Types of viral encephalitis Flashcards

1
Q

what part of the brain is affected by viral encephalitis

A

brain parenchyma

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2
Q

what are the most frequent etiology of viral encephalitis

A

Arbovirus

HSV-1

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3
Q

What is the key in signs and symptoms of viral encephalitis

A

to determine whether signs and symptoms is focal or diffused

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4
Q

what are etiologic agents of diffused encephalitis besides arbovirus

A

HSV1

non-polio enterovirus

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5
Q

what are etiologic agents of focal encephalitis besides HSV-1

A

arbovirus
non-polio enterovirus
rarely polio virus or rabies

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6
Q

if one of the viral encephalitis agents produces an asymptomatic infection does the infection spread to the CNS

A

NO

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7
Q

What are togaviridiae group of arbovirus

A

comprised most arthropod-borne virus, also rubella

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8
Q

what are categories of togaviridae

A

Alphavirus and flavivirus

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9
Q

what are examples of alphaviruses

A

EEEV, WEEV, VEEV

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10
Q

what are examples of flavivirus

A

SLEvirus
WNEvirus
POWvirus

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11
Q

what are examples of bunyavirus

A

Hantavirus

California Virus, Jamestown canyon virus, LaC virus

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12
Q

where is the highest incidence of California encephalitis serogroup

A

California, Midwest, SE U.S.

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13
Q

what are examples of reoviridae

A

rotovirus, CLTFvirus

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14
Q

arbovirus causes what two primary syndromes

A

hemorrhagic fever

encephalitis/meningitis

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15
Q

what is the seasonality of arbovirus

A

varies annually, peak in summer months when animals are out

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16
Q

what is the primary cause of epidemic encephalitis

A

arbovirus

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17
Q

what are the principle arthropod vectors

A

mosquitoes and ticks

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18
Q

what are CLFV and POW virus spread by and what about the rest

A

ticks

Rest is spread by mosquitoes

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19
Q

what are the principle reservoir of arbovirus

A

birds and small mammals

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20
Q

how is arbovirus transmitted to humans

A

tangent transmission

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21
Q

what is the age and gender relationship in arbovirus

A

primarily children others in elderly

N/A gender

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22
Q

what is the seasonality of arbovirus

A

sporadic epidemic occur in summer months when reservoir vector and humans are out doors

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23
Q

what is the RF for arbovirus in individuals

A

summer exposure to mosquitoes and ticks, age

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24
Q

for creation of arbovirus epidemic what is needwed

A

large reservoir (birds), large vector (mosquitoes), favorable climate

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25
Q

how do you monitor the arbovirus activity in the US

A

sample mosquitoes,
wild birds are captured and bleed
sick dying animals are observed

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26
Q

what is the pathogenesis of arboviris

A

primary viral replication causes none/mild symptoms

secondary replication causes viremia attacks brain and other organs

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27
Q

what is the most common clinical manifestation of arbovirus

A

asymptomatic infection most common result

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28
Q

what are possible disease outcomes of arbovirus

A

self-limiting flu
self-limiting aseptic meningitis
encephalitis and death +/- flaccid paralysis

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29
Q

how do diagnose arbovirus

A

CSF
Serological
EEG
CT

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30
Q

what is the treatment of arbovirus

A

supportive

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31
Q

what is the prevention of arbovirus

A

goal is limiting the vector population and education and precaution (DEET)

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32
Q

What type of immunity is there against arbovirus

A

specific and life long
2 vaccines for horse
US military vaccine against EEV and WEEV

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33
Q

what geographical location does EEEV predominate

A

East Coast , wooded areas near swamps and marshes

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34
Q

what arbovirus has the worst mortality rate and more likely to manifest with neurological sequelae

A

EEEV

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35
Q

How is EEEV unique to other arboviruses

A

asymptomatic is not the norm. Norm is Eastern Equine Encephalitis

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36
Q

what geographical location does WEE predominate

A

west of Mississippi River highest in rural residence

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37
Q

what age does most WEEV occur

A

50% in children <1yo

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38
Q

what arbovirus is the most benign form of encephalitis

A

WEEV

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39
Q

what geographical location does SLEV predominate

A

Midwest

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40
Q

What age does most SLEV occur

A

varies due to herd immunity
Children in West
Elderly in East

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41
Q

what is the leading cause of epidemic arboviral encephalitis before WNEV in 2002

A

SLEV

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42
Q

What agent does WNEV relate to

A

SLEV

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43
Q

what is the geographic distribution of WNEV

A

Africa, Europe, middle east, west Asia, Australia. North america

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44
Q

what is the most common arbovirus in the US today

A

WNEV

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45
Q

how else can WNEV be transmitted beside mosquitoes

A

transfusions, in utero

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46
Q

what are s&s of West Nile Fever

A

flu symptoms, muscle aches, nausea, maculopapular rash, frontal HA, eye pain

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47
Q

what are S&S of West Nile Encephalitis

A

West nile fever with at least one of the following:

meningitis, encephalitis, parkinsonism, focal muscle weakness

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48
Q

what is treatment of WNEV

A

Ribavirin useful in vitro

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49
Q

where does CAL serogroup predominate

A

California, East of Mississippi

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50
Q

What is the age relationship in CAL serogroup

A

almost all occur in children and adolescents

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51
Q

what is the most important cause of arbovirus pediatric encephalitis in the USA

A

LAC

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52
Q

what symptom of CAL serogroup is unique and can occur as a sequelae

A

siezures

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53
Q

what is poliomyelitis

A

acute infection systemic infectious disease destroying motor neurons in the spinal cord results in flaccid, ascending, asymmetrical paralysis

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54
Q

what is the morphology of Polio virus

A

enterovirus, non-enveloped, + sense RNA virus

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55
Q

which serotype of Polio virus is responsible for most of the paralytic polio

A

type 1

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56
Q

what serotype of Polio virus is often isolated in vaccine-associated poliomyelitis

A

types 2 and 3

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57
Q

why is Polio virus rare in us today

A

vaccine

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58
Q

what was the original though of Polio virus

A

disease of developed countries in older populations, but child and young adults present with serious disease

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59
Q

where is paralytic polio still a significant concern

A

underdeveloped counyties

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60
Q

what is the transmission of Polio virus

A

fecal oral route through water. Virus in stool for 3-6 weeks

less so through respiration (oral-oral)

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61
Q

what is the host of Polio virus

A

humans

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62
Q

what are the reservoir of Polio virus

A

humans and water

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63
Q

how infectious is Polio virus

A

highly communicable

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64
Q

what population is primarily infected by Polio virus

A

<3yo children, but young adults, prego, and elderly can be susceptible as well

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65
Q

what is the relationship with severity of polio/paralytic polio and age

A

severity and chance of getting paralytic polio increases with age

66
Q

what is the seasonality of polio

A

summer-fall

67
Q

what is the pathogenesis of Polio virus

A

incubation is long

infected cells train to lymph nodes along GI, first pharynx then intestine, shed in resp. weeks shed in feces for months

68
Q

is Polio virus lytic or lysogenic

69
Q

what is a rare occurrence of Polio virus in the body

A

entering cns is rare

70
Q

what happens if Polio virus enters cns

A

but if it does it spread through neural routes and pns like rabies and herpes destroys nerve fiber pathway
results in flaccid paralysis with no sensory lose (unlike GBS)

71
Q

what is the most common clinical syndrome in Polio virus

A

asymptomatic

72
Q

what are signs of minor poliomyelitis

A

fever, malaise, HA, muscle aches, pharyngitis, nausea, abd pain, constipation last 72 hours

73
Q

what are signs of aseptic meningitis in Polio virus without paralysis

A

signs of minor poliomyelitis and
pain in neck, back, and leg
muscle stiffness and tenderness or spasm lasts 1-2weeks

74
Q

what are signs of paralytic poliomyelitis

A

initial like aseptic meningitis
paralysis after that complete by fever break, muscle spasms, loss of superficial and deep tendon reflex, abnormal sensations

75
Q

what are three forms of paralytic poliomyelitis

A

spinal
bulbar polio
bulbospinal polio

76
Q

what is post polio syndrome

A

survivors of paralytic polio fatigue, new muscle weakness/pain, progressive atrophy
happens in 30-40yo not activation of latent virus but to over use

77
Q

how do you diagnose Polio virus

A

stool sample
PCR
partial genomic sequencing of stool

78
Q

what is the treatment of polio virus

A

supportive

79
Q

what is the prevention of polio

A

vaccine, IPV, eIPV

80
Q

what is needed after Polio virus vaccine especially in developing countries

A

booster, 4th booster in developing countries

81
Q

how does oral polio vaccine differ from parental polio vaccine

A

oral is live attenuated. can put unvaccinated at risk

82
Q

what is rabies

A

acute, fatal. fulminant, focal encephalitis and myelitis

83
Q

what are characteristic of rabies

A

rhabdoviridae, lyssavirus, -ssRNA, bullet shaped

84
Q

how many serotypes of rabies

85
Q

what is a negri body

A

eosinophilic cytoplasmic inclusions of viral nucleoptoteins

86
Q

what is the incidence rate of rabies

A

low because of control of cats and dogs

87
Q

what is the transmission of rabies

A

animal bite or scratch

88
Q

what is the reservoir of rabies

A

dogs cats, skunks, fox, racoon. bat, wolves others

89
Q

what is the geographic distribution of rabies

A

in the us, rabies is epizootic

90
Q

what is the age/gender relationship in rabies

91
Q

what is the seasonality of rabies

92
Q

what are RF of rabies

A

uncontrolled animals

93
Q

what animal is the most common source of rabies in US

94
Q

what is pathogenesis of rabies

A

virus enters PNS at unmyelinated sensory terminals and nm junctions
retrograde axoplasmic flow to spinal cord then brain

95
Q

what part of the brain does rabies predominate

A

gray matter , but localizes in limbic system

96
Q

when is a rabies pt potentially infectious

A

from 2 weeks before onset of symptoms to death

97
Q

what is the point of no return for rabies

A

moment the virus enters sensory terminals and NM junctions

98
Q

Can the rabies virus be isolated in blood

99
Q

what is the prodrome of rabies

A

flu like symptoms for 2 to 4 days

100
Q

what length of rabies disease is always fatal

A

5 to 6 days

101
Q

what forms of rabies disease cab be seen

A

paralytic/dumb form

Excititation-furious form

102
Q

What is paralytic/dumb rabies

A

signs are similar to viral encephalitis
paralysis extremity to trunk
hypoventilation and hypotension to coma and death

103
Q

what is excitation-furious rabies

A

photo/phonophoba

hyperactivity sexual agressive, agitation anxiety, insomnia. confusion, foaming at mouth to coma and death

104
Q

which rabies form is more common

A

excitation-furious rabies

105
Q

how is rabies diagnosed

A

csf, DFA of cytoplasmic inclusions, isolation of virus via mouse inoculation

106
Q

what is treatment for rabies

107
Q

wat is prevention of rabies

A

vaccination pre and post exposure

108
Q

where should you never inject rabies vaccine

A

gluteal injections

109
Q

what should you do after exposure

A

clean wound, tetanus prophylaxis, Vaccination AND antiserum two diff sites

110
Q

what agent cause 20% of all cases of viral encephalitis in the US and most common cause of all non epidemic/ sporadic focal encephalitis

111
Q

who does HSV have peak incidence in

A

nenates with infected mother

young adults/elderly via reactivation of latency

112
Q

what is the transmission of hsv

A

saliva, vagina secretion (esp. post partum), semen

in utero but rare

113
Q

what is the pathogenesis of hsv

A

spread to the CNS by retrograde axoplasmic flow

114
Q

is hsv lytic or lysogenic

115
Q

what is hsv manifestation in adults

A

focal encephalopathy in one lobe usually temporal.
memory defect, psychosis, slurred speech, personality changes
relapse and death is high

116
Q

in adults primary genital herpes infections can result in?

A

a benign, aseptic meningitis

117
Q

what are the 3 possible presentations of HSV in neonate

A

Local herpes infection, SEM
Disseminated
CNS disease

118
Q

what is the etiologic agent in bells palsy

A

hsv and vsv

119
Q

how is hsv diagnosed

A

symptoms presentation
CSF- viral glucose protein levels, mononuclear pleocytosis and lost of RBCs
Other Tests

120
Q

what is treatment for hsv

A

antivirals and nucleoside analogs, not a cure

121
Q

where is the most common hsv infection in children from infected mother

A

intrapartum

122
Q

how is hsv diagnosed in pregnant women

A

clinical exam plus one of the following
Swab- PCR or viral culture
or Serology for type specific AB test

123
Q

what is tx of hsv in prego women

A

suppressive on in last 4 weeks of pregnancy
acyclovir daily
discuss delivery stategy
Csection if virus was aquired 3rd trimester or lesion is present

124
Q

What does HAND stand for

A

HIV associated neurocognative disorders

125
Q

what does HAD stand for

A

HIV associated dementia

126
Q

what is HAND

A

it is a slowly progressobe demylenation of disease with neuronal loss of the CNS

127
Q

what is the incidence of cns disease of HIV pts pre-HAART

A

60% will show evidence of neuropathy

128
Q

what is RF of HAND

A

IVDA even despite HAART

129
Q

what is a good prognostic indicator of pts who have HAND

A

plasma and viral load supression

130
Q

what is the pathogenesis of HAD

A

direct infection of cns and pns occurs early in HIV infection

131
Q

what cells does HIV replicate and infect in HAD pathology

A

monocyte, macrophage, microglia of CNS

132
Q

what cells does HIV not infect

A

neurons and oligodendrocytes

133
Q

hiv in the CNS is M-trophic which utilizes which receptor as a cofactor

134
Q

what is hiv related neuronal damage due to

A

gp120 or Tat proteins

135
Q

HAD is NOT due to

A

autoimmune, lymphoma, infection (other than HIV of course)

136
Q

HAD is characterized by

A

, astrocytosis, micrglial nodules, diffuse or focal myelin pallor or neuronal loss

137
Q

what are manifestation of of HIV associated CNS

A

peripheral neuropathy, aseptic meningitis, acute encephalitis, HIV motor complex, vacuolar neuropathy, sensory pain of feet

138
Q

what is asymptomatic neurocognative impairment (ANI)

A

impairments seen through testing but are symptomatic in their daily life

139
Q

what is HIV associated mild neurocognative disorder (MND)

A

impairments causing mild disturbances in daily life

140
Q

what Hiv associated cns disease is more common in the new area of HAART

A

ANI -> NMD

141
Q

what type of changes are seen in HAD pts

A

Early: Cognitive, Motor, Behavioral
Late: Progression, mute, spasticity, death

142
Q

how is hiv associated cns disease diagnosed specifically HAD

A

if pts have one or more (pleocytosis, abnormal CSF ig recoverable HIV in CNS)
Use HAD Scale

143
Q

what should imaging studies show in HAD

A

cortical atrophy, enlarged ventricles , demylenation of white matter, abscence of focal abnormalities

144
Q

what is the treatment of CNS HIV disease

A

HAART, could cause increase in sensory neuropathy and should be able to cross BBB

145
Q

what does PML stand for

A

progressive multifocal leukoencephalopathy

146
Q

what kind of disease is PML

A

uncommon, subacute, progressive demyelination of CNS

147
Q

what is the etiologic agent in PML

A

papovavirus

148
Q

what is the morphology of papovavirus

A

naked dsDNA with icosahedral symmetry

149
Q

what are examples of papovavirus

A

Polymavirus (JC virus, BK virus, SV40)

HPV

150
Q

what is the result of PML in immunocompetant

A

common asymptomatic infection

151
Q

what percentage of people world wide are positive for BK virus

152
Q

how can JC and BK virus become fatal

A

underlyining disorder which causes reactivation of virus through immunosuppression

153
Q

what does BKV cause

A

a fatal opportunistic kidney disease in renal transplant pts

or severe UTI in HIV

154
Q

what does JCV cause

A

a rare opportunisitic CNS reactivation of disease in advanced HIV/AIDS and pts on Natalizumab

155
Q

what is the pathogenesis of JCV

A

invades oligodendrocytes cause cell death and causes infection along the myelin tract and infects astrocytes

156
Q

what virus is present in most pediatric brain tumors

157
Q

what part of the brain is most affected by JVC

A

subcortical white matter

158
Q

what would cells would be affected by JVC

A

abscence of oligodendrocytes, abnormal astrocytes, sparing of neuron and axons, enlarged oligodendritic cells with inclusions
INFLAMMATORY CELLS ARE ABSENT

159
Q

What are the clinical manifestation of JVC disease

A

Rapid, Muscle weakness, ataxia, cognitive/speech impairments, visual loss

160
Q

how do you diagnose pml

A

clinical signs, PCR of CSF, Neuroimaging of demyelnation, pathology seen in brain biopsy

161
Q

what is the tx for pml

A

cidofovir
HAART in aids pts.
Prognosis good if HAART is started when CD4>100