Iatrogenic Botulism Research Articles

Case of iatrogenic botulism after botulinotherapy in clinical practice

Case of iatrogenic botulism after botulinotherapy in clinical practice

Identification of Cross Reactive Antigens of C. botulinum Types A, B, E & F by Immunoproteomic Approach.

Diseases triggered by microorganisms can be controlled by vaccines, which need neutralizing antigens. Hence, it is very crucial to identify extremely efficient immunogens for immune prevention. Botulism, a fatal neuroparalytic disease, is caused by botulinum neurotoxins produced by the anaerobic, Gram-positive spore-forming bacteria, Clostridium botulinum. Food-borne botulism and iatrogenic botulism are caused by botulinum toxin. Wound botulism, infant botulism, and adult intestinal botulism are caused by primarily C. botulinum followed by secondary intoxication. To identify protective antigens, whole cell proteome of C. botulinum type B was separated by two-dimensional gel electrophoresis. 2-D gel of whole cell proteins was probed with hyper immune sera of whole cell proteins of C. botulinum types A, E, and F. Six cross immunoreactive proteins were identified. These immunoreactive proteins will be further tested for developing vaccines and serodiagnostic markers against botulism.

Myasthenia Gravis after Botulinum Toxin Type A Injection

Botulinum toxin type A (BoNT type A) is a neurotoxin produced by Clostridium botulinum, which causes paralysis by presynaptically binding to the cholinergic nerve terminals at the neuromuscular junction and decreasing the release of acetylcholine (1). BoNT type A, first used to treat strabismus, is now widely used to treat dystonia, spasticity, and other movement disorders, and also autonomic nervous system disorders including hyperhidrosis and sialorrhea (2). As with the effects of the toxin, the adverse effects are also reversible. The most common and severe adverse effects of the toxin are unwanted and excessive weakness of muscle after injection, paralysis of adjacent muscles caused by diffusion of the toxin and iatrogenic botulism characterized by widespread paralysis including the bulbar muscles. Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction, which is caused by antibodies produced against acetylcholine receptors. Fluctuating weakness is the main characteristic of the disease. A woman aged 80 years who presented with forceful contractions of the jaw and tongue, which caused difficulty in opening the mouth, was diagnosed as having oromandibular dystonia. Ten MU (mouse units) of BoNT type A was administered to each hypoglossal muscle once every 3 months. The patient was admitted to the emergency service with bilateral dropping of the eyelids, diplopia, dysphagia, general weakness, and shortness of breath, ten days after the 9th injection. Neurologic examination showed right dominant bilateral ptosis, mild restriction of lateral gaze of the right eye, isochoric pupils, and weakness of eye tightening. Her speech had a nasal quality. The masseter muscles, tongue, and the flexors of neck were weak. Motor examination of other muscles was normal. Generalized botulism, a rare adverse effect of BoNT type A injection, was considered in the patient. Supportive treatment and pyridostigmine 60 mg 5 times per day were given. Worsening of the symptoms, fluctuating weakness, and inadequate response to pyridostigmine suggested the diagnosis of MG. Repetitive nerve stimulation performed 6 weeks after BoNT type A injection revealed dysfunction of neuromuscular junction and autoantibodies against acetylcholine receptors were found positive in serum. Thorax computerized tomography performed for diagnosis of thymoma was normal. Treatment of 0.5 mg/kg/d prednisolone following 0.4 g/kg/d intravenous immunoglobulin was given because dysphagia and shortness of breath worsened. In time, necessity for pyridostigmine decreased and a significant improvement in neurologic status was achieved. Neurologic examination after 6 months was normal except bilateral mild ptosis. Unfortunately, the patient died of acute myocardial infarction 3 weeks after her last follow-up examination. After BoTN type A injection, symptoms including unilateral ptosis, diplopia, and dysphagia can occur and mimic MG (3). Patients with MG are rarely reported to show movement disorders including blepharospasm and cervical dystonia in the literature (4). The occurrence of symptoms of MG after BoTN type A injection

102. Timing of neurophysiological abnormalities in iatrogenic botulism

We have previously demonstrated lacking of facilitation on repetitive nerve stimulation (RNS) due to structural blockage by botulinum toxin. In the current study we aimed to assess timing of the neurophysiological findings induced by botulinum toxin A. After inoculation of 15 U botulin toxin type A in extensor brevis digitorum (EDB), 10 healthy volunteers were evaluated by weekly EMG, SFEMG, and 3 and 20 Hz RNS examinations, for 12 consecutive weeks. All subjects showed reduced cMAP by one week after inoculation, with subsequent normalization within 12 weeks. No decrement at 3 Hz and no facilitation at 20 Hz RNS were observed. Abnormal jitter and blocking were mostly recorded between the 5th and 8th week, always associated with denervation/reinnervation EMG findings. Low cMAP is an early finding in iatrogenic botulism with no evidence of facilitation. Jitter abnormalities are concomitant with denervation/reinnervation findings. We speculate that the increase in jitter and blocking induced by botulinum toxin could be due to nerve terminal sprouting in addition to the formation of new neuromuscular junctions.

Iatrogenic Botulism After the Therapeutic Use of Botulinum Toxin-A

Local injection of botulinum toxin-A is an accepted treatment for hyperhidrosis. We report 2 cases of primary hyperhidrosis who developed iatrogenic botulism after the therapeutic dose of onabotulinumtoxinA (Botox). This case report highlights the necessity of clinicians having sufficient information of potentially adverse effects, optimal dose, and correct preparation and injection of botulinum toxin-A.

Poster 86: The Diagnosis, Symptomatic Treatment, and Course of Iatrogenic Botulism: A Case Report

Poster 86: The Diagnosis, Symptomatic Treatment, and Course of Iatrogenic Botulism: A Case Report

Iatrogenic Botulism After Botulinum Toxin Type A Injections

Therapeutic use of botulinum toxin type A (BT/A) is well known, effective, and safe. Iatrogenic botulism that presents with generalized weakness, dysphagia, and respiratory distress is a rare but significant complication in BT/A treatment. In this study, we report 4 patients who developed iatrogenic botulism after receiving therapeutic doses of BT/A for spasticity and blepharospasm. One patient was placed in intensive care unit, but consequently, every patient recovered fully. The cause of BT/A as an adverse effect is most likely hematological spread of the toxin.

Iatrogenic Botulism in a Child With Spastic Quadriparesis

Botulinum toxins are potent neurotoxins used in a variety of neurological disorders. Few pediatric reports have been published to date regarding the potential hazards of therapeutic use of botulinum toxins. We describe the case of a 10-year-old boy who developed systemic weakness following treatment of spasticity with botulinum toxin type B. The patient developed iatrogenic botulism with ptosis, facial diplegia, neck flexor and extensor weakness, and profound hypopharyngeal laxity with respiratory compromise from which he eventually recovered. Clinicians should be mindful of the risk for systemic botulism when using local injections of the neurotoxin.

Iatrogenic Botulism Due to Therapeutic Botulinum Toxin A Injection in a Pediatric Patient

Botulinum toxin A is commonly used to reduce spasticity and dystonia in children with cerebral palsy. We report a pediatric patient who developed systemic botulism as a result of a severe overdose of the injected toxin (40 U/kg). This case highlights the importance of physicians having adequate knowledge of primate and human literature on the lethal dose, 50% of botulinum toxin A before injecting children.

Iatrogenic botulism in an amateur weight‐lifter

Movement DisordersVolume 21, Issue 7 p. 1056-1056 Letter to the Editors Iatrogenic botulism in an amateur weight-lifter Philip Duffey FRCP, Philip Duffey FRCP phil.duffey@york.nhs.uk Department of Neurology, York Hospital, York, United KingdomSearch for more papers by this authorCaroline Brown BSc, Caroline Brown BSc Department of Neurology, York Hospital, York, United KingdomSearch for more papers by this author Philip Duffey FRCP, Philip Duffey FRCP phil.duffey@york.nhs.uk Department of Neurology, York Hospital, York, United KingdomSearch for more papers by this authorCaroline Brown BSc, Caroline Brown BSc Department of Neurology, York Hospital, York, United KingdomSearch for more papers by this author First published: 25 April 2006 https://doi.org/10.1002/mds.20903Citations: 10Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume21, Issue7July 2006Pages 1056-1056 RelatedInformation

Botulism

Botulism is a rare disease with 4 naturally occurring syndromes: foodborne botulism is caused by ingestion of foods contaminated with botulinum toxin, wound botulism is caused by Clostridium botulinum colonization of a wound and in situ toxin production, infant botulism is caused by intestinal colonization and toxin production, and adult intestinal toxemia botulism is an even rarer form of intestinal colonization and toxin production in adults. Inhalational botulism could result from aerosolization of botulinum toxin, and iatrogenic botulism can result from injection of toxin. All forms of botulism produce the same distinct clinical syndrome of symmetrical cranial nerve palsies followed by descending, symmetric flaccid paralysis of voluntary muscles, which may progress to respiratory compromise and death. The mainstays of therapy are meticulous intensive care (including mechanical ventilation, when necessary) and timely treatment with antitoxin.