Cases reported "Botulism"

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1/9. Transient paralysis of the bladder due to wound botulism.

    In the last 10 years, wound botulism has increasingly been reported and nearly all of these new cases have occurred in injecting-drug abusers. After absorption into the bloodstream, botulinum toxin binds irreversibly to the presynaptic nerve endings, where it inhibits the release of acetylcholine. diplopia, blurred vision, dysarthria, dysphagia, respiratory failure and paresis of the limbs are common symptoms of this intoxication. Surprisingly and despite the well-known blocking action of the botulinum toxin on the autonomic nerve system, little attention has been paid to changes in the lower urinary tract following acute botulinum toxin poisoning. Here we report a case of bladder paralysis following wound botulism. early diagnosis and adequate management of bladder paralysis following botulism is mandatory to avoid urologic complications. Accordingly, the prognosis is usually favorable and the bladder recovery complete.
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2/9. 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.
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3/9. 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.
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4/9. Cardiovascular-reflex testing and single-fiber electromyography in botulism. A longitudinal study.

    Four patients with botulism were studied on admission and at different times after intoxication, using a battery of cardiovascular autonomic tests. The results were compared with clinical status and single-fiber electromyographic findings. In the early stage of intoxication, the control of heart-rate and blood-pressure responsivity was markedly impaired, as was the neuromuscular transmission. At follow-up, results of sympathetic tests normalized earlier than those of parasympathetic tests. The recovery of autonomic function was slower than that of neuromuscular transmission in three patients. Monitoring autonomic derangement in botulism adds further information on the course of the disease and may identify patients at risk for cardiac or respiratory arrest. Further clinical investigation can help in determining more precisely the autonomic sites where the toxin acts.
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5/9. Two fatal cases of type E adult food-borne botulism with early symptoms and terminal neurologic signs.

    Type E botulism, one of the least common forms of botulinal intoxication on the East Coast of the united states, is described for two elderly patients with chronic underlying disease. Both patients consumed tainted kapchunka, a salted, ungutted whitefish. Gastrointestinal symptoms and signs were prominent, but neurologic complaints, although noted soon after the consumption of the fish in one patient, did not progress until late in the course of the patient's illness. One patient exhibited both urinary retention, which was reported mainly in one outbreak of type E botulism (M.G. Koenig, A. Spickard, M.A. Cardella, and D.E. Rogers, medicine [baltimore] 43:517-545, 1964), and muscular fasciculations, which have been rarely reported.
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6/9. 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.
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7/9. 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.
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keywords = intoxication
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8/9. tracheotomy for infant botulism.

    botulism is a serious intoxication caused by ingestion of food containing preformed botulinus toxin and characterized by rapidly progressive bulbar paralysis, generalized weakness, and respiratory insufficiency. In 1976 a distinct clinical entity of infant botulism was recognized. The disease apparently results from intraintestinal toxin production which produces a defect in neuromuscular transmission by interfering with release of acetylcholine at cholinergic synapses. Five cases of infant botulism were identified at the Children's Hospital of philadelphia between 1975 and 1977. Initial symptoms included constipation, slow feeding, lethargy and weak cry. Four of the patients progressed to respiratory insufficiency requiring nasotracheal intubation. Three of the infants with respiratory failure required tracheotomy. Because infants with respiratory failure may require support for months, we recommend that a tracheotomy be performed early in the management to avoid the complications associated with prolonged intubation. The effectiveness of antitoxin or antibiotics to treat infant botulism remains questionable and therefore prolonged respiratory supportive care is the mainstay of therapy. In addition, we offer guidelines for decannulation in cases of infant botulism. None of the patients in our series could be decannulated prior to initial discharge from the hospital.
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9/9. Quantitative evidence of intestinal colonization by clostridium botulinum in four cases of infant botulism.

    infant botulism is an infectious form of a disease heretofore principally known as food-borne intoxication. Previous epidemiologic and laboratory studies have shown that infant botulism results from the ingestion of spores of clostridium botulinum that subsequently germinate in the infant intestine and produce botulinal toxin. A quantitative study of the fecal microflora of four infants with infant botulism revealed the presence of C. botulinum in numbers as high as 6.0 x 10(8) colony-forming units (cfu)/g. At various times after the onset of illness, the numbers of C. botulinum that were recovered from feces ranged from 10(3) to 10(8) cfu/g and constituted from 0.01% to 3.3% of the total fecal flora. It was concluded that the large numbers of C. botulinum found in patients' feces could occur only as a consequence of in vivo spore germination and outgrowth.
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