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Infant botulism (IB) is an intestinal toxemia that manifests as descending paralysis, constipation, and, in some cases, respiratory failure. Laboratory-confirmed IB cases are rare, and recent data in Israel are lacking. We conducted a national multicenter retrospective study of laboratory-confirmed IB cases reported in Israel during 2007-2021. A total of 8 cases were reported during the study period. During 2019-2021, incidence may have increased because of a cluster of 5 cases. Infant median age for diagnosis was 6.5 months, older than previously reported (3 months). Most cases occurred during March-July. Honey consumption was reported in 1 case, and possible environmental risk factors (living nearby rural or construction areas, dust exposure, and having a father who works as a farmer) were reported in 6 cases. Although IB is rare, its incidence in Israel may have increased over recent years, and its epidemiology and risk factors differ from cases reported previously in Israel.

Botulism is a severe neuroparalytic disorder that can be potentially life-threatening. In Barcelona, Spain, no outbreaks had been reported in the past 25 years. However, in September 2011, two outbreaks occurred involving two different families. A rare case of Clostridium baratii which produced a neurotoxin F outbreak was detected in five family members who had shared lunch, and several days before that another family was affected by C. botulinum toxin A which was probably present in homemade pâté.

Botulism is a rare but severe disease which is characterized by paralysis and inhibition of secretions. Only a few cases had been reported at the end of the 19th century in France. The disease was frequent during the second world war, and then the incidence decreased progressively. However, human botulism is still present in France with 10–25 cases every year. Food-borne botulism was the main form of botulism in France, whereas infant botulism (17 cases between 2004 and 2016) was rare, and wound and inhalational botulism were exceptional. Type B was the prevalent botulism type and was mainly due to consumption of home-made or small-scale preparations of cured ham and to a lesser extent other pork meat products. In the recent period (2000–2016), a wider diversity of botulism types from various food origin including industrial foods was reported. Severe cases of type A and F botulism as well as type E botulism were more frequent. Albeit rare, the severity of botulism justifies its continued surveillance and recommendations to food industry and consumers regarding food hygiene and preservation practices.

Background: Botulism is a low incidence but potentially fatal infectious disease caused by neurotoxins produced mainly by Clostridium botulinum. There are different routes of acquisition, food-borne and infant/intestinal being the most frequent presentation, and antitoxin is the treatment of choice in all cases. In Spain, botulism is under surveillance, and case reporting is mandatory. Methods: This retrospective study attempts to provide a more complete picture of the epidemiology of botulism in Spain from 1997 to 2019 and an assessment of the treatment, including the relationship between a delay in antitoxin administration and the length of hospitalization using the Cox proportional hazards test and Kruskal–Wallis test, and an approach to the frequency of adverse events, issues for which no previous national data have been published. Results: Eight of the 44 outbreaks were associated with contaminated commercial foods involving ≤7 cases/outbreak; preserved vegetables were the main source of infection, followed by fish products; early antitoxin administration significantly reduces the hospital stay, and adverse reactions to the antitoxin affect around 3% of treated cases.

Key Points Botulinum neurotoxins (BoNTs) are produced by neurotoxigenic clostridia and are a diverse group that consists of approximately 40 different BoNT types (and various subtypes), all of which cause persistent paralysis of peripheral nerve terminals — a condition known as botulism. Recent studies have solved various structures of BoNT complexes, which has provided insights into their modes of entry into the general circulation as well as the ability of these toxins to survive for long periods of time in the ex vivo environment. The molecular basis of the specificity of BoNT binding to nerve terminals is explored, as well as the ensuing cellular events, including toxin endocytosis and the targeting and cleavage of SNARE proteins. A molecular model for the essential process of membrane translocation of the metalloprotease domain of BoNTs into the neuronal cytosol is presented. Open questions and future areas of research are outlined with respect to the development of novel therapeutic agents that are based on BoNTs. Botulinum neurotoxins, which are the most powerful known toxins, are produced by toxigenic clostridia and cause persistent paralysis of peripheral nerve terminals by blocking neurotransmitter release. In this Review, Montecucco and colleagues discuss recent structural and molecular insights into the mechanisms of toxin entry into nerve terminals, membrane translocation and neuroparalysis. Botulinum neurotoxins (BoNTs) are produced by anaerobic bacteria of the genus Clostridium and cause a persistent paralysis of peripheral nerve terminals, which is known as botulism. Neurotoxigenic clostridia belong to six phylogenetically distinct groups and produce more than 40 different BoNT types, which inactivate neurotransmitter release owing to their metalloprotease activity. In this Review, we discuss recent studies that have improved our understanding of the genetics and structure of BoNT complexes. We also describe recent insights into the mechanisms of BoNT entry into the general circulation, neuronal binding, membrane translocation and neuroparalysis.

Botulinum neurotoxins are known to have seven serotypes (BoNT/A–G). Here we report a new BoNT serotype, tentatively named BoNT/X, which has the lowest sequence identity with other BoNTs and is not recognized by antisera against known BoNTs. Similar to BoNT/B/D/F/G, BoNT/X cleaves vesicle-associated membrane proteins (VAMP) 1, 2 and 3, but at a novel site (Arg66-Ala67 in VAMP2). Remarkably, BoNT/X is the only toxin that also cleaves non-canonical substrates VAMP4, VAMP5 and Ykt6. To validate its activity, a small amount of full-length BoNT/X was assembled by linking two non-toxic fragments using a transpeptidase (sortase). Assembled BoNT/X cleaves VAMP2 and VAMP4 in cultured neurons and causes flaccid paralysis in mice. Thus, BoNT/X is a novel BoNT with a unique substrate profile. Its discovery posts a challenge to develop effective countermeasures, provides a novel tool for studying intracellular membrane trafficking, and presents a new potential therapeutic toxin for modulating secretions in cells. There are seven well-established types of Botulinum neurotoxins (BoNTs). Here the authors report the identification and characterization of a new type of BoNT—BoNT/X—which cleaves a different site on canonical BoNTs substrates and targets SNARE family members not cleaved by known BoNTs.

Background and ImportanceInfant botulism (IB) is a potentially life-threatening disorder that is caused by the ingestion of Clostridium botulinum spores, that consequently colonise and produce neurotoxins in the colon. IB occurs in children younger than 12 months, being more frequent in children younger than 6 months. The initial symptoms are constipation in 90%of cases, followed by neuromuscular paralysis, which begins with the cranial nerves and progresses to the peripheral and respiratory muscles. Clinical diagnosis is made through laboratory identification of the toxin or microorganisms in the faeces. Treatment is carried out after hospitalisation, with supportive measures, and should begin as soon as the diagnosis is suspected. Specific treatment is carried out with human botulism immune globulin (BIG-IV) and the earlier it is administered, the more effective it is and the lower the mortality rate.Aim and ObjectivesPresentation of three cases of IB in a paediatric hospital and description of the procedures leading to their resolution.Materials and MethodsAdmission of three infants with IB in three different years (2009, 2022 and 2023), aged less than or equal to 6 months. During the respective hospitalisations and after clinical suspicion of IB, the California Department of Health Services world reference centre was contacted to obtain guidelines for acquiring BIG-IV, since botulinum antitoxin from the national strategic reserve (RENAB) is only indicated from 12 months of age. After obtaining the appropriate authorisations from the Pharmacy and Therapeutics Committee, the hospital’s Board of Directors and INFARMED, as well as finalising the administrative procedures, the process of sending the medication to Portugal was set in motion.ResultsClinical improvement in all three cases after the administration BIG-IV.Conclusion and RelevanceThe administration of BIG-IV should be carried out as early as possible, as soon as there is clinical suspicion of infant botulism. Although RENAB has been set up to provide equine botulinum antitoxin (DGS Guideline 001/2020 of 16/01/2020), it is not indicated for children under 1 year of age, so it is essential to create a National Reserve that includes BIG-IV indicated for this age group.References and/or AcknowledgementsDGS Guideline 001/2020 of 16/01/2020Rao AK, et al. Clinical guidelines for diagnosis and treatment of botulism, 2021. Centres for Disease Control and Prevention, Recommendations and Reports, Vol. 70, No. 2, May 7.Antonucci L, et al. Infant botulism: an underestimated threat. Infectious Diseases, 2021;53:9, 647–660. https://doi.org/10.1080/23744235.2021.1919753Fox, CK, Keet, CA, Strober, JB. Recent advances in Infant Botulism. Pediatr Neurol 2005;32:149–154.Monography BAT, 9 May 2007.Monography BabyBIG, June 2021.

Infant botulism in a 4-month-old boy in China who continued to excrete toxins for over a month despite antitoxin therapy was further treated with fecal microbiota transplantation. After treatment, we noted increased gut microbial diversity and altered fecal metabolites, which may help reduce intestinal pH and enhance anti-inflammatory capabilities.

Botulinum neurotoxins (BoNTs) produced by Clostridia species are the most potent identified natural toxins. Classically, the toxic neurological syndrome is characterized by an (afebrile) acute symmetric descending flaccid paralysis. The most know typical clinical syndrome of botulism refers to the foodborne form. All different forms are characterized by the same symptoms, caused by toxin-induced neuromuscular paralysis. The diagnosis of botulism is essentially clinical, as well as the decision to apply the specific antidotal treatment. The role of the laboratory is mandatory to confirm the clinical suspicion in relation to regulatory agencies, to identify the BoNTs involved and the source of intoxication. The laboratory diagnosis of foodborne botulism is based on the detection of BoNTs in clinical specimens/food samples and the isolation of BoNT from stools. Foodborne botulism intoxication is often underdiagnosed; the initial symptoms can be confused with more common clinical conditions (i.e., stroke, myasthenia gravis, Guillain–Barré syndrome—Miller–Fisher variant, Eaton–Lambert syndrome, tick paralysis and shellfish or tetrodotoxin poisoning). The treatment includes procedures for decontamination, antidote administration and, when required, support of respiratory function; few differences are related to the different way of exposure.