Botulinum neurotoxin is produced by the anaerobic bacterium Clostridium botulinum. It is the most poisonous biological substance known. Very small amounts of botulinum toxin can lead to botulism, a descending paralysis with prominent bulbar symptoms and often affecting the autonomic nervous system. Botulism can occur in two ways. It can result from infection with bacterial spores that produce and release the toxin in the body—as in enteric infectious botulism, when the bacteria grow in the intestine, and in wound botulism, when the wound becomes infected. Alternatively, botulism occurs after ingestion of the toxin (food borne botulism).1

Botulism has been recognised since the early 19th century, and there was speculation about what caused the condition. In 1822 it was suggested that a “fatty acid” in sausages was the culprit,2 and this led to the term botulism (botulus being the Latin word for sausage). In 1897, Van Ermengen related botulism to a bacterial toxin.3

The discovery that botulinum toxin blocks neuromuscular transmission4 and thereby causes weakness laid the foundation for its development as a therapeutic tool. In 1981, the ophthalmologist Alan Scott pioneered treatment with botulinum toxin when he used it to treat strabismus.5 He paved the way for clinical research in many specialties.