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Neuroscience > Microbiology and Immunology > Flashcards

Microbiology and Immunology Flashcards

0
Q

Which bacteria are the most common causes of bacterial meningitis?

A
  • H. influenza
  • N. meningitidis
  • S. pneumoniae
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1
Q

What is the most common aetiology of meningitis?

A

Viral - usually enterovirus

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2
Q

Why are H. influenza, N. meningitidis and S. pneumoniae the most common causes of bacterial meningitis?

A

They are encapsulated bacteria

Can avoid complement fixation and phagocytosis

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3
Q

What are the most common bacterial causes of meningitis in neonates?

A

Mostly from birth canal:

  • E. coli
  • Klebsiella
  • Group B strep
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4
Q

What is the pathogenesis of bacterial meningitis?

A
  1. Colonisation of nasopharyngeal mucosa
  2. Invasion of bloodstream
  3. Survival and multiplication
  4. Crossing of BBB
  5. Invasion of meninges and CNS
  6. Increased permeability of BBB
  7. /8. Pleocytosis (abnormal number of cells in CSF) and increased ICP
  8. Release of pro-inflammatory cytokines into CSF
  9. Neuronal injury
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5
Q

What are common symptoms of meningitis in adults?

A
  • Fever
  • Nausea/vomiting
  • Headache
  • Stiff neck
  • Altered mental state
  • Photophobia
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6
Q

What are common symptoms of meningitis in children?

A
  • Fever
  • Irritable/unsettled
  • Refusing food/drink
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7
Q

What are the normal values of CSF?

A

-Pressure 60%

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8
Q

What are the typical values of CSF associated with viral meningitis?

A
  • Normal pressure
  • Clear appearance
  • WCC >100 x 10^6 /L
  • RCC 0
  • Gram stain negative
  • Protein 0.4-1.0 g/L
  • Glucose >60%
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9
Q

What are typical CSF values associated with bacterial meningitis?

A
  • Pressure >150 mm H2O
  • Cloudy appearance
  • WCC >1000 x 10^6
  • RCC positive
  • Protein > 1.0 g/L
  • Glucose <40%
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10
Q

What are typical CSF values associated with TB infection?

A
  • Pressure > 150 mm H2O
  • Cloudy appearance
  • WCC >100 x 10^6
  • RCC 0
  • ZN stain positive
  • Protein 1.0-5.0 g/L
  • Glucose <30%
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11
Q

Why must CSF analysis for suspected meningitis be conducted immediately?

A

CSF cell counts rapidly decline due to cell lysis

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12
Q

Why must CSL values be obtained multiple time?

A

Initial CSF values cannot distinguish between bacterial and viral meningitis

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13
Q

What is the treatment plan for meningitis?

A
  • Resuscitation/life support
  • Fluids
  • Antibiotics
  • Steriods
  • Contact prophylaxis
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14
Q

What are possible complications of bacterial meningitis?

A
  • Cognitive deficits
  • Seizures
  • Hearing loss
  • Motor deficits
  • Visual disturbances
  • Behavioural problems
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15
Q

How do encephalitis compare to meningitis?

A
  • Encephalitis is inflammations of the brain due to direct invasion of the parenchyma while meningitis is inflammation of the meninges
  • Encephalitis almost always has a viral aetiology (HSV) while meningitis can be caused by viral or bacterial infection
  • Patients tend to present with an altered conscious state due to brain parenchyma involvement whereas patients with meningitis have normal conscious state since the brain isn’t affected
  • Usually tx of encephalitis is with acyclovir
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16
Q

What is a neurotropic virus?

A

Capable of replicating in nerve cells

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17
Q

What is a neuroinvasive virus?

A

Capable of entering or infecting the CNS

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18
Q

What is a neurovirulent virus?

A

Capable of causing disease within the CNS

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19
Q

What is primary viral encephalitis?

A

Direct viral infection of the spinal cord and brain

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20
Q

What is secondary encephalitis?

A

Post-infectious encephalitis: results from complications of a current viral infection in which virus spreads to the brain

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21
Q

What is the main cause of viral meningitis?

A

Enterovirus

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22
Q

What are common causes of viral encephalitis?

A
  • HSV 1 and 2
  • Rabies virus
  • Arbovirus
  • Enterovirus
  • Mumps virus
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23
Q

What pathology is associated with post-infectious encephalomyelitis?

A

Inflammation and demyelination - possibly autoimmune

No virus present

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24
Q

What is Guillan-Barre syndome?

A

Acute inflammatory demyelinating disease following viral infection
Often results in reversible partial or total paralysis
Does not require an active infection

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25
Q

What is Reye’s syndrome?

A

Post-infection with influenza or chickenpox in children
Cerebral oedema but no inflammation
Associated with administration of aspirin for fever

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26
Q

How might a virus spread to the brain?

A
  • Viruses may travel via axon fibres of peripheral nerves to the CNS (e.g. rabies virus, HSV 1&2)
  • Enter CNS directly via blood stream (e.g. mumps, measles, poliovirus)
  • Via olfactory bulb (e.g. coronavirus, HSV)
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27
Q

How are viruses carried in peripheral nerves?

A

Whole virions or uncoated nucleocapsids carried passively along axons/dendrites

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28
Q

Why are viruses protected from attack by cytotoxic lymphocytes in peripheral nerves?

A

Nerve cells do not display MHC Class I molecules

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29
Q

Where does viral replication take place in a nerve?

A

Replication occurs in the soma because protein synthesis occurs here

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30
Q

What kind of virus is the rabies virus?

A
  • negative stranded RNA virus
  • Helical capsid
  • Enveloped
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31
Q

What is the pathogenesis of rabies infection?

A

Virus in saliva of an infected animal can enter another animal via a puncture wound
Rabies virus replicates in local myocytes and enters peripheral nerve endings
Nucleocapsid can travel into spinal cord
Virus can travel into CNS along via neuronal processes causing neuronal dysfunction
Virus travels along peripheral nerves from the CNS and invates salivary glands
Virus replicates in acinar cells of salivary glands and virus is shed in saliva

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32
Q

T/F rabies virus hides from the immune system in nerve cells

A

False - replication in nerve bodies leads to glycoprotein displayed on the cell surface
Infected cells are targeted by complement and antibodies causing subsequent neuronal death

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33
Q

How long does rabies virus generally take to reach the CNS?

A

60 day window of opportunity to receive vaccination

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34
Q

T/F rabies virus is both highly neuroinvasive and neurovirulent

A

True

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35
Q

T/F alpha herpesviruses are both highly neuroinvasive and neurovirulent

A

False - low neuroinvasiness and highly neurovirulent

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36
Q

What kind of viruses are alpha herpesviruses?

A
  • Linear ds DNA
  • Icosahedral virion
  • Enveloped
37
Q

What is the pathogenesis of HSV?

A

Break in skin or mucous membranes (HSV1: mouth, throat, eyes; HSV2: genital region) allows HSV to enter and locally multiply
Can cause primary disease (10-15%) at the site of infection then enter adjacent nerve endings, migrate along axons to reach trigeminal or sacral ganglia where the virus remains latent
Virus may reactivate and migrate along axons then multiple causing disease recurrence and may eventually cause sporadic encephalitis
OR virus can multiply in regional lymph nodes (80-95%) and result in an inapparent infection which can spread to the blood and distant organs (rare) and may cause sporadic encephalitis

38
Q

What occurs in latency?

A

No structural genes expresses
However latency activated mRNA transcripts (LATs) are expressed
But not protein products identified from LATs

39
Q

What is the pathogenesis of VZV?

A

Infection of conjuntiva or URT mucosa
Virus replicates in regional lymph nodes
Virus spread via blood (primary viraemia)
Replication can occur in spleen and liver
Virus spread via blood (secondary viraemia)
Infection of skin leading to the appearance of vesicular rashes
From the rashes, virus can enter ganglia and become latent
Virus may reactivate, travel to spinal cord and travel along peripheral nerve roots back to the skin causing shingles to particular dermatomes

40
Q

T/F Growth in nerve cells is an obligatory part of the poliovirus lifecycle

A

False

41
Q

T/F Poliovirus is poorly neuroinvasive and highly neurovirulent

A

True

42
Q

T/F Growth in nerve cells is not an obligatory part of herpesviruses life cycles

A

False

43
Q

T/F Growth in nerve cells is an obligatory part of the rabies virus lifecyles

A

True

44
Q

What kind of virus is poliovirus?

A
  • Positive-stranded RNA virus
  • Icosahedral capsid
  • Non enveloped
  • Member of enterovirus genus
  • cytocidal
45
Q

What is the pathogenesis of poliovirus?

A

Virus is ingested and reaches GALT
Virus invades the gut and replicates (can be excreted into faeces)
Virus travels to regional lymph nodes and replicates
Virus travels into blood (plasma viraemia) and can cross the BBB
Virus replicates in anterior horn cells
(If invades CNS, total paralysis may ensue)
Subsequent neuronal damage and death causing paralysis

46
Q

Which virus does not require growth in nerve cells as part of life cycle?

A

Poliovirus

47
Q

Which virus affecting the CNS is a negative stranded RNA virus?

A

Rabies virus

48
Q

Which virus affecting CNS does not have an envelope?

A

Poliovirus

49
Q

Which virus affecting the CNS has a helical capsid?

A

Rabies virus

50
Q

Which viruses have a linear dsDNA genome?

A

Alpha herpesvirusess (HSV 1&2, VZV)

51
Q

Where does central tolerance occur?

A

Thymus -T cells

Bone marrow -B cells

52
Q

Where does peripheral tolerance occur?

A
  • Secondary lymphoid organs

- Peripheral tissues

53
Q

What are the mechanisms implemented to induce tolerance?

A
  • Delete
  • Anergize
  • Ignore
  • Regulate
54
Q

How does a mature B cell become clonally ignorant during central tolerance?

A

If a B cell has LOW-AFFINITY interactions with self-antigen, antigen might bind with one Fc receptor but affinity is too low to allow cross-linking and activation of the B cell.
B cell will be allowed to mature but because of the low affinity interaction it has with self-antigen, this B cell can never be trigger

55
Q

How does a B cell become anergic during central tolerance?

A

Serum proteins in the circulation (soluble self molecules) may be able to trigger inappropriate activation of immature B cells even if cross-linking is inefficient. Since these B cells can be activated, they are turned off.

55
Q

How does deletion of immature B cells occur during central tolerance?

A

Multivalent self-molecules may be expressed on cell surfaces and can efficiently cross-link with Fc receptors on immature B cells. Because of the efficient activation of the B cell, apoptosis is induced.

56
Q

What signals are necessary for a mature B cell to respond and survive?

A
  1. Surface ligation of Ig receptor with antigen at B cell surface leading to cross-linking
  2. T cell help is necessary for affinity maturation and differentiation
57
Q

What happens during the double negative thymocyte stage in T cell development?

A

The double negative thymocyte (DN) is committed to T cell lineage but it doesn’t yet express co-receptors.
At this stage, the beta chain is rearranged.
If the cell is functional after rearrangement, the cell is then committed to the double positive stage in which the alpha-chain-beta-heterodimer receptor (TCR) is expressed

58
Q

What is the main mechanism by which T cells are deleted?

A

If T cell reacts too well to self MHC and self peptides, it is negatively selected during the double positive thymocyte stage.

59
Q

What are the selection processes that double positive thymocytes undergo following expression of a TCR?

A

Positive and negative selection

60
Q

What is the process of positive selection?

A

Thymocytes which express TCRs that are capable of recognising self-MHC with some affinity are selected to survive.
If a double positive (DP) thymocytes isn’t able to recognise self-MHC, death from neglect occurs

61
Q

What is the Goldilocks theory?

A

T cell selection is dependent on receptor affinity for self protein MHC:
If there insufficient interaction between T cell and MHC, no positive selection occurs and the cell dies by neglect.
If there is low-intermediate interaction between immature T cell and self-MHC, it is positively selected.
If the T cell has high affinity for self-MHC, it is negatively selected and apoptosis is induced.

62
Q

What controls the expression of tissue specific self-antigens in the thymus?

A

Tissue-specific antigens expressed in thymic epithelial cells are under the control of AIRE (autoimmune regulator of expression) transcription factor

63
Q

Where is AIRE expressed and what does it do?

A

It is uniquely expressed in medullary epithelial cells of the thymus.
It can randomly distribute itself wherever DNA is accessible and non-specifically turn on gene-expression

64
Q

What is a possible consequence of a defect in AIRE?

A

Defects lead to failure of negative selection from some antigens which results in autoimmunity

65
Q

How is T cell tolerance to tissue specific antigens (e.g. pancreatic tissue antigens like insulin) induced?

A

AIRE can turn on gene expression of tissue specific antigens so that these antigens are expressed in the thymus by medullary epithelial cells. These peptide antigens will be processed and presented by resident dendritic cells in the thymus to immature T cells. If an immature thymocyte sees the self-antigen, apoptosis will occur.

66
Q

Where does anergy occur for T cells?

A

Peripheral tissues

67
Q

Where does anergy for B cells occur?

A

Bone marrow

68
Q

What is the mechanism of T cell anergy?

A

Normally, activation of T cells requires 3 signals:

  • TCR recognises MHC+peptide (signal 1)
  • Co-stimulatory molecule on T cell interacts with receptor on APC
  • Co-stimulatory molecule on APC (upregulated when APC recognises PAMPs) interacts with receptor on T cell

Since there are no PAMPs associated with self-antigen, APC does not upregulate co-stimulatory molecules. So when an APC presents self-peptide to immature T cell, there is no co-stimulatory signal and the T cell is inactive.

69
Q

What transcription factor is associated with the expression of Tregs?

A

foxp3

70
Q

What is the role of Tregs?

A

Suppression of all TH responses and CD8 responses

Involved in tolerance and attenuating inflammatory responses

71
Q

What immunosuppressive cytokines do Tregs secrete?

A

IL-10 and TGF-beta

72
Q

What are nTregs?

A

Derived from thymus during T cell development

73
Q

What are iTregs?

A

induced following the activation of naive CD4 T cells in the presence of TGFbeta

74
Q

How do iTregs inhibit T cell activation?

A

Tregs express CTLA4 which competes with CD28 for B7 (CD80/86) on dendritic cells.
High levels of CTLA4 expressed on the surface of Tregs inhibit naive T cell activation by preventing co-stimulation

75
Q

What are the 3 components of autoimmune disease?

A
  • Genetic susceptibility
  • Environmental factors (e.g. stress and malnutrition)
  • Loss of self-tolerance
76
Q

Why can we have some autoreactive lymphocytes circulating that aren’t activated?

A
  • Antigen may not be available (e.g.immunologically privileged sites such as eye)
  • Absence of signal 2
  • Might have autoreactive B cells but no autoreactive T cells to a particular antigen
77
Q

Why are viral infections thought to trigger autoimmune diseases?

A

During infection/inflammation, damaged tissues can create an environment that promotes lymphocyte activation by releasing co-stimulatory molecules and self-antigens (DNA/nuclear associated proteins). Self-reactive B cells in periphery respond to tissue antigens. If CD4 T cell is also self-reactive, it can help self-reactive B cell affinity maturation and differentiation. Autoantibodies are then generated

78
Q

What are the consequences of a defect in AIRE gene?

A
  • Decreased central tolerance
  • Multi-system autoimmunity
  • “APECED”
79
Q

What are the consequences of a defect in Foxp3?

A
  • “IPEX”
  • Loss of Tregs
  • Loss of peripheral tolerance
  • Multi-system autoimmunity
80
Q

What is type III hypersensitivity?

A

Immune complex deposition

81
Q

What is type II hypersensitivity?

A

Autoantibodies

82
Q

What is are examples of type II hypersensitivities (B cell-mediated autoimmunity)?

A

Graves’ disease - stimulatory antibodies to TSH receptor

Myasthenia gravis - inhibitory antibodies to ACh receptor

83
Q

What autoimmune disease is an example of type III hypersensitivity?

A

Systemic lupus erythematosus (SLE)

Damage to kidney caused by immune complex deposition

84
Q

What is IDDM?

A

Organ specific, T cell mediated autoimmune disease

Destruction of pancreatic beta cells resulting in the loss of insulin secretion

85
Q

What haplotypes are associated with IDDM?

A

HLA DR3-DQ2 and HLA DR4-DQ8

86
Q

What is multiple sclerosis?

A

Organ-specific, T cell mediated autoimmune disease
Degenerative disorder of CNS:
CD4 T cells target myelin antigens
Th1 and Th17 responses implicated (IFNgamma and IL-17)
Associated with dysregulation of Tregs

87
Q

Which haplotypes are associated with MS?

A

HLA-DR15 and HLA-DQ6

88
Q

What is the role of infection in initiating autoimmune disease?

A

Microbes may infect dendritic cells that are presenting self-antigens
TLRs are triggered and co-stimulatory molecules are upregulated
CD4 T cells are now able to provide necessary help for adequate B cell activation

89
Q

What is the role of molecular mimicry in autoimmune disease?

A

Antigens from pathogens may be similar in shape to autoantigens
These antigens are able to cross react with autoreactive T and B cells
e.g. rheumatic heart disease (M protein of S. pyogenes is similar to proteins on myocytes)

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