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David D. Yu, MD; Michael A. Lemp, MD; William D. Mathers, MD; Mark Espy, MS; Thomas White, PhD
Washington, DC; Iowa City, Iowa; Rochester, Minn

Arch Ophthalmol. 1993;111(2):167-168.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Disciform keratitis is a well-known sequela of herpes zoster ophthalmicus (HZO) and varicella.¹ The clinical course can persist for many years with longterm dependence on low-dose topical steroids to suppress recurrent inflammation. The mechanism for disciform keratitis development is not known but is thought to be a delayed hypersensitivity reaction to varicella-zoster virus (VZV) antigen in the cornea. Using the polymerase chain reaction, we have demonstrated the presence of VZV DNA in the cornea of a patient who underwent penetrating keratoplasty 2 years following development of HZO.

Report of a Case.

—A 47-year-old woman was afflicted with HZO in V-1 and V-2 dermatomes on the left side in October 1989. Zoster keratouveitis resulted in secondary, open angle glaucoma. The patient presented in February 1991 with disciform keratitis and Streptococcus viridans corneal ulceration that was successfully treated with topical vancomycin (50 mg/mL) and topical penicillin G (100000 U/mL) (Fig 1). . . . [Full Text PDF of this Article]

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