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,
• 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, 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 polio with destruction of spinal anterior horn cells as apposed to GBS

Differential Diagnosis

• Meningitis
• SAH
• Lyme disease
• Brain abscess
• Bacterial endocarditis
• Toxic / metabolic encephalopathy

Altered mental status and fever

• Infectious
  • Sepsis
  • Meningitis
  • Encephalitis
  • Cerebral malaria
• Other
  • Neuroleptic malignant syndrome
  • Serotonin syndrome
  • Malignant hyperthermia
  • Sympathomimetic toxicity (cocaine, amphetamine, ketamine)
  • Anticholinergic toxicity
  • Heat stroke
  • Delirium tremens
  • Hypothalamic stroke
  • Pheochromocytoma
  • Thyroid storm

Evaluation

• Perf wbc count normal or sl elevated
• CSF - pleocytosis with lymphocyte predominance and elevated protein
• CT head neg
• MRI brain usually neg 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, balance problem most common neuro finding after dc to home
• Initial severe encephalopathy did not mean poor neuro outcome
• Acute flaccid paralysis typically has very poor recovery

Disposition

Admit

See Also

• Encephalitis

Authors

Ross Donaldson