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Neuromuscular Junction Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Diana Mnatsakanova, Qin Li Jiang
The mainstay of treatment for severe botulism is intensive care unit monitoring with close observation of respiratory and cardiac functions. The use of antitoxin is controversial due to its lack of benefit in many cases and high risk of side effects. It must be given within 24 hours of symptom onset when toxins are still in the circulation. Equine serum antitoxin is used in babies older than 1 year of age and adults. There is a 2% risk of anaphylaxis with equine serum antitoxin. A human-derived antitoxin is used in babies less than 1 year of age. Antitoxin can only be obtained from the Center for Disease Control, Department of Public Health in Alaska and California.29
Inherited Defects in Immune Defenses Leading to Pulmonary Disease
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Serum antibodies play at least four major roles in bacterial infections: toxin neutralization; bacteriolysis in the presence of complement; opsonization of bacteria prior to phagocytosis; and formation of immune complexes which generate chemotactic cleavage products of complement. Antitoxins prevent tissue damage which facilitates the growth and spread of Clostridia, diptheria Corynebacteria, tetanus bacteria, and other infectious agents. Bacteriolysis of gram-negative bacilli may be brought about by IgM and IgG. IgA class antibodies activate complement by the alternate but not by the classical pathway [14,15]. Bacteriolysis may be enhanced by lysozyme. Pneumococcal virulence is correlated with presence of capsular protein which inhibits phagocytosis. Small amounts of type-specific antibody will accelerate phagocytosis and prolong host survival. The interactions of group- and type-specific antibody are illustrated by a series of studies of meningococcal antibody. The chick embryo lacks complement and primarily relies on phagocytic mechanisms for protection. Group Β polysaccharide antibody, which is an effective opsonin, was protective in the chick embryo, while serotype antibody, which was bactericidal and complement dependent, was not. Group- and type-specific protection were synergistic [16].
Chemical and Biological Threats to Public Safety
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Supportive care and maintenance of vital functions, especially respiration, is of the utmost importance in treatment. Specific antitoxin is available for some of the neurotoxin types (A, B, and E). With good supportive care and antitoxin administration, the mortality rate is reduced to 25%. Prolonged or permanent muscle paralysis may persist indefinitely.
Early recovery of botulism: one decade of experience
Published in Clinical Toxicology, 2021
Firouze Hatami, Shervin Shokouhi, Masoud Mardani, Minoush Shabani, Latif Gachkar, Ilad Alavi Darazam
Throughout the world, different formulation of antitoxin are available. In the EU trivalent antitoxin and heptavalent antitoxin are available. In March 2018, the European Association of Poison Center and Clinical Toxicology (EAPCCT) collected antitoxin availability data in poison centers/poisoning treating facilities (PCs) in different countries, trivalent equine antitoxin (A, B, E) was available in the EU, and the administration doses, formulation and total amount of antitoxin (IU) were varied in countries. In Poland, the recommended dosage of trivalent antitoxin (each vial 10 mL contains 5000 Units (U) serotype A, 5000 U serotype B, and 1000 U serotype E) was 1–5 vial. In Germany, the recommended dosage of trivalent antitoxin (each bottle 250 mL contains 187,500 U serotype A, 125,000 U serotype B, and 12,500 U serotype E) was two bottles [9,32].
Application of proteomics in studying bacterial persistence
Published in Expert Review of Proteomics, 2019
Jordy Evan Sulaiman, Henry Lam
The toxin-antitoxin (TA) systems, which constitute a maintenance mechanism in bacteria, are perceived to be the key players of the formation of persisters [30]. It consists of a stable toxin that targets essential cellular processes and an unstable antitoxin which prevents the toxin protein from functioning [31]. So far, there are two types of TA modules related to persistence that has been widely discussed, classified based on the antitoxin’s mechanism of action. In type I TA modules, the antitoxin counteracted the toxin actions as antisense RNAs, and most of the toxin’s in type I TA modules are membrane-associated peptides that form pores in the cell membrane to decrease ATP synthesis. Examples of these pore-forming peptides are Hok [32] and TisB toxins [33]. Besides forming pores, other type I toxins act by inducing nucleoid condensation (e.g. DinQ [34] and LdrD toxins [35]). Unlike type I antitoxins, type II antitoxins are proteins that inactivate the toxin by forming an inactive protein complex through direct protein–protein interaction. Type II toxins function by inhibiting replication or translation, usually by cleaving mRNA (RelE, MqsR, MazF toxins) and inactivating ribosome elongation factors (Doc toxin) [36–38]. Certain environmental cues such as antibiotic treatment, phagocytosis by immune cells, or biofilm formation will trigger a cascade of activation and inhibition that leads to the activation of the TA modules [20]. The increase in toxin level inside the cells will interfere with essential cellular processes and inhibit their growth, thus leading to the formation of persisters.
Foodborne botulism in Turkey, 1983 to 2017
Published in Infectious Diseases, 2019
Hasan Karsen, Mehmet Resat Ceylan, Hasan Bayındır, Hayrettin Akdeniz
Ninety-five cases of botulism were diagnosed on the basis of clinical picture and on the history of consumption of foods capable of supporting botulism neurotoxin-producing. In 71 cases electromyogram and epidemiological investigations supported the clinical diagnosis. Laboratory confirmation was performed only in 19 cases (in 9 cases detecting BoNTs in biological specimens by mouse inoculation bioassay and in 10 cases detecting type A BoNT in leftover foods by ELISA). For treatment, 56 patients were given trivalent botulism antitoxin. In 13 cases, a statement on antitoxin therapy was missing and moreover, 26 patients were left untreated because of toxin unavailability.