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Immunology > Scientific Basis of Vaccines > Flashcards

Scientific Basis of Vaccines Flashcards

1
Q

What is variolation?

A

Variolation (with variola minor) and Vaccination (vaccinia) - taking scabs from mild disease and inoculating people

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2
Q

What are the scientific principles learnt about vaccines from Jenner’s experiments?

A
  1. Challenge dose – proves protection from infection
  2. Concept of attenuation
  3. Concept that prior exposure to agent boosts protective response
  4. Cross-species protection – antigenic similarity
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3
Q

How was smallpox eradicated?

A
  • Vaccination programmes
  • case finding (surveillance)
  • and movement control
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4
Q

Why was smallpox eradication possible?

A
  1. No subclinical infections (mild / full blown)
  2. After recovery, the virus was eliminated - no carrier states
  3. No animal reservoir
  4. Effective vaccine (live vaccinia virus)
  5. Slow spread, poor transmission
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5
Q

What is a vaccine?

A

Material from an organism that will actively enhance adaptive immunity

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6
Q

How do vaccines provide immunity?

A

Produces an immunologically “primed” state that allows for a rapid secondary immune response on exposure to antigen - drives T cell memory

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7
Q

What is the role of vaccines?

A

Prevention of DISEASE not infection

  • can’t stop people getting infected but can stop disease symptoms occurring
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8
Q

How do we achieve long lasting immunity with vaccines?

A

Long lasting - requires immunological memory

Antibodies and/or T cells (humoral and cell mediated immunity)

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9
Q

What are the aims of vaccines?

A
  • Protection of the individual: ↓rate/severity
  • Protection of the population: Herd Immunity
  • Eradication of disease
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10
Q

What factors determine eradication of a disease?

A

Eradication requires balance between the epidemic risk to individuals and a population

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11
Q

What is the am of the rubella vaccine?

A

Rubella: a mild disease. Aim is to prevent congenital damage, not protect population

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12
Q

How is immunity memory maintained?

A

Herd Immunity memory boosted by periodic outbreaks of disease in community and vaccines

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13
Q

Why are booster vaccines required?

A

As disease rates decline - no natural boosting

Increases importance of vaccination uptake rates

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14
Q

Outline the risks and benefits of vaccination against measles

A

Infection Complications

  • 1/15 pneumonia, otitis media, bronchitis
  • 1/5000 encephalitis (15% mortality)

Vaccination Damage

  • 1/1000 fever/convulsions
  • 1/400,000 meningo encephalitis
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15
Q

What are the risks and benefits of vaccinating against diphtheria?

A

Infection Complications
- 5% mortality

Vaccination Damage
- Occasional swelling

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16
Q

Outline the risks and benefits of the whooping cough vaccination

A

Infection Complications

  • 0.1% mortality
  • frequent pneumonia

Vaccination Damage
- 1 / 600,000 encephalopathy

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17
Q

What are the different types of active immunity?

A
  • Innate / Adaptive (Cell Mediated Immunity; antibodies)
  • Natural exposure (carriage)
  • Infection
  • Vaccination

Long effect

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18
Q

What are the different types of passive immunity?

A

Antibody from another source: serum

  • Prophylaxis and/or treatment

Short effect

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19
Q

Describe the primary immune response to antigens

A

Primary exposure 5-7 days → antibody response
2 weeks for a full response
- IgM to IgG switching
- memory B and T cells

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20
Q

How long does a secondary immune response last?

A

Secondary response 2 days for full protective response (prior exposure)

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21
Q

How do we remain protected against pathogens after exposure?

A

Post-exposure immunoprotection due to response vs specific antigens

e. g. surface proteins, polysaccharides, toxins
- good targets for vaccine candidates

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22
Q

What are the general principles of vaccines?

A
  1. Induce correct TYPE of response
    - antibodies / cell mediated
  2. Induce response in RIGHT PLACE
    - mucosal sIgA / systemic
  3. Duration of protection
  4. Age of vaccination
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23
Q

Why are antibody vaccines insufficient for systemic infections?

A

Antibodies aren’t sufficient for systemic infections as they can’t enter host cells or viruses

24
Q

What are the different durations of vaccines?

A

Short-term (travel) antibody sufficient
Long-term memory essential

Boosters - natural (seasonal epidemics; carriage)
- vaccines

25
Q

How does the type of infection effect the duration of the vaccine?

A

long incubation time (systemic) - measles

short incubation time (surface) - cholera

26
Q

How are neonates protected against infection?

A

Maternal antibodies present in neonates for protection

sIgA in milk lasts for ~ 6 months

27
Q

Why are maternal antibody presence in neonates a problem for some vaccines?

A

Problem for live attenuated vaccines e.g. MMR
Virus neutralised by maternal antibody → no protection ∴ need to wait until maternal ab cleared before administering live attenuated vaccines in babies

28
Q

When should young babies first be vaccinated with live attenuated vaccines?

A

Vaccinate > 9 months

But many babies are infected by then in endemic areas

29
Q

What are the different natures of antigens?

A

Monotypic (measles) - get once

Polytypic (flu, gonorrhoea) - multiple

30
Q

What factors make vaccine production difficult?

A

Antigen variation + Genetic diversity makes it difficult to produce vaccinations

31
Q

How do antigens effect the immune system?

A

Most antigens are immunogenic but NOT immuno-protective

Unless their surface components can neutralise the effect of the organism by preventing adherance or neutralizing its toxins

32
Q

What is a live attenuated vaccine?

A

One or more components of a microorganism

e.g. BCG, polio(Sabin), MMR, yellow fever, VZV

33
Q

How is a live attenuated vaccine produced?

A
  • serial passage,
  • low temperature adaptation,
  • recombinant genetics
    ( S.typhi Ty21a; galE + aroA/B/C mutant)
  • selection of natural attenuated strains
34
Q

Why are booster injections given?

A

3 separate doses to overcome strain antagonism and ensure adequate immune response against each type

35
Q

What are the different types of vaccines?

A
  1. live, attenuated
  2. Killed, whole organism
  3. Sub-unit vaccines
36
Q

Name examples of killed, whole organism vaccines

A

e.g. pertussis, flu (old type), polio (Salk type), cholera, HepA

37
Q

What are the considerations of a killed, whole organism vaccine?

A

reactogenicity

boosting required

38
Q

What are subunit vaccines composed of?

A

Individual components

  • proteins
  • toxoids (diphtheria; tetanus)
  • peptides (synthetic)
  • polysaccharide
  • recombinant proteins (cloned into bacteria / yeast)
  • subcellular fractions
  • surface antigens
    e. g. Hep B; Flu H; menB
  • virulence determinant
    e. g. aP-pertussis:- adhesin + toxoid + OMP
39
Q

Describe the effectiveness of polysaccharide subunit vaccines

A

Poor antigens

Conjugated to toxoid + outer membrane protein (e.g. MenC; Hib;)

40
Q

What are the effects of bacterial toxins?

A

Toxin normally causes direct tissue damage and disease e.g. tetanus , diphtheria

41
Q

What is a toxoid?

A

By purifying the toxin and activating it chemically, we produce a toxoid - used in vaccine

42
Q

What is the effect of toxoids on the body?

A

Toxoids neutralise toxins when exposed

43
Q

Why are bacterial capsular polysaccharides poor antigens as vaccines?

A

short term memory

no T-cell immunity

44
Q

Why are bacterial polysaccharides less immunogenic in children <2yrs?

A

Poor IgG2 responses (IgG2 promotes opsonisation

and major recognition of polysaccharides; also B cells less mature)

45
Q

How is bacterial polysaccharides immunogenicity increased?

A

Enhance immunogenicity by protein conjugation with toxoids D/T + outer membrane proteins

46
Q

How does conjugation of bacterial polysaccharides effect the immunogenic response in children?

A

Long lasting immunity and response in children

47
Q

Name examples of conjugated vaccines

A

Neisseria meningitidis Group C MenC vaccine

Haemophilus influenzae Type B Hib vaccine

48
Q

How does conjugtion work?

A

Conjugation links polysaccharide antigen to protein carrier (e.g. diphtheria or tetanus) that the infant’s immune system already recognises in order to provoke an immune response

49
Q

Outline how bacterial polysaccharides act as antigens

A

> poor memory
Polysaccharide binds to B-Cell Receptor, but children <2 recognise PS very poorly ∴ produce v. poor antibodies due to poro recognition and no memory associated

50
Q

How do conjugates act as antigens?

A

> good memory

By linking PS to a protein, the B cell recognises the protein well and will present it to a T cell

51
Q

What is the role of CD4 T cells activated by conjugates?

A

The Th cells recruit cytokines that aid the B cell to produce high affinity antibodies at higher levels - potent response

52
Q

What are adjuvants?

A

Chemical / lipid structures that enhance the immune response using the vaccine components

53
Q

What is the effect of vaccine adjuvants in delivery of immune response?

A
  • enhance immune response to antigen
  • promote uptake and antigen presentation
  • stimulate correct cytokine profiles
54
Q

Name an example of an adjuvant

A

Aluminium salts (Alum)

  • form trapped particles (depot)
  • slow release of Ag
  • large number of Mp’s exposed
55
Q

Outline the features of a live attenuated vaccine

A
  • Long lived immunity
  • Good immune response; IgG, IgA; CMI
  • Requires cold chain
  • Insufficient attenuation
  • Reversion
  • Immunosuppressed; Risk of persistent infection
  • Foetal damage
56
Q

Outline the features of a Killed, whole vaccine

A
  • Short or long lived immunity
  • IgG - needs boosters
  • Poor CMI
  • Stable
  • Inactivation and immunogenicity
  • Contamination
  • toxicity/allergy
  • Autoimmunity

Immunology (14 decks)

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