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Risk factors for bacterial keratitis include contact lens wear—especially overnight wear—and corneal trauma, including refractive surgery. The pathogens most commonly isolated are staphylococci, including MRSA; streptococci; and Pseudomonas aeruginosa, Moraxella species, and other gram-negative bacilli. The cornea has an epithelial defect and an underlying opacity. Hypopyon may be present (eFigure 7–23). Topical fluoroquinolones, such as levofloxacin 0.5%, ofloxacin 0.3%, norfloxacin 0.3%, or ciprofloxacin 0.3%, are commonly used as first-line agents as long as local prevalence of resistant organisms is low (Table 7–2). For severe central ulcers, diagnostic scrapings can be sent for Gram stain and culture. Treatment may include compounded high-concentration topical antibiotic drops applied hourly day and night for at least the first 48 hours. Fourth-generation fluoroquinolones (moxifloxacin 0.5% and gatifloxacin 0.3%) are also frequently used in this setting. Although early adjunctive topical corticosteroid therapy may improve visual outcome, it should be prescribed only by an ophthalmologist.

eFigure 7–23.

Central corneal ulcer and hypopyon due to Pseudomonas keratitis. (Reproduced with permission from Riordan-Eva P, Augsburger JJ. Vaughan & Asbury's General Ophthalmology, 19th ed. McGraw-Hill, 2018.)

When to Refer

Any patient with suspected bacterial keratitis must be referred emergently to an ophthalmologist.

Jin  H  et al. Evolving risk factors and antibiotic sensitivity patterns for microbial keratitis at a large county hospital. Br J Ophthalmol. 2017;101:1483.
[PubMed: 28336675]  
Lin  A  et al; American Academy of Ophthalmology Preferred Practice Pattern Cornea and External Disease Panel. Bacterial keratitis: Preferred Practice Pattern®. Ophthalmology. 2019;126:P1.
[PubMed: 30366799]  
Peng  MY  et al. Bacterial keratitis: isolated organisms and antibiotic resistance patterns in San Francisco. Cornea. 2018;37:84.
[PubMed: 29053557]  


Primary ocular herpes simplex virus infection may manifest as lid, conjunctival, or corneal ulceration (eFigure 7–24). The ability of the virus to colonize the trigeminal ganglion leads to recurrences that may be precipitated by fever, excessive exposure to sunlight, or immunodeficiency. Herpetic corneal disease is typically unilateral but can be seen bilaterally in the setting of atopy or immunocompromise. The dendritic (branching) corneal ulcer is the most characteristic manifestation of herpetic corneal disease (eFigure 7–25). More extensive (“geographic”) ulcers also occur, particularly if topical corticosteroids have been used. The corneal ulcers are most easily seen after instillation of fluorescein and examination with a cobalt blue light. Resolution of corneal herpetic disease is hastened by treatment with topical antiviral agents (eg, trifluridine drops, ganciclovir gel, acyclovir ointment) or oral antiviral agents (eg, acyclovir, 400–800 mg five times daily or valacyclovir 500–1000 mg three times daily for 7–14 days). Topical antiviral agents may cause corneal toxicity after approximately 10–14 days of therapy and for that reason are not commonly used ...

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