Foodborne Botulism Research Articles

Foodborne botulism in Canada, 1985-2005.

During 1985–2005, a total of 91 laboratory-confirmed outbreaks of foodborne botulism occurred in Canada; these outbreaks involved 205 cases and 11 deaths. Of the outbreaks, 75 (86.2%) were caused by Clostridium botulinum type E, followed by types A (7, 8.1%) and B (5, 5.7%). Approximately 85% of the outbreaks occurred in Alaska Native communities, particularly the Inuit of Nunavik in northern Quebec and the First Nations population of the Pacific coast of British Columbia. These populations were predominantly exposed to type E botulinum toxin through the consumption of traditionally prepared marine mammal and fish products. Two botulism outbreaks were attributed to commercial ready-to-eat meat products and 3 to foods served in restaurants; several cases were attributed to non-Native home-prepared foods. Three affected pregnant women delivered healthy infants. Improvements in botulism case identification and early treatment have resulted in a reduction in the case-fatality rate in Canada.

Case report with sequential nerve conduction studies: A very old patient with atypical foodborne botulism type a with pupil sparing treated with botulinum antitoxin

Case report with sequential nerve conduction studies: A very old patient with atypical foodborne botulism type a with pupil sparing treated with botulinum antitoxin

Molecular assembly of botulinum neurotoxin progenitor complexes

Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum and associates with nontoxic neurotoxin-associated proteins to form high-molecular weight progenitor complexes (PCs). The PCs are required for the oral toxicity of BoNT in the context of food-borne botulism and are thought to protect BoNT from destruction in the gastrointestinal tract and aid in absorption from the gut lumen. The PC can differ in size and protein content depending on the C. botulinum strain. The oral toxicity of the BoNT PC increases as the size of the PC increases, but the molecular architecture of these large complexes and how they contribute to BoNT toxicity have not been elucidated. We have generated 2D images of PCs from strains producing BoNT serotypes A1, B, and E using negative stain electron microscopy and single-particle averaging. The BoNT/A1 and BoNT/B PCs were observed as ovoid-shaped bodies with three appendages, whereas the BoNT/E PC was observed as an ovoid body. Both the BoNT/A1 and BoNT/B PCs showed significant flexibility, and the BoNT/B PC was documented as a heterogeneous population of assembly/disassembly intermediates. We have also determined 3D structures for each serotype using the random conical tilt approach. Crystal structures of the individual proteins were placed into the BoNT/A1 and BoNT/B PC electron density maps to generate unique detailed models of the BoNT PCs. The structures highlight an effective platform that can be engineered for the development of mucosal vaccines and the intestinal absorption of oral biologics.

Botulism Associated with Commercially Canned Food

Foodborne botulism is rare in the United States, and almost all cases are caused by improperly prepared home-processed foods. During one week in July

Foodborne Botulism Treated with Heptavalent Botulism Antitoxin

To report a case of foodborne botulism and subsequent use of the investigational heptavalent botulism antitoxin (H-BAT). A 60-year-old man was hospitalized with blurred vision, diplopia, and dysarthria. On hospital day 2, the patient was transferred to the intensive care unit for progressive fatigable weakness with ptosis, dysphagia, dysarthria, and nausea. Secondary to worsening respiratory distress, the patient was intubated and placed on a ventilator. The patient could open his eyes only with assistance but still had normal strength in all extremities. H-BAT was administered 48 hours after presentation for possible botulism. The patient then revealed that he consumed home-canned corn several days prior to admission. On hospital day 8, botulinum neurotoxin was confirmed in the patient's serum and the home-canned corn. The patient slowly regained muscle strength and was discharged to a long-term acute care facility on hospital day 22. Foodborne botulism is caused by a neurotoxin from Clostridium botulinum and usually occurs after the consumption of improperly prepared home-canned food. Botulism is characterized by symmetrical descending paralysis that may progress to respiratory arrest. The standard confirmatory test for botulism is a mouse bioassay to prove the presence of botulinum neurotoxin. Outside of supportive care, the treatment options for botulism are limited. Individuals with botulism often require intensive care unit monitoring and potentially ventilatory support. H-BAT, the only treatment available for botulism in patients older than 1 year, is a purified and despeciated equine-derived immunoglobulin active against all known botulinum neurotoxins. H-BAT's despeciation significantly reduces the risk of hypersensitivity reactions, anaphylaxis, and serum sickness. In a confirmed case of foodborne botulism treated with H-BAT, the patient tolerated H-BAT and did not develop any hypersensitivity reactions or serum sickness.

An Outbreak of Foodborne Botulism in Surat Thani Province, Thailand, 2012

An Outbreak of Foodborne Botulism in Surat Thani Province, Thailand, 2012

Google botulism: an annotated database

Botulism risk information is available on government websites such as USFDA, USDA, CDC, Canadian Food Inspection Agency (Canadian CFIA), European Centre for Disease Prevention and Control (ECDC), and Health Canada. State health departments and university websites contain consumer-based information about botulism. Outbreaks of botulism are quickly investigated, and appropriate measures are coordinated among public health and regulatory agencies. Here, we compiled a list of publically reported botulism outbreaks. The data includes published reports from all countries but reports were mostly from USA. The database focuses initially on the 17-year period from 1994 to 2010 throughout the world, but has been and will be updated and expanded. The data will be publically accessible for viewing and analysis. This botulism web-based data source representing a tool for scientists and epidemiologists is both feasible and practical and is a step toward improving the understanding and knowing the occurrence of foodborne botulism worldwide.

Antagonistic effect of different bacteria on Clostridium botulinum types A, B, D and E in vitro

Clostridium botulinum is an anaerobic, Gram-positive, spore-forming rod that produces a potent neurotoxin. Seven types (A, B, C1+2, D, E, F and G) of C botulinum are recognised, based on...

National Outbreak of Type A Foodborne Botulism Associated With a Widely Distributed Commercially Canned Hot Dog Chili Sauce

On 7 and 11 July 2007, health officials in Texas and Indiana, respectively, reported 4 possible cases of type A foodborne botulism to the US Centers for Disease Control and Prevention. Foodborne botulism is a rare and sometimes fatal illness caused by consuming foods containing botulinum neurotoxin. Investigators reviewed patients' medical charts and food histories. Clinical specimens and food samples were tested for botulinum toxin and neurotoxin-producing Clostridium species. Investigators conducted inspections of the cannery that produced the implicated product. Eight confirmed outbreak associated cases were identified from Indiana (n = 2), Texas (n = 3), and Ohio (n = 3). Botulinum toxin type A was identified in leftover chili sauce consumed by the Indiana patients and 1 of the Ohio patients. Cannery inspectors found violations of federal canned-food regulations that could have led to survival of Clostridium botulinum spores during sterilization. The company recalled 39 million cans of chili. Following the outbreak, the US Food and Drug Administration inspected other canneries with similar canning systems and issued warnings to the industry about the danger of C. botulinum and the importance of compliance with canned food manufacturing regulations. Commercially produced hot dog chili sauce caused these cases of type A botulism. This is the first US foodborne botulism outbreak involving a commercial cannery in >30 years. Sharing of epidemiologic and laboratory findings allowed for the rapid identification of implicated food items and swift removal of potentially deadly products from the market by US food regulatory authorities.

Intestinal Abscess Caused by Botulism

Introduction: Botulism is a rare but life threatening neuroparalytic condition caused by bacterium Clostridium botulinum. We report a case of a middle-aged male who developed intestinal abscesses that were secondary to Botulism. Case: A 43-year-old male was admitted to our institution with abdominal pain, blurred vision and dysarthria for one day duration. He denied any fever, headache or neck stiffness. Past medical history was significant for diabetes mellitus, hypertension and gout. Examination revealed normal vital signs, inability to protrude the tongue with no evidence of palpable adenopathy or rash. MRI brain was unremarkable. Laboratory values showed leukocytosis of 20.3 K/microliter and platelet count of 602 K/microliter. CT scan abdomen and pelvis showed multiloculated gas containing fluid collections in the perigastric area and in left anterior abdominal wall. Abscesses were incised and drained and culture from the abscess was positive for Clostridium botulinum type A toxin. Serum, stool and gastric aspirate were assayed using mouse bioassay which were positive for type A botulinum toxin. Subsequently, patient developed respiratory failure and was intubated requiring mechanical ventilatory support. The patient got botulinum antitoxin and was treated with imipenem. Subsequently, his condition started improving and is recovering neurologically in the last three weeks of follow-up. Discussion: Botulism is an acute neuroparalytic condition characterized by cranial nerve palsies followed by descending symmetrical flaccid paralysis which can cause respiratory arrest and can be fatal. Botulism is caused by botulinum neurotoxin types A, B, E or F and G produced by Clostridium species (C. botulism, C. baratti, C. butyricum). Three major forms of botulism are: 1) Food borne botulism from ingestion of food contaminated by preformed botulism neurotoxin. 2) Intestinal botulism caused by colonization from Clostridium botulinum followed by in situ production of toxin. 3) Wound botulism caused by contamination of wound by Clostridium botulinum and production of neurotoxin in situ. A careful history and physical examination, serum assays, analysis of stool and suspected food item may also reveal neurotoxin which is diagnostic when coupled with appropriate clinical and neurological findings. If clinical suspicion for botulism is high, Centers for Disease Control and Prevention (CDC) should be contacted for administration of botulism antitoxin which is the standard of care followed by antibiotics. To summarize, our case reiterates the importance of early and prompt diagnosis of botulism which is a fatal disease to initiate therapy in a timely fashion.

Toxin Detection in Patients' Sera by Mass Spectrometry during Two Outbreaks of Type A Botulism in France

In two outbreaks of food-borne botulism in France, Clostridium botulinum type A was isolated and characterized from incriminated foods. Botulinum neurotoxin type A was detected in the patients' sera by mouse bioassay and in vitro endopeptidase assay with an immunocapture step and identification of the cleavage products by mass spectrometry.

Treatment of foodborne botulism in current clinical toxicology: authors' reply.

Dr. Zamani pointed out the role of the wholebowel irrigation (WBI) with polyethylene gly-col as an appropriate adjunctive option of gas-trointestinal decontamination in severe botu-lism poisoning. Secondly, the author underlinethe early administration of trivalent antitoxinas soon as clinical suspicion of botulism poi-soning is made.[...]

Positive ice pack test in a case of food-borne botulism: a clinical note

Positive ice pack test in a case of food-borne botulism: a clinical note

Treatment of Foodborne Botulism in Current Clinical Toxicology

We read with interest the case presented byLonati D. et al.entitled Fatal course of food-borne botulism in an eight-month old infantbeing published in one of the recent issues ofPediatr Report.[...]

Clinical and Electrodiagnostic Features of an Outbreak of Foodborne Botulism Due to Home-Brew Alcohol among Prisoners (P04.093)

Objective: Describe the epidemiological, neurological and electrodiagnostic features of 12 prisoners with food borne botulism from self-made alcohol. Background Botulism causes rapidly progressive weakness with prominent dysphagia, ophthalmoparesis, and autonomic dysfunction including pupillary abnormalities. Nerve conduction studies (NCS) typically reveal reduced compound muscle action potential (CMAP) amplitudes with an incremental response to rapid (30-50 hertz) repetitive nerve stimulation (RNS) in 50%. Design/Methods: Twelve adult prisoners developed confirmed botulism after consuming alcohol made from fresh and canned fruit and potatoes (Pruno). All patients were triaged in the emergency department or via teleconference in the prison infirmary; 8 were admitted. Clinical and electrodiagnostic features are reported on the admitted patients. Each underwent NCS including 3 and 50 hertz RNS of the median and ulnar nerves. Results: Serial neurologic examinations revealed bulbar weakness with a notable lack of pupillary abnormalities. Three patients had rapidly progressive respiratory failure requiring intubation, and two developed descending proximal predominant weakness. Determination of the C. Botulinum subtype is pending at the time of submission. NCS were normal in 5 patients. The three most severely affected had mildly reduced compound muscle action potential amplitudes. No patient had CMAP facilitation following exercise, and only the weakest had a 30% increment following 50 hertz RNS. Conclusions: We present features of an outbreak of Pruno associated botulism. Although pupillary findings are commonly cited in the literature as a core feature of botulism, they were uniformly absent. The classic electrodiagnostic features of reduced CMAP amplitudes and incremental response to rapid RNS were also absent in all but 1 patient. These findings emphasize the fact that botulism remains a clinical diagnosis. Absence of pupillary and NCS abnormalities do not exclude botulism and patients with a suspicious exposure history and clinical examination should undergo serum testing and appropriate therapy. Supported by: R01DK064814 (AGS, JRS). Disclosure: Dr. Chung has nothing to disclose. Dr. Burbank has nothing to disclose. Dr. Afra has nothing to disclose. Dr. Hoesch has nothing to disclose. Dr. Singleton has received personal compensation for activities with Medical Review Institute. Dr. Leydard has nothing to disclose. Dr. Dolan has nothing to disclose. Dr. Smith has received personal compensation for activities with Allergan, Baxter Bioscience, Merz, Pfizer and NeurogesX as a consultant. Dr. Smith has received personal compensation in an editorial capacity for serves as the Associate Editor for Education at AAN.com. Dr. Smith has nothing to disclose.

Formes graves de botulisme du nouveau-né et du nourrisson : trois observations récentes et algorithme de prise en charge

Botulism rarely involves young children. Food borne botulism is a direct toxin contamination that can affect infants following the ingestion of a food product contaminated by botulinum toxin. Infant botulism occurs after intestinal colonisation by Clostridium botulinium and secondary toxin production in children less than 12 months of age. Both forms lead to a presynaptic blockage of the neuromuscular junction. In its natural course, the disease ultimately resolves completely, but some patients will require ventilatory and nutritional support, thus experiencing intensive care complications. Early administration of intravenous antitoxin has been proved to accelerate recovery, which requires physicians to be aware of this rare disease. Here we report three recent cases of botulism in young children that are especially relevant, and propose guidelines to optimise diagnosis and treatment.

Rapid Detection of Foodborne Botulism Outbreaks Facilitated by Epidemiological Linking of Cases: Implications for Food Defense and Public Health Response

The main objective of this study was to develop an understanding of the descriptive epidemiology of foodborne botulism in the context of outbreak detection and food defense. This study used 1993-2008 data from the Centers for Disease Control and Prevention (CDC) Annual Summaries of Notifiable Diseases, 2003-2006 data from the Bacterial Foodborne and Diarrheal Disease National Case Surveillance Annual Reports, and 1993-2008 data from the Annual Listing of Foodborne Disease Outbreaks. Published outbreak investigation reports were identified through a PubMed search of MEDLINE citations for botulism outbreaks. Fifty-eight foodborne botulism outbreaks were reported to CDC between 1993 and 2008. Four hundred sixteen foodborne botulism cases were documented; 205 (49%) were associated with outbreaks. Familial connections and co-hospitalization of initial presenting cases were common in large outbreaks (>5 cases). In these outbreaks, the time from earliest exposure to outbreak recognition varied dramatically (range, 48-216 h). The identification of epidemiologic linkages between foodborne botulism cases is a critical part of diagnostic evaluation and outbreak detection. Investigation of an intentionally contaminated food item with a long shelf life and widespread distribution may be delayed until an astute physician suspects foodborne botulism; suspicion of foodborne botulism occurs more frequently when more than one case is hospitalized concurrently. In an effort to augment national botulism surveillance and antitoxin release systems and to improve food defense and public health preparedness efforts, medical organizations and Homeland Security officials should emphasize the education and training of medical personnel to improve foodborne botulism diagnostic capabilities to recognize single foodborne botulism cases and to look for epidemiologic linkages between suspected cases.

Diplopia as the primary presentation of foodborne botulism

Foodborne botulism is a serious condition caused by Clostridium botulinum neurotoxin. Clinically, botulism presents as bilateral cranial nerve neuropathy and descending paralysis. We report a unique presentation of botulism to remind clinicians of this potentially fatal condition. In this observational case report initial evaluation showed only esodeviation. This progressed to unilateral cranial nerve six (CN VI) paresis along with systemic signs. Clinical diagnosis was made based on in-depth history and concurrent symptoms in three other patients. Foodborne botulism presenting as diplopia and unilateral motility deficits is rare and can represent a diagnostic and therapeutic challenge to the ophthalmologist.

Two cases of food-borne botulism in Finland caused by conserved olives, October 2011

In October 2011 in Finland, two persons fell ill with symptoms compatible with botulism after having eaten conserved olives stuffed with almonds. One of these two died. Clostridium botulinum type B and its neurotoxin were detected in the implicated olives by PCR and mouse bioassay, respectively. The olives were traced back to an Italian manufacturer and withdrawn from the market. The public and other European countries were informed through media and Europe-wide notifications.

An outbreak of food-borne botulism in Scotland, United Kingdom, November 2011

An investigation is currently underway to explain an outbreak of food-borne botulism in Scotland. Three children in the same family were confirmed as having botulism following consumption of a meal made with a jar of korma sauce. Residual sauce from the jar, the jar lid and a remnant of the meal, all tested positive for Clostridium botulinum type A toxin. The children are recovering, although two remain ventilated and in intensive care unit.