1
Q

What are virulence factors?

A

➝ components that drive pathogenic processes

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2
Q

What is virulence?

A

➝ the degree to which a pathogen causes disease

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3
Q

What 3 things do virulence factors mainly do?

A

➝ promote adherence or receptor binding
➝ allow bacteria to colonise
➝ promote tissue damage - toxins

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4
Q

What are the 5 roles of the complement?

A
➝ Activate, promote and regulate the inflammatory process
➝ increase phagocytosis by opsonization
➝ increasing vascular permeability 
➝ mast cell degranulation
➝ lysis of cell membranes
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5
Q

How does the complement activate, promote and regulate the inflammatory process?

A

➝ Releasing factors that chemo attract effector cells like macrophages and neutrophils

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6
Q

How does the complement increase phagocytosis by opsonization?

A

➝ binding to the surface of bacteria and viruses allowing them to be phagocytosed by macrophages

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7
Q

Why is complement sometimes unable to bind to bacteria?

A

➝ They have polysaccharide capsuled on their surface and endotoxins
➝ they don’t allow the early stages of the complement cascade to bind to their surfaces

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8
Q

What happens if bacteria can bind to factor H?

A

➝ it can stop the complement activating on the surface

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9
Q

How do some bacteria stop C3B binding?

A

➝ they coat themselves in non-fixing IgA

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10
Q

What is C3B ?

A

➝ a powerful opsonin which allows opsonisation into macrophages

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11
Q

When is C5A released?

A

➝ after the complement is activated

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12
Q

What is C5A?

A

➝ a chemoattractant

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13
Q

What are 3 intracellular pathogens?

A

➝ mycobacterium tuberculosis
➝ listeria
➝ salmonella

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14
Q

What is used by bacteria to avoid phagocytosis?

A

➝ capsules

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15
Q

What is protein A?

A

➝ binds antibodies the wrong way round

➝ they have Fc receptors that bind the antibody by the Fc region not the epitope

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16
Q

How does staph damage immune cells?

A

➝ they produce extracellular toxins that damage the membrane of white cells
➝they prevent opsonization by complement

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17
Q

How does M.tuberculosis prevent phagocytosis?

A

➝ blocks the phago-lysosome formation and stops acidification of the endosome

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18
Q

How does Listeria prevent phagocytosis?

A

➝ escapes the phago-lysosome into the cytoplasm

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19
Q

How do some bacteria neutralise the ROS made in the phago-lysosome?

A

➝ some bacteria produce catalases and peroxidases

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20
Q

How do microbes make Fc receptors?

A

➝ they have proteins on their surface that encode mimics of the Fc receptors

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21
Q

Why are microbe Fc receptors effective?

A

➝ Even if the immune system generates antigen specific antibodies the Fc receptors will bind the antibodies the wrong way round
➝ they can no longer be phagocytosed and killed

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22
Q

What are the 4 ways pathogens conceal antigens?

A

➝ hide inside cells
➝ privileged sites
➝ block MHC antigen presentation
➝ Surface uptake of host molecules - CMV

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23
Q

What virus blocks MHC antigen presentation?

A

➝ Herpes

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24
Q

What are 4 ways that pathogens cause immunosuppression?

A

➝ Decreased MHC
➝ downregulate receptors like interferon gamma, apoptosis, cytokine switch, IgA proteases
➝ Antigenic variation
➝ Persistence/latency/reactivation

25
Q

What pathogen is the common cause of lobar pneumonia?

A

➝ Streptococcus pneumoniae

26
Q

How is streptococcus pneumoniae breathed in?

A

➝ through the nasopharynx

27
Q

How does streptococcus pneumoniae prevent antibody degradation?

A

➝ by secreting IgA proteases

28
Q

What disease does streptococcus pneumoniae often follow and why?

A

➝ A viral infection because it will have damaged the structure of the defense mechanisms in the respiratory tract

29
Q

What are the main defense mechanisms against streptococcus pneumoniae?

A

➝ Surfactant and mucus in the lungs

30
Q

How does streptococcus pneumoniae invade the lungs?

A

➝produces IgA proteases which cleave antibodies
➝ Induces and switches on the genes for pneumolysin which is a toxin that lyses the membranes and causes pores in pneumocytes of the lungs

31
Q

How many serotypes of streptococcus pneumoniae are there?

A

➝ 80-90

32
Q

How can streptococcus pneumoniae escape phagocytosis?

A

➝ they have capsules

33
Q

What are 4 ways that pathogens can evade the immune system?

A

1) Latency
2) decreased antigen presentation
3) decreased MHC expression
4) mutation of epitopes

34
Q

What 2 pathogens can become latent and why?

A

➝ VZV, HSV

➝ if the virus were to infect everybody at the same time then the virus would die out

35
Q

Where do latent viruses usually affect and why?

A

➝ Nerve cells

➝ they have very little immune surveillance so they can exist undisturbed

36
Q

Which virus decreases antigen presentation and how?

A

➝ HPV

➝ binds to the TAP protein and blocks antigen transfer to MHC molecules

37
Q

Which virus decreases MHC expression?

A

➝ CMV

38
Q

Why do viruses mutate epitopes?

A

➝ so the B cell antibodies can’t work

➝ they evade the immune cells

39
Q

What is antigenic diversity?

A

➝ Genetically stable and alternative forms of antigens in a population of microbes

40
Q

What is antigenic variation?

A

➝ Successive expression of alternative forms of an antigen in a specific clone or its progeny

41
Q

How is antigenic variation done?

A

➝ Pathogens can switch antigens on or off at low frequency

42
Q

What kind of an infection is gonorrhoea?

A

➝ Inflammatory and pyogenic infection of the anterior urethra

43
Q

Where does gonorrhoea infect?

A

➝ mucosal surfaces with a columnar epithelium

➝ urethra, cervix, rectum , pharynx, conjunctiva

44
Q

What are the 4 symptoms of gonorrhoea?

A

➝ Dysuria
➝ Redness
➝ swelling
➝ pain on urination

45
Q

What are the 9 pathologies that can occur as a result of gonorrhoea?

A
➝ Destruction of mucosa 
➝ prostatitis
➝ orchitis
➝ strictures
➝ ovaritis
➝ fistulas
➝ PID 
➝ proctitis
➝ sterility
46
Q

What are three disseminated infections that can occur as a result of gonorrhoea?

A

➝ Arthritis
➝ Endocarditis
➝ Meningitis

47
Q

Which structures of gonorrhoea can undergo phase variation?

A
➝ Capsule
➝ pilus
➝ outer membrane
➝ Opa 
➝ Inner membrane
48
Q

What are the two components of the influenza virus?

A

➝ Haemagglutinin

➝ Neuraminidase

49
Q

How many haemagglutinin types are there?

A

➝ 15

50
Q

How many neuraminidase types are there?

A

➝ 9 types

51
Q

What kind of genome does the influenza virus have?

A

➝ segmented negative ssRNA genome

➝ 8 segments, 10 genes

52
Q

What causes epidemics?

A

➝ Antigenic drift

53
Q

What is antigenic drift?

A

➝ as the virus replicates itself it has errors

➝ if there is a mutation then antibodies do not recognise it

54
Q

What causes pandemics?

A

➝ Antigenic shift

55
Q

What is antigenic shift?

A

➝ Two viruses infecting a single cells
➝ they undergo recombination of the genome
➝ There are combinations that are new and the population has not seen before

56
Q

What are the 6 ways that viruses avoid the adaptive immune system?

A

➝ MHC mimics - block killing by NK cells
➝ downregulate MHC
➝ Block antigen processing by TAP
➝ induce immune suppression by decreasing cell mediated immunity and CD4+ cells
➝ host mimicry
➝ cytokine binding mimics and binding proteins

57
Q

What are the 2 ways that viruses avoid innate immunity?

A

➝ Latency reactivation

➝ Rapid growth and transmission prior to adaptive immunity

58
Q

What are the 3 ways that bacteria avoid the adaptive immune system?

A

➝ Inhibition of antigen presentation
➝ superantigens and inappropriate immune activation
➝ induction/inhibition of apoptosis

59
Q

What are the 4 ways that bacteria avoid the innate immune system?

A

➝ Prevent opsonin binding
➝ C3a and C5A proteases, anti-inflammatory and anti chemoattractant
➝ inhibits opsonisation
➝ inhibits complement activation