Botulism is a neuroparalytic disease caused by neurotoxins produced by Clostridium botulinum, and classically presents as palsies of cranial nerves and acute descending flaccid paralysis. Food-borne botulism is the most common form of botulism, and caused by preformed neurotoxins produced by Clostridium botulinum. Electrophysiological studies play an important role in the early diagnosis. Confirmation of the diagnosis is based on the detection of botulinum toxins in the patient's serum or stool. In Japan, decades ago, botulism type E occurred, though only sporadically, almost every year, but in recent years, has dramatically decreased in frequency. Botulism is a curable disease when treated early and adequately. Differential diagnosis of cranial nerves and limb muscle palsies with rapid exacerbation should include food-borne botulism.
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Preventive Effects of Botulinum Neurotoxin Long-Term Therapy: Comparison of the 'Experienced' Benefits and 'Suspected' Worsening Across Disease Entities.
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January 2025
Department of Neurology, University of Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, Germany.
Repetitive intramuscular injections of botulinum neurotoxin (BoNT) have become the treatment of choice for a variety of disease entities. But with the onset of BoNT therapy, the natural course of a disease is obscured. Nevertheless, the present study tries to analyze patients' "suspected" course of disease severity under the assumption that no BoNT therapy had been performed and compares that with the "experienced" improvement during BoNT treatment.
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Division of High-Risk Pathogens, Department of Laboratory Diagnosis and Analysis, Korea Disease Control and Prevention Agency, KDCA, Cheongju 28159, Republic of Korea.
Background: Botulinum neurotoxins (BoNTs), produced by , are potent protein toxins that can cause botulism, which leads to death or neuroparalysis in humans by targeting the nervous system. BoNTs comprise three functional domains: a light-chain enzymatic domain (LC), a heavy-chain translocation domain (HC), and a heavy-chain receptor-binding domain (HC). The HC domain is critical for binding to neuronal cell membrane receptors and facilitating BoNT internalization via endocytosis.
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Institut für Zellbiochemie, OE 4310, Medizinische Hochschule Hannover, 30623, Hannover, Germany.
Botulinum neurotoxins (BoNT) are established biopharmaceuticals for neuromuscular and secretory conditions based on their ability to block neurotransmitter release from neurons by proteolyzing specific soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins. Recently, a mutant catalytic domain of serotype E (LC/E) exhibiting 16 mutations was reported to cleave the phosphatase and tensin homolog (PTEN). This molecule represents an attractive new target in neurons as several reports support PTEN knockdown as a strategy to stimulate axonal regeneration after injury.
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Background: This is the first study to examine a cohort that engages in the practice of immunization with snake venoms. In this practice, either fresh wet venom or venom reconstituted from freeze-dried form is used in vaccination protocols to produce hyper-immunity to venom.
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Botulinum neurotoxins exploit host digestive proteases to boost their oral toxicity via activating OrfXs/P47.
Nat Struct Mol Biol
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Department of Physiology and Biophysics, University of California, Irvine, Irvine, CA, USA.
Botulinum neurotoxins (BoNTs) rank among the most potent toxins and many of them are produced by bacteria carrying the orfX gene cluster that also encodes four nontoxic proteins (OrfX1, OrfX2, OrfX3 and P47). The orfX gene cluster is also found in the genomes of many non-BoNT-producing bacteria, often alongside genes encoding oral insecticidal toxins. However, the functions of these OrfXs and P47 remain elusive.
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