Cases reported "Botulism"

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1/15. AAEM case report 16. botulism. American association of Electrodiagnostic medicine.

    early diagnosis of botulism is essential for effective treatment. Electrophysiologic testing can be of major help to establish a prompt diagnosis, but the classic electrodiagnostic features of botulism are often elusive. Decrement or increment of compound muscle action potential (CMAP) amplitudes to slow or fast rates of nerve stimulation are often unimpressive or totally absent. Reduction of CMAP amplitudes, denervation activity, or myopathic-like motor unit potentials in affected muscles are found more frequently but they are less specific. In general, the electrophysiologic findings taken together suggest involvement of the motor nerve terminal, which should raise the possibility of botulism. The case reported here illustrates a common clinical presentation of botulism. This study emphasizes realistic expectations of the electrodiagnostic testing, the differential diagnosis, and the potential pitfalls often encountered in the interpretation of the electrophysiologic data.
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2/15. Wound botulism in drug addicts in the United Kingdom.

    Clostridium novyi has recently been identified as the causative organism responsible for the deaths of 35 heroin addicts who had injected themselves intramuscularly. We present two heroin addicts who developed C. botulinum infection following intramuscular or subcutaneous injection of heroin. Like C. novyi, this grows under anaerobic conditions and clinical presentation may be similar; however, descending motor or autonomic signs are invariably present in botulism. The prognosis is good if the diagnosis is made early and appropriate treatment commenced.
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3/15. in vitro microelectrode study of neuromuscular transmission in a case of botulism.

    We performed in vitro microelectrode studies in the anconeus muscle biopsy of a 6-week-old infant intoxicated with clostridium botulinum toxin B. The most striking abnormalities were the severe reduction of the endplate potential (EPP) quantal content and the marked variability of EPP latencies. The increased variability was often limited to a "single quantum" component of the EPP. Neither the amplitudes nor the frequencies of spontaneous miniature endplate potentials (MEEPs) were decreased. However, there was a wide range of amplitudes and frequencies of MEPPs. This unique combination of electrophysiologic findings indicates a severe presynaptic failure of neuromuscular transmission, which appears to result from an impairment of the process of synaptic vesicle release taking place after the stimulus induced influx of calcium into the motor nerve terminals.
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4/15. Severe botulism after eating home-preserved asparagus.

    OBJECTIVE: To present a case of adult botulism acquired in queensland. CLINICAL FEATURES: After eating home-preserved asparagus, a 33-year-old man presented with internal and external ophthalmoplegia, bilateral facial nerve palsies, and descending muscle weakness culminating in a sudden respiratory arrest. Electrophysiological testing demonstrated normal nerve conduction velocities and an incremental response of evoked motor potentials on repetitive stimulation, confirming the clinical diagnosis of botulism. INTERVENTION AND OUTCOME: Treatment with trivalent antitoxin, oral treatment with vancomycin and supportive mechanical ventilation for four weeks resulted in complete clinical recovery. plasmapheresis was also used but its contribution to the patient's improvement is dubious. CONCLUSIONS: Although botulism is rare in australia, clinicians should be aware of the clinical presentation and the rapidity of confirmation of the diagnosis by electrophysiological testing. patients should be nursed in an intensive care setting. Regular testing of vital capacity should be performed to determine the need for mechanical ventilation.
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5/15. food-borne botulism cases in Van region in eastern turkey: importance of electromyography in the diagnosis.

    OBJECTIVES: food-borne botulism is an acute form of poisoning that results from ingestion of a toxin produced by clostridium botulinum. botulism toxin causes its major effect by blocking neuromuscular transmission in autonomic and motor nerve terminals. methods: In this study, we present the features of eleven cases of food-borne botulism admitted to our hospital in 2001. All of the cases were caused by home-prepared foods; green beans. In these cases, the main symptoms and signs were generalized muscular weakness, dry mouth, dysphagia, disponea and diplopia. Electrophysiological studies were performed on four patients. RESULTS: Motor conduction studies showed that compound muscle action potentials were decreased with normal latencies and conduction velocities. The needle electromyography showed signs of denervation potentials like fibrillation and positive waves in four patients. Repetitive nerve stimulation with high frequency (20 Hz) induced an increment close to 100% in the amplitudes in 2 of 4 patients. CONCLUSION: Although toxin could not be detected in the patients, the electromyographic findings supported our diagnosis. We concluded that electromyography has an important role in diagnosis of botulism, especially in the condition that serologic tests are negative or cannot be performed.
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6/15. Descending polyneuropathy in an intravenous drug user.

    A 27-year-old male intravenous drug user presented to the Emergency Department of St James's Hospital with a 1-week history of progressive dysphasia, dysphagia and difficulty 'holding his head up' and 'keeping his eyes open'. He also complained of increasing weakness in his upper limbs, as a result of which he kept dropping things. He was on a methadone program but was using both intravenous heroin and cocaine at the time of presentation. Examination of his motor function revealed generalized hypotonia, hyporeflexia and reduced power in both upper limbs. No sensory loss was observed. Co-ordination was intact. The clinical picture of a proximal symmetrical descending weakness and an absence of sensory loss was suggestive of botulism. clostridium botulinum is a spore-forming, obligate anaerobe. The three forms of human botulism are food-borne, wound and intestinal. A fourth man-made form is produced from aerosolized botulinum toxin and results in inhalational botulism. A little as 1 g of aerosolized botulinum toxin has the potential to kill 1.5 million people. Toxin is detected in serum or stool specimens in only approximately 46% of clinically diagnosed cases. Treatment involves supportive care and early passive immunization with equine antitoxin. patients should be regularly assessed for loss of gag and cough reflex, control of oropharyngeal secretions, oxygen saturation, vital capacity and inspiratory force. When respiratory function begins to deteriorate, anticipatory intubation is indicated. Early symptom recognition and early treatment with antitoxin are essential in order to prevent mortality, and to prevent additional cases, it is important to ascertain the presence of similar symptoms in contacts of the patient and local public health officials must be notified as one case may herald an outbreak. Given the continued threat of bioterrorism, the Centre for disease Control Surveillance System in the united states must also be notified of any cases of botulism.
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7/15. infant botulism due to consumption of contaminated commercially prepared honey. First report from the Arabian Gulf States.

    OBJECTIVE: To report the first case of infant botulism in Arabian Gulf States. CLINICAL PRESENTATION AND INTERVention: A 6-week-old infant, presenting with signs of sepsis, was intubated and ventilated due to progressive weakness. infant botulism was suspected with acute flaccid paralysis and a history of honey consumption. An electromyogram showed decreased amplitude of compound muscle action potential in all motor nerves, preserved sensory responses; the motor terminal latencies and motor conduction velocities were normal. blood, stool and honey samples were sent for culture. Stool and honey cultures showed two identical strains of clostridium botulinum. CONCLUSION: This case shows that the infant botulism occurred from the ingested contaminated honey. Hence vigilance should be maintained when a baby is fed honey and shows signs of progressive weakness because the disease can quickly progress to respiratory failure.
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8/15. botulism: electrophysiological studies.

    In a patient with botulism type B, electrophysiological studies showed: (1) a pattern in the repetitive nerve stimulation test resembling that found in the Eaton-Lambert syndrome but without any significant increment at high rates of stimulation or posttetanic exhaustion phenomenon; (2) a prominent response to guanidine hydrochloride; (3) a short mean duration of motor unit potentials that reversed with recovery; (4) a mild, prolonged latency and low amplitude of the h-reflex; (5) mild peripheral nerve dysfunction; and (6) a long-lasting persistence of abnormalities beyond the time of clinical recovery. The literature reports two types of responses in the repetitive nerve stimulation test in botulism: in the severe form one obtains a low-amplitude muscle potential, a decremental response at low rates of stimulation, and an insignificant incremental response at high rates of stimulation; in the mild form a normal amplitude of muscle potential occurs together with a normal response to low rates of stimulation and a significant incremental response at high rates of stimulation.
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9/15. 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.
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10/15. Acute infantile motor unit disorder. Infantile botulism?

    Eight infants with an acute reversible motor unit disorder are described, including two infants from whom Clostridum botulinum type A was isolated from stool specimens. The clinical spectrum includes constipation, cranial nerve deficits, pupillary involvement, and generalized hypotonic weakness. There were no deaths, and all infants have had complete clinical recovery. A characteristic electromyographic (EMG) pattern was present in part until clinical recovery. This distinctive pattern consisted of brief, small, abundant for power exerted motor unit potentials. This EMG pattern in the context of the clinical syndrome may well be diagnostic for acute infantile motor unit disorder.
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