Systemic and Ophthalmic Manifestations of West Nile Virus Infection

Yos Priestley; Marcia Thiel; Steven B. Koevary


Expert Rev Ophthalmol. 2008;3(3):279-292. 

In This Article

Long-term Effects of Systemic & Ophthalmic Disease

One of the most common symptoms reported by patients with WNF and neuroinvasive disease is extreme fatigue; others, as mentioned previously, include weakness, muscle pain, headache, memory problems, excessive sleepiness and problems concentrating.[79,80,81,82] Patients recovering from WNM often suffer from many of these same symptoms. WNE is associated with the highest mortality and morbidity rates compared with other forms of the infection, with death due to disease occurring up to 1 year following diagnosis.[47,82] Some of the most common longer-lasting symptoms of WNE include persistent tremors, bradykinesia, parkinsonism and ataxia. Many patients require months of intensive care and ventilator support, and rehabilitation may include intense physical, occupational and speech therapy. The initial severity of WNE does not necessarily predict neurological outcome; even patients who suffer severe encephalopathy and neurological symptoms may experience full recovery. In general, functional recovery following WNV tends to be more complete in younger patients.[47,82]

Although rare, WNP is associated with the highest mortality and morbidity among all WNV-infected individuals. Patients who were successfully extubated following WNP may still experience dyspnea and require supplemental oxygen for many years. Muscle strength usually returns after 6-8 months and may continue to improve over time; the level of improvement following physical and occupational therapy has been variable. Patients recovering from neuroinvasive disease may continue to show motor impairment and compromised dexterity over time.[82] Finally, depression has also been a reported outcome in approximately a third of patients with WNV.[83]

Ophthalmic manifestations associated with WNV have only relatively recently been recognized, making the long-term prognosis in these patients difficult to predict. Most patients presenting with chorioretinitis show improvement over time, with visual acuity returning to baseline after a few months. An interesting case was reported of late-onset choroidal neovascularization (CNV) following a history of WNV chorioretinitis[84] in a man of 81 years of age with a history of diabetes, nonproliferative retinopathy, hyperstension, coronary artery disease and pseudophaki who was diagnosed with serologically confirmed WNV encephalitis. The patient developed bilateral mild vitritis and chorioretinal lesions characteristic of WNV. Within 4-5 months, the patient's vision returned to baseline and chorioretinal scars developed. After 5 years, the patient presented with reduced vision to hand motion in his left eye at 60.96 cm. Fundoscopic examination revealed the presence of a 2 disk-diameter area of subretinal fluid centered on the fovea OS with a subretinal hemorrhage surrounding it. FA and ICG (Figure 4), as well as OCT all confirmed the diagnosis of CNV. The patient was treated with 1.25 mg of the anti-VEGF compound bevacizumab intravitreally in his left eye. After 4 weeks, the patient's intraretinal fluid resorbed but his visual acuity failed to improve. To date, there have been only two other reported cases of CNV to our knowledge,[12,29] both of whom had a history of diabetes and presented with chorioretinitis. Presentation with CNV seems to occur between 6 months and 5 years following the development of WNV chorioretinitis.[84] In light of this, CNV should be considered as a possible late manifestation of WNV chorioretinitis, especially in patients with diabetes.

Figure 4.

Late onset choroidal neovascularization in a patient with prior confirmed West Nile virus infection. (A) Red-free photograph of left fundus. (B) Early- and (C) late-phase fluorescence angiography shows late leakage perifoveally with hypofluorescence corresponding to hemorrhage, and late hyperfluorescence of the West Nile virus chorioretinal scars. (D) Late phase indocyanine green angiography showing foveal hyperfluorescence, and hypofluorescence of the West Nile virus chorioretinal scars. Reproduced with permission from.[84]


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