Original ArticleSevere Reactive Ischemic Posterior Segment Inflammation in Acanthamoeba Keratitis: A New Potentially Blinding Syndrome
Section snippets
Patients and Methods
A retrospective record review was conducted for patients with the diagnosis of Acanthamoeba keratitis between January 1, 1995, and December 1, 2005, at the University of Texas Southwestern Medical Center at Dallas. Inclusion criteria included a diagnosis of Acanthamoeba keratitis confirmed by either corneal culture and biopsy or in vivo tandem-scanning confocal microscopy and enucleation of the involved eye. Five of 118 eyes met both criteria. The study was performed with institutional review
Patient 1
A 68-year-old woman had a 5-month history of pain and redness in the left eye. She had been treated for iritis and presumptive Herpes simplex keratitis before presentation. Her medical history was positive for type 2 diabetes mellitus. Her best-corrected visual acuity was 20/25 in the right eye and counting fingers at 2 inches in the left eye. A slit-lamp examination showed a large central corneal ulcer in the left eye with a ring infiltrate and marked corneal edema with Descemet’s folds (Fig 1
Discussion
Involvement of the posterior ocular structures in amebic infections was reported first in 1975 in a previously healthy 7-year-old boy with uveitis before keratitis.17 The patient experienced fatal meningoencephalitis. Histopathologic examination showed Acanthamoeba trophozoites in the ciliary body and chronic perivascular inflammation of the retina and optic disc edema. The infective organism was identified as A. polyphagia. Heffler et al18 subsequently reported a case of Acanthamoeba
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Cited by (40)
Advances in the management of Acanthamoeba keratitis: A review of the literature and synthesized algorithmic approach: Advances in the Management of Acanthamoeba
2022, Ocular SurfaceCitation Excerpt :Extra-corneal disease may accompany AK and manifestations include Acanthamoeba sclerokeratitis (ASK) [67,68], Acanthamoeba endophthalmitis [69,70], severe ischemic posterior segment inflammation [71], and adnexal disease (dacryoadenitis and extraocular muscle inflammation) [72]. Severe reactive inflammation secondary to adjacent extensive corneal disease (i.e. ring infiltrate in advanced stromal keratitis) is thought to be the predominant mechanism for ASK and severe posterior segment inflammation [67,71]. However, Acanthamoebal scleral invasion has also been demonstrated [69].
The biology of Acanthamoeba keratitis
2021, Experimental Eye ResearchIn vitro effects of environmental isolates of Acanthamoeba T4 and T5 over human erythrocytes and platelets
2020, Experimental ParasitologyAcanthamoeba keratitis – Clinical signs, differential diagnosis and treatment
2019, Journal of Current OphthalmologyCitation Excerpt :In about 23% of the cases,2,31,44–46 a mixed infection with virus, bacteria, or fungi is present. Clinical signs of acanthamoeba keratitis are the following44–55 (Table 2): Chameleon-like epithelial changes ("dirty epithelium", pseudodendritiformic epitheliopathy, epithelial microerosions, and microcysts) (Fig. 1A)
Acanthamoeba sclerokeratitis: Epidemiology, clinical features, and treatment outcomes
2014, OphthalmologyCitation Excerpt :All the patients included in our series were immunocompetent at the time of the onset of scleritis. In our opinion, the scleral inflammation in immunocompetent patients with ASK is usually an inflammatory process in which Acanthamoeba-driven antigen mimicry or a T-cell-mediated vasculitic response (similar to that observed in the ischemic posterior inflammation reported by Awwad et al13) could be the underlying cause of scleral inflammation. However, in light of the few reported cases of scleral invasion and because of the potential for the active Acanthamoeba trophozoite to spread into the sclera as a result of the introduction of immunosuppressive therapy, we used prophylaxis with oral itraconazole or voriconazole in recently treated cases and recommend this for all cases.28–31
Manuscript no. 2006-167.
Supported in part by the National Eye Institute, Bethesda, Maryland (grant nos.: EY10738 [HDC], EY016664); Pearle Vision Foundation, Dallas, Texas; and an unrestricted grant from Research to Prevent Blindness, Inc., New York, New York.