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At least 19 recordsLinked to original sources
PubMed1991

Distinction between Clostridium botulinum type A strains associated with food-borne botulism and those with infant botulism in Japan in intraintestinal toxin production in infant mice and some other properties.

Two strains of Clostridium botulinum type A associated with food-borne botulism and six strains associated with infant botulism in Japan were compared in intraintestinal toxin production in infant mice, in vitro toxin and hemagglutinin production, molecular sizes of the toxins, and some other properties. The infant botulism-associated strains, producing M toxin (Mr 300 kDa) but no hemagglutinin, showed significantly lower 50% infective doses in infant mouse intestines. The antigenicities of the toxin differed between the two groups, while the biochemical properties of the cultures did not. Besides infant botulism-associated strains, this set of properties were found only in a strain isolated from honey of South American origin.

Animals↗
PubMed1977

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↗
PubMed2026

Tracing and characterization of a family outbreak of subtype B2 botulism linked to homemade pickled eggs in Jinan, China.

Foodborne botulism (FB) results from the ingestion of food contaminated with botulinum neurotoxin. Here, we report a family outbreak of foodborne botulism caused by Clostridium botulinum subtype B2 linked to homemade pickled eggs. On August 13, 2024, the Jinan Center for Disease Control and Prevention and the Shanghe County Center for Disease Control and Prevention collaborated to investigate an outbreak of botulism poisoning related to a family gathering in Shanghe County, Jinan City. A total of 4 people attended the family gathering, three of whom developed clinical symptoms of botulism after consuming pickled eggs. The diagnosis of botulism was suspected through collaborative efforts by the Qilu Medical Prevention and Control Innovation Integration Mechanism and multidisciplinary consultations across multiple hospitals. We detected the bont gene using real-time quantitative PCR (qPCR) in Jinan CDC, determined the toxin serotype by mouse bioassay (MBA) in China CDC and performed whole-genome sequencing of bacterial strains isolated from patient feces, the homemade pickled eggs and soil in both laboratories. It was shown that the toxin type and bont gene were subtype B2, belonging to the ha gene cluster. The Clostridium botulinum strains isolated from two patients were closely related to the strains from the homemade pickled eggs through whole-genome single nucleotide polymorphism analysis. We also found that Clostridium botulinum strains from soil clustered into one branch with those from patients and food, suggesting that the source of Clostridium botulinum contamination may be from soil, although the contamination pathway was not clear. Importantly, our findings provided a basis for clinical antitoxin treatment, in which one patient successfully gave birth after recovery. These results underscore the importance of strengthening public education about the health risks associated with consuming homemade fermented or preserved foods and enhancing the laboratory detection capabilities.

Botulism↗
PubMed1992

Characterization of the neurotoxin isolated from a Clostridium baratii strain implicated in infant botulism.

Botulism is widely known to result from ingestion of food containing botulinum neurotoxin produced in situ by certain strains of Clostridium botulinum. Infant botulism caused by C. botulinum, unlike the food-borne intoxication, is the toxicoinfectious form of botulism (S. S. Arnon, p. 331-345, in G. E. Lewis, ed., Biomedical Aspects of Botulism, 1981). The strain of Clostridium baratii implicated in infant botulism produced a neurotoxin that was neutralized with antiserum for botulinum neurotoxin serotype F (J. D. Hall, L. M. McCroskey, B. J. Pincomb, and C. L. Hatheway, J. Clin. Microbiol. 21:654-655, 1985). We developed a procedure to culture the toxigenic C. baratii (strain 6341) in dialysis bags and a simple purification scheme (precipitation of 900-ml culture supernatant with ammonium sulfate and two anion-exchange chromatographic steps at pH 5.5 and 8.0) that yielded up to 150 micrograms of purified neurotoxin. It is an approximately 140-kDa single-chain protein and has the following sequence of amino acid residues at the N terminus: Pro-Val-Asn-Ile-Asn-Asn-Phe-Asn-Tyr-Asn-Asp-Pro-Ile-Asn-Asn-Thr-Thr-Ile- Leu. Comparison of this amino acid sequence with those of the botulinum neurotoxin serotypes A, B, and E showed 40 to 50% identical residues in comparable positions. The specific toxicity of the neurotoxin, approximately 2 x 10(6) 50% lethal doses for mice per mg of protein injected, was not enhanced significantly by mild trypsinization, although the protease cleaved the neurotoxin within a disulfide loop that generated at least two primary fragments, approximately 47 and approximately 86 kDa, that remained linked by an interchain disulfide. These two fragments resembled the light and heavy chains of the well-characterized neurotoxin serotypes A, B, C, D, E, and F produced by C. botulinum.

Amino Acid Sequence↗
PubMedDate not supplied

Tracheotomy for infant botulism.

Botulism is a serious intoxication caused by ingestion of food containing preformed botulinus toxin and characterized by rapidly progressive bulbar paralysis, generalized weakness, and respiratory insufficiency. In 1976 a distinct clinical entity of infant botulism was recognized. The disease apparently results from intraintestinal toxin production which produces a defect in neuromuscular transmission by interfering with release of acetylcholine at cholinergic synapses. Five cases of infant botulism were identified at the Children's Hospital of Philadelphia between 1975 and 1977. Initial symptoms included constipation, slow feeding, lethargy and weak cry. Four of the patients progressed to respiratory insufficiency requiring nasotracheal intubation. Three of the infants with respiratory failure required tracheotomy. Because infants with respiratory failure may require support for months, we recommend that a tracheotomy be performed early in the management to avoid the complications associated with prolonged intubation. The effectiveness of antitoxin or antibiotics to treat infant botulism remains questionable and therefore prolonged respiratory supportive care is the mainstay of therapy. In addition, we offer guidelines for decannulation in cases of infant botulism. None of the patients in our series could be decannulated prior to initial discharge from the hospital.

Botulism↗
PubMed1992

[Botulism: a case report].

Botulism is an acute form of poisoning that results from ingestion of a toxin produced by Clostridium botulinum. Botulism toxin causes their major effect by blocking neuromuscular transmission in autonomic and motor nerve terminals. Guillain Barre Syndrome, Myasthenia Graves, Lambert Eaton Myasthenic Syndrome, acute poliomyelitis and diphtheria must be considered in the differential diagnosis. Electrodiagnostic studies have been shown to be of value in differentiating botulism from other paralytic diseases. Identification of the toxin in the patients serum is diagnostic. The treatment of botulism is mainly supportive. In this study we have discussed a patient who was treated in our clinic as a botulism from unknown source, the differential diagnosis from other paralytic diseases.

Botulism↗
PubMed1991

[Botulism in the Czech Republic].

In a retrospective study the authors analyzed 76 cases of botulism reported in 1961-1989 in the Czech Republic. The analysis of descriptive data pertained to the annual incidence of botulism with a maximum of cases in 1966, 1973 and 1984 (11, 7 and 6 cases); geographical distribution with a maximum incidence in the South and Central Bohemian region (100,000 population); age distribution with a predominance in subjects above 15 years. The dominating vehicle of botulism was in 61% of the notified cases a home-prepared food; usually a galantine, aspic, liver paste, pork with vegetables, and smoked pork. In 1966 and 1973 a processed food predominated as vehicle: pickled herring and tomato, red peppers and sausage. The results of the retrospective study were compared in the discussion with the problem of botulism in other countries. The authors discuss the danger of undetected botulism and the necessity of an anti-botulin serum (Bossea).

Adolescent↗
PubMed1979

Honey and other environmental risk factors for infant botulism.

Infant botulism results from the in vivo production of toxin by Clostridium botulinum after it has colonized the infant's gut. Epidemiologic and laboratory investigations of this recently recognized disease were undertaken to identify risk factors and routes by which C. botulinum spores might reach susceptible infants. Clostridium botulinum organisms, but no preformed toxin, were identified in six different honey specimens fed to three California patients with infant botulism, as well as from 10% (9/90) of honey specimens studied. By food exposure history, honey was significantly associated with type B infant botulism (P = 0.005). In California, 29.2% (12/41) of hospitalized patients had been fed honey prior to onset of constipation; worldwide, honey exposure occurred in 34.7% (28/75) of hospitalized cases. Of all food items tested, only honey contained C. botulinum organisms. On household vacuum cleaner dust specimens and five soil specimens (three from case homes, two from control homes) contained Clostridium botulinum. The known ubiquitous distribution of C. botulinum implies that exposure to its spores is universal and that host factors contribute importantly to the pathogenesis of infant botulism. However, honey is now an identified and avoidable source of C. botulinum spores, and it therefore should not be fed to infants.

Botulism↗
PubMed1992

A recent reminder of botulism.

Botulism is a rare yet potentially common form of food poisoning that can be fatal. (1) Few documented cases of botulism exist in Australia (2,3,4) and New Zealand (5), emphasising how infrequently it is encountered. The recent admission to our Intensive Care Unit (ICU) of a man suspected of having botulism was a timely reminder of just how dangerous this condition can be. This paper will review the contemporary knowledge and interventions necessary in the management of botulism. It will also utilise anecdotes from our recent experience to illustrate some of the clinical scenarios and potentially fatal complications seen in this condition.

Australia↗
PubMedDate not supplied

Laboratory procedures for cases of suspected infant botulism.

The recent development and evaluation of procedures for examination of fecal specimens for botulinal toxin and Clostridium botulinum have provided the means by which infant botulism can be recognized. The toxicity for mice of fecal extracts containing botulinal toxin can be neutralized with specific botulinal antitoxin. The presence of C. botulinum in the feces is detected by demonstrating the presence of botulinal toxin in enrichment culture supernatant by means of toxicity tests in mice. C. botulinum is isolated by streaking enrichment cultures on egg yolk agar and picking typical lipase-positive colonies. The experience of both the Center for Disease Control (CDC) Botulism Laboratory and other laboratories has been that botulinal toxin and C. botulinum are rarely, if ever, found in the feces of humans (infants or older people) not afflicted with botulism. Results of the examination in the CDC laboratory of specimens from 24 babies with infant botulism are given.

Animals↗
PubMedDate not supplied

Food and environmental aspects of infant botulism in California.

In an effort to identify vehicles by which Clostridium botulinum spores might have reached the intestine of patients with infant botulism, 555 samples of foods, drugs, and environmental specimens were examined. Of the food items, C. botulinum was only found in nine of 90 (10%) honey specimens. Five patients had been exposed to honey that contained C. botulinum, and ingestion of honey was found to be a significant risk factor for type B infant botulism (P = 0.005). In addition, C. botulinum was isolated from five samples of soil (three from case homes, two from control homes) and from vacuum cleaner dust from one case home. In every instance in which C. botulinum was isolated from a specimen of honey, soil, or duct associated with a case of infant botulism, the type of toxin (A or B) in the honey, soil, or dust isolate matched the type of toxin of the organism recovered from the infant. Isolation of C. botulinum from the soil of homes of control infants emphasizes the ubiquitous distribution of and exposure to this organism and suggests that host factors are important in the development of illness. Prevention of infant botulism will depend on the identification of these host factors, as well as on the identification of other vehicles that, like honey, may convey C. botulinum spores to susceptible infants.

Botulism↗
PubMed1991

[Botulism in cattle, a review].

Botulism in cattle is reviewed in the present paper. General information concerning the aetiology and symptomatology of the disease is followed by a discussion of the epidemiological situation in the Netherlands. Since 1975 several outbreaks of botulism type C or D have occurred. Poultry litter in which toxic carcasses were present, was the most important source of the toxin. An increasing number of cases of botulism type D was reported in recent years, which was probably due to the fact that poultry is not susceptible to toxin type D and therefore the presence of type D toxin is difficult to recognise timely. In addition, atypical cases of type B botulism occurred in the Netherlands during the period from 1977 to 1978, which were caused by supplementary feeding of brewer's grains. Finally, the diagnostic problems, differential diagnosis, prevention, treatment and public health aspects are discussed.

Animals↗
PubMed1976

[Contamination of fish by agents of botulism type F and differentiating it from type E].

A total of 1859 samples of fish and various sea animals were examined for contamination with causative agent of botulism. The cultural fluid of 4--5-day cultures of the samples was tested in the reaction of neutralization with the diagnostic antitoxic antibotulin sera. types A, B, C, E. The causative agents of botulism (types A--7,B--16, C--5, E--128) were revealed in 156 samples. The sera were diluted to the concentration of 1 IU/ml for differentiation of the toxins types B and F in the neutralization test. Of 128 samples which gave a positive reaction with the serum of type E, 75 were identified as type F. In connection with the aforesaid the authors recommended in all the cases of botulism of type E in man to carry out differential diagnosis between the causative agents of botulism of types E and F and, on the basis of these data, to solve the problem on the necessity of production of therapeutic antibotulin serum of type F.

Animals↗
PubMed2026

A single-case foodborne botulism outbreak caused by Clostridium botulinum type A1(B5) in diced garlic in Newfoundland and Labrador, 2024.

Foodborne botulism is a severe neuroparalytic disease caused by ingestion of foods containing botulinum neurotoxins, produced by Clostridium botulinum. In 2024, a 74-year-old woman from Newfoundland and Labrador with complete bilateral flaccid paralysis and respiratory distress was hospitalized and required intubation. From the broader differential diagnosis list, botulism was favoured prior to laboratory confirmation. Serum and feces samples initially tested negative for botulinum neurotoxins by mouse bioassay, yet viable C. botulinum type A was recovered from the feces. Food history investigation included some diced garlic in a repurposed coffee container that tested negative for botulinum neurotoxins by mouse bioassay, but viable C. botulinum type A was recovered from the sample. Both the fecal and garlic enrichment cultures were positive for bont/A and bont/B genes by real-time PCR. Whole genome sequencing revealed that both fecal and garlic isolates were highly similar with conserved gene synteny, including an intact bont/A1 gene and a disrupted (silent) bont/B5 gene encoded on the chromosome. This single-case foodborne botulism outbreak from Newfoundland and Labrador in 2024 was caused by C. botulinum type A1(B5) in diced garlic.

Aged↗
PubMed1977

Infant botulism. Epidemiological, clinical, and laboratory aspects.

Clostridium botulinum organisms and toxin were identified in the feces of six infants, aged 5 to 20 weeks, who had illnesses clinically consistent with botulism. Five of the infants lived in California and became ill within a six-month period in 1976; one infant became ill in New Jersey in 1975. Three cases were type A botulism, and three were type B. No source of ingested botulinal toxin could be found in any case. However, one infant with type B botulism had ingested a food containing C botulinum type B organisms, and no toxin was found in it. The clinical findings in these cases include constipation, weak sucking and crying ability, pooled oral secretions, cranial nerve deficits, generalized weakness, and, on occasion, sudden apnea. A characteristic electromyographic pattern termed "brief, small, abundant, motor-unit action potentials" (BSAP) was observed. The sources of C botulinum toxin for these six infants is thought to have been in vivo (gastrointestinal) production following ingestion of C botulinum organisms. Studies are underway to determine the full clinical spectrum, incidence, and potential public health importance of this infectious disease newly recognized in infants.

Age Factors↗
PubMed1979

Botulism, type A, and treatment with guanidine.

In a double-blind crossover study in which patients received placebo or active drug for varying periods, we evaluated the ability of guanidine hydrochloride (20 to 35 mg/kg per day perorally) to improve the rate of recovery in patients with moderate or severe botulism, type A, intoxication. Among 14 patients who received conventional botulism therapy, there was no improvement in recovery rate in those who received guanidine compared with the nontreated group. Individual patients in the treated group showed neither an acceleration in their rate of improvement when they received guanidine nor a regression in their progress when the drug was stopped. Individual patients, likewise, noted no subjective improvement when they received the drug compared with the placebo. Treatment with guanidine does not enhance recovery from botulism.

Botulism↗