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. (See image below.)
Bacterial keratitis remains one of the most important potential complications of contact lens use and refractive corneal surgery. Keeping this in mind, early diagnosis and treatment are key to minimizing any visual-threatening sequelae. In addition, close follow-up, attention to laboratory data, and changing antimicrobials if no clinical improvement is evident are important elements for successful outcome.
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.
Approximately 25,000 Americans develop bacterial keratitis annually.
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.
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.
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