Foodborne Botulism Research Articles

Foodborne botulism due to ingestion of home-canned green beans: two case reports

BackgroundFoodborne botulism is a life-threatening, rapidly progressive disease. It has an incidence of less than 10 cases per year in Germany and mostly affects several previously healthy people at the same time. The only specific treatment is the administration of botulism antitoxin. According to the German guidelines administration of antitoxin is recommended only in the first 24 hours after oral ingestion of the toxin.Case presentationA 47-year-old white woman and her 51-year-old white husband presented with paralysis of multiple cranial nerves and rapidly descending paralysis approximately 72 hours after ingestion of home-canned beans. The disease was complicated by autonomic changes like hypertension, febrile temperatures, and a paralytic ileus. The diagnosis was confirmed by identification of botulinum neurotoxin type A in the serum of the woman. In accordance with the German guidelines, antitoxin was not given due to the prolonged time interval at diagnosis. Both patients had a long intensive care unit course requiring ventilation for approximately 5 months. Finally they recovered completely.ConclusionsA full recovery from foodborne botulism is possible even in patients with intensive care lasting several months. There are only case reports indicating that administration of antitoxin may shorten the course of the disease, even if given later than 24 hours after intoxication. Due to the rarity of the disease and its rapid course there are no randomized controlled trials. Thus, evidence of the superiority of this treatment is lacking. However, the prevailing view according to the German guidelines to administer antitoxin only within 24 hours after ingestion of the toxin should be questioned in the case of progression of the disease with proof of remaining toxin in the blood.

Clinical Features of Foodborne and Wound Botulism: A Systematic Review of the Literature, 1932-2015.

Botulism is a rare, potentially fatal paralytic illness caused by neurotoxins. To inform the evaluation of patients with suspected botulism, we conducted a systematic review to describe the clinical features of botulism. We searched Medline Ovid, Embase Dialog, Embase Ovid, Cumulative Index to Nursing and Allied Health Literature (CINAHL) EBSCO, Global Health Ovid, Cochrane Library, Scopus, and ClinicalTrials.gov for English language articles through May 2015. Information abstracted included demographics, signs and symptoms, laboratory results, and clinical outcome for foodborne and wound botulism patients confirmed by laboratory testing, epidemiologic link, or association with an outbreak. The review followed PRISMA guidelines and was registered with PROSPERO (CRD42015024784). We identified 402 patients from 233 articles published in English between 1932 and 2015. Most cases (n = 346 [86%]) were foodborne botulism and most (n = 263 [65%]) were associated with an outbreak. The median incubation period was 1 day, and the median time from illness onset to hospital admission was 2 days. Shortness of breath, dyspnea, or respiratory distress or failure at hospital admission was reported in 169 (42%) patients; 71 (42%) reported respiratory involvement without report of extremity weakness. Among 154 patients for whom the hospital day of intubation was reported, 134 (87%) were intubated on the first or second hospital day. Botulism patients can experience a range of signs and symptoms. Respiratory involvement may occur early in the illness and can occur without preceding extremity weakness. Clinicians and public health departments preparing for and responding to botulism events should use this information to guide the evaluation of suspected botulism patients.

Efficacy of Antitoxin Therapy in Treating Patients With Foodborne Botulism: A Systematic Review and Meta-analysis of Cases, 1923-2016.

Botulism is a rare, potentially severe illness, often fatal if not appropriately treated. Data on treatment are sparse. We systematically evaluated the literature on botulinum antitoxin and other treatments. We conducted a systematic literature review of published articles in PubMed via Medline, Web of Science, Embase, Ovid, and Cumulative Index to Nursing and Allied Health Literature, and included all studies that reported on the clinical course and treatment for foodborne botulism. Articles were reviewed by 2 independent reviewers and independently abstracted for treatment type and toxin exposure. We conducted a meta-analysis on the effect of timing of antitoxin administration, antitoxin type, and toxin exposure type. We identified 235 articles that met the inclusion criteria, published between 1923 and 2016. Study quality was variable. Few (27%) case series reported sufficient data for inclusion in meta-analysis. Reduced mortality was associated with any antitoxin treatment (odds ratio [OR], 0.16; 95% confidence interval [CI], .09-.30) and antitoxin treatment within 48 hours of illness onset (OR, 0.12; 95% CI, .03-.41). Data did not allow assessment of critical care impact, including ventilator support, on survival. Therapeutic agents other than antitoxin offered no clear benefit. Patient characteristics did not predict poor outcomes. We did not identify an interval beyond which antitoxin was not beneficial. Published studies on botulism treatment are relatively sparse and of low quality. Timely administration of antitoxin reduces mortality; despite appropriate treatment with antitoxin, some patients suffer respiratory failure. Prompt antitoxin administration and meticulous intensive care are essential for optimal outcome.

The Epidemiology of Foodborne Botulism Outbreaks: A Systematic Review.

We performed a systematic review of foodborne botulism outbreaks to describe their clinical aspects and descriptive epidemiology in order to inform public health response strategies. We searched seven databases for reports of foodborne botulism outbreaks published in English from database inception to May 2015. We summarized descriptive characteristics and analyzed differences in exposure and toxin types by geographic region. We performed logistic regression to assess correlations between exposure source, implicated food, and outbreak size. There were 197 outbreaks reported between 1920 and 2014. The median number of cases per outbreak was 3 (range 2-97). The majority of reported outbreaks (109; 55%) occurred in the United States. Toxin types A, B, E, and F were identified as the causative agent in 34%, 16%, 17%, and 1% of outbreaks, respectively. The median duration between exposure and symptom onset was approximately 1 day. The mean percentage of cases requiring mechanical ventilation per outbreak was 34%. Seventy percent of all outbreaks and 77% of small outbreaks (≤11 cases) originated from point source exposures, while commercial foods were significantly (odds ratio, 6.9; 95% confidence interval, 2.2-21.1) associated with large outbreaks (≥12 cases). Toxin type A accounted for half of outbreaks, and these outbreaks had a higher proportion of patient ventilatory failure. Most outbreaks were due to point source exposures, while outbreaks due to commercial food were larger. For effective responses to foodborne botulism outbreaks, these findings demonstrate the need for timely outbreak investigation and hospital surge capacity.

Detection and Quantification of Biologically Active Botulinum Neurotoxin Serotypes A and B Using a Förster Resonance Energy Transfer-Based Quantum Dot Nanobiosensor.

Botulinum neurotoxin (BoNT) is the most potent toxin known. The ingestion of food contaminated with biologically active BoNT causes foodborne botulism, which can lead to respiratory paralysis, coma, and death after ingestion of as little as 70 μg for a 70 kg human. Because of its lethality and challenges associated with current detection methods, there is an urgent need for highly sensitive rapid screening techniques capable of detecting biologically active BoNT. Here, we describe a Förster resonance energy transfer-based nanobiosensor that uses quantum dots (QDs) and two specific quencher-labeled peptide probes to detect and differentiate two biologically active forms of BoNT, serotypes A and B, which were responsible for 80% of human foodborne botulism cases in the U.S. from 2012 to 2015. Each peptide probe contains an enzymatic cleavage site specific to only one serotype. QDs were selected based on the spectral overlap with the quenchers. In the presence of the target BoNT serotype, the peptide probe is cleaved and the quenching of QD photoluminescence (PL) is reduced, giving a signal that is easily detected by a PL spectrophotometer. This sensor performance was evaluated with light chains of BoNT/A and BoNT/B (LcA and LcB), catalytic domains of the respective serotypes. LcA and LcB were detected in 3 h with limits of detection of 0.2 and 2 ng/mL, respectively. The specificity of the sensor was evaluated, and no cross-reactivity from nontarget serotypes was observed with 2 h of incubation. Because each serotype-specific peptide is conjugated to a QD with a unique emission wavelength, multiple biologically active BoNT serotypes could be detected in one PL spectrum. The sensor was also shown to be responsive to BoNT/A and BoNT/B holotoxins. Good performance of this sensor implies its potential application as a rapid screening method for biologically active BoNT/A and BoNT/B in the laboratory and in the field.

Botulism: Diagnosis and Therapy

Background Botulism is a rare, life-threatening, time-critical neuroparalytic disease that is frequently a subject of differential diagnostic considerations. But there is much uncertainty regarding diagnosis and therapy. Rapid diagnosis, early antitoxin dose, consistent food hygiene and the sensitization of the population can help to reduce incidence, morbidity and mortality. Methods This overview is based on an epidemiological data inquiry (RKI, ECDC, CDC, WHO) and a selective literature research (pubmed till March 2017). Additionally, the German botulism guideline (2012) and own diagnostical experiences were taken into account. Results The incidence of botulinum toxin intoxication induced by ubiquitous spore-forming Clostridium botulinum (main representative) is < 0.01/100 000 EU citizens. Foodborne botulism is a pure intoxication syndrome (most common form) due to improperly prepared or incorrectly stored food. Wound and infant botulism are kinds of "toxico-infections". A "bulbar" neuroparalysis is a main symptom progressing to a flaccid tetraparesis up to respiratory paralysis. Infant botulism is presented non-specific and is treated only symptomatically; but a special human-derived antitoxin is available at international pharmacies. In case of suspected foodborne or wound botulism antitoxin must be administered as soon as possible, which may also be effective 24 hours after symptoms onset. There is no evidence for adjuvant treatment except of intensive care unit (ICU) therapy. Conclusion Despite typical symptomatology botulism is often diagnosed too late. Early antitoxin administration and ICU therapy are crucial for survival. A consultant laboratory should be contacted for advice.

Genome Sequence of Clostridium botulinum Strain Adk2012 Associated with a Foodborne Botulinum Case in Tottori, Japan, in 2012

ABSTRACTWe report here a draft genome sequence of Clostridium botulinum Adk2012 responsible for a foodborne botulism case that occurred in Tottori, Japan, in 2012. Its genome size was 2,904,173 bp, with 46 rRNAs and 54 tRNAs, at a coverage of 14.5×.

Reoccurrence of botulinum neurotoxin subtype A3 inducing food-borne botulism, Slovakia, 2015.

A case of food-borne botulism occurred in Slovakia in 2015. Clostridium botulinum type A was isolated from three nearly empty commercial hummus tubes. The product, which was sold in Slovakia and the Czech Republic, was withdrawn from the market and a warning was issued immediately through the European Commission’s Rapid Alert System for Food and Feed (RASFF). Further investigation revealed the presence of botulinum neurotoxin (BoNT) subtype BoNT/A3, a very rare subtype implicated in only one previous outbreak (Loch Maree in Scotland, 1922). It is the most divergent subtype of BoNT/A with 15.4% difference at the amino acid level compared with the prototype BoNT/A1. This makes it more prone to evading immunological and PCR-based detection. It is recommended that testing laboratories are advised that this subtype has been associated with food-borne botulism for the second time since the first outbreak almost 100 years ago, and to validate their immunological or PCR-based methods against this divergent subtype.

Botulism in Italy, 1986 to 2015.

Botulism is a rare but severe neuroparalytic disease caused by botulinum toxins. Because of its high potential impact on public health, botulism is a closely monitored communicable disease in Europe. In Italy, which has one of the highest incidence rates in Europe (0.03 cases per 100,000 population), botulism is monitored through a case-based passive surveillance system: the front-line physician who diagnoses a suspected case must notify the Local Health Units immediately, and the Ministry of Health's office within 12 hours. From 1986 to 2015, 466 confirmed cases of botulism were recorded in Italy (of 1,257 suspected cases). Of these, 421 were food-borne (the most frequently seen form of botulism due to the consumption of improperly home-canned foods), 36 were infant botulism, which accounts for ca 50% of all these types of cases registered in Europe, six were wound-related and three were due to adult intestinal colonisation. This scenario suggests that stronger efforts should be made towards raising public awareness of the risk of food-borne botulism, especially with respect to home-preserved foods, as well as improving the training of front-line medical personnel, to ensure that a quick and accurate diagnosis of botulism can be made.

Clinical analysis of 53 patients with Clostridium botulinum food poisoning

To analyze the epidemiologic data of patients with Clostridium botulinum food poisoning, and to improve the understanding, diagnosis and treatment of food borne botulism. A retrospective study was conducted. Fifty-three patients with Clostridium botulinum food poisoning admitted to Chinese PLA Center of Poisoning and Treatment from January 2009 to December 2016 were enrolled, and they were divided into mild, moderate, and severe groups according to the severity of disease. The clinical data including medical history, epidemiology data, routine blood test and blood biochemistry at hospital admission, the vital signs and arterial blood gas analysis before and after treatment, as well as the occurrence frequency of symptom and sign on set were collected. Fifty-three patients with food borne botulism were enrolled, with 33 patients in mild group, 13 in moderate group, and 7 in severe group. Most of the patients were female, the age distribution was in large span, the outbreak of disease was in groups mainly with the family, and patients were mainly located in Hebei Province, Beijing and Henan Province. The outbreaks were mainly happened in Spring and Summer, and homemade fermentation products were still the first cause of poisoning with the average latent period of (51.01±4.78) hours. The majority of patients with botulism were in mild resulted from the type A toxin. With the aggravation of disease, hospitalization time was gradually increased, white blood cell (WBC) and neutrophils (NEUT) at hospitalization admission, and respiratory rate (RR), heart rate (HR), fraction of inspired oxygen (FiO2) before the treatment were shown in obviously rising trend, albumin (ALB) at hospitalization admission and pH, arterial partial pressure of oxygen (PaO2), arterial oxygen saturation (SaO2) before treatment were in decline. The parameters in severe group were most severe, and had significant differences as compared with those of mild group [hospitalization time (days): 72.57±39.52 vs. 6.61±3.72, WBC (×109/L): 13.01±6.44 vs. 6.85±2.07, NEUT: 0.85±0.07 vs. 0.63±0.14, RR (bpm): 32.14±4.33 vs. 15.18±1.70, HR (bpm): 132.29±5.19 vs. 75.54±8.24, FiO2: 0.32±0.05 vs. 0.21±0.00, ALB (g/L): 38.57±4.65 vs. 42.09±4.57, pH: 7.08±0.10 vs. 7.38±0.07, PaO2 (mmHg, 1 mmHg = 0.133 kPa): 75.16±5.24 vs. 98.39±1.50, SaO2: 0.78±0.06 vs. 0.97±0.02, all P < 0.05]. The symptom and sign on set of 53 patients with food borne botulism was dizziness, followed by fatigue, blurred vision, nausea, and other symptoms and signs were lower than 50%, and the occurrence of dizziness with rank one happen rate was significantly higher than blurred vision and nausea (χ 2 values were 7.209 and 10.502 respectively, and P values were 0.007 and 0.004 respectively). After the on time prescription of botulinum antitoxins treatment, the clinical symptoms of patients could be relived quickly. All the patients were discharged without deaths. In order to improve the recovery of the food borne botulism poisoning patients, adequate antitoxin and the related organ supports should be prescribed on time.

Botulinum neurotoxin type B uses a distinct entry pathway mediated by CDC42 into intestinal cells versus neuronal cells.

Botulinum neurotoxins (BoNTs) are responsible for severe flaccid paralysis by inhibiting the release of acetylcholine at the neuromuscular junctions. BoNT type B (BoNT/B) most often induces mild forms of botulism with predominant dysautonomic symptoms. In food borne botulism and botulism by intestinal colonisation such as infant botulism, which are the most frequent naturally acquired forms of botulism, the digestive tract is the main entry route of BoNTs into the organism. We previously showed that BoNT/B translocates through mouse intestinal barrier by an endocytosis-dependent mechanism and subsequently targets neuronal cells, mainly cholinergic neurons, in the intestinal mucosa and musculosa. Here, we investigated the entry pathway of BoNT/B using fluorescent C-terminal domain of the heavy chain (HcB), which is involved in the binding to specific receptor(s) and entry process into target cells. While the combination of gangliosides GD1a /GD1b /GT1b and synaptotagmin I and to a greater extent synaptotagmin II constitutes the functional HcB receptor on NG108-15 neuronal cells, HcB only uses the gangliosides GD1a /GD1b /GT1b to efficiently bind to m-ICcl2 intestinal cells. HcB enters both cell types by a dynamin-dependent endocytosis, which is efficiently prevented by Dynasore, a dynamin inhibitor, and reaches a common early endosomal compartment labeled by early endosome antigen (EEA1). In contrast to neuronal cells, HcB uses a Cdc42-dependent pathway to enter intestinal cells. Then, HcB is transported to late endosomes in neuronal cells, whereas it exploits a nonacidified pathway from apical to basal lateral side of m-ICcl2 cells supporting a transcytotic route in epithelial intestinal cells.

Adult food borne botulism in Australia: The only 2 cases from the last 15 years

Highlights: Consider botulism in a patient with weakness, ptosis, internal and external ophthalmoplegia and autonomic features. In contrast to acute neuropathies (e.g. Miller Fisher syndrome), the reflexes are usually preserved. Toxin serotype may predict clinical course and severity. An anti-toxin is available and should be given early and rigorous case follow-up is vital in food borne outbreaks. With good supportive care, the prognosis is excellent but recovery is often protracted over many months.

Preventing the outbreaks of food-borne botulism and minimizing the risk of fatality

Preventing the outbreaks of food-borne botulism and minimizing the risk of fatality

A case of foodborne botulism in the province of Viterbo

A 57 years-old woman with gastrointestinal pain, dysphagia, diplopia, dry mouth, was diagnosed with foodborne botulism caused by Clostridium Botulinum toxin. In this case, a jar of vegetables preserved in oil was identified as the source of the intoxication. Canned peppers were produced at home by the patient according to traditional techniques, deemed appropriate as established use. Despite this, the procedure proved to be a health hazard.The present article follows the diagnostic therapeutic pathway of the patient, highlighting the critical points not only related to the clinic but also to the ministerial procedures for reporting a case of botulism. This case provides an opportunity to emphasize the need for greater awareness about how to prevent and correctly manage the cases of botulism, both by the general population and by physicians who faced a patient with suspected poisoning by Botulinum toxin.[Article in Italian]

Diversity of Group I and II Clostridium botulinum Strains from France Including Recently Identified Subtypes.

In France, human botulism is mainly food-borne intoxication, whereas infant botulism is rare. A total of 99 group I and II Clostridium botulinum strains including 59 type A (12 historical isolates [1947–1961], 43 from France [1986–2013], 3 from other countries, and 1 collection strain), 31 type B (3 historical, 23 recent isolates, 4 from other countries, and 1 collection strain), and 9 type E (5 historical, 3 isolates, and 1 collection strain) were investigated by botulinum locus gene sequencing and multilocus sequence typing analysis. Historical C. botulinum A strains mainly belonged to subtype A1 and sequence type (ST) 1, whereas recent strains exhibited a wide genetic diversity: subtype A1 in orfX or ha locus, A1(B), A1(F), A2, A2b2, A5(B2′) A5(B3′), as well as the recently identified A7 and A8 subtypes, and were distributed into 25 STs. Clostridium botulinum A1(B) was the most frequent subtype from food-borne botulism and food. Group I C. botulinum type B in France were mainly subtype B2 (14 out of 20 historical and recent strains) and were divided into 19 STs. Food-borne botulism resulting from ham consumption during the recent period was due to group II C. botulinum B4. Type E botulism is rare in France, 5 historical and 1 recent strains were subtype E3. A subtype E12 was recently identified from an unusual ham contamination. Clostridium botulinum strains from human botulism in France showed a wide genetic diversity and seems to result not from a single evolutionary lineage but from multiple and independent genetic rearrangements.

A cluster of three cases of botulism due to Clostridium baratii type F, France, August 2015

A cluster of three cases of food-borne botulism due to Clostridium baratii type F occurred in France in August 2015. All cases required respiratory assistance. Consumption of a Bolognese sauce at the same restaurant was the likely source of contamination. Clostridium baratii was isolated both from stool specimens from the three patients and ground meat used to prepare the sauce. This is the second episode reported in France caused by this rare pathogen.

Microepidemia familiar de botulismo alimentario en la Comunidad de Madrid

Botulism is a syndrome caused by the toxin of the bacillus Clostridium botulinum. The toxin acts by blocking the presynaptic cholinergic endings of the neuromuscular junction and of the parasympathetic nervous system, and gives rise to a flaccid paralysis and parasympathetic failure. The most common way to catch the disease is by ingestion of the preformed toxin present in badly sterilised home-made preserves, although other mechanisms are also possible. Its incidence in Spain today is very low. We report the case of three members of a family living together who presented a clinical picture of food-borne botulism. The initial clinical symptoms showed a predilection for ocular paresis and for dysautonomic symptoms of little specificity, and the familial aggregation was the fundamental evidence that suggested the diagnosis. Later, the patients' state got worse and two of them presented involvement of the respiratory function and required a lengthy stay in the intensive care unit. After a period of convalescence the three patients recovered without any sequelae. Botulinum toxin was detected by bioassay in some food samples, which allowed the diagnosis to be categorised as confirmed. The familial microepidemic reported here is a case of predominantly ocular and dysautonomic involvement. Likewise, it illustrates several aspects that are typical of the disease: the suspected diagnosis in cohabiting patients who visit at the same time for a similar clinical picture, the characteristic complications of the process and its treatment, the laboratory diagnosis and its natural history towards resolution.

New Elements To Consider When Modeling the Hazards Associated with Botulinum Neurotoxin in Food.

Botulinum neurotoxins (BoNTs) produced by the anaerobic bacterium Clostridium botulinum are the most potent biological substances known to mankind. BoNTs are the agents responsible for botulism, a rare condition affecting the neuromuscular junction and causing a spectrum of diseases ranging from mild cranial nerve palsies to acute respiratory failure and death. BoNTs are a potential biowarfare threat and a public health hazard, since outbreaks of foodborne botulism are caused by the ingestion of preformed BoNTs in food. Currently, mathematical models relating to the hazards associated with C. botulinum, which are largely empirical, make major contributions to botulinum risk assessment. Evaluated using statistical techniques, these models simulate the response of the bacterium to environmental conditions. Though empirical models have been successfully incorporated into risk assessments to support food safety decision making, this process includes significant uncertainties so that relevant decision making is frequently conservative and inflexible. Progression involves encoding into the models cellular processes at a molecular level, especially the details of the genetic and molecular machinery. This addition drives the connection between biological mechanisms and botulism risk assessment and hazard management strategies. This review brings together elements currently described in the literature that will be useful in building quantitative models of C. botulinum neurotoxin production. Subsequently, it outlines how the established form of modeling could be extended to include these new elements. Ultimately, this can offer further contributions to risk assessments to support food safety decision making.

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FigureFigureFigureA 5-month-old boy with no notable medical history presented with weakness, poor feeding, and constipation. His poor feeding had gradually progressed over two weeks: he would tire easily and cough when trying to swallow. He had had constipation for seven to eight days, and had grown progressively weaker, now unable to lift his head off the bed. His family denies fever, vomiting, focal weakness, and seizure-like activity. Vaccinations are up to date, and his mother said he was born full-term through an uncomplicated vaginal delivery. The family lives on a farm with various livestock. Find the diagnosis and case discussion on p. 16. Diagnosis: Infant Botulism Unlike its better-known brethren, foodborne botulism, which is caused by the ingestion of preformed botulin toxins in tainted foods (e.g., home canning), infant botulism is caused by the ingestion of the entire Clostridium botulinum spore. Most commonly seen between the first and sixth month of life, infant botulism, though rare, can be life-threatening. The C. botulinum spores colonize the infant's intestinal tract, allowing the toxin to be produced. This potent toxin prevents the release of multiple neurotransmitters, most notably acetylcholine, and the blockage of these cholinergic synapses causes a symmetric, descending motor weakness and flaccid paralysis with autonomic dysfunction. (BMC Microbiol 2010;10:267.) Infants are at increased risk because studies have shown that the absence of competitive microbial flora enables the growth of the ingested spores. (Clin Microbiol Rev 2006;19[2]:298.) As a result, infants, who have not yet become colonized with normal gut flora, are at high risk of becoming colonized with the botulinum spores. (Clin Microbiol Rev 2006;19[2]:298.) Despite its common association with honey, C. botulinum is actually most often linked to soil and dust exposure. Living in a rural area and with someone who works with soil are risk factors for bacterial colonization. (Pediatr Neurol 2005;32[3]:149.) The first clinical symptom of infant botulism is constipation. Infants then experience loss of head control (from weakness of the neck muscles), followed by symmetric, descending hypotonia and weakness, ultimately progressing to involve the diaphragmatic muscles. (Annu Rev Med 1980;31:541.) Infant botulism is distinguished from other neurological disorders by the presence of symmetric cranial nerve palsies. These include ptosis, fatigable pupillary response to light, ophthalmoplegia, poor suck, decreased gag reflex, difficulty swallowing, and expressionless facies. (Pediatrics 2007;119[4]:826.) Diagnosis of infant botulism is achieved via bioassay, and this study unsurprisingly may take many days to return, leaving the treatment team with the dilemma of treating without a conclusive diagnosis. This is complicated even more so because the definitive treatment, intravenous botulism immunoglobulin (BabyBIG), is only available through the California Department of Public Health, so infant botulism remains a clinical diagnosis. Supportive care should pay special attention to airway protection, whether there is a need for mechanical ventilation, positioning to decrease aspiration risks, and urinary retention. This patient was admitted to the PICU to monitor his airway while awaiting BabyBIG, which was administered the following day. Two weeks later, the immunoassay returned positive for botulism toxin, and he made a full recovery. Differential Diagnosis for Infant Weakness Sepsis Electrolyte abnormalities Meningitis Botulism metabolic abnormalities Muscular dystrophies Myasthenia gravis Spinal cord trauma Share this article on Twitter and Facebook. Access the links in EMN by reading this on our website or in our free iPad app, both available at www.EM-News.com. Comments? Write to us at [email protected].

Biphasic botulism diagnosed by electromyogram

Botulism is an acute, flaccid paralytic illness caused by the neurotoxin produced by Clostridium species . Three forms of botulism are known; infant botulism, food borne, and wound botulism. We report an 11-year-old boy with food borne botulism diagnosed on electromyography. Although his clinical findings improved in 10 days, his symptoms recurred, showing a biphasic course. After 3 weeks, he was symptom free. His electromyography findings were also normal on the 3rd week. After 3 weeks, he was discharged without clinical symptoms.