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At least 235 records · Page 13Linked to original sources
PubMed1988

AAEE case report #16: Botulism.

Botulinal toxin causes a marked reduction in the number of quanta released by autonomic and motor nerve terminals. As a result it causes blurred vision, inability to move the eyes, weakness of other cranial nerve-innervated muscles, dyspnea progressing to apnea, and generalized weakness. Electrodiagnostic findings in severe botulism can be relatively nonspecific, with low amplitude and short duration motor unit action potentials and small M wave amplitudes. A modest increment in M wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction. Identification of the toxin in the patient's serum is diagnostic. The treatment of botulism is mainly supportive.

Adolescent↗
PubMed1993

A case of infant botulism associated with honey feeding in Italy.

A case of infant botulism in a 9 week-old female is described. A strain of C. botulinum type B was isolated from the feces of the baby. The epidemiologic study detected in a sample of home canned honey Clostridium botulinum spores of the same serotype that was isolated from the patient. The honey had been used only to sweeten the pacifier of the baby. This is the first case of infant botulism in Europe linked conclusively to honey.

Botulism↗
PubMed1986

Single fiber EMG and cardiovascular reflexes in botulism: a follow-up study.

A patient with botulism was studied at different times after intoxication using various autonomic tests of the cardiovascular reflexes, and by single fiber EMG (SFEMG). The control of heart rate and blood pressure appeared markedly impaired in the early stage of the disease as well as SFEMG. Autonomic function recovered more slowly as neuromuscular transmission. Monitoring autonomic derangement in botulism may give the opportunity to select patients at risk for cardiac or respiratory arrest.

Autonomic Nervous System↗
PubMed2000

Electrophysiological studies of a child with presumed botulism.

Electrophysiological studies of a child with presumed botulism showed that the amplitude of the serially and electrically elicited blink reflexes Rl, R2 and R2' was reduced during recovery. These findings suggest a conduction block of the facial nerves. Other nerve conduction studies and an incremental response to repetitive stimulation demonstrated a block of the presynaptic neuromuscular transmission. Results of the biological tests were negative, but those of electrodiagnosis and clinical examination favored a diagnosis of botulism. A combination of electrically elicited blink reflexes and rapid repetitive stimulation of the peripheral nerves was found to be a sensitive method of assessing the integrity of neuromuscular junctions and the subclinical impairment of muscle nerves.

Blinking↗
PubMed2006

A case of recurrent Miller Fisher syndrome mimicking botulism.

Miller Fisher syndrome (MFS) is a rare and usually monophasic polyradiculoneuropathy characterised by ophthalmoplegia, decreased or absent tendon reflexes, and ataxia. The objective of this study was to report a case of recurrent MFS with a clinical presentation virtually indistinguishable from botulism. The patient was a young man with two episodes of increasing external ophthalmoplegia, ptosis, and ataxia with a long asymptomatic interval in between. The second episode occurred after consumption of rotten fish and was accompanied by gastrointestinal symptoms and an anticholinergic syndrome. Very rarely, MFS can present with a recurrent course. The importance of this case of recurrent MFS lies not only in its long asymptomatic period and identical clinical presentation, but also in its instructiveness regarding the differential diagnosis of MFS, particularly life-threatening botulism.

Acute Disease↗
PubMed1983

Human botulism (type F)--a rare type.

An unusual presentation of type F botulism (one of the world's three reported outbreaks) is described. The diagnosis was complicated by the presence of pre-existing Adie's myotonic pupil. There was also a history of self-inflicted small-caliber gunshot wound to the right brain 10 years before the onset of the botulism. Post-traumatic seizure disorder, also present in this patient, was under good control. No offending food was ever discerned, despite exhaustive study.

Botulism↗
PubMed1987

Ultrastructural study of the motor end-plate in botulism and Lambert-Eaton myasthenic syndrome.

The motor end-plate fine structure was studied in 3 patients with type A botulism and compared with that in 4 patients with Lambert-Eaton myasthenic syndrome (LES). In the botulism cases a biopsy of the biceps brachii muscle was performed at the chronic stage. The skeletal muscle showed a neurogenic change. The nerve terminal area had decreased and the postsynaptic regions had been denuded of their nerve terminals in 16% of the regions (9.8% in control). No highly simplified postsynaptic regions were observed. The findings are consistent with those observed at the motor end-plates in motoneuron diseases. By contrast, in LES no changes were observed in the presynaptic region. In the postsynaptic region, the postsynaptic membrane length and membrane density decreased and hypertrophy of the junctional folds was not observed.

Action Potentials↗
PubMed1990

Distinct characters of Clostridium botulinum type A strains and their toxin associated with infant botulism in Japan.

Four strains of Clostridium botulinum type A having been associated with infant botulism in Japan, and another strain isolated from honey not associated with infant botulism, were found to be hemagglutinin (HA) negative. These strains do not produce L (Mr 500 kDa) nor LL toxin (Mr 900 kDa) but M toxin (Mr 300 kDa) only. No marked difference was found between the HA-positive and HA-negative strains in other biochemical properties, but the HA-negative strains tended to colonize more easily in the intestines of infant mice than did HA-positive strains. The toxin of HA-positive strains and that of HA-negative strains differed in the antigenicity of part of the toxic component and that of the nontoxic component, and in the molecular size of the toxic component.

Botulinum Toxins↗
PubMed1986

The mechanism of botulism.

Botulism is induced by botulinum toxin and the mechanism of the disease is unknown. In another study, a fatal autoimmune disease was produced in animals by immunization with a fraction of choline acetyltransferase. When these two syndromes are compared, numerous similarities are observed. It is postulated that botulism toxin acts as an initiator for the autoimmune disease by catalyzing in vivo the formation of the pathogenic fraction of choline acetyltransferase.

Animals↗
PubMed1985

Emergency department presentation of type A botulism.

In October 1983, 28 people became ill with type A botulism in a common-source, food-borne outbreak. Thirteen of these patients presented to an emergency department for initial medical evaluation. The records of these thirteen patients were examined retrospectively in an attempt to characterize the initial presenting symptoms. All patients complained of at least three of four symptoms (generalized weakness, diplopia, dry mouth, and difficulty speaking). Emergency physicians can play a pivotal role in limiting the extent of common-source botulism outbreaks by early recognition of the disease and immediate mobilization of community public health resources.

Botulism↗
PubMed1993

Sequence of the gene coding for the neurotoxin of Clostridium botulinum type A associated with infant botulism: comparison with other clostridial neurotoxins.

The neurotoxin gene from a strain of Clostridium botulinum type A causing infant botulism was cloned as a series of overlapping polymerase chain reaction (PCR) fragments generated using primers designed to conserved regions of published botulinal toxin (BoNT) sequences. Translation of the nucleotide sequence derived from cloned PCR fragments demonstrated that the toxin gene encodes a protein of 1,296 amino acid residues. Comparative alignment of the derived infant BoNT/A sequence with those of other published neurotoxins revealed highest sequence relatedness with BoNT/A of classical food-borne botulism. The sequence identity between infant and classical BoNT/A was 94.9% for the light chain (corresponding to 23 amino acid changes) and 87.1% for the heavy chain (corresponding to 109 amino acid changes).

Bacterial Proteins↗
PubMed2000

Serum positive botulism with neuropathic features.

A 32-year-old man presented with multiple cranial neuropathies and his serum was positive for botulism type B. However, serial electrodiagnostic studies were consistent with a primarily neuropathic process, such as Fisher syndrome, rather than a neuromuscular junction disorder. Electrodiagnostic study findings in patients with presumed neuromuscular junction disorders may mimic findings suggestive of a neuropathic process, or the bioassay for botulism may be falsely positive in patients with Fisher Syndrome.

Adult↗
PubMed1992

Electrodiagnosis reliability in the diagnosis of infant botulism.

Infant botulism is confirmed by isolation of Clostridium botulinum from stool culture or by toxin assay. Although electrodiagnosis has been described as a diagnostic tool in infant botulism, our 11-year review of toxin-confirmed cases suggests that electrodiagnosis is not a reliable tool. In the case report presented, results of electrodiagnosis were negative but enema effluent contained adequate concentrations of organism and toxin to confirm the diagnosis.

Botulinum Toxins↗
PubMed1993

Early severe infantile botulism.

Two neonates with a history of diarrhea, abrupt apnea, and suspected sepsis were proved to have infantile botulism. Initial symptoms in both infants suggested other diagnoses. Electrophysiologic studies were important in confirming the diagnosis. Early severe infantile botulism may be rare but should be considered in neonates who have hypotonia and respiratory arrest or a sepsis-like clinical picture.

Acute Disease↗
PubMed1982

Protective role of human milk against sudden death from infant botulism.

We examined the possibility that human milk and formula milk might differentially affect the severity of the infant botulism because they differ in immunologic composition and in influence on the normal intestinal microflora against which Clostridium botulinum must compete. A beneficial effect of human milk was suggested by the different feeding experiences of the moderate, hospitalized patients and the sudden death cases. Of patients hospitalized in California, 66% (33/50) were still being nursed at onset of illness, a percentage significantly greater than that of matched controls (P less than 0.01). In contrast, all ten California cases of sudden infant death attributable to C. botulinum infection were being fed iron-supplemented formula milk at death) unlike their controls, P less than 0.02) and had received no human milk within ten weeks of death. A beneficial effect of human milk was also observed in differences in mean age at onset; hospitalized breast-fed patients were almost twice as old (13.8 +/- 6.7 weeks) as were hospitalized formula-fed patients (7.6 +/- 2.9 weeks) (P less than 0.01). Human milk (or possibly other factors associated with breast-feeding) appeared to have moderated the severity at onset of infant botulism, allowing time for hospital admission, whereas for some infants with this illness, formula milk (or possibly other factors associated with formula feeding) was linked to sudden unexpected death.

Botulism↗
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↗
PubMed2004

Fatal type A botulism in South Africa, 2002.

Although wildfowl and domestic livestock botulism has been recognized as a problem in southern Africa, very few human cases have ever been described in the region. In late February 2002, two siblings aged eight and 12 years developed acute flaccid paralysis and died. Mouse bioassays revealed the presence of type A botulinum toxin in the serum of both children, and in the retrieved remains of the implicated food. The implicated vehicle of the toxin was tinned fish in tomato sauce, commercially produced in South Africa. Type A Clostridium botulinum was cultured from the food. The most likely scenario was that corrosion damage had allowed entry of environmental organisms, including Clostridium botulinum, to the tinned food. This is the first outbreak of human type A botulism in southern Africa to be documented, and the first fatal outbreak described; previous human cases in this region have involved type B botulinum toxin, which tends to produce milder disease. A few other outbreaks elsewhere in Africa have been published, the most extensive being a type E epidemic in Egypt. Commercially tinned products were not involved in any of those outbreaks.

Animals↗
PubMed1989

Outbreak of botulism in north west England and Wales, June, 1989.

The clinical features of 27 patients identified in an outbreak of botulism in Lancashire, England, and North Wales are reviewed. All but 1 of the patients (age range 14 months to 74 years) were admitted to hospital: 12 were treated in intensive care units, and 8 received positive pressure ventilation. 1 patient died with an aspiration pneumonia. The clinical presentations contained several unusual features, with evidence of segmental demyelination in some patients and drowsiness, sore throats, and fever in others. The widely dispersed source of intoxication with patients presenting singly to several hospitals added to the difficulties of diagnosis. Successful clinical management depends on full and early recognition both of the dangers of impaired oropharyngeal function and of the rapid neurological changes in botulism.

Adolescent↗