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Acanthamoeba keratitis occurs in association with contact lens use, minor corneal trauma, or contact of the eye with contaminated water. It is a relatively uncommon but potentially sight-threatening keratitis. In mild to moderate cases, medical treatment alone can eradicate the infection; however, in severe cases surgical treatment is usually required.1 Other members of the ameba family rarely cause ocular infection. A case of contact lens–related amebic keratitis due to a mixed infection of Vahlkampfia and Hartmannella was recently reported.2 Both patients were contact lens wearers.
We report herein the second case of amebic keratits secondary to Vahlkampfia infection. To our knowledge, this is the first case of amebic keratitis following minor corneal trauma in a patient who did not wear contact lenses, and the first report of a non-Acanthamoeba amebic keratitis in the United States.
Report of a Case
A 30-year-old man came to our institution with severe pain and irritation in the right eye. One month previously he had sustained corneal abrasion to the right eye from fiberglass while working on his boat and subsequently self-irrigated the eye with tap water. He was then seen by his private ophthalmologist and was treated with a combination ointment of neomycin sulfate, polymyxin B sulfate, and bacitracin zinc (Neosporin, Glaxo Wellcome Inc, Research Triangle Park, NC) after yields from a corneal culture were examined. No organism was isolated from the initial corneal cultures. No notable improvement of his symptoms and corneal findings was noted after 1 month. He was referred to our institution for further evaluation. On ophthalmic examination, his best-corrected visual acuity was 20/50 OD and 20/20 OS. Intraocular pressure was normal in both eyes. Slitlamp examination of the right eye revealed a midstromal infiltrate with an overlying epithelial defect and localized corneal edema (Figure 1). No other ocular abnormality was noted. Corneal scrapings were obtained for culture and the patient was given empiric treatment with ciprofloxacin under the assumption that he had bacterial keratitis. The patient continued to have persistent intraocular inflammation with stromal infiltrates. Two weeks later, a second set of scrapings was obtained, and the patient's treatment was switched to fortified vancomycin hydrochloride and ceftazidime. Yields from routine culturing of both sets of corneal scrapings we obtained were negative for organisms. Despite intensive antibiotic treatment, he remained symptomatic. One week later, yields from an agar-agar culture obtained from a third set of corneal scrapings revealed a moderate amount of cysts and trophozoites. The organisms were also identified by Giemsa stain (Figure 2) in both scraping and culture yields. They appeared smaller and morphologically distinct from Acanthamoeba and were identified as Vahlkampfia. The patient subsequently began receiving routine antiamebic treatment that included propamidine; polyhexamethyl biguanide (Bacquacil); the combinarion ointment of neomycin sulfate, polymyxin B sulfate, and bacitracin zinc; and clotrimazole every 2 hours with rapid resolution of symptoms. He was maintained on a regimen of promamidine (Brolene) and Bacquacil for a month. His final visual acuity was 20/20 with complete resolution of the stromal infiltrate.
Clinical appearance of the Vahlkampfia keratitis.
Giemsa stain of corneal scraping shows free-living ameba morphologically consistent with a Vahlkampfia cyst (original magnification ×1000).
Vahlkampfia is a free-living ameba found in water and soil, and it belongs to the same family as Naegleria.3 Two cases of encephalitis presumably due to Vahlkampfia have been reported.2 The first case of Vahlkampfia keratitis was in a 24-year-old contact lens wearer from whom amebas were isolated from the corneal biopsy tissue, contact lens, case, and home water supply.2 He was treated with amphotericin B; the combination ointment of neomycin sulfate, polymyxin B sulfate, and bacitracin zinc, and propamidine. However, eventual penetrating keratoplasty secondary to central corneal scarring was required. In our case, corneal abrasion and self-irrigation with tap water predisposed the patient to such an unusual infection. The Vahlkampfia was finally isolated only after repeated corneal scrapings, emphasizing the difficulty in culturing these organisms. Given the difficulty growing and identifying these amebic organisms, it is impossible to know the prevalence of non-Acanthamoeba amebic keratitis. Special techniques such as the polymerase chain reaction or organism-specific immunohistochemistry may facilitate identifying this kind of unusual amebic keratitis.4 Our patient's rapid response to the standard treatment for Acanthamoeba keratitis indicates that Vahlkampfia is also sensitive to these medications. To the best of our knowledge, this case is the first report in the United States of keratitis due to an ameba other than Acanthamoeba, and the first case not associated with contact lens usage.
Corresponding author: Andrew J. W. Huang, MD, MPH, Bascom Palmer Eye Institute, 900 NW 17th St, Miami, FL 33136 (e-mail address: email@example.com).
Alexandrakis G, Miller D, Huang AJW. Amebic Keratitis Due to Vahlkampfia Infection Following Corneal Trauma. Arch Ophthalmol. 1998;116(7):950–951. doi:
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