A case of type A botulism

The neurotoxin produced by Clostridium botulinum, is responsible for botulism. The clinical signs are digestive disorders, pupillar alterations, and peripheral muscular weakness. The failure of thoracic muscles is responsible for the severity of botulism. We describe a case of a 74 year old woman who presented a severe form of botulism, requiring a prolonged intensive care unit stay.     

Open Tibial Fracture Complicated by Wound Botulism: A Case Study

Botulism is a neuroparalytic disease most commonly caused by foodborne ingestion of neurotoxin types A, B, and E, and is often fatal if untreated. Clinicians should be able to recognize the classic symptoms of botulinum intoxication (12). Owing to its rarity, there are a limited number of studies evaluating the clinical care of patients with wound botulism (10). We present an infected tibial non-union with botulism who underwent a successful radical excision and bone transport. The patient tolerated the procedure well.     

Botulism

Opinion statement Botulinum toxin is the most potent toxin known to humans and as little as 100 ng can be lethal. The toxin blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system by introducing an endopeptadase enzyme into the presynaptic side of the synapse. The endopeptadase cleaves acetylcholine vesicle docking proteins that are required for the synapse to release acetylcholine into the synaptic cleft. Botulism occurs from consumption or inhalation of preformed botulinum toxin or growth of Clostridium botulinum bacteria in the infant gastrointestinal tract or within a wound. Growth of C. botulinum in the immature gut or wound will release botulinum toxin that reaches the circulation. All forms of botulism cause progressive weakness, bulbar signs (blurred vision, diplopia, mydriasis, dysphagia, and dysarthria), and respiratory failure with normal sensation and mentation. Treatment is aimed at 1) maintaining respiration via intubation and mechanical ventilation, 2) stopping progression of weakness by administration of botulinum antitoxin (equine trivalent botulinum antitoxin for adults and botulism immune-globulin intravenous-human for infant botulism), and 3) preventing complications from weeks of paralysis with good supportive care. The source of the botulinum toxin should be identified to prevent additional cases. Patients can recover normal muscle strength within weeks to months, but usually complain of fatigue for years.     

Two cases of foodborne botulism with home-preserved asparagus

Botulism is a rare but potentially fatal disease caused by toxins produced by Clostridium botulinum. We report botulism in two adult females, one of them just tasting from "bad" asparagus and the other eating the full portion. Both patients survived after intermittent mechanical ventilation and trivalent antitoxin administration. The diagnosis was confirmed by detection of botulinum toxin. Acute onset of bilateral cranial neuropathies associated with symmetric descending weakness as well as some key features of the botulism syndrome including absence of fever, symmetric neurologic deficits, the patients remaining responsive and no sensory deficits, with the exception of blurred vision, led to the clinical diagnosis in the first presenting case which was then easily made in the second. Despite the fact that amount of toxin ingested, time-to-symptom development, and time-to-recovery markedly differed in the two patients, their maximal disease severity was similar.     

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.     

Mechanisms of action of intravesical botulinum treatment in refractory detrusor overactivity

Urinary retention is one of a multitude of autonomic deficits resulting from acute botulism (oral botulinum intoxication). The powerful influence of botulinum-A neurotoxin (BoNT-A) on autonomic function has now been harnessed to the benefit of patients with detrusor overactivity (DO), by injecting the agent intramurally, with consequent improvement in urodynamic and clinical variables. Nonetheless, the complexity of bladder cellular physiology and putative mechanisms underlying the pathophysiological basis of DO even now render the precise mechanisms of clinical response to intravesical BoNT-A uncertain. In this review, the processes by which BoNT-A affects nerve function and the state-of-the-art in the physiological understanding of bladder dysfunction are discussed together, conveying how much must be reckoned when attempting to understand the mechanisms by which this powerful agent can improve refractory and bothersome DO.     

Botulism toxin,bioterrorist weapon

BOTULISM AND BIOWARFARE: Botulism is a severe neuro-paralysing infection due to a toxin produced by Clostridium botulinum. The use of the botulinum toxin for terrorist aims in the form of aerosols is a perfectly credible eventuality. The botulinum toxin is the most potent toxin known; it is easy to produce and can lead to massive destruction. DEPENDING ON THE CONTAMINATION: The clinical forms of botulism depend on the mode of contamination. Botulism through inhalation can only be the result of a deliberate act using an aerosol. The clinical symptomatology is identical to that of the other forms. PREVENTION: In the case of a bio-terrorist attack with an aerosol of botulinum toxin, the subjects exposed should be vaccinated as a prophylactic measure with trivalent antitoxin vaccine (types A, B and E). This vaccine must be administered as rapidly as possible in symptomatic patients. A single case of botulism acquired by inhalation corresponds to an act of terrorism.     

肉毒毒素注射引起的不良反应

肉毒毒素注射引起的不良反应,是药物本身的组成成分引起的与用药目的无关的有害反应,与医生注射方式和注射技术无关。尽管肉毒毒素生产厂家的药品说明书上也有提示,但其所提供的信息不够全面,也未必能引起医生的足够重视。目前文献上多为散发病例。为此作者对过去20年有关肉毒毒素注射引起的过敏反应、肉瘤样肉芽肿、眼睑水肿、流感样症状等相关不良反应的临床表现、发病机制与治疗方法进行综述。     

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.     

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.     

The basic science of botulinum toxin

Understanding the basic science of botulinum toxin should serve as a fundamental first step for clinical therapy. This article endeavors to cover many aspects of basic research that also have clinical import. The two principal toxins of the clostridial family, Clostridium tetani and C botulinum, are described in detail. The five clinical manifestations of botulism poisoning are also outlined, and structural aspects and the mechanism of action of botulinum toxin are then presented. Finally, the immunologic and pharmacologic principles that define the various serotypes of botulinum toxin are set forth.     

Botulinum neurotoxin and other treatments for fissure-in-ano and pelvic floor disorders

BACKGROUND: The management of disorders of the lower gastrointestinal tract, such as chronic anal fissure and pelvic floor dysfunction, has undergone re-evaluation recently. To a large extent this is due to the advent of neurochemical treatments, such as botulinum neurotoxin injections and topical nitrate ointment. METHODS AND RESULTS: This review presents, inter alia, current data on the use of botulinum neurotoxin to treat lower gastrointestinal tract diseases, such as chronic anal fissure for which it promotes healing and symptom relief in up to 70 per cent of cases. This agent has also been used selectively to weaken the external anal sphincter and puborectalis muscle in constipation and in Parkinson's disease. Symptomatic improvement can also be induced in anterior rectocele by botulinum neurotoxin injections. CONCLUSION: Botulinum neurotoxin appears to be a safe therapy for anal fissure. It is more efficacious than nitrate application and does not require patient compliance to complete treatment. While it may also be a promising approach for the treatment of chronic constipation due to pelvic floor dysfunction, further investigation of its efficacy and safety in this role is needed before general usage can be advocated.     

Passive mechanical properties and related proteins change with botulinum neurotoxin A injection of normal skeletal muscle

The effects of botulinum neurotoxin A on the passive mechanical properties of skeletal muscle have not been investigated, but may have significant impact in the treatment of neuromuscular disorders including spasticity. Single fiber and fiber bundle passive mechanical testing was performed on rat muscles treated with botulinum neurotoxin A. Myosin heavy chain and titin composition of single fibers was determined by gel electrophoresis. Muscle collagen content was determined using a hydroxyproline assay. Neurotoxin‐treated single fiber passive elastic modulus was reduced compared to control fibers (53.00 kPa vs. 63.43 kPa). Fiber stiffness and slack sarcomere length were also reduced compared to control fibers and myosin heavy chain composition shifted from faster to slower isoforms. Average titin molecular weight increased 1.77% after treatment. Fiber bundle passive elastic modulus increased following treatment (168.83 kPa vs. 75.14 kPa). Bundle stiffness also increased while collagen content per mass of muscle tissue increased 38%. Injection of botulinum neurotoxin A produces an effect on the passive mechanical properties of normal muscle that is opposite to the changes observed in spastic muscles. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:497–502, 2012     

Botulinum neurotoxin A: A review

Despite its ubiquity in cosmetic circles and broad general awareness, a literature search of botulinum neurotoxin in JPRAS and BJPS yielded a mere 4 articles germane to cosmesis. A pair each detailing its application in masseteric hypertrophy(1,2) and the use of cryoanalgesia.(3,4) Given that botulinum neurotoxin A is the most commonly used cosmetic treatment, with American figures being most accurate,(5) a review of the background, development and scientific evidence would be perhaps useful, if not overdue, as Plastic Surgeons increasingly incorporate non-surgical interventions into their practices as part of a comprehensive facial rejuvenation strategy.     

Complications with the Use of Botulinum Toxin Type A in Facial Rejuvenation: Report of 8 Cases

The botulinum toxin A is produced by Clostridium botulinum and causes a reversible, selective muscle relaxation that leads to a temporary flattening of the mechanical component of wrinkling without the stigmata of invasive surgery. Since the end of the 1980s, this neurotoxin has been used to treat mimic facial lines with good results. Although this is considered a safe therapy, with adverse effects typically self-limited, more severe complications have been observed when it is used by nonskilled physicians or in improper dosages. This article reports eight patients treated with botulinum toxin A for aesthetic purposes who developed different complications. Treatment of the complication included the use of electrical stimulation, lymphatic drainage, antiinflammatory therapy, dipivefrine cloridrate drops, and other approaches. With specific treatment for each patient, the lengths of these complications seemed to be reduced.     

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.     

Current practices in the use of botulinum toxin A in the management of facial lines and wrinkles.

Botulinum toxin A (BTX-A) is a potent neurotoxin produced by the bacterium Clostridium botulinum. There are eight antigenically distinct serotypes, and they share a similar structure--a light chain with an associated molecule of zinc and a heavy chain linked by a disulfide bond. Each serotype has a separate site of action within the nerve ending. Only serotype A (Botox, Allergan, Irvine, CA) is available for clinical use in the United States.     

Bupivacaine-induced myotoxicity and its effect on botulinum toxin paresis

PURPOSE: To determine the effect of the coinjection of bupivacaine with botulinum toxin type A on the degree of muscular paralysis. Enhancement of paralysis could allow a decreased dose of neurotoxin treatment, thus reducing the risk for neutralizing antibody formation. METHODS: Prospective, randomized, double-blind study. Sixteen consecutive patients undergoing treatment of glabellar furrows received botulinum toxin A reconstituted with bupivacaine 0.75% to one corrugator muscle and botulinum toxin A reconstituted with nonpreserved normal saline to the contralateral muscle. Patients were evaluated on days 0 (injection day), 3, 7, 30, 60, and 90. Patients also completed a questionnaire each visit regarding their assessment of paralysis, asymmetry, and adverse effects. RESULTS: At 1 week after botulinum toxin A injection, 68.8% of the patients showed greater weakness on the bupivacaine-reconstituted side as opposed to 25.0% of patients showing greater weakness on the saline-reconstituted side. At 1 and 3 months, there was no statistical difference in weakness between the saline and the bupivacaine sides. The survey revealed that 56% of the patients had greater pain on the saline side, 31% on the bupivacaine side, and equal pain in 13%. CONCLUSIONS: Reconstituting botulinum toxin A with bupivacaine is safe, does not limit efficacy, and does not reduce the degree or relative duration of muscular paralysis. Reconstituting botulinum toxin A with bupivacaine results in faster onset of paresis, possibly due to a synergistic effect of bupivacaine induced myotoxicity. Utilizing bupivacaine may result in less pain for patients.     

Botulinum toxin for the treatment of lower urinary tract symptoms: a review

AIMS: To review the available literature on the application of botulinum toxin in the urinary tract, with particular reference to its use in treating detrusor overactivity (DO). METHODS: Botulinum toxin, overactive bladder (OAB), detrusor instability, DO, detrusor sphincter dyssynergia (DSD), and lower urinary tract dysfunction were used on Medline Services as a source of articles for the review process. RESULTS: DO poses a significant burden on patients and their quality of life. Traditionally patients have been treated with anti-cholinergic drugs if symptomatic, however, a significant number find this treatment either ineffective or intolerable due to side effects. Recent developments in this field have instigated new treatment options, including botulinum toxin, for patients' refractory to first line medication. Botulinum toxin, one of the most poisonous substances known to man, is a neurotoxin produced by the bacterium Clostridium botulinum. Botulinum toxin injections into the external urethral sphincter to treat detrusor sphincter dyssynergia has been successfully used for some years but recently its use has expanded to include voiding dysfunction. Intradetrusal injections of botulinum toxin into patients with detrusor overactivity and symptoms of the overactive bladder have resulted in significant increases in mean maximum cystometric capacity and detrusor compliance with a reduction in mean maximum detrusor pressures. Subjective and objective assessments in these patients has shown significant improvements that last for 9-12 months. Repeated injections have had the same sustained benefits. CONCLUSIONS: Application of botulinum toxin in the lower urinary tract has produced promising results in treating lower urinary tract dysfunction, which needs further evaluation with randomised, placebo-controlled trials.