Vitritis and Chorioretinitis in a Patient With West Nile Virus Infection FREE

ALTHOUGH INFECTION with the West Nile virus has been endemic to areas of Africa, Asia, and Europe, it was first documented in the United States in 1999 with its appearance in New York, NY.^{1 - 3} This single-stranded RNA flavivirus belongs to the Japanese encephalitis virus serocomplex, which contains both the Japanese and St Louis encephalitis viruses as well as others that cause encephalitis in humans.⁴ West Nile virus is spread via an enzootic cycle involving mosquitoes and birds that often crosses over to humans and other animals.^{3 ,5} Although the incubation period of the virus is not precisely known, it is thought to range from 3 days to 2 weeks. Only an estimated 20% of infected persons become symptomatic with fever, and typically only half of them are ill enough to seek medical attention.⁶ More severe symptoms include fever, malaise, anorexia, nausea, vomiting, eye pain, headache, myalgia, arthralgia, rash, and lymphadenopathy. Age older than 50 years is a significant risk factor for more severe neurologic disease such as encephalitis or meningitis.^{6 - 8}

The West Nile virus has been isolated and identified since 1937 and is endemic in various parts of the world; however, a search of the MEDLINE literature failed to yield any reports of intraocular findings associated with West Nile virus infection. We report a case of West Nile virus infection in which the patient developed ocular symptoms early in the course of the disease and was found to have bilateral vitritis and chorioretinitis before the serologic diagnosis of West Nile virus infection was made.

The patient was a 62-year-old woman residing in a suburb of Chicago, Ill, who had a 2-week history of floaters in her left eye along with symptoms of fatigue, a left-sided frontal headache, and a low-grade fever for 1 week. On examination, she had a temperature of 38.6°C. Her vision was 20/25 OD and 20/40 OS. A slitlamp examination was notable for rare anterior chamber cells in the left eye along with a few keratic precipitates. There were a few anterior vitreous cells in the right eye and 2+ anterior vitreous cells in the left eye. An ophthalmoscopic examination revealed deep, flat, creamy whitish-yellow outer chorioretinal lesions measuring 500 to 750 µm and extending superiorly in a linear radial pattern from the optic nerve head of the left eye (Figure 1A), with less extensive, faint but similar lesions in the right eye. The lesions were actively inflammatory, and there was moderate vitritis overlying the optic disc and superior retina of the left eye. There were several small, 200-µm superior intraretinal hemorrhages in the right eye and similar small, faint hemorrhages associated with some of the lesions in the left eye. No vascular sheathing, cystoid macular edema, microangiopathy, disc edema, perifoveal changes, or subretinal fluid were present. Fluorescein angiography was notable for blocked fluorescence by the small intraretinal hemorrhages as well as late leakage of the lesions (Figure 1B). The view of the left optic nerve was partially obscured by the overlying vitritis. Minimal staining of both optic nerves was seen, with no significant leakage.

The patient was given 1% prednisolone acetate 4 times a day in both eyes. The following day, the left keratic precipitates had resolved but the vision had worsened to 20/60 OS, and the patient's temperature was 39.2°C. The systemic workup, including serologic testing for syphilis, antinuclear antibody, and Bartonella henselae, was normal with the exception of 10 to 25 white blood cells present per high-power field on urinalysis. Bacterial blood cultures showed no growth. Although the patient was treated with an oral course of levofloxacin, the fever and symptoms of fatigue persisted. Clinical suspicion led to serologic testing for the West Nile virus immunoglobulin M (Ig M); the results were found to be positive for this disease.

Two weeks after the patient's initial symptoms, the vision had improved to 20/30 OS, the floaters had diminished, the chorioretinal lesions were pigmented, and the vitritis was improved (Figure 2).Fluorescein angiography demonstrated a marked decrease in late-phase leakage of lesions, with staining of most chorioretinal lesions. The chorioretinitis healed and the patient recovered.

West Nile virus infection is a relative newcomer to the United States. Physicians are still learning to include West Nile virus in the differential diagnosis of suspicious febrile illnesses and obtain appropriate serologic tests. In our case, the West Nile Ig M serologic test was performed as part of an arbovirus panel that also included Ig M tests for St Louis encephalitis, eastern equine encephalomyelitis, and California encephalitis. The test results are reported as positive, negative, or equivocal. In this case, in addition to the positive findings of the serologic test for West Nile virus Ig M, there was an equivocal positive result for St Louis equine virus Ig M, a cross-reactive pattern sometimes noted by local infectious disease specialists. Detection of Ig M in the cerebrospinal fluid is diagnostic for central nervous system West Nile virus infection. Positive serum Ig M test results are strongly suggestive of acute West Nile virus infection and can be followed by confirmatory tests that are performed at the Centers for Disease Control (Atlanta, Ga). These results typically are not available for several months.

There is very limited information on appropriate treatment of identified cases; generally, only supportive care is used. Despite encouraging results in vitro, attempts to treat patients in uncontrolled trials with agents such as ribavirin and interferon alfa-2b have demonstrated no efficacy.^{9 - 10}

We believe that this case provides the first documentation of ocular involvement by West Nile virus. Although presumptive, the diagnosis was based on the close temporal relationship between active ocular inflammation and the systemic manifestations and serologic diagnosis of West Nile virus. Illinois is presently experiencing the largest number of cases of West Nile virus in the country. The patient specifically recalled being awakened at night by numerous mosquito bites approximately 7 to 10 days prior to the onset of symptoms. The findings presented in this article may lay the foundation for a more systematic ocular evaluation of patients with West Nile virus infections. As this case illustrates, the eye findings along with associated systemic signs and symptoms potentially provide a tool for the diagnosis of infection with West Nile virus.

Corresponding author and reprints: Jeffrey R. Parnell, MD, Retina Services Ltd, 7447 W Talcott Ave, Suite 461, Chicago, IL 60631 (e-mail: j.parnell@attbi.com).

Submitted for publication September 24, 2002; final revision received November 7, 2002; accepted November 12, 2002.

This study was supported in part by an unrestricted grant (Northwestern University, Chicago, Ill) from Research to Prevent Blindness, Inc, New York, NY.

We thank Jonathan Shankle and John Gerty for their fundus photography and preparation of prints.