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West Nile virus has been described in Africa, Europe, the Middle East, west and central Asia, Oceania, and has emerged in recent years in temperate regions of Europe and North America.1 West Nile virus was first isolated from a febrile adult woman in the West Nile District of Uganda in 1937 and became recognised as a cause of severe human meningoencephalitis in elderly patients during an outbreak in Israel in 1957.2 In 1999, the plight of city birds and a collection of human encephalitis cases in New York heralded the arrival of West Nile virus on this side of the Atlantic. From 1999 through 2001, there were 149 cases of human West Nile virus infection in the United States, including 18 deaths, but in 2002 alone more than 3500 cases and 200 deaths were reported.3 In 2003, over 9000 cases were reported with more than 300 cases of neuroinvasive disease.3
The Centers for Disease Control notes that neuroinvasive disease includes those cases resulting in meningitis, encephalitis, or meningoencephalitis.3 Cases with ocular involvement should probably be included in this category as well. As our clinical experience in such cases evolves so does our understanding of the ophthalmic manifestations of the disease. Here, we present a case of ocular involvement with West Nile virus, highlighting the typical ocular findings.
An 80 year old man convalescing in a nursing home from neurological complications of recently acquired West Nile virus meningoencephalitis presented with bilateral visual loss of unspecified duration. The patient had been hospitalised 4 months previously for serologically confirmed West Nile virus encephalitis. His infectious course was complicated by residual right sided paresis, dysarthria, and generalised mental status changes with dementia. Over the following months as he regained his mental faculties he complained to family members of decreased vision and central scotomas, worse in his left eye than right. His best corrected visual acuity at this time was 20/40 in the right eye and 20/60 in the left eye. The patient’s ophthalmic and medical histories were otherwise non-contributory. Biomicroscopic examination revealed normal anterior segments without inflammation and moderate nuclear sclerotic and cortical changes involving both crystalline lenses. Funduscopic examination revealed mild vitreous debris with moderately large areas of retinal pigment epithelial and choroidal atrophy in the posterior segment (fig 1A and B, right and left eyes, respectively) in addition to partially atrophic and pigmented chorioretinal foci throughout the retinal periphery (fig 2A and B, right and left eyes, respectively).
Over the next 3 months the patient developed problems with his activities of daily living at night and glare with lighting. Subsequent examination revealed progression of the lenticular changes and the patient was referred for cataract extraction. He returned 3 months later after uneventfully cataract surgery. He was not on any medications at this time. Best corrected visual acuity measured 20/30 in the right eye and 20/40 in the left eye. Normal anterior segments without inflammation and well placed posterior chamber intraocular lenses were noted. The vitreous debris persisted and his funduscopic examination was without change bilaterally. Examination 6 months later and approximately 16 months after initial West Nile virus infection demonstrated stable ophthalmic findings and visual acuity.
Although ocular symptoms associated with West Nile virus were first reported in 1956 ocular findings in West Nile virus infection were first described in the medical literature soon after the West Nile virus epidemic in North America in 2002.4–8 Initial reports described analogous clinical findings consisting of mild anterior segment inflammation, vitritis, and discrete nummular outer retinal/choroidal lesions which were often linear in distribution and varied in appearance from “creamy whitish-yellow” to atrophic with various degrees of pigmentation.5–7,9 Mild retinal haemorrhage was also occasionally present. Fluorescein angiography revealed these “target” lesions to be hypofluorescent centrally and hyperfluorescent peripherally. Leakage from the optic nerve is sometimes present as optic neuritis and papilloedema may be associated with contiguous central nervous system involvement.8,9,10 Later reports confirmed these findings and suggested that active lesions associated with vitritis may appear “creamy” in nature eventually progressing to foci of well circumscribed chorioretinal atrophy as the disease becomes inactive and subsequently becoming more prominent with time.9,10 Occlusive vasculitis without chorioretinal findings has also been noted in an isolated case.11
Various ocular inflammatory and infectious processes such as toxoplasmosis and juvenile rheumatoid arthritis have been associated with periods of recurrence and exacerbation after intraocular surgery.12 This highlights an important issue with regard to West Nile virus infection as the risk for neuroinvasive disease is higher for people 50 years of age and older, many of whom are currently or soon will be candidates for cataract extraction. Our patient did well with routine postoperative care and surveillance after uncomplicated cataract extraction in an eye previously affected by West Nile virus chorioretinitis. The eye remained quiescent without evidence of uveitis or reactivation of previously affected fundus lesions. Although surveillance would be recommended for these patients, our findings suggest that chorioretinitis associated with West Nile virus appears to be an acute self limited process without residual sequelae after subsequent intraocular surgery.
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