Botulism

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.

Treatment of Foodborne Botulism in Current Clinical Toxicology: Authors’ Reply

“… 1 In fact, the antitoxin should be administered also before the laboratory results, immediately as soon as clinical suspicion of botulism poisoning is suspected. 4 In our case: i) a positive history for food consumption was not promptly reported on hospital admission, ii) the clinical suspicion for botulism poisoning was difficult and unfortunately hypothesized late and iii) antitoxin research was performed only after laboratory confirmation: these aspects made the diagnosis and the treatment of this case of severe foodborne botulism complicated and not as timely and prompt as theoretically desired.…”

“…About the timing of antidote administration, it should keep in mind that the aim of the antitoxin therapy consists in neutralizing the circulating toxin molecules still unbound to the nerve endings: this mechanism of action limits the involvement of new nerve endings, but cannot reverse the paralysis nor neutralize the toxins already bound to the nerve receptors. 4 The clinical picture of our baby was severe still at admission (severe respiratory failure with hypoxemia and metabolic acidosis) and rapidly worsening consistent with the ingestion of a large dose of type A toxin, the most potent type of botulinum neurotoxins. In our case, trivalent antitoxin was administered about 10 hours after laboratory confirmation.…”

“…3 However, these procedures may be difficult and their efficacy may be reduced in the presence of drug- or toxin-induced ileus. 4 In some cases prostigmine, which inhibits the enzymatic degradation of acetylcholine, appears to be useful in reversing ileus. 5 In our case, the prolonged absence of peristalsis and the gastric stasis made cathartic agents administration difficult; in fact gastrointestinal decontamination with nasogastric tube, activated charcoal oral administration and intravenous prostigmine were performed to reduce the toxin absorption and to promote the gut peristalsis.…”

Fatal Course of Foodborne Botulism in an Eigth-Month Old Infant

“…The ‘infant’ form is reported the most frequently under one year of age. 1 , 2 , 4 In one case of foodborne botulism described in the US, the patient (a six month-old infant) gradually recovered from a severe neuroparalytic picture after a 6-week period of intensive care. 5 Foodborne cases have also been reported in 1 to 2 year-old infants (2 fatal and 3 non-fatal cases) mostly due to ingestion of home-canned baby food.…”

“…The human botulism is primarily related to types A, B, E and rarely to type F. All forms of botulism (foodborne, wound, infant botulism, adult intestinal toxemia, inhalational and iatrogenic botulism) are characterized by the same clinical syndrome, including an acute/subacute afebrile condition and symmetric descending flaccid paralysis. 1 Foodborne botulism is caused by ingestion of preformed toxin in food. The onset of clinical manifestations can be rapid and dramatic, differing from the infant form which usually develops less rapidly as the result of progressive intestinal colonization by neurotoxigenic clostridia and subsequent intraluminal production and absorption of toxin.…”