Microbial and Fungal Toxins Flashcards

1
Q

WHat 2 types of microbial toxin exist?

A
> Endotoxin (LPS) 
- part of the outermembrane of G- bacteria
- Lipid A part specifically (O some chains largely irrelevant) 
- heat stable
- hydrophobic
> exotoxins 
- secreted or released on lysis 
- proteins(so heat labile)
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2
Q

How is LPS toxic?

A
  • molecular structure recognised by PRRs on macrophages etc. as a sign of bacterial infection
  • macrophage receptors ocmplexes CD14, TLR4, MD2 cause release of cytokines TNFa[tumour necrosis factor], IL-1
  • > fever, hypotension, and other pathophysiological effects
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3
Q

Give 7 examples of exotoxins

A
  • cytolytic toxins
  • enzymes
  • enterotoxins
  • neurotoxins
  • superantigens
  • ADP-ribosylation toxins
  • Type 3 secretion systems
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4
Q

Give an examples of cytolytic toxins

A
  • Heamolysins eg Streptolysin S (Strep equi)

- leukocidins e.g. APXIII of a. pleuropneumoniae

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5
Q

Give examples of enzymes

A
  • phospholipase C of Clostridium. perfringens (alpha toxin)
  • hyaluronidase
  • collagenase
  • protease
  • lipase
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6
Q

e.g.. of enterotoxins

A
  • act in the GIT
  • ADP-ribosylation toxins - Latbile enterotoxin (LT) of E. COli (similar to cholera toxin, attaches brush border of SI cells, -> secretion of CL- (+ therefore Na+) -> secretory D+ via cAMP and G protein receptors)
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7
Q

eg. of neurotoxin

A

> Botulinum toxin
- blocks release of ACh at synapse and NMJ -> flaccid paralysis and death
- often source is a dead and rotting small animal in a bale of silage
wild fowl also get botulism (“limber neck”)
Tetanus toxin
- blocks release of NTs for inhibitory synapses (GABA and glycine)
- uncontrolled exitatory synaptic activity

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8
Q

Why is botulism a public health risk?

A

Gets into milk

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9
Q

What are super antigens?

A
  • eg. staph aureus TSST-1
  • immunomodulators, induce massive T-cell activation and cytokine release
  • toxin binds to invariable regions on MHC Class 2 on APC
  • > short circuiting of the normal T cell activation pathway
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10
Q

What are ribose transferases?

A
  • add one/more ADP-ribose moieties to a protein
  • affect cell signalling and gender regulation
  • toxicity of cholera toxin, diphtheria toxin and enterotoxins
  • may types of exotoxin act this way eg. pertussis toxin, pseudomonas exotoxin A, diptheria, cholera, E.Coli LT
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11
Q

Outline the pathogenesis of salmonella. Clinical signs?

A
  • > bloody mucoid D+ +- septicaemia
  • Type 3 secretion systems (Injectosomes)
  • needle like structure used as sensory probe to detect eukaryotic cells and then secret proteins into cells
  • exert effects that help pathogen to survive and evade the immune response (uptake into host cell blebosome) initiate apoptosis of host cell
  • T3SS proteins = structural proteins (syringe) efector proteins (contents) and chaperonins (protectors) contained in the Salmonella Pathogenicity Island
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12
Q

Egs. of toxins used as vaccine agents

A

> neutrolising Ab production to the toxoid (formalin treated toxin)

  • tetanus
  • diptheria
  • clostridial
  • pasteurella osteolytic tocin (atrophic rhinitis)
  • APX1,2,3
  • Anthrax toxin
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13
Q

3 classes of mycotoxin?

A
  1. toadstool poisoning
  2. ingestion of plant pathogenic fungi (ergotism)
    - ingestion of mouldy feed (mycotoxicosis)
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14
Q

What colour is amanita phalloides? COmmon name?

A

Orange

- death cap

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15
Q

What is ergotism? Clinical signs

A
  • ergot poisoning
  • sclerotium forms in grass and cereal
  • ergots contain vasoactive alkaloids (eg. ergotamine)
  • ingestion -> constriction of arterioles in extremitis -> gangrene and lameness, convulsions, halucinations and pain
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16
Q

Outline the lifecycle of ergot

A

eg. claviceps purpurea
- sclerotium overwinters in soil
- in spring, ergot germinates -> tiny toadstools produce sexual spores (ascospores) inside the perithecium
- ascospores infect the floret of wheat etc (ovary colonised by the fungus)
- conidiospores (asexual spores) produced from mycelium
- honeydew exudes from infected floret, attracting flies
- conidiospres SPREAD TO OTHER FLORETS (warm spring encourages spread)
- grain replaced by compacted mycelium (ergot)

17
Q

What is mycotoxicsosis? eg? How can this be identified?

A
  • toxins produced in feed moulded after harvest
    > eg. AFLAtoxin (not alfa)
    -> turkey X disease d/t aspergillus flavus (hence afla)
  • fluoresces blue or green
    -eg. also aspergillus fumigatus (sporing heads with conidiospores)
    > trichothecenes
  • grain moulded with fusarium sp. in the field
    -> alimentary toxis aleukia in humans
    > zearalonone
  • oestrogenic factor
  • pigs, mouldy grain
    > ochratoxins
  • Denmark, pigs
  • nephritis
  • coffee beans?
18
Q

How common is aflatoxin poisoning? Clinical signs/path?

A

Now rare, young animals most susceptible

-> liver damage, tumours and teratogenic

19
Q

What toxin does aspergillus flavus produce?

A

Aflatoxin B1

20
Q

What toxin does aspergillus versicolorproduce?

A

Sterigmatocystin

21
Q

What toxin does penicillum viridicatum produce?

A

Ochratoxin

22
Q

What toxin does fusarium sporotrichoides produce?

A

Trichothecens (T-2)

23
Q

What toxin does fusarium graminearum produce?

A

Zearalonone