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MICB 308 > Toxins: BoNT, TeNT, Anthrax > Flashcards

Toxins: BoNT, TeNT, Anthrax Flashcards

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1
Q

clostridial neurotoxins (2)

A
  • botulinum toxin (BoNT)
  • tetanus toxin (TeNT)
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2
Q

botulinum toxin (BoNT): bacterium

A
  • clostridium botulinum
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3
Q

botulinum toxin: serotypes

A
  • A-G
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4
Q

BoNT: serotype A (3)

A
  • one of the most potent toxins for humans
  • extremely toxic lethal dose
  • half life of several months
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5
Q

BoNT: symptoms (2)

A
  • flaccid paralysis; body goes limp
  • muscles relax with no contractions
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6
Q

tetanus toxin: bacterium

A
  • clostridium tetani
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7
Q

TeNT: symptoms (2)

A
  • spastic paralysis; muscle spasms
  • muscles contracting excessively
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8
Q

C. botulism (3)

A
  • strict anaerobe
  • spore-former
  • gram positive
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9
Q

botulism types (4)

A
  • food botulism
  • infant botulism
  • wound botulism
  • cosmetic botulism
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10
Q

food botulism (2)

A
  • ingestion of toxin
  • bacteria grow in food anaerobically, producing toxin in the food
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11
Q

infant botulism (2)

A
  • ingestion of bacterial spores
  • bacteria grows in gastrointestinal tract
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12
Q

wound botulism (2)

A
  • puncture with bacterial spore
  • bacteria grows in wound
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13
Q

cosmetic botulism

A
  • injection of toxin for cosmetic reasons
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14
Q

progenitor BoNT structure (3)

A
  • heterodimer
  • active (derivative) BoNT protein
  • non-toxic protein similar to BoNT (missing active site)
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15
Q

progenitor BoNT structure (3)

A
  • heterodimer
  • active (derivative) BoNT protein
  • non-toxic protein similar to BoNT (missing active site)
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16
Q

progenitor BoNT: non-toxic component (2)

A
  • likely protects active protein from stomach acids and proteases
  • active component eventually dissociates from complex
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17
Q

BoNT structure (3)

A
  • single protein with multiple domains
  • HC (heavy chain) and LC (light chain)
  • held together via disulfide bonds
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18
Q

BoNT structure: HC

A
  • B subunit
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19
Q

BoNT strucutre: LC (2)

A
  • A subunit
  • zinc-endopeptidase, a protease
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20
Q

BoNT target cell

A
  • binds neurons in the peripheral nervous system
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21
Q

BoNT receptor

A
  • “B” subunit binds to pre-synaptic membrane receptors
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22
Q

BoNT: mechanism of intoxication (5)

A
  1. HC binds receptor and is taken up into the neuron in an endosome
  2. disulfide bonds are reduced when pH drops
  3. LC subunit translocates via HC to the cytosol
  4. depending on serotype, LC cleaves different SNARE proteins
  5. fusion of vesicle with pre-synaptic membrane is prevented and no neurotransmitters are released
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23
Q

BoNT: what SNARE proteins are cleaved (3)

A
  • Synaptobrevin
  • SNAP25
  • Syntaxin
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24
Q

Synpatobrevin (2)

A
  • a VAMP
  • found on vesicles containing neurotransmitters
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25
VAMP
- vesicle associated membrane protein
26
SNAP25
- found on pre-synaptic membrane
27
Syntaxin
- found on pre-synaptic membrane
28
what is the molecular results of BoNT intoxication (2)
- blockage of the release of neurotransmitters from neuromuscular junctions in the peripheral nervous system - BoNT prevents normal contraction of muscles upon stimulation
29
BoNT: severe condition (2)
- respiratory failure - death
30
BoNT: 'mild' conditions (5)
- neurological symptoms - headache - slurred speech - double vision - nausea
31
BoNT recovery
- over a year, depending on severity
32
how are BoNT and TeNT related (3)
- structurally very similar - both are clostridial neurotoxins - have opposite mechanism/effects
33
TeNT target cells
- neurons of the central nervous system
34
what activity does TeNT exhibit (2)
- zinc-endopeptidase activity - cleaves synaptobrevin (VAMP)
35
what are the molecular results of TeNT intoxification
- prevention of the release of neurotransmitters from inhibitory neurons in the spinal cord
36
TeNT mechanism of intoxication (2)
- TeNT must be retrogradely transported to motorneuron cell body - here, it can access inhibitory neurons of the spinal cord
37
anthrax toxin bacterium
- caused by bacillus anthracis
38
B. anthracis routes of infection (3)
- cutaneous - gastrointestinal - pulmonary
39
B. anthracis: cutaneous (3)
- skin lesions - accounts for 95% of all cases of anthrax - 20% get septicemia
40
B. anthracis: gastrointestinal (2)
- rare - from eating poorly cooked meet from infected animal
41
B. anthracis: pulmonary (2)
- inhalation disease - lung is not the site of infection
42
pulmonary anthrax: within minutes (3)
- spores are inhaled - spores are phagocytosed by macrophages - macrophages travel to lymph nodes
43
pulmonary anthrax: within minutes to hours (2)
- spores germinate in the macrophage and become vegetative bacilli - bacilli escape from macrophage
44
pulmonary anthrax: within hours (3)
- bacilli produce toxins and resist phagocytes - fatal bacteremia, toxemia, or septicemia develops - edema
45
pulmonary anthrax: within days (3)
- edema - meningitis - death 1-7 days after exposure
46
pulmonary anthrax: mortality rate
- 80% mortality rate
47
why do vegetative spores bacilli become spores in the environment
- due to nutrient deprivation
48
B. anthracis: virulence factors (2)
- capsule - tri-partite toxin
49
B. anthracis: capsule virulence factor (2)
- poly-γ-D-glutamic acid - anti-phagocytic
50
B. anthracis: tri-partite toxin (2)
- 3 different proteins - protective antigen (PA), lethal factor (LF) and edema factor (EF)
51
B. anthracis: tri-partite toxin; protective antigen (2)
- "B" subunit - heptamer
52
B. anthracis: tri-partite toxin; "A" subunit
- LF and EF are A "subunits"
53
what is the receptor for the anthrax PA subunit
- anthrax toxin receptor (ATR)
54
anthrax toxin: what is the difference between PA and PA' (2)
- PA' is made from PA after the host cell protease, furin, cleaves it - PA is PA83, while PA' is PA63
55
anthrax toxin: mechanism of intoxication; adhesion/invasion (4)
1. PA binds to its receptors 2. PA is cleaved by a host protease (furin), changing into PA' 3. PA' forms a heptamer that LF and EF can now bind to 4. the entire complex is endocytosed
56
anthrax toxin: mechanism of intoxication: survival (3)
1. when pH drops to 5, the PA' heptamers form a pore in the endosome membrane 2. LF and EF unfold and translocated through pore 3. LF and EF re-fold in the cytosol
57
anthrax toxin: mechanism of intoxication; LF subunit (2)
- zinc metalloprotease - cleaves MAP kinases
58
anthrax toxin: mechanism of intoxication; EF subunit (3)
- calmodulin-dependent adenylate cyclase toxin - requires host protein calmodulin to become activated - leads to increase in cAMP levels inside the cell
59
anthrax toxin: result of LF intoxication (2)
- septic shock - death
60
anthrax toxin: results of EF intoxication (3)
- increase in water secretion - affects chemotaxis of monocytes and neutrophils - affects phagocytosis, aiding in immune evasion
61
anthrax toxin: what does EF subunit increase in water secretion affect (2)
- affects water homeostasis in the body - leads to massive edema
62
what kind of effects do EF and LT have
- pleiotropic effects
63
what systems does EF affect (3)
- immune system - cardiovascular system - endocrine system
64
what systems does LF affect (4)
- immune system - cardiovascular system - endocrine system - nervous system
65
why might anthrax toxin be difficult to study (2)
- they act on key signaling pathways present in many cells types across different systems - complicates understanding of effects as pathways targeted can cause unique effect for different cells/organs
66
what was previously found in anthrax toxin that was found to be untrue
- rapid death from LT injection was due to increased cytokine production from macrophages
67
what was more recently found in anthrax toxin that replaced old research (2)
- hypoxic response proteins rapidly increase after LT injection - LT predominantly suppresses pro-inflammatory cytokine production

MICB 308 (22 decks)

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