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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↗
PubMed1987

[A case of botulism in a 11-month-old infant].

We report a case of botulism in a 11 month-old infant. Hypotonia complicated by progressive bulbar paralysis revealed the disease. Botulism B toxin was present in serum on the 8th day of the disease. On the occasion of this case report the clinical, diagnostic, epidemiological and pathophysiologic aspects of infant botulism are reviewed. The relationship between sudden infant death and botulism is discussed.

Botulism↗
PubMedDate not supplied

Botulism in China.

During the period 1958-1983, 986 outbreaks of botulism occurred in China, affecting 4,377 individuals and resulting in 548 deaths. The initial cases of botulism were found in Xinjiang province, where the incidence was highest. Outbreaks have occurred in all of the northern provinces and in some of the southern provinces of China. The toxin found most frequently in the northwest region of China was type A; in north China, type B; and in the northeast, type E. The most frequently offending food was home-made strong-smelling preserved bean curd, which was implicated in 74% of the outbreaks. The complex clinical manifestations of botulism can be grouped into those affecting the eyes, the mouth, the pharynx, and the skeletal muscles. Following the institution of effective methods of prevention and treatment, epidemics of botulism in China have been controlled and the mortality rate reduced from 41% (1950s) to 7.6% (1983).

Animals↗
PubMed1973

Botulism--diagnosis, management and public health considerations.

Botulism is an uncommon but often fatal disease associated with ingestion of a potent neurotoxin present in improperly preserved foods. Exposures to commercially preserved foods with an odd or peculiar taste almost never represent exposure to botulism toxin. Improperly prepared home-canned products which are tasted or consumed without heating are more likely to be associated with botulism. The management of suspect and confirmed cases of botulism is presented by medical epidemiologists in the State Department of Public Health, Bureau of Communicable Disease Control, to provide physicians in California with a practical approach to this problem.

Botulism↗
PubMed1983

Early and late pulmonary complications of botulism.

Pulmonary complications of botulism were studied in an outbreak of 34 cases of type A botulism in New Mexico in 1978. Hospital record review, standardized questionnaires, and pulmonary function tests were used to define pulmonary complications during the acute illness and the patient's status one year later. Pulmonary involvement was documented in 81% of patients. Ventilatory failure occurred in 11, aspiration pneumonia in nine, and death in two patients. Difficulties in the diagnosis of ventilatory insufficiency were identified. At one year, most patients had residual symptoms, including easy fatigability in 68% and exertional dyspnea in 46%. However, only minor pulmonary function abnormalities were present. This study confirms the generally favorable prognosis of botulism and provides clinical guidance for the diagnosis and management of pulmonary complications in botulism.

Adolescent↗
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↗
PubMed1994

Wound botulism.

All published cases of wound botulism were reviewed to describe the epidemiology, clinical manifestations, diagnosis, and treatment of this rare infection. The MEDLINE data base of English-language literature was searched from 1966 to 1992, using the keywords "wound botulism". Cases published during this period were identified, and the bibliographies of these articles were used to identify cases published before MEDLINE's search limit of 1966. Because of the limited number of published cases, all were reviewed. Data related to epidemiology, clinical manifestations, diagnosis and treatment were collected on each case. When possible, cross-references from case series or reviews were used to corroborate and supplement data for a given case. There were 40 cases identified as wound botulism. The case fatality rate was 10%. The 36 survivors had significant morbidity requiring prolonged medical care. Wound botulism is a rare life-threatening complication of trauma and i.v. drug abuse. The diagnosis should be considered in any patient with either of these risk factors who develop paresis of cranial nerves and a descending pattern of weakness. Treatment, including administration of antitoxin, should be initiated prior to definitive diagnosis by microbiologic laboratory tests.

Botulism↗
PubMed1998

[Botulism in newborn infants].

Infant botulism, first described in 1976, is the most common form of botulism. The majority of cases are reported from the USA. The disease is rare in Europe, and this article describes the first patient reported in Norway. A three-month-old boy of Norwegian origin who had been fed Argentinian honey developed symptoms of botulism. Electromyography showed presynaptic neuromuscular dysfunction. The diagnosis was confirmed by the demonstration of Clostridium botulinum type A neurotoxin in the faeces. After supportive treatment, breast-milk feeding and lactobacillus supplementation he made a complete recovery. If spores of C. botulinum are ingested, they can bind to the epithelium, germinate and produce toxin which causes botulism. Because of the composition of their intestinal flora, children below one year of age are at risk. Ingestion of honey is a well known risk factor. Contamination of Norwegian honey has never been reported but we recommend that honey should not be given to children during their first year of life.

Botulinum Toxins, Type A↗
PubMed1998

[Wound botulism in heroin addiction].

Botulism is a rare disease which usually is caused by preformed botulinum toxin in food. However, this article describes a case of wound botulism in a 29-year-old male heroin addict who developed progressive diplopia, dysphagia and proximal weakness of skeletal limb muscles. He needed mechanical ventilation for two weeks. The clinical diagnosis of botulism was supported by neurophysiological tests. Assays for detection of botulinum toxin and Clostridium botulinum were negative. The patient had not eaten any contaminated food the last two weeks before symptoms appeared, but he had multiple contaminated skin wounds. After treatment with botulinum antitoxins and antibiotics he gradually recovered, and six weeks later he was discharged from hospital in good condition. To the best of our knowledge this is the first case of wound botulism reported in Norway.

Adult↗
PubMed2003

Botulism.

Botulinum toxin is the most potent toxin known to humans and as little as 100 ng can be lethal. The toxin blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system by introducing an endopeptadase enzyme into the presynaptic side of the synapse. The endopeptadase cleaves acetylcholine vesicle docking proteins that are required for the synapse to release acetylcholine into the synaptic cleft. Botulism occurs from consumption or inhalation of preformed botulinum toxin or growth of Clostridium botulinum bacteria in the infant gastrointestinal tract or within a wound. Growth of C. botulinum in the immature gut or wound will release botulinum toxin that reaches the circulation. All forms of botulism cause progressive weakness, bulbar signs (blurred vision, diplopia, mydriasis, dysphagia, and dysarthria), and respiratory failure with normal sensation and mentation. Treatment is aimed at 1) maintaining respiration via intubation and mechanical ventilation, 2) stopping progression of weakness by administration of botulinum antitoxin (equine trivalent botulinum antitoxin for adults and botulism immune-globulin intravenous-human for infant botulism), and 3) preventing complications from weeks of paralysis with good supportive care. The source of the botulinum toxin should be identified to prevent additional cases. Patients can recover normal muscle strength within weeks to months, but usually complain of fatigue for years.

Journal Article↗
PubMed2006

An outbreak of botulism in Thailand: clinical manifestations and management of severe respiratory failure.

BACKGROUND: Northern Thailand's biggest botulism outbreak to date occurred on 14 March 2006 and affected 209 people. Of these, 42 developed respiratory failure, and 25 of those who developed respiratory failure were referred to 9 high facility hospitals for treatment of severe respiratory failure and autonomic nervous system involvement. Among these patients, we aimed to assess the relationship between the rate of ventilator dependence and the occurrence of treatment by day 4 versus day 6 after exposure to bamboo shoots (the source of the botulism outbreak), as well as the relationship between ventilator dependence and negative inspiratory pressure. METHODS: We reviewed the circumstances and timing of symptoms following exposure. Mobile teams treated patients with botulinum antitoxin on day 4 or day 6 after exposure in Nan Hospital (Nan, Thailand). Eighteen patients (in 7 high facility hospitals) with severe respiratory failure received a low- and high-rate repetitive nerve stimulation test, and negative inspiratory pressure was measured. RESULTS: Within 1-65 h after exposure, 18 of the patients with severe respiratory failure had become ill. The typical clinical sequence was abdominal pain, nausea and/or vomiting, diarrhea, dysphagia and/or dysarthria, ptosis, diplopia, generalized weakness, urinary retention, and respiratory failure. Most patients exhibited fluctuating pulse and blood pressure. Repetitive nerve stimulation test showed no response in the most severe stage. In the moderately severe stage, there was a low-amplitude compound muscle action potential with a low-rate incremented/high-rate decremented response. In the early recovery phase, there was a low-amplitude compound muscle action potential with low- and high-rate incremented response. In the ventilator-weaning stage, there was a normal-amplitude compound muscle action potential. Negative inspiratory pressure variation among 14 patients undergoing weaning from mechanical ventilation was observed. Kaplan-Meier survival analysis identified a shorter period of ventilator dependency among patients receiving botulinum antitoxin on day 4 (P=.02). CONCLUSIONS: Patients receiving botulinum antitoxin on day 4 had decreased ventilator dependency. In addition, for patients with foodborne botulism, an effective referral system and team of specialists are needed.

Botulism↗
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↗
PubMed1999

Stimulation single-fiber EMG in infant botulism.

The principal electrodiagnostic feature of infant botulism, an incremental response on high rates of repetitive nerve stimulation, has variable sensitivity and may not always be useful as a diagnostic test given the vagaries of test timing and severity of illness. We report the use of stimulation single fiber EMG (S-SFEMG) in making this clinical diagnosis. Four infants between 1 and 5 months of age presented with rapidly progressive bulbar and limb weakness, internal and external ophthalmoplegia, areflexia, and compromised ventilation. Incremental response with high-rate repetitive nerve stimulation and a typical clinical course for infant botulism confirmed the diagnosis in all; stool toxin studies were positive for type B botulinum in 2 of the 3 cases in which they were obtained. S-SFEMG was performed by surface stimulation of median and ulnar nerves and recording with a single fiber needle in the thenar, hypothenar, or first dorsal interosseous muscles. A total of eight single fiber recordings were studied at rates of 2, 5, 10, and 20 Hz. All single fibers studies showed an improvement with higher rates of stimulation, beginning at 10 Hz and peaking at 20 Hz. Compared to baseline study at 2 Hz (100%), the mean percent changes in jitter at 5, 10, and 20 Hz were 109, 60, and 47, respectively. This is the first report of the usefulness of S-SFEMG in the diagnosis of infant botulism.

Botulism↗
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↗
PubMed1984

Descending paralysis resulting from occult wound botulism.

A 30-year-old male drug abuser developed ophthalmoplegia, bulbar paralysis, and limb weakness responsive to edrophonium. However, potentiation of a low-amplitude evoked muscle action potential was produced with repetitive nerve stimulation at 10 Hz, and the clinical and electrophysiological data suggested the diagnosis of botulism. The source of botulism type B toxin was a clinically obscure cyst produced by subcutaneous infiltration of cocaine two weeks prior to the onset of symptoms. The patient improved with chronic administration of pyridostigmine bromide and plasmapheresis. Wound botulism may be underdiagnosed because of confusion with inflammatory neuropathy or myasthenia gravis. Neuromuscular transmission studies in patients with acute craniosomatic paralysis can prevent such oversights.

Adult↗
PubMed1990

Relapse of infant botulism.

We report on 3 infants who had relapse of infant botulism after apparent resolution of clinical symptoms. This group represented 5% of the infants with confirmed infant botulism who were treated at our institution since 1976. The exact cause for these relapses was unclear, but three potential mechanisms are examined. There were no historical, clinical, or electrophysiological predictors of relapse. Although at the time of writing recovery from relapse appeared complete, close follow-up of patients recovering from a bout of infant botulism is necessary.

Botulism↗
PubMed1992

Wound botulism: clinical and microbiological findings of an Italian case.

A case of wound botulism in a 41-year old man is reported. The patient had accidently been wounded when he fell on an iron bar. Some days later he developed typical clinical manifestations of botulism. Wound botulism was confirmed by detection and quantification of type B botulinal toxin in the serum. Ventilatory supportive care was necessary and botulinal antitoxin was not given. The patient was hospitalized for 30 days and recovery was complete.

Adult↗