[Evolution of botulism. IV. Epidemiological prerequisites for acquisition of resistance to botulism by ancestors of modern man].
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Biological Evolution↗
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Botulism among Cape Dorset Eskimos and suspected botulism at Frobicher Bay and Wakeham Bay.
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Adolescent↗
Type C botulism in cattle in association with a botulism die-off in waterfowl in Saskatchewan.
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Animals↗
Clinical spectrum of botulism.
Botulism is a paralyzing disease caused by the toxin of Clostridium botulinum. The toxin produces skeletal muscle paralysis by producing a presynaptic blockade to the release of acetylcholine. Recent studies have pinpointed the site of action of the several types of botulinum neurotoxin at the nerve terminal. Since the discovery of the toxin about 100 years ago, five clinical forms of botulism have been described: 1) classic or foodborne botulism; 2) wound botulism; 3) infant botulism; 4) hidden botulism; 5) inadvertent botulism. A clinical pattern of descending weakness is characteristic of all five forms. Almost all human cases of botulism are caused by one of three serotypes (A, B, or E). Classic and wound botulism were the only two forms known until the last quarter of this century. Wound botulism was rare until the past decade. Now there are increasing numbers of cases of wound botulism in injecting drug users. Infant botulism, first described in 1976, is now the most frequently reported form. In infant botulism spores of Clostridium botulinum are ingested and germinate in the intestinal tract. Hidden botulism, the adult variant of infant botulism, occurs in adult patients who usually have an abnormality of the intestinal tract that allows colonization by Clostridium botulinum. Inadvertent botulism is the most recent form to be described. It occurs in patients who have been treated with injections of botulinum toxin for dystonic and other movement disorders. Laboratory proof of botulism is established with the detection of toxin in the patient's serum, stool, or wound. The detection of Clostridium botulinum bacteria in the stool or wound should also be considered evidence of clinical botulism. Electrophysiologic studies can provide presumptive of botulism in patients with the clinical signs of botulism. Electrophysiologic testing can be especially helpful when bioassay studies are negative. The most consistent electrophysiologic abnormality is a small evoked muscle action potential in response to a single supramaximal nerve stimulus in a clinically affected muscle. Posttetanic facilitation can be found in some affected muscles. Single-fiber EMG studies typically reveal increased jitter and blocking, which become less marked following activation. The major treatment for severe botulism is advance medical and nursing supportive care with special attention to respiratory status.
Botulinum Toxins↗
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.
Antitoxins↗
[Clinical and epidemiological characteristics of botulism in France].
Botulism is still found in France. Botulism is life-threatening and may have epidemic occurrences, which justifies an epidemiological watch with systematic notification of cases. In order to complete these recent epidemiological data, older cases since 1940 have been reviewed through a survey sent to the French Ministry of Health and the Pasteur Institute (National Reference Center). A Medline search has also been completed. In France, foodborne botulism is the main source of contamination. Type B is nearly always involved but type E botulism has been regularly reported. Fatal outcome due to botulism-induced respiratory muscle weakness can now be avoided by mechanical ventilation, leading to better prognosis. Microbiological diagnosis has been confirmed in two-thirds of the cases by isolation of toxin in the patient's serum. It is important to identify the foodstuff incriminated to prevent the development of a botulism outbreak. Foodstuffs responsible for foodborne botulism are the same since 1940. However, the increased consumption of vacuum-packed foodstuffs might facilitate the persistence of botulism. In conclusion, this review points out the significance of epidemiological screening of foodstuffs in the alimentary chain as well as the systematic notification of botulism. The regular educational information for young physicians regarding botulism should be continued.
Adult↗
Botulism: the present status of the disease.
The main form of human botulism throughout the world is the classic foodborne intoxication. Would botulism is very rare, and most of the documented cases have been found in the United States. While infant botulism remains rare throughout the world, it has become the most frequent form of the disease in the United States in recent years. On very rare occasions botulism results from growth and toxin production in humans other than infants. Botulism occurs in animals with much higher frequency. The causative organisms constitute a diverse group of clostridia, resulting in nomenclature problems. Human botulism is largely limited to toxin types A, B, and E, while type C botulism predominates in avian and nonhuman mammalian species. The diagnosis of botulism is made on the basis of the neurologic signs and symptoms that it causes in humans and animals. The diagnosis is confirmed by tests that identify the toxin and toxigenic organisms in patient and food specimens. Treatment includes supportive intensive care and use of therapeutic antitoxin.
Animals↗
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.
Age of Onset↗
Signs and symptoms predictive of death in patients with foodborne botulism--Republic of Georgia, 1980-2002.
Foodborne botulism is a severe, potentially fatal disease characterized by cranial nerve palsies and descending paralysis. Little is known about signs and symptoms predictive of death from botulism. We studied patients with botulism in the Republic of Georgia, which has the highest reported rate of foodborne botulism in the world. After abstracting medical records of patients with botulism who were hospitalized during 1980-2002, we performed classification-and-regression-tree analysis to identify clinical syndromes predictive of survival and death. We identified records for 706 patients hospitalized for foodborne botulism from 1980-2002. Trivalent antitoxin was administered to 623 patients (88%). Fifty-four (8%) died. Patients with shortness of breath and impaired gag reflex and without diarrhea were 23 times more likely to die than were patients without this syndrome. Validating this clinical prediction rule may help reduce mortality from botulism in Georgia. Validation in other settings could help public health preparations for large outbreaks of naturally occurring or bioterrorism-related botulism.
Adolescent↗
Botulism.
Botulism is a rare disease with 4 naturally occurring syndromes: foodborne botulism is caused by ingestion of foods contaminated with botulinum toxin, wound botulism is caused by Clostridium botulinum colonization of a wound and in situ toxin production, infant botulism is caused by intestinal colonization and toxin production, and adult intestinal toxemia botulism is an even rarer form of intestinal colonization and toxin production in adults. Inhalational botulism could result from aerosolization of botulinum toxin, and iatrogenic botulism can result from injection of toxin. All forms of botulism produce the same distinct clinical syndrome of symmetrical cranial nerve palsies followed by descending, symmetric flaccid paralysis of voluntary muscles, which may progress to respiratory compromise and death. The mainstays of therapy are meticulous intensive care (including mechanical ventilation, when necessary) and timely treatment with antitoxin.
Botulinum Antitoxin↗
Use of enzyme-linked immunoassays for antibody to types C and D botulinum toxins for investigations of botulism in cattle.
The development of specific enzyme-linked immunosorbent assays (ELISA) for antibody to types C and D Clostridium botulinum toxins for investigation of botulism in cattle is described. Partially purified type C and D toxins were used as antigens to develop these ELISAs. Specificity of the ELISAs was evaluated on sera from 333 adult beef and dairy cattle from areas with no history or evidence of botulism in animals or water birds. The test was also evaluated on sera from 41 herds that included herds vaccinated against botulism, confirmed botulism cases and herds from areas where the disease is considered endemic. The ELISAs detected the presence of antibody to botulinum toxins in samples from vaccinated cattle and both convalescent and clinically normal animals from unvaccinated herds with outbreaks of botulism. Antibody was also found in unvaccinated animals from herds in which there had been no diagnosed botulism cases in areas where botulism was considered endemic. Sera from some unvaccinated cattle with high ELISA reactivity was shown to be protective for mice in botulinum toxin neutralisation tests. The use of these tests in investigations of botulism in cattle is discussed.
Animals↗
Long-term follow-up of symptoms, pulmonary function, respiratory muscle strength, and exercise performance after botulism.
Respiratory muscle weakness occurs commonly at presentation in patients with botulism. Although clinical improvement occurs over several months, symptoms such as fatigue and dyspnea persist in many patients in the long term. To determine whether continued respiratory muscle weakness might contribute to these symptoms, we compared lung function tests, respiratory muscle strength, and exercise performance in 13 patients 2 years after type B botulism. We found that residual symptoms including dyspnea and fatigue were common in botulism patients at 2 years postintoxication. Lung function tests had returned to normal in all patients. Maximal inspiratory and expiratory pressures were similar between botulism patients and control subjects. Evaluation of individual results showed evidence of inspiratory muscle weakness in four of 13 patients with botulism (Plmax less than 65% predicted). Maximal oxygen consumption and maximal workload during exercise were reduced in botulism patients in comparison to control subjects. During exercise, botulism patients had a more rapid and shallow breathing pattern and a higher dyspnea score at a given minute ventilation in comparison to control subjects. Reasons for premature exercise termination in botulism patients were multifactorial. Although respiratory muscle weakness may have been contributory in some patients, most appeared to be limited by reduced cardiovascular fitness, leg fatigue, or reduced motivation.
Adult↗
Foodborne botulism in the Republic of Georgia.
Foodborne botulism is a potentially fatal, paralytic illness that can cause large outbreaks. A possible increase in botulism incidence during 2001 in the Republic of Georgia prompted this study. We reviewed surveillance data and abstracted records of patients with botulism who were hospitalized from 1980 to 2002. During this period, 879 botulism cases were detected. The median annual incidence increased from 0.3 per 100,000 during 1980 to 1990 to 0.9 per 100,000 during 1991 to 2002. For 706 botulism patients hospitalized from 1980 to 2002, 80% of their cases were attributed to home-preserved vegetables. Surveillance evaluation verified that botulism incidence varied greatly by region. Georgia has the highest nationally reported rate of foodborne botulism in the world. A strategy addressing individual behaviors in the home is needed to improve food safety; developing this strategy requires a deeper understanding of why botulism has increased and varies by region.
Adolescent↗
An outbreak of type A botulism associated with a commercial cheese sauce.
BACKGROUND: Although botulism is rare, recognition of a possible case of this illness represents a public health emergency. To prevent more cases, prompt investigation must be done to determine whether illness is linked to commercial product or restaurant. Botulism can masquerade as other illnesses, and seemingly unlikely foods can harbor botulinum toxin. OBJECTIVE: To confirm the diagnosis and determine the cause and extent of an outbreak of botulism associated with food served at a delicatessen. DESIGN: Retrospective cohort study of patrons of the delicatessen; laboratory analysis of food, serum samples, and stool samples; and traceback of implicated food. SETTING: Community in Georgia. PARTICIPANTS: Patrons of the delicatessen. MAIN OUTCOME MEASURES: Botulinum toxin in food, serum, or stool and Clostridium botulinum in food and stools. RESULTS: 8 of 52 patrons (15%) met the case definition for botulism. In 4 of the 8 patrons, and illness other than botulism was initially diagnosed. Five of the 8 were hospitalized, and 1 died. Stool cultures from 4 patrons yielded type AC. botulinum, and two serum samples contained botulinum toxin. All ill persons ate food from the delicatessen on 1 October 1993. Of the 22 persons who ate at the delicatessen that day, all 8 ill persons but none of the 14 well persons ate a potato stuffed with meat and cheese sauce. An open can of cheese sauce contained type A botulinum toxin and yielded C botulinum on culture. Cheese sauce experimentally inoculated with C botulinum spores became toxic after 8 days at a temperature of 22 degrees C (room temperature). CONCLUSIONS: A commercial, canned cheese caused a botulism outbreak. This product readily becomes toxic when contaminated by C botulinum spores and left at room temperature. Mild botulism caused by unusual vehicles may be misdiagnosed. Botulism should be included in the differential diagnosis of persons with signs or symptoms of acute cranial nerve dysfunction.
Adult↗
Coproexamination for botulinal toxin and clostridium botulinum. A new procedure for laboratory diagnosis of botulism.
Stool or serum specimens or both from 318 persons pertaining to 165 botulism investigations over a three-year period were examined. Botulinal toxin was detected in stools of 19 of 56 patients and in sera of 20 of 60 patients with clinical botulism; it was not detected in specimens from 246 persons with an illness other than botulism or well contacts of patients. Clostridium botulinum was identified in stools of 36 of 60 clinical botulism patients and in four of 27 asymptomatic contacts of patients with botulism victims, but not in stools of 65 persons not associated with confirmed botulism. When stool and serum samples were examined, confirmatory evidence was obtained for 72.9% of the botulism cases. Detection of botulinal toxin or C botulinum in the stool of a persons should be considered evidence supporting the clinical diagnosis of botulism.
Bacteriological Techniques↗
Botulism in 4 adults following cosmetic injections with an unlicensed, highly concentrated botulinum preparation.
CONTEXT: Botulism is a potentially lethal paralytic disease caused primarily by toxins of the anaerobic, spore-forming bacterium Clostridium botulinum. Although botulinum toxin A is available by prescription for cosmetic and therapeutic use, no cases of botulism with detectable serum toxin have previously been attributed to cosmetic or therapeutic botulinum toxin injections. On November 27, 2004, 4 suspected botulism case-patients with a link to cosmetic botulinum toxin injections were reported to the Centers for Disease Control and Prevention. OBJECTIVE: To investigate the clinical, epidemiological, and laboratory aspects of 4 suspected cases of iatrogenic botulism. DESIGN, SETTING, AND PATIENTS: Case series on 4 botulism case-patients. MAIN OUTCOME MEASURES: Clinical characteristics of the 4 case-patients, epidemiological associations, and mouse bioassay neutralization test results from case-patient specimens and a toxin sample. RESULTS: Clinical characteristics of the 4 case-patients were consistent with those of naturally occurring botulism. All case-patients had been injected with a highly concentrated, unlicensed preparation of botulinum toxin A and may have received doses 2857 times the estimated human lethal dose by injection. Pretreatment serum toxin levels in 3 of the 4 case-patients were equivalent to 21 to 43 times the estimated human lethal dose; pretreatment serum from the fourth epidemiologically linked case-patient was not available. A 100-microg vial of toxin taken from the same manufacturer's lot as toxin administered to the case-patients contained a toxin amount sufficient to kill approximately 14,286 adults by injection if disseminated evenly. CONCLUSIONS: These laboratory-confirmed cases of botulism demonstrate that clinical use of unlicensed botulinum toxin A can result in severe, life-threatening illness. Further education and regulation are needed to prevent the inappropriate marketing, sale, and clinical use of unlicensed botulinum toxin products.
Botulinum Toxins, Type A↗
Is there a link between infant botulism and sudden infant death? Bacteriological results obtained in central Germany.
UNLABELLED: Despite the fact that botulism was described in Germany for the first time by Kerner in 1820, the disease is almost forgotten in this country. Only about 10-20 cases of classical botulism (intoxication) are recorded every year, including 1-2 cases of clinical infant botulism. As we assumed a high incidence of botulism to be connected with cases of sudden infant death (SID), we undertook the research work presented here. From every case of unexpected infant death up to 12 months of age, standardised specimens (blood, liver and intestine) were taken at autopsy. They were tested for the presence of botulinum neurotoxin (BoNT) and/or bacterial forms of Clostridium botulinum with subsequent BoNT neutralisation tests by the international standard mouse bioassay. Age, sex, pathological findings and season were recorded. Over a 5-year period, 75 samples including 57 SID cases were tested. Free toxin was found in nine and bacterial forms were detected in six samples. Toxin neutralisation revealed the definite presence of BoNT/BoNT producing bacteria (mainly type E), whereas another 11 toxin tests were inconclusive. According to international literature, these 15 cases are to be interpreted as infant botulism. CONCLUSION: the results show a remarkable incidence of infant botulism without any known previous medical history, partly hidden as sudden infant death. We propose to systematically search for botulism in connection with sudden infant death.
Animals↗
Botulism in foals less than 6 months of age: 30 cases (1989-2002).
Botulism has been recognized as a clinical entity in foals since the 1960s. Also known as "Shaker foal" disease, the toxicoinfectious form of botulism affects foals, with the highest incidence in the United States seen in Kentucky and the mid-Atlantic region. The disease is characterized by progressive muscular weakness caused by the action of botulism neurotoxin at cholinergic neuromuscular junctions. Increased number of episodes and duration of recumbency, muscular trembling, and dysphagia are seen in affected foals. Left untreated, the disease can be rapidly fatal, with death occuring secondary to respiratory muscle paralysis within 24 to 72 hours of the onset of clinical signs. Very mildly affected foals can survive with minimal treatment Despite advances made in treatment of these foals, including administration of botulism antitoxin early in the course of the disease, there is still an impression that the disease carries a high mortality rate. The purpose of this study was to evaluate outcome in 30 foals <6 months of age diagnosed with botulism between 1989 and 2002 at the George D. Widener Large Animal Hospital, New Bolton Center. Two foals were euthanized for economic reasons early in the disease course, and I died while being treated. Survival of treated cases was greater than 96%. Approximately 50% of the cases required oxygen therapy, whereas 30% required mechanical ventilation. All foals, excepting 1 mildly affected foal, received botulism antitoxin. Mean duration of hospitalization was 14 days. With appropriate treatment, foals with botulism have a high survival rate.
Animals↗