mymedschool.orgU01.03.017 Bacteria with exotoxins

Exotoxins are secreted proteins produced by bacteria that disrupt host cell function. They often act enzymatically, interfere with cell signaling, or lyse cells. Many are AB toxins, where the B (binding) subunit mediates attachment and endocytosis, and the A (active) subunit performs the toxic enzymatic function.

1. Inhibit Protein Synthesis (AB toxins targeting ribosomes)

Bacterium	Toxin	Mechanism	Clinical Manifestation	Mnemonic
Corynebacterium diphtheriae	Diphtheria toxin	ADP-ribosylates EF-2, halting protein synthesis	Pharyngitis with pseudomembranes, lymphadenopathy (“bull neck”), myocarditis	“Diphtheria → Death of cells”
Pseudomonas aeruginosa	Exotoxin A	ADP-ribosylates EF-2, host cell death	Tissue necrosis, systemic infection	Similar to diphtheria
Shigella spp.	Shiga toxin	Inactivates 60S ribosome	Dysentery; HUS (especially EHEC O157:H7)	“Shiga → Stop protein synthesis”
Enterohemorrhagic E. coli (EHEC)	Shiga-like toxin	Inactivates 60S ribosome	Hemolytic-uremic syndrome (HUS); does not invade cells	“Like Shigella but no invasion”

2. Increase Fluid Secretion (Enterotoxins)

Bacterium	Toxin	Mechanism	Clinical Manifestation	Mnemonic
Enterotoxigenic E. coli (ETEC)	LT (heat-labile)	↑ adenylate cyclase → ↑ cAMP → ↑ Cl⁻ secretion	Watery diarrhea	“Labile → Adenylate cyclase”
	ST (heat-stable)	↑ guanylate cyclase → ↑ cGMP → ↓ NaCl resorption	Watery diarrhea	“Stable → Guanylate cyclase”
Vibrio cholerae	Cholera toxin	Permanently activates Gs → ↑ cAMP	“Rice-water” diarrhea	Think cholera → watery floods
Bacillus anthracis	Anthrax toxin	Mimics adenylate cyclase → ↑ cAMP	Edematous borders of cutaneous anthrax eschar	Edema + anthrax

3. Inhibit Phagocytic Ability

Bacterium	Toxin	Mechanism	Clinical Manifestation	Mnemonic
Bordetella pertussis	Pertussis toxin	Inactivates Gi → ↑ cAMP	Whooping cough, posttussive vomiting, 100-day cough	“Pertussis → Persistent cough”

4. Inhibit Neurotransmitter Release

Bacterium	Toxin	Mechanism	Clinical Manifestation	Mnemonic
Clostridium tetani	Tetanospasmin	Cleaves SNARE proteins → inhibits GABA & glycine release	Spastic paralysis, risus sardonicus, trismus	“Tetanus → Tight”
Clostridium botulinum	Botulinum toxin	Cleaves SNARE proteins → inhibits ACh release	Flaccid paralysis, infant botulism, foodborne botulism	“Botulism → Floppy”

5. Lyse Cell Membranes

Bacterium	Toxin	Mechanism	Clinical Manifestation	Mnemonic
Clostridium perfringens	Alpha toxin	Phospholipase → membrane destruction	Myonecrosis (“gas gangrene”), hemolysis	“Perfringens → Perforates membranes”
Streptococcus pyogenes	Streptolysin-O	Pore-forming → lyses RBCs	Beta-hemolysis; ASO antibodies used in rheumatic fever	“Strepto → Stab RBCs”

6. Superantigens (Massive Cytokine Release)

Bacterium	Toxin	Mechanism	Clinical Manifestation	Mnemonic
Staphylococcus aureus	TSST-1	Cross-links the TCR β region to MHC II	Toxic shock syndrome: fever, rash, shock	“TSST → Toxic Shock”
Streptococcus pyogenes	Erythrogenic exotoxin A	Superantigen	Scarlet fever, toxic shock-like syndrome	“Scarlet A”

High-Yield AB Toxin Note:

A subunit: Active/enzymatic → disrupts host cell function
B subunit: Binding → mediates uptake into host cell

Learning Objective: Identify major exotoxins, their mechanism of action, and clinical manifestations, focusing on high-yield Step 1 associations.