West Nile encephalitis is a viral encephalopathy caused by the West Nile virus and transmitted primarily by the Culex mosquito. West Nile virus is a part of the Flaviviridae family and is endemic to parts of Africa and Asia.
West Nile encephalitis (WNE) is one of the illnesses caused by West Nile virus (WNV) infection. Most individuals infected with WNV are asymptomatic, some develop West Nile fever, and a small percentage develop neuroinvasive disease. WNV is transmitted to humans mainly via mosquito bites. The incubation period ranges from 2 days to 2 weeks [1]. WNE can present in a number of ways, albeit similar to other types of viral encephalitis. Patients usually have a fever, headache, and altered mental status.
Initial symptoms and signs of illness may include myalgia, arthralgia, or pharyngitis and are often nonspecific. Those at the extremes of age have more pronounced symptoms. Aseptic meningitis may occur simultaneously with encephalitis, resulting in signs of meningism. The severity of illness is proportional to the extent of viral invasion. Changes in the mental status range from acute confusion to coma.
Gastrointestinal upset (nausea and vomiting) is common. Gait instability, coarse tremor, and bulbar palsy have been described [2]. Less frequently reported are seizures and cerebral edema [3]. Parkinsonism, extrapyramidal manifestations, myoclonus, and muscle weakness mimicking lower motor neuron lesions, also form part of the clinical picture [4].
WNE could present with acute flaccid paralysis, which is also directly caused by WNV infection. The presence of muscle weakness distinguishes WNE from other encephalitides. Facial nerve palsies present acutely or over the course of a few weeks [5]. Elderly individuals are at an increased risk [6].
Further presenting features of WNE are ophthalmologic manifestations, lymphadenopathy (especially of the submental nodes), and a maculopapular rash on the trunk [5].
The main diagnostic test for WNV infection is the IgM antibody-capture enzyme-linked immunosorbent assay (MAC-ELISA) [7]. IgM antibodies may be detected in serum, however, when they are present in cerebrospinal fluid (CSF) this indicates central nervous system (CNS) invasion by the virus (as IgM does not cross the blood-brain barrier). Eventually, this confirms the diagnosis of West Nile encephalitis. The majority of patients will test positive at the time of presentation [8]. Moreover, nearly all patients are MAC-ELISA positive after a week of symptomatic illness.
Immunological assays may be supplemented by the use of nucleic acid amplification test (NAAT), thus improving the detection rate to over 90%. One advantage that NAAT has over immunology is that it can detect viral infection even in immunosuppressed patients who may produce a scarce amount of antibodies.
Raised white blood cell count may be a feature of WNE, although it is not always present. Increased leukocytes, either neutrophils or lymphocytes, and elevated protein level are some of the CSF findings [9]. T2-weighted magnetic resonance imaging (MRI) may sometimes reveal brainstem and periventricular lesions [10] [11].