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Immunology > Lecture 17 - Bacteria And Toxins > Flashcards

Lecture 17 - Bacteria And Toxins Flashcards

1
Q

What are toxins?

A

Poisonous substance produced by certain microorganism Often main contributor of microbes pathogenic properties Can block protein synthesis, destroy blood cells, blood vessels, disrupt the nervous system of the immune response Can produce fever, cardiovascular problems, diarrhoea, shock Toxins are the most powerful human poison known

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2
Q

What are some examples of human poison ?

A

Botulinum Diphtheria Tetanus Toxins

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3
Q

What is 1mg of botulinum toxin enough to kill?

A

1 million guinea pigs

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4
Q

What are the different criteria of Toxins?

A

Activity, cell target Producer Order of discovery

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5
Q

What are examples of activity, cell target?

A

Neurotoxin Enterotoxin Cytotoxin

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6
Q

What is an example of producer?

A

Cholera toxin Tetanus toxin Diphtheria

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7
Q

What are the order of discovery?

A

a, b, d (specific to species)

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8
Q

What are two main types of toxins?

A

Endotoxins Exotoxins

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9
Q

What is endotoxin?

A

Cell walls component Lipopolysaccharide (LPS) + peptidoglycan, techoid acid

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10
Q

Where is endotoxin released from?

A

Growing bacteria Bacteria laser by host defences(e.g. lysosomes) Upon antibiotic treatment

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11
Q

Where is Exotoxins released from?

A

Live bacteria

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12
Q

What are the 3 main types of bacteria in exotoxins?

A

Cytolysins with cell membrane targets A-B toxins: intracellular targets Toxins acting on host defences (superantigens)

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13
Q

Endotoxin

A

Integral part of the bacterium

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14
Q

What does injection of purified LPS in experimental animal cause?

A

Large spectrum of pathophysiological reactions

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15
Q

What does LPS in the other membrane have?

A

Toxic systems effect Fever, sepsis, change in blood pressure, septic shock

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16
Q

Are endotoxins easily denatured or destroyed by heat ?

A

No

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17
Q

What is Lipid A?

A

Gram negative bacteria Toxic portion Activates complement and stimulated production of cytokines

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18
Q

What are also considered endotoxin?

A

Peptidoglycan fragments and techoid acid from gram positive organisms

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19
Q

When Lipid A from LPS is bound to LPB, where is it directed to?

A

TLR4/ CD14

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20
Q

What are the effects of TLR4/CD14?

A

Signal transduction to cytoplasm (NFKB + MAPK) Activation of complement cascade Increased vascular permeability and activation of coagulation cascade Amplified inflammatory response (septic shock)

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21
Q

What is LPS net effect?

A

Induction of fever inflammation Intravascular coagulation

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22
Q

What does LPS net effect lead to?

A

Haemorrhage and septic shock

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23
Q

What does endotoxin (Lipid A) do?

A

Activate macrophages Activate complement Activate tissue factors

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24
Q

What is examples of activated macrophages?

A

IL-1/ IL-6 (fever) TNF (fever and hypotension) NO (hypotension)

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25
Q

What is example of activates complement ?

A

C3a ( hypotension, Edema) C5a (neutrophil chemotaxis)

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26
Q

What is example of activated tissue factor?

A

Coagulation cascade (DIC)

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27
Q

Where are bacterial Exotoxins Produced?

A

By bacteria

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28
Q

Where is bacterial Exotoxins released?

A

Into surrounding area and cause disease

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29
Q

What are the 3 classes of bacterial Exotoxins?

A

Toxins that damage membranes Toxins that act as enzymes Toxins that activate immune response

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30
Q

What happens when toxins are inserted into the membrane?

A

Form transmembrane pores - this leads to influx of water (endosmosis), resulting in cellular swelling and lysis

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31
Q

What are the 3 classes of bacterial Exotoxins?

A

Toxins that damage membranes Toxins that act as enzymes Toxins that activate immune response

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32
Q

What happens when toxins are inserted into the membrane?

A

Form transmembrane pores - this leads to influx of water (endosmosis), resulting in cellular swelling and lysis

33
Q

What attaches to cell membrane cholesterol and takes part in the pathogenesis of gas gangrene ?

A

Perfringolysin O from clostridium perfringens

34
Q

What does alpha-haemolysis (alpha-toxin, Hla) do?

A

Binds to ADAM10 at cell membrane Cause cell lysis Later signalling pathways (influx of ca2+) and contribute to disease

35
Q

How do you form small pore-forming toxins?

A

Polymerisation 2 subunits Pores 1 to 1.5nm with selective permeability for small ions and nucleotides

36
Q

What is the consequence of small pore-forming toxins?

A

Disruption membrane permeability Activation of endonucleases Cytokine production Initiation of Apoptosis

37
Q

What induces cell death?

A

High concentration of toxins

38
Q

What is an example of high concentration of toxins?

A

Alpha toxin staphylococcus aureus

39
Q

What are the 2 subunits of A/B toxins?

A

A - enzymatic activity B - binding to membrane receptor and translocation of A subunit

40
Q

A-(5)B

A

2 subunits independently produced and non-covalently associated during secretion

41
Q

A+B

A

2 proteins which interact at cell host surface

42
Q

A/B

A

1 polypeptide former by 2 domains separated by proteolysis

43
Q

What is Diphtheria?

A

Gram positive, rod-like organism

44
Q

What is Diphtheria infection?

A

Upper respiratory tract, with systemic effects on heart, liver, kidney and nervous system

45
Q

What does Diphtheria infection lead to?

A

High children mortality in the past, before introduction of vaccination

46
Q

What are the symptoms of Diphtheria?

A

Sore throat Airway obstructing pseudomrmbrane Enlarged lymph nodes in neck (bull-neck appearance)

47
Q

What does Diphtheria toxin do?

A

Block protein synthesis

48
Q

What is Diphtheria toxin (DT)?

A

ADP-ribosyltransferase

49
Q

What is the process of inhibiting protein synthesis by DT?

A

DT targets elongation factor (EF-2) EF-2 is required for protein synthesis DT inactivates EF-2 by ADP-ribosylation Inhibition of protein synthesis leads to cell death and damaged to infected tissue

50
Q

What can Diphtheria toxin razchV

A

Blood steam and target nerves, heart and kidney

51
Q

What is vibrio cholera ?

A

Acute diarrheal illness Severe dehydration caused by intestinal infection

52
Q

What is vibrio cholera made from?

A

Gram-negative curved bacteria

53
Q

How is vibrio cholera transmitted?

A

Ingestion of contaminated food or water

54
Q

What does severe cholera cause?

A

Diarrhoea (profuse rice like water stools) Vomiting Dessication Hypotension

55
Q

What does the lack of therapy cause in vibrio cholera?

A

Acute renal failure, coma, shock and death

56
Q

What is the treatment of cholera?

A

Salt solution Intravenous fluid Antibiotic

57
Q

What happens in the large intestine?

A

1) bacteria multiply rapidly 2) toxins from bacteria penetrates cells of intestinal wall 3) toxins prevent intestine from absorbing water from digested food

58
Q

What does cholera toxin speed up?

A

Normal excretory process leading to massive fluid loss with diarrhoea and severe dehydration

59
Q

What is the mode of action of cholera toxin?

A

Cholera toxin ADP-ribosylates large G proteins that regulates cyclic AMP via adenylate cyclase High levels of CAMP secretion stimulate chloride ion secretion via cystic fibrosis transmembrane conductance regulator chloride Chanel Water and other electrolytes osmotically follow which cause diarrhoea

60
Q

What does cholera toxin inactivate ?

A

GTPase intrinsic activity of large G protein Galpha subunit preventing its regulation

61
Q

What are the 3 forms of Anthrax disease?

A

Cutaneous Intestinal Inhalation

62
Q

Which form of anthrax disease is fatal?

A

Inhalation: severe breathing problems and shock

63
Q

How does contamination of Anthrax occur?

A

Via spores

64
Q

What is the mechanism of Anthrax?

A

1) sneaking in - anthrax spores are inhaled and swept into the lungs 2) beating the defence white blood cells - attack the spores killing only a few 3) growing - spores collect in the lymph nodes and develop. The immune system of vaccinated people can defeat the infection at this point. 4) striking - toxins released by the bacteria spread via the lymphatic system. The poison causes internal bleeding and severe damage to the tissue of major organs. Once the poison has circulated, antibiotics will not save the victim

65
Q

What does Botulinum neurotoxin block?

A

The release of acetylcholine (muscle contraction) - flaccid paralysis

66
Q

What do Botulinum neurotoxins contain?

A

Zn metalloproteases - cleave SNARE proteins - block exocytosis

67
Q

What is SNARE?

A

Membrane anchorage of vesicles containing neurotransmitter

68
Q

What does BoNT A target and cleave?

A

SNAP 25

69
Q

What are SNARE necessary for?

A

Vesicular transport Fusion between plasma membrane and vesicles

70
Q

Where does Antigen presented by MHC II bind? (Normal situation)

A

Antigen-binding-groove (ABG) of the TCR

71
Q

Where does superantigens bind?

A

Outside the ABG and cause widespread non-specific stimulation of T cells Leads to immunological dysfunction (IFN Gamma, IL-2, TNF alpha)

72
Q

What is the consequence of immunological dysfunction?

A

Fever, vomitting, diarrhoea, shock with circulation/organ failure, death

73
Q

What are the main producers of superantigen toxins?

A

Streptococcus pyogenes Staphylococcus aureus

74
Q

What does streptococcus pyogenes produce?

A

Pyrogenic Exotoxins that Cause streptococcal toxic shock syndrome (STSS)

75
Q

What does staphylococcus aureus produce?

A

Toxic shock syndrome toxin (TSST-1) that bind TCR and MHC Ii - cause toxic shock syndrome

76
Q

What is staph.aureus leucotoxins?

A

Beta-pore forming toxin formed by 2 subunits LukS- PV and LukF-PV

77
Q

Where is staph. Aureus leucotoxins present?

A

MRSA - Increase virulence

78
Q

Staph. Aureus leucotoxins

A

Target host defence cells: white blood cells, monocytes and macrophages Cause necrotic lesions in lung ( necrotising pneumonia)

Immunology (20 decks)

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