Food-borne Botulism Cases Research Articles

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.

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.

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.

Fatal Course of Foodborne Botulism in an Eigth-Month Old Infant

An 8-month old girl, weighing 9 kg, was brought by her parents at 8.15 am to the Emergency Department (ED) for a progressive worsening of weakness and acute respiratory failure. On admission, the baby presented with poor oral intake, a weak cry and extremely weak muscular body control. Poor gag and suck, unreactive mydriasis, hypotonia, lethargy and absence of peristalsis were noted. Laboratory data showed severe respiratory acidosis. Chest X-ray, electroencephalography, encephalic CT scan and MRI were all normal, as were cerebrospinal fluid analysis and viral tests. Orotracheal intubation and continuous mechanical ventilation were applied. The patient received fluids, corticosteroids, aerosol therapy, large-spectrum antibiotics and enteral-nutrition. Further investigation revealed ingestion of an improperly prepared home-canned homogenized turkey meal. Type A botulinum neurotoxin was identified. Trivalent botulinum antitoxin, prostigmine and oral activated charcoal were administered. Generalized flaccid paralysis, areflexic bilateral mydriasis, gastric stasis and deep coma persisted for the duration of the hospital stay, and the patient died of severe respiratory failure and cardiac arrest 12 days after ED admission. Botulism poisoning should be suspected in any infant presenting with feeding difficulties, constipation, descendent paralysis or acute respiratory failure. Supportive treatment and antidotal therapy should be performed as soon as a clinical diagnosis is made. We describe a case of foodborne botulism in an 8-month old infant caused by ingestion of an improperly prepared home-canned homogenized turkey meal, representing the youngest fatal case reported in medical literature.

Dry mouth as an initial sign of food-borne botulism: a case report and review of the literature

Botulism is a rare neuroparalytic disease caused by a potent neurotoxin produced by Clostridium botulinum. There are different clinical types of botulism. Early diagnosis of the condition is essential for effective treatment. We report a case of food-borne botulism in identical twins characterized by severe initial oral involvement and a review of the literature about the condition.

Multiplex Detection of Microbial and Plant Toxins by Immunoaffinity Enrichment and Matrix-Assisted Laser Desorption/Ionization Mass Spectrometry

Plant and microbial toxins such as ricin, staphylococcal enterotoxin B (SEB), and the botulinum neurotoxins (BoNT) are considered as potential biological warfare agents. Specific screening methods are, therefore, required that enable unambiguous and sensitive identification of these biohazards, particularly for the occurrence of the toxins in complex sample matrixes. The present study describes a combination of a multiplex-immunoaffinity purification approach, followed by matrix-assisted laser desorption/ionization (MALDI)-based detection for the simultaneous identification of ricin, SEB, BoNT/A, and BoNT/B. The method comprises an affinity enrichment step, using specific monoclonal antibodies for each of the four toxins which have been selected from a pool of antibodies. The selected antibodies allow for specific and simultaneous capture of ricin, SEB, BoNT/A, BoNT/B, and the corresponding BoNT complexes. These were subsequently identified by MALDI time-of-flight (TOF) mass spectrometry (MS), following tryptic digest. The sensitivity of the technique was approximately 500 fmol for each of the toxins. These toxins were detectable within 8 h, even when present in complex matrixes such as milk or juice. Furthermore, the MALDI-based multiplex assay allowed for the discrimination of closely related BoNT sero- and subtypes, including a real case of food-borne botulism in Germany.

Le botulisme alimentaire au Maroc, à propos de 15 cas. Valeur diagnostique de l’électrophysiologie

Botulism is a rare but serious disease, which affects the peripheral autonomous nervous system, potentially with a fatal outcome. In Morocco, botulism is exceptional. This was a prospective analysis of the epidemiological, clinical, neurophysiological and toxicological features of 15 cases of food-borne botulism identified among a series of 45 highly suspect cases collected in Morocco during an epidemic in August1999. The 15 patients (eight females, seven males) included in the protocol were aged 3 to 49 years (average 18.8 years). One-third of the cases occurred in a familial context. The clinical presentation was typical and complete in nine cases; respiratory failure was noted in four patients. Botulinum toxins were found in nine cases. Outcome was less than favorable, with total recovery in seven cases, persistence of motor sequelae in three and death in five. Electrophysiological investigations showed an incrementing response at high frequency in 73.3%, a decrement at lower frequency in 60% and low motor amplitudes in 93%. These findings constituted a very sensitive and specific triad for botulism diagnosis. These findings illustrate the gravity of botulism and the important diagnostic value of neurophysiological results, especially incrementation, which can provide a very pertinent diagnostic contribution, especially in seronegative patients.

Diagnosis and Treatment of Botulism: A Century Later, Clinical Suspicion Remains the Cornerstone

ically defined cases of wound botulism. Wheeler and colleagues surely know wound botulism when they see it, because they consult on most wound botulism cases, and to the mind of most experts familiar with the diagnostic challenges of botulism, they are fully justified in using clinical diagnosis as the gold standard against which to measure the mouse bioassay’s limited sensitivity. The sensitivity calculated in the article is not the intrinsic sensitivity of a test under ideal laboratory conditions, but rather that of the clinical setting, calculation of which depends on a complicated set of real-world factors. This calculation must take into account the quality of the gold standard clinical diagnosis, which depends on the initial astuteness of the admitting physician and the diagnostic skill of the California Department of Public Health consultant, and variations in toxin levels in clinical samples, which depend on the timeliness of sample collection, the size of the Clostridium botulinum colony in the infected wound, kinetics of toxin absorption from the abscess, its migrations to the extracirculatory compartment, and possibly other factors. One must also keep in mind that the sensitivity of mouse bioassay results may be different for the other principal forms of botulism—foodborne botulism and infant botulism. Most foodborne botulism cases are diagnosed by other expert con

Recurrent Episodes of Food Borne Botulism in a 7-Year Old Boy

Objective Botulism is the acute, descending, flaccid paralysis that results when the neurotoxin of Clostridium botulinum blocks neuromuscular transmission. C botulinum toxin is the most poisonous substance that blocks neuromuscular transmission and causes death through airway and respiratory muscle paralysis; all forms of botulism manifest neurologically as asymmetric, descending, flaccid paralysis beginning with the cranial nerve musculature. Food-borne botulism results from the ingestion of food in which C botulinum has multiplied and produced its toxin. Patient We report a new case of food-borne botulism in a 7 year old boy with recurrent episodes of weakness, difficulty in wallowing and speech; bilateral ptosis and mydriasis. He had positive history of the same symptoms, documented twice before. The patient's samples were sent for detection of toxin of Clostridium botulinum, and toxin of C. botulinum, type A was found in his stool sample, confirming our diagnosis. This case was unusual report because our patient has not history of canned food ingestion and also because recurrent episodes of paralysis in this case are unusual findings in botulism. Conclusion In this report we want to emphasize that canned-food ingestion is not necessary for diagnosis of food-borne botulism and because delayed treatment leads to increase mortality and morbidity, treatment should be initiated promptly on the basis of clinical suspicion.

Botulism: Cause, Effects, Diagnosis, Clinical and Laboratory Identification, and Treatment Modalities

Botulism is a neuroparalytic disease caused by neurotoxins produced by the bacteria Clostridium botulinum. Botulinum neurotoxins (BoNTs) are among the most potent naturally occurring toxins and are a category A biological threat agent. The 7 toxin serotypes of BoNTs (serotypes A-G) have different toxicities, act through 3 different intracellular protein targets, and exhibit different durations of effect. Botulism may follow ingestion of food contaminated with BoNT, from toxin production of C botulinum present in the intestine or wounds, or from inhalation of aerosolized toxin. Intoxication classically presents as an acute, symmetrical, descending flaccid paralysis. Early diagnosis is important because antitoxin therapy is most effective when administered early. Confirmatory testing of botulism with BoNT assays or C botulinum cultures is time-consuming, and may be insensitive in the diagnosis of inhalational botulism and in as many as 32% of food-borne botulism cases. Therefore, the decision to initiate botulinum antitoxin therapy is primarily based on symptoms and physical examination findings that are consistent with botulism, with support of epidemiological history and electrophysiological testing. Modern clinical practice and antitoxin treatment has reduced botulism mortality rates from approximately 60% to < or =10%. The pentavalent botulinum toxoid is an investigational product and has been used for more than 45 years in at-risk laboratory workers to protect against toxin serotypes A to E. Due to declining immunogenicity and potency of the pentavalent botulinum toxoid, novel vaccine candidates are being developed.

Botulism Associated With Commercially Canned Chili Sauce—Texas and Indiana, July 2007

On July 7 and July 11, 2007, public health officials in Texas and Indiana, respectively, reported to CDC four suspected cases of foodborne botulism, two in each state. Investigations conducted by state and local health departments revealed that all four patients had eaten brands of Castleberry's hot dog chili sauce before illness began. Botulinum toxin type A was detected in the serum of one Indiana patient and in a leftover chili mixture obtained from his home. CDC informed the Food and Drug Administration (FDA) of the apparent link between illness and consumption of the chili sauce. On July 18, FDA issued a consumer advisory, and the manufacturer, Castleberry's Food Company (Augusta, Georgia), subsequently recalled the implicated brand and several other products produced in the same set of retorts (commercial-scale pressure cookers for processing canned foods) at the same canning facility. Examination of the canning facility in Georgia during the outbreak investigation had identified deficiencies in the canning process. On July 19, the U.S. Department of Agriculture Food Safety and Inspection Service (FSIS) issued a press release that announced a recall of chili and certain meat products from the Castleberry canning facility and provided recommendations to consumers. That recall was expanded on July 21 to include additional canned products. A fifth case of botulism potentially linked to one of the recalled products is under investigation in California. This report describes the ongoing investigation by members of OutbreakNet and others and the measures undertaken to control the outbreak, which is the first outbreak of foodborne botulism in the United States associated with a commercial canning facility in approximately 30 years. Clinicians should be vigilant for symptoms of botulism, including symmetric cranial nerve palsies, especially if accompanied by descending flaccid paralysis. Consumers should not eat any of the recalled chili sauce or other recalled products and should carefully dispose of all recalled products. Information regarding product disposal is available at http://www.cdc.gov/botulism/botulism_faq.htm.

Two Cases of Foodborne Botulism with Home-preserved Asparagus

Botulism is a rare but potentially fatal disease caused by toxins produced by Clostridium botulinum. We report botulism in two adult females, one of them just tasting from "bad" asparagus and the other eating the full portion. Both patients survived after intermittent mechanical ventilation and trivalent antitoxin administration. The diagnosis was confirmed by detection of botulinum toxin. Acute onset of bilateral cranial neuropathies associated with symmetric descending weakness as well as some key features of the botulism syndrome including absence of fever, symmetric neurologic deficits, the patients remaining responsive and no sensory deficits, with the exception of blurred vision, led to the clinical diagnosis in the first presenting case which was then easily made in the second. Despite the fact that amount of toxin ingested, time-to-symptom development, and time-to-recovery markedly differed in the two patients, their maximal disease severity was similar.

ProteolyticClostridium botulinumType B in the Gastric Content of a Patient with Type E Botulism Due to Whitefish Eggs

Whitefish eggs were confirmed by pulsed-field gel electrophoresis to cause type E foodborne botulism in a 54-year-old patient in Finland. Botulinum neurotoxin and/or nonproteolytic Clostridium botulinum type E organisms were detected in fecal and gastric samples from the patient and in suspected whitefish eggs. Apart from C. botulinum type E, proteolytic type B organisms were detected in the patient's gastric content. This was considered to be insignificant with respect to the clinical disease, suggesting botulinal spores to be occasionally present in the human gastrointestinal tract without any apparent clinical significance. This is the first domestic case of foodborne botulism in Finland.

Food-borne botulism: review of five cases

Food-borne botulism is a disease caused by the ingestion of food contaminated with botulinum toxin, often present in smoked meat, canned food and preserved food; it can occur as sporadic case or as an outbreak. In the last decades there has been an increasing incidence of food-borne botulism in Portugal. The authors do a review of five cases of food-borne botulism, three isolated cases and 2 familiar. Four were associated with the ingestion of smoked ham and one of canned tunafish. The incubation period was 48 hours in one patient and 4 days in another, in the remaining patients it was not possible to determine this period. The clinical picture was dominated in all patients by diplopy, dysphagia, dizziness, blurred vision, dry mouth and constipation, and in two patients there were gastrointestinal complains. In one patient the electromyography findings were compatible with pre-synaptic neuromuscular blockage. A toxin type B was found in the serum of one patient and in the food involved in the two familiar cases. All patients experienced complete recovery with only symptomatic treatment. With this article the authors intend to call attention to this diagnosis, which is not rare, but difficult for someone not familiar with its presentation, being of notice that the diagnosis is essentially clinic with a strong epidemiological history, confirmed by typical electromyography findings and by the identification of the toxin involved. In Portugal there is only descriptions of clinical cases associated with the type B and the type E toxins, not being necessary the resource to the antitoxin therapy.

Foodborne botulism in a six-month-old infant caused by home-canned baby food

Previously reported cases of botulism in infants have been diagnosed as infant botulism; that is, botulism caused by intestinal colonization by Clostridium botulinum with intraluminal production and absorption of toxin. Foodborne botulism is caused by ingestion of preformed toxin. We describe an unusual case of foodborne botulism in a 6-month-old infant caused by the ingestion of improperly prepared home-canned baby food. This represents the youngest age of onset for foodborne botulism in the United States of which we are aware and illustrates the need to rule out foodborne botulism, which represents a public health emergency, regardless of the patient's age. The diagnosis could have been readily missed or delayed in this case because the weakness was rapidly progressive rather than insidious, as is typical of infant botulism. [Ann Emerg Med. 2003;42:226-229.]

Botulism Due to Clostridium baratii Type F Toxin

Botulism results from consumption of preformed toxin or in vivo toxin elaboration in wounds or intestine. Of U.S. food-borne botulism cases since 1950, the majority were due to toxin A, but a significant number of suspect cases were never confirmed by culture or toxin detection. We report here a possible case of food-borne botulism attributed to toxin F production by a Clostridium baratii organism isolated from food consumed by the patient. The isolation of a toxin-producing Clostridium species other than Clostridium botulinum from food and stool requires deviation from the usual laboratory protocols, which may account for the lack of complete laboratory confirmation of clinically diagnosed cases.

Foodborne Botulism From Eating Home-Pickled Eggs—Illinois, 1997

During November 1997, the Illinois Department of Public Health was notified by a local physician about a possible case of foodborne botulism. This report summarizes the case investigation, which implicated home-pickled eggs as the cause.

Botulism in the United States: a clinical and epidemiologic review.

Botulism is caused by a neurotoxin produced from the anaerobic, spore-forming bacterium Clostridium botulinum. Botulism in humans is usually caused by toxin types A, B, and E. Since 1973, a median of 24 cases of foodborne botulism, 3 cases of wound botulism, and 71 cases of infant botulism have been reported annually to the Centers for Disease Control and Prevention (CDC). New vehicles for transmission have emerged in recent decades, and wound botulism associated with black tar heroin has increased dramatically since 1994. Recently, the potential terrorist use of botulinum toxin has become an important concern. Botulism is characterized by symmetric, descending, flaccid paralysis of motor and autonomic nerves, usually beginning with the cranial nerves. Blurred vision, dysphagia, and dysarthria are common initial complaints. The diagnosis of botulism is based on compatible clinical findings; history of exposure to suspect foods; and supportive ancillary testing to rule out other causes of neurologic dysfunction that mimic botulism, such as stroke, the Guillain-Barré syndrome, and myasthenia gravis. Laboratory confirmation of suspected cases is performed at the CDC and some state laboratories. Treatment includes supportive care and trivalent equine antitoxin, which reduces mortality if administered early. The CDC releases botulism antitoxin through an emergency distribution system. Although rare, botulism outbreaks are a public health emergency that require rapid recognition to prevent additional cases and to effectively treat patients. Because clinicians are the first to treat patients in any type of botulism outbreak, they must know how to recognize, diagnose, and treat this rare but potentially lethal disease.

Recovery of a strain of Clostridium botulinum producing both neurotoxin A and neurotoxin B from canned macrobiotic food

A rare strain of Clostridium botulinum subtype Ab was isolated from a canned macrobiotic food suspected of being linked to a fatal case of food-borne botulism. The strain was recovered and identified by conventional methods modified by the inclusion of a PCR assay (G. Franciosa, J.L. Ferreira, and C.L. Hatheway, J. Clin. Microbiol. 32:1911-1917, 1994). The titers of neurotoxins produced by the strain were evaluated by a mouse bioassay.

Foodborne Botulism—Oklahoma, 1994

On July 2, 1994, the Arkansas Department of Health and the Oklahoma State Department of Health were notified about a possible case of foodborne botulism. This report summarizes the investigation, which implicated consumption of improperly stored beef stew.