West Nile virus
Revision as of 13:52, 28 November 2015 by Neil.m.young (talk | contribs)
Background
Virolgy
- RNA virus
- Virus family assoc with St Louise encephalitis, Japanese encephalitis, Murray Vallen enceph, and Kunjin enceph
- 2 lineage of WNV - only lineage 1 assoc with human dz 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 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 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 Transmission
- Most from mosq 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, nv, eye pain, HA, myalgia, rash
- 20% of infc people 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, sz
- 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 dysfnctn and absence of pain or sens 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
- Brain abscess
- Other
Diagnosis
- 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 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
- Acute flaccid paralysis typically has very poor recovery