Introduction
Background
Bacterial keratitis is a sight-threatening process. A particular feature of bacterial keratitis is its rapid progression; corneal destruction may be complete in 24-48 hours with some of the more virulent bacteria. Corneal ulceration, stromal abscess formation, surrounding corneal edema, and anterior segment inflammation are characteristic of this disease.
Pathophysiology
Interruption of an intact corneal epithelium and/or abnormal tear film permits entrance of microorganisms into the corneal stroma, where they may proliferate and cause ulceration. Virulence factors may initiate microbial invasion, or secondary effector molecules may assist the infective process. Many bacteria display several adhesins on fimbriated and nonfimbriated structures that may aid in their adherence to host corneal cells. During the initial stages, the epithelium and stroma in the area of injury and infection swell and undergo necrosis. Acute inflammatory cells (mainly neutrophils) surround the beginning ulcer and cause necrosis of the stromal lamellae.
Diffusion of inflammatory products (including cytokines) posteriorly elicits an outpouring of inflammatory cells into the anterior chamber and may create a hypopyon. Different bacterial toxins and enzymes (including elastase and alkaline protease) may be produced during corneal infection, contributing to the destruction of corneal substance.
The most common groups of bacteria responsible for bacterial keratitis are as follows: Streptococcus, Pseudomonas, Enterobacteriaceae (including Klebsiella, Enterobacter, Serratia, and Proteus), and Staphylococcus species.
Up to 20% of cases of fungal keratitis (particularly candidiasis) are complicated by bacterial coinfection.
Frequency
United States
Approximately 25,000 Americans develop bacterial keratitis annually.
International
Incidence of bacterial keratitis varies considerably, with less industrialized countries having a significantly lower number of contact lens users and, therefore, significantly fewer contact lens-related infections.
Mortality/Morbidity
In cases of severe inflammation, a deep ulcer and a stromal abscess may coalesce, resulting in thinning of the cornea and sloughing of the infected stroma. These processes may create some of the following complications:
- Corneal leukoma: Scar tissue formation with the presence of corneal vascularization may be the end result of a bacterial keratitis. Depending on the location and depth of stromal involvement, the resulting corneal leukoma may be visually significant and necessitate corneal surgery for visual rehabilitation (including phototherapeutic keratectomy [PTK] or penetrating keratoplasty [PK]).
- Irregular astigmatism: Another possible complication of these infections is uneven healing of the stroma, resulting in irregular astigmatism (that may require a gas-permeable contact lens or PTK to improve vision).
- Corneal perforation: This is one of the most feared complications of bacterial keratitis that may result in secondary endophthalmitis and possible loss of the eye.
Clinical
History
Patients with bacterial keratitis usually complain of rapid onset of pain, photophobia, and decreased vision. It is important to document a complete systemic and ocular history in these patients to identify any potential risk factors that would have made them susceptible to develop this infection, including the following:
- Contact lens wear (Note the type of lens, wearing time, and type of disinfection system.)
- Trauma (including previous corneal surgery)
- Use of contaminated ocular medications
- Decreased immunologic defenses
- Aqueous tear deficiencies
- Recent corneal disease (herpetic keratitis, neurotrophic keratopathy)
- Structural alteration or malposition of the eyelids
Physical
External and biomicroscopic examination of these patients reveals some or all of the following features:
- Ulceration of the epithelium; corneal infiltrate with no significant tissue loss; dense, suppurative stromal inflammation with indistinct edges; stromal tissue loss; and surrounding stromal edema
- Increased anterior chamber reaction with or without hypopyon
- Folds in the Descemet membrane
- Upper eyelid edema
- Posterior synechiae
- Surrounding corneal inflammation that is either focal or diffuse
- Conjunctival hyperemia
- Adherent mucopurulent exudate
- Endothelial inflammatory plaque
Causes
Any factor or agent that creates a breakdown of the corneal epithelium is a potential cause or risk factor for bacterial keratitis. Furthermore, exposure to some virulent bacteria that may penetrate intact epithelium (eg, Neisseria gonorrhoeae) also may result in bacterial keratitis.
- By far the most common cause of trauma to the corneal epithelium and the main risk factor for bacterial keratitis is the use of contact lenses, particularly extended-wear contact lenses. Of patients with bacterial keratitis, 19-42% are contact lens wearers. Incidence of bacterial keratitis secondary to use of extended-wear contact lenses is about 8,000 cases per year. The annual incidence of bacterial keratitis with daily-wear lenses is 3 cases per 10,000.
- Contaminated ocular medications or contact lens solutions
- Decreased immunologic defenses secondary to malnutrition, alcoholism, and diabetes (Moraxella)
- Aqueous tear deficiencies
- Recent corneal disease (including herpetic keratitis and secondary neurotrophic keratopathy)
- Structural alteration or malposition of the eyelids (including entropion with trichiasis and lagophthalmos)
- Chronic dacryocystitis
- Use of topical corticosteroids
More on Keratitis, Bacterial |
 Overview: Keratitis, Bacterial |
| Differential Diagnoses & Workup: Keratitis, Bacterial |
| Treatment & Medication: Keratitis, Bacterial |
| Follow-up: Keratitis, Bacterial |
| References |
| Next Page » |
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Further Reading
Keywords
corneal ulcer, ulcerative keratitis
