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SEM 4: Medical Microbiology > Microbial Immune Evasion > Flashcards

Microbial Immune Evasion Flashcards

1
Q

Properties of the microbe (Pathogenic mechanisms)

A
  • Adhesions
  • Toxins
  • Capsule
  • etc
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2
Q

Properties of the host (Defensive mechanisms)

A
  • Natural barriers
  • Defensive cells
  • Complement
  • Immune Response
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3
Q

What is balanced pathogenicity?

A

The properties of the microbe to cause disease and the properties of the host to defend the body are balanced.

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4
Q

What happens when the balanced pathogeneicity is out of balance?

A

It is not an all or nothing response.
Overcoming or avoiding the immune response within an infected individual and within a population will lead to clinical course of disease. This will be different in each person depending on their immune system.

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5
Q

What are virulence factors?

A

Components of organisms that drive the pathogenic process are called virulence factors.

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6
Q

What are the different mechanisms of action of virulence factors?

A
  • Promote colonisation and adhesion
  • Evade host defences
  • Promote tissue disease
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7
Q

How do viruses promote colonisation and adhesions?

A

Viruses can bind to receptors on host cells and change the intracellular processes.

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8
Q

How do viruses promote tissue damage?

A

Viruses will promote the production of toxins. The toxins can lead to direct effect on the tissue by damaging it or can lead to electrolyte balance and change the pharmacological aspects of the cell.

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9
Q

How do vaccines work?

A

They generate an immune response which will protect from the disease.

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10
Q

What happens if a pathogen is not able to evade the innate and adapted immune system? How have pathogens evolved to counteract this?

A

It will not be able to survive and cause disease. This is why most pathogens have evolved to be infer with those mechanisms of defence.

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11
Q

What do bacteria need to overcome?

A

Bacteria need to be able to overcome complement.

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12
Q

What is complement and what are their roles?

A

Complement is a very important component of the innate immune system. The roles of complement include:

  • Induces inflammatory response
  • Promotes chemotaxis
  • Increases phagocytosis by opsonisation - very important
  • Increases vascular permeability
  • Causes mast cell degradation
  • Lysis of the cell membrane
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13
Q

What are the mechanisms of how bacteria overcome complement?

A
  • Fail to activate/trigger the complement pathway
  • Factor H sequestration
  • Coating with non-fixing with IgA
  • Capsule blocks C3b binding
  • C5a proteases
  • Hide inside macrophages - intracellular pathogens
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14
Q

How does bacteria stop the activation of the complement pathway?

A
  • These bacteria have polysaccharide capsules and like polysaccharide capsules (LPS) on their surface that prevent the binding of the early molecules that trigger the complement cascade pathway.
  • This means that the pathway is suppressed.
  • Also stops the bacteria/complement complex from building up on surfaces.
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15
Q

How does bacteria sequest Factor H to overcome complement?

A
  • Some bacteria such as one that causes meningitis have a protein which is encoded by the genome that binds to factor H.
  • Factor H is a negative regulator of the complement cascade.
  • Therefore, if a bacteria has a protein that binds to factor H which negatively regulates the complement pathway, it means it will stop the pathway from taking place.
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16
Q

How does bacteria oppose the binding of antibodies to overcome complement?

A
  • Certain antibodies help the binding of the bacteria to the complement by promoting opsonisation such as IgG and IgN, however some do the opposite.
  • Certain antibodies can prevent the binding of the bacteria to the complement such as IgA.
  • And therefore, they cannot be opsonised by the complement.
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17
Q

How does a bacteria LPS capsule block C3b binding to overcome complement?

A
  • The LPS capsules on bacteria can prevent C3b binding.
  • This is a molecule which is released once the complement cascade is triggered.
  • It is a potent opsonising molecule which allows the binding to surfaces of macrophages.
  • And therefore, preventing this allows the bacteria to survive.
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18
Q

What is C5a protease and how bacteria use this to overcome complement?

A
  • C5a is a molecule which is released after the complement pathway is triggeredc.
  • It is a chemoattract factor and is very important for the inflammatory response.
  • Some bacteria encode proteins /enzymes which breaks it down.
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19
Q

What is the benefit of bacteria hiding in a macrophage?

A
  • Some bacteria such as Mycobacterium tuberculosis, listeria and salmonella are able to survive and hide inside the macrophage.
  • This makes it very hard of the cell to kill it as it is hidden from serum killing, complement and antibodies.
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20
Q

What else does bacteria need to overcome to survive?

A

Needs to be able to avoid phagocytosis

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21
Q

What are some of the ways bacteria avoids phagocytosis?

A
  • Release leucocidins
  • Prevent opsonisation (antibody mediated opsonisation)
  • Block contact
  • Hide inside the macrophage - intracellular pathogens
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22
Q

Describe how bacteria avoids phagocytes by releasing leucocidins

A
  • These are toxins which the bacteria can release to kill leukocytes (WBCs).
  • This means that when macrophages are recruited to the site of infection, they are destroyed by the toxins and therefore phagocytosis cannot occur.
  • An example of this is staphs bacteria.
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23
Q

How does bacteria avoid phagocytosis by preventing opsonisation?

A

Can be done the same as preventing the binding to complement.

  • It can also produce protein A which binds antibodies the wrong way around.
  • Therefore, instead of the antibody binding to the bacteria via its epitope recognition site;
  • It binds to the Fc portion of the antibody and therefore it blocks the ability of the antibody to have its affect as it has not lost the Fc active receptor and cannot be opsonised by a macrophage.
  • An example of this is Staphs again.
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24
Q

How does bacteria avoid phagocytosis by blocking contact?

A
  • Polysaccharides capsules on the surface of bacteria which again prevent opsonisation and phagocytosis.
  • Example of this is meningococcus (causes meningitis and septicaemia) and Hib.
25
Q

What happens normally when a bacteria is in a macrophage?

A

When it is in a macrophage, phagosome is created, and the bacteria is broken down.

26
Q

How does bacteria avoid phagocytosis by hiding in the macrophage?

A
  • Some bacteria can enter the macrophage via different kind of receptors that do not activate the respiratory burst (rapid release of reactive oxygen species which would kill the bacteria).
  • Some bacteria can inject proteins into the macrophages which act as receptors on the macrophage, so the bacteria can then bind to those receptors and be internalised in a way which doesn’t activate the macrophage killing (phagosome) process.
  • Some bacteria can block the phagolysosome complex by secreting certain proteins and also block acidification which occurs after the phagolysosome complex is made.
  • Some bacteria can escape the phagolysosoome by staying in the cytoplasm of the macrophage where it grows and replicates.
  • Some bacteria can generate their own enzymes which neutralise the enzymes that are generated in the phagolysosome.
27
Q

Examples of bacteria that have mechanisms of hiding in the macrophage to prevent degradation

A

Shigella
M. tuberculosis
Listeria
Prevent degradation once inside the macrophage

28
Q

How does bacteria protect against antibodies?

A

They produce Fc receptors by microbes. Antibodies are antigen specific high affinity receptors.
1. Once the antibody binds to the bacterium, the Fc receptor binds to the macrophage.

  1. The bacterium gets internalised and killed.
  2. However, certain bacteria and viruses such as staphs, streps, herpes, VZV and CMV have proteins on their receptors which mimic the Fc receptor.
  3. So even if the immune system generates antigen specific antibodies, the antibody will bind to the fake receptor.
  4. This means the complex can no longer be opsonised, and therefore this acts as a protective method against neutralisation by antibodies.
29
Q

What is the adaptive immunity?

A

Involves T cell mediated responses that are antigen specific.

30
Q

How are T cells and B cells recruited in adaptive immunity?

A
  • These are recruited by antigen presentation by macrophages on MHC complexes.
  • These are then recruit clonal T cells that are antigen specific, which then expand to produce cytotoxic T cells that recognise these antigens and destroy them.
  • They also drive the recruitment of helper T cells which produce cytokines that recurrent and allow B cells to clonally expand. These B cells then produce plasma cells which produce antigen specific antibodies.
31
Q

How can pathogens evade the adaptive immunity?

A
  • Hide within cells like TB bacteria
  • Go to immunological privileged sites in the body
  • Block MHC antigen presentation
  • Immunosuppression
  • Antigenic variation
  • Persistence/latency/reactivation
32
Q

Why do some viruses go to immunological privileged sites in the body?

A

Viruses go because for example immune cells cannot cross the blood brain barrier as they are too big. So some viruses stay in the neurons for years , until it is safe for them to come out for example where there is immunodeficiency. For example, herpes virus.

33
Q

How do pathogens block MHC antigen presentation?

A

They do this by lowering the number of antigens which are present on the surface of antigen presenting cells.
This is done by inhibiting TAP proteins, which is the protein associated with adding a small peptide to the MHC molecule before it is presented on the cell and recruiting cytotoxic cells e.g. herpes

34
Q

How do pathogens cause immunosuppression?

A
  • Downregulating MHC and receptors
  • Trigger apoptosis of immune cell, so they die without triggering inflammation, this allows the pathogen to spread to other parts of the body.
  • Interfere with the cytokine balance which means the host immune system has now lost its balance which is needed for an effective immune response.
  • Damage secretory IgA that is a key antibody for the defence mechanism in all out mucosal surfaces, therefore for a pathogen to adhere to a mucosal surface it needs to destroy IgA via secreting IgA proteases.
35
Q

Latency of a virus

A

Virus will infect the host then lay latent until the body is immunodeficient.

36
Q

Infection that Streptococcus pneumonia and how does it cause infection

A

An organism that causes septicaemia, otitis media and meningitis. It causes infection by by-passing defencees, colonises, survives and causes damage.

37
Q

What is the pathogenic mechanism for streptococcus pneumonia?

A
  1. There is colonisation of nasopharynx which causes otitis media (inflammation) in the nasopharynx and aerosol.
  2. Leads to inhalation of the bacteria into the lungs (or causes bacteraemia that leads to meningitis + septicaemia).
  3. It by-passes the defences and surfactant and reaches the lungs.
  4. In the lungs, it escapes phagocytosis, causes inflammation leading to lung damage and damage to endothelial cells.
  5. These affects cause pneumonia leading to bacteraemia.
  6. Eventually leading to meningitis + septicaemia with the symptoms of inflammation and toxic shock.
38
Q

How does bacteria cause otitis media?

A
  • It lives in the nasopharynx where it colonises causing otitis media.
  • This is because they have specific adherence molecules which allow them to adhere there.
  • They also produce IgA proteases which breakdown IgA that is secreted in order to help bind the bacteria to the complement
  • This allows them to stay there and colonise waiting for the right moment (typically after viral damage) to evade further and cause disease.
  • This can lead to the development of otitis media (middle ear infection).
39
Q

What happens when s. pneumonia spreads to the lungs?

A
  • Damages the structures of the defence mechanism of the respiratory system and the bacterium can follow to a viral infection.
  • It overcomes the surfactants molecules which are defence mechanisms in the lungs by producing IgA proteases (again) and pneumolysin.
  • Pneumolysin is toxin released by the bacteria which lysis the membrane of the pneumocytes.
  • Once this happens then all the defence mechanisms in the lungs are overcome and the bacteria can replicate there, and cause an inflammatory process.
40
Q

How does the s. pneumonia overcome the inflammatory response?

A
  • An inflammatory response due to the damage to the pneumocytes will be triggered.
  • However, the bacteria are able to overcome this because it contains a capsule.
  • The capsule blocks complement and antibody binding which prevents phagocytosis from taking place.
  • Bacteria produces teichoic acids which allows the bacteria to have an immune-defence mechanism.
  • Due to the pneumolysin being produced as well, any immune cells which is recruited is being lysed and therefore its able to evade the immune system even further.
41
Q

How does s. pneumonia cause pneumonia, meningitis and septicaemia?

A
  • Causes pneumonia as the bacteria has overcome the immune system.
  • Can spread to the blood and cause septicaemia
  • Can then spread to the spinal cord and the meninges to cause meningitis
  • Can cause toxic shock, organ failure and death.
42
Q

Why does s. pneumonia have different serotypes of bacteria?

A
  • More than 80 different serotypes which means it can survive in a population via antigenic diversity
  • This is because the bacteria relied on only surviving in one individual, eventually that individual (if survived pneumonia) will create an immune response and the bacteria would no longer be able to survive there.
  • By having multiple different antigen, it is able to survive in the population.
43
Q

Describe how microbes (VZV) remain latent

A
  1. During this, the persistent microbe varicella zoster virus infects the cell.
  2. The microbe then remains latent.
  3. It is then reactivated and infects the next general of susceptibles.
  4. This allows the virus to exist in small populations, because if the virus infected everyone at the same time, then you would get a population which is completely immune, and the pathogen would due out.
  5. Therefore for a population to be persistent, it needs to be able to develop latency strategy to evade immune-clearance within a population.
44
Q

Examples of microbes that remain latent

A

VZV (shingles/chicken pox) and herpes simples

45
Q

What are some viral immune evasion mechanisms?

A
  • Latency
  • Reduce antigenic presentation
  • Downregulate MHC expression
  • Mutations of epitopes
46
Q

How do viruses reduce antigenic presentation?

A
  • Such as herpes.
  • They lower the number of antigens which are presented on the surface of antigen presenting cells.
  • This is done by inhibiting TAP proteins, which is the protein associated with adding a small peptide to the MHC molecule before.
47
Q

Example of a virus that downregulate MHC expression

A
  • Such as Cytomegalovirus which is part of the herpes family
48
Q

What are epitopes?

A

The sites that the antigens on the virus which are recognised by either the antibodies or the T cell receptors

49
Q

What is mutations of epitopes?

A
  • If it escapes the B cells, it is called neutralisation escape.
  • If it escapes the T cells, it is called CD8+ escape mutants
    Example is HIV.
50
Q

What phenotype changes occur to pathogens? Why do they occur?

A
  • Colony morphology
  • Virulence
  • Serotype
  • Loose flagella
  • Change surface sugars
  • This is a strategy for immune evasion and pathogenesis
51
Q

Why is it important for a vaccine to work on the different serotypes of viruses?

A
  • There are a lot of genetically stable and alternative forms of antigens in a population of microbes.
  • For example, different serotypes of strep. pneumonia.
  • Therefore, a vaccine against this virus needs to be able to work on the different serotypes.
52
Q

What is antigenic variation?

A

When one organism can express different antigens on its surface.

53
Q

What is phase variation? Why is it important?

A

When a bacteria is able to switch on/off its antigen. Therefore, even if there is specific immune response against this bacterium, the ability to carry out phase variation means the immune response is not going to recognise it. This occurs during course of infection in an individual host and during spread of microbe through a community.

54
Q

Example of a antigenic variation virus

A

Gonorrhoea

55
Q

Structure of the influenza/flu virus

A
  • A segmented negative ssRNA virus
  • Contains around 10 genes which code for surface proteins called haemagglutinin and neuramindase
  • There are different types of the 2 types of proteins
56
Q

How does the flu virus able to evade the immune system?

A

Evade the immune system on a population level via antigenic drift

57
Q

What causes epidemics?

A
  • There is a series of mutations.
  • As the virus replicates itself, they make error/mutations to the components/ proteins expressed on the surface.
  • Therefore, the ones that the immune system are able to recognise normally, are now different and therefore it cannot recognise them anymore.
  • The antigens on the surface of the virus change, meaning the antibodies made over the years are not effective.
  • This is why in the population, there is continuous infection of the flu and the flu jab needs to be taken every year.
  • This causes epidemics.
58
Q

What causes pandemics?

A
  • Caused by viruses able to carry out antigenic shift
  • This is when 2 viruses infect one cell and undergo recombination of the genome
  • This means there are now genes and proteins that the immune system has not see before (a new virus particle)
  • This means this virus has the ability to infect a population and no one will have an immune response to it.

SEM 4: Medical Microbiology (15 decks)

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