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
What pathogen is the common cause of lobar pneumonia?
➝ Streptococcus pneumoniae
26
How is streptococcus pneumoniae breathed in?
➝ through the nasopharynx
27
How does streptococcus pneumoniae prevent antibody degradation?
➝ by secreting IgA proteases
28
What disease does streptococcus pneumoniae often follow and why?
➝ A viral infection because it will have damaged the structure of the defense mechanisms in the respiratory tract
29
What are the main defense mechanisms against streptococcus pneumoniae?
➝ Surfactant and mucus in the lungs
30
How does streptococcus pneumoniae invade the lungs?
➝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
How many serotypes of streptococcus pneumoniae are there?
➝ 80-90
32
How can streptococcus pneumoniae escape phagocytosis?
➝ they have capsules
33
What are 4 ways that pathogens can evade the immune system?
1) Latency 2) decreased antigen presentation 3) decreased MHC expression 4) mutation of epitopes
34
What 2 pathogens can become latent and why?
➝ VZV, HSV | ➝ if the virus were to infect everybody at the same time then the virus would die out
35
Where do latent viruses usually affect and why?
➝ Nerve cells | ➝ they have very little immune surveillance so they can exist undisturbed
36
Which virus decreases antigen presentation and how?
➝ HPV | ➝ binds to the TAP protein and blocks antigen transfer to MHC molecules
37
Which virus decreases MHC expression?
➝ CMV
38
Why do viruses mutate epitopes?
➝ so the B cell antibodies can't work | ➝ they evade the immune cells
39
What is antigenic diversity?
➝ Genetically stable and alternative forms of antigens in a population of microbes
40
What is antigenic variation?
➝ Successive expression of alternative forms of an antigen in a specific clone or its progeny
41
How is antigenic variation done?
➝ Pathogens can switch antigens on or off at low frequency
42
What kind of an infection is gonorrhoea?
➝ Inflammatory and pyogenic infection of the anterior urethra
43
Where does gonorrhoea infect?
➝ mucosal surfaces with a columnar epithelium | ➝ urethra, cervix, rectum , pharynx, conjunctiva
44
What are the 4 symptoms of gonorrhoea?
➝ Dysuria ➝ Redness ➝ swelling ➝ pain on urination
45
What are the 9 pathologies that can occur as a result of gonorrhoea?
``` ➝ Destruction of mucosa ➝ prostatitis ➝ orchitis ➝ strictures ➝ ovaritis ➝ fistulas ➝ PID ➝ proctitis ➝ sterility ```
46
What are three disseminated infections that can occur as a result of gonorrhoea?
➝ Arthritis ➝ Endocarditis ➝ Meningitis
47
Which structures of gonorrhoea can undergo phase variation?
``` ➝ Capsule ➝ pilus ➝ outer membrane ➝ Opa ➝ Inner membrane ```
48
What are the two components of the influenza virus?
➝ Haemagglutinin | ➝ Neuraminidase
49
How many haemagglutinin types are there?
➝ 15
50
How many neuraminidase types are there?
➝ 9 types
51
What kind of genome does the influenza virus have?
➝ segmented negative ssRNA genome | ➝ 8 segments, 10 genes
52
What causes epidemics?
➝ Antigenic drift
53
What is antigenic drift?
➝ as the virus replicates itself it has errors | ➝ if there is a mutation then antibodies do not recognise it
54
What causes pandemics?
➝ Antigenic shift
55
What is antigenic shift?
➝ 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
What are the 6 ways that viruses avoid the adaptive immune system?
➝ 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
What are the 2 ways that viruses avoid innate immunity?
➝ Latency reactivation | ➝ Rapid growth and transmission prior to adaptive immunity
58
What are the 3 ways that bacteria avoid the adaptive immune system?
➝ Inhibition of antigen presentation ➝ superantigens and inappropriate immune activation ➝ induction/inhibition of apoptosis
59
What are the 4 ways that bacteria avoid the innate immune system?
➝ Prevent opsonin binding ➝ C3a and C5A proteases, anti-inflammatory and anti chemoattractant ➝ inhibits opsonisation ➝ inhibits complement activation