From encounter to disease - Bacteriology II Flashcards

This deck contains the pneumococcal vaccine lecture and the nasal carriage of S.Aureus

1
Q

Which two kinds of S.pneumoniae vaccines are there?

A
  • Whole cell vaccines
  • Polysaccharide vaccines
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2
Q

Disadvantage of polysaccharide vaccines

A
  • Not effective in kids < 2 years old
  • Do not generate a T cell response
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3
Q

Why are polysaccharide vaccines not effective in kids <2 years old?

A

B cells under the age of 2 really need T cell help to do anything

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4
Q

Why do polysaccharide vaccines don’t elicit a T cell response?

A

It’s a sugar instead of a protein:
- No generation of peptides –> no presentation to T cells

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5
Q

What does the pneumococcal conjugate vaccine consist of?

A

10 or 13 different purified capsular polysaccharides conjugated to carrier proteins

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6
Q

What are examples of carrier proteins?

A

Diphteria toxoid, tetanus toxoid or Haemophilus influenzae protein D

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7
Q

Which vaccine is recommended for elderly?

A

PPV23

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8
Q

What does aluminum phosphate do in the pneumococcal vaccine?

A

T helper cell 2 (Th2) adjuvant –> to increase
antibody response

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9
Q

Describe the mechanism of protection of PPSV

A
  • Polysaccharide binds to BCR
  • Differentiation into plasma cells
  • No production of memory B cells
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10
Q

Describe the mechanisms of protection of PCV?

A
  • Polysaccharide + protein antigen bind to BCR
  • Polysaccharide specific B cell generates antibody- AND memory response
  • Protein antigen can be presented to T cell –> T cell help
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11
Q

What is opsonophagocytosis?

A

Antibody-complement-mediated phagocytosis

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12
Q

Limitation of current pneumococcal vaccines (3)

A
  • Protection against a limited number of serotypes
  • Designed and based on prevalence in US and Europe
  • Expensive and complex
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13
Q

Name the requirements of an improved vaccine (5)

A
  • Broadly protective
  • Affordable
  • Target groups
  • Reduction of carriage
  • Identify conserved proteins required for colonization
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14
Q

What are the three routes of administration?

A
  • Parental
  • Intranasal (mucosal)
  • Oral (mucosal)
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15
Q

For what kind of infections are oral vaccinations used?

A

Infections that infect us in the GI-tract

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16
Q

What are factors you have to take into account about mucosal (intranasal) vaccines? (3)

A
  • Provides local and systemic immunity
  • Prevents disease and infection
  • Asymptomatic colonization causes natural immunization
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17
Q

Which antibody is involved in the opsonophagocytosis?

A

IgG, IgM, complement

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18
Q

Which antibody is involved in blocking the interaction with the epithelium?

A

IgA

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19
Q

Which antibody is involved in agglutination?

A

IgG

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20
Q

Describe Th17 T cell immunity against colonizing pneumococci

A
  • Th17 cells below the epithelial surface secrete IL17A
  • Recruiting/secreting AMPs, neutrophils, IgA –> killing/clearance of pneumococci
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21
Q

Why is it important to vaccinate mucosally?

A

You want to have memory T cells

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22
Q

Delivery systems: efficacy of intranasal vaccines depends on immune activation. How? (2)

A
  • Penetration of epithelial barrier
  • Attraction of immune cells
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23
Q

What can be used as particles for delivery during intranasal vaccination? (3)

A
  • Lipids
  • Immune particles
  • Outer membrane vesicles
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24
Q

What are two characteristics of OMVs?

A
  • Contain multiple PAMPs
  • Possibility for surface display of antigens
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25
Q

What is the advantage of using OMVs?

A

Antigen delivery and adjuvanticity combined

26
Q

Name examples of virulence factors of S. Aureus (4)

A
  • PVL
  • TSST
  • Exfoliate toxins
  • Enterotoxins
27
Q

What causes toxic shock syndrome?

A

Enterotoxins (superantigen)

28
Q

What is a superantigen?

A

A molecule that is able to elicit T-lymphocyte responses by circumventing normal antigen processing and presentation functions

29
Q

How can viral-bacterial co-infections occur?

A

Influenza damages your lung epithelium, upon which bacterial co-infections can occur

30
Q

Which bacteria are often involved in viral-bacterial co-infections?

A
  • Pneumococcal
  • S. Aureus
31
Q

True or false: “S. Aureus can be tackled with antibiotics”

A

False. S. Aureus is resistant to all antibiotics

32
Q

Which kind of S.Aureus strains can you encounter?

A
  • Community-acquired MRSA
  • Methilicin resistant SA
  • Vancomycin resistant SA
33
Q

Where can S. Aureus be found in the body?

A

General population:
Nasal carrier: majority in the nose

34
Q

Describe the nasal carriage rate vs. age

A

7 min

35
Q

Where is S. Aureus located if you are a nasal carrier? Why?

A

Border of your skin and nasal mucosa. This is because of how the setup of the epithelium is.

36
Q

What happens if you eradicate S. Aureus from the nose?

A

It will disappear from other sites as well

37
Q

What happens if you eradicate S. Aureus from the nose in a hospital setting?

A

Clear reduction in endogenous infections in these patients.

38
Q

Replacement?

A
39
Q

Name two kinds of carriage patterns

A
  • Persistent (positive every time you make a nose swab)
  • Non- and intermittent carriers (negative every time you make a nose swab)
40
Q

How many percent of nasal carriers are persistenly colonized with one unique S.Aureus strain?

A

98%

41
Q

How many persistent nasal carriers intermittenly carries a second S. Aureus strain?

A

1 in 6

42
Q

What suggestsa single focus or low-grade persitent carriage?

A

58% of intermittent carriers are colonized with a unique
S. aureus genotype

43
Q

Risk of infection amongst the carrier groups

A

Persistent - risk high

Intermediate/non carrier –> risk lower/risk the same between these groups

44
Q

Intermittent carrier, why?

A

They see a persistent carrier, take up strain from the environment, but loose this strain

45
Q

Name the categories of mechanisms associated with S. Aureus nasal carriage (4)

A

General
Exposure
Adherence
(Evading) immune response

46
Q

Some examples of those categories

A
47
Q

Describe the difference in resistance between non-carriers and persistent carriers

A
  • Non- Carriers seem to be ‘resistant’ to colonization with S. aureus
  • Persistent carriers seem to be ‘resistant’ to colonization with a different strain of S. aureus
48
Q

What could cause this difference?

A

Host Factor or bacterial interference?

49
Q

Describe the association between the proportion of persistent S. Aureus nasal carriage and the fasting serum glucose level

A

The sweeter the environment, the better S. Aureus can adhere

50
Q

What is the role of ethnicity in nasal carriage?

A

Persistent carriage rates vary
between different ethnic groups

51
Q

Which HLA molecule is associated with persistent carriage?

A

HLA-DR3

52
Q

What can be said about the properties of nasal fluid from non-carriers

A

It is bactericidal against S. Aureus

53
Q

Persistent carriers: Name a host factor involved in generating a locally immune suppressed state

A

Nasal secretions lacks antimicrobial activity against S. aureus

54
Q

Persistent carrier: What is the contribution of S. Aureus to staying in the nose?

A

It induces a suppressing interaction with the local immune system

55
Q

Describe the relation between pneumococcal and S. Aureus carriage

A

Inverse relation between pneumococcal- and S. Aureus carriage during age

56
Q

Losing a-virulent bacteria could lead to elimination of S. Aureus from the nose, why?

A
57
Q

What is ecological richness?

A

Diversity of different types in your microbiota

58
Q

What is the level of ecological richness in hospitalized patients? Why?

A

Very much reduced. Treatment/surgery

59
Q

True or False: “Hospitalized patients are less prone to be carrying S. Aureus.”

A

False. Hospitalized patients are more prone to be carrying S. Aureus

60
Q

Which factors are involved in the multifactorial genesis underlying S. Aureus nasal carriage?

A
  • Host/Human
  • Microbe/Microbiota
  • Host-Microbiota interaction