Host cornea stained with Gomori methenamine silver, demonstrating numerous Acanthamoeba cysts (original magnification ×400).
Slitlamp photograph of the patient's left eye, revealing a clear corneal graft with a hypopyon.
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Davis MJ, Packo KH, Epstein RJ, Grostern RJ, Cohen JA. Acanthamoeba Endophthalmitis Following Penetrating Keratoplasty for Acanthamoeba Keratitis. Arch Ophthalmol. 2010;128(4):505–506. doi:10.1001/archophthalmol.2010.33
We report a case of culture-positive Acanthamoeba endophthalmitis in a patient with a history of Acanthamoeba keratitis. To our knowledge, there is only 1 previous report1 in the English literature.
A 61-year-old female soft contact lens wearer had a 10-day history of progressively worsening pain, redness, and blurred vision in the left eye. Her visual acuity was 20/20 OD and 20/40 OS. She was initially diagnosed with possible herpes simplex keratitis. Over the next 2 months, she was treated with topical trifluridine, prednisolone acetate, and oral famciclovir. Her symptoms continued to worsen, and her visual acuity decreased to counting fingers.
Two months later, she was seen at our center. She had significant pain and her visual acuity was hand motions. Examination revealed multiple epithelial defects and diffuse anterior keratitis with a ring infiltrate. Confocal microscopy revealed probable Acanthamoeba cysts. Corneal scrapings were performed for culture. Treatment with trifluridine, prednisolone, and famciclovir was discontinued, and treatment with propamidine isethionate, polyhexymethylene biguanide, chlorhexidine gluconate, neomycin sulfate, and atropine sulfate eyedrops was started.
Over the next 4 months, there was fluctuation of the keratitis and anterior chamber inflammation, with a persistent epithelial defect. Treatment was continued with various anti-Acanthamoeba agents without resolution. Because of a concern for impending perforation, a therapeutic penetrating keratoplasty was performed. Histological analysis of the corneal button demonstrated widespread Acanthamoeba cysts, including at the margin of resection (Figure 1).
Fifteen days later, the patient reported seeing a “white dot in her cornea.” Visual acuity was 20/400. The corneal graft was clear but the anterior chamber had 4+ cells with a hypopyon (Figure 2). She was seen in consultation by a retina specialist and began treatment with oral prednisone for presumed sterile inflammation. The inflammation initially improved and the prednisone dosage was decreased. However, 2 days later, the hypopyon increased in size and a vitreous tap with injection of antibiotics was performed. The oral prednisone dosage was increased as well. The inflammation initially improved, but it worsened a few days later. The patient underwent a vitrectomy, lensectomy, and anterior chamber washout. Aqueous and vitreous cultures were performed.
Postoperatively, the corneal graft remained clear; however, the intraocular inflammation increased and vitreous cultures were positive for Acanthamoeba. Subsequently, the eye was enucleated. Pathological analysis revealed Acanthamoeba in the cornea, extending into the anterior sclera but not within the posterior segment. All other cultures were negative. The patient has done well since the enucleation, with no further sequelae.
Acanthamoebae are ubiquitous protozoans found in various aquatic habitats. They are known to cause keratitis in contact lens wearers.2 They have rarely been reported to cause intraocular infection. There is 1 pathologically confirmed case of chorioretinitis associated with Acanthamoeba keratitis.1 The patient underwent 4 penetrating keratoplasties, followed by enucleation. Analysis of the pathological specimen revealed cysts consistent with Acanthamoeba throughout the globe. It was concluded that the spread of Acanthamoeba was via direct extension through the interior of the eye. Additionally, there are 2 cases of systemic Acanthamoeba infection with secondary ocular involvement.3,4 A case of sterile panophthalmitis from Acanthamoeba keratitis without pathological or culture evidence has also been described.5
A study to determine why Acanthamoeba keratitis does not spread intraocularly was published.6 It was found that the trophozoites could progress beyond the Descemet membrane and endothelium, but in the anterior chamber a neutrophilic response rapidly cleared the organisms.
Our patient had intraocular inflammation with a hypopyon. Acanthamoeba was isolated from the vitreous culture with no other organisms isolated. Intraocular spread was likely due to direct extension from the cornea. As our patient developed endophthalmitis secondary to Acanthamoeba keratitis, this should be considered in patients with intraocular inflammation associated with Acanthamoeba keratitis.
Correspondence: Dr Epstein, Chicago Cornea Consultants, Ltd, 806 Central Ave, Ste 300, Highland Park, IL 60035 (firstname.lastname@example.org).
Previous Presentation: This paper was presented at the 43rd Annual Meeting of the Ocular Microbiology and Immunology Group; October 23, 2009; San Francisco, California.
Financial Disclosure: None reported.
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