[Factors affecting the seeding of the causative agents of botulism in raw and preserved foods].
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Clostridium botulinum↗
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[Change in the level group B vitamins during the cultivation of the causative agent of types A and B botulism].
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Botulinum Toxins↗
[The effect of various amino acids on growth and toxin formation by the agents of botulism types A, B, C and E and their toxins].
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Amino Acids↗
[Development of new generation of vaccine against pertussis, cholera, botulism, tetanus, and diphtheria toxins].
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Bacterial Toxins↗
[Bilateral laryngeal movement disorder and synkinesia: value of botulism toxin. Apropos of a case].
Several years after a subtotal thyroidectomy complicated by bilateral vocal cord paralysis, the patient presented with progressive dyspnea due to laryngeal synkinesis. The impairement of the ventilation status, in spite of laser arytenoidectomy, followed by contralateral posterior transverse cordotomy, suggested a botulinum toxin injection in the intrinsic adductor laryngeal muscles. The rapid improvement in ventilation without phonatory impairement is discussed in the following report.
Adult↗
[Botulinum toxin: from poison to drug. A historical review].
Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning. The first case of botulism is believed to have occurred in 1735. An epidemic in Southern Germany in 1793 claimed the death of over the half of those patients who had become ill through eating uncooked blood sausages. The term "pharmakon" is Greek and implicates that a drug originates from poison (potion, remedy). Theophrastus Bombast von Hohenheim known as Paracelsus (1493/94-1541) first described this duality with his dictum "alle ding sind gift und nichts on gift; alein die dosis macht das ein ding kein gift ist" (only the dose makes a remedy poisonous). In Baden-Württemberg in 1817, the poet and physician Dr. Justinus Christian Kerner described the symptoms of botulism, so that at this time botulism was also called Kerner disease. Until the turn of the century the reason for poisoning was not known. Van Ermengem succeeded in isolating the anaerobic bacterium causing botulism, but the specific mechanism of BTX was only established after the second World War. In the late seventies the ophthalmologist Dr. Alan Scott used BTX the first time in the treatment of strabismus. The drug was then used in the treatment of several muscle spasticities such as, for example, torticollis or hemifacial spasm. Only recently BTX has been successfully used for focal hyperhidrosis. We review the history of botulinum toxin from its discovery in the nineteenth century and the research into its effect in the middle of the 20th century up to its clinical use at the present time.
Botulinum Toxins↗
Improved selective medium for the isolation of lipase-positive Clostridium botulinum from feces of human infants.
Isolation of lipase-positive Clostridium botulinum from fecal specimens establishes the diagnosis of infant botulism, contributes to the diagnosis of food-borne botulism, and is most easily accomplished by use of selective media. Modification of an available selective medium, C. botulinum inhibitory medium (CBI), enabled more rapid isolation of C. botulinum. The modified medium (botulinum selective medium [BSM] contained (per liter) 25 g of dehydrated heart infusion broth, 20 g of agar, 30 ml of egg yolk suspension, 250 mg of cycloserine, 76 mg of sulfamethoxazole, 4 mg of trimethoprim, and 100 IU of thymidine phosphorylase at pH 7.4. The two media were compared by using 15 fresh fecal specimens from infant botulism patients (10 type A and 5 type B) and a C. botulinum isolate that had been obtained from an infant botulism patient and that was mixed into a fresh stool specimen from a healthy human infant. In comparison to CBI, BSM always provided better suppression of the nonbotulinum fecal flora and earlier emergence of lipase-positive colonies. Diagnosis of infant botulism was accomplished sooner with BSM than with CBI because isolation of lipase-positive C. botulinum was easier.
Botulism↗
Botulin toxin: a weapon in terrorism.
Clostridium botulinum, the causative agent of botulism is an anaerobic, spore forming gram-positive bacillus. C. botulinum causes three types of botulism; foodborne botulism, wound botulism, and infant botulism. Most strains of the bacterium produce a potent, muscle-paralyzing neurotoxin. Respiratory failure secondary to paralysis of the respiratory muscles can lead to death unless appropriate therapy is promptly initiated. Due to the severity and potency of this neurotoxin, its importance as a biological weapon is of major concern to public health officials.
Bioterrorism↗
Occurrence of toxigenic Clostridium botulinum type C in the soil of wetlands in Saskatchewan.
Mouse-lethal toxin identified as that of Clostridium botulinum type C by antitoxin neutralization was present in cultures of 38.0% of 326 soil samples collected from 28 wetlands in Saskatchewan. There was no difference in prevalence of toxicity between samples collected in spring and summer, and no relationship was evident between the occurrence of toxicity and water salinity, marsh type or water depth. There was a strong association between the prior occurrence of avian botulism in a marsh and the presence of toxin in cultures from soil; 59.2% of soil samples from marshes with a known history of botulism produced toxin, whereas only 6.2% of soil samples from marshes with no history of the disease produced toxin. Eight of the 10 soil samples collected from a marsh that had been dry for several years, and from another marsh that had not had a recognized outbreak of botulism for 11 yr produced toxin, indicating a long residual effect after a botulism outbreak. The results suggest that any wetland with a history of botulism is likely to suffer repeated occurrences because of heavy contamination of the soil with spores, and should be managed to control the disease.
Botulinum Toxins↗
Botulinum toxin.
Botulinum toxin is regarded as the most lethal substance known. It is estimated that the human LD50 for inhalation botulism is 1 to 3 nanograms of toxin/kilogram body mass. Although only three cases of inhalational botulism have been described, an understanding of the pathophysiology of food-borne outbreaks, wound botulism, and infant botulism, and their therapies, enables the medical community to plan treatment in the event of an aerosol release of botulinum toxin. Antitoxin, vaccine, and F(ab')2 immune fragment therapies are discussed as adjuncts to supportive therapy.
Bioterrorism↗
Descending polyneuropathy in an intravenous drug user.
A 27-year-old male intravenous drug user presented to the Emergency Department of St James's Hospital with a 1-week history of progressive dysphasia, dysphagia and difficulty 'holding his head up' and 'keeping his eyes open'. He also complained of increasing weakness in his upper limbs, as a result of which he kept dropping things. He was on a methadone program but was using both intravenous heroin and cocaine at the time of presentation. Examination of his motor function revealed generalized hypotonia, hyporeflexia and reduced power in both upper limbs. No sensory loss was observed. Co-ordination was intact. The clinical picture of a proximal symmetrical descending weakness and an absence of sensory loss was suggestive of botulism. Clostridium botulinum is a spore-forming, obligate anaerobe. The three forms of human botulism are food-borne, wound and intestinal. A fourth man-made form is produced from aerosolized botulinum toxin and results in inhalational botulism. A little as 1 g of aerosolized botulinum toxin has the potential to kill 1.5 million people. Toxin is detected in serum or stool specimens in only approximately 46% of clinically diagnosed cases. Treatment involves supportive care and early passive immunization with equine antitoxin. Patients should be regularly assessed for loss of gag and cough reflex, control of oropharyngeal secretions, oxygen saturation, vital capacity and inspiratory force. When respiratory function begins to deteriorate, anticipatory intubation is indicated. Early symptom recognition and early treatment with antitoxin are essential in order to prevent mortality, and to prevent additional cases, it is important to ascertain the presence of similar symptoms in contacts of the patient and local public health officials must be notified as one case may herald an outbreak. Given the continued threat of bioterrorism, the Centre for Disease Control Surveillance System in the United States must also be notified of any cases of botulism.
Adult↗
Clostridium botulinum: an increasing complication of heroin misuse.
Wound botulism is a rare infectious disease due to neurotoxin release from the anaerobic, spore-forming bacterium Clostridium botulinum that is becoming an ever more frequent complication of parenteral drug abuse in the Western world. Before the year 2000, no such cases had been reported in the UK and Ireland, but since then the number of proven and suspected cases of wound botulism occurring in parenteral drug users has increased markedly. The diagnosis is often difficult, based on a high degree of clinical suspicion and if not considered in the initial differential diagnosis, then considerable delays in treatment may result. This is the case report of a male heroin user who presented three times to an Emergency Department in the UK before a diagnosis of wound botulism was made and treatment commenced. It is important that emergency clinicians are aware of the possibility of wound botulism in parenteral drug users that present with unusual neurological or respiratory symptomatology.
Adult↗
Clostridium botulinum and the safety of minimally heated, chilled foods: an emerging issue?
Foodborne botulism is caused by consumption of preformed botulinum neurotoxin, with as little as 30 ng of neurotoxin being potentially lethal. Consumption of minute quantities of neurotoxin-containing food can result in botulism. In view of the severity of foodborne botulism, it is essential that new foods be developed safely without an increase in incidence of this disease. Minimally heated, chilled foods are a relatively new type of food, sales of which are currently increasing by about 10% per annum. These products meet consumer demand for high-quality foods that require little preparation time. Their safety and quality depends on mild heat treatment, chilled storage, restricted shelf life and sometimes on intrinsic properties of the foods. The principal microbiological hazard is nonproteolytic Clostridium botulinum, and there is a concern that this may become an emerging issue. A considerable amount of research and development over the last 15 years has underpinned the safe production of commercial, minimally heated, chilled foods with respect to foodborne botulism, and it is essential that safe food continues to be developed. In particular, the desire to use lighter heat processes and a longer shelf life presents a challenge that will only be met by significant developments in quantitative microbiological food safety.
Botulism↗
Watershed issues associated with Clostridium botulinum: a literature review.
Botulism the disease, the related organism (Clostridium botulinum) and toxin have gained renewed attention in these times of heightened homeland security and bioterrorism preparedness. Since C. botulinum is ubiquitous in nature, botulism outbreaks resulting from environmental exposure can be of concern to watershed managers and drinking water utilities. This paper reviews aspects of naturally occurring C. botulinum in light of concerns for source water watersheds. Information regarding sources and occurrence of botulism, C. botulinum and botulism toxins are discussed. Ecology and physiology of environmental C. botulinum and cycles of disease are reviewed. Finally, the effectiveness of water treatment and disinfection measures is discussed.
Animals↗
Ability of physicians to diagnose and manage illness due to category A bioterrorism agents.
BACKGROUND: Early recognition of a terrorist attack with biologic agents will rely on physician diagnosis. Physicians' ability to diagnose and care for patients presenting after a bioterror event is unknown. The role of online case-based didactics to measure and improve knowledge in the diagnosis and treatment of these patients is unknown. METHODS: A multicenter online educational intervention was completed by 631 physicians at 30 internal medicine residency programs in 16 states and Washington, DC, between July 1, 2003, and June 10, 2004. Participants completed a pretest, assessing ability to diagnose and manage potential cases of smallpox, anthrax, botulism, and plague. A didactic module reviewing diagnosis and management of these diseases was then completed, followed by a posttest. Pretest performance measured baseline knowledge. Posttest performance compared with pretest performance measured effectiveness of the educational intervention. Results were compared based on year of training and geographic location of the residency program. RESULTS: Correct diagnoses of diseases due to bioterrorism agents were as follows: smallpox, 50.7%; anthrax, 70.5%; botulism, 49.6%; and plague, 16.3% (average, 46.8%). Correct diagnosis averaged 79.0% after completing the didactic module (P<.001). Correct management of smallpox was 14.6%; anthrax, 17.0%; botulism, 60.2%; and plague, 9.7% (average, 25.4%). Correct management averaged 79.1% after completing the didactic module (P<.001). Performance did not differ based on year of training (P = .54) or geographic location (P = .64). Attending physicians performed better than residents (P<.001). CONCLUSIONS: Physician diagnosis and management of diseases caused by bioterrorism agents is poor. An online didactic module may improve diagnosis and management of diseases caused by these agents.
Anthrax↗
Intestinal infection and toxin production by Clostridium botulinum as one cause of sudden infant death syndrome.
The spontaneous production of botulinum toxin in the infant gut by ingested Clostridium botulinum organisms is the underlying cause of infant botulism, recognised as an infectious disease only in late 1976. Because of the recognition of the pathophysiology of this disease and because the known potency and action of botulinum toxin can lead to rapid respiratory arrest, it appeared possible that the in-vivo production of botulinum toxin could cause the sudden death of some infants. To test this hypothesis, serum, selected tissues, and bowel contents from 280 dead infants were examined for the presence of C. botulinum toxin and/or organsisms. We found C. botulinum organisms in 10 infants, all of whom died suddenly and unexpectedly. 9 of these deaths were classified by the forensic pathologist as sudden infant death syndrome (S.I.D.S. or crib death). In 2 of these 10 sudden deaths both C. botulinum organisms and botulinum toxin were identified, and from the spleen of 1, C. botulinum organisms were isolated. Faecal specimens from 160 age-matched healthy infants who served as controls in studies of inpatient infant botulism cases were negative for both C. botulinum organisms and toxin, except for one specimen that contained only C. botulinum type A organisms. The 9 S.I.D.S. cases with evidence of C. botulinum infection comprised 4.3% of the 211 S.I.D.S. cases examined over 12 months. These findings suggest that intestinal production of botulinum toxin by C. botulinum is one cause of S.I.D.S. The strikingly similar age-distribution of 62 inpatient infant botulism cases and the 211 S.I.D.S. cases is also consistent with this concept. The possibility that in-vivo production of botulinum toxin may account for a larger proportion of S.I.D.S. cases is discussed.
Botulinum Toxins↗
Bacterial meningitis and diseases caused by bacterial toxins.
Bacterial meningitis most commonly occurs in young calves secondary to septicemia. Clinical signs of hyperirritability are usually seen. Meningitis can be confirmed by cerebrospinal fluid analysis and culture or by necropsy. Intoxications by the exotoxins of Clostridium perfringens types C and D, C. botulinum, and C. tetani are difficult to confirm. The clinical signs of these intoxications vary from flaccid paralysis (botulism) to muscular rigidity (tetanus). Treatment of affected cattle has been unrewarding in botulism and enterotoxemia, whereas early aggressive treatment of tetanus cases can often be successfully resolved. Botulism and enterotoxemia can be proved using mouse inoculation tests, whereas tetanus is diagnosed largely by ruling out other diseases.
Animals↗
Detection of Clostridium botulinum types C and D toxin by ELISA.
An ELISA to detect Clostridium botulinum type D toxin was developed using polyclonal antibodies to a semi-purified toxic complex of the neurotoxin. Sensitivity of the ELISA for detecting type C and type D toxin compared with mouse inoculation was 70% and specificity 96% on samples from animals with botulism diagnosed on clinical signs and herd history. However, both mouse inoculation and the ELISA failed to detect toxin in many animals with a presumptive diagnosis of botulism. Some cross-reaction was seen with Clostridium novyi type A, but not with other clostridial species. While the ELISA described here cannot replace mouse inoculation for the diagnosis of botulism, it is a useful additional test.
Animals↗