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PubMed2006

Botulism: the challenge of diagnosis and treatment.

Botulism is a rare paralytic disease caused by a neurotoxin produced from the spore-forming bacterium Clostridium botulinum and in rare cases Clostridium butyricum and Clostridium baratii. Botulism has 4 naturally occurring syndromes: foodborne, wound, infant botulism, and adult intestinal toxemia. Inhalational botulism could result from aerosolization of botulinum toxin, and iatrogenic botulism can result from injection of toxin. All of these produce the same clinical syndrome of symmetrical cranial nerve palsies followed by descending, symmetric flaccid paralysis of voluntary muscles, which may progress to respiratory compromise and death. Treatment includes meticulous intensive care that includes mechanical ventilation, when necessary, and administration of antitoxin.

Botulinum Toxins↗
PubMed1991

[Botulism in the Czech Republic].

In a retrospective study the authors analyzed 76 cases of botulism reported in 1961-1989 in the Czech Republic. The analysis of descriptive data pertained to the annual incidence of botulism with a maximum of cases in 1966, 1973 and 1984 (11, 7 and 6 cases); geographical distribution with a maximum incidence in the South and Central Bohemian region (100,000 population); age distribution with a predominance in subjects above 15 years. The dominating vehicle of botulism was in 61% of the notified cases a home-prepared food; usually a galantine, aspic, liver paste, pork with vegetables, and smoked pork. In 1966 and 1973 a processed food predominated as vehicle: pickled herring and tomato, red peppers and sausage. The results of the retrospective study were compared in the discussion with the problem of botulism in other countries. The authors discuss the danger of undetected botulism and the necessity of an anti-botulin serum (Bossea).

Adolescent↗
PubMed1980

Infant botulism: clinical spectrum and epidemiology.

Between 1977 and 1979, 12 cases of infant botulism were diagnosed in Utah, and 87 control patients (normal, nonbotulism neurologic disease, and nonbotulism systemic disease) were evaluated. Observations from these patients suggest an expanded clinical spectrum of infant botulism including asymptomatic carriers of organism; mild hypotonia and failure to thrive; typical cases with constipation, bulbar weakness, and hypotonia; and children with a picture compatible with sudden infant death syndrome. Clostridium botulinum was isolated from the stools of three normal control infants and nine control infants who had neurologic diseases that were clearly not infant botulism. These infants were termed "asymptomatic carriers" of the organism. The occurrence of the asymptomatic carrier state suggests that a diagnosis of infant botulism cannot be made on a basis of culture results alone, but must rest in historical documentation and physical confirmation of progressive bulbar and extremity weakness with ultimate complete resolution of symptoms and findings over a period of several months. A common set of environmental features characterizes the home environment of children with infant botulism and "asymptomatic carriers" and includes: nearby constructional or agricultural soil disruption, dusty and windy conditions, a high water table, and alkaline soil conditions.

Botulinum Toxins↗
PubMed2006

[Sarcoidal granulomas following injections of botulic toxin A (Botox) for corrections of wrinkles].

BACKGROUND: The introduction of foreign material into the skin can lead to sarcoidal reactions. Such a reaction is reported, consecutive to injections of botulic toxin A (Botox). CASE REPORT: A 57-year-old woman, noticed the occurrence of frontal and glabellar nodules, 3 weeks after the injection of botulic toxin A (Botox), for the correction of wrinkles. Histopathological examination revealed a sarcoidal granuloma. Clinical and biological investigations were negative, ruling out the hypothesis of systemic sarcoidosis. The lesion could be reproduced experimentally by an intradermal injection of botulic toxin A on the volar aspect of the forearm. Corticosteroids per os associated with intralesional injections of triamcinolone acetonide were followed by a complete regression of the nodules. DISCUSSION: The occurrence of sarcoidal granulomas at the sites of injection of botulic toxin A (Botox(R)) has not been reported - so far - in the literature. Systemic sarcoidosis has been ruled out. The sarcoidal reaction has been reproduced experimentally by the intradermal injection of botulic toxin A, but not by saline. This leads to think that the sarcoidal reaction was provoked by antigenic stimulation, comparable to the Kveim reaction, and did not correspond to "scar sarcoidosis".

Botulinum Toxins, Type A↗
PubMed2000

AAEM case report 16. Botulism. American Association of Electrodiagnostic Medicine.

Early diagnosis of botulism is essential for effective treatment. Electrophysiologic testing can be of major help to establish a prompt diagnosis, but the classic electrodiagnostic features of botulism are often elusive. Decrement or increment of compound muscle action potential (CMAP) amplitudes to slow or fast rates of nerve stimulation are often unimpressive or totally absent. Reduction of CMAP amplitudes, denervation activity, or myopathic-like motor unit potentials in affected muscles are found more frequently but they are less specific. In general, the electrophysiologic findings taken together suggest involvement of the motor nerve terminal, which should raise the possibility of botulism. The case reported here illustrates a common clinical presentation of botulism. This study emphasizes realistic expectations of the electrodiagnostic testing, the differential diagnosis, and the potential pitfalls often encountered in the interpretation of the electrophysiologic data.

Adult↗
PubMed2004

Historical notes on botulism, Clostridium botulinum, botulinum toxin, and the idea of the therapeutic use of the toxin.

Food-borne botulism probably has accompanied mankind since its beginning. However, we have only few historical sources and documents on food poisoning before the 19th century. Some ancient dietary laws and taboos may reflect some knowledge about the life-threatening consumption of poisoned food. One example of such a dietary taboo is the 10th century edict of Emperor Leo VI of Byzantium in which manufacturing of blood sausages was forbidden. Some ancient case reports on intoxications with Atropa belladonna probably described patients with food-borne botulism, because the combination of dilated pupils and fatal muscle paralysis cannot be attributed to an atropine intoxication. At the end of the 18th century, some well-documented outbreaks of "sausage poisoning" in Southern Germany, especially in Württemberg, prompted early systematic botulinum toxin research. The German poet and district medical officer Justinus Kerner (1786-1862) published the first accurate and complete descriptions of the symptoms of food-borne botulism between 1817 and 1822. Kerner did not succeed in defining the suspected "biological poison" which he called "sausage poison" or "fatty poison." However, he developed the idea of a possible therapeutic use of the toxin. Eighty years after Kerner's work, in 1895, a botulism outbreak after a funeral dinner with smoked ham in the small Belgian village of Ellezelles led to the discovery of the pathogen Clostridium botulinum by Emile Pierre van Ermengem, Professor of bacteriology at the University of Ghent. The bacterium was so called because of its pathological association with the sausages (Latin word for sausage = "botulus") and not-as it was suggested-because of its shape. Modern botulinum toxin treatment was pioneered by Alan B. Scott and Edward J. Schantz.

Animals↗
PubMedDate not supplied

Botulism as a cause of respiratory failure in injecting drug users.

BACKGROUND: Wound botulism occurs as a consequence of inoculation of Clostridium botulinum spores into a wound. AIM: To describe such a case of wound botulism. RESULTS: A 23-year-old drug-injecting user presented with bulbar symptoms and progressive signs over a three-day period. The diagnosis of botulism was suspected and was treated with large doses of penicillin and botulinum antitoxin. The diagnosis was confirmed by the presence of serum botulinum toxin A. CONCLUSION: Physicians should be aware of the association of botulism in injecting drug users, particularly in Ireland.

Adult↗
PubMed2001

Two cases of foodborne botulism type E and review of epidemiology in France.

In 1999, two new cases of type E botulism were observed in French hospitals. Since this type of botulism is uncommon in France, the cases prompted a national epidemiological study. Sixteen cases of type E botulism, including the two cases reported here, occurred between 1952 and 1999. The clinical and treatment characteristics of all cases were evaluated, and the results suggest that, despite its rarity, type E botulism should be considered by clinicians in France. Changes in the eating habits of people in France, as in the rest of Europe, with the increased consumption of vacuum-packed fish from endemic areas and decreased consumption of local foodstuffs, could explain the occurrence of the most recent cases.

Adult↗
PubMed1984

Equine antitoxin use and other factors that predict outcome in type A foodborne botulism.

The use of trivalent equine antitoxin in treating foodborne botulism has not been adequately assessed. One hundred thirty-two cases of type A foodborne botulism reported to the Centers for Disease Control in the period from 1973 to 1980 are reviewed to evaluate the effect of antitoxin therapy and other factors on the outcomes of patients with botulism. The fatality rates were higher in patients over 60 years old and in those who were index patients (the first or only patient in an outbreak). The clinical course was longer in patients over 60 years old, patients whose incubation period was less than 36 hours, and index patients. Patients who had received trivalent equine antitoxin had a lower fatality rate and a shorter course than those who did not receive antitoxin, even after controlling for age and incubation period. Patients who received antitoxin in the first 24 hours after onset had a shorter course but about the same fatality rate as those who received antitoxin later. These results suggest that trivalent antitoxin has a beneficial effect on survival and shortens the course of patients with type A botulism.

Age Factors↗
PubMed1989

Histological examination of the central nervous system in the diagnosis of botulism.

Type C botulinum toxin was given to mice by mouth or intraperitoneal injection. The central nervous system (CNS) of control and affected mice was examined by histological methods such as would be used in a field investigation of botulism. The only change definitely associated with intoxication was microscopic haemorrhage and vascular engorgement; other changes were considered incidental or artefactual. The results are discussed in the light of other descriptions of botulism in animals. It is concluded that non-specific petechiation and vascular engorgement sometimes occur in the CNS in botulism but that the only way routine histology may support a diagnosis of botulism is by exclusion of other diseases.

Administration, Oral↗
PubMed2005

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.

Acute Disease↗
PubMed2005

Recent advances in infant botulism.

Since infant botulism was first identified three decades ago, our understanding of botulinum toxins and the organisms that produce them has grown. A newer classification system now recognizes Clostridium baratii and Clostridium butyricum along with Clostridium botulinum as causative agents. Recently, increasing therapeutic use of botulinum toxins has sparked substantial new research into their mechanisms of action. This research, and some case reports from infants sickened by unusual botulinum toxins suggest that disease caused by different toxin types may result in varying clinical presentations. Perhaps most significantly for pediatricians and child neurologists, a specific treatment for infant botulism has just been approved. This article reviews the clinical presentation, diagnosis, and treatment of infant botulism, including human botulism immune globulin, and discusses the various organisms and toxins that cause this disease.

Bacterial Proteins↗
PubMed1979

Honey and other environmental risk factors for infant botulism.

Infant botulism results from the in vivo production of toxin by Clostridium botulinum after it has colonized the infant's gut. Epidemiologic and laboratory investigations of this recently recognized disease were undertaken to identify risk factors and routes by which C. botulinum spores might reach susceptible infants. Clostridium botulinum organisms, but no preformed toxin, were identified in six different honey specimens fed to three California patients with infant botulism, as well as from 10% (9/90) of honey specimens studied. By food exposure history, honey was significantly associated with type B infant botulism (P = 0.005). In California, 29.2% (12/41) of hospitalized patients had been fed honey prior to onset of constipation; worldwide, honey exposure occurred in 34.7% (28/75) of hospitalized cases. Of all food items tested, only honey contained C. botulinum organisms. On household vacuum cleaner dust specimens and five soil specimens (three from case homes, two from control homes) contained Clostridium botulinum. The known ubiquitous distribution of C. botulinum implies that exposure to its spores is universal and that host factors contribute importantly to the pathogenesis of infant botulism. However, honey is now an identified and avoidable source of C. botulinum spores, and it therefore should not be fed to infants.

Botulism↗
PubMed1994

Wound botulism.

Wound botulism is a rare infectious and toxicologic complication of trauma and i.v. drug abuse. Only 39 cases have been reported in detail in the English literature. This case report describes a patient with wound botulism who presented to four medical facilities before receiving definitive diagnosis and treatment. Although his history and physical examination were consistent with wound botulism, diagnosis and therapy were delayed because this rare disease was not considered initially in the differential diagnosis. Wound botulism should be considered in trauma patients and i.v. drug abusers who present with cranial nerve palsies and descending paresis.

Abscess↗
PubMed2001

Wound botulism associated with black tar heroin and lower extremity cellulitis.

Wound botulism is a rare and potentially fatal disease. The use of black tar heroin has spawned an increase in the incidence of the disease, with the majority of cases occurring in California. The use of botulism antitoxin and surgical debridement are recommended to decrease hospital stay. For this to be effective, the diagnosis of wound botulism first must be considered, followed by an aggressive search for any area of infection that may be debrided. This case report demonstrates several factors to consider in patients presenting with symptoms of botulism poisoning: occurrence away from the Mexico border, no obvious abscess, and the need for prolonged ventilatory support. This case report documents a prolonged hospital stay, possibly caused by delay in administration of antitoxin in a patient with cellulitis that was not considered appropriate for debridement.

Botulism↗
PubMed2001

Botulism in the horse.

Botulism should be considered in cases where weakness, paralysis, or intolerance to exercise might be seen in the horse. Dysphagia may also be present, although it is not a consistent finding. Potential sources include carrion in hay, moldy or otherwise rotted vegetation or forage, birds carrying material from animal burial or other similar sites, and contaminated carcasses on-site. Horses, especially foals, may also suffer from toxicoinfectious botulism, a condition where the C. botulinum might colonize and produce toxin within the gastrointestinal tract. Wounds also may harbor the organism and otherwise promote botulism. Diagnosis of botulism is often a clinical diagnosis backed up by elimination of other possible infectious, injurious, or toxic causes of weakness of the horse. Definitive diagnosis and type identification in the laboratory are difficult and usually require a suitable sample of the source material. Treatment often is unrewarding unless a case is identified early and the proper antitoxin is readily available. Prevention involves common sense approaches to feeding and care of the horse and, where possible, judicious use of vaccination in endemic areas.

Animals↗
PubMed1997

[Importance of electromyography in the diagnosis of botulism].

Botulism is a cause of neuromuscular transmission impairment. We report here an electrophysiological study of the neuromuscular junction in a patient presenting with botulism. Repetitive stimulation of a motor nerve showed a characteristic triad, indicating presynaptic block of neuromuscular transmission: the muscle action potential amplitude was low; repetitive high frequency stimulation (20 Hz) induced a more than 100% increment in the amplitude; low frequency repetitive stimulation (3 Hz) induced a more than 10% decrement in the amplitude. Progressive clinical improvement spontaneously occurred and the electrophysiological control recording that was done 1 month later was normal. Botulism toxin reduces acetylcholine quanta released in the autonomic and neuromuscular junction, causing presynaptic block. Electrophysiological recordings associated with clinical data contributed more to the diagnosis of botulism than serological analysis, which remained negative in this patients.

Adolescent↗
PubMed1992

A recent reminder of botulism.

Botulism is a rare yet potentially common form of food poisoning that can be fatal. (1) Few documented cases of botulism exist in Australia (2,3,4) and New Zealand (5), emphasising how infrequently it is encountered. The recent admission to our Intensive Care Unit (ICU) of a man suspected of having botulism was a timely reminder of just how dangerous this condition can be. This paper will review the contemporary knowledge and interventions necessary in the management of botulism. It will also utilise anecdotes from our recent experience to illustrate some of the clinical scenarios and potentially fatal complications seen in this condition.

Australia↗