Clostridium botulinum and Botulinum toxin Clostridium botulinum is Clostridium botulinum, the two are synonymous. Clostridium is a genus of Bacillus family, is able to form bacilli, anaerobic growth of Gran stain positive large bacilli, because its bacilli are often larger than the body, resulting in the body is shuttle-shaped and named, there are Chen anaerobic bacillus genus, to avoid ambiguity, now collectively referred to as botulinum. Botulinum toxin, short for botulinum toxin, is also often referred to as botulinum toxin or botulinum toxin, which is an extracellular toxin produced by Clostridium botulinum in the process of reproduction. Botulinum toxin is not released by the living Clostridium botulinum, but the non-toxic precursor toxin is first produced in Clostridium botulinum cells, and after the death of Clostridium botulinum and autolysis, the precursor toxin is free and activated by trypsin in the intestine or protease produced by bacteria, before it becomes toxic. Different strains can produce different subtypes of neurotoxins. Among them, botulinum toxin type A is the most virulent, the most studied and the most widely used. Usually, the botulinum toxin we use in our cosmetic clinical practice is type A botulinum toxin. Botulinum toxin type A is a 150kD polypeptide consisting of a 100kD heavy chain and a 50kD light chain linked by a disulfide chain, and is one of the most toxic natural substances known. Botulinum toxin type A for clinical use is a complex of neurotoxin, hemagglutinin and hemagglutinin protein. Neurotoxin plays a therapeutic role, and hemagglutinin maintains the morphology and spatial structure of the toxin to keep the toxin stable and toxic. Mechanism of action Botulinum toxin mainly inhibits the release of acetylcholine from nerve endings, causing muscle relaxation and paralysis. Under normal conditions, the process of muscle contraction is: nerve impulse → acetylcholine → end plate potential → muscle action potential → muscle contraction. Botulinum toxin acts on the endings of cholinergic motor nerves, and by antagonizing the effect of calcium ions, it infects the release of acetylcholine from motor nerve endings, thus blocking the conduction of nerve impulses to muscles and causing muscle paralysis.