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MICR3330 Final Exam > Toxins > Flashcards

Toxins Flashcards

(39 cards)

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1
Q

Endotoxins

A

•heat stable
•lipid A portions of lipopolysaccharides
•from Gram negative bacteria

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2
Q

Exotoxins

A

•heat labile
•proteins
•released/secreted

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3
Q

Exotoxins can be named according to:

A

•the host cells they attack
•the species that produces them or the disease they cause
•their enzymatic activity

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4
Q

Which toxin does Bordetella pertussis produce?

A

Adenylate cyclase

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5
Q

What does adenylate cyclase do

A

•enters eukaryotic cells
•produces cAMP
•cell loses ability to control flow of ions
•respiratory problems
•whooping cough

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6
Q

What toxin does Clostridium perfringens produce

A

Lecithinase or phospholipase C

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7
Q

What does lecithinase do

A

•alpha toxin
•hydrolyses lecithin in cell membrane
•lyses cells
•gas gangrene

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8
Q

What is a type I toxin

A

•binds to host cell surface but doesn’t enter cell
•acts extracellularly

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9
Q

What are superantigens

A

•secreted proteins that cause massive non-specific inflammatory response

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10
Q

Which superantigens do Staphylococcus aureus produce

A

Toxic shock syndrome toxin (TSST-1)
•causes toxic shock
•shock, respiratory distress, intravenous coagulation, renal failure
•5% fatality

Staphylococcal enterotoxins A-I
•food poisoning

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11
Q

Which superantigens do streptococcus pyogenes produce

A

Spe exotoxins
•streptococcal toxic shock syndrome
•30% fatality

•necrotising fasciitis
•inflammatory destruction of connective tissue

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12
Q

What do superantigens bind to

A

•MHC II on macrophages
•T cell receptors that interact with MHC

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13
Q

What happens in a superantigen inflammatory response

A

•more macrophages and T-cell pairs than normal (10-20% of T cells)
•high levels of cytokines released by T-cells
•nausea, vomiting, fever

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14
Q

What are type II toxins

A

•act extracellularly
•destroy eukaryotic cells integrity
•form pores or phospholipase that damages cell membranes

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15
Q

How do cytotoxic type II toxins work

A

•bind to cholesterol
•causes proteins to polymerise and form a large pore
•cell becomes permeable
•cell death

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16
Q

What are some examples of cytotoxic type II toxins

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A

Streptolysin O
•produced by Streptococcus pyogenes
•beta hemolysis

•listeriolysin O
•pneumolysin
•alpha hemolysin (E coli)

17
Q

How do phospholipase type II toxins work

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A

•removes the charged polar head from phospholipid
•destabilises the membrane
•lysis

18
Q

What are some examples of phospholipase type II toxins

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A

•alpha toxin
•lecithinase
•phospholipase C (C perfringens)

19
Q

What is a type III toxin

Study These Flashcards
A

•proteins with an A-B structure
•the Binding region recognises a receptor
•the Active region acts intracellularly

20
Q

Describe the structure of a simple A-B toxin

Study These Flashcards
A

•synthesised as a single chain
•the two subunits are cleaved by protease
•theyre re-attached by a disulphide bond

21
Q

What are some examples of simple A-B toxins

Study These Flashcards
A

•diphtheria toxin
•botulinum toxin
•tetanus toxin
•exotoxin A (AB)

22
Q

Describe the structure of compound A-B toxins

Study These Flashcards
A

•multiple B subunits
•1 or more A subunits
•linked non-covalently

23
Q

What are some examples of compound A-B toxins

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A

•cholera toxin
•pertussis toxin
•LT
•shiga toxin (A1B5)
•anthrax toxin (A3B7)

24
Q

Which pathogen produces diphtheria toxin

Study These Flashcards
A

•Corynebacterium diphtheriae
•gram positive
•aerobic rod, distinctive club shape

25
What does a diphtheria infection look like
•respiratory disease, mainly of children •sore throat, swollen glands, fever, breathing difficulties •colonisation of the throat, pseudomembrane forms •DT inhibits protein synthesis and induces leukocyte response, necrosis
26
Which receptor does the B domain of diphtheria toxin bind to
Heparin-binding epidermal growth factor
27
How does diphtheria toxin cause cell death
•DT enters cell by receptor-mediated endocytosis •DT inside vacuole •endosome vacuole acidified and toxin unfolds •hydrophobic residues of translocation domain become exposed •hydrophobic residues bind to vacuole membrane and form a pore •A chain can then translocate and escape vacuole into cytoplasm •A chain catalyses ADP-ribosylation of EF-2 •damages EF-2, inhibits protein synthesis -> death
28
Which pathogen causes whooping cough
•Bordetella pertussis •gram negative coccobacillus •pertussis toxin accelerates mucous secretion and alters water transport
29
How does pertussis toxin deregulate adenylate cyclase
•B domain (S2, S3, 2 S4, S5) binds to surface receptor •toxin internalised by endocytosis •A domain (S1) ADP-ribosylates host Gi protein •inactivation of Gi •host adenylate cyclase makes cAMP •Gi inactivates adenylate cyclase when there's enough cAMP •so when PT destroys Gi, cAMP is uncontrolled
30
Which receptor does the B domain of cholera toxin bind to
•monosialosyl ganglioside (GM1) •intestinal cells
31
How does cholera toxin produce symptoms
•A1 enters cell and ADP-ribosylates Gs •Gs stimulates adenylate cyclase to make cAMP •ADP-ribosylation of Gs permanently activates Gs and stimulates adenylate cyclase resulting in increased cAMP •cAMP affects CFTR ion channels •massive secretion of Cl- through CFTR into lumen •flow of ions and water into lumen due to osmotic gradient caused by Cl- •diarrhea
32
What toxin does Clostridium botulinum produce and what are its effects
•botulinum toxin •C botulinum doesn't colonise, symptoms are caused by the toxin •BT attacks neurons and blocks acetylcholine release •prevents muscle contraction •causes flaccid paralysis
33
What toxin does Clostridium tetani produce and what are its effects
•tetanus toxin •TT binds to neurons and enter •prevents neurons from signalling relaxation •acetylcholine continually produced
34
What are the similarities between BT and TT
•both neurotoxins •have sequence homology •both zinc requiring proteases •cleave SNARE proteins needed for neurotransmitter release
35
What are the differences between BT and TT
•TT cleaves SNARE protein synaptobrevin •when cleaved, inhibitory neurotransmitter can't be released •acetylcholine continually released •TT targets CNS neurons •BT cleaves SNARE protein SNAP-25 •prevents release of acetylcholine •BT targets peripheral neurons
36
Endotoxins
•LPS from OM of gram neg bacteria •less toxic, less specific, more heat stable •lipid A is the toxic moiety
37
Endotoxin effect on host and mechanism of action
•inflammation, tissue damage, fever, septic shock •overstimulation of immune system during systemic infection •cytokine production, activation of complement and coagulation cascades, B cell mitogen
38
39
Examples of endotoxins when bacteria lyse
•lipoteichoic acid (gram pos pathogens) •peptidoglycan fragments •tracheal cytotoxin (TCT)

MICR3330 Final Exam (11 decks)

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