeae*. Tetracycline 1% or erythromycin 0.5% ointment

Most of the acute viral conjunctivitis forms are self‐limited and treatment is aimed to decrease discomfort and prevent secondary infection. Topical antibiotic such as sulfacetamide 10% (Sulfacid®) qid may be applied. In G6PD and sulfa‐sensitive patients, other antibiotics such as Gatifloxacin (Zymar®) bid, a quinolon, may be prescribed. It is best to defer topical corticoste‐ roid for a week to ascertain that the conjunctivitis is not herpetic or adenoviral. If no improve‐ ment is observed after a week, topical corticosteroid such as fluorometholone (FML®) 0.1% qid may be used for 1–2 weeks in tapered dosage. Patients should be instructed to prevent eye‐ finger‐eye contact (and other contact means) especially with adenoconjunctivitis. The disease

hyperemia is accompanied by subconjunctival hemorrhages.

6 Advances in Common Eye Infections

The general name for corneal infection or inflammation is keratitis. The conjunctiva is usually secondarily involved as conjunctival hyperemia. The clinical manifestations vary and include corneal ulcer, abscess and/or infiltrate [10]. Corneal ulcer is distinguished from abscess and infiltrate by its staining with fluorescein. Abscess and infiltrate do not stain. The clinical findings may overlap between different etiologies.

The diagnosis of all corneal infections is based on scrapping for direct staining with hema‐ toxylin and eosin or Giemsa, and cultures, which should be taken routinely before com‐ mencing with empiric broad‐spectrum topical antibiotics. The only exceptions for obtaining corneal scarps and cultures are a marginal (near the limbus) smaller than 3 mm width flat ulcer(s) and certain typical findings such as dendrite suggesting herpetic keratitis or bilater‐ al multiple epithelial minute defects (epitheliopathy) suggesting adenoviral (epidemic) keratoconjunctivitis.

**Figure 3.** *Pseudomonas aeruginosa* corneal ulcer at the acute stage.

Bacterial keratitis or bacterial ulcer is usually a single solid ulcer with distinctive borders (**Figure 3**). Its size and depth may vary. It may be accompanied by an infiltrate in its base or by localized corneal edema. Infiltrate is white, more dense and distinct and is well localized in contrast to the grayish appearance and less distinctive borders of edema. A grayish, glistening appearance with secretions is a common manifestation of Pseudomonas ulcer. Flare and cells or hypopyon may accompany bacterial ulcer and they may be sterile or infected. If they appear under treatment, they indicate worsening of the infectious process. Any flare or

cells in the vitreous in phakic or pseudophakic eyes indicates the development of endoph‐ thalmitis. Predisposing factors for corneal ulcer include contact lens wear, ocular trauma, dry eyes and long use of topical antibiotics and/or corticosteroids.

Herpetic keratitis a characterized by dendrites in the secondary infection. In Herpes simplex, dendrites vary in number (usually 1–3). They are coarse with widening of their ends (terminal bulbs) (**Figure 4**). Thus, they differ from Herpes zoster dendrites, which are usually numerous, small, thin and without terminal bulbs (**Figures 5**, **6**). Involvement of the tip of the nose (Hutchison's sign) indicates an involvement of the eye on the same side of herpes zoster (**Figure 7**). In repeated Herpes simplex infections, the epithelial defects may form a geographic pattern and may accompanied by corneal vascularization. An important clinical test is corneal sensitivity, which is reduced in recurrent infections. Another finding is patchy sectorial atrophy of the iris that occurs mainly in the midperiphery after herpetic keratouveitis or uveitis.

**Figure 4.** Corneal scar as a result of the ulcer seen in **Figure 3**.

**Figure 5.** Recurrent herpetic keratitis with dendrite in corneal graft. The dendrite is large and has terminal bulbs.

**Figure 6.** Corneal dendrites in herpes zoster. The dendrites are multiple and very fine. They represent immunologic reaction rather than true infection.

Fungal keratitis appears usually as multiple foci of feathery opacification of the cornea with satellites (**Figures 8** and **9**). Hyphae and yeast may be identified by confocal microscopy in the affected cornea.

**Figure 7.** Herpes zoster ophthalmicus. The vesicular rash involves the dermatome innervated by the ophthalmic branch of the trigeminal nerve. Involvement of the tip of the nose indicates involvement of the eye (Hutchison's sign).

**Figure 8.** Fungal keratitis. Note the multiple foci.

cells in the vitreous in phakic or pseudophakic eyes indicates the development of endoph‐ thalmitis. Predisposing factors for corneal ulcer include contact lens wear, ocular trauma, dry

Herpetic keratitis a characterized by dendrites in the secondary infection. In Herpes simplex, dendrites vary in number (usually 1–3). They are coarse with widening of their ends (terminal bulbs) (**Figure 4**). Thus, they differ from Herpes zoster dendrites, which are usually numerous, small, thin and without terminal bulbs (**Figures 5**, **6**). Involvement of the tip of the nose (Hutchison's sign) indicates an involvement of the eye on the same side of herpes zoster (**Figure 7**). In repeated Herpes simplex infections, the epithelial defects may form a geographic pattern and may accompanied by corneal vascularization. An important clinical test is corneal sensitivity, which is reduced in recurrent infections. Another finding is patchy sectorial atrophy of the iris that occurs mainly in the midperiphery after herpetic keratouveitis or uveitis.

**Figure 5.** Recurrent herpetic keratitis with dendrite in corneal graft. The dendrite is large and has terminal bulbs.

eyes and long use of topical antibiotics and/or corticosteroids.

8 Advances in Common Eye Infections

**Figure 4.** Corneal scar as a result of the ulcer seen in **Figure 3**.

Acanthamoeba infection may vary in presentation. The earliest clinical signs include multiple corneal epithelial cell swellings (as seen in adenoviral keratoconjunctivitis but here they are unilateral) and/or corneal edema. Late signs include perineural sheathing and stromal ring(s) (**Figure 10**). Acanthamoeba cysts may be identified by confocal microscopy. A history of contact lens wear and/or bathing in pools or sea is common and symptoms of pain are more striking than the clinical appearance. When diagnosis by cultures is impossible especially in recurrent disease, polymerase chain reaction of the involved tissue may establish the diagnosis.

**Figure 9.** Fungal keratitis with multiple foci and indistinct borders.

**Figure 10.** Immune ring in Acanthamoeba keratitis.

Corneal co‐infections as other co‐infections or mixed infections should be suspected when the course of the disease is atypical or when the condition deteriorates despite of treatment according to cultures and sensitivities. In such cases, repeated cultures should be obtained and broaden accordingly.

All corneal infections may result in either scarring (**Figure 10**) or melting and perforation.

The treatment approach differs between central and peripheral ulcers. Central ulcers are treated with topical antibiotics and are followed frequently to monitor their size and depth. Peripheral ulcers are treated with topical antibiotics and corticosteroids may be cautiously added. Treatment includes broad‐spectrum topical antibiotics such as fortified cefazolin and gentamicin or moxifloxacin (Vigamox®) 0.5% every 30 min–1 h until sensitivity is obtained. Then antibiotic treatment is dictated by the sensitivity of the microorganism. In cases of pain and/or flare and cells in the anterior chamber, topical cycloplegic agent (e.g. cyclopentolate hydrochloride 1% tid) is added to decrease the pain originating from the ciliary body and/or prevention of posterior synechiae. Suspicion of infection other than bacteria should be made when no response is achieved or when the condition worsens under treatment. Additional treatment modalities include topical autologous serum, antipolymorphonuclear migration agents such as tetracycline 1% and/ or citrate 10%, which cause decrease of collagenase activity by chelating free calcium ions that are required for collagenase activity. Vitamin A (ascorbic acid) either topically 10% and/or PO (Vitamin A 500 mg bid). Liberal use of partial tarsorrhaphy is useful especially in recurrences of ulcers, exposure, dryness, corneal anesthesia or trophic ulcers and deep ones. All these means should be used in severe ulcer. Topical corticosteroids should be avoided at the acute phase of the keratitis and when the epithelium is not intact because they cause potentiation of collagenase that may lead to perforation and may also promote secondary infection. They may be used in later stage only after the epithelium healed (no corneal staining) to decrease stromal scarring. If descemetocele occurs, several surgical options exist and include anterior corneal grafts such as deep anterior lamellar keratoplasty (DALK) or non‐Descemet's membrane endothelial keratoplasty (DMEK). A relatively historic treatment is placement of histoacryl for corneal perforation or descematocele. This promotes healing but also corneal vascularization, which impairs vision. Conjunctival flap (Gunderson operation) is indicated for perforation only for eyes with no potential for vision.
