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At least 343 records · Page 19Linked to original sources
PubMed1990

Outbreak of type A botulism caused by a commercial food product in Taiwan: clinical and epidemiological investigations.

In late September 1986, we found 7 patients from a printing factory in Chang-Hwa city who developed an endemic disease manifested by general malaise, ptosis, double vision, dysarthria, dysphagia, and proximal limb weakness. After clinical, epidemiological, microbiological, and toxicological investigations, an outbreak of botulism was confirmed 2 weeks later, Commercially canned peanuts made by an unlicensed cannery were identified as the vehicle of botulinum toxin transmission. Antitoxin was given to 2 patients who needed ventilator support. One of the 7 victims died from medical complications and the remaining 6 patients recovered. Several administrative problems exposed in this outbreak were the poor governmental supervision of canned food, the inadequate quantities of "orphan drugs" stored in this country, the inefficient system for recalling the problem products, and the delayed broadcasting of warnings to the public. Since commercially processed food is increasingly popular with modernization, the possibility of future botulism outbreaks should not be overlooked.

Adolescent↗
PubMed1989

[Comparative analysis of disorders of neuromuscular conduction in patients with botulism and Eaton-Lambert myasthenic syndrome].

The analysis of conduction at neuromuscular junctions was performed in 25 patients with botulism and 31 patients with Lambert-Iton syndrome. These groups showed apparent differences in mechanisms of recruitment and posttetanic facilitation of the neurotransmitter release. Prolonged stimulation with the rate of 6 imp/s in ischemic muscles pointed to essential differences in the mechanisms facilitating the transmitter release. These differences of neuromuscular conduction disorders in botulism and Lambert-Iton syndrome are supposedly connected with affliction of different mechanisms of conduction facilitation in the neuromuscular synapses.

Botulism↗
PubMed1985

Food-borne botulism in Canada, 1971-84.

Sixty-one outbreaks of food-borne botulism involving a total of 122 cases, of which 21 were fatal, were recorded from 1971 to 1984 in Canada. Most occurred in northern Quebec, the Northwest Territories or British Columbia. Of the 122 victims 113 were native people, mostly Inuit. Most of the outbreaks (59%) were caused by raw, parboiled or "fermented" meats from marine mammals; fermented salmon eggs or fish accounted for 23% of the outbreaks. Three outbreaks were attributed to home-preserved foods, and one outbreak was attributed to a commercial product. The causative Clostridium botulinum type was determined in 58 of the outbreaks: the predominant type was E (in 52 outbreaks), followed by B (in 4) and A (in 2). Renewed educational efforts combined with a comprehensive immunization program would significantly improve the control of botulism in high-risk populations.

Animals↗
PubMed1977

Type A and type B botulism in the North: first reported cases due to toxin other than type E in Alaskan Inuit.

Botulism outbreaks shown to be due to type A and type B toxin occurred in Alaska, a region previously known for only type E botulism. The outbreak due to type A toxin involved three people, two of whom died. The outbreak due to type B toxin involved nine people, none of whom died. Both outbreaks were in Inuit villages, and native foods were incriminated. The occurrence of these outbreaks strongly suggests that Clostridium botulinum, types A and B are indigenous to Alaska. The outbreaks underscore the need for initial treatment of patients with antitoxin that is trivalent (ABE), even in Arctic regions.

Adolescent↗
PubMed1986

[Botulism].

In view of large-scale outbreaks of botulism among waterfowl and farm animals in the Netherlands, studies were done designed to estimate the risks incurred by man. The presence of C. botulinum in the environment as well as contamination cycles and the potential for multiplication were studied. Raw materials used in the production of food were frequently found to be contaminated with types of C. botulinum pathogenic for man. The growth of C. botulinum in foods and meat preservatives other than nitrite were examined. To reduce the use of laboratory animals in research on botulism, immunological methods to detect botulinum toxins were developed.

Animals↗
PubMed1979

Ocular findings in botulism type B.

In April 1977, fifty-nine persons became ill with type B botulism in a large, common-source outbreak. A combination of signs and symptoms that should make the clinician strongly suspect botulism was derived from the histories and ocular findings of these persons. Certain signs of third cranial nerve dysfunction reliably predicted in which patients ventilatory insufficiency would develop.

Botulism↗
PubMed1986

[Type-C botulism in dogs].

Twelve dogs died from an outbreak of type-C botulism. The origin of the outbreak was found to consist in feeding the dogs broiler carcasses contaminated with Clostridium botulinum type-C. High concentrations of toxin type-C could be detected in the stomach contents. Botulism in dogs was only fatal when large amounts of toxin had been produced.

Animal Feed↗
PubMed1985

Botulism among penned pheasants and protection by vaccination with C1 toxoid.

Fifty to 100 per cent of about 8000 penned pheasants raised on a farm in Hiroshima Prefecture died annually for three years. Deaths were ascribed to type C botulism. Vaccination of four groups of pheasants with partially purified C1 toxoid effectively protected them against type C botulism. The protective efficacy of the toxoid was emphasised by the relatively high susceptibility of the pheasant to C1 toxin.

Animals↗
PubMed1985

Botulism intoxication after surgery in the gut.

Botulism intoxication is described in a 45-year-old woman who was hospitalized with symptoms suggesting an intestinal obstruction. At intervention a 20-cm length of necrotic small intestine was excised and prophylactic antibiotics were given. Five days after surgery--during which time the patient was fed only parenterally--dryness of the mouth, difficulty in swallowing, general weakness, and difficulty with speech and in keeping her eyes open were noted. The patient was alert and well oriented. The clinical symptoms and the electrophysiological studies suggested the diagnosis of botulism. A serum sample caused death in mice upon inoculation and two samples of feces were positive for the presence of Clostridium botulinum organisms. Supportive treatment with botulinum antitoxin was given and the patient was discharged in good condition.

Anti-Bacterial Agents↗
PubMed1979

[First case of type D botulism in cattle in the Netherlands (author's transl)].

Report on an outbreak of botulism in six cows, in which Cl. botulinum toxin type D was found to be the cause for the first time in the Netherlands. Epidemiological studies showed that this outbreak of type D botulism was due to the fact that the litter used in the cubicles of the cows had been taken from a poultry farm in which cadavers of chicken were present, which contained up to 2 x 10(5) LD100 of Cl botulinum toxin type D per gram.

Animals↗
PubMed1977

Type B botulism outbreak caused by a commercial food product. West Virginia and Pennsylvania, 1973.

In the week of May 7, 1973, seven persons contracted botulism after eating together. The most common symptoms were vomiting, constipation, dry mouth, dysphagia, and dysphonia. All were treated with trivalent botulinal antitoxin, and none died. Serum specimens obtained from all seven patients were negative for botulinal toxin, but stool specimens from three patients were positive for type B toxin. Electromyographic studies performed on five patients documented the neurophysiologic abnormalities of botulism. Commercially canned peppers in oil were implicated epidemiologically, and type B toxin was identified in leftover peppers. The processor voluntarily recalled the pepper product, and no further cases were reported.

Botulinum Antitoxin↗
PubMed1982

Outbreaks of type C botulism in waterfowl in Japan.

Four outbreaks of botulism in waterfowl were encountered over a five-year period of 1973 to 1977 in Japan. In all the outbreaks toxin was detected from all 12 sera, twenty-three of 24 gizzard contents from diseased or dead birds and one of three maggots. It was neutralized with Clostridium botulinum type C antitoxin serum, regardless of its origin. By using CO2 gas jet method, C. botulinum was isolated from four of 11 gizzards from diseased birds, five of 7 ones from dead birds, one of one maggot and one of one sludge sample, that is, eleven of 20 specimens in total. All 20 strains were identical with C. botulinum type C in biological properties. Most of the isolates showed a toxin titer ranging from 1,000 to 200,000 LD50 for mice. Four of them were identified as type C by mouse neutralization tests with antitoxin sera. The toxic suspensions of a strain 1-15 were administered orally to Chinese spot-billed ducks, which died when more than 200,000 LD50 mouse toxin was administered. Environmental conditions for occurrences of waterfowl botulism were discussed.

Animals↗
PubMed1982

Infant botulism--the first five years.

In 1976 physicians in California reported the presence of botulism in infancy. Over a period of a few days infants developed generalized weakness and lost autonomic functions. The severity of infant botulism has varied from feeding difficulties to paralysis. No toxin was found in the infants' food, but it was detected in the stool along with C. botulinum spores and organism. This suggested that infants consumed the spores, which germinated into organisms, which produced the toxin.

Animals↗
PubMed1978

[Type B botulism in cattle, caused by feeding grass silage. Report of a case (author's transl)].

An outbreak of type B botulism in cattle, caused by feeding grass silage, is reported. The clinical features were completely identical with those in cases of type B botulism, which occurred when abnormal brewers' grains were fed. 36.5 mouse LD50 type B toxin was found to be present in each gramme of grass silage, the bacterial count being 10(4) Cl. botulinum type B per gramme.

Animal Feed↗
PubMed1980

Toxicoinfectious botulism in foals and adult horses.

Toxicoinfectious botulism was proved to be the cause of a neuromuscular paralytic syndrome in foals and adult horses. In eight successive cases, Clostridium botulinum type B was isolated at necropsy. Foals were either found dead without premonitory signs of illness or, most often, they had signs of progressive and symmetric motor paralysis. Stilted gait, muscular tremors, and the inability to stand longer than 4 to 5 minutes were the salient clinical signs. Other clinical manifestations included dysphagia, constipation, mydriasis, and frequent urination. As the disease progressed, dyspnea with extension of the head and neck, tachycardia, and respiratory arrest occurred. Death occurred most often 24 to 72 hours after the onset of clinical signs. The most consistent postmortem findings were congestion and edema of the lungs and excessive pericardial fluid, which contained free-floating strands of fibrin. Gastric ulcers, foci of necrosis in the liver, abscesses in the navel and lungs, and wounds of the skin and muscle were predisposing sites for development of toxicoinfectious botulism.

Animals↗
PubMed1980

Botulism: a case report.

The 4th case of botulism in South Africa is reported. Unusual features are the detection of toxin in the patient's serum 7 weeks after the onset of the illness and the need for 14 weeks' intermittent positive pressure ventilation. Symptomatic treatment and meticulous nursing resulted in complete recovery. The microbiology, pathophysiology, clinical features, diagnosis and management of botulism are briefly reviewed.

Adult↗
PubMed1978

Botulism and guanidine. Ten years later.

Guanidine hydrochloride was introduced as an adjunct in the treatment of botulism in 1968. It has been reported to be of benefit in 39 cases and of no benefit in 13 cases. No serious side effects have occurred with the short-term therapy required in botulism. Our two cases are similar to earlier cases in that the improvement seen with quanidine therapy is most notable in ocular muscles and least notable in respiratory muscles. Electrophysiological findings again showed an increase in the amplitude of evoked muscle-action potentials after guanidine administration.

Adolescent↗