Botulism is described as nerve paralysis due to toxin buildup. Which mechanism explains this paralysis?

Botulism is described as nerve paralysis due to toxin buildup. Which mechanism explains this paralysis?

• A. The toxin blocks the release of acetylcholine in the synapse
• B. The toxin destroys myelin
• C. The toxin attacks muscle fibers directly
• D. The toxin reduces nerve conduction velocity

Answer: (A)

Botulism causes paralysis by blocking acetylcholine release at the neuromuscular junction. The botulinum toxin enters motor nerve terminals and cleaves SNARE proteins needed for vesicle fusion, so acetylcholine-containing vesicles cannot fuse with the presynaptic membrane and release its signal into the synaptic cleft. Without acetylcholine, the muscle fiber at the motor end plate can’t be stimulated, so it cannot contract, leading to flaccid paralysis. This mechanism is presynaptic and neurotransmitter-specific rather than damaging nerve myelin, the muscle fibers themselves, or the speed of nerve conduction along the axon. If myelin were destroyed, or muscle fibers were directly damaged, or nerve conduction were simply slowed, the pattern of weakness and physiology would be different from the orderly, transmitter-release–blocked paralysis seen with botulism.

Botulism causes paralysis by blocking acetylcholine release at the neuromuscular junction. The botulinum toxin enters motor nerve terminals and cleaves SNARE proteins needed for vesicle fusion, so acetylcholine-containing vesicles cannot fuse with the presynaptic membrane and release its signal into the synaptic cleft. Without acetylcholine, the muscle fiber at the motor end plate can’t be stimulated, so it cannot contract, leading to flaccid paralysis.

This mechanism is presynaptic and neurotransmitter-specific rather than damaging nerve myelin, the muscle fibers themselves, or the speed of nerve conduction along the axon. If myelin were destroyed, or muscle fibers were directly damaged, or nerve conduction were simply slowed, the pattern of weakness and physiology would be different from the orderly, transmitter-release–blocked paralysis seen with botulism.