Visual Loss with West Nile Virus Infection: A Wider Spectrum of a “New” Disease
- William Havener Eye Center, Department of Ophthalmology, Ohio State University Medical Center, Columbus, Ohio
- Reprints or correspondence: Dr. William Anninger, William Havener Eye Center, Dept. of Ophthalmology, Ohio State University Medical Center, Columbus, OH 43210 (wva.dms01{at}alum.Dartmouth.org).
Abstract
We describe a case of severe visual loss as a result of West Nile virus (WNV) infection. Associated headache and fever led to the proper diagnosis and management, but the findings of optic neuritis, retinitis, and uveitis were a surprising and prominent component of the patient's meningitis syndrome. Physicians diagnosing and treating patients with WNV infection should be alerted to the possibility of ocular and optic nerve involvement, which may leave permanent neuropathic residua.
West Nile virus (WNV) has spread quickly throughout the United States since its arrival in New York City in 1999. [1, 2] The virus, which is maintained in an enzootic cycle of mosquitoes and birds, has now affected humans in 42 states [3]. Recent reports suggest that the syndrome can include permanent visual loss and eye pain from retinitis, optic neuritis, and uveitis [4–10]. This report concerns a patient who presented with visual clouding and ocular pain early in the course of WNV meningoencephalitis.
Ten days after a weekend of camping in central Ohio, a 55-year-old woman with a history of insulin-dependent diabetes mellitus presented to her doctor with a fever (temperature, 39.4°C). She complained of severe headache, right eye pain and visual field loss, nausea, chills, night sweats, and intermittent poor balance. She was referred to the emergency department. A head CT was performed, the findings of which were unremarkable, and evaluation of a CSF specimen revealed a WBC count of 265 cells/µL (57% segmented neutrophils, 34% lymphocytes, and 9% unspecified), a glucose level of 106 mg/dL (normal range, 45–80 mg/dL), and a protein level of 119 mg/dL (normal range, 15–45 mg/dL). She was given a dose of ceftriaxone in the emergency department and was admitted to the hospital with suspected meningitis. Evaluation of a serum sample showed a WNV IgM titer of 3.88 (normal, <2.00), and “probable WNV encephalitis” was diagnosed [11]. On the second day of hospitalization, the patient developed “clouding of vision” in both eyes, which was greater in the right eye than in the left eye. During her hospital stay, she received supportive care. Her 1-week hospital stay was remarkable for transient ataxia and mild confusion, both of which had resolved by the time of discharge.
One week after hospital discharge, the patient presented to her ophthalmologist complaining of a “black fog” in both eyes dating from the first days of her hospital stay. Her visual acuity was 20/80 in the right eye and 20/40 in the left eye, down from 20/25 in each eye several months earlier. A dilated fundus examination revealed pale optic nerves, vitreous cavity cells, and creamy yellow-colored lesions averaging 500 µm in diameter diffuse through the retina and choroid of both eyes. Visual field evaluation was remarkable for prominent loss of peripheral vision in both eyes (greater in the right than the left eye). The patient was not given any medical treatment. Her clinical course has been consistent with a resolving multifocal choroiditis and optic neuritis. A year after the original infection, the patient recovered her central visual acuity in the left eye, but visual acuity is still 20/60 in the right eye. The visual fields have shown mild improvement since the acute illness, but the patient continues to have significant visual field loss, with optic atrophy, which is worse in the right eye (figure 1).
Figure 1
Visual fields (i.e., what the patient sees) in a 55-year-old woman 1 year after having West Nile virus meningoencephalitis. The small cross represents central target fixation.
The recent rapid spread of WNV infection throughout the United States has made it an important addition to the differential diagnosis of a summertime febrile illness. Approximately 20% of infected humans experience symptoms after a 2–14-day incubation period. Uncomplicated WNV fever is characterized by fever, headache, myalgia, and nausea that resolve in 1 week. The infection can progress to meningoencephalitis, with the additional findings of stiff neck, weakness, and confusion. The rare fatalities are attributed to progressive meningoencephalitis in very old or very young persons [11, 12].
The clinical spectrum of illness due to WNV infection continues to evolve. Up until the mid-1950s, it was believed that the WNV had very low affinity for the CNS and that it classically caused fever, headache, lymphadenopathy, and skin rash [10]. In more recent epidemics, rash and lymphadenopathy have become less common, and the prevalence of meningoencephalitis cases has increased [10, 12]. The reason for this change is unknown; it may be in part due to evolution of the virus or the naive immunity characteristics of the host population.
The patient we describe had, in addition to headache and fever, the unexpected signs and symptoms of optic neuritis, uveitis, and chorioretinitis. In addition, she has neuropathic residua of her WNV infection, with visual acuity loss, visual field loss, and optic atrophy. These changes are compatible with the neuropathologic patterns reported in autopsies of WNV-infected patients, which reveal leptomeningeal perivascular infiltration, as well as axonal loss [13]. This case helps us recognize a broader spectrum of WNV disease and demonstrates persistent neuroocular residua in a “recovered” patient.
- Received September 20, 2003.
- Revision received October 7, 2003.
- Accepted March 16, 2004.
- © by the 2004 Infectious Diseases Society of America
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