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PA20351 > Determinants of infectious disease II > Flashcards

Determinants of infectious disease II Flashcards

1
Q

What must pathogens must do in order to grow and colonise?

A

Find an appropriate niche that is optimal. This may involve the formation of biofilms.

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2
Q

What are biofilms?

A

When bacteria attach to a surface and become enveloped in a matrix.

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3
Q

What is the purpose of a biofilm?

A

To protect the bacteria from phagocytosis, antibiotics and disinfectants.

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4
Q

What are some infections relating to biofilms?

A

Endocarditis, dental plaque, cystic fibrosis, UTIs from urinary catheters.

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5
Q

What is a common bacteria normally formed in the gut that forms a biofilm?

A

Enterococcus faecalis.

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6
Q

What is the main nutrient that is a limiting factor for bacteria in the host?

A

Iron.

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7
Q

What happens to iron in aerobic conditions?

A

It is oxidised in ferric form and has low solubility.

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8
Q

What happens to iron in the body?

A

It is complexed to proteins such as transferrin, lactoferrin, ferritin and haemoglobin.

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9
Q

How do bacteria gain iron?

A

Uptake of free iron or iron complexes such as direct contact using cell surface proteins or secreting small compounds with high affinity for iron that capture iron from host proteins/insoluble ferric acids.

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10
Q

What compounds with high affinity for iron can bacteria secrete to gain iron?

A

Siderophores.

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11
Q

What cell surface proteins can be used to gain iron in bacteria?

A

Transferrin binding protein (TBP) and haemoglobin binding protein (HBP).

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12
Q

When are siderophores produced?

A

When the concentration of iron is low.

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13
Q

What is an example of a siderophore?

A

Enterobactin.

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14
Q

How does the siderophore dependet iron transport work?

A

The sid gains iron from an iron source ((Fe(OH)3, ferritin, transferrin)) to form Fe(III)Sid. It then travels through a transporter system into the cell and Fe(II) is released. Conditions inside the cell are much more reducing, and the affinity for ironII is much lower so is released inside the cell.

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15
Q

What are the defences hosts have that bacteria need to overcome?

A

Physical barriers, the innate immune system and the adaptive immune system.

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16
Q

What are the avoidance strategies bacteria have to avoid host defence mechanisms?

A

The evade complement, resisting phagocytosis, intracellular survival and evading the host antibody response.

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17
Q

What is the complement system?

A

It is an important part of the immune system that enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism.

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18
Q

What are the ways in which bacteria can evade the complement?

A

Capsules - thick polysaccahride layer around the cells prevents complement activation. LPS O-antigen - elongated O chains prevent complement activation.

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19
Q

How can phagocytosis be resisted?

A

Prevent effective contact with the phagocyte, affect phagocyte migration and destroy phagocytes.

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20
Q

How can effective contact with the phagocyte be prevented?

A

Biofilms, capsules/specific proteins.

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21
Q

How can phagocyte migration be affected?

A

S. pyogenes peptidase cleaves a complement factor.

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22
Q

How can phagocytes be destroyed?

A

Using toxins such as leukocidins.

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23
Q

How can bacteria survive inside cells?

A

Some pathogens can be phagocytosed but survive and some pathogens invade non-phagocytic cells.

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24
Q

How can pathogens be phagocytosed but survive?

A

Survive phagolysosome, prevent formation of phagolysosome or destroy/escape from the phagosome and live in the cytosol.

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25
Q

How can pathogens evade the host-antibody response?

A

Bind to host proteins and produce surface protein which bind antibodies backwards.

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26
Q

What are examples of host proteins?

A

Fibronectin, albumin.

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27
Q

What pathogen surface protein can bind host proteins?

A

Streptococcus pyogenes.

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28
Q

What pathogen can produce surface protein that binds antibodies backwards?

A

Staphylococcus aureus/streptococcus pyogenes.

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29
Q

What is opsinisation?

A

Labelling for phagocytosis - labelled using antigens.

30
Q

How can opsinisation be avoided?

A

Antibodies being the wrong way around - so it cannot be recognised as a target for destruction. Protien A form S.aureus can cause this anti-opsinisation.

31
Q

Why is damage a result of toxins being present?

A

Damage is created to obtain nutrients and to spread around rather than to purposefully harm the host.

32
Q

What are toxins?

A

Products of bacteria that cause immediate host damage and induce inflammation.

33
Q

What is exotoxin?

A

It is actively secreted during growth - usually proteins.

34
Q

What is endotoxin?

A

The structural part of bacteria that is only released during bacterial lysis - not protein.

35
Q

How are exotoxins transmitted?

A

Ingestion of pre-formed exotoxin or colonisation followed by exotoxin production.

36
Q

Give examples in the ways exotoxins can be transmitted.

A

Food poisoning or infection followed by toxin production.

37
Q

What is specific about ingestion of pre-formed exotoxin?

A

There is no adherence/colonisation/growth of the pathogen in the host.

38
Q

What does heat labile mean?

A

Can be changed due to heat - e.g. denaturing.

39
Q

What are host-site specific exotoxins?

A

Exotoxins that only affect specific cells such as neurotoins, enterotoxins and cytotoxkins. Many are AB toxins.

40
Q

What are AB toxins?

A

The A subunit is toxin and the B subunit is for targeting.

41
Q

What are the three main types of exotoxins?

A

Host-site specific exotoxins, membrane disrupting toxins and superantigen type.

42
Q

What are some examples of membrane disrupting toxins?

A

Leukocidins, haemolysins and phospholipases.

43
Q

How do superantigen type exotoxins work?

A

They stimulate T cells to release cytokines. This is normally released in response to infection, but there is a large amount of aspecific cytokines produced - the body cannot deal with this and there is damage to organs.

44
Q

What do haemolysins do?

A

They kill off red blood cells.

45
Q

What do phospholipases do?

A

Kill the phospholipid bilayer.

46
Q

How do Pore Forming Toxins (PFTs) work?

A

The exotoxin (haemolysin or leukocidin) forms a pore in the membrane. Water enters uncontrollably and the cell swells and bursts - lysis.

47
Q

What happens in bilayer disruption?

A

Phospholipase exotoxin causes disruption of bilayer, which then leads to cell lysis.

48
Q

How can haemolysis be seen in bacteria?

A

Bacteria is plated on agar containing blood - haemolysis can be seen due to clearing zones around colonies. This is visible due to iron being used around these areas.

49
Q

What are superantigens produced by?

A

Staphylococci/streptococci.

50
Q

How many exotoxins are produced by staphylococci?

A

8 enterotoxins (including toxic shock syndrome toxin, TSST).

51
Q

How many exotoxins are produced by streptococci?

A

6 pyrogenic exotoxins.

52
Q

What are enterotoxins?

A

Toxins produced that affect the intestines.

53
Q

What does pyrogenic mean?

A

Inducing fever.

54
Q

What do superantigens lead to?

A

Massive non-specific inflammatory response that leads to endothelial damage, circulatory shock and multi-organ failure.

55
Q

What is LPS?

A

Lipopolysaccharide found in the outer membrane of gram negative bacteria.

56
Q

Where is endotoxin found?

A

It is the lipid A component of the LPS.

57
Q

When is endotoxin released?

A

Only when bacteria burst open/lyse.

58
Q

What do endotoxins induce?

A

Fever (pyrogenic), initiates complement and clotting cascades - toxic shock.

59
Q

What can antibiotic treatment lead to?

A

Some antibiotics cause lysis of bacterial cells that will lead to release of LPS, causing toxic shock.

60
Q

How do endotoxins differ to exotoxins in terms of stability?

A

Endotoxins are heat stable.

61
Q

How do pathogens regulate virulence factors?

A

As bacteria have to cope with very different conditions such as nutrients, oxygen and temperature. The pathogens can sense the environment to regulate the expression of virulence genes such as in the early steps producing adhesins and in the later steps producing exotoxins and downregulating adhesins that may be targets for host defence.

62
Q

What are Fur proteins involved in?

A

Controlling the intracellular iron concentration in bacteria.

63
Q

In terms of the Fur protein, what happens if there is low iron?

A

It remains in the apo Fur state and gene expression is switched on - there is de-repression of genes.

64
Q

In terms of the Fur protein, what happens if there is high iron?

A

The Fur protein changes into the ferric form and will bind to iron - this complex will recognise specific sequences upstream of particular genes that are behind it. The sequences that it recognises will bind to to prevent transcription of genes behind it.

65
Q

Why does the ferric form of Fur prevent gene transcription?

A

The Fur complex is in the way of RNA polymerase.

66
Q

What is the idea of quorum sensing?

A

That many pathogenic bacteria produce virulence factors only until a quorum (minimal number) of cells is present. Producing virulence factors is costly, and only worthwhile when there are a large number of pathogenic cells to cause harm. Before this minimal number of cells is reached, energy will be used to increase the population size.

67
Q

What are examples of quorum sensing?

A

VIbrio fisheri - lux genes and pseudomonas aeruginosa - haemolysin

68
Q

What are the components involved in quorum sensing?

A

Autoinducer and R protein.

69
Q

What is an autoinducer?

A

A small diffusable molecule that can diffuse through the inside and outside of cells.

70
Q

What is the function of the R protein?

A

It activates the transcription of genes when the R protein binds to the autoinducer. This binding only occurs at high concentrations of the autoinducer, and this only happens at high cell densities.

71
Q

How are biofilms involved in quorum sensing?

A

As there is a high cell density in biofilms, the formation of biofilms often leads to the expression of virulence factors through quorum sensing.

72
Q

What is a short summary of the process of bacteria invading skin?

A

Bacteria invade the skin and adhere to bone because of adhesins. They start to form a biofilm (microcolony) and they start to divide to get bigger and bigger. There is switched off expressions of adhesins and upregulation of toxins.

PA20351 (11 decks)

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