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Flashcards in lecture 11 Deck (69):
1

what is the tetanus mortality rate?

81%

2

what is the diphtheria mortality rate?

10%

3

how many cases of measles was there in the us?

550,000

4

how many cases of smallpox was there in the us?

30,000

5

what is the Spanish flu?

influenza pandemic

6

when did the Spanish flu happen?

1918-1919

7

how many people did the Spanish flu kill around the world

25 million

8

did the Spanish flu kill more people than WW1?

yes

9

did the Spanish flu kill more people in the US?

yes

10

how does vaccination work (basic answer)

Provoke an immune response without causing an infection
Immunological memory:
- Ability of the immune system to respond quicker and better to pathogens that have been encountered previously
- E.g. bacteria and viruses

11

what are the Key features of Immunological memory:

1. Long lived
2. Maintained in absence of antigen
3. Antigen specific
- As opposed to non-specific antigen immunity  the characteristic of innate immunity
4. Immunological memory is the privilege of adaptive immune system

12

How does Vaccination work?

 Expose the immune system to a less virulent or inactivated pathogen [or killed one]
 Leads to innate immune response [ pathogen recognition receptor – not very specific for a antigen – recognises specific patterns on the surface of pathogen triggering innate immunity through Toll-like receptors]
 If you have a cut – clotting cascade starts to function trying to seal the cut from outside environment
- Neutrophils arrive [ numerous in peripheral circulation – last 48 hours and produced continuously]
- Passing antibodies can neutralize the pathogen

13

what happens after Passing antibodies neutralize the pathogen

- Adaptive immunity happens: split into B and T cells
• Occurs in the lymph node
• APC will phagocytose the pathogen in the context of MHC class I/MHC class II and present it to the nearest lymph node
• Presentation to B and T cells
• It takes 3 weeks to produce antibodies
• Natural B cells produce IgM antibodies [ not of high affinity/specifity]
• Bacteria staphylococcus needs B cell immunity to produce antibodies
• T cell also gets stimulated

14

what happens if you do not have good robust immune response

end up with toxic shock syndrome [over stimulation of T cells through MHC class molecules)

15

B cell memory

by generating B cell memory is the frequency of antigen specific B cell

16

In staphylococcus, how many b cells are found

1 in 10,000 or even less frequency

17

After immunisation how many b cells are found

1 in 100/1000

18

where do be b cells switch their class

-Occurs in the germinal centre [maturation/ somatic hypermutation]

19

in the germinal centre what do b cells switch their class to?

In the germinal centre you go from Igm to igG or igA

20

How sticky the antibody is with target antigen improves?

T cell help: interaction between MHC class II on T cell and CD80/86 on the B cell

21

in the primary response what is the main source of antibodies

IgM

22

what happens during the second exposure of an antigen

After second exposure: you have enough IgG to be used

23

what happens during the third exposure of an antigen

in 3rd exposure: the response is even more quicker and higher

24

what happens after 3 weeks during this response?

After 3 weeks, the IgG starts to be produced

25

what are antibodies produced by?

b-cells / plasma cells

26

what is Neutralisation

Preventing viral entry and actions of bacterial toxins

27

what is Antibody dependent cytotoxicity

- Phagocytes recognise antibodies bound to extracellular pathogens
- Antibodies have Fc receptors
- With one side on the FAB they attach to the pathogen and Fc receptor trigger cells like NK cells and CD8 cells to function as cytotoxic cells
- These cells either phagocytose the target bacteria or produce cytokines that can facilitate the process

28

what occurs during Activation of the classical complement cascade

- Binding of C1q to antibody-antigen complexes
- Some of the antibodies have complement receptors and can activate the complement cascade
- Functions as a general inflammatory response – perpetuate the response by anaphylatoxins C3A and C5A – more B cells goes to the site of infection

29

what is CD4 T helper cell function

CD4 T helper cell which will coordinate all the immune response including B cells

30

in the context of viral infections what do CD8 T cell do

-take up the pathogen and destroy by phagocytosis
-Cytotoxic T cells recognise and destroy infected cells

31

in general what do T helper cells do?

stimulate the immune response of other cells
- Stimulate B cells to produce antibodies
- Activate phagocytes to destroy pathogens they have taken up

32

what do Memory T cells do

Increased frequency of cells (100-1000-fold higher) – first time exposure of the host
-Increased survival characteristics e.g. increase in BCL2

33

can memory t-cells be re stimulated more easily?

yes as the requirement for co-stimulation is much reduced

34

will the response be faster with memory t-cells?

yes

35

does 2nd/3rd exposure require co-stimulation/second stimulation

no

36

what does Costimulation do

The principle of the Costimulation is that it always provokes longer lasting immunity

37

what will CD4 produce

interferons

38

what is one cytokine example cd4 will produce

IFN-gamma

39

what year was the phenomena of immune memory described?

429BC

40

what did thucydides notice?

people who survive ‘’smallpox’’ do not get re-infected

41

what did the Chinese discover

variolation

42

what year did the chinese discover variolation?

900AD:

43

what did the chinese do?

- Exposing healthy people to tissue from the scabs from patients with small pox (variola virus) – by putting scabs under the skin or up the nose prevented small pox

44

what is Variola: Latin derived from

- derived from varius (‘’spotted’’) or varus (‘’pimple’’)

45

what year did variolation arrive in England

1721:

46

who discovered the vaccine?

Edward Jenner

47

what year did edward jenner discover vaccine

1796

48

what did edward jenner observe

milkmaids who contracted cowpox seemed less likely to get smallpox

49

what was Edwards jenner intervention

used pus from blisters of patients with cowpox

50

what was edwards jenners results

if those vaccinated got cowpox it was less serve than small pox

51

what did Louis Pasteur discover

vaccination against rabies

52

what year did Pasteur discover vaccination against rabies

1880

53

what year did vaccinations become widely available ?

1920

54

what year was smallpox eradicated from the world?

1980

55

what are Viruses that causes cowpox called

called vaccinia from Latin Vacca [it affects the cows]

56

what is the Difference between vaccination and immunisation

- Vaccination is when you take a vaccine and inject an individual
- Immunisation is the process of developing immunological memory through vaccination [artificial] or by natural infection

57

why is smallpox bad

-Major killer
-One of the most infectious diseases in the world
- high mortality

58

What are the features of an effective vaccine?

1.Safety
- The vaccine must not itself cause illness or death

2.Protection
- The vaccine must protect against exposure to the pathogen

3.Longevity
- The vaccine should give long-lasting protection

4.Neautralizing Antibodies
- these must be induced to protect against pathogens

5.Protective T cells
-these must be induced to protect against pathogens such as TB

6.Practicality
- the vaccine must be cheap to produce and easy to administer

59

what is herd / community immunity

if someone with measles is surrounded by people who are vaccinated against measles, the disease cannot be passed to anyone and will quickly disappear

60

who does herd / community immunity give protection against?

vulnerable people such as:
1) elderly people
2) new born babies
3) those too sick to be vaccinated

61

what is Active immunisation

Divides into inactivated vaccines (e.g. heat treated) or attenuated vaccines (e.g. ‘’a weaker strain’’

62

what is passive immunisation:

- antibodies being transferred to a person who is exposed to a pathogen and does not have immunity against pathogens e.g. a serum from a different individual
- or passive transfer of maternal immunity to the baby – last 3 months of trimester

63

list 4 modern vaccines

1. from recombinant technology
2. recombinant peptide vaccines
3. DNA vaccines
4. Therapeutic vaccines

64

when is passive immunisation given ?

 This type of immunisation is often given to counteract insect/animal venoms (e.g. spider or snake venum)

65

what type of serum is used in passive immunisation

Usually horse serum is used

66

what is the problem with passive immunisation
two reasons

immunisation effects only lasts for as long as the antibody stays alive- hence doesnt provide long last long protection

it can cause serum sickness as the patient makes immune response against serum

67

Whole organisms used

- Live but attenuated
- Killed/inactivated

68

subunits used

- Peptide
- Polysaccharide
- Conjugate

69

what are the issues with live vaccine

Issues with live vaccines
 Probably the most potent of vaccines, as best recapitulates/ mimics natural infection
 BUT
- Although attenuated, there is still the potential to cause disease
- Akin to variolation resulting in small pox in a proportion of recipients
- The risk of disease is small
- But is increased in the immunocompromised