32 Viral Flashcards

1
Q

Predictors of bacterial meningitis:

A
  • Low CSF glucose
  • High CSF protein
  • High CSF WBC count
  • High CSF neutrophil count
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2
Q

can present similarly to viral meningitis:

A

partially treated bacterial meningitis

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3
Q

clinical course of viral meningitis:

A

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

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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)
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5
Q

Outcome for a patient with viral meningitis?

A

resolves without significant neurologic sequalae

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6
Q

Recurrent viral meningitis can result from:

A

persistent or latent infections

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7
Q

Viruses causing meningitis:

A

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

10% attributed to Mumps (without MMR vaccine)

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8
Q

Viruses causing recurrent aseptic meningitis:

A

HSV-2 (genital herpes), HIV, VZV

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9
Q

Viruses causing Viral encephalitis:

A

arborviruses
enteroviruses
HSV-1

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10
Q

Transmission of arbovirus?

A

mosquitos, ticks (**seasonality)

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11
Q

MC affected by arbovirus?

A

old + young

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12
Q

Cause of enterovirus inf?

A

family

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13
Q

Types of HSV encephalitis?

A

acute

reactivated latent

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14
Q

Characteristic site of damage in HSV encephalitis?

Lab/imaging?

A

temporal lobe

necrosis in temporal lobe, RBC in CSF

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15
Q

Dx of HSV encephalitis?

A

PCR (false neg happen though)

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16
Q

Prognosis of HSV encephalitis?

A

Curable if treated early

Devastating if treatment is delayed

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17
Q

Structure of Flaviviridae?

A

Small, enveloped, nonsegmented, (+) strand RNA

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18
Q

Diseases caused by Flaviviridae?

A

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

Hepatitis C virus

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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

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20
Q

What is notable about genome of Flaviviridae?

A

contains 5’- cap

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21
Q

Transmission of Flaviviridae?

A

insect vectors

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22
Q

Initial location of Arbovirus replication?

A

site of inoculation (endothelium or epithelial cells

surrounding bite site) and establish transient primary viremia

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23
Q

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

A

macrophages, spleen, or lymph nodes

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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
Geographical location of St. Louis encephalitis epidemics?
North, Central, and South America | Colorado, California, Florida, Texas, and Arkansas
26
Clinical syndromes that occur with St. Louis encephalitis?
1) Febrile headache 2) Aseptic meningitis 3) Encephalitis
27
Onset of StLE is characterized by:
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
The most effective means of control of StLE is:
reduction of the mosquito vector population.
29
Symptoms of a mild form of West Nile virus?
febrile HA myalgia occ. rash + LAD
30
Symptoms of a severe form of West Nile virus?
- Severe HA with high fever - Neck stiffness, muscle weakness - Stupor, disorientation, convulsions, tremors - Coma, paralysis, and, rarely, death.
31
Structure of Togaviridae?
Small, enveloped, nonsegmented, (+) strand RNA viruses
32
Types of Togaviridae?
Rubiviruses (Rubella) | Alphaviruses
33
Initial site of replication of Togaviridae?
muscle + fibroblasts of numerous organs
34
Progression of Togaviridae?
infection --> repl in muscle/fibroblasts --> viremia w/ CNS invasion --> neuron destruction
35
Symptoms of Togaviridae?
1. fever x2wks 2. Dizziness + Incr LOC 3. Encephalitis w/ coma --> death
36
Structure of Bunyaviridae?
Enveloped, spherical particles with segmented (2-3), single-strand, negative-sense RNA genomes
37
Types of Bunyaviridae causeing CNS infections?
a) California encephalitis virus | b) La Crosse encephalitis virus
38
Location of replication of Bunyaviridae?
exclusively in the cytoplasm | mRNAs are not spliced
39
MC cause of rboviral-induced pediatric encephalitis in the U.S.? Symptoms?
LaCrosse virus seizures and focal neurological signs
40
Structure of Rhabdoviridae?
Enveloped, nonsegmented, negative-strand RNA viruses | "bullet-shaped"
41
Human disease-causing genera of Rhabdoviridae?
Vesiculoviruses --> vesicular stomatitis virus Lyssaviruses --> rabies virus
42
Replication/dissemination of Rhabdoviridae?
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
During the final stages | of the disease, Rabies Virus is found replicating in high concentrations in:
the salivary glands | Efferent nerves transport virus to the submaxillary salivary glands
44
Primary mechanism of Rabies spread?
saliva (animal bite) | open wound
45
Prognosis of untreated Rabies?
death
46
Once infected, Rabies virus predominates in:
neurons of the limbic system, midbrain, and hypothalamus.
47
Phases of Rabies symptoms?
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
Trx of Rabies?
washing of the wound instillation of wound with human anti- rabies Ig administration of multiple doses of inactivated vaccine (thigh or deltoid)
49
Why is vaccination an effective trx?
long incubation period
50
Structure of arenaviridae?
- Enveloped - Contain 2 ambisense RNA segments (encoding 4 proteins) - Often contain host cell ribosomes
51
Cell entry of arenaviridae?
pH-dependent pathway following endocytosis
52
Replication of arenaviridae?
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
Transmission of arenaviridae?
inhalation of aerosolized virus from rodent excreta and saliva
54
Progression of Lymphocytic choriomeningitis virus infection?
1. ever, headache, nausea, and vomiting which coincides with viremia 2. aseptic meningitis usually begins about 10 days later
55
Possible side-effect of Lymphocytic choriomeningitis virus infection?
sudden-onset deafness can occur during the meningeal phase
56
Neurologic complications occur in __% of AIDS patients
40
57
Direct neuro effects of HIV inf?
- Acute aseptic meningitis (at seroconversion) - Chronic meningitis - HIV dementia complex - Vacuolar myelopathy - Peripheral neuropathy - Cranial neuropathy - Inflammatory myopathy
58
Indirect neuro effects of HIV inf?
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)