Botulism

Abstract

Abstract Botulism is a paralytic illness caused by botulinum neurotoxins (BoNTs) produced by three clostridium species ( Clostridium botulinum, Clostridium butyricum and Clostridium baratii ). Seven immunological BoNTs, (A–G) have been recognized. Human botulism has been mainly caused by type‐A, B, E and rarely by F neurotoxins. BoNT is a simple dichain polypeptide that consists of a 100 kDa ‘heavy’ chain joined by a single disulfide bond to a 50 kDa ‘light’ chain. The toxin's light chain is a Zn 2+ ‐containing endopeptidase that blocks acetylcholine‐containing vesicles from fusing with the terminal membrane of the peripheral cholinergic terminals, resulting in flaccid muscle paralysis and alteration of autonomic functions. Three common and naturally occurring botulism types have been identified: foodborne, wound and intestinal botulism (including infant and adult forms). Two other forms are man‐made: inhalation botulism could result from aerosolization of BoNTs from laboratory accidents or deliberate dissemination, whereas iatrogenic botulism is related to incorrect usage of injected BoNTs for cosmetic or therapeutic purposes. The clinical syndrome is characterized by symmetrical cranial nerve palsies followed by a descending, symmetrical, flaccid paralysis that may progress to respiratory compromise and death. The diagnosis is essentially clinical and can be confirmed by the detection of BoNTs in human or in food samples; in the infant and intestinal forms, BoNTs‐producing Clostridia can be isolated from stools. Current management is based on supportive treatment (including respiratory support in severe cases) and antitoxin administration that, if early practised, may prevent or limit the extent of the paralysis, but will not reverse it.