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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
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↗
PubMed1975

A continuing common-source outbreak of botulism in a family.

In December, 1974, three cases of botulism occurred in a family; two were fatal. The first patient died after a 10-day illness without botulism being suspected. 4 days later, after a 2-day illness, the second patient was diagnosed as having botulism after a cardiorespiratory arrest; she died 3 days later. In the third patient, the only symptom was dysphagia. Clostridium botulinum type B was found in stool specimens from all three patients. Home-canned (bottled) mushrooms, which were found to contain C. botulinum type B and its toxin, were believed to be responsible for the outbreak; mushrooms were found at necropsy in the gastrointestinal tracts of both patients who died. Heat treatment of the mushrooms during canning had been inadequate.

Adult↗
PubMedDate not supplied

Differential diagnosis of infant botulism.

Clinical investigations of infants hospitalized with botulism demonstrate a remarkable uniformity of complaints and physical findings. Constipation precedes a course of progressive weakness and cranial nerve dysfunction. Examination reveals hypotonia, hyporeflexia, and a variable pattern of involvement of the motor cranial nerves. Initial laboratory investigations should include electrodiagnostic tests, because findings of an incremental response to rapid, repetitive nerve stimulation and of brief, small-amplitude motor units on electromyography are virtually pathognomonic of botulism in the infant. Differential diagnosis includes disorders that may produce generalized depression of the central nervous system, such as septicemia, meningitis, metabolic disturbances, and intoxications. Specific involvement of the neuromuscular system includes acute polyneuropathies, diseases of the anterior horn cell, congenital myopathies or muscular dystrophy, and neonatal myasthenia gravis. Recent studies have expanded the clinical spectrum of infant botulism to include some cases of sudden infant death syndrome and otherwise nonspecific constipation.

Action Potentials↗
PubMedDate not supplied

Laboratory aspects of infant botulism in California.

Infant botulism is the newly recognized form of the disease in which illness results from the production of toxin in the infant's intestines. Between the recognition of infant botulism as a distinct clinical entity in 1976 and the end of 1978, 50 cases were identified in California. The diagnosis of botulism was established by the identification of botulinal toxin in and the isolation of Clostridium botulinum from stool specimens of the affected infants. Thirty cases were type A and 20 were type B. Fecal excretion of toxin and organisms was monitored during hospitalization and after discharge from the hospital. Stools from family members and from 160 age-matched control infants did not contain botulinal toxin. A total of 396 food and drug samples, as well as 159 environmental and miscellaneous items, were examined. None of the foods or drugs tested contained preformed toxin. However, C. botulinum organisms were isolated from the nine samples of honey, five of soil, and one of vacuum cleaner dust.

Botulinum Toxins↗
PubMed1978

Botulism type B: epidemiologic aspects of an extensive outbreak.

Between March 31 and April 6, 1977, 59 individuals developed type B botulism. All ill persons had eaten at the same Mexican restaurant and all had consumed a hot sauce made with improperly home-canned jalapeno peppers, either by adding it to their food, or by eating a nacho that had had hot sauce used in its preparation. There was a highly significant association between illness and consumption of hot sauce when a comparison was made between ill persons and well controls: 4% of all restaurant patrons eating at the restaurant during the outbreak period became ill with botulism; however, approximately two-thirds of those actually exposed to the toxic hot sauce became ill. Disease severity was statistically correlated with incubation periods. No differences in disease severity were found between persons of different age groups. The full clinical spectrum (mild symptomatology with neurologic findings through life-threatening ventilatory paralysis) of type B botulism was documented.

Adolescent↗
PubMed1979

Prolonged respiratory paralysis in wound botulism.

Two patients had wound botulism with longer duration of respiratory paralysis than previously described. Each sustained extensive trauma to soft tissues and grossly contaminated wounds when thrown from a vehicle in a rural area. Progressive muscular weakness and respiratory distress occurred 8 and 13 days after injury, in the presence of infected wounds and clinical and laboratory findings characteristic of botulism. Spontaneous vital capacity and inspiratory effort served as bedside indicators of ventilatory function throughout 11 weeks of ventilatory support in each case and paralleled other clinical assessments of progress and recovery. Wound botulism may result in neuromuscular paralysis for a prolonged period. These cases illustrate the primary role of scrupulous nursing and respiratory care throughout such a period of ventilatory insufficiency.

Adult↗
PubMed1975

[Botulism. Therapeutic management. Apropos of 36 cases].

Botulism is relatively common in the Vienne department as we have observed 36 cases over a peroid of 7 years. Other French cases, published over the last 10 years, included 10 to 19 cases in the largest series. In a total of 10 series, there were 105 cases. Botulism is caused, in most cases, by eating ham prepared on the farm. It gives rise to the usual clinical picture including paralysis of accommodation, dysphagia, digestive symptoms with abdominal pain and constipation and finally, bladder paralysis. The mild forms are fairly common. We did not observe any severe cases. Our patients were treated in two homogeneous series of 17 cases each ; two patients were given no treatment. Patients treated by sero-anatoxin therapy according to classical methods, evolved towards a cure within 21 days on average. Patients treated by sulfguanidin were cured within 24 days. This study permitted us to confirm that sero-anatoxin therapy is not essential. The disadvantages are the number of injections, the possibility of sometimes fatal hyper-sensitive reactions which, in the opinion of many authors, justifies routine cover with cortisone. This attitude does not seem to us justified owing to the usually benign nature of the botulism. The treatment with sulfaguanidin is well tolerated and is not of any risk to the patient.

Botulinum Antitoxin↗
PubMed1977

[Contribution to the aetiology and epidemiology of botulism in broiler chickens (authors transl)].

The second outbreak of botulism in broiler chickens diagnosed in the Netherlands is reported. In this case, the source of botulinum toxin was positively located. Despite the fact that the owner had emphatically assured that all sick and dead broilers had been carefully removed, several carcasses of broilers, almost unrecognizable at first sight, were found to be present in the litter covering the floor, particularly at the rear of the fowl house. The concentration of toxin in the carcasses in the area surrounding this source of infection averaged well over 1,000,000 LD50 per gram of tissue. This is more than sufficient to account for the outbreak of botulism as the oral MLD of the strain of Cl. botulinum type C isolated in previous studied had been found to be well over 4,000,000 LD50 per kg of body weight for chickens, the oral MLD of the strain of Cl. botulinum type C isolated in the second outbreak being found to be 2,000,000 LD50 per kg. of body weight. In discussing the origin of the infection, attention is finally drawn to the possible relationship with the fact that botulism has become increasingly common among waterfowl in the Netherlands since 1970.

Animal Husbandry↗
PubMed1975

Guanidine in type B botulism.

On two occasions, guanidine produced clinical and electrophysiological improvement in a 54-year-old man with botulism, type B. However, guanidine was ineffective for autonomic dysfunction. There were no intolerable side effects. Our experience showed that guanidine is also effective in botulism, type B, as adjunctive therapy.

Botulism↗