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PubMed1986

Determination of soluble antigens of Clostridium botulinum A by chemiluminescent--immunosorbent assay (CLISA).

The chemiluminescent--immunosorbent assay (CLISA) was adopted for Cl. botulinum A soluble toxic antigens determination. Luminol (ABEI) labelled botulinum antitoxin globulins showed a strongly positive specific immunochemiluminescent reactions with the native botulinum toxin preparations coupled (adsorbed) on polystyrene balls. The sensitivity of the reaction reached 20 DLM/ml (5,000 light impulses per 40 sec) in comparison with 2 X 10(6) DLM (57,000 impulses), control preparations (1,500 impulses) and the background (150-300 impulses). The results give a perspective further investigations with the CLISA for rapid indication of Cl. botulinum toxic antigens.

Antigens, Bacterial↗
PubMed1982

Botulism in an Oregon dairy cow herd.

Of 18 sick cows in a 100-cow dairy herd in Oregon, 14 died despite treatment. The cows were being fed high-moisture whole corn and alfalfa and rye haylage from pit silos. Signs of illness were anorexia, severe depression, and reduced milk production. Necropsy revealed only hyperemia of the abomasal mucosa and dilated, gas filled large intestine. On the basis of response to treatment, laboratory findings, necropsy findings, and herd history, a tentative diagnosis of botulism was made. This diagnosis was confirmed by results of mouse inoculation tests. Injections of extract from the corn killed mice that were not protected by botulinum antitoxin.

Animal Feed↗
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↗
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↗
PubMed1995

[Epidemic of type B botulism: Sion, December 1993-January 1994].

12 cases of food-borne botulism were registered in Sion, Switzerland, between 31 December, 1993 and 12 January, 1994. A type B toxin was isolated from the serum of one patient and from the incriminated ham. Clinical data of 10 male patients aged 21 to 54 years and some epidemiologic data are reported. The clinical course was mild to moderate with predominant autonomic and gastro-intestinal symptoms and signs: blurred vision (10 patients of 10), dry mouth with dysphagia (9/10), asthenia (7/10), diarrhea and/or constipation (7/10), nausea and vomiting (6/10), abdominal cramps (5/10), impaired sexual function (5/10), dilated pupils (4/10). Some discomfort (mainly blurred vision, asthenia and impaired sexual function) persisted for several months in most patients. Neuromuscular involvement was never the reason for seeking medical assistance and had often disappeared at the time of the first visit. Two patients were hospitalized, one for transient ileus of unknown origin and the second (first suspected case) for monitoring and infusion of trivalent equine botulinum antitoxin. This treatment was administered on day eight after intoxication and had no effect on this patient's outcome when compared with others. No patient died. Epidemiology, diagnosis, treatment and prognosis of botulism are discussed.

Adult↗
PubMed1989

Complete bilateral internal ophthalmoplegia as sole clinical sign of botulism: confirmation of diagnosis by single fibre electromyography.

A case of complete bilateral internal ophthalmoplegia as the sole clinical sign of botulism is reported. Diagnosis was immediately confirmed by single-fibre electromyography (SFEMG), which revealed abnormally high blocking (14.3%), contrasting with moderately increased jitter (mean consecutive difference in the extensor digitorum communis muscle, 43.9 microseconds). After giving equine botulinum antitoxin and simultaneous forced emptying of the bowels, ocular symptoms completely disappeared within 2 days. Six days, 5 weeks and 6 months after the first SFEMG study, the jitter was still abnormal, even becoming more so with time. Blocking, however, was only rarely observed in the follow-up studies. It is concluded that SFEMG may serve as a useful and sensitive method for the rapid diagnosis of botulinum intoxication, even in cases where no clinical signs of general muscular weakness are apparent.

Adult↗
PubMed1998

Transient tonic pupils in botulism type B.

We report a 29-year-old woman who developed unilateral unreactive mydriasis and cycloplegia after 5 days of persistent constipation. During the next hours the patient complained of dry mouth and difficulties in swallowing food; iris and ciliary muscle palsies spread over the second eye. Ocular motility was normal and there were no clinical signs of neuromuscular involvement. Conventional electromyography and evoked muscle action potentials following repetitive nerve stimulation were normal; single-fiber electromyography showed normal jitter and absence of blocking. The diagnosis of botulism was considered as most likely, and the patient was given botulinum antitoxin. The post-treatment course was characterized by bilateral tonic pupillary reaction to near, sectoral iris contractions to light and pupillary constriction to 2 mm in 40 min following topical instillation of 0.1% pilocarpine. Ocular manifestations completely disappeared within 5 weeks. Botulism type B toxin was demonstrated in the pretreatment stool of the patient but not the serum.

Adult↗
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↗
PubMed2001

Foodborne Illnesses.

Foodborne illnesses cause a substantial human and financial burden. Despite sanitary infrastructure improvements, the incidence of foodborne bacterial infections due to non-typhoidal salmonellae (NTS), Campylobacter jejuni, and enterohemorrhagic Escherichia coli (EHEC) has risen over the last two decades. Overall, viruses account for two thirds of all foodborne illness. Most foodborne illnesses are self-limited. Supportive therapy with rehydration and the correction of electrolyte abnormalities is usually sufficient. Antibiotics play a beneficial role in the treatment of patients with certain foodborne diseases, such as listeriosis and typhoid fever, and all patients with tissue invasive or bloodstream infections. Immunocompromised patients should be treated presumptively. Antibiotics are of variable efficacy for the treatment of many infections limited to the gastrointestinal tract, and recommendations differ between pathogens. Antibiotics are generally helpful for shigellosis and cholera, and possibly beneficial for campylobacteriosis. However, antibiotics are potentially harmful in uncomplicated NTS and EHEC gastroenteritis and generally should not be used. Toxin-mediated food poisoning usually does not require specific therapy. The exception is botulism, for which botulinum antitoxin is highly efficacious if used early in the course of illness. Empiric therapy for gastroenteritis is possibly beneficial, though the magnitude of benefit is modest and incurs the risk of inadvertently treating NTS or EHEC. The choice of antibiotic should be based on local resistance patterns and the results of susceptibility testing.

Journal Article↗
PubMed1982

Botulinum toxin type A: kinetics of calcium dependent paralysis of the neuromuscular junction and antagonism by drugs and animal toxins.

The effect of botulinum Toxin (BoTx), which blocks the mechanism of release of acetylcholine at neuromuscular junctions and induces paralysis of muscles stimulated by nerves, is known to be Ca2+-dependent. Amplitude of muscular contractions evoked by nerve impulse was studied in BoTx poisoned preparations. The present report notes that an increase in Ca2+ concentration in vitro delays paralysis of muscular contractions of the frog evoked by nerve impulse. The restorative effect of different drugs on this paralysis has been tested: 4-aminopyridine, ATXII (toxin isolated and purified from the sea anemone Anemonia sulcata tentacles) and a crude venom isolated from the scorpion Androctonus australis antagonize the BotX induced paralysis at physiological concentrations of Ca2+ (Cao2+ = 2 mM), whereas the restorative effect observed with tetra-ethylammonium or guanidine occurs at higher concentrations of Ca2+ (Cao2+ = 4 mM), as in mammals. ATXII restores in vivo the activity of a BoTx paralysed muscle of guinea pig and this effect is more efficient if the interval between the injection of BoTx and ATXII is shortened. These results on the frog and guinea pig are in agreement with those obtained on other biological preparations by several investigators. Moreover it is suggested that the antagonism of BoTx induced paralysis is a consequence of the increase in Ca2+ at the nerve ending. The efficiency of 4-aminopyridine and animal toxins is explained by an action on the nerve ending, by increasing Ca2+ from an interval compartment of the cell, whereas antagonism produced by guanidine and tetraethylammonium involves uptake of Ca2+ from the external medium. The bathing medium must be at a higher concentration of Ca2+ than usual. This explains the differences in antagonism obtained by these drugs and toxins in vitro and in vivo.

Animals↗
PubMed1980

Interaction between Clostridium botulinum neurotoxin and gangliosides.

The effect of gangliosides on Clostridium botulinum type A neurotoxin was examined in terms of detoxification. The molar concentrations of gangliosides necessary to detoxify 50% of 1 M Cl. botulinum neurotoxin were as follows: GM1, 2073; GM2, 2439; GM3, 6098; GD1a, 610; GD1b, 488; GT1a, 829; GT1b, 6 and GQ1b, 27. Inhibition by gangliosides of the neurotoxin binding to synaptosomes showed that GT1b was highly effective, but the others were not. Low-temperature treatment inhibited the detoxification of neurotoxin by GT1b and the binding of 125I-labelled neurotoxin to the synaptosome fraction. 125I-labelled neurotoxin was mixed with GM1 or GT1b and their molecular size was estimated by sucrose-density-gradient centrifugation. When 125I-labelled neurotoxin was incubated with GM1, a single radioactive peak having a sedimentation coefficient of 7.3 S appeared. When incubated with GT1b, however, 125I-labelled neurotoxin gave three peaks having sedimentation coefficients 14, 10 and 7.3 S, respectively. The present results indicated that the location and the number of sialic acids in ganglioside molecules are of significance in the detoxification and the binding of Cl. botulinum neurotoxin with ganglioside molecules.

Animals↗
PubMed2005

Submolecular recognition profiles in two mouse strains of non-protective and protective antibodies against botulinum neurotoxin A.

We have used a set of synthetic overlapping peptides encompassing the entire heavy (H) chain of botulinum neurotoxin serotype A (BoNT/A) to map, in two mouse strains (BALB/c, H2d, and SJL, H2S), the regions on the H-chain recognized by Abs in the last bleed of non-protective anti-BoNT/A antisera and in the bleed of protective antisera immediately following it in the bleeding schedule. Although the protective antisera bound slightly higher amounts of total (IgG+IgM) Abs, non-protective and protective BALB/c antisera showed similar peptide-binding profiles involving peptides N6/N7, N25, C2/C3, C9/C10/C11, C15, C18, C24, C30, and C31 and, at lower amounts of bound Abs, peptides N19, C6/C7, and C28. IgG+IgM antibodies of the protective SJL antisera recognized peptides N5, N22, and C21, and these peptides were only slightly recognized (N22, C21) or unrecognized (N5) by the non-protective antisera. Additionally, peptides N7/N8, N25, C11, C15, and less so N27/N28 bound two-fold or more Abs from the SJL protective antisera than the non-protective antisera. The Abs bound to peptides C4 and C29 were of relatively lower affinity. Peptides C2/C3, C7, C18/C19, C24, C30, and C31 bound higher amounts of Abs in the SJL protective versus the non-protective antisera, but the differences were less than double. We also mapped the binding profiles of the IgG Abs in these sera. BALB/c and SJL had 13-36-fold higher of IgG Abs that bound to BoNT/A in the protective antisera relative to non-protective antisera. The IgG Abs in the protective antisera of each mouse haplotype bound to the same peptides that bound total Abs in the correlate antiserum. But in both mouse strains, the non-protective Abs showed little or no IgG Abs that bound to these peptides. In the SJL haplotype, the IgG response to peptide N5 was transient, appearing strongly in early protective Abs and disappearing by day 70. It is not clear whether the response to region N5 plays a role in initiating and contributing to the protective activity of the toxin in the SJL strain in the early stages but is not needed in later hyperimmune stages of the Ab response. It is concluded that the switch in BALB/c and SJL mice from non-protective to protective Abs is not associated with major changes in the epitope-recognition profiles. Although some slight differences between non-protective and protective antisera appeared in their levels of Abs that were bound by some peptides, these differences are not sufficient to explain differences in the protection properties. Protection was mostly associated with the immunoglobulin class of the antibodies. IgM antibodies were non-protective, while IgG Abs produced after the switch were protective.

Amino Acid Sequence↗
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↗