27 Vaccination Flashcards

1
Q

what is active immunisation

A

Administration of antigen in order to induce active production (takes time to generate response) of immunity and thus protection from disease

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2
Q

what immunity is created following active immunisation

A

specific for antigen given

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3
Q

is immunological memory is induced following active immunisation

A

yes

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4
Q

what does immunity involve for active immunisation

A

AB and/or T cell responses

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5
Q

what immunity can be induced following active vaccination

A

systemic and/or mucosal immunity

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6
Q

when is the protection in place following active immunisation

A

not immediate

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7
Q

what is the first ever virus eradicated

A

small pox

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8
Q

what is variolation

A

in china - potentially dangerous, scrap the scab and powder it in hope it would act as a protection

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9
Q

what was the cowpox vaccine like

A

not variolation - as not using material from the organism itself

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10
Q

why did the cowpox cure smallpox

A

elicit proteins of cowpox, can bind to smallpox virus and stop it infecting

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11
Q

what is the initial response following infection/vaccination

A

IgM

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12
Q

whay is herd immunity

A

more vaccinated against it in community the harder it is to spread

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13
Q

what are live attenuated vaccines

A

Organisms whose virulence has been reduced e.g. by repeated culture in vitro

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14
Q

what do live attenuated vaccines cause

A

Multiply in host, mimicking natural infection but causing no/mild symptoms
Immune response mimics that generated by natural infection

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15
Q

what are the risks of live attenuated vaccines

A
  • potential for severe infection in immunodeficiency
  • potential to revert to virulent strain
  • storage conditions critical for stability
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16
Q

what immunity is induced following live attenuated vaccines

A

systemic/mucosal immunity

long lasting memory

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17
Q

what is the problem with live attenuated vaccines

A

not suitable/possible for all viruses

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18
Q

examples of live attenuated vaccines

A

MMR

BCG

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19
Q

what is the effect when vaccinated with killed viruses

A

Preparations of whole inactivated virus/bacteria

Don’t multiply in host

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20
Q

what is the immunity induced following killed vaccines

A

Usually only systemic immunity induced

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21
Q

how many doses of live attenuated are required

A

one

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22
Q

how many doses of killed vaccines are required

A

several doses

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23
Q

what is the risk with killed vaccines

A

Large amount of antigen needed – risk of reaction – partly overcome by using adjuvants

  • inactivation process may alter structure
  • not suitable for all organisms
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24
Q

what are the ‘no risks’ with killed vaccines

A

no risk of infection (unless faulty inactivation)
no risk of reversion to virulence
tend to be more stable for storage

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25
Q

examples of killed vaccines

A
killed polio (salk)
influenza
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26
Q

what is the effect mixing an antigen with adjuvant

A

good response

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27
Q

what is the adjuvant mechanisms of action

A
  1. sustained release of antigen at site of infection
  2. upregulation of cytokines and chemokines
  3. cellular recruitment at infection site
  4. increase antigen uptake and presentation to APC
  5. activation and maturation of APC (increased MHC class II and costimulatory molecules expression) and migration to draining lymph nodes
  6. activation of inflammasomes
28
Q

example of adjuvant

A

alum - aluminium hydroxide

29
Q

what happens when alum mixed with killed vaccine materials

A

Triggers NLRP3 inflammasome which turns on inflammatory markers = increase response
Local cytokine production

30
Q

what are subunit vaccines made of

A

Consist of parts of organisms/products of organisms

31
Q

effect after subunit vaccine

A

Immunisation doesn’t mimic natural infection but induces a response which prevents disease

32
Q

what immunity is induced after subunit vaccine

A

usually only systemic immunity induced

33
Q

how many doses are required following subunit vaccine

A

several

34
Q

what is required in subunit vaccine

A

adjuvant

35
Q

what are the ‘no risks’ of subunit vaccines

A
  • no risk of infection
  • no risk of reversion to virulence
  • no unwanted components in vaccine
36
Q

examples of subunit vaccines

A

tetanus toxoid
Hep B
Group C meningococcus

37
Q

examples of subunit conjugate vaccines

A

meningococcal group C vaccine

38
Q

what is the response to polysaccharide antigen conjugated to protein

A

(e.g. Dip toxoid or tetanus toxoid)

seeing polysaccharide not protein of the conjugate, gives T cell help, can get AB that are specific to polysaccharide

39
Q

what is genetic shift

A

genetic reassortment

40
Q

what does genetic shift cause

A
  • pandemics

- cross-species mixing of virus genes

41
Q

what is genetic drift

A

continuous mutational changes

42
Q

what does genetic drift cause

A
  • seasonal/epidemic
43
Q

what is antigenic drift

A

neutralising AB against hemagglutinin block binding to cells –> mutations after epitopes in hemagglutinin so that neutralising AB no longer binds

44
Q

what is antigenic shifr

A

antigenic shift occurs when RNA segments are exchanged between viral strains in secondary host –> no cross-protection immunity to virus expressing a novel hemagglutinin

45
Q

all vaccines - contraindications to immunisation

A
  • acute illness

- severe reaction to previous dose of same vaccine

46
Q

live vaccines - contraindications to immunisation

A
  • pregnancy
  • primary immunodeficiency
  • secondary immunodeficiency e.g. high dose steroids, cancer chemotherapy, HIV infection
47
Q

allergic - contraindications to immunisation

A

Patient known to be allergic to vaccine/component

  • influenza may contain traces of egg protein
  • some viral vaccine contain traces of AB e.g. polymyxin or neomycin
48
Q

what does poliovirus consist of

A

Poliovirus consists of RNA genome enclosed in protein shell capsid

49
Q

how does poliovirus infect

A

oral-faecal route

50
Q

what are the polioviruses that naturally occur

A

wild polioviruses

51
Q

what are the serotypes of wild poliovirus

A
  • type 1
  • type 2
  • type 3
52
Q

how do the wild serotypes of poliovirus differ

A

slightly different capsid protein

53
Q

what % of infected people with poliovirus not show symptoms

A

90

54
Q

what is the route of infection for poliovirus

A

oral-faecal

  • enters body via mouth
  • replicated in intestine
  • shed from body via faeces
55
Q

what is iPV

A

inactivated polio vaccine

56
Q

what is the problems with IPV

A
  • relatively expensive

- little immunity in intestine

57
Q

what is the benefits of IPV

A

extremely safe

58
Q

what is OPV

A

live oral polio vaccine

59
Q

what are the benefits of OPV

A

relatively cheap

good immunity in intestine – stop transmission

60
Q

how is IPV administered

A

injection

61
Q

how is OPV administered

A

orally

62
Q

what are the problems with OPV

A

very safe, can revert to disease-causing form

63
Q

what is OPV trivalent

A

protects against all 3 strains

64
Q

what is OPV bivalent

A

protects against 1 and 3

65
Q

what is OPV monovalent

A

protects against strain 1 or 3

66
Q

which is the least effective OPV

A

trivalent

bivalent = 30% more effective than trivalent
and monovalent more effective than trivalent