West Nile virus
Virolgy
- rna virus
- virus family assoc with St Louise encephalitis, Japanese encephalitis, Murray Vallen enceph, and Kunjin enceph
- 2 lineage of west nile- only lineage 1 assoc with human dz- originated in middle east/ isreal
Ecology
- bird- mosquito- bird cycle
- passerine birds are amplification host
- starts in spring, ends in fall when mosquitos dormant
- Culex mosquitos
- Unclear if human infc from culex bite or other bridge vector mosq 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 (west nile virus) in birds feces and oral secretions
- Bird to bird xmission possible in lab
- Birds can be infected by eating infc mosquitoes, infc birds and infc rodents but importance of oral spread in nature unclear
Epidemiology
- found in Africa, middle east, Russia, australia,
- most human infc in August and Sept but can happen from May to Dec
Human Xmission
- most from mosq bites
- maternal fetal
- breast milk
- blood xfsn
- percutaneous lab infc
Clinical Illness
- most people assymptomatic
- severity increases with age
- 2- 14 day incubation
- illness for 3- 6 days
- malaise, anorexia, nv, eye pain, HA, myalgia, rash
- 20% of infc people get west nile fever
- <1% get severe neuro problem- encephalitis, meningitis, acute flaccid paralysis (afp)
- can also get movement disorder- tremor, myoclonus, parkinsonism, bradykinesia
- weakness from afp asymmetric, can affect upper or lower limbs and can happen without meningitis
- afp also gets hypo/ areflexic, acute bowel and bladder dysfnctn and absence of pain or sens changes
- afp csf has increased protein, and pleocytosis
- afp not like gullain barre but more like polio with destruction of spinal anterior horn cells
- can also have cranial nerve, optic neuritis, sz
- also myocarditis, pancreatitis, fulminant hepatitis
Clinical Outcome
- 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 pts 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
- afp pts have v poor recovery
Pathogenesis
- mosq bite- then virus replicates in skin and LN's- makes primary viremia that seeds reticuloendothelial system
- secondary viremia seeds other organs and cns
- viremia disappears after symtom onset and concomitant rise in IGM and neutralizing abx
- immune compromised pt can have long viremia
- risk for neuro infc and death is age, immune senescence and change in blood brain barrier
- involvement of basal gang, thalamus, pons causes tremor and parkinsons sxs
Diagnosis
- perf wbc count normal or sl elevated
- csf- pleocytosis with lymphocyte predominance and elevated protein
- ct neg
- mri usually neg but can show focal lesion in pons, basal gang, thal
- dx 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
Treatment and Prevention
- supportive
- can vaccinate horses but not avail for human yet
- no studies to support ribavirin, interferon, gamma globulin, steroids, anticonvulsants, or osmotic agents
- avoid mosq