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I&I WC1 > Organ-specific immunity: BRAIN - Disease > Flashcards

Organ-specific immunity: BRAIN - Disease Flashcards

This deck contains the lectures about viral encephalitis, bacterial meningitis, models to study MS and the immunopathogenesis of MS

1
Q

What is encephalitis?

A

An acute inflammation of the brain parenchyma

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2
Q

What is the most common cause of encephalitis?

A

Viral infection

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3
Q

What are the symptoms of viral encephalitis? (6)

A
  • Fever
  • Headache
  • Behavioral changes
  • Altered level of consciousness
  • Focal neurologic deficits
  • Seizures
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4
Q

Which common human viruses can cause viral encephalitis? (3)

A
  • Predominantly: herpesviruses
  • Rare: Entero/Paramyxoviruses
  • Very rare: influenza viruses
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5
Q

Which zoonotic viruses can cause viral encephalitis? (3)

A
  • Arboviruses
  • Rabiesvirus
  • Nipahvirus
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6
Q

What are the two main routes of viral entry into the CNS?

A
  • Hematogenous
  • Migration via peripheral nerves
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7
Q

Which viruses take the hematogenous entry route into the CNS?

A

Entero- and Arboviruses

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8
Q

Which viruses take the peripheral nerve entry route into the CNS?

A

Herpes- and Rabies virus

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9
Q

What are the three mechanisms of neurovirulence?

A
  • Cytopathic effect
  • Antiviral immune responses
  • Exacerbated immune response due to viral infection of microglia
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10
Q

What is the cytopathic effect of a virus?

A

Direct death of virus-infected neurons

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11
Q

Which viruses cause mild meningitis? (2)

A
  • Enteroviruses
  • Measles virus
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12
Q

Which viruses cause fatal encephalitis?

A
  • Arboviruses
  • Herpes Simplex
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13
Q

What are the major Arbovirus families causing encephalitis? (3)

A
  • Flaviviridae (West-Nile virus)
  • Togaviridae
  • Buyaviridae
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14
Q

Which human herpes viruses are neurotropic?

A

Alphaherpesviruses

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15
Q

Which two clinical manifestations of herpes simplex viruses are there?

A
  • Herpetic stromal keratitis
  • Herpes labialis
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16
Q

Why is getting herpes labialis bad luck?

A

This is an opthalmic branch latency manifestation

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17
Q

What is meningitis?

A

Inflammation (swelling) of the protective membranes covering the brain and spinal cord

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18
Q

Which three divisions can be made when considering meningitis?

A
  • Acute/chronic
  • Infectious/non-infectious
  • Bacterial/viral/fungal/protozoa
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19
Q

Which two pathogens are the predominant causes of bacterial meningitis?

A
  • S. pneumonia
  • N. meningitidis
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20
Q

What are the initial clinical features of acute bacterial meningitis? (5)

A
  • Headache, fever
  • Nausea, vomiting
  • Photophobia
  • Neck stifness
  • Altered mental status
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21
Q

What is petechiae? During which kind of meningitis do you see this?

A
  • Pinpoint-sized spots of bleeding under the skin or mucous membranes
  • N. meningitidis
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22
Q

Describe the immunopathogenesis of community-acquired bacterial meningitis (3)

A
  • Attachment and interaction with nasopharyngeal epithelium
  • Survival in bloodstream
  • Crossing of blood-brain barrier
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23
Q

Which factors affect the intravascular survival of bacteria that cause meningitis? (2)

A
  • Capsule
  • Acquisition of iron from transferrin
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24
Q

What are the most frequent systemic complications of bacterial meningitis? (3)

A
  • Cardiorespiratory failure
  • Hyponatremia
  • Disseminated intravascular coagulation
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25
Q

What are the most frequent neurological complications of bacterial meningitis? (6)

A
  • Cerebrovascular complications
  • Meningo-encephalitis
  • Seizures
  • Hearing loss
  • Brain oedema
  • Hydrocephalus
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26
Q

What are the major intracranial complications in bacterial meningitis? (3)

A
  • Posterior brain ischemia
  • Brain infarction
  • Obliteration cerebral artery
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27
Q

What is the treatment for (suspected) bacterial meningitis?

A

Antibiotics in combination with dexamethasone

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28
Q

What is MS (multiple sclerosis)?

A

Most common inflammatory disease of the CNS

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29
Q

What are risk factors for MS? (4)

A
  • EBV
  • Smoking
  • Vitamin D
  • Genetics/HLA –> especially MHC-II
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30
Q

Which HLA-molecule is mostly associated with development of MS?

A

HLA-DRB1*15:01

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31
Q

How do you diagnose MS? (3)

A
  • Clinical profile (RR-MS or (S/P)P-MS)
  • Cerebral/spinal cord MRI
  • Presence of oligoclonal bands/ increased IgG index supportive
32
Q

How do you treat MS? (3)

A
  • Symptomatic/supportive
  • Disease modifying drugs
  • Steroids
33
Q

What are the three clinical representations of MS?

A
  • Relapsing-remitting MS
  • Secondary-progressive MS
  • Primary-progressive MS
34
Q

What are the characteristics of relapsing-remitting MS?

A

Relapse periods (clinical symptoms) that go away again

35
Q

What are the characteristics of secondary-progressive MS?

A
  • Patients start of with RR-MS
  • Then: less and less of the relapses, more of a steady decline of neurological functions
36
Q

What are the characteristics of primary-progressive MS?

A
  • Patients do not start with RR-MS first
  • A fairly steady, gradual change in functional ability over time without any remissions
37
Q

What are the pathological hallmarks of MS? (3)

A
  • Demyelination –> loss of the myelin sheet
  • CNS inflammation –> influx of peripheral immune cells
  • Neurodegeneration –> loss of axons, synapses and neurons
38
Q

Can you cure MS with a stem-cell transplantation?

A

No

39
Q

Describe the dominant MS phenotypes across for a younger- and older age

A
  • Younger age: mostly attacks of neurological disability –> make new MRI lesions
  • Older people: Not that many attacks, more prominent progression of disability –> very resistant to almost any drug
40
Q

Which different tests can you do across the lifespan?

A
  • Bloodwork
  • Genetics
  • CSF analysis
41
Q

What do you need to bear in mind about post-mortem autopsy?

A

These are performed really at the end of MS –> will not really learn you a lot about how the immune system drives the start of disease

42
Q

Which lesions drive relapsing-remitting MS?

A

New inflammatory lesions in white matter

43
Q

What is EAE particularly suitable for?

A

To study inflammatory white matter lesions

44
Q

What drives axonal degeneration in inflammatory white matter lesions?

A

Influx of extracellular Ca2+ through a leaky membrane

45
Q

What drives progressive MS?

A
  • Brain atrophy
  • Neurodegeneration
46
Q

What drives cortical neurodegeneration in progressive MS?

A
  • Microglial activation
  • Meningeal inflammation
47
Q

Which cells are the central cells in MS?

A

Memory B cells are the niche for MS

48
Q

What is the lymphocyte distribution in the normal blood?

A
  • Mostly CD4+
  • Some CD8+
  • Lots of naïve cells
  • Lots of B cells
49
Q

What is the lymphocyte distribution in the CSF?

A
  • No naive cells in your CNS
  • Central memory cells most prominent in CSF
  • Hardly any B cells found
50
Q

What do T cells in the CNS prevent?

A

Neurotropic viruses

51
Q

Phenotypic adaptations during normal immune surveillance are depend on..?

A

Border organ such as the choroid plexus and meninges

52
Q

Where does the expression of CD69 mostly occur?

A

CSF and white matter

53
Q

What are the three options for the start of an MS-attack?

A
  • Antigens from the periphery
  • Activation of CNS patrolling immune cells
  • Presentation of CNS antigens in the periphery
54
Q

After initiation of an MS-attack, what happens next? (3)

A
  • APC with peptide ends up in cervical lymph node
  • Interaction with naive or memory populations
  • Migrate out of LN Into bloodstream and move to border BB-barrier to infiltrate
55
Q

Disease modifying therapies for MS can act on the sequence of events in the lymph nodes. Describe the sequence of events on which these drugs can act.

A
  • Activation
  • Clonal expansion
  • Migration
  • Depletion
  • Trafficking intro CNS
56
Q

Which event is the most logical target for disease modifying therapies in MS?

A

Depletion

57
Q

Do you see lesions in the grey matter in E-MS?

A

Far less pronounced

58
Q

Which kind of lesions do you see more at the start of MS?

A

Far more white matter inflammation than grey matter inflammation

59
Q

Which three factors mediate the recovery after an MS attack?

A
  • Resolving inflammation
  • Remyelination of lesions
  • Compensation for loss of function - using larger brain networks
60
Q

About ⅘ patients (when they die) still have active lesions in the CNS. Which cells populate these lesions?

A

MHC class II positive cells → not driven by cells infiltrating from the periphery

61
Q

True or False: “Lesions from people with advanced MS show higher numbers of T cells present in the context of these lesions”

A

True. These cells ended up in the PVS once and kept contributing by making pro-inflammatory mediators

62
Q

True or False: “The majority of lesions from people with advanced MS do not contain B cells.” + Explain what this does to the prognosis.

A

False. Many of them do contain B cells, which continuously produce immunoglobulins –> prognostic unfavorable factor.

63
Q

What is a likely driver of the ongoing antibody synthesis during progressive MS?

A

Local interaction of CD4+ T cells and B cells

64
Q

What are the 2 stages of axonal degeneration?

A

1: Focal swelling and 2: fragmentation

65
Q

What is the EAE model?

A

A mouse model in which an autoimmune response is induced against myelin, by injecting myelin protein with immune activators

66
Q

What predicts axonal fate?

A

Ca2+

67
Q

What is the source of increased Ca2+?

A

Extracellular influx

68
Q

What drives cortical pathology?

A

The immune cells in the meninges (meningial inflammation) that stimulate and activate the microglia

69
Q

What is the phenotype of MS2 (MS specific) microglia that is not found in other neurodegenerative diseases?

A

High branching, low homeostatic markers and low inflammatory markers (HLAII low)

70
Q
A
70
Q

What is the CMI?

A

A chronic meningeal inflammation model to study cortical pathology in progressive MS

71
Q
A
72
Q
A
72
Q
A
73
Q
A
74
Q
A

I&I WC1 (25 decks)

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