Unilateral reactivation of West Nile virus chorioretinitis with occlusive vasculitis
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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.