Tetanus toxin versus botulinum toxin
Tetanus toxin (usually entering after a contaminated wound) and botulinum toxin (which can be swallowed in food) are related enzymes at different synapses, giving rigid muscles and floppy weakness.
Remember
Tetanus toxin removes the brakes on the nerve cells that drive muscles, so the muscles go rigid. Botulinum toxin blocks acetylcholine release at the nerve ending, so the muscles go floppy.
Memory aid
tetanus removes the brakes, whereas botulism cuts the accelerator cable
Brakes removed gives rigid muscles, while a cut accelerator cable gives floppy muscles.
Both toxins are zinc-dependent proteases, which are enzymes that cut proteins. Each one cuts SNARE proteins, the machinery that pulls a vesicle (a tiny membrane bubble full of transmitter, the chemical messenger of a nerve ending) against the nerve membrane so that the two can fuse. If the vesicle cannot fuse, the transmitter is not released. The chemistry is shared, so the difference lies in where each toxin goes.
After a contaminated wound, tetanus toxin is taken up at peripheral nerve endings and carried backwards along the nerve into the spinal cord. There it blocks transmitter release from the inhibitory interneurones, the small spinal nerve cells that calm motor neurones (the nerve cells that drive muscles). Their release of glycine and GABA, the main inhibitory transmitters, is reduced, so the brake is lost. The motor neurones fire without restraint and the muscles become stiff and rigid, a picture called spastic paralysis.
Botulism is the disease caused by botulinum toxin, which can be swallowed in improperly preserved food. The toxin stays at the peripheral nerve endings of the neuromuscular junction (the synapse between motor nerve and muscle). It blocks acetylcholine release, so the muscle receives a weaker command or none at all and becomes floppy, a picture called flaccid paralysis. The weakness is typically descending, starting with the cranial nerves.
Same chemistry, different address, opposite result.
Key facts
- Shared mechanism
- both toxins are zinc-dependent proteases that cut the SNARE proteins that a nerve ending needs to release its transmitter.
- Tetanus site
- the toxin is carried backwards along nerves to the spinal cord and reduces glycine and GABA release from inhibitory interneurones.
- Tetanus result
- motor neurones fire unopposed, giving rigid (spastic) paralysis.
- Botulinum site
- the toxin stays at the neuromuscular junction and blocks acetylcholine release.
- Botulinum result
- the muscle receives a weaker command or none at all and goes floppy (flaccid paralysis), typically with a descending pattern that starts in the cranial nerves.
Exam traps
- Blocking acetylcholine release at the neuromuscular junction is the action of botulinum toxin, not tetanus toxin, and it causes flaccid weakness rather than rigidity.
- Tetanus toxin does not block glycine receptors on the receiving neurone; instead it prevents the release of inhibitory neurotransmitters from the sending nerve ending.
- Inhibiting acetylcholinesterase, the enzyme that clears acetylcholine, would leave acetylcholine in the synaptic gap for longer and increase stimulation, which is the opposite of botulism: botulinum toxin does not act on that enzyme but acts earlier, by stopping acetylcholine being released.
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