63539
Gastrointestinal Infections: Toxins
- C. Botulinum
- Neurotoxin: Inhibits acetylcholine
release from nerve endings, flaccid
paralysis
- Heavy (100kDa) & Light Chain (50kDa,
metalloprotease, HexxH zinc-binding motif,
cleaves SNARE complex, ie SNAP-25,
synaptobrevin, or syntaxin)
- Heavy (100kDa) & Light Chain (50kDa,
metalloprotease, HexxH zinc-binding motif,
cleaves SNARE complex, ie SNAP-25,
synaptobrevin, or syntaxin)
- Types A-G but food-bourne usually
A,B,D, E (marine)
- Therapy= antitoxins
to mop up free toxin
- Difficult to diagnose: Similar to stroke
symptoms. Need to isolate toxin from
faeces/CSF/serum, takes 2+ days to show!
- Mouse bioassay (4
days), new PCR
developed
- Mouse bioassay (4
days), new PCR
developed
- G+ve, spore forming (survive high temps),
anaerobe
- Outbreaks through contaminated food-
preserving/canning process inadequate
- Incubation:
6hrs-16days
- Vaccine for high risk
workers,e.g. scientists
- Infant botulism: Linden
flowers implicated,
natural sedative
- Neurotoxin: Inhibits acetylcholine
release from nerve endings, flaccid
paralysis
- S. aureus
- G+, coccus,
facultative anaerobe
- Stable over range of
pH/salt/temps
- Staph enterotoxin, heat-resistant
- Abdominal pain, vomiting, fever
- Catalase +ve,
coagulase/DNAse
+ve
- 20-100ng enough to
cause infection
- Protein-rich foods, e.g.
dairy/meat
- Incubation:
1-6hrs,
infection:<48hrs
- Enter text here
- G+, coccus,
facultative anaerobe
- B. cereus
- Cereulide (emetic
toxin), cyclic
dodecadepsipeptide
- Highly resistant to
acid/proteolysis,
heat
- Bind 5HT3 receptor on vagus
afferents (nerve fibres) to
stimulate sickness
- Inhibits fatty acid oxidation in
mitochondria, possible liver
toxicity
- Encoded on a
megaplasmid, via
ces genes
- PlcR regulated
expression
- Highly resistant to
acid/proteolysis,
heat
- 103-108 infectious
dose (high)
- Can cause meningitis,
UTIs, RTIs, HAIs!
- RTIs: carries anthracis pX01
plasmid (but no pX02- required for
capsule+positive regulator of toxin genes
on pX01)
- HAIs: amongst
immunosuppressed patients,
equipment contaminated e.g.
ventilators, intravenous
catheters, etc
- Meningitis, meningoencephalitis, brain abscess,
etc. Abdominal pain before bacteremia-->brain.
Risk factors include intrathecal induction
chemotherapy
- UTIs: Contaminant on catheter
(forms biofilm)--->pyelonephritis.
- RTIs: carries anthracis pX01
plasmid (but no pX02- required for
capsule+positive regulator of toxin genes
on pX01)
- Diarhoeal toxins
- Tripartite (Cytotoxin K
& Nonhaemolytic
Enterotoxin)
Nota:
- NHe most dominant!!
- L1, L2 (lytic) & B (binding) subunits
(CytK), NHeA, NHeB,
NHeC (NHe)
- NHe= pore former
- Oligomeric B-barrel
pore-forming
(Haemoysin bl & CytK)
- Cerelysin O
- Haemolysin II
- HlyIIR, dimeric
transcriptional
regulator (repressor)
- HlyIIR, dimeric
transcriptional
regulator (repressor)
- InhA2
- phospholipase C
- Tripartite (Cytotoxin K
& Nonhaemolytic
Enterotoxin)
- G+ve, facultative-to-aerobic,
spore-forming (resistant to gamma
radiation/pasteurisation), non-mannitol
fermentor
- Some strains produce negligible
amounts of toxin & authorised for
use as probiotic!
- Vomiting infection:
8-10hours, diarrhoeal
infection: 20-36hrs
- Cereulide (emetic
toxin), cyclic
dodecadepsipeptide
- C.perfringens
- G+ve,
spore-forming,
anaerobic
- IN NORMAL
FAECAL FLORA
- Incubation:
8-14hrs, infection:
24hrs
- Peaks in
autumn
(stews)
- Toxins
- CPE (enterotoxin)
- Bind claudin -3, -4, -8, -14
- Oligomerises into hexamer (CH1)
- Influx of Ca2+ into cell--> apoptotic pathway
- Influx of Ca2+ into cell--> apoptotic pathway
- CH2
- Internalises occludin
- Histopathologic damage
to cells--> diarrhoea
- Internalises occludin
- Oligomerises into hexamer (CH1)
- Cytoplasmic C and N termini,
4 transmembrane domains
- Bind claudin -3, -4, -8, -14
- Iota toxin
- ADP-ribosyltransferase
- CD44 binding implicated
- ADP-ribosyltransferase
- CPE (enterotoxin)
- Non-motile
- G+ve,
spore-forming,
anaerobic
- V. cholerae
- C. Difficile
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