Bacterial Toxins

There are now more than 240 well-recognized bacterial toxins. A few of these are entirely responsible for the patterns of clinical illness (e.g. botulinum toxin in botulinum poisoning), but the majority are important components in the spectum of virulence factors that a pathogenic bacterium uses to cause disease. Some of the most important toxins are listed in the table below.

There are numerous ways to classify toxins:

Pattern of release, e.g. endotoxin or exotoxin
Structural model:
Subunit toxins:
- enzymatic component (A)
- adhesin component (B)
Cellular / tissue target, e.g. enterotoxins, neurotoxins, leukotoxins, haemolysins, etc.
Mechanism of action:
- membrane damaging toxins (cytolysins)
- receptor modulating toxins
- internalised / enzymatic toxins
- ADP-riboslylating toxins
- Adenylate cyclase toxins etc
Major biological effects, e.g. dermonecrotic, oedema-producing, haemolytic, diarrhoea-producing etc.

Some important bacterial toxins:

Name:	Micro-organism:	Structure:	Target/receptor:	Mode of action:	Biological effect:
Membrane damaging (Pore-forming) toxins:
Pneumolysin	Streptococcus pneumoniae	-	Bind cholesterol	Form aggregates, membrane spanning pores	decreased efficiency phagocytosis; cell death
Receptor targeting toxins:
TSST-1 (superantigen)	Staphyloccus aureus	_	HLA-DR & DQ (MHC Class II)	Widespread T-cell activation then deletion	greatly increased cytokine production; shock
Internalised / enzymatic toxins:
Adenylate cyclase toxins:
Oedema factor	Corynebacterium anthacis	A+B	Unknown glycoprotein	Calmodulin-activated adenylate cyclase.	increased target cell cAMP
RNA glycosidase toxins:
Shiga toxin	Shigella dysenteriae	A+5B	Globotriaosylceramide	N-glycosidase cleavage of rRNA	decreased protein synthesis results in cell death
Metalloprotease toxins:
Tetanus toxin	Clostridium tetani	A/B	Probably ganglioside	Zn2+-dependant protease cleavage of synaptobrevin	decreased gamma-aminobutyric acid release (esp. interneural synapses) results in spastic paralysis
Botulinum toxin	Clostridium botulinum	A/B	Probably ganglioside	Zn2+-dependant protease cleavage of synaptobrevin	decreased acetyl choline release (esp. neuromuscular synapses) results in flaccid paralysis
ADP-ribosylating toxins:
Cholera toxin	Vibrio cholerae	A+5B	GM1 ganglioside	Stimulation and stabilisation of Gs-alpha (Stimulatory G protein)	Activation adenylate cyclase results in increased cAMP leading to secretory diarrhoea
Pertussis toxin	Bordetella pertussis	A+5B	Glycoprotein / glycolipids?	Fixation of Gi-alpha in inactive form(Inhibitory G-protein)	Loss of adenylate cyclase inhibition results in inhibition of signal transduction
Diphtheria toxin	Corynebacterium diphtheriae	A/B	Erythrocyte Growth Factor (EGF)-like precursor	ADP-ribosylation of elongation factor II	Inhibition protein synthesis results in cell death

Bacterial Toxins

Some important bacterial toxins:

See also: "The Bad Bug Book"

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