Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro II > 32 Viral > Flashcards

32 Viral Flashcards

1
Q

Predictors of bacterial meningitis:

A
  • Low CSF glucose
  • High CSF protein
  • High CSF WBC count
  • High CSF neutrophil count
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

can present similarly to viral meningitis:

A

partially treated bacterial meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

clinical course of viral meningitis:

A

self-limited, with complete recovery in 7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Appearance of a patient with viral meningitis?

A

does’t appear extremely ill (not encephalopathic)

  • Fever & malaise
  • HA
  • Neck stiffness
  • Low back pain (overshadowed by HA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Outcome for a patient with viral meningitis?

A

resolves without significant neurologic sequalae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Recurrent viral meningitis can result from:

A

persistent or latent infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Viruses causing meningitis:

A

80% caused by enterovirus (Echo, Coxsackie, Enterovirus 71)

10% attributed to Mumps (without MMR vaccine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Viruses causing recurrent aseptic meningitis:

A

HSV-2 (genital herpes), HIV, VZV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Viruses causing Viral encephalitis:

A

arborviruses
enteroviruses
HSV-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Transmission of arbovirus?

A

mosquitos, ticks (**seasonality)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MC affected by arbovirus?

A

old + young

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cause of enterovirus inf?

A

family

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Types of HSV encephalitis?

A

acute

reactivated latent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Characteristic site of damage in HSV encephalitis?

Lab/imaging?

A

temporal lobe

necrosis in temporal lobe, RBC in CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dx of HSV encephalitis?

A

PCR (false neg happen though)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prognosis of HSV encephalitis?

A

Curable if treated early

Devastating if treatment is delayed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Structure of Flaviviridae?

A

Small, enveloped, nonsegmented, (+) strand RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diseases caused by Flaviviridae?

A

Flaviviruses: St. Louis encephalitis, West Nile, Japanese encephalitis

Hepatitis C virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Replication of Flaviviridae?

A

a) R-mediated endocytosis –> nucleocapsid delivered into cytoplasm following pH- dependent fusion
b) RNA translated by host ribosomes –> polyprotein –> cleaved by a combination of viral (cis-cleavage) and host (trans-cleavage) proteases
c) Viral polymerase replicates genomic RNA
d) Structural proteins (capsid and envelope glycoproteins) assemble genomic RNA into virions –> bud into ER/Golgi –> enveloped viruses released during transport at cell surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is notable about genome of Flaviviridae?

A

contains 5’- cap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Transmission of Flaviviridae?

A

insect vectors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Initial location of Arbovirus replication?

A

site of inoculation (endothelium or epithelial cells

surrounding bite site) and establish transient primary viremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Location of Arbovirus replication 3-7d post-exposure?

A

macrophages, spleen, or lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Progression of arbovirus infection?

A
  1. mild systemic disease (most infections do not progress beyond this point)
  2. If infection not controlled by immune response, secondary viremia ensues and results in severe systemic disease (e.g. encephalitis)
25
Q

Geographical location of St. Louis encephalitis epidemics?

A

North, Central, and South America

Colorado, California, Florida, Texas, and Arkansas

26
Q

Clinical syndromes that occur with St. Louis encephalitis?

A

1) Febrile headache
2) Aseptic meningitis
3) Encephalitis

27
Q

Onset of StLE is characterized by:

A
  1. generalized malaise, fever, headache, sore throat or cough
  2. followed in 1 to 4 days by acute or subacute meningeal and neurological signs
28
Q

The most effective means of control of StLE is:

A

reduction of the mosquito vector population.

29
Q

Symptoms of a mild form of West Nile virus?

A

febrile HA
myalgia
occ. rash + LAD

30
Q

Symptoms of a severe form of West Nile virus?

A
  • Severe HA with high fever
  • Neck stiffness, muscle weakness
  • Stupor, disorientation, convulsions, tremors
  • Coma, paralysis, and, rarely, death.
31
Q

Structure of Togaviridae?

A

Small, enveloped, nonsegmented, (+) strand RNA viruses

32
Q

Types of Togaviridae?

A

Rubiviruses (Rubella)

Alphaviruses

33
Q

Initial site of replication of Togaviridae?

A

muscle + fibroblasts of numerous organs

34
Q

Progression of Togaviridae?

A

infection –> repl in muscle/fibroblasts –> viremia w/ CNS invasion –> neuron destruction

35
Q

Symptoms of Togaviridae?

A
  1. fever x2wks
  2. Dizziness + Incr LOC
  3. Encephalitis w/ coma –> death
36
Q

Structure of Bunyaviridae?

A

Enveloped, spherical particles with segmented (2-3), single-strand, negative-sense RNA
genomes

37
Q

Types of Bunyaviridae causeing CNS infections?

A

a) California encephalitis virus

b) La Crosse encephalitis virus

38
Q

Location of replication of Bunyaviridae?

A

exclusively in the cytoplasm

mRNAs are not spliced

39
Q

MC cause of rboviral-induced pediatric encephalitis in the U.S.?
Symptoms?

A

LaCrosse virus

seizures and focal neurological signs

40
Q

Structure of Rhabdoviridae?

A

Enveloped, nonsegmented, negative-strand RNA viruses

“bullet-shaped”

41
Q

Human disease-causing genera of Rhabdoviridae?

A

Vesiculoviruses –> vesicular stomatitis virus

Lyssaviruses –> rabies virus

42
Q

Replication/dissemination of Rhabdoviridae?

A
  1. enters muscle cells (pH-dependent manner following endocytosis)
  2. transported through periph sensory nerves to spinal ganglia (neuronal cell replication)
  3. travels up spinal cord, disseminates once reaches brain
43
Q

During the final stages

of the disease, Rabies Virus is found replicating in high concentrations in:

A

the salivary glands

Efferent nerves transport virus to the submaxillary salivary glands

44
Q

Primary mechanism of Rabies spread?

A

saliva (animal bite)

open wound

45
Q

Prognosis of untreated Rabies?

A

death

46
Q

Once infected, Rabies virus predominates in:

A

neurons of the limbic system, midbrain, and hypothalamus.

47
Q

Phases of Rabies symptoms?

A
  1. Prodromal (mild, nonspecific symptoms; abn sensation around bite)
  2. Acute neurologic phase (anxiety, agitation, paralysis, delirium, hydrophobia)
  3. Coma (up to 30 days, death from resp arrest)
48
Q

Trx of Rabies?

A

washing of the wound

instillation of wound with human anti- rabies Ig

administration of multiple doses of inactivated vaccine (thigh or deltoid)

49
Q

Why is vaccination an effective trx?

A

long incubation period

50
Q

Structure of arenaviridae?

A
  • Enveloped
  • Contain 2 ambisense RNA segments (encoding 4 proteins)
  • Often contain host cell ribosomes
51
Q

Cell entry of arenaviridae?

A

pH-dependent pathway following endocytosis

52
Q

Replication of arenaviridae?

A

nonconventional “ambi-sense” transcr/transl:

  1. Either L (long) or S (short) RNA segment used as a template for transcription –> NP and L mRNAs
  2. polymerase then produces a full-length antigenome for each of the segments
  3. ”(+)”-sense antigenome used as a template for transcription of the glycoprotein mRNA
  4. Assembly + release via budding
53
Q

Transmission of arenaviridae?

A

inhalation of aerosolized virus from rodent excreta and saliva

54
Q

Progression of Lymphocytic choriomeningitis virus infection?

A
  1. ever, headache, nausea, and vomiting
    which coincides with viremia
  2. aseptic meningitis usually begins about 10 days later
55
Q

Possible side-effect of Lymphocytic choriomeningitis virus infection?

A

sudden-onset deafness can occur during the meningeal phase

56
Q

Neurologic complications occur in __% of AIDS patients

A

40

57
Q

Direct neuro effects of HIV inf?

A
  • Acute aseptic meningitis (at seroconversion)
  • Chronic meningitis
  • HIV dementia complex
  • Vacuolar myelopathy
  • Peripheral neuropathy
  • Cranial neuropathy
  • Inflammatory myopathy
58
Q

Indirect neuro effects of HIV inf?

A
  1. opportunistic infections (CMV encephalitis, PML, etc)
  2. Neoplasms (1’ CNS lymphoma, metastatic Karposi’s)
  3. Nutritional and metabolic disorders (drug toxicity of anti-retrovirals)

Neuro II (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions