Review on Foodborne Botulism: Historical Notes, Diagnosis and Treatment

Abstract

It is likely that mankind has been plagued by food-borne botulism since the beginning of time. Prior to the 19th century, food poisoning was only documented in a few historical sources. There is evidence that some ancient dietary laws and taboos were based on a knowledge of the life-threatening effects of poisoned food. Botulism was first described in 1735. However, in 1793, another intoxication occurred in Wildbad, in Baden-Württemberg, Germany, when six persons over 13 died. The cause of the intoxication was a popular blood sausage (black pudding). Blood sausages were prohibited by the edict of Emperor Leo VI of Byzantium in the 10th century. Atropine intoxication cannot result in dilated pupils combined with fatal muscle paralysis as described in some ancient case reports on Atropa belladonna intoxications. The discovery of botulinum toxin in Southern Germany at the end of the 18th century was spurred by well-documented outbreaks of “sausage poisoning” in Württemberg. Between 1817 and 1822, Justinus Kerner (1786-1862) published the first accurate and complete description of the symptoms of foodborne botulism. Clostridia species produce botulinum neurotoxins (BoNTs), which are the most potent natural toxins known. An acute symmetric descending flaccid paralysis is a classic symptom of toxic neurological syndrome (afebrile). In most cases, botulism occurs as a result of food poisoning. A toxin-induced neuromuscular paralysis causes all forms of the disease to exhibit the same symptoms. The diagnosis of botulism and the choice of antidote are essentially clinical decisions. Labs are mandatory in confirming clinical suspicions to regulatory agencies, identifying the BoNTs involved, and identifying the source of intoxication. Detection of BoNTs in clinical specimens/food samples and isolation of BoNTs from stool are the two steps in the diagnosis of foodborne botulism in the laboratory. The initial symptoms of foodborne botulism can be confused with more common clinical conditions (stroke, myasthenia gravis, Guillain-Barré syndrome-Miller-Fisher variant, Eaton-Lambert syndrome, tick paralysis, and shellfish or tetrodotoxin poisoning). As part of the treatment, decontamination procedures, antidotes are administered, and, when necessary, respiratory support is provided; little difference is related to the way that the patient was exposed to the substance.