Botulism Poisoning: A Case Study

An unlikely substance for humans to willingly inject into themselves, botulinum toxin is the endotoxin produced by the gram-negative, acidophilic anaerobe Clostridium botulinum. This neurotoxin, which causes muscular paralysis and can result in death due to respiratory failure, is extremely potent; just 50 grams would be enough to kill every person on the planet (Lindsay, 2013). The earliest recorded case of botulism poisoning occurred in 1735 in Europe. Assumed to be associated with a batch of sausage, it was named for the German word for sausage, “botulus (Sterba, 1982).” Botulism poisoning still occurs today, though with careful food preparation techniques it is incredibly rare. With modern medical attention, the case fatality rate of botulism

botulinum was first isolated and identified in 1895. Immediately, intrigue regarding possible therapeutic value of the bacterium’s potent neurotoxin led to extensive research, and ultimately, the pharmacological empire that exists today. The toxin itself was first isolated in the 1920s. By the 1950s, a medical doctor named Vernon Brooks discovered that the toxin blocked the release of acetylcholine from motor nerve endings, which temporarily reduced muscular activity when injected into a hyperactive muscle. Studies conducted by Alan B. Scott, M.D. in the 1960s showed that, in monkeys, intramuscular injection of minute quantities of purified toxin realigned the crossed eyes associated with strabismus. Shortly thereafter, Dr. Scott began testing the toxin on human volunteers (History and Development,

As seen by Blasi (1993) found that the light chain acts as a zinc-dependent protease. It targets and cleaves at the carboxy terminus of the SNARE protein SNAP-25. The destruction of this SNARE protein causes the inability for the neurotransmitter vesicles to localize via the synaptobrevin-SNAP 25 interaction. It also disables the SNARE complex from docking or fusing any vesicles. Without neurotransmitter release into the synaptic cleft, there can be no muscular contraction. The neuron still receives the signals from the central nervous system, but is no longer able to pass the signal on though the neuromuscular junction, thus paralyzing the muscles innervated by neurons affected by the