Viral Infections fo the CNS Flashcards

1
Q

acute viral meningitis usually

A

mild and self-resolving completely in 7-10 days

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2
Q

acute bacterial meningitis

A

life threatening

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3
Q

most common cause of meningitis

A

viral

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4
Q

predictors of BACTERIAL MENINGITIS

A

LOW CSF GLUCOSE
HIGH PROTEIN
HIGH CSF WBC COUNT
HIGH PMN COUNT

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5
Q

patients with viral meningitis present

A

not severely ill looking-not encephalopathic

HA, Low Back Pain, neck stiffness, fever mailaise

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6
Q

viral types of meningitis

A

80%-entero (echo, cocksack, entero 71
10% mumps
10% aseptic

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7
Q

recurrent aseptic meningitis due to

A

HSV2, HIV, VZV

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8
Q

viruses causing ecephalitis

A

30%-arborviruses
23%-enteroviruses
27%-HSV1

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9
Q

treatable with acylovir and causes encephalitis

A

HSV1

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10
Q

seen in family outbreaks via URI of GI infections-also causes encephalitis

A

enteroviruses

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11
Q

encephalitis cause-seen with high seasonality, transmitted by misquitos or ticks-most common in very old and young

A

arborviruses

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12
Q

HSV encephalitis more commonly caused by

A

reactivation of latent infections over primary infection

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13
Q

Diagnostic signs present in HSV encephalitis

A
  1. MRI shows necrosis of temporal lobe,
  2. RBC’s in CSF=necrosis

*HSV tropic for temporal lobe

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14
Q

three families of mosquito borne encephalitis viruses

A

Flavaviridae
Togaviridae
Bunyaviridae

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15
Q

classificiation features of flavaviridae

A

small, ENVELOPED, non-segmented, +RNA virus

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16
Q

three genera of family flavaviridae

A

Flavaviruses
Pestiviruses
Hep C

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17
Q

Main players in Flavavirus genera

A

St. Louis encephalitis
West Nile
Japanese ecephalitis

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18
Q

after endocytosis and fusion related nucleocapsid release–> poly protein made by host ribosomes) is cleaved by viral (cis0cleavage) and host (trans cleavage) poteases

A

flavaviruses

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19
Q

all _____ viruses are transmitted by insects and are found thruout the world

A

flavaviruses

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20
Q

most important type of arboviruses

A

flavaviruses

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21
Q

secondary viremia (flavavirus not contained in spleen or in lymphnodes) what happens

A

secondary viremia can occure and encephalitis can happen

this is a minority of cases

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22
Q

3 clinical syndromes occuring with SLE

A

febrile headache
aseptic meningitis
encephalitis

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23
Q

most effective means of control for SLE

A

control mosquito population

there are no effective antivirals or vaccines

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24
Q

transmision via Culex species of mosquito

A

west nile virus

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25
Q

transmission cylce of west nile

A

culex mosq, takes blood meal from infected birds, virus localizes to salivary gland of mosq, transmission to humans as incidental hosts

only 1% will get seriously ill if infected

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26
Q

mild WNV

A

fever, headache skin rash, LAN, mylagia

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27
Q

severe WNV infection

A

severe HA, high fever, neck stiffness, muscle weakness, stupor, tremors, disorientation, sonvulsions tremors, soma paralysis, rarely death

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28
Q

tx for WNV

A

NON-SUPPORTIVE FLUIDS HOSPITALIZATION, CONTROL MOSQUITO POPO

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29
Q

JAPANESE ECEPH

A

IF YOU GOING TO SE ASIA OR INDIA OR USSR FOR OVER ONE MONTH GET VACCINE

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30
Q

CLASS CHARACTERS OF TOGAVIRIDAE

A

small, enveloped, non-segmented, positive sense RNA

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31
Q

two genera that make up togaviridae

A

rubiviruses

alphaviruses

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32
Q

only member of rubivirus family

A

rubella

*limited host range

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33
Q

genera in alphaviruses

A

Western Equine encephalitis, EEE, VEE,

34
Q

raplication for alphaviruses

A

witt is a fag and says “go look at rubella”

wiki has a fucking 90 page thing

but the answer will be somehting wih E1 and E2 proteins and the capsid protein having a diff,. fucniton…i dk my bff rose

35
Q

initially replicates in muscle and fibroblasts of various organs

A

alphaviruses

36
Q

after replicating in muscles and fibroblasts, aslpha viruses sometimes

A

induce low level viremia within 24 hours, invade CNS-destroy neurons

37
Q

usually fever for 2 weeks–> then encephalitis

A

alpha viruses

38
Q

after encephalopathy of ALPHA viruses begins..describe clinical course

A

usually become comatose and die within first few days of hospitalization

fever, diziness, LOC

39
Q

enveloped, spherical particles with segmented, ssRNA, negative sense

A

Bunyaviruses

40
Q

genera of bunyaviruses causing CNS infection (2/5)

A

California Encephalitis Virus

La Cross Encephalitis Virus

41
Q

genes found on 2-3 separat segments

A

bunyavirus

otherwise replication like other negative sense viruses

42
Q

similar to influenza except replicaiton occurs entirely in the cytoplasm and mRNAs are not spliced

A

bunyaviridae

CEV
LCEV

43
Q

most common cause of arboviral pediatric encephalitis in US

A

La Cross Virus–> bunyaviridae

44
Q

manifest as seizures and focal neurological signs in children mainly

A

Lacross virus

45
Q

Animal Vector Encphalitis Virses

A
  1. Rhabdoviridae
46
Q

can reassort based on segmentation

A

bunyaviruses

47
Q

enveloped, nonsegmented, negative sense ssRNA, with bullet shaped morphology

A

rhabdovirus-RABIES

48
Q

bullet shaped morphology

A

rabies

49
Q

rahbdo genera that cuase dz in humans

A

vesiculoviruses

lyssaviruses

50
Q

which one is the rabies im thinking of

A

lyssvirus

rhabdoviridae

51
Q

cell entry hinges on single glycoprotein with pH dependent fusion activity

A

rhabdoviridae-enter in pH dependent manner

otherwise like paramyxoviruses

52
Q

replication of rabies-just like a paramyxovirus

A

The virions attach to the surface of a host cell, and the envelope fuses to the plasma membrane. The nucleocapsid is released into the cell. The negative-sense RNA is transcribed into individual messenger RNAs and a positive-sense RNA template, which is used to create negative-sense RNA. Assembly occurs, and new viruses bud from the cell membrane (which is how they become enveloped).

53
Q

rabies replication exclusive to …

A

neurons-but once it reached brain it goes to other organs

54
Q

during final stages, rabies found in high concentration in the

A

salivary glands

55
Q

uniformly fatal it post exposure treatment not given

A

rabies

56
Q

incubation of rabis typically

A

long 2-3 months

can be a week tho

57
Q

after entry/replication in the muscle after a bit, rabies virus

A

transported through peripheral sensory nerves to spinal ganglia where it replicated and travels up cord to brain

58
Q

rabies tropic for neurons in which parts of the brain

A

limbic system, midbrain, and hypothalamus

59
Q

early prodromal rabies

A

mild, nonspecific

*caution if itching, burning, numbness around bite locally

60
Q

acute neurological phase of rabies

A

Nervous system dysfunction

anxiety agitation, paralysis, delirium

“furious rabies”-agitation predom
“dumb rabies” somnolence predom

61
Q

hydrophobia, exaggerated gag reflex to protect airway seen in

A

rabies-lyssavirus

62
Q

2-7 days after neurologic phase–rabies patients fall into

A

comadeath from rabies usually due to

respiratory depression

63
Q

post exposure prophyllaxis of rabies

A

clean wound

intra-wound introduciton of human-anti rabies Ig and multiple doses of rabies vaccine

64
Q

rabies vaccine is a

A

inactivated vaccine

65
Q

enveloped, segmented, ambisense RNA
virus

another animal borne ecephalopathic virus

A

arenaviridae

66
Q

virus contains 2 rna segments coding for 4 proteins

A

Lymphocytic choriomeningitis virus
LCMV

Aerenaviridae

67
Q

member of arenaviridae

A

LCMV

lymphocytic choriomenigitic virus

68
Q

LCMV-arenavirus-non-conventuional ambisense replication strategy–describe this shit

A
  1. genome used as template for transcription and the NP and M MRNAs produced frmo either the long or the short RNA segment

polymerase produces full length antigenome for each segment

positive sense antigenome is then used as a template for transcription of glycoprotein mRNA

assembly and exit

69
Q

can cause sudden onset of deafness in meningeal pahse of dz

A

LCMV

70
Q

transmitted form rodent excreta and saliva

A

arenavirus-LCMV

71
Q

HIV can case acute asceptic meningitis at

A

serovonversion-primary viremia

72
Q

most common opportunistic infection in AIDS pt.s

A

toxoplasmosis

73
Q

JC virus in HIV can cause

A

PML

progressive multifocal leukodystrophy

74
Q

Mollerate cells in CSF

A

recurrent HSV2 meningitis

75
Q

HSV1 responds to

A

acyclovir

76
Q

CMV responds to

A

GANCICLOVIR

77
Q

WHICH VIRUSES HAVE A POOR PROGNOSIS ONCE ENCEPHALITIS DEVELOPS

A

LACROSS
CALIFORNIA ENCV
EEV
WEST NILE

78
Q

UNIFORMLY LETHAL IF NOT TREATED

A

RABIES

79
Q

“NECROSIS IN TEMPORAL LOBE”

A

HSV1

80
Q

MISQUITO BORN VIRUS FAMILIES

A

FLAVA
ALPHA (TOGA)
BUNYA

81
Q

ANIMAL TRANSMITTED VIRUSES

A

RABIES

ARENA (LCMV)