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MIIM20002 - Microbes, Infections, Responses > Lecture 22 - S. pneumoniae Vaccination > Flashcards

Lecture 22 - S. pneumoniae Vaccination Flashcards

(66 cards)

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0
Q

What receptors do neutrophils have?

A
  • FcR

* CR (complement receptors)

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1
Q

What receptors do neutrophils have?

A
  • FcR

* CR (complement receptors)

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2
Q

What is the function of NETS?

A

Contain bacteria at the site of infection

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3
Q

What is the makeup of a NET?

A
  • DNA
  • Histoproteins
  • Granule contents
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4
Q

What is the name for the production of NETS?

A

NETosis

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5
Q

What are cathelicidins?

A

Antimicrobial proteins in a neutrophil

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6
Q

Describe what is important about colonial selectin

A

Only the B lymphocyte that has the specific TCR appropriate for the antigen will be selected

Then expansion occurs

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8
Q

Describe the concentration of antibody in the blood over time

A
  • Before immunisation: none
  • First immunisation: rapid increase, then decline to a low number
  • Interim: low number (memory)
  • Second immunisation: more antibody made, more quickly
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8
Q

What is the central principle of vaccination?

A

Vaccination will be the first exposure

When we are exposed to the antigen again, the immune response will be heightened and rapid

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9
Q

Describe the magnitude of e response the second time we are exposed to an antigen

A
  • Greater magnitude

* More rapid response

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11
Q

Describe the differentiation of naive cells after exposure to antigen:
• first immunisation
• second immunisation

A

First: naive differentiates into:
• memory
• effector

Second:
• memory cells differentiate into many more effector cells

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12
Q

Which diseases are caused by S. pneumoniae

A

• Pneumonia

  • Septicaemia
  • Meningitis
  • Otitis media
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13
Q

Why vaccinate against TB?

A
  • Most important pathogen for children under 5
  • Debilitating and permanent sequelae
  • Disease occurs in the healthy as well as the immuno compromised
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13
Q

What is the primary site of replication of S. pneumonia

A

Nasopharynx

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14
Q

What we need to know when making a vaccine?

A
  • Pathogenesis of bacterium
  • Nature of immune response which will give protection (B cell, CD4+, CD8+, IgA?)
  • Ensuring response to antigen is immunogenic, not pathogenic
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15
Q

To where does S. pneumonia disseminate?

A

Ears
Lungs
Blood
Meninges

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17
Q

What does the S. pneumoniae vaccine need to protect?

How do we do this?

A 
IgG:
• Blood
• Meninges
IgA:
• Mucosa
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18
Q

What are the virulence factors of S. pneumonia?

A
  • Adhesins
  • Pneumolysin
  • Capsule (critical for virulence)
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19
Q

Describe the functions of pneumolysin

A
  • cilia inhibition
  • cytotoxic to alveolar / endothelial cells
  • triggers C’ cascade
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19
Q

What are the innate immune functions that allow us to recover from infection?

A

Phagocytes
Spleen
PRRs (TLR2, NOD2)

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20
Q

Why is the capsule virulent?

A
  • Allows the bacterium to survive in the blood
  • Masks underlying structures
  • Reduces efficiency of phagocytosis
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21
Q

What are the adaptive immune responses that lead to recovery from infection

A

Antibodies against capsule

–> opsonisation

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23
Q

Why is the spleen important in recovery?

A

Spleen receives antigens from the blood

It is thus a major site of:
• antibody production
• removal of old cells
• removal of antigens

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23
Q

What happens to people without spleens?

A

Suffer from overwhelming infections, due to lack of antigen and immune complex removal

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24
Describe how immune complexes are removed from the blood
1. In tissue, circulation: • Red blood cells have C3bR which bind complement in the immune complexes RBCs + Immune Complexes circulate to spleen 2. In spleen: • Splenic macrophages express C3bR and FcR • Endocytosis of complexes; removal
25
What will the ideal prophylactic vaccine induce?
IgA (mucosa) | IgG (meninges and blood)
27
What will an ideal theraputic vaccine induce?
Innate and adaptive responses: • splenic macrophages • antibody against capsule
28
Describe the first pneumococcal vaccine
* Whole killed vaccine * Sir Almroth Wright * South African miners * Success questioned
28
How was the whole killed vaccine improved upon?
The whole killed vaccine elicited undesirable reactions They extracted just capsular antigens
29
Describe the vaccine in 1983
Pneumococcal polysaccharide vaccine • just capsular polysaccharide antigens Vaccine contains 23 of the most common serotypes 80% of infection prevented
30
Describe the structure of a native antigen
T cell determinant B cell determinant
31
Describe the effects of vaccination with capsular antigens (1983)
Adults: • 80% effective in immunocompetent • Short lived response (no memory) Elderly, Children, immunocompromised: • Variable / poor response
32
How are B cells activated to produce antibodies
1. Take up, process antigen, present on MHC II 2. Th cell activated by macrophage 3. Th cell activates B cell with presentation of antigen, costimulation and cytokines 4. B cell makes antibodies
33
What is required for isotype switching and high affinity antibodies?
T cell help | --> presentation of antigen on MHC II
35
What does T cell help bring about
Memory High affinity antibody Isotype switching
36
Can we launch an immune response against polysaccharide at all?
Yes
37
Describe how B cells respond to polysaccharide
1. Repetitive antigens 2. Cross linking to receptors on B cells 3. B cells activated NB not T cell help
38
What is produced by B cells that are activated by polysaccharide?
IgM A little IgG
39
Why are highly repetitive polysaccharides required?
Only repetitive sugars can cross link on the B cell receptors Cross linking is required for activation
40
Compare the type of molecule in T cell dependent and T cell independent antigen
TD: protein TI: polysaccharide, lipids, nucleic acids
41
Compare repeating epitopes in T cell dependent and T cell independent antigen
TD: no TI: yes
42
Compare response in infants in T cell dependent and T cell independent antigen Explain this
TD: yes TI: no In infants, the immune system has not yet developed to be able to response to TI antigen
43
Compare isotype switching in T cell dependent and T cell independent antigen
TD: yes TI: no (some IgG)
44
Compare antibody affinity in T cell dependent and T cell independent antigen
TD: high TI: low
45
Compare memory in T cell dependent and T cell independent antigens
TD: yes TI: no
46
How do we change our antigens so that the vaccine is more effective?
Chemically connect a protein antigen to a polysaccharide antigen Perform conjugation, because T cell reacts to protein B cells react to polysaccharide
47
What is the connection of TD and TI called?
Conjugation
48
What does a B cell do to a conjugate antigen? What is the significance of this?
BCR recognises polysaccharides Takes it up whole thing up Presents the protein on MHC II Now, Th cells can recognise this B cell --> isotype switching, affinity, memory
49
What is the antigen specificity of the antibodies?
The capsular polysaccharide Because the initial B cell receptor recognised the polysaccharide
50
What is the specificity of the T cell receptor?
The protein from the conjugated antigen
51
When were conjugated vaccines first licensed in Australia? Which proteins are used?
2001 By 2005, on the national vaccination program Tetanus toxoid or diphtheria toxoid
52
How many serotypes in the new generation conjugate S. pneumoniae vaccine?
Heptavalent - 7 serotypes Now, 13
53
What are the pros and cons of conjugate S. pneumoniae vaccine?
Pros: - response in children Cons: - expensive
54
What is the result of the conjugate vaccine?
Children: 72% efficacy against IPD Adults: Reduced incidence of pneumonia --> if children don't have it, their parents won't New disease, serotype 19A: From serotypes that aren't in the vaccine, esp. 19A
55
What is serotype replacement? Give an example
This is when a non-vaccinated serotype starts to cause the majority of infections For example: 19A infection rate has increased since vaccination was brought in, because it was not in the vaccine
56
Describe the effect of the vaccine on under 2s from 2001 to 2006
Dramatic decrease in IPD Indigenous communities: still have a higher rate of infection than other groups
57
Why was there also a decrease in IPD in elderly when the children were infected?
The children were no longer transmitting the bacteria to their grandparents HERD IMMUNITY
58
What is herd immunity?
This is when vaccinating one group has effects on another group
59
What happened to incidence of IPD due to non 7vPCV serotypes after vaccination?
Increase in incidence Due to serotype replacement
60
Why did the vaccine elicit such a poor response?
The vaccine contained only polysaccharide, not protein. Since there was no antigen presented on MHC, no T cells were activated. Low affinity antibodies, no isotype switching, no memory
61
WHat are some possibilities of new vaccines?
1/ Less antigenic variation - pneumolysin 2/ Protein antigens
62
How is it that B cells can be helped by T cells that recognise an internal part of the antigen?
B cells take up the antigen, degrade it and express the internal antigen on their MHC II. Th cells recognise this with their TCR
63
What does H. influenzae cause in children?
Meningitis
64
Describe the mode of action of the Hib vaccine
(vaccine against H. influenzae type b) • Conjugate vaccine: polysaccharide antigen + toxoid protein • BCR binds polysaccharide • TCT recognises toxoid protein • B cell present toxoid on BCR --> T cell help • high affinity, isotype switching, memory
65
What have been the outcomes in the community since the use of the Hib conjugate vaccine?
Big decrease in incidence of childhood H. influenzae infection
66
What is the protein that is conjugated onto the polysaccharide antigens?
A toxoid: • Diphtheria • Tetanus

MIIM20002 - Microbes, Infections, Responses (32 decks)

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