Exudative complications after photodynamic therapy.

Nile virus ranges from 3 to 14 days. Two serosurveys have shown that approximately 1 in 150 infections resulted in meningitis or encephalitis, but most human infections remain subclinical. The reported symptoms and signs associated with West Nile virus infection include fever, malaise, anorexia, nausea, vomiting, headache, myalgia, rash, and lymphadenopathy. The frequencies of various symptoms and signs are poorly defined. Many patients with West Nile virus infection complain of severe muscle weakness. Acute flaccid paralysis similar to that associated with Guillain-Barré and poliomyelitis-like syndromes has been reported. Although our patient had a long history of mitochondrial myopathy, an acute change in muscle pain and fatigue had occurred. This would not be typical for a mitochondrial cytopathy, which is characterized by slowly progressive myogenic weakness. Nash and colleagues described the clinical characteristics of 59 patients hospitalized with West Nile virus infection in the New York City area in 1999. Fourteen percent of patients had symptoms of photophobia, and 3% of patients had conjunctivitis. Marberg et al described 70 patients with West Nile fever. Forty-five percent reported ocular pain, and 60% had conjunctival hyperemia. Neither study commented on visual acuity or ophthalmologic examination findings. Although uveitis may have been the cause of the ocular findings, it was not specifically identified as such. Meningitis alone can cause photophobia and ocular pain. An Israeli patient developed signs and symptoms of meningitis, blurred vision, photophobia, and ocular pain. Ophthalmologic examination revealed visual dysfunction, bilateral optic nerve edema, and hemorrhages, but no uveitis. It is conceivable that the visual field defect in our patient was representative of a subclinical optic neuropathy secondary to the virus infection. We postulate that some of the patients with photophobia, conjunctival hyperemia, and ocular pain may have had uveitis, but they were not examined by an ophthalmologist or with appropriate magnification. The patient described herein had anterior and posterior uveitis. Although acute hyperglycemia may cause uveitis, our patient had normal blood glucose levels throughout the observation period. Theoretically, our patient’s uveitis could have occurred via human T-lymphotropic virus type 1 infection in the setting of Graves disease. This is unlikely to occur at the same time as her acute West Nile virus infection; furthermore, she does not live in an endemic region for human Tlymphotropic virus type 1 or have any risk factors for the infection. Although idiopathic bilateral uveitis can occur, the temporal relationship to the acute West Nile virus infection in our patient suggests a relationship to the viral infection. In addition, some flaviviruses can cause uveitis. Advanced age is the most significant risk factor for the development of severe neurologic disease, long-term morbidity, and death associated with these viruses. Diabetes mellitus is also associated with death in this infectious setting. A similar finding was noted during the 1996 Romanian outbreak of West Nile encephalitis. Our patient’s medical conditions, including the presence of diabetes mellitus, may have predisposed the development of symptomatic West Nile virus infection, including uveitis. Based on a MEDLINE search, we believe this represents the first report of uveitis associated with confirmed West Nile virus infection. Patients with a confirmed infection and ocular symptoms may warrant an ophthalmologic opinion. Patients with uveitis in endemic areas and with systemic symptoms may deserve West Nile virus testing.