West Nile virus

Background

Virolgy

  • RNA virus
  • Virus family associated with St Louise encephalitis, Japanese encephalitis, Murray Vallen enceph, and Kunjin enceph
  • 2 lineage of WNV - only lineage 1 associated with human disease originating in Middle East/Israel

Ecology

  • Bird- mosquito- bird cycle
  • Passerine birds are amplification host
  • Starts in spring, ends in fall when mosquitos dormant
  • Culex mosquitos
  • Unclear if human infection from culex bite or other bridge vector mosquito species
  • House sparrows have high level of viremia and are amplifiers
  • Humans and horses also but viremia is low so are not important amplifiers
  • WNV in birds feces and oral secretions
  • Bird to bird transmission possible in lab
  • Birds can be infected by eating infected mosquitoes, birds or odents but importance of oral spread in nature unclear

Epidemiology

  • Found in Africa, Middle East, Russia, Australia
  • First appeared in eastern US in 1999 but now found nationwide[1]
  • Most human infections occur in August and Sept but can happen from May to Dec
  • Human Transmission
    • Most from mosquito bites
    • Maternal fetal
    • Breast milk
    • Blood transfusion
    • Percutaneous lab infection

Clinical Features

  • Most people asymptomatic
  • Severity increases with age
  • 2-14 day incubation
  • Illness for 3-6 days
  • Malaise, anorexia, nausea/vomiting, eye pain, headache, myalgia, rash
  • 20% of infected patients get West Nile fever
  • <1% get severe neuro problem- encephalitis, meningitis, acute flaccid paralysis
  • Can also get movement disorder- tremor, myoclonus, Parkinsonism, bradykinesia
  • Can also have cranial nerve involvement, optic neuritis, seizure
  • Myocarditis, pancreatitis, fulminant hepatitis
  • Acute flaccid paralysis
    • Weakness can affect upper or lower limbs and can happen without meningitis
    • Can become hypo/areflexic, acute bowel and bladder dysfunction, absence of pain, or sensory changes
    • CSF has increased protein and pleocytosis
    • Similar to polio with destruction of spinal anterior horn cells as opposed to GBS

Differential Diagnosis

Altered mental status and fever

Evaluation

  • WBC count normal or slightly elevated
  • CSF - pleocytosis with lymphocyte predominance and elevated protein
  • CT head- negative
  • MRI brain usually negative but can show focal lesion in pons, basal gang, thal
  • Confirmation by blood or CSF IgM
    • IgM does not cross BBB so CSF IgM indicated CNS infc
  • False positive is recently vaccinated for yellow fever, Jap enceph, or recently infected with relate flavivirus- St Louse, Dengue
  • Confirmation by 4X increase of acute/ conv titres of antibodies

Management

  • Supportive
  • No studies to support ribavirin, interferon, gamma globulin, steroids, anticonvulsants, or osmotic agents

Prognosis

  • 4- 18% fatality
  • Older age greatest risk for death
  • Risk for poor neuro outcome and death- encephalitis, severe muscle weakness, AMS, DM, immune suppression
  • Can have significant morbidity and loss of function even in those patients that survive and are discharged to home
  • Parkinsons, tremor, gait instability, balance problems are most common neuro findings after discharge to home
  • Initial severe encephalopathy did not mean poor neuro outcome
  • Acute flaccid paralysis typically has very poor recovery

Disposition

Admit

https://www.cdc.gov/westnile/index.html

See Also

References

  1. West Nile virus. Centers for Disease Control and Prevention website. Accessed January 15, 2021.
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