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Michel R. Popoff, Botulinum Neurotoxins: More and More Diverse and Fascinating Toxic Proteins, The Journal of Infectious Diseases, Volume 209, Issue 2, 15 January 2014, Pages 168–169, https://doi.org/10.1093/infdis/jit505
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(See the major articles by Barash and Arnon on pages 183–91and Dover et al on pages 192–202,and the editorial commentaries by Hooper and Hirsch on page 167and Relman on pages 170–2.)
Botulism is a rare but severe disease mainly resulting from food poisoning or intestinal colonization. Food poisoning, including botulism, certainly occurred in ancient times. However, this disease was not recognized as a distinct pathological entity until the latter half of the 18th century. A first detailed description of the clinical symptoms was provided by Kerner in Germany (1815–1817), who investigated numerous cases in southwest Germany resulting from the consumption of blood sausage. The disease was called “sausage poisoning”. Notably, Kerner concluded that a toxin develops in blood sausage under anaerobic conditions that it is lethal at very small doses and induces flaccid paralysis. He speculated that this toxin may have a therapeutic application in suppressing muscle tonicity or hypersecretion of body fluids of neurological disorders manifesting by overactivity. In 1895, van Emmingen identified the causative agent, Bacillus botuliinum, later renamed Clostridium botulinum, which he isolated from a ham and from a human who died from botulism during a severe outbreak in Belgium. He found that the culture filtrates administrated to experimental animals induce the symptoms of botulism and lead to death. A few years later (1904), Landman isolated a strain from canned beans, which caused a German botulism outbreak. This was a unique event showing that botulism is a disease not only of meats or fish, but also of vegetables. Leuch (1910), from the Royal Institute of Infections in Berlin, found on the basis of the absence of cross-neutralization that the 2 strains produce distinct toxins. From the end of 18th century to the beginning of the 19th century, numerous cases have also been reported in the United States, mainly due to the consumption of heat-treated canned vegetables, which was a novel mode of food preservation at that time. It appeared that the botulinum toxin (BoNT) produced by the American strains differed from that of the European strains. The strains from canned vegetables were designated type A, and those from ham were designated type B [1].
