Cases reported "Botulism"

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1/26. Severe adult botulism.

    A case of severe adult botulism with paralysis, respiratory failure and cranial nerve palsies is presented. The pathophysiology, clinical manifestations, diagnosis and treatment options for botulism are discussed.
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2/26. 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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3/26. 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.
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4/26. Wound botulism in the UK and ireland.

    There are three main, naturally occurring, epidemiological types of botulism: food-borne, intestinal colonization (infant botulism) and wound botulism. The neurological signs and symptoms are the same for all three epidemiological types and may include respiratory paralysis. Wound botulism is caused by growth of cells and release of toxin in vivo, is associated with traumatic wounds and abscesses and has been reported in drug users, such as those injecting heroin or sniffing cocaine. Up to the end of 1999 there were no confirmed cases of wound botulism in the UK. Between the beginning of 2000 and the end of December 2002, there were 33 clinically diagnosed cases of wound botulism in the UK and ireland. All cases had injected heroin into muscle or by 'skin popping'. The clinical diagnosis was confirmed by laboratory tests in 20 of these cases. Eighteen cases were caused by type A toxin and two by type B toxin.
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5/26. A case of type F botulism in southern california.

    BACKGROUND: botulism caused by type F botulinum toxin accounts for less than 0.1% of all human botulism cases and is rarely reported in the literature. CASE REPORT: A 45-year-old woman presented to an emergency department complaining of blurred vision, difficulty focusing, and dysphagia. The treating physician initially considered the possibility of paralytic shellfish poisoning due to a report of shellfish ingestion, which was later determined to be frozen shrimp and a can of tuna, but no gastroenteritis or paresthesias were present. During the emergency department observation, the patient developed respiratory distress with hypercapnea and required intubation and mechanical ventilation. Within hours, ptosis, mydriasis, and weakness in the arms and legs developed. Bivalent (A, B) botulinum antitoxin was administered approximately 24 h from the onset of initial symptoms, but over the next two days complete paralysis progressed to the upper and lower extremities. Shortly thereafter a stool toxin assay demonstrated the presence of type F botulinum toxin. The patient subsequently received an experimental heptavalent botulinum antitoxin on hospital day 7 but paralysis was already complete. Her three-week hospital course was complicated by nosocomial pneumonia and a urinary tract infection, but she gradually improved and was discharged to a rehabilitation facility. Anaerobic cultures and toxin assays have yet to elucidate the source of exposure. CONCLUSION: We report a rare case of type F botulism believed to be foodborne in etiology. Administration of bivalent botulinum antitoxin did not halt progression of paralysis.
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6/26. infant botulism, type F, presenting at 54 hours of life.

    We report a case of botulism in a 54-hour-old infant with rapidly progressive fulminant paralysis and rapid spontaneous recovery atypical for infant botulism. Clostridium baratii and type F botulinum neurotoxin were isolated from the patient's stool. This unique presentation with rapid recovery is consistent with pharmacokinetics of type F botulinum neurotoxin. Interestingly, a muscle biopsy also revealed pathologic changes early in the disease course. This article reports the youngest known case of infant botulism and only the third reported case of this disease caused by type F neurotoxin. botulism should be considered in patients of any age with subacute or acute neuromuscular weakness.
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7/26. Acute paralysis following "a bad potato": a case of botulism.

    PURPOSE: Intensivists often encounter patients with respiratory failure as a result of neuromuscular disease, however, acute neuro-muscular syndromes are less common. We present a case of food borne Clostridium botulism and discuss the diagnostic and therapeutic considerations. CLINICAL FINDINGS: A 35-yr-old healthy male presented with abdominal pain and blurred vision 12 hr after ingesting a "bad" potato. During the next 17 hr, the patient demonstrated a gradual descending paralysis which ultimately resulted in no cranial nerve function and 0/5 strength in all extremities. sensation was intact. The patient required intubation and mechanical ventilation. His blood count, biochemical profile, computerized tomography and magnetic resonance imaging of the head were normal. A lumbar puncture revealed no abnormalities. Due to the rapid deterioration and presentation of 'descending' paralysis, botulism was suspected. The patient was treated empirically with botulinum anti-toxin. Samples of blood, stool and gastric contents were cultured for the presence of clostridium botulinum and its toxin and these tests were positive for botulinum toxin A 12 days later. The patient's neuromuscular function gradually improved over a prolonged period of time. Six and one-half months after his initial presentation, the patient was discharged home after completing an aggressive rehabilitation program. CONCLUSIONS: botulism is a rare syndrome and presents as an acute, afebrile, descending paralysis beginning with the cranial nerves. If suspected, botulinum anti-toxin should be considered, particularly within the first 24 hr of onset of symptoms. Confirmation of the presence of botulinum requires days therefore the diagnosis and management rely on history and physical examination.
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8/26. A rare differential diagnosis in dysphagia: wound botulism.

    The incidence of wound botulism is increasing dramatically among intravenous drug users. Efficient intensive care and early treatment with antitoxin is essential to avoid lethal courses. The clinical picture of botulism is of descending, symmetric, flaccid paralysis. Early symptoms include cranial nerve palsies resulting in blurred vision and diplopia, difficulty in focusing, ptosis, facial weakness, dysphagia, dysphonia, and dysarthria. Because patients presenting with dysarthria and dysphagia will often be seen by an ear, nose and throat specialist initially, this rare but upcoming neurologic disease must be considered in the differential diagnoses.
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9/26. 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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10/26. 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.
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