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At least 19 recordsLinked to original sources
PubMed1990

Titration of botulinum antitoxin of low levels by the score method.

Botulinum antitoxin is commonly titrated by injecting a mixture of toxin and antitoxin into mice and by utilizing deaths as a marker to measure the amount of unneutralized toxin. We attempted to titrate antitoxin by converting the severity of symptoms (notably palsy) and time-to-death in days into scores. In neutralization tests with toxin levels at 5.9 LD50 and 23.5 LD50, a linear relationship was obtained for antitoxin dose in a range between 0.03 to 0.003 IU/ml. Statistical analysis showed that homogeneity of variance or slope was not denied for the scores obtained on any day from the first to the fourth days after injection, demonstrating that this method can titrate accurately antitoxin of such a low level as 0.003 IU/ml within 4 days after injection.

Animals↗
PubMed1976

Botulinum antitoxins and antibacterial IgM and IgG antibodies in sera of persons immunized with botulinum polytoxoid combined with cholera vaccine. II. Response to cholera vaccine.

The response of humans to cholera vaccine was very heterogeneous. The proportion of IgG vibriocidal antibodies was high in persons having previous natural or artificial contact with V. cholerae antigens. Predominance of IgM antibody response was seen in persons vaccinated for the first time. This type of response was sometimes evoked by unspecific stimuli such as botulinum polytoxoid without cholera vaccine. Antibodies passively protecting mice were found both in IgM and IgG globulins but the activity of these antibodies was higher in IgG than in IgM globulins.

Adult↗
PubMed1976

Botulinum antitoxins and antibacterial IgM and IgG antibodies in sera of persons immunized with botulinum polytoxoid combined with cholera vaccine. I. Response to botulinum toxoid.

Two groups of subjects were immunized with combined vaccine containing aluminum hydroxide-adsorbed botulinum toxoids, types A, B, and E, and 4 mld of formaldehyde-inactivated V. cholerae Inaba and Ogawa organisms. The first group included laboratory workers who were previously immunized against cholera and had professional contact with botulinum toxins and viable V. cholerae organisms. The second group included young men who were never vaccinated against botulism or cholera. The three-dose immunization schedule with combined vaccine resulted in clear-cut antitoxin response; after the third dose, the A, B, and E antitoxin level ranged from 0-2 to 10 IU/ml. Immunity against botulinum toxins lasted at least one year. Distribution of the antitoxins among IgM and IgG globulin classes resembled that in the case of response to other toxoids; 21 days after the third immunization antitoxin activity was found in IgG globulins.

Adult↗
PubMed1975

Preparation, measurement and possible use of human antitoxin against Cl. botulinum A, B, and E toxins.

Human antibodies against botulinum toxins A, B, and E have been raised by repeated injections of pentavalent toxoid in a healthy volunteer. The final titer was 3.2 U anti-A, 0.4 U anti-B, and 2.5 U anti-E/ml. In mice, the efficacy of the antitoxin decreases with the time between poisoning and application of the antiserum. The dose recommended for prophylactic purposes in man is 1 ml/kg. In overt poisoning, therapy should be started with higher titer animal serum since in animal experiments high titer sera can stop (although not reverse) the symptoms of overt botulism within an-admittedly not too broad-rnage of time and dosage. Later on, therapy can be continued with human antiserum. An inverse radioimmunassay for botulinum A antitoxin using labeled botulinum toxin and antibody-coated tubes is described. The serum is available upon request from the author.

Animals↗
PubMed1978

[1st stage of infectious allergy].

In administration of bacterial exotoxins (diphtheria, botulinic) to guinea pigs in doses of 1/100 Dlm at an interval of one hour there developed a typical sickness with the lethal outcome in the course of 2-3 days from the beginning of the exotoxin administration. Low bacterial exotoxin doses induced allergic reaction of the organism before the cell producing specific antibodies began to act in defence. Lymphatic system cells responded rapidly to the low doses of bacterial exotoxins, but the process of formation of cells producing antibodies failed to reach mature plasmocytes, and no antibodies formed. With increase of the interval between the administration of low bacterial exotoxin doses to 24 hours specific antibodies did form, but these antibodies failed to protect the animals which were in the state of infectious allergy. The first stage of infectious allergy induced by low bacterial doses was nonspecific. Animals which were in the state of infectious allergy to diphtheria exotoxin perished of low botulinic (exotoxin) doses, and vice versa.

Antibodies, Bacterial↗
PubMed1991

Lectins from Triticum vulgaris and Limax flavus are universal antagonists of botulinum neurotoxin and tetanus toxin.

Lectins from Anguilla anguilla, Artocarpus integrifolia, Canavalia ensiformis, Datora stramonium, Glycine max, Limax flavus, Ricinus communis and Triticum vulgaris were tested for their abilities to antagonize the binding of botulinum neurotoxin and tetanus toxin to rat brain membranes and to antagonize the ability of these toxins to block neuromuscular transmission in mouse phrenic nerve-hemidiaphragm preparations. Lectins from Limax flavus and Triticum vulgaris, both of which have affinity for sialic acid, were antagonists of the various serotypes of botulinum neurotoxin and tetanus toxin. When tested against the high affinity binding site for botulinum neurotoxin type B, the lectin from Limax flavus had a Ki of 3.1 x 10(-7) M and the lectin from Triticum vulgaris had a Ki of 3.75 x 10(-7) M. When tested against the high affinity binding site for tetanus toxin, the lectins from Limax flavus and Triticum vulgaris had Ki values of 1.5 x 10(-7) and 1 x 10(-6) M, respectively. In all cases the lectins behaved as competitive antagonists. In reverse experiments, neither botulinum toxin nor tetanus toxin was a very effective antagonist of lectin binding to brain membranes. Studies on isolated neuromuscular preparations showed that the lectin from Triticum vulgaris did not affect transmission at concentrations of 10(-6) to 10(-3) M, but at a concentration of 3 x 10(-5) M the lectin produced highly statistically significant antagonism of the neuromuscular blocking properties of botulinum neurotoxin types A, B, C, D, E and F as well as tetanus toxin. The lectin did not antagonize beta-bungarotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Infant botulism.

Infant botulism is a unique neuromuscular disease affecting infants less than six months old. It is the result of intraintestinal toxin production by C. botulinum (toxi-infection). Characteristic symptoms include constipation, lethargy, and decreased feeding. Physical examination often reveals generalized hypotonia with cranial nerve impairment. Recovery is dependent on supportive care in an intensive care setting. The relationship of this disease to the sudden infant death syndrome requires further study.

Botulinum Antitoxin↗
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↗
PubMed1991

Infant botulism with Down syndrome.

A 4-month-old boy with Down syndrome and infant botulism is reported. He was admitted to our hospital with stridor and developed respiratory failure and generalized paralysis. Laboratory examination revealed botulinal toxin type A in his blood and feces. Clostridium botulinum organisms were found in the feces and in the honey which he had been fed. Anti-botulinal toxin was administered on the 10th day of illness. Artificial ventilation was given for 87 days and he survived. This is the 11th known case of infant botulism in Japan. It is possible that other cases remain undiagnosed.

Botulinum Antitoxin↗
PubMed1977

Cultural and physiological characteristics of Clostridium botulinum type G and the susceptibility of certain animals to its toxin.

Strain 89 of Clostridium botulinum type G, isolated by Gimenez and Ciccarelli in 1969, was characterized culturally, biochemically, and toxigenically. It was motile, hemolytic asaccharolytic, weakly proteolytic, lipase and lecithinase negative, and it produced acetic, isobutyric, butyric, and isovaleric acids in peptone-yeast extract-glucose broth. No spores were seen in smears from solid or liquid media. Very low levels of toxin were produced in regular broth cultures, but dialysis cultures yielded 30,000 mouse 50% mean lethal doses (LD50 per kg, orally and subcutaneously, respectively; and for guinea pigs, 10,000 to 20,000 and 100 mouse LD50 per kig, intragastrically and intraperitoneally, respectively.

Animals↗
PubMed1976

Phage conversion to hemagglutinin production in Clostridium botulinum types C and D.

Five toxigenic strains of Clostridium botulinum types C and D were incubated at 37 degrees C for 7 days in 15 ml of the following media: LYG medium, cooked-meat medium, egg meat medium, and N-Z-amine medium. The supernatants of these cultures were tested for hemagglutinin production with 1% erythrocytes obtained from mice, guinea pigs, chickens, sheep, monkeys, and humans. Four toxigenic strains produced hemagglutinin. The highest hemagglutinin titer was obtained with a combination of human erythrocytes and cultures incubated in LYG medium. When the same experiment was carried out with many nontoxigenic strains, hemagglutination was observed in only one strain, C-N71. Strains producing hemagglutinin also produced phages. The phages obtained from toxin- and hemagglutinin-producing strains converted nontoxigenic indicator strains to produce both toxin and hemagglutinin. The phage obtained from a toxin-positive hemagglutinin-negative strain could only induce cultures to produce toxin, and the phage from a toxin-negative hemagglutinin-positive strain could only induce production of hemagglutinin. These studies suggest that the production of hemagglutinin by C. botulinum types C and D is governed by bacteriophages and that hemagglutinin production can be transmitted separately or concomitantly with toxin production.

Bacteriophages↗
PubMed1975

On the question of permeability of the blood-brain barrier to botulinum toxin.

The clinical symptoms of botulinum intoxication suggest that besides the involvement of the peripheral nervous system, the central nervous system is also affected. Studies were undertaken to determine whether pure toxin of Clostridium botulinum type A could be demonstrated in the brains of poisoned mice. With the aid of autoradiography of the toxin marked with 125-I and indirect fluorescent labeling it was possible to show the presence of the toxin in the parenchyma of the brain.

Animals↗