Brainscape's Knowledge GenomeTM

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


See full index

Neurology Micro > Viral Infections > Flashcards

Viral Infections Flashcards

1
Q

T or F. Bacterial Meningitis is more common than viral meningitis

A

False

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

What are predictors of bacterial meningitis?

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

What normally happens w/ viral meningitis?

A

usually self-limited w/ complete recovery in 7-10 days. A partially treated bacterial meningitis can present similarly to viral meningitis.
- generally resolves w/ out significant neurologic sequalae

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

What type of patients are generally not considered to be encephalopathic

A

Those that don’t appear extremely ill. Normal pts usually have fever, malaise, headache, neck stiffness, low back pain usually overshadowed by headache

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

What are the common causes of viral meningitis?

A
  1. 80% -Enterovirus such as Echo, Coxsackie, and Enterovirus
  2. 10% - attributed to Mumps w/out MMR vaccine
  3. recurrent aspetic meningitis usually due to HSV2, HIV, and VZV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are causes of viral encephalitis?

A
  1. 30% - Arborviruses
  2. 23% - Enteroviruses
  3. 27% - HSV 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

vectors for Arborviruses?

A

Mosquitos or ticks - strong seasonality, most often affects elderly and young kids

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

When do enteroviruses usually cause problems?

A

present as epidemics via URI or GI infections

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

DDx for viral encephalitis

A 
bacterial meningitis
fulminant TB or fungal meningitis
RMSF, Lyme dz
Brain abscess
Postinfectious or post-vaccinial immune mediated
Bacterial endocarditis
CNS vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where is a common site of damage w/ HSV encephalitis

A
  • temporal lobe
  • MRI findings of necrosis in temporal lobe
    RBCs in CSF = sign of necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What provides definite dx of HSV encephalitis

A

PCR but false negatives can occur

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

What is crucial to know about HSV encephalitis

A
  • curable if treated early w/ acyclovir but devastating if treatment is delayed (70% morality w/out treatment)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

micro details of Flavivirdae

A

Small, enveloped, nonsegmented, positive strand RNA virus

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

What are examples of Flavivirdae

A
  1. Flaviviruses - St Louis Encephalitis, West Nile, Japanese encephalitis
  2. Pestiviruses - cow, pig, and sheep pathogens
  3. Hep C virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the replication cycle for Flavivirdae?

A
  1. entry via R- mediated endocytosis and nucleocapsid is delivered into cytoplasm following pH dependent fusion event
  2. genomic RNA translated by host ribosomes to make single polyprotein which is then cleaved cis and trans via proteases
  3. viral polymerase replicates genomic RNA
  4. Structural proteins assemble genomic RNA into virions, which bud into ER or Golgi and enveloped viruses released during transport at cell surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how are flaviviruses transmitted

A

insect vectors, humans aren’t primary hosts

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

How do Arboviruses reach target organ?

A

initially replicate at site of inoculation (endothelium or epithelial cells surrounding bite site) and establish transient primary viremia

  • replicates in reticuloendothelial system 3-7 days post exposure. Most infections don’t progress beyond this point.
  • if infection is not controlled by immune responses then secondary viremia ensues and leads to systemic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 3 clinical syndromes w/ St Louis Encephalitis

A
  1. Febrile headache
  2. Aseptic meningitis
  3. Encephalitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the incubation period of St Louis Encephalitis

A

4-21 days
- onset characterized by malaise, fever, headache, sore throat or cough – followed by acute or subacute meningeal/neurologic signs 1-4 days after

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

What is the outcome of St Louis Encephalitis

A

50% of pts w/ fatal infections die w/in 1 week of onset
80% die w/in 2 weeks
fatality rate is low
- no vaccine or antivirals
- most effective means of control is reduction of mosquito vector population

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

What is the transmission cycle of West Nile virus?

A

Mosquitoes (Culex sp) take blood meal from infected birds.

  • virus localizes in salivary glands of mosquito
  • only 1% of those infected get severely ill
22
Q

What usually happens w/ West Nile virus infxn?

A

relatively mild symptoms including febrile headache, myalgia, and at time skin rash and swollen lymph nodes

23
Q

What are some severe symptoms of West nile virus

A
  1. severe headache w/ high fever
  2. neck stiffness, muscle weakness
  3. stupor, disorientation, convulsions, tremors
  4. coma, paralysis, and rarely death
24
Q

What is the typical treatment for West Nile virus

A

supportive therapy - hospitalization, IV fluids, respiratory support

25
Q

Micro details for Togaviridae

A
  • small, enveloped, nonsegmented, positive strand RNA virus
26
Q

What are the 2 genera for Togaviridae

A
  1. Rubiviruses - Rubella

2. Alphaviruses - western equine encephalitis, EEE, VEE

27
Q

What is the spectrum of alphavirus disease?

A

Can go from Asx to undifferentiated febrile illness to devastating encephalitis.

  • dependent on dose and age of individual
  • initially virus replicates in muscle and fibroblasts of numerous organs
  • low level viremia then occurs (w/in 24 hrs) w/ simultaneous invasion of CNS leading to destruction of neurons
28
Q

What are symptoms of Alphavirus infxn

A
  • fever for 2 wk, abrupt onset of encephalitis characterized by fever, dizziness, increasing loss of consciousness
  • become comatose and die w/in 1st few days of hospital but incidence is quite low
29
Q

How can alphaviruses be treated

A

no vaccine for humans

30
Q

Micro details of Bunyaviridae

A
  • enveloped, spherical particles w/ segmented, SS and negative RNA
31
Q

What are specific viruses of Bunya that cause CNS diseases in human

A

California encephalitis virus

La Crosse encephalitis virus

32
Q

What is the replication strategy of Bunya

A
  • like other negative strand RNA viruses except genes are found on 2-3 separate RNA segments
  • like influenze, except replication occurs only in cytoplasm — mRNAs aren’t spliced
33
Q

What is the MCC of arboviral-induced pediatric encephalitis in the US

A

LaCrosse Virus

  • produces seizures and focal neurologic signs manifested in kids w/ low mortality rate
  • no vaccine available
34
Q

Micro details of Rhabdoviridae - Rabies virus

A

enveloped, nonseg, negative strand RNA

- characteristic bullet shaped morphology

35
Q

What are the types of Rhabdoviridae

A
  1. vesiculoviruses - vesicular stomatitis virus and related virus
  2. Lyssaviruses - rabies virus and related virus
36
Q

What is the replication cycle for Rhabdoviridae

A

same as paramyxoviruses except they enter cell in pH dependent manner following endocytosis (single glycoprotein)

37
Q

Why does Lyssavirus cause slow progressive disease that involves the CNS? (rabies)

A
  • due to specific neurotropism of rabies
  • replication only in neuronal cells but once it reaches the brain it is disseminated to other organs
  • virus found in high [ ]s in salivary glands during final stages of disease
  • uniformly fatal is post-exposure treatment is not administered
38
Q

Incubation period of Lyssavirus

A
  • usually long but can be as short as 1 week

- depends on bite site and proximity to CNS

39
Q

What happens to rabies virus after a bite

A
  • enters muscle and replicates locally
  • transported through peripheral sensory nerves to spinal ganglia and replicates and travels up to spinal cord to brain
  • virus predominates in neurons of limbic system, midbrain, and hypothalamus
  • efferent nerves transport virus to submaxillary salivary glands and replicates in high concentrations
40
Q

What is the prodrome period of Rabies?

A

2-10 days after exposure

  • symptoms mild and nonspecific (malaise, chills, fever, headache)
  • specific early symptom is abnormal sensations around bite site (itching, burning, numbness)
41
Q

What is the acute neurologic phase of rabies?

A
  • nervous system dysfunction (anxiety, agitation, paralysis, episodes of delirium)
  • hyperactivity = furious rabies
  • paralytic or dumb rabies
  • common sign is hydrophobia –> caused by exaggerated gag or respiratory tract protective reflex
42
Q

What is the coma phase of rabies?

A
  • after 2-7 days following acute neurologic phase and can last from 3-30 days
  • death typically follows from respiratory arrest
43
Q

What is the usual rabies treatment?

A
  1. postexposure prophylaxis - wash wounds, instillation of wound w/ human anti rabies Ig and admin of multiple doses of rabies vaccine
  2. Vaccine if effective due to long incubation period - all are inactivated vaccine
  3. control measures aimed at herd immunization of animal vector - either recombinant vaccinia virus or recombinant adenoviruses
44
Q

Micro detail of Arenaviridae

A

LCMV

  • enveloped, segmented, ambisense RNA
  • virion contain 2 RNA segments encoding 4 proteins
  • virions often contain host cell ribosomes
45
Q

Arenaviridae replication scheme

A
  • pH dependent pathway following endocytosis
  • following uncoating transcription and replication occurs by nonconventional ambisense strategy
    1. genome 1st used as template for transcription. NP and L mRNAs produced from either L or S RNA segment
    2. polymerase produces full length antigenome
    3. positive sense antigenom used to make glycoprotein mRNA
    4. virus particles then assembled and releases from cell surface by budding
46
Q

How are Arenaviridae transmitted?

A
  • inhalation of aerosolized virus from rodent excreta and saliva
  • no current vaccines
47
Q

What are the 2 phases of arenaviridae (LCMV)

A
  1. prodrome of fever, headache, N/V - all coincides w/ viremia
  2. Aseptic meningitis begins 10 days later
  3. most recover w/out serious neurologic problems but sometimes sudden onset deafness can occur during meningeal phase of disease
48
Q

What are the direct effects of neurologic complications of HIV

A 
acute aseptic meningitis
chronic meningitis
HIV dementia complex
Vacuolar myelopathy
peripheral myelopathy
cranial neuropathy
inflammatory myopathy
49
Q

What are the indirect effects of neurologic complications of HIV

A

due to immunosuppression

  • opportunistic infections
  • toxoplasmosis
  • cryptococcal meningitis
  • TB
  • JC virus –> progressive multifocal leukodystrophy
  • CMV encephalitis
50
Q

What are cancers associated w/ HIV

A

Primary CNS lymphoma

Metastatic Kaposi’s sarcoma (rarely goes to brain)

Neurology Micro (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions