West Nile virus: Difference between revisions

Revision as of 05:48, 28 March 2011

Background

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

Diagnosis

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

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

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
afp pts have v poor recovery

Authors:

@@ Line 1: / Line 1: @@
-Virolgy
+==Background==
+===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
-- rna virus
+===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
-- virus family assoc with St Louise encephalitis, Japanese encephalitis, Murray Vallen enceph, and Kunjin enceph
+===Epidemiology===
+# found in Africa, middle east, Russia, australia,
-- 2 lineage of west nile- only lineage 1 assoc with human dz- originated in middle east/ isreal
+# most human infc in August and Sept but can happen from May to Dec
-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
-- most from mosq bites
+==Diagnosis==
+# most people assymptomatic
-- maternal fetal
+# severity increases with age
+# 2- 14 day incubation
-- breast milk
+# illness for 3- 6 days
+# malaise, anorexia, nv, eye pain, HA, myalgia, rash
-- blood xfsn
+# 20% of infc people get west nile fever
+# <1% get severe neuro problem- encephalitis, meningitis, acute flaccid paralysis (afp)
-- percutaneous lab infc
+# 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
-Clinical Illness
+# afp not like gullain barre but more like polio with destruction of spinal anterior horn cells
+# can also have cranial nerve, optic neuritis, sz
-- most people assymptomatic
+# also myocarditis, pancreatitis, fulminant hepatitis
-- 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
+# 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==
+# 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
+# afp pts have v poor recovery
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