West Nile virus: Difference between revisions

No edit summary
No edit summary
Line 1: Line 1:
==Background==
==Background==
===Virolgy===
===Virolgy===
# rna virus
*RNA virus
# virus family assoc with St Louise encephalitis, Japanese encephalitis, Murray Vallen enceph, and Kunjin enceph
*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
*2 lineage of WNV - only lineage 1 assoc with human dz originating in Middle East/Israel


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


===Epidemiology===
===Epidemiology===
# found in Africa, middle east, Russia, australia,
*Found in Africa, middle east, Russia, australia,
# most human infc in August and Sept but can happen from May to Dec
*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


Human Xmission
==Clinical Features==
# most from mosq bites
*Most people asymptomatic
# maternal fetal
*Severity increases with age
# breast milk
*2-14 day incubation
# blood xfsn
*Illness for 3-6 days
# percutaneous lab infc
*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
 
{{AMS and fever DDX}}


==Diagnosis==
==Diagnosis==
# most people assymptomatic
*Perf wbc count normal or sl elevated
# severity increases with age
*CSF - pleocytosis with lymphocyte predominance and elevated protein
# 2- 14 day incubation
*CT head neg
# illness for 3- 6 days
*MRI brain usually neg but can show focal lesion in pons, basal gang, thal
# malaise, anorexia, nv, eye pain, HA, myalgia, rash
*Confirmation by blood or CSF IgM
# 20% of infc people get west nile fever
**IgM does not cross BBB so CSF IgM indicated CNS infc
# <1% get severe neuro problem- encephalitis, meningitis, acute flaccid paralysis (afp)
*False positive is recently vaccinated for yellow fever, Jap enceph, or recently infected with relate flavivirus- St Louse, Dengue
# can also get movement disorder- tremor, myoclonus, parkinsonism, bradykinesia
*Confirmation by 4X increase of acute/ conv titres of antibodies
# 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
 
# 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==
==Management==
# supportive
*Supportive
# no studies to support ribavirin, interferon, gamma globulin, steroids, anticonvulsants, or osmotic agents
*No studies to support ribavirin, interferon, gamma globulin, steroids, anticonvulsants, or osmotic agents


==Prognosis==
===Prognosis===
# 4- 18% fatality
*4- 18% fatality
# older age greatest risk for death
*Older age greatest risk for death
# risk for poor neuro outcome and death- encephalitis, severe muscle weakness, ams, DM, immune suppression
*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
*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
*Parkinsons, tremor, gait, balance problem most common neuro finding after dc to home
# initial severe encephalopathy did not mean poor neuro outcome
*Initial severe encephalopathy did not mean poor neuro outcome
# afp pts have v poor recovery
*Acute flaccid paralysis typically has very poor recovery


==See Also==
==See Also==
*[[Encephalitis]]
*[[Encephalitis]]
[[Category:ID]]
[[Category:ID]]

Revision as of 13:52, 28 November 2015

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

Altered mental status and fever

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

See Also