Table 1. Epidemiology, Clinical Features, Pathophisiology, MRI findings, and Diagnosis of West Nile Encephalitis .

CSF: Cerebrospinal fluid, US: United States, IgM: Immunoglobulin M, WNV: West Nile virus

Epidemiology, Clinical Features, Pathophisiology, MRI findings, and Diagnosis of West Nile Encephalitis
Epidemiology [1]	Endemic in the US. Only 20% of patients develop West Nile Fever. Neuroinvasive disease is seen in less <1%, with a mortality rate of 10%. Old age increases the risk of developing WNV encephalitis
Clinical Features [7]	West Nile Fever: headache, fever, myalgia, generalized weakness, skin rash, lymphadenopathy, vomiting, and diarrhea. WNV encephalitis: West Nile meningitis and encephalitis: fever, signs of meningeal irritation like headache, nuchal rigidity, Kernig’s and Brudzinski’s signs on physical exam, altered level of consciousness, disorientation, and focal neurological signs and symptoms (eg, dysarthria, seizures, tremor) Acute flaccid paralysis: mild flu-like symptoms including headache, fever, malaise, gastrointestinal symptoms precede the onset of paralysis in which the most prominent feature is the limb weakness. Sensory examination and deep tendon reflexes are usually preserved.
Pathophisiology [7]	WNV is transmitted through infected mosquito bites. In the skin, WNV replicates in the dendritic cells. The cells then spread the infection to the regional lymph nodes and from there into the bloodstream. The mechanism of neural transmission is still unclear. However, theories propose a retrograde axonal transport of WNV in the peripheral nervous system. CNS expression of CCR5 and its ligand CCL5 is upregulated by WNV. The secretion of chemokine CXCL10 stimulates the influx of immune cells that express CCR5, mostly CD4+, CD8+, and macrophages, into the CNS by WNV infected neurons. The infiltration of lymphocytes in the CNS is the leading cause of neurological damage, which results in the clinical manifestation of WNV encephalitis.
MRI Findings [7]	Normal in most patients. Lesions were noticed on T2-weighted images in the basal ganglia (substantia nigra) pons, and thalamus. In the spinal cord, lesions consistent with anterior horn damage were also reported in patients who developed paralysis.
Diagnosis [5]	Clinical Criteria: Having the classical clinical features of encephalitis, acute flaccid paralysis, meningitis, or other central or peripheral nervous signs. These clinical signs need to be present in the absence of a better explanation. Having the following related symptoms help yield the diagnosis: myalgia, vomiting, paresis, arthralgia and or nuchal rigidity. Laboratory criteria: Isolation of the virus in the blood, CSF, or other body fluid. In the serum the IgM is detected while in the CSF is addition to the IgM, pleocytosis and negative results for arbovirus.