Clostridium botulinum is the Gram-positive soil bacterium most famous in the cosmetic world for its ability to produce the highly sought after neurotoxins. Seven serotypes of C. botulinum exist, each giving rise to an antigenically distinct botulinum toxin, botulinum neurotoxin (BoNT) type A, B, C1, D, E, F, and G (serotype C2 exists but is cytotoxic and not neurotoxic). All toxins have the ability to bind to motor nerve terminals, become internalized, and block the release of acetylcholine (Ach). However, a complex interplay of several factors, including toxin serotype, potency, duration of action, preparation, volume of dilution, and protein load, creates variation among the neurotoxins. Of the seven distinct neurotoxin serotypes, BoNT type A has been the most scrutinized, studied, and therapeutically successful commercially available form.

The history of how this deadly toxin became available to use as medicine is fascinating and includes work done by many dedicated and astute physicians and scientists. The toxic effect of botulinum toxin was first noted in 1822 by a German physician, Kerner, who described food poisoning caused by ingestion of sausages. It was not until some years later, in 1895, that a Belgian microbiologist, Professor van Ermengen, identified that a bacterium producing a neurotoxin was the cause of botulism in Belgium musicians who became ill after eating sausages. Progress in research was possible after researchers, including Professor Ed Schantz and his colleagues, purified botulinum toxin A in sufficient amount for research.