Letteratura scientifica selezionata sul tema "Clostridium botulinum"
Cita una fonte nei formati APA, MLA, Chicago, Harvard e in molti altri stili
Consulta la lista di attuali articoli, libri, tesi, atti di convegni e altre fonti scientifiche attinenti al tema "Clostridium botulinum".
Accanto a ogni fonte nell'elenco di riferimenti c'è un pulsante "Aggiungi alla bibliografia". Premilo e genereremo automaticamente la citazione bibliografica dell'opera scelta nello stile citazionale di cui hai bisogno: APA, MLA, Harvard, Chicago, Vancouver ecc.
Puoi anche scaricare il testo completo della pubblicazione scientifica nel formato .pdf e leggere online l'abstract (il sommario) dell'opera se è presente nei metadati.
Articoli di riviste sul tema "Clostridium botulinum"
1
Harris, Richard A., Fabrizio Anniballi e John W. Austin. "Adult Intestinal Toxemia Botulism". Toxins 12, n. 2 (24 gennaio 2020): 81. http://dx.doi.org/10.3390/toxins12020081.
Testo completoAbstract (sommario):
Intoxication with botulinum neurotoxin can occur through various routes. Foodborne botulism results after consumption of food in which botulinum neurotoxin-producing clostridia (i.e., Clostridium botulinum or strains of Clostridium butyricum type E or Clostridium baratii type F) have replicated and produced botulinum neurotoxin. Infection of a wound with C. botulinum and in situ production of botulinum neurotoxin leads to wound botulism. Colonization of the intestine by neurotoxigenic clostridia, with consequent production of botulinum toxin in the intestine, leads to intestinal toxemia botulism. When this occurs in an infant, it is referred to as infant botulism, whereas in adults or children over 1 year of age, it is intestinal colonization botulism. Predisposing factors for intestinal colonization in children or adults include previous bowel or gastric surgery, anatomical bowel abnormalities, Crohn’s disease, inflammatory bowel disease, antimicrobial therapy, or foodborne botulism. Intestinal colonization botulism is confirmed by detection of botulinum toxin in serum and/or stool, or isolation of neurotoxigenic clostridia from the stool, without finding a toxic food. Shedding of neurotoxigenic clostridia in the stool may occur for a period of several weeks. Adult intestinal botulism occurs as isolated cases, and may go undiagnosed, contributing to the low reported incidence of this rare disease.
2
Nguyen, Duc, Thu Nguyen e Huu Nguyen. "Investigation of botulism in free-range ducks farming in the Mekong Delta, Vietnam". Open Veterinary Journal 12, n. 5 (2022): 632. http://dx.doi.org/10.5455/ovj.2022.v12.i5.7.
Testo completoAbstract (sommario):
Background: One of the most common diseases in free-range ducks in the Mekong Delta is “botulism”. Botulism is a poultry disease caused by botulinum exotoxin of Clostridium botulinum. Aim: The purpose of the investigation was to evaluate the prevalence of botulism in free-range ducks in the Mekong Delta and the risk of infection by determining the presence of Clostridium botulinum in the farming environment. Methods: Research on 200 duck flocks with 187050 individuals raised freely in the fields in the provinces of the Mekong Delta including An Giang, Can Tho, Hau Giang, and Kien Giang. The ducks were diagnosed with botulism based on clinical symptoms. To demonstrate the presence of botulinum neurotoxins and identify serotype, samples of serum and/or gut were analyzed by mouse bioassay. Samples of soil (n=600), water (n=600), crabs (n=216), and snails (n=400) were taken from the grazing regions for Clostridium botulinum analysis by PCR assay. Results: There were 1.19% (2235/187050) free-range ducks in the Mekong Delta positive for botulism. Clinical symptoms of botulism including limberneck, drooping eyelids - enlarged pupils, and leg paralysis were prevalent across free-range ducks, with the frequency of 87.92% (1965/2235), 90.07% (2013/2235), and 79.78% (1783/2235), respectively. The lesions of pulmonary edema – hemorrhage, hemorrhagic liver, and gas-producing intestines were common, accounting for 86.19% (362/420), 95.48% (401/420), and 92.14% (387/420), respectively. Botulin toxin type C was found in a considerable number of serum samples, accounting for 40.48% (51/126). Meanwhile, the percentage of serum samples containing botulin toxin types E and D was 28.57% (36/126) and 25.40% (32/126), respectively. Clostridium botulinum was detected in the farming environment specifically 17.5% (105/600) in soil, 19.67% (118/600) in water, 8.33% (18/216) in crabs, and 3.00% (12/400) in snails. Conclusion: The free-range ducks in the Mekong Delta were at high risk of botulism because of the latent presence of Clostridium botulinum in the farming environment.
3
Mubarik Ali e Norina Jabeen. "Botulism a Major Risk in Animals After Flood in Pakistan; A Review". Indus Journal of Agriculture and Biology 1, n. 1 (31 dicembre 2022): 1–7. http://dx.doi.org/10.59075/ijab.v1i1.139.
Testo completoAbstract (sommario):
Flooding has affected and will likely continue to alter the occurrence, distribution, and prevalence of animal diseases, including botulism, according to a growing body of evidence. The pathogen Clostridium botulinum is thought to be one of several species that can produce the A–H-coded botulinum toxins. These toxins (BoNT) are thought to be the most harmful elements found in nature. The poison hits nerves that are firing more frequently, which causes the pattern of damage. The toxin specifically affects synapses and neuromuscular junctions by preventing the generation or release of acetylcholine there. The majority of animals who contract botulism die from it; it affects the breathing, chewing, and swallowing muscles as well as the diaphragm and intercostal muscles, leading to flaccid paralysis and respiratory arrest. The neurotoxins types C and D produced by the bacterium Clostridium botulinum in an animal or plant substance, during decomposition, are the cause of the condition in cattle. Failure of the respiratory system causes death. The toxin that causes botulism, also known as botulinus poisoning, is produced by the bacterium Clostridium botulinum. There are few available treatment options for the neuroparalytic disease botulism, which impacts the livestock business globally and has been documented in a number of nations.
4
Franciosa, Giovanna, Manoocheher Pourshaban, Alessandro De Luca, Anna Buccino, Bruno Dallapiccola e Paolo Aureli. "Identification of Type A, B, E, and F Botulinum Neurotoxin Genes and of Botulinum Neurotoxigenic Clostridia by Denaturing High-Performance Liquid Chromatography". Applied and Environmental Microbiology 70, n. 7 (luglio 2004): 4170–76. http://dx.doi.org/10.1128/aem.70.7.4170-4176.2004.
Testo completoAbstract (sommario):
ABSTRACT Denaturing high-performance liquid chromatography (DHPLC) is a recently developed technique for rapid screening of nucleotide polymorphisms in PCR products. We used this technique for the identification of type A, B, E, and F botulinum neurotoxin genes. PCR products amplified from a conserved region of the type A, B, E, and F botulinum toxin genes from Clostridium botulinum, neurotoxigenic C. butyricum type E, and C. baratii type F strains were subjected to both DHPLC analysis and sequencing. Unique DHPLC peak profiles were obtained with each different type of botulinum toxin gene fragment, consistent with nucleotide differences observed in the related sequences. We then evaluated the ability of this technique to identify botulinal neurotoxigenic organisms at the genus and species level. A specific short region of the 16S rRNA gene which contains genus-specific and in some cases species-specific heterogeneity was amplified from botulinum neurotoxigenic clostridia and from different food-borne pathogens and subjected to DHPLC analysis. Different peak profiles were obtained for each genus and species, demonstrating that the technique could be a reliable alternative to sequencing for the rapid identification of food-borne pathogens, specifically of botulinal neurotoxigenic clostridia most frequently implicated in human botulism.
5
Popoff, Michel R., e Holger Brüggemann. "Regulatory Networks Controlling Neurotoxin Synthesis in Clostridium botulinum and Clostridium tetani". Toxins 14, n. 6 (24 maggio 2022): 364. http://dx.doi.org/10.3390/toxins14060364.
Testo completoAbstract (sommario):
Clostridium botulinum and Clostridium tetani are Gram-positive, spore-forming, and anaerobic bacteria that produce the most potent neurotoxins, botulinum toxin (BoNT) and tetanus toxin (TeNT), responsible for flaccid and spastic paralysis, respectively. The main habitat of these toxigenic bacteria is the environment (soil, sediments, cadavers, decayed plants, intestinal content of healthy carrier animals). C. botulinum can grow and produce BoNT in food, leading to food-borne botulism, and in some circumstances, C. botulinum can colonize the intestinal tract and induce infant botulism or adult intestinal toxemia botulism. More rarely, C. botulinum colonizes wounds, whereas tetanus is always a result of wound contamination by C. tetani. The synthesis of neurotoxins is strictly regulated by complex regulatory networks. The highest levels of neurotoxins are produced at the end of the exponential growth and in the early stationary growth phase. Both microorganisms, except C. botulinum E, share an alternative sigma factor, BotR and TetR, respectively, the genes of which are located upstream of the neurotoxin genes. These factors are essential for neurotoxin gene expression. C. botulinum and C. tetani share also a two-component system (TCS) that negatively regulates neurotoxin synthesis, but each microorganism uses additional distinct sets of TCSs. Neurotoxin synthesis is interlocked with the general metabolism, and CodY, a master regulator of metabolism in Gram-positive bacteria, is involved in both clostridial species. The environmental and nutritional factors controlling neurotoxin synthesis are still poorly understood. The transition from amino acid to peptide metabolism seems to be an important factor. Moreover, a small non-coding RNA in C. tetani, and quorum-sensing systems in C. botulinum and possibly in C. tetani, also control toxin synthesis. However, both species use also distinct regulatory pathways; this reflects the adaptation of C. botulinum and C. tetani to different ecological niches.
6
Lindström, Miia, e Hannu Korkeala. "Laboratory Diagnostics of Botulism". Clinical Microbiology Reviews 19, n. 2 (aprile 2006): 298–314. http://dx.doi.org/10.1128/cmr.19.2.298-314.2006.
Testo completoAbstract (sommario):
SUMMARY Botulism is a potentially lethal paralytic disease caused by botulinum neurotoxin. Human pathogenic neurotoxins of types A, B, E, and F are produced by a diverse group of anaerobic spore-forming bacteria, including Clostridium botulinum groups I and II, Clostridium butyricum, and Clostridium baratii. The routine laboratory diagnostics of botulism is based on the detection of botulinum neurotoxin in the patient. Detection of toxin-producing clostridia in the patient and/or the vehicle confirms the diagnosis. The neurotoxin detection is based on the mouse lethality assay. Sensitive and rapid in vitro assays have been developed, but they have not yet been appropriately validated on clinical and food matrices. Culture methods for C. botulinum are poorly developed, and efficient isolation and identification tools are lacking. Molecular techniques targeted to the neurotoxin genes are ideal for the detection and identification of C. botulinum, but they do not detect biologically active neurotoxin and should not be used alone. Apart from rapid diagnosis, the laboratory diagnostics of botulism should aim at increasing our understanding of the epidemiology and prevention of the disease. Therefore, the toxin-producing organisms should be routinely isolated from the patient and the vehicle. The physiological group and genetic traits of the isolates should be determined.
7
Long, Sharon C., e Tiffany Tauscher. "Watershed issues associated with Clostridium botulinum: A literature review". Journal of Water and Health 4, n. 3 (1 aprile 2006): 277–88. http://dx.doi.org/10.2166/wh.2006.016b.
Testo completoAbstract (sommario):
Botulism the disease, the related organism (Clostridium botulinum) and toxin have gained renewed attention in these times of heightened homeland security and bioterrorism preparedness. Since C. botulinum is ubiquitous in nature, botulism outbreaks resulting from environmental exposure can be of concern to watershed managers and drinking water utilities. This paper reviews aspects of naturally occurring C. botulinum in light of concerns for source water watersheds. Information regarding sources and occurrence of botulism, C. botulinum and botulism toxins are discussed. Ecology and physiology of environmental C. botulinum and cycles of disease are reviewed. Finally, the effectiveness of water treatment and disinfection measures is discussed.
8
Lanci, Aliai, Riccardo Rinnovati, Fabrizio Anniballi, Bruna Auricchio, Concetta Scalfaro, Marika Menchetti, Alessandro Spadari e Jole Mariella. "The First Case of Botulism in a Donkey". Veterinary Sciences 6, n. 2 (15 maggio 2019): 43. http://dx.doi.org/10.3390/vetsci6020043.
Testo completoAbstract (sommario):
Botulism, a severe neuroparalytic disease that can affect humans, all warm-blooded animals, and some fishes, is caused by exotoxins produced by ubiquitous, obligate anaerobic, spore-forming bacteria belonging to the genus Clostridium and named botulinum neurotoxin (BoNT)-producing clostridia. This report presents the case of a 3-year-old donkey mare referred for progressive and worsening dysphagia of four days’ duration. Her voluntary effort in eating and drinking was conserved, and she was able to slow chew without swallowing. A complete neurological examination was performed, and botulism was strongly suspected. The ability to swallow feed and water returned on the tenth day of hospitalization and improved progressively. The jenny was discharged from the hospital after fifteen days. During the hospitalization, the Italian National Reference Centre for Botulism confirmed the diagnosis: mare’s feces were positive for BoNT/B and Clostridium botulinum type B.
9
Pohanka, Miroslav. "Botulinum Toxin as a Biological Warfare Agent: Poisoning, Diagnosis and Countermeasures". Mini-Reviews in Medicinal Chemistry 20, n. 10 (27 maggio 2020): 865–74. http://dx.doi.org/10.2174/1389557520666200228105312.
Testo completoAbstract (sommario):
Botulinum toxin is a neurotoxin produced by Clostridium botulinum and some other relative species. It causes a lethal disease called botulism. It can enter the body via infections by Clostridium (e.g. wound and children botulism) or by direct contact with the toxin or eating contaminated food (food-borne botulism). Botulinum toxin is also considered as a relevant biological warfare agent with an expected high number of causalities when misused for bioterrorist or military purposes. The current paper surveys the actual knowledge about botulinum toxin pathogenesis, the manifestation of poisoning, and current trends in diagnostics and therapeutics. Relevant and recent literature is summarized in this paper.
10
HAUSCHILD, A. H. W., R. HILSHEIMER, K. F. WEISS e R. B. BURKE. "Clostridium Botulinum in Honey, Syrups and Dry Infant Cereals". Journal of Food Protection 51, n. 11 (1 novembre 1988): 892–94. http://dx.doi.org/10.4315/0362-028x-51.11.892.
Testo completoAbstract (sommario):
A total of 150 honey, 43 syrup and 40 dry cereal samples were analyzed for Clostridium botulinum spores, each in triplicate quantities of 25 g. The foods were sampled randomly, except for two lots of honey which were potentially associated with illness. Botulinal spores were detected in a sample of honey associated with infant botulism and in a single sample of rice cereal.
Tesi sul tema "Clostridium botulinum"
1
Sharma, Davinder Kumar. "Toxin production by Clostridium botulinum". Thesis, University of East Anglia, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301991.
Testo completoAbstract (sommario):
The endopeptidase activity assay developed for measurement of purified botulinum neurotoxin type A (BoNT/A) in clinical therapeutic preparations has been adopted to provide a specific measure of BoNT/A activity in culture supernatants of proteolytic C. botulinum type A. Electrophoretic studies and inhibition of BoNT/A activity by anti-A antibody confirmed the specificity of the assay. The minimum detection limit was 0.2 MLD50/ml indicating the assay as more sensitive than the standard mouse bioassay or any other in vitro assay available to date. Whilst the assay did not exhibit any cross reactions with non-proteolytic (saccharolytic) clostridia, proteolytic C. botulinum types B and F and C. sporogenes showed some cross reactions. The endopeptidase assay was used to investigate physiological aspects of BoNT/A production by proteolytic C. botulinum type A strain NCTC 7272. Growth studies at 15°C, 25°C and 37°C with strain NCTC 7272 demonstrated that the first appearance of BoNT/A (0.1-1.0 MLD50 ml) occurred during mid-late exponential or early stationary phase of growth. Extracellular BoNT/A formation was not proportional to viable count. Slightly more BoNT/A was detected at 25°C than 37° or 15°C. The results of BoNT/A formation by one of the growth curves at 25°C measured by the endopeptidase assay and mouse bioassays were very similar confirming the specificity of the assay. A simple method was developed to lyre the cells so that BoNT/A formation could be subsequently measured in the endopeptidase assay. The data obtained following lysis of cells and measurement of intracellular BoNT/A showed that both intracellular BoNT/A and total BoNT/A formation is not constitutive but are more closely proportional to viable count than extracellular BoNT/A. Release of BoNT/A from cells was not associated with autolysis. The conversion of BoNT/A from the single-chain to dichain form during growth has been measured. The use of the endopeptidase assay has been also exploited to study BoNT/A formation by this strain within the population of cells. There was only a four-fold difference in BoNT/A production by cells of strain NCTC 7272, and further work in this area is warranted. Attempts were made to use MAPs for the production of monoclonal antibodies to SNAP-25 following cleavage by BoNT/E. Whilst the outcome was unsuccessful, the soundness of the principle was demonstrated
2
Raffestin, Stéphanie. "Régulation de la toxinogenèse chez Clostridium botulinum et Clostridium tetani". Paris 7, 2005. http://www.theses.fr/2005PA077044.
Testo completo
3
Davis, Tom Owen. "Regulation of botulinum toxin complex formation in Clostridium botulinum : type A NCTC 2916". Thesis, Open University, 1998. http://oro.open.ac.uk/57744/.
Testo completoAbstract (sommario):
Genomic DNA fragments encoding the silent type B neurotoxin gene from Clostridium botulinum NCTC 2916 have been cloned and the complete nucleotide sequence determined. The translated sequence revealed that the gene encoded a neurotoxin which was closely related to type B neurotoxin genes from Group I Clostridium botulinum. However among the nucleotide sequence differences, aG to T transition has interrupted the coding sequence with the formation of a stop codon. In addition the deletion of an adenine residue has resulted in a frame-shift mutation. Analysis of the DNA sequence contiguous with the silent type B neurotoxin gene revealed the presence of a gene encoding a Nontoxic-Nonhaemagglutinin protein which appears to share a bicistronic mRNA transcript with the type B neurotoxin gene. In the reverse orientation, the partial sequence of a gene encoding a haemagglutinin protein was found, typical of type A and B botulinal neurotoxin complexes. Separating the genes encoding the 'components of the neurotoxin complex was a gene of 178 amino acids which possessed features commonly associated with transcriptional factors. To facilitate the in vivo study of botulinal neurotoxin complex regulation, a gene transfer system using clostridial components has been developed. The minimal replicon of the cryptic plasmid pCB 102 from Clostridium butyricum NCIB 7423 was located to 1.6 kb DNA fragment by deletion analysis, enabling the identification of hitherto undiscovered putative ORFs and secondary structures, consistent with a replicative function. The replicon has been incorporated in to a number of Escherichia coli vectors resulting in a versatile series of shuttle vectors which have demonstrated high structural and segregational stabilities in a heterologous host Clostridium beyerinckii NCI NIB 8052. Gene transfer of a Group I Clostridium botulinum type A strain was demonstrated with a representative pCB 102-derived shuttle vector, pMTL540E. In addition, a 5.9 kb plasmid indigenous to C. hotulimun NCTC 2916 was cloned and the complete nucleotide sequence determined. Eight putative ORFs have been identified, including a putative replication protein and recombinase.
4
Cooksley, Clare Marie. "Characterisation of a putative agr system in Clostridium botulinum and Clostridium sporogenes". Thesis, University of Nottingham, 2008. http://eprints.nottingham.ac.uk/11463/.
Testo completoAbstract (sommario):
Botulinum neurotoxin induces a potentially fatal paralytic condition in humans and various animal species collectively known as 'botulism'. It consequently poses a major problem to the food industry, due to the ability of its spores to survive in cooked foods. The incidence of wound botulism has also suffered a recent increase in the UK. The genome sequence of the C botulinum Group I strain ATCC 3502 has recently been determined. In silico analysis has revealed the presence of two distinct loci capable of encoding proteins with homology to AgrB and AgrD of the Staphylococcus aureus agr quorum sensing system. The functional characterisation of these genes has been carried out in order to determine whether they play a role in quorum sensing. To simplify laboratory procedures, C. sporogenes, the non-toxic counterpart of C. botulinum, was initially focused on. The agr regions in C. sporogenes were sequenced and their proteins compared with those of C. botulinum and other Gram-positive bacteria. Regions of conservation were observed amongst the clostridia and, to a lesser extent, between clostridia and staphylococci. Transcriptional linkage assays showed some of the genes of the C sporogenes agr regions to be co-expressed, and Real-Time RT-PCR demonstrated the maximal expression of these genes during late exponential growth. Modulation of the expression of the identified agr genes is a prerequisite to determining their function. Due to an initial lack of an effective gene knockout tool, antisense RNA expression was used for this purpose in C sporogenes, and showed that down regulation of the agrB genes affects sporulation. The development of an integrative vector system for gene inactivation in C sporogenes was also attempted. Knockout mutants in C botulinum and C sporogenes were later constructed using the newly-developed ClosTron system. These mutants were used to demonstrate that AgrDl, AgrD2 and an orphan sensor kinase protein all play a role in the control of sporulation in C. botulinum and C. sporogenes.
5
Hielm, Sebastian. "Molecular detection, typing and epidemiology og Clostridium botulinum". Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/ela/elint/vk/hielm/.
Testo completo
6
Connan, Chloé. "Neurotoxinogénèse et Passage des neurotoxines botuliques à travers la barrière intestinale". Thesis, Paris 11, 2013. http://www.theses.fr/2013PA114830/document.
Testo completoAbstract (sommario):
Les neurotoxines botuliques (BoNTs), produites par C. botulinum, sont responsables du botulisme humain et animal. Dans sa forme naturelle, le botulisme résulte le plus souvent d’une absorption des toxines botuliques à partir du tube digestif après ingestion d’aliments contaminés par la toxine et C. botulinum. L’intoxination peut être divisée en 4 grandes étapes : production de toxine par la bactérie, ingestion d’aliments contenant la toxine préformée, passage de la neurotoxine à travers la barrière intestinale et action protéolytique aux terminaisons nerveuses. La régulation de la production des toxines et le passage des neurotoxines botuliques à travers la barrière intestinale sont mal compris. BoNT s’associe à des protéines non toxiques (NAPs) pour former des complexes de différentes tailles. Les gènes codant les BoNTs et NAPs sont regroupés sur le locus botulique et leur expression est contrôlée positivement par le facteur sigma alternatif BoTR/A. La toxinogénèse chez C. botulinum est contrôlée par un réseau complexe de régulateurs incluant au moins 3 systèmes à deux composants (TCS), identifiés pas la méthode d’ARN antisens, qui régulent positivement la production de complexe botulique indépendamment de BoTR/A. D’autre part, l’entrée de BoNT/B dans la barrière intestinale a été suivie à l’aide du fragment HcB marqué en fluorescence dans une anse intestinale ligaturée de souris. Des analyses en microscopie à fluorescence, immunohistochimie et microscopie électronique ont permis de mettre en évidence que HcB transcytose à travers les entérocytes par une voie d’endocytose dépendante de la dynamine. HcB cible les terminaisons nerveuses acétylcholinergiques de la lamina propia des villosités et gagne les neurones acétylcholinergiques et sérotoninergiques de la sous-muqueuse et de la musculeuse en seulement 10 minutes. Une étude in vitro réalisée sur cellules intestinales (m-ICcl2) montre que l’entrée de HcB est dépendante de récepteurs gangliosidiques GD1b/GT1b présents à la surface des cellules mais pas de la synaptotagmine II qui est requise pour l’entrée de BoNT/B dans les cellules neuronalesBotulinum neurotoxins (BoNTs), produced by C. botulinum, are responsible for animal and human botulism. In its natural form, botulism is mostly acquired after absorption of BoNTs in the digestive tract after ingestion of food contaminated with C. botulinum and its toxins. The intoxination can be divided in 4 major steps: toxin production, ingestion of food contaminated with BoNTs, passage of BoNTs through the intestinal barrier, and proteolytic activity on nerve endings. Regulation of toxin production and passage of BoNTs through the intestinal barrier are poorly understood. BoNT associates with non toxic protein (NAPs) to form complexes of various sizes. The BoNTs and NAPs genes are clustered in the botulinum locus and are positively regulated by an alternative sigma factor BotR/A. Toxinogenesis in C. botulinum is regulated by a complex regulatory network containing at least 3 two components systems (TCS), identified by antisens RNA strategy, which regulate the production of botulinum complex independently of BotR/A. On the other hand, BoNT/B entry was monitored with fluorescent HcB fragment in ligatureted mouse intestinal loop. Fluorescent imaging analysis, immunohistochemistry and electron microscopy, have evidence that HcB is transcytosed through enterocytes cells by an endocytosis dynamin dependant. HcB targets acetylcholinergic nerves localized in lamina propria of villi then reaches serotoninergic and acetylcholinergic nerve endings in the submucosa and musculosa within 10 minutes. In vitro experiments performed on intestinal cell line (m-ICcl2) shows that the endocytosis of HcB is dependent on the GD1b/GT1b gangliosidic receptors on the cell surface but not on the synaptotagmine II protein which is recquiered HcB entry in neuronal cells
7
Masuyer, Geoffrey. "Structure and activity of Clostridium botulinum neurotoxin functional fragments". Thesis, University of Bath, 2012. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.557825.
Testo completoAbstract (sommario):
Botulinum neurotoxins (BoNTs) cause flaccid paralysis by inhibiting neurotransmission at cholinergic nerve terminals. BoNTs consist of three essential domains for toxicity: the cell binding domain (Hc), the translocation domain (Hn) and the catalytic domain (LC). The binding function of the Hc domain is essential for BoNTs to bind the neuronal cell membrane, therefore removal of the Hc domain results in a product that retains the endopeptidase activity of the LC but is non-toxic. Functional derivatives (LHn) of the parent neurotoxin composed of Hn and LC domains have been recombinantly produced and characterised. The crystallographic structures of LHn from serotypes A and B are reported here and demonstrate the stability of the LHn fragment in comparison to the full length toxins. The activity of LHn has been assessed on recombinant substrates and on cultured neuronal cells. LHn retains the capacity to internalise and cleave its intracellular SNARE substrate when applied to the cells at high concentration. These activities demonstrate the utility of engineered botulinum neurotoxin fragments as analytical tools to study the mechanisms of action of BoNT neurotoxins and of SNARE proteins. Targeted secretion inhibitors (TSI) are a new class of engineered biopharmaceutical molecules derived from the botulinum neurotoxins. These functional derivatives are expressed as single-chain proteins and require post-translational activation into di-chain molecules for function. A range of BoNT derivatives are presented and demonstrate the successful use of engineered SNARE substrate peptides at the LC-Hn interface to give these molecules self-activating capabilities while retaining the functions of LHn. Several novel molecules with therapeutic potential have been produced and their crystallisation for structural investigation is reported. These results provide an understanding of the structural implications and challenges of engineering therapeutic molecules that combine functional properties of the LHn fragment from BoNTs with specific ligand partners to target different cell types.
8
Woudstra, Cedric. "Clostridium botulinum, du génotypage de la toxine en passant par les flagellines jusqu'au séquençage de génomes : un aperçu de la diversité génétique des Clostridies associés au botulisme animal et humain". Thesis, Paris Est, 2016. http://www.theses.fr/2016PESC1020/document.
Testo completoAbstract (sommario):
Le botulisme est une maladie nerveuse, commune à l’homme et aux animaux, due à l’action de la toxine botulique produite par Clostridium botulinum. Il existe 8 types de toxines dénommées A à H. Les bactéries capables de produire cette toxine se différencient en six groupe sur la base de leurs caractéristiques phénotypiques et biologiques. Les souches de C. botulinum responsables du botulisme humain appartiennent aux groupes I et II selon qu’elles soient protéolytiques ou non. Elles produisent les toxines A, B, E et F, ainsi que le nouveau type H récemment découvert. C. butyricum et C. baratii sont également capables de produire les toxines botuliques de type F et E et appartiennent au groupe V et VI. C. argentinense appartient au groupe IV et est capable de synthétiser la toxine de type G. Elle a été soupçonnée d’être impliquée dans des cas de botulisme infantile en Argentine. Les souches de C. botulinum responsables du botulisme animal appartiennent au groupe III (C. novyi sensu lato) et produisent les toxines C, D et leurs formes mosaïques C/D et D/C. La toxine botulique est le poison le plus puissant connu à ce jour. La dose létale nécessaire pour tuer une personne en bonne santé par intoxication alimentaire est de 70 µg seulement. C’est pourquoi cette toxine a fait l’objet d’études particulièrement approfondies, notamment celles impliquées dans des cas de botulisme humain. Elle peut également être utilisée pour le traitement de certaine pathologie ou la chirurgie esthétique (Botox). Malheureusement, elle peut également être utilisée à mauvais escient, en tant qu’arme de guerre ou à des fins de bioterrorisme. C’est pourquoi l’emploi de la toxine botulique ou de sa bactérie productrice fait l’objet d’une législation particulièrement stricte. Mon projet de doctorat s’est organisé autour de plusieurs projets de recherche visant à développer des méthodes de détection et de typage de du germe et de sa toxine (projets Européens BIOTRACER et AniBioThreat ; projets NRBC-bio ; LNR botulisme aviaire en France). Lors de mes recherches j’ai concentré mon travail sur le développement de méthodes capable de suivre et remonter à la source d’une contamination, qu’elle soit délibérée, accidentelle ou naturelle. Afin d’y parvenir j’ai investigué les gènes des flagellines de C. botulinum groupe I à III, responsables du botulisme humain et animal. L’analyse des gènes flaA et flaB a mis en évidence 5 groupes majeurs et 15 sous-groupes, certain étant spécifiques de régions géographiques. FlaB s’est montré spécifique de C. botulinum type E. Les gènes flagellines fliC, spécifiques à C. botulinum du groupe III, se divisent 5 groupes, avec fliC-I et fliC-IV associés aux types mosaïques C/D et D/C. J’ai étudié la prévalence des souches productrices de toxine de type mosaïques chez les volailles et les bovins. Les résultats montrent que les types C/D et D/C sont majoritaires en Europe. Enfin, j’ai séquencé 17 génomes provenant de souches responsables de botulisme animal en France (14 types C/D et 3 types D/C). Leur analyse montre que ces souches sont très proche génétiquement, entre elles et avec les souches Européennes. Grâce à ces données j’ai mis en évidence un large contenu extra chromosomique dans les souches C/D, qui peut être utilisé pour créer une carte d’identité génétique. D’autre part, l’étude des séquences Crisps à des fins de typage ne s’est pas avérée suffisamment résolutive, du fait de système Crispr-Cas déficient chez les souches C/D. Enfin, un très haut degré de discrimination a été atteint par typage SNP, qui a permis de distinguer jusqu’à l’origine de chaque souche. L’ensemble de ces résultats est développé dans le présent manuscritClostridium botulinum is the etiologic agent of botulism, a deadly paralytic disease that can affects both human and animals. Different bacteria, producing neurotoxins type A to H, are responsible for the disease. They are separated into different groups (I to VI) on the basis of their phenotypical and biological characteristics. Human botulism is mainly due to Groups I and II producing neurotoxins A, B, E and F, with type H recently discovered. Also C. butyricum and C. baratii species (Groups V and VI), producing toxins type F and E respectively, are scarcely reported. C. argentinense Group IV, producing toxin type G, which has been suspected to be associated with infant botulism in Argentina. Animal botulism is mainly due to Group III, which is constituted by C. novyi sensu lato species. They produce toxin types C, D and their mosaic variants. Botulinum neurotoxins are the most powerful toxin known to date with as little as 70 µg enough to kill a person by food poisoning. Therefore, it received a great deal of attention. Botulinum neurotoxins have been deeply studied, especially human related toxins compared to animal. The toxins found to be useful for medical or cosmetic (Botox) treatments, but it was also used as a biological warfare agent, and for bioterrorism. Its extreme potency is equal to its dangerousness. Therefore, governments show concerns of its potential misuse as a bioterrorism weapon; research programs are funded to study and raise awareness about both the toxins and the producing organisms. My PhD work was structured by the different projects I was involved in, which were related to C. botulinum detection and typing, like BIOTRACER and AniBioThreat European projects, the French national CBRN program, or the NRL for avian botulism. The main transversal objective I followed lead me to develop new methods to trace back the origin of C. botulinum contamination, in case of a deliberate, accidental or naturally occurring botulism outbreak. I investigated flagellin genes as potential genetic targets for typing C. botulinum Group I-II and III, responsible for human and animal botulism respectively. Flagellin genes flaA and flaB showed the investigated C. botulinum Group I and II strains to cluster into 5 major groups and up to 15 subgroups, some being specific for certain geographical areas, and flaB being specific to C. botulinum type E. Flagellin fliC gene investigated in C. botulinum Group III showed to cluster into five groups, with fliC-I and fliC-IV associated to type C/D and D/C respectively, being not discriminative enough to differentiate highly genetically related strains. I also studied the prevalence of mosaic toxin genes in C. botulinum Group III in animal botulism, mainly in poultry and bovine. The results brought out the mosaic toxin types C/D and D/C to be predominant in the samples investigated throughout Europe. Finally, I explored the full genome sequences of 14 types C/D and 3 types D/C C. botulinum Group III strains, mainly originating from French avian and bovine botulism outbreaks. Analyses of their genome sequences showed them to be closely related to other European strains from Group III. While studying their genetic content, I was able to point out that the extrachromosomal elements of strains type C/D could be used to generate a genetic ID card. Investigation of Crispr typing method showed to be irrelevant for type C/D, due to a deficient Crispr-Cas mechanism, but deserve more investigation for type D/C. The highest level of discrimination was achieved while using SNP core phylogeny, which allowed distinguishing up to the strain level. Here are the results I’m going to develop in this manuscript
9
Bradbury, Mark. "Genomic and flow cytometric studies of Clostridium sporogenes, a non-toxigenic surrogate for Clostridium botulinum". Thesis, Federation University Australia, 2014. http://researchonline.federation.edu.au/vital/access/HandleResolver/1959.17/97216.
Testo completoAbstract (sommario):
Clostridium sporogenes and Group I Clostridium botulinum are two bacterial species belonging to the same phylogenetic group, primarily differentiated by the expression of botulinum neurotoxin. Both organisms are of significant commercial importance in regards to the spoilage of and/or disease in thermally processed food products due to their ability to form heat resistant spores. As such, these species are often used as the target organism for the design of thermal inactivation processes, particularly in regards to thermal sterilisation. Two specific aspects pertaining to these organisms were investigated to further enhance knowledge with respect to their use in thermal processing studies: the genetic relationship between C. sporogenes and Group I C. botulinum; and the mechanism of heat resistance in spores of C. sporogenes. The first part of this thesis describes the assembly, annotation and analysis of the draft genome of C. sporogenes PA 3679 (the most widely used surrogate for Group I C. botulinum). These data allowed identification of unique variants genes related to spore germination, analogous toxin regions and mobile elements between species. MLST analysis revealed that phylogeny was an ineffective indicator of toxigenicity in this group and thus prompted a pan-genomic analysis. The pan-genome of C. sporogenes/Group I C. botulinum was found to consist of 8799 coding sequences (CDS’s) and a core genome consisting of 1590 CDS’s. Analysis of this pan-genome revealed the significant role that mobile genetic elements have played in genetic diversity within this group of organisms. The second part of this thesis investigated the heat inactivation of C. sporogenes PA 3679 spores in regards to structural variation and population heterogeneity. A novel flow cytometric approach was developed and utilised to investigate isothermal spore inactivation; and implications of the impact of NaCl on the intrinsic variability throughout this process and during a subsequent recovery period. Based on these approaches a possible mechanistic description for the thermal inactivation of spores was developed. Together, these studies present significant evidence supporting the continued suitability of C. sporogenes as a surrogate for Group I C. botulinum, whilst also enhancing the understanding of clostridial spore inactivation during a moist heat process.Doctor of Philosophy
10
Bucknavage, Martin M. "Growth and survival of Clostridium botulinum type E in pasturized oysters". Thesis, This resource online, 1988. http://scholar.lib.vt.edu/theses/available/etd-04122010-083636/.
Testo completoLibri sul tema "Clostridium botulinum"
1
Smith, Louis DS. Botulism: The organism, its toxins, the disease. 2a ed. Springfield, Ill., USA: Thomas, 1988.
Cerca il testo completo
2
Hauschild, Andreas H. W., 1929- e Dodds Karen L. 1957-, a cura di. Clostridium botulinum: Ecology and control in foods. New York: M. Dekker, 1993.
Cerca il testo completo
3
National Institutes of Health (U.S.). Office of Medical Applications of Research, a cura di. Consensus statement. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, Office of Medical Applications of Research, 1993.
Cerca il testo completo
4
O, Sang-sŏk. Chŏ sansŏng milbong pʻojang sikpʻum ŭi kijun, kyugyŏk kukchehwa saŏp =: Establishment of global standards for low acid canned foods in hermetically sealed container. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.
Cerca il testo completo
5
Rasetti-Escargueil, Christine, e Susanne Surman-Lee. Clostridium botulinum: A spore forming organism and a challenge to food safety. New York: Nova Science Publishers, 2012.
Cerca il testo completo
6
Szczawiński, Jacek. Wpływ peklowania, pasteryzacji i napromieniowania mięsa na wytwarzanie toksyny przez Clostridium botulinum. Warszawa: Wydawn. SGGW-AR, 1987.
Cerca il testo completo
7
Sharkey, Freddie. Toxin gene expression in clostridium botulinum type E under different growth conditions. 2S.l: The author], 2002.
Cerca il testo completo
8
Sharkey, Freddie. Toxin gene expression in clostridium botulinum type E under different growth conditions. [S.l: The author], 2002.
Cerca il testo completo
9
Sharkey, Freddie. Toxin gene expression in clostridium botulinum type E under different growth conditions. 2S.l: The author], 2002.
Cerca il testo completo
10
Loch, Petra Vera. Kulturell-biochemische und molekularbiologische Untersuchungen sowie Pathogenitätsprüfung von Clostridium botulinum-Stämmen: Ein Beitragzur Taxonomie. Hannover: [s.n.], 2000.
Cerca il testo completoCapitoli di libri sul tema "Clostridium botulinum"
1
Stechenberg, Barbara. "Clostridium botulinum". In The Neurological Manifestations of Pediatric Infectious Diseases and Immunodeficiency Syndromes, 235–38. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-391-2_21.
Testo completo
2
Abbasi, Adeel, Francis DeRoos, José Artur Paiva, J. M. Pereira, Brian G. Harbrecht, Donald P. Levine, Patricia D. Brown et al. "Clostridium botulinum". In Encyclopedia of Intensive Care Medicine, 567. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1363.
Testo completo
3
Schütt-Gerowitt, Heidi. "Clostridium botulinum". In Lexikon der Infektionskrankheiten des Menschen, 173–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-39026-8_198.
Testo completo
4
Lund, Barbara M., e Michael W. Peck. "Clostridium botulinum". In Guide to Foodborne Pathogens, 91–111. Oxford: John Wiley & Sons, 2013. http://dx.doi.org/10.1002/9781118684856.ch6.
Testo completo
5
Peck, Michael W. "Clostridium botulinum". In Pathogens and Toxins in Foods, 31–52. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815936.ch3.
Testo completo
6
Johnson, Eric A. "Clostridium botulinum". In Food Microbiology, 441–63. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818463.ch17.
Testo completo
7
Johnson, Eric A. "Clostridium botulinum". In Food Microbiology, 487–512. Washington, DC, USA: ASM Press, 2019. http://dx.doi.org/10.1128/9781555819972.ch18.
Testo completo
8
Brüggemann, Holger, Antje Wollherr, Christelle Mazuet e Michel R. Popoff. "Clostridium botulinum". In Genomes of Foodborne and Waterborne Pathogens, 185–212. Washington, DC: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816902.ch13.
Testo completo
9
Bhunia, Arun K. "Clostridium botulinum, Clostridium perfringens, Clostridium difficile". In Foodborne Microbial Pathogens, 209–28. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7349-1_12.
Testo completo
10
Allerberger, F., K. Pfaller e M. P. Dierich. "Clostridium botulinum und Botulismus". In Infektiologie Aktuelle Aspekte, 65–74. Vienna: Springer Vienna, 2001. http://dx.doi.org/10.1007/978-3-7091-6236-1_8.
Testo completoAtti di convegni sul tema "Clostridium botulinum"
1
Lorenzo-Lozano, Paloma, Oscar Jiménez-Mateo, Juan Carlos Cabria-Ramos e María del Valle Jiménez-Pérez. "Development of PCR for simultaneously detection of Clostridium botulinum types A, B, E, and F". In MICROBES IN APPLIED RESEARCH - Current Advances and Challenges. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814405041_0050.
Testo completo
2
Benvenuto, Brendo Bezerra, Pedro Henrick Guimarães Carvalho, Matheus Procópio Guimarães, Tereza Cristina Batista Dias, Renner Cassio Nunes de Lucena, Tiago Lameque de Sousa e. Silva, Maria Eduarda Medeiros Martins, Fabricia dos Santos Almeida, Eric Cymon do Vale Beserra e Iury Hélder Santos Dantas. "Botulism in the southeast region of Brazil: an epidemiological analysis from 2007 to 2021". In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.631.
Testo completoAbstract (sommario):
Introduction: Botulism is a rare, serious neurological disease caused by a toxin produced by Clostridium botulinum. Although rare, it has a high lethality rate, reaching up to 15%. The Southeast region of Brazil is the most populous and may have more cases. Epidemiological analysis is essential to understand its occurrence, identify risk groups, and adopt preventive measures. Objectives: To perform an epidemiological analysis of botulism in the Southeast of Brazil between 2007 and 2021, in order to evaluate its incidence, geographic and temporal distribution. Methods: Data on botulism cases in the Southeast region of Brazil were obtained from the Brazilian Ministry of Health’s Notifiable Diseases Information System (SINAN). The study included confirmed cases between 2007 and 2021 and analyzed the number of cases per year, gender, age range, and mode of transmission. Results: 41 cases of botulism were reported, with an average of 2.73 cases per year. The year 2009 presented the highest number of cases (n = 6), followed by 2007 and 2008 (n = 5 in each year). The majority of cases occurred in males (n = 29, 70.7%) and the most affected age group was 30 to 59 years old (n = 21, 51.2%). The most frequent mode of transmission was foodborne (n = 39, 95.1%). No significant correlations were found between the number of cases and gender, age range, or mode of transmission. Conclusion: Botulism in Southeast Brazil has the highest incidence in the country, with a variable temporal and geographic distribution. Foodborne transmission is the most common and predominantly affects young adult males. Health professionals must be vigilant for early diagnosis and treatment, and prevention measures must be intensified, particularly for proper food handling and storage.
3
Rodrigues, Pedro Vitor Ferreira, Amanda Pereira Sindeaux Pinheiro, Raoni de Oliveira da Silva Domingues, Leonardo José Rodrigues de Araújo Melo e Cássia Caroline Aguiar da Ponte. "Epidemiologic review: an analysis of the incidence of botulism in southeast Brazil from 2011-2021". In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.345.
Testo completoAbstract (sommario):
Introduction: Botulism is a rare life-threatening condition caused by Clostridium Botulinum bacteria toxins, which attack the various parts of the nervous system, like nerves, spinal cord and brain, causing symptoms, like dry mouth, facial weakness, trouble breathing and, in the worst cases, even paralysis. Being, for all the risks that this disease represents, a very important object of study and observation. Objectives: Analyze the epidemiological profile of confirmed cases of botulism in the Southeast region of the country during the years 2011–2021. Methods: This work was made using the data, from the Information System for Notifiable Diseases of the Information Department of the Unified Health System of Brazil, about the botulism. The data has been selected to represent only the 4 states, São Paulo (SP), Rio de Janeiro (RJ), Minas Gerais (MG) and Espírito Santo (ES), of the southeast region. Results: The Brazil had 60 cases of botulism in the analyzed period, with 41.5% of them being in the Southeast region. SP had the most cases in the region with 56% of them, followed by MG with 24% and by RJ with 20%. No cases have been reported in ES. 92% of the reports were foodborne botulism showing an absolute prevalence of this spread form. With a deviation of ±1.35 in the botulism cases over the years. Among those diagnosed, 48% were women and 52% men. Still, 56% of the people were white. Conclusion: With the data collected, it is possible to perceive a stable wave of incidence throughout the entire period, with major regional distortions. In addition, the overwhelming prevalence of the foodborne form of the disease is noticeable. however, due to the small number of cases, much of the data suffer from poor sampling and therefore may be biased, such as gender and race data, thus requiring more longitudinal studies to reach relevant numbers for this type of analysis.
4
Artin, Ingrid, Maria Lövenklev, Peter Rådström e Elisabet Holst. "Development of an in vitro method for detection of Clostridium botulinum types A and E using real-time PCR". In Second International Symposium on Epidemiology and Control of Salmonella in Pork. Iowa State University, Digital Press, 2003. http://dx.doi.org/10.31274/safepork-180809-467.
Testo completo
5
Gomes, Maria Clara Cavalcante, Nathaly Bruna de Oliveira Silva, João Lucas Pessoa de Vasconcelos, Saulo Brivaldo Mendonça da Silva, Mariana Souza Bezerra Cavalcanti e Ana Bárbara Xavier da Silva. "USO DA TOXINA BOTULÍNICA COMO TERAPIA COADJUVANTE EM PACIENTES COM DOENÇA DE PARKINSON, DISFUNÇÕES TEMPOROMANDIBULARES E BRUXISMO". In XXVII Semana de Biomedicina Inovação e Ciência. Editora IME, 2021. http://dx.doi.org/10.51161/9786588884119/46.
Testo completoAbstract (sommario):
Introdução: A toxina botulínica é uma neurotoxina produzida pelo Clostridium botulinum, causador do botulismo, doença neuroparalítica grave(1,3). Esta, é uma proteinase de zinco que realiza a clivagem de proteínas associadas a vesículas neuronais, responsáveis pela liberação de acetilcolina na junção neuromuscular(1). A doença de Parkinson (DP), afeta significativamente a vida dos pacientes, alguns não respondem às opções terapêuticas aplicadas costumeiramente, prejudicando ainda mais essa situação(2). Ademais, disfunções temporomandibulares (DTMs) e bruxismo do sono (BS), são condições que prejudicam significativamente os pacientes, causando dores e movimentos mandibulares restritos(4). A utilização da toxina botulínica, é vista ligada principalmente a fins estéticos, contudo sua utilidade vai muito além disso. Objetivos: Este resumo possui como objetivo avaliar e correlacionar o uso da toxina botulínica à doença de Parkinson, DTMs e Bruxismo como uma possível alternativa terapêutica. Métodos: Foi realizada uma pesquisa de artigos científicos nas plataformas Pubmed e Sciencedirect, buscando por meio dos descritores “botulinum toxin AND parkinsonism, botulinum toxin AND bruxism”, onde foi encontrado os artigos utilizados. Resultados: O uso de toxina botulínica mostrou diversos benefícios quando avaliado em pacientes com DP, DTMs e BS. Isso foi evidente ao avaliar a sialorréia, que acomete 86% dos pacientes com DP, caracterizando a incapacidade de controlar as secreções orais, que após a aplicação da toxina botulínica nas glândulas salivares houve a inibição da transmissão colinérgica parassimpática e simpática pósganglionar, promovendo a diminuição da secreção salivar(2). Além disso, a disfunção urinária ligada a DP também mostrou bons prognósticos quando submetidos à aplicação da toxina, agindo no músculo detrusor podendo trazer benefício por até 6 meses(2).Em pacientes com DTMs e BS, submetidos a uma sessão de injeção da toxina nos músculos temporal e masseter, foi possível observar uma melhora considerável nos níveis de dor, como também nos movimentos mandibulares, avaliados no pós-operatório, em um, três e seis meses após o tratamento(4). Conclusões: Dessa forma, é possível concluir que o uso da terapia com toxina botulínica nos distúrbios de parkinsonismo, disfunções temporomandibulares e bruxismo tem uma grande importância terapêutica coadjuvante auxiliando de forma significativa no tratamento dos sintomas dessas síndromes. Porém, mais estudos são necessários para melhor compreender os mecanismos dessa toxina em cada síndrome, bem como buscar a padronização de doses nas mesmas, além de sua utilização em outras enfermidades.
6
Aversa, Felipe Pires De Campos, Renato Massaharu Hassunuma e Patrícia Carvalho Garcia. "PRODUÇÃO DE SCRIPTS PARA ESTUDO TRIDIMENSIONAL DA ESTRUTURA DA NEUROTOXINA BOTULÍNICA DO SOROTIPO A". In II Congresso Brasileiro de Bioquímica Humana On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbraqui/7.
Testo completoAbstract (sommario):
Introdução: A neurotoxina botulínica do sorotipo A (BoNT/A) é a uma metaloproteinase dependente de zinco e corresponde a um dos sete tipos sorológicos produzidos pela bactéria Clostridium botulinum. Dos sete tipos sorológicos, a BoNT/A é a mais utilizada com finalidades estéticas e está presente em várias marcas comerciais como Botox®, Dysport®, Xeomin®, entre outras. Objetivos: Nesta pesquisa foram desenvolvidos scripts para produção de imagens no software RasMol 2.7.4.2, com o objetivo de visualização da estrutura bioquímica da BoNT/A, seus domínios e subdomínios. Material e métodos: Inicialmente foi realizado um levantamento de arquivos do tipo PDB no site Protein Data Bank sobre a BoNT/A. Após a seleção dos melhores arquivos, foram desenvolvidos vários scripts para a observação da estrutura e domínios da BoNT/A. Resultados: Nos scripts produzidos foi observado que a BoNT/A é formada 1296 resíduos de aminoácidos, organizados em três domínios: 1) o domínio de ligação com o receptor: que é formado pelos resíduos de aminoácidos 873-1295 e corresponde a região responsável pela ligação da BoNT/A com o terminal pré-sináptico do neurônio; 2) o domínio de translocação: que é formado pelos resíduos 448-872 e é responsável por perfurar a membrana do endossomo e expor o domínio catalítico ao citossol, após a toxina ser endocitada; e 3) o domínio catalítico: que é formado pelos resíduos 1-437. É nesta região em que se encontra o sítio catalítico dependente de zinco. É esta região da BoNT/A que desempenha o efeito de bloqueador neuromuscular ao degradar a proteína associada ao sinaptossoma de 25 kDa (SNAP-25). Conclusão: Os scripts desenvolvidos produziram imagens que puderam demonstrar os domínios e subdomínios da BoNT/A. O estudo estrutural da BoNT/A é importante para compreender melhor a função de cada parte da molécula no processo de bloqueio neuromuscular da toxina. O desenvolvimento de futuras pesquisas na área de Bioinformática podem ser importantes para produção de novas moléculas sintéticas, biologicamente mais seguras, que possam ser utilizadas em procedimentos estéticos.
Rapporti di organizzazioni sul tema "Clostridium botulinum"
1
Swaminathan, Subramanyam. Structural Studies on Intact Clostridium Botulinum Neurotoxins Complexed With Inhibitors Leading to Drug Design. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2003. http://dx.doi.org/10.21236/ada411713.
Testo completo
2
Swaminathan, Subramanyam. Structural Studies on Intact Clostridium botulinum Neurotoxins Complexed with Inhibitors Leading to Drug Design. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2009. http://dx.doi.org/10.21236/ada504608.
Testo completo
3
Swaminathan, Subramanyam. Structural Studies on Intact Clostridium Botulinum Neurotoxins Complexes with Inhibitors Leading to Drug Design. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2004. http://dx.doi.org/10.21236/ada422765.
Testo completo
4
Swaminathan, S. Structural Studies on Intact Clostridium botulinum Neurotoxins Complexed with Inhibitors Leading to Drug Design. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2007. http://dx.doi.org/10.21236/ada466176.
Testo completo
5
Swaminathan, Subramanyam. Structural Studies on Intact Clostridium Botulinum Neurotoxins Complexed with Inhibitors Leading to Drug Design. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2006. http://dx.doi.org/10.21236/ada466700.
Testo completo
6
Swaminathan, Subramanyam. Structural Studies on Intact Clostridium botulinum Neurotoxins Complexed with Inhibitors Leading to Drug Design. Fort Belvoir, VA: Defense Technical Information Center, febbraio 2008. http://dx.doi.org/10.21236/ada482360.
Testo completo
7
Botulinum Neurotoxin-Producing Clostridia, Working Group on. Report on Botulinum Neurotoxin-Producing Clostridia. Food Standards Agency, agosto 2023. http://dx.doi.org/10.46756/sci.fsa.ozk974.
Testo completoAbstract (sommario):
In 1992 a working group of the UK Advisory Committee on the Microbiological Safety of Food presented a report on Vacuum Packaging and Associated Processes regarding the microbiological safety of chilled foods. The report supported subsequent guidance provided by the UK Food Standards Agency for the safe manufacture of vacuum packed and modified atmosphere packed chilled foods. In 2021 the ACMSF requested that a new subgroup should update and build on the 1992 report as well as considering, in addition to chilled foods, some foods that are intended to be stored at ambient temperatures. The new subgroup agreed a scope that includes the conditions that support growth and/or neurotoxin formation by C. botulinum, and other clostridia, as well as identification of limiting conditions that provide control. Other foodborne pathogens that need to be considered separately and some foods including raw beef, pork and lamb were explicitly excluded. The subgroup considered the taxonomy, detection, epidemiology, occurrence, growth, survival and risks associated with C. botulinum and other neurotoxin-forming clostridia. There has been no significant change in the nature of foodborne botulism in recent decades except for the identification of rare cases caused by neurotoxigenic C. butyricum, C. baratii and C. sporogenes. Currently evidence indicates that non-clostridia do not pose a risk in relation to foodborne botulism. The subgroup has compiled lists of incidents and outbreaks of botulism, reported in the UK and worldwide, and have reviewed published information concerning growth parameters and control factors in relation to proteolytic C. botulinum, non-proteolytic C. botulinum and the other neurotoxigenic clostridia. The subgroup concluded that the frequency of occurrence of foodborne botulism is very low (very rare but cannot be excluded) with high severity (severe illness: causing life threatening or substantial sequelae or long-term illness). Uncertainty associated with the assessment of the frequency of occurrence, and with the assessment of severity, of foodborne botulism is low (solid and complete data; strong evidence in multiple sources). The vast majority of reported botulism outbreaks, for chilled or ambient stored foods, are identified with proteolytic C. botulinum and temperature abuse is the single most common cause. In the last 30 years, in the UK and worldwide where a cause can be identified, there is evidence that known controls, combined with the correct storage, would have prevented the reported incidents of foodborne botulism. The subgroup recommends that foods should continue to be formulated to control C. botulinum, and other botulinum neurotoxin-producing clostridia, in accordance with the known factors. With regard to these controls, the subgroup recommends some changes to the FSA guidelines that reflect improved information about using combinations of controls, the z-value used to establish equivalent thermal processes and the variable efficacy associated with some controls such as herbs and spices. Current information does not facilitate revision of the current reference process, heating at 90°C for 10 minutes, but there is strong evidence that this provides a lethality that exceeds the target 6 order of magnitude reduction in population size that is widely attributed to the process and the subgroup includes a recommendation that the FSA considers this issue. Early detection and connection of cases and rapid, effective coordinated responses to very rare incidents are identified as crucial elements for reducing risks from foodborne botulism. The subgroup recommends that the FSA works closely with other agencies to establish clear and validated preparedness in relation to potential major incidents of foodborne botulism in the UK.
8
Cairo, Jessica, Iulia Gherman e Paul Cook. The effects of consumer freezing of food on its use-by date. Food Standards Agency, luglio 2021. http://dx.doi.org/10.46756/sci.fsa.ret874.
Testo completoAbstract (sommario):
The current Food Standards Agency consumer guidance states that consumers can freeze pre-packed food right up to the “use-by” date and, once food has been defrosted, it should be consumed within 24 hours. This strategic review has collated relevant data to determine whether there is an increased risk in relation to freezing ready-to-eat and non-ready-to-eat foods on the use-by date compared to the day before the use-by date. The review has focused on how the shelf-life of a food is determined and the effects of freezing, thawing and refrigeration on foodborne pathogens, including Bacillus spp., Campylobacter spp., Clostridium botulinum, Clostridium perfringens, Listeria monocytogenes, Salmonella, pathogenic Escherichia coli and Shigella spp. In the UK, food business operators are responsible for setting the safe shelf-life of a food which, in practice, should take into consideration the consumer habits, as well as the factors affecting shelf-life, such as food product characteristics, food processing techniques, transport, retail and domestic food storage temperatures, and type of packaging. Some countries, such as Ireland, New Zealand and Canada specifically recommend including safety margins within shelf lives. This is used to maintain brand integrity because it ensures that the food is consumed in its optimum condition. The FSA has collaborated with other organisations in the production of several guidance documents; however, there is no explicit requirement for the consideration of a margin of safety when setting shelf-life. There is also no legal requirement in the UK to consider a safety margin when setting shelf-life. According to regulations, pathogens should not be present in sufficient levels to cause foodborne illness on the use-by date, as food should still be safe to eat on that day. Given that these requirements are met, the risk assessed in this report arises from the processes of freezing, thawing and subsequent refrigerated storage for a further 24 hours, and the potential for these to increase pathogen levels. In this review, it was found that there is a risk of additional growth of certain pathogens during the refrigerated storage period although the impact of freezing and thawing on the extent of this growth was not readily evident. This risk would relate specifically to ready-to-eat foods as cooking of non-ready-to-eat foods after defrosting would eliminate pathogens. This report explores the potential issues related to consumer freezing on the use-by date and identifies additional information or research required to understand the risks involved. Overall, there is little evidence to suggest a significant change in risk between consumers freezing ready-to-eat food on the use-by date compared to freezing the food on the day before the use-by date. Specific areas that merit further research include the risks due to low temperature survival and growth of L. monocytogenes. There is also a lack of research on the effects of freezing, defrosting and refrigeration on the growth and toxin production of non-proteolytic C. botulinum, and the growth of Salmonella during domestic freezing and thawing. Finally, more information on how food business operators set shelf-life would enable a better understanding of the process and the extent of the safety margin when determining shelf-life of ready-to-eat and non-ready-to-eat foods.