West Nile virus
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West Nile virus (WNV) is an arbovirus and one of the Flavivirus genus known to cause neuroinvasive disease, including Flavivirus encephalitis. According to the CDC, the majority of mosquito-borne disease in the continental United States is attributed to West Nile virus infection 1.
Epidemics have occurred along the migratory routes of birds in the US, Europe, Africa, the Middle East and West Asia 2. In recent history, frequency and severity of West Nile virus outbreaks are increasing 3. Of note, West Nile virus is implicated in the majority of viral encephalitis cases in the US 5.
Presentation varies with the severity of response to West Nile virus infection. The majority will remain asymptomatic. Approximately 20% will develop classical symptoms of a viral fever - or West Nile fever in this case - including fever, malaise, fatigue, myalgia, arthralgia, retro-orbital pain, maculopapular rash and lymphadenopathy 3,4.
Less than 1% of those infected will present with neuroinvasive disease, often in the context of advanced age or immunodeficiency 4:
- neuromuscular involvement
- most commonly a poliomyelitis-like syndrome, with acute onset, asymmetric flaccid paralysis of one or more limbs
- encephalitis, bowel and bladder dysfunction often occur in conjunction
- myalgia and somatosensory disturbance are less common
- may be mistaken for Guillain-Barré syndrome
- encephalitis, meningitis or encephalomeningitis
- presenting symptoms including headache, neck stiffness, somnolence, coma, movement disorder, confusion and seizures 3,4
CSF sampling typically demonstrates an abnormally high lymphocyte count, or pleocytosis, with high total protein and WNV-specific IgM antibodies 4.
West Nile virus is a single-stranded RNA of the genus Flavirirus and family Flaviviridae. Birds are the host organism and mosquitos, via their salivary glands, the vector of disease transmission.
- hyperintensity within deep brain structures, including the thalami, basal ganglia and midbrain structures 5; the latter includes the red nucleus, cerebral peduncle and substantia nigra
- increased signal intensity in the mesial temporal structures has been described in a number of cases 5
- high diffusion signal has been reported within the basal ganglia and disseminated throughout the white matter 5
- interestingly, DWI may detect inflammation prior to signal intensity changes detected using T2/FLAIR 5
History and etymology
The first isolation of West Nile virus dates to 1937, from the West Nile district of Northern Uganda 3.
Infection by one of the pathogenic members of the Flavivirus genus may present similarly, including:
- Japanese encephalitis virus (Asia)
- tick-borne encephalitis virus
- Murray Valley encephalitis (Australia, New Zealand, Papua New Guinea)
- St Louis encephalitis virus (United States of America)
- Rocio virus (Brazil)
- Powassan virus (United States of America)
- of note, the Kunjin virus would be on this list but it was reclassified as a subtype of West Nile virus in 1999
In addition, basal ganglia T2 hyperintensity has numerous differential diagnoses, notably including:
- autoimmune encephalitis
- Creutzfeldt-Jakob disease
- neurotoxicity secondary to organophosphate poisoning
- anoxic-ischemic encephalopathy
- toxic leukoencephalopathy
- hypoglycemic encephalopathy
- herpes-simplex encephalitis (note the increased signal intensity of mesial temporal structures in both herpes simplex virus and West Nile virus encephalitis)