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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
What is example of activates complement ?
C3a ( hypotension, Edema) C5a (neutrophil chemotaxis)
26
What is example of activated tissue factor?
Coagulation cascade (DIC)
27
Where are bacterial Exotoxins Produced?
By bacteria
28
Where is bacterial Exotoxins released?
Into surrounding area and cause disease
29
What are the 3 classes of bacterial Exotoxins?
Toxins that damage membranes Toxins that act as enzymes Toxins that activate immune response
30
What happens when toxins are inserted into the membrane?
Form transmembrane pores - this leads to influx of water (endosmosis), resulting in cellular swelling and lysis
31
What are the 3 classes of bacterial Exotoxins?
Toxins that damage membranes Toxins that act as enzymes Toxins that activate immune response
32
What happens when toxins are inserted into the membrane?
Form transmembrane pores - this leads to influx of water (endosmosis), resulting in cellular swelling and lysis
33
What attaches to cell membrane cholesterol and takes part in the pathogenesis of gas gangrene ?
Perfringolysin O from clostridium perfringens
34
What does alpha-haemolysis (alpha-toxin, Hla) do?
Binds to ADAM10 at cell membrane Cause cell lysis Later signalling pathways (influx of ca2+) and contribute to disease
35
How do you form small pore-forming toxins?
Polymerisation 2 subunits Pores 1 to 1.5nm with selective permeability for small ions and nucleotides
36
What is the consequence of small pore-forming toxins?
Disruption membrane permeability Activation of endonucleases Cytokine production Initiation of Apoptosis
37
What induces cell death?
High concentration of toxins
38
What is an example of high concentration of toxins?
Alpha toxin staphylococcus aureus
39
What are the 2 subunits of A/B toxins?
A - enzymatic activity B - binding to membrane receptor and translocation of A subunit
40
A-(5)B
2 subunits independently produced and non-covalently associated during secretion
41
A+B
2 proteins which interact at cell host surface
42
A/B
1 polypeptide former by 2 domains separated by proteolysis
43
What is Diphtheria?
Gram positive, rod-like organism
44
What is Diphtheria infection?
Upper respiratory tract, with systemic effects on heart, liver, kidney and nervous system
45
What does Diphtheria infection lead to?
High children mortality in the past, before introduction of vaccination
46
What are the symptoms of Diphtheria?
Sore throat Airway obstructing pseudomrmbrane Enlarged lymph nodes in neck (bull-neck appearance)
47
What does Diphtheria toxin do?
Block protein synthesis
48
What is Diphtheria toxin (DT)?
ADP-ribosyltransferase
49
What is the process of inhibiting protein synthesis by DT?
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
What can Diphtheria toxin razchV
Blood steam and target nerves, heart and kidney
51
What is vibrio cholera ?
Acute diarrheal illness Severe dehydration caused by intestinal infection
52
What is vibrio cholera made from?
Gram-negative curved bacteria
53
How is vibrio cholera transmitted?
Ingestion of contaminated food or water
54
What does severe cholera cause?
Diarrhoea (profuse rice like water stools) Vomiting Dessication Hypotension
55
What does the lack of therapy cause in vibrio cholera?
Acute renal failure, coma, shock and death
56
What is the treatment of cholera?
Salt solution Intravenous fluid Antibiotic
57
What happens in the large intestine?
1) bacteria multiply rapidly 2) toxins from bacteria penetrates cells of intestinal wall 3) toxins prevent intestine from absorbing water from digested food
58
What does cholera toxin speed up?
Normal excretory process leading to massive fluid loss with diarrhoea and severe dehydration
59
What is the mode of action of cholera toxin?
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
What does cholera toxin inactivate ?
GTPase intrinsic activity of large G protein Galpha subunit preventing its regulation
61
What are the 3 forms of Anthrax disease?
Cutaneous Intestinal Inhalation
62
Which form of anthrax disease is fatal?
Inhalation: severe breathing problems and shock
63
How does contamination of Anthrax occur?
Via spores
64
What is the mechanism of Anthrax?
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
What does Botulinum neurotoxin block?
The release of acetylcholine (muscle contraction) - flaccid paralysis
66
What do Botulinum neurotoxins contain?
Zn metalloproteases - cleave SNARE proteins - block exocytosis
67
What is SNARE?
Membrane anchorage of vesicles containing neurotransmitter
68
What does BoNT A target and cleave?
SNAP 25
69
What are SNARE necessary for?
Vesicular transport Fusion between plasma membrane and vesicles
70
Where does Antigen presented by MHC II bind? (Normal situation)
Antigen-binding-groove (ABG) of the TCR
71
Where does superantigens bind?
Outside the ABG and cause widespread non-specific stimulation of T cells Leads to immunological dysfunction (IFN Gamma, IL-2, TNF alpha)
72
What is the consequence of immunological dysfunction?
Fever, vomitting, diarrhoea, shock with circulation/organ failure, death
73
What are the main producers of superantigen toxins?
Streptococcus pyogenes Staphylococcus aureus
74
What does streptococcus pyogenes produce?
Pyrogenic Exotoxins that Cause streptococcal toxic shock syndrome (STSS)
75
What does staphylococcus aureus produce?
Toxic shock syndrome toxin (TSST-1) that bind TCR and MHC Ii - cause toxic shock syndrome
76
What is staph.aureus leucotoxins?
Beta-pore forming toxin formed by 2 subunits LukS- PV and LukF-PV
77
Where is staph. Aureus leucotoxins present?
MRSA - Increase virulence
78
Staph. Aureus leucotoxins
Target host defence cells: white blood cells, monocytes and macrophages Cause necrotic lesions in lung ( necrotising pneumonia)

Immunology (20 decks)

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