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Unilateral reactivation of West Nile virus chorioretinitis with occlusive vasculitis

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Quoi:
Paper Presentation | Présentation d'article
Quand:
2:27 PM, Vendredi 14 Juin 2019 (8 minutes)
Thème:
Uvéite

Author Block: Maryam I. T. Al-Najjar, Marie Josee Aubin, Cristina Bostan
Author Disclosure Block: M.I.T. Al-Najjar: None. M. Aubin: Any direct financial payments including receipt of honoraria; Name of for-profit or not-for-profit organization(s); Honoraria: University of Ottawa Eye Institute, Gilead. Membership on advisory boards or speakers’ bureaus; Name of for-profit or not-for-profit organization(s); PeriPharm; Gilead. C. Bostan: None.

Abstract Body:

Purpose: To report a case of unilateral reactivation with occlusive vasculitis after West Nile virus (WNV) meningoencephalitis and bilateral chorioretinitis resolution.
Study Design: Case report.
Methods: Retrospective medical chart review. Ophthalmologic examination included Snellen visual acuity (VA), complete ocular examination, macular optical coherence tomography (OCT), fundus fluorescence angiography (FFA), and Humphrey standard 24-2 visual fields.
Results: A 63-year-old immunocompetent diabetic Caucasian male was seen in the Ophthalmology Department three weeks after hospital admission for fever and lethargy. A diagnosis of meningo-encephalitis secondary to WNV had been retained following serologic confirmation of infection. The patient’s neurological status had been improving with supportive therapy. A consultation in ophthalmology was requested for new onset of decreased vision. The initial evaluation revealed pinhole VA 20/30 in the right eye (OD) and 20/50 in the left eye (OS), bilateral punched-out inactive chorioretinal lesions distributed in a linear pattern in the posterior pole and mid-periphery, and macular edema OS, but no signs of vasculitis in either eye. Topical prednisolone acetate 1% and nepafenac 0.1% were started OS. At follow-up two weeks later, there was further reduction in VA OS to 20/70. Examination revealed mild posterior vitritis, diffuse retinal arterioral attenuation and sheathing, scattered cotton-wool spots and intra-retinal hemorrhages OS. Vascular leakage and areas of capillary non-perfusion, but no macular ischemia, were evident on FFA. A tapering regimen of oral prednisone was started. Two months later, the occlusive vasculitis had resolved, the VA had recovered to baseline levels, but scotomas corresponding to involved retinal areas persisted on the patient’s visual field OS, while his visual field OD showed no deficits.
Conclusions: WNV infection is associated with ocular manifestations, of which chorioretinitis is the most common, occurring in up to 80% of patients with neuroinvasive disease. Reactivation of WNV-associated ocular involvement after resolution of the systemic disease has only been reported in one case. Although rare, occlusive vasculitis can be a late-onset feature of WNV infection and may be more common in diabetics. Continued follow-up after resolution of the systemic disease is important, as early detection and treatment of ocular recurrences may reduce irreversible vision loss.

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