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Infection And Immunity > Neurotoxins and other toxins > Flashcards

Neurotoxins and other toxins Flashcards

1
Q

what causes Tetanus?

A

Clostridium tetani, Gram positive, anaerobic

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2
Q

how does Tetanus cause death?

A

• Spores enter wounds, germinate at low oxygen tension
• Toxin synthesised at approach to stationary phase
i.e. toxico-infection
• Death from exhaustion, respiratory failure

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3
Q

what are the Clinical symptoms of tetanus?

A

muscular spasms, fluctuation in blood pressure, irregular heartbeat, sweating dehydration

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4
Q

describe the Tetanus toxin

A

• Synthesised as a 150-kDa pro-toxin, protease cleaved to give:
- 50-kDa light chain
- 100-kDa heavy chain - disulphide bond
• Heavy chain mediates binding to GT1 gangliosides on peripheral nerve endings
• Conformational changes allow internalisation into nerve cells
• Retrograde axonal transport

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5
Q

whats the Action of tetanus toxin

A
  • Normally signals across synapses are controlled by excitatory and inhibitory neurotransmitters
  • Tetanustoxin blocks release of inhibitory neurotransmitters (e.g. glycine, g-amino-butyric acid)
  • Continuous stimulation - SPASTIC PARALYSIS
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6
Q

what causes Botulism

A

Clostridium botulinum, Gram positive, anaerobic, spore forming

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7
Q

how does botulism cause infection?

A

• Spores present in food, germinate in anaerobic conditions
• Toxin released into food
• If not destroyed by heating, toxin is ingested, absorbed in gut, enters bloodstream
i.e. intoxication

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8
Q

what are the symptoms of botulism

A

vomiting, headaches, slurred speech, generalised flaccid paralysis, progressive weakness of muscles, impaired organ functions, death

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9
Q

describe the movement of the toxin

A
  1. PROGENITOR TOXIN- ingested, passes through stomach,
    subunits dissociate in small intestine
  2. DERIVATIVE TOXIN- proteolytically cleaved in small intestine
  3. ACTIVE TOXIN- enters blood, targets peripheral neurones and enters synaptic vesicles
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10
Q

what happens after the botulism toxin is activated?

A
  • Toxin binds ganglioside receptors on neurone surface via C-terminus of large subunit
    • pH changes at cell surface enhance toxin hydrophobicity, penetrates membrane
    • N-terminus of large subunit inserts into membrane of synaptic vesicle, forms pores
    • pH changes disrupt disulphide bond
    • small (toxic) subunit passes into synaptic vesicle
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11
Q

describe the Action of botulinum toxin?

A

• Normally stimuli cause release of stimulatory neurotransmitter acetylcholine (A)
• Acetylcholine crosses synaptic space,
interacts withreceptors, trans-stimulus to neurones or to muscle
• Botulinum toxin prevents release of acetylcholine
• Inhibits stimulatory activity - FLACCID PARALYSIS

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12
Q

what is the Botulinum toxin used for?

A

• Used to treat disorders that involve muscle hyperactivity
- e.g. laryngeal dystonia, tremors, facial tics
- induces paralysis of target hyperactive muscle
• Cosmetic use - reduce deep wrinkles caused by contraction of facial muscles (Botox)

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13
Q

what are the similarities between Tetanus and botulinum toxins?

A

Both are ‘zinc endopeptidases’ and cleave synaptobrevins (vesicle- associated membrane proteins, VAMPS), inhibiting release of neurotransmitters

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14
Q

why are Tetanus and botulinum toxins Effects different?

A
  • tetanus toxin acts at nerve junctions

- botulinum toxin acts at junctions between nerves and muscles

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15
Q

name an enzyme toxin

A

• Clostridium perfringens a-toxin - phospholipase C
• Cleaves phospholipids at phosphodisester linkage - phosphatidylcholine to phosphorylcholine + a diglyceride
- sphingomyelin to phosphorylcholine + ceramide
• Causes localised cell and tissue destruction  gas gangrene
• Bacteria enter bloodstream, release more toxin (toxaemia)
• Only treatment is radical surgery

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16
Q

explain the action of Hyaluronidase enzyme toxin?

A
  • produced by Group A streptococci, Bacteroides gingivalis, staphylococci
    • Catalyses breakdown of hyaluronic acid, a component of connective tissue
    • Sub-epidermal injection of cell free hyaluronidase causes a diffuse area of tissue damage
    • Called ‘spreading factor’ – allows pathogens greater access to colonise tissues
17
Q

what is the enzyme toxin of Pseudomonas aeruginosa?

A
  • causes lung infections in immunocompromised patients, particular problem in cystic fibrosis
    • Produces elastase, a protease specific for elastin, major component of connective tissue - disrupts ciliary function of respiratory epithelium and hence clearance of mucus/bacteria
18
Q

whats the enzyme toxin associated with Streptococcus pneumoniae

A
  • produces proteases specific for secretory IgA

• Degrade antibodies, prevent recognition by macrophages, so reducing phagocytosis

19
Q

what are the 4 types of Membrane damaging toxins

A
  1. Non-enzymatic proteins cause lysis of erythrocytes and other cell types
  2. Immunologically cross-reactive, similar structures
  3. Toxins bind to cholesterol in target cell membranes,
    insert as rings of oligomers forming pores
  4. Efflux of small molecules, breakdown of membrane electrical potential
20
Q

name 2 Non-enzymatic proteins cause lysis of erythrocytes

A
  • pneumolysin of Streptococcus pneumonia

- streptolysin of Streptococcus pyogenes

21
Q

describe the action of a-hemolysin (HlyA) of E. coli

A
  • One of the first pore-forming toxins described
  • Synthesised as pro-toxin acylated (i.e. attachment of fatty acids) and secreted (107-kDa)
  • Inserts into eukaryotic membranes of erythrocytes, leukocytes, lymphocytes, epithelial and endothelial cells
  • Small amounts induce cytokine production and inflammatory response
  • Large amounts cause cell lysis
22
Q

what happens at Low HlyA

A

Interaction with host proteins
e.g. GTPase RhoA
Changes Ca2+ levels
Causes cytokine induction (IL-1, TNF)

23
Q

what happens at High HlyA

A

Pore formation

Alters osmotic balance Causes cell lysis

24
Q

what are the Functions of HlyA

A

+ In UTI isolates work in combination with cytotoxic necrotizing factor 1 to cause sloughing of uroepithlium, bladder hemorrhage and inflammation
+ May enhance spread by disrupting epithelial cells in gut lining, providing nutrients and inactivating immune effector cells

25
Q

what is Streptococcus pyogenes

A
  • Human pathogen
  • Mild diseases - pharyngitis and impetigo
  • Severe, life-threatening diseases - necrotizing fasciitis
  • Post-infection sequelae - glomerulonephritis and rheumatic fever
  • Rheumatic fever is often associated with heart disease and is a hypersensitive reaction mediated by cross-reactive antibodies
26
Q

what are S. pyogenes virulence factors

A

• M-protein – fibronectin-binding protein for
adhesion and inhibition of phagocytosis
• Hyaluronic acid capsule – inhibits phagocytosis
• Streptokinase, steptodornase, hyaluronidase and streptolysins – invasion, tissue damage and spread
• Pyrogenic toxin – causes scarlet fever rash and toxic shock

27
Q

what is the role of Streptolysin O and SPN in Virulence

A
  1. SLO induces pro-inflammatory cytokines (IL1b, IL6 and IL8)
  2. the absence of SPN helps to resolve the infection.
  3. double-mutant lacks mitigating effect is more virulent.
  4. In wt, the combination of both genes results in strong pathogenic effect.
28
Q

summarise Neurotoxins and other toxins

A
  1.  Neurotoxins cause tetanus and botulisum, two component molecules, inhibit release of neurological signalling molecules
  2.  Enzymatic toxins disrupt host tissues facilitating spread or inhibiting clearance
  3.  Membrane-damaging (pore forming) toxins perturb host immune responses influencing clearance, competition and transmission

Infection And Immunity (16 decks)

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