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PubMed1993

[Clinico-epidemiological study of botulism poisoning in La Rioja (1979-1990)].

BACKGROUND: The aim of the present study was to evaluate botulinic poisoning requiring hospital admission in La Rioja (Spain) during one decade from a clinical-epidemiologic point of view. METHODS: Chart records from patients admitted to the departments of Internal Medicine, Neurology, the ICU, and the Neurophysiology and Preventive Medicine files of the reference hospital between 1979 and 1990 were retrospectively reviewed. RESULTS: Fifteen cases were identified. Home preserves of vegetables were most frequently the foods responsible for the poisoning. The presentation as a sole case constituted half of this series. The most frequent symptomatology was neuro-ophthalmologic and digestive. All the cases were type B. Neurophysiologic studies were compatible with the diagnosis in all the cases in which they were performed. Two cases (13.3%) required intensive care and death occurred in one (6.6%). CONCLUSIONS: a) The habit of home preserves was responsible for the presentation of botulism in this environment. b) Early diagnosis was based on complementary clinical tests together with the neurophysiologic study. c) The mild forms were most frequent. Death in this series was 6.6%.

Adolescent↗

PubMed1997

Botulism outbreak associated with poultry litter consumption in three Brazilian cattle herds.

One hundred fifty-five of 201 cattle from 3 different farms showed clinical signs and died of botulism after eating the same batch of poultry litter contaminated with poultry and rodent carcasses. The cattle had access to poultry litter for only 1 d; afterwards it was removed from the diet. Death occurred over a period of 17 d after the poultry litter intake. The peak mortality was on day 4; 20 animals died within 10 d of the ingestion. The greater the intake of poultry litter, the higher the cattle mortality. Three steers which died on the first day had peracute effects while the remaining cattle showed classical signs. Twenty-five of the 46 surviving cattle had mild clinical signs, but recovered in a few days. Type C Clostridium botulinum toxin was found in extracts of the poultry litter, carcasses and cattle intestinal contents. Nutrient composition of the poultry litter was normal but pH was lower (6.9) than usual (7.5 to 9.3).

Animal Feed↗

PubMed1977

[Changes in the electrogenic properties of striated muscle fibers during experimental botulism].

Changes in the electrical parameters of fibers of fast and slow muscles of rats during development of local botulism were studied. At the early stage of intoxication a decrease of the membrane potential of the fast and slow muscle fibers was found. At the stage of intoxication, alongside with an expressed membrane depolarization, there was a change of the input resistance, of the membrane electrical time constant, the threshold currents and the amplitude of action potentials, caused by direct intra-cell stimulation. Changes in the electrical parameters are more expressed in the fibers of the fast muscle.

Animals↗

PubMed1995

The metallo-proteinase activity of tetanus and botulism neurotoxins.

Tetanus and botulinum neurotoxins are produced by several Clostridia and cause the paralytic syndromes of tetanus and botulism by blocking neurotransmitter release at central and peripheral synapses, respectively. They consist of two disulfide-linked polypeptides: H (100 kDa) is responsible for neurospecific binding and cell penetration of L (50 kDa), a zinc-endopeptidase specific for three protein subunits of the neuroexocytosis apparatus. Tetanus neurotoxin and botulinum neurotoxin serotypes B, D, F and G cleave at single sites, which differ for each neurotoxin, VAMP/synaptobrevin, a membrane protein of the synaptic vesicles. Botulinum A and E neurotoxins cleave SNAP-25, a protein of the presynaptic membrane, at two different carboxyl-terminal peptide bonds. Serotype C cleaves specifically syntaxin, another protein of the nerve plasmalemma. The target specificity of these metallo-proteinases relies on a double recognition of their substrates based on interactions with the cleavage site and with a non-contiguous segment that contains a structural motif common to VAMP, SNAP-25 and syntaxin.

Amino Acid Sequence↗

PubMed2002

[Results of using botulism toxin in the treatment of spasmodic dysphonia].

Spasmodic Dysphonia (SD) is a dystonia involving laryngeal musculature thus causing a characteristic voice disorder. Two main types of SD have been described. The adductor type is the commonest and it is characterized by a strain-strangle, choked voice. The abductor type can be distinguished from the previous one by episodes of a blown and whispering voice, interrupting speech. Botulism toxin (BTX) has demonstrated to be the most effective treatment for this condition. Thirty patients diagnosed of SD (twenty-nine adductor type/one abductor type) were included. Their degree of dysphonia was evaluated using both functional and visual-analogue scales. They were treated with BTX vocal cord injections using a percutaneous technique under EMG guidance. Improvements up to a 100% of the normal vocal function were obtained, with an average of 82% in the adductor type. The adverse effects were mild and transient. Hypophonia affected 61.3% of patients lasting an average of 11.3 days. Dysphagia was reported in 44.1% of cases lasting an average of 5.8 days.

Adult↗

PubMed1994

Detection of type A, B, and E botulism neurotoxin genes in Clostridium botulinum and other Clostridium species by PCR: evidence of unexpressed type B toxin genes in type A toxigenic organisms.

We studied the effectiveness of the PCR in detecting the type A, B, and E botulism neurotoxin genes in 209 strains of Clostridium botulinum and 29 strains of other Clostridium spp. All 79 strains that produced type A toxin, 77 strains that produced type B toxin, and 51 organisms that produced type E toxin (46 C. botulinum and 5 C. butyricum) were PCR positive in reactions with primers targeting sequences specific for their respective toxin genes. The PCR for type A toxin was positive for one type B toxin-producing strain that produced a small amount of type A toxin in addition to a large amount of type B toxin. Surprisingly, the type B toxin gene was detected in addition to the type A toxin gene in 43 type A toxin-producing strains, only 1 of which could be shown by bioassay to produce biologically active type B toxin in culture. The type B gene was also detected in two strains of C. subterminale, which were determined to be nontoxigenic by bioassay. While the PCR was sensitive and specific in detecting the neurotoxin genes, the discovery of unexpressed toxin genes indicates that PCR results may not be adequate for establishing type B neurotoxigenicity.

Base Sequence↗

PubMed1996

Tetanus and botulism neurotoxins: a novel group of zinc-endopeptidases.

Tetanus and botulinum neurotoxins are produced by bacteria of the genus Clostridium and cause the paralytic syndromes of tetanus and botulism with a persistent inhibition of neurotransmitter release at central and peripheral synapses, respectively. These neurotoxins consist of two disulfide-linked polypeptides: H (100 kDa) is responsible for neurospecific binding and cell penetration of L(50 kDa), a zinc-endopeptidase specific for three protein subunits of the neuroexocytosis apparatus. Tetanus neurotoxin and botulinum neurotoxins serotypes B, D, F, and G cleave at single sites, which differ for each neurotoxin. VAMP/synaptobrevin, a membrane protein of the synaptic vesicles. Botulinum A and E neurotoxins cleave SNAP-25, a protein of the presynaptic membrane, at two different carboxyl-terminal peptide bonds. Serotype C cleaves specifically syntaxin, another protein of the nerve plasmalemma. The target specificity of these metallo-proteinases relies on a double recognition of their substrates based on interactions with the cleavage site and with a non contiguous segment that contains a structural motif common to VAMP, SNAP-25 and syntaxin.

Amino Acid Sequence↗

PubMed1964