West Nile virus

Background

Virolgy

1. rna virus
2. virus family assoc with St Louise encephalitis, Japanese encephalitis, Murray Vallen enceph, and Kunjin enceph
3. 2 lineage of west nile- only lineage 1 assoc with human dz- originated in middle east/ isreal

Ecology

1. bird- mosquito- bird cycle
2. passerine birds are amplification host
3. starts in spring, ends in fall when mosquitos dormant
4. Culex mosquitos
5. Unclear if human infc from culex bite or other bridge vector mosq species
6. House sparrows have high level of viremia and are amplifiers
7. Humans and horses also but viremia is low so are not important amplifiers
8. Wnv (west nile virus) in birds feces and oral secretions
9. Bird to bird xmission possible in lab
10. Birds can be infected by eating infc mosquitoes, infc birds and infc rodents but importance of oral spread in nature unclear

Epidemiology

1. found in Africa, middle east, Russia, australia,
2. most human infc in August and Sept but can happen from May to Dec

Human Xmission

1. most from mosq bites
2. maternal fetal
3. breast milk
4. blood xfsn
5. percutaneous lab infc

Diagnosis

1. most people assymptomatic
2. severity increases with age
3. 2- 14 day incubation
4. illness for 3- 6 days
5. malaise, anorexia, nv, eye pain, HA, myalgia, rash
6. 20% of infc people get west nile fever
7. <1% get severe neuro problem- encephalitis, meningitis, acute flaccid paralysis (afp)
8. can also get movement disorder- tremor, myoclonus, parkinsonism, bradykinesia
9. weakness from afp asymmetric, can affect upper or lower limbs and can happen without meningitis
10. afp also gets hypo/ areflexic, acute bowel and bladder dysfnctn and absence of pain or sens changes
11. afp csf has increased protein, and pleocytosis
12. afp not like gullain barre but more like polio with destruction of spinal anterior horn cells
13. can also have cranial nerve, optic neuritis, sz
14. also myocarditis, pancreatitis, fulminant hepatitis

1. perf wbc count normal or sl elevated
2. csf- pleocytosis with lymphocyte predominance and elevated protein
3. ct neg
4. mri usually neg but can show focal lesion in pons, basal gang, thal
5. dx by blood or csf igm
6. igm does not cross BBB so csf igm indicated cns infc
7. false positive is recently vaccinated for yellow fever, Jap enceph, or recently infected with relate flavivirus- St Louse, Dengue
8. confirmation by 4X increase of acute/ conv titres of antibodies

Treatment

1. supportive
2. no studies to support ribavirin, interferon, gamma globulin, steroids, anticonvulsants, or osmotic agents

Prognosis

1. 4- 18% fatality
2. older age greatest risk for death
3. risk for poor neuro outcome and death- encephalitis, severe muscle weakness, ams, DM, immune suppression
4. can have significant morbidity and loss of function even in those pts that survive and are discharged to home
5. parkinsons, tremor, gait, balance problem most common neuro finding after dc to home
6. initial severe encephalopathy did not mean poor neuro outcome
7. afp pts have v poor recovery

See Also

• Encephalitis