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At least 487 records · Page 27Linked to original sources
PubMed1990

Suspected botulism in cattle associated with poultry litter.

Botulism was diagnosed clinically in grazing cattle on three closely sited dairy farms. The evidence suggests that the source of the toxin was poultry carcases containing types C and D Clostridium botulinum. These organism were also found in the alimentary tract of affected animals. Silage is suspected as having acted as a vehicle for the organisms and, or, toxins in cases which occurred later in housed cattle on one of the farms.

Animal Husbandry↗
PubMed1989

[Food-borne botulism and its epidemiological features as seen in our country during the last few years].

We evaluated and presented here, the features of the eleven cases of food-borne botulism who admitted to the Infectious Diseases Department of Ibni Sina Hospital of Ankara University. Three of the cases admitted in 1984 and eight of them admitted in 1987. All of the cases were caused by home-prepared foods which had been eaten without cooking; the types of the food were green beans and pepper with sauce. In these cases the main symptoms and signs were generalized muscular weakness, dry mouth, dysphagia, diplopia, ptosis of the eyelids; besides these the other clinical symptoms and signs were seen in some patients. Although toxin couldn't be detected in the patients' sera by mouse-toxin neutralization, the EMG findings supported our diagnoses. To the three patients in the first group, botulinal anti-toxin was not given and two of them died. Anti-toxin was administered to the seven patients in the second group, none of them died.

Adolescent↗
PubMed1989

[Botulism in infancy].

The authors describe a case of botulism in a 3-month-old infant infected with Clostridium botulinum type A. Symptomatology developed within four days, persisted for two weeks, then regressed. Symptoms were paresis of face muscles, hyporeactive pupils, loss of succion and deglutition, axial hypotonia, weakness of peripheral muscles, lability of the autonomic nervous system with acute episodes of bradycardia and constipation. Anomalies of the electroen-cephalogram and of the auditory evoked responses suggest that the toxin penetrated the central nervous system. Treatment was symptomatic, without need for assisted ventilation. It was not possible to detect the source of infection.

Botulinum Toxins↗
PubMedDate not supplied

[A clinical case of botulism].

A patient with botulism (type E) has been subject to complex therapy, which involved specific serotherapy, infusion therapy, and controlled lung ventilation with the following assisted lung ventilation.

Botulinum Antitoxin↗
PubMed1989

[A patient with botulism caused by Clostridium botulinum type B].

A case of botulism type B acquired in The Netherlands is presented. The diagnosis was made on clinical grounds and positive mouse bio-assay. The patient was a man aged 37 years. Additional evidence was obtained by electromyography, single fibre electromyography and autonomic function tests. Antitoxin was administered without side effects. The clinical outcome was good.

Adult↗
PubMed1986

Electrophysiological evidence of peripheral nerve dysfunction in six dogs with botulism type C.

In six dogs with botulism type C electrophysiological examinations showed: fibrillation potentials and prolonged insertional activity; low amplitude of the evoked muscle action potential; decrease in amplitude of the compound muscle action potential with slow repetitive stimulation; slowing of motor and sensory velocities in the peripheral nerve; and restoration of velocity and amplitude corresponding to clinical improvement. These findings indicate peripheral nerve dysfunction which cannot be explained adequately by current knowledge of the action of botulinum toxin on cholinergic nerve endings. It is therefore suggested that botulinum toxin also interferes with peripheral nerve conduction.

Action Potentials↗
PubMed1977

[Botulism in a number of yearlings (author's transl)].

An outbreak of botulism in four yearlings of a single herd is reported. One animal recovered spontaneously. The other animals underwent euthanasia (animal A) or were slaughtered (animals B and C). Cl. botulinum toxin type C was detected in the sera of animals A and B as well as in the liver and abomasal contents of animal A. In addition, Cl. botulinum was isolated from the liver of animal A. The symptoms are described. Total muscular weakness, also resulting in lingual paralysis and inability to swallow, was the most important clinical feature. The mechanism of action of Cl. botulinum toxin, possible methods of treatment and aspects of meat inspection are discussed.

Abomasum↗
PubMed1986

[First outbreak of botulism caused by Clostridium botulinum subtype Af].

In December 1982 an outbreak of foodborne botulism presumably produced by the ingestion of home-made pickled trout occurred in San Rafael, province of Mendoza, Argentina. The toxin detected in blood serum and feces samples of the sole affected patient was preliminarily typed as a plain type A. A strain of Clostridium botulinum was isolated from feces which, after culture by the dialysis method, produced 1 x 10(7) LD50/mouse per ml. Quantitative neutralization tests carried out at different levels of toxin concentration, showed that this toxin consists of a major type A antigenic component (about 99% of the complex) and a minor type F component, defining its identity as a subtype Af. A rabbit antiserum obtained from this toxin neutralizes A and F reference toxins. Despite the antitoxic and supportive treatment, the patient died as a consequence of the poisoning. The polyvalent antiserum administered contained A, B and E antitoxins. Death could be due to the lethal effect of the A fraction, the F fraction or to a combined effect of both toxic components of the toxin. This is the first detection of an outbreak produced by C. botulinum subtype Af, serotype described in Argentina fifteen years ago, and not detected until now in other parts of the world.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Food-borne botulism. A review of 13 outbreaks.

Thirteen outbreaks of food-borne botulism occurred between 1970 and 1984. Fifty patients were affected, with 30 of them requiring hospitalization. The number of patients per outbreak ranged from one to ten (mean, 3.8). All outbreaks were caused by home-prepared foods: nine by smoked ham, one by bacon, one by sausage, and one by mussels; contaminated food was not found in one outbreak. Bacteriologic study was performed in 11 outbreaks and type B toxin, the only found, was detected in eight of them. Generalized muscular weakness, visual disturbances, extreme dry mouth, and severe constipation were observed in all inpatients. Palpebral ptosis, dysphonia, urinary retention, postural hypotension, and respiratory impairment were also reported, but not in all inpatients. Identical, but less severe, manifestations were registered in the 20 ambulatory patients. Electromyographic study showed decreased motor action potential and posttetanic facilitation. Pulmonary function, studied in four inpatients, was decreased in three. All patients recovered fully. Management consisted of supportive measures, symptomatic treatment, and nursing care. Equine antitoxin was not administered and assisted ventilation was unnecessary.

Adolescent↗
PubMed1987

Botulism as a sequel to open castration in a horse.

Clostridium botulinum and type-B C botulinum toxin were isolated from a necrotic wound that developed subsequent to castration in a 2-year-old Thoroughbred gelding. The horse had clinical signs of botulism and was successfully treated with wound debridement, C botulinum type-B antitoxin, potassium penicillin, and supportive care.

Animals↗
PubMed1985

Botulism in New Zealand.

Two patients with botulism with recovery are described. These are the first reported cases in New Zealand.

Adult↗
PubMed1985

Clinical, laboratory, and environmental features of infant botulism in Southeastern Pennsylvania.

Forty-four cases of botulism occurred in infants in Southeastern Pennsylvania between 1976 and 1983. Forty-three were caused by Clostridium botulinum type B. Progressive weakness necessitated ventilatory support in 39 infants. Complications during hospitalization included otitis media in 13 patients and aspiration pneumonia in 11. Eight infants developed the syndrome of inappropriate secretion of antidiuretic hormone and two developed adult respiratory distress syndrome. One infant died of progressive bradycardia despite adequate control of ventilation. Manifestations of autonomic nervous system dysfunction recognized on admission to the hospital were constipation, distention of the urinary bladder, and decreased salivation and tearing. During hospitalization, some infants had unexpected fluctuations of skin color, blood pressure, and heart rate. Infants' strength improved despite persistent intestinal elaboration of toxin. C botulinum was isolated from seven of nine home or work environments sampled. All 44 infants were white and were receiving breast milk at the time of onset of symptoms. The majority had first feedings of nonhuman food substances within 4 weeks prior to onset of symptoms. Delineation of fecal flora in seven infants revealed predominance of enterobacteriaceae. Perturbations of intestinal flora during infancy, especially at weaning, may cause transient permissiveness to colonization by C botulinum.

Botulinum Toxins↗
PubMed1985

Type A botulism from sauteed onions. Clinical and epidemiologic observations.

Twenty-eight persons were hospitalized in Illinois with neurologic signs and symptoms compatible with botulism in October 1983. Twelve patients required ventilatory support, and 20 patients were treated with trivalent ABE antitoxin; one patient died while still in the hospital six months after onset of illness. Type A toxin and/or type A Clostridium botulinum were subsequently identified in specimens from 18 patients. Case-control studies implicated sauteed onions made from fresh raw onions and served on a patty-melt sandwich in a local restaurant as the vehicle of transmission. Although the original sauteed onions were not available for toxin testing, type A toxin was detected in washings from a wrapper in which a patty-melt sandwich was taken home by one of the ill persons. Also, type A C botulinum was cultured from five of 75 raw onions taken from the restaurant. This outbreak implicated an unusual vehicle for botulinal toxin that was initially not suspected and demonstrates the importance of considering all theoretically possible food items as potential vehicles for toxin until epidemiologic and laboratory data have been collected and analyzed.

Adult↗
PubMed1985

[Description of a case of type E botulism in Italy].

The authors report the first documented italian case of type E botulism. The initial symptoms were typical permitting prompt diagnosis; the symptoms became severe and the patient had to be moved to intensive care. Biological tests on guinea-pigs showed the presence of type E botulin toxin in the tuna (stored in oil) which the patient had eaten 24 hours prior to admission. This tuna had been caught near the mediterranean coast of Spain several months earlier and canned at home. The authors emphasize that, even though this fish was imported, there is a danger that this intoxication could, in the future, be more widely observed.

Adult↗
PubMed1974

Human botulism in Canada (1919-1973).

Since 1919, in Canada, 62 authenticated outbreaks of human botulism have affected 181 persons, with 83 deaths, a fatality rate of 46%. Among these, 41 outbreaks were bacteriologically determined (31 in one laboratory) as six type A, four type B, one both A and B, and 30 type E. About two thirds of the total outbreaks, cases and deaths involved Eskimos and Pacific coast Indians consuming raw marine mammal products and salmon eggs, respectively. Other parts of Canada recorded seven occurrences due to miscellaneous vehicles, three being type B. Since January 1961 there have been 38 outbreaks, involving 94 cases with 33 deaths. These include 18 outbreaks among Eskimos, affecting 51 persons (of whom 24 died) in Labrador, southern Baffin Island, northern Quebec, and the Mackenzie area. Also, putrid salmon eggs caused 15 outbreaks among Pacific coast Indians, totalling 35 cases, of whom only six died, the low fatality rate reflecting the introduction of type E botulinus antitoxin during 1961.

Animals↗
PubMedDate not supplied

[Mechanism of the change in energy and electrolyte metabolism in the respiratory musculature in experimental botulism].

Distinct decrease in concentrations of creatine phosphate and K+ was observed in various respiratory muscles of cat in generalized botulism, accompanied by the syndrom of asphyxia. Content of glycogen and Na+ was unaltered in these cases. In local botulinic paralysis concentrations of creatine phosphate, glycogen and K+ were decreased in the respiratory muscles. Accumulation of Na+ was observed in diaphragm and intercostal muscles. Content of K+ and creatine phosphate was partially restored in respiratory muscles after intraperitoneal administration of guanidine HCl/50 mg/kg of body weight/.

Animals↗
PubMed1978

[Clinical and EMG study of botulism (case report) (author's transl)].

The Authors describe the clinical and electromyographic findings of a case of botulism with complete recovery. Therapy was based on anti-cholynesterasic drugs, on guanidine (at dosage of 30 mg/kg/day) and on antibotulinic serum. The neuromuscular transmission was assessed with the Desmedt's test: during the disease the EMG showed a tipical pattern of facilitation of motor units potentials during stimulation at 30 per second, becoming normal after recovery.

Adult↗