Cases reported "Botulism"

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1/18. Infantile botulism: clinical and laboratory observations of a rare neuroparalytic disease.

    A 3-month-old male infant was admitted to the University Hospital of Los Andes with a history of constipation, weak crying, poor feeding, flaccidity and later bilateral ptosis and hyporeflexia. The admission diagnosis was septicaemia until an electrophysiological study reported postetanic facilitation with 50 Hz/seg stimulations four days later. The Clostridium botulinum toxin type B was isolated from the infant's stool samples and the organism grew in anaerobic cultures. The patient recovered completely and was discharged 2 months later. Although infant botulism is an uncommon disease in our environment, this diagnosis must be suspected in all afebrile infants with constipation, affected cranial nerves and generalized hypotonia. The principal differential diagnoses are Landry-guillain-barre syndrome, poliomyelitis, myasthenia gravis and infant muscular atrophy.
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2/18. botulism due to Clostridium baratii type F toxin.

    botulism results from consumption of preformed toxin or in vivo toxin elaboration in wounds or intestine. Of U.S. food-borne botulism cases since 1950, the majority were due to toxin A, but a significant number of suspect cases were never confirmed by culture or toxin detection. We report here a possible case of food-borne botulism attributed to toxin F production by a Clostridium baratii organism isolated from food consumed by the patient. The isolation of a toxin-producing Clostridium species other than Clostridium botulinum from food and stool requires deviation from the usual laboratory protocols, which may account for the lack of complete laboratory confirmation of clinically diagnosed cases.
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3/18. 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.
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4/18. 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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5/18. 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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6/18. 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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7/18. 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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8/18. arm abscesses caused by Clostridium botulinum.

    Wound botulism is an uncommon disorder that continues to be rarely reported in the united states. A 34-year-old intravenous heroin user was admitted to the loma Linda, Calif., veterans Administration hospital with multiple abscesses on his forearms. His clinical course was compatible with botulism, and his culture and serum were positive for Clostridium botulinum toxin type A. Early culture and/or serum identification can lead to prompt diagnosis, treatment, and improvement in the morbidity and mortality rates of this disease.
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9/18. Type A botulism from commercially canned beef stew.

    Two of three persons who ate lunch together became ill with symptoms characteristic of botulism. One died before botulism was suspected and before specimens could be collected for laboratory testing, but a serum specimen from the other patient, who survived, yielded botulinal toxin, type A. The third person remained asymptomatic, but clostridium botulinum type a was cultured from his stool. The three persons had shared two canned foods: home-canned green beans and commercially canned beef stew. The green beans were initially assumed to be the cause of the outbreak. However, the empty stew can was recovered from the garbage, and washings from the can yielded C botulinum, type A, and its toxin.
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10/18. Two cases of type E infant botulism caused by neurotoxigenic clostridium butyricum in italy.

    The first two confirmed cases of type E infant botulism occurred in two 16-week-old girls in Rome, italy. The original diagnosis for the first patient was intestinal blockage due to an ileocecal invagination, which was treated surgically. Postoperatively, the patient became unresponsive and required ventilatory assistance. A diagnosis of infant botulism was then made. The second infant presented to the same hospital 7 1/2 months later with profound weakness, hypotonicity, mydriasis, and areflexia. This case was recognized as possible botulism at admission. Both cases were confirmed by detection and identification of type E botulinal toxin in stool specimens and in enrichment cultures of those specimens. The toxigenic organisms isolated were quite different from clostridium botulinum type e. The apparent causative organism in each case resembles clostridium butyricum but produces a neurotoxin that is indistinguishable from type E botulinal toxin by its effects on mice and by its neutralization with type E botulinal antitoxin.
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