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Botulism treatment

Centers for Disease Control and Prevention (CDC). (2006), Botulism Treatment Overview for Clinicians. Atlanta, GA, Centers for Disease Control and Prevention, June 14. Last viewed October 10, 2006, http / www.bt.cdc.gov/agent/Botulism/clinicians/treatment.asp... [Pg.709]

The onset of botulism occurs generally between 18 and 36 hours after consumption of food products containing botulin toxin. However, it may affect patients earlier or later, even on the tenth day after food consumption. The first symptoms include stomach ache, nausea, vomiting, and diarrhea, followed by neurological disorders. Other symptoms include, skin, mouth and throat dryness, diplopia, blurred vision, dysphonia, dysarthria, dysphagia, and peripheral weakness. In lethal cases of botulism, respiratory muscles are involved. This leads to respiratory failure and death. Because all the symptoms are connected with toxemia, the first step of medical treatment is to provide a patient with antiserum. [Pg.201]

Botulism Botulism antitoxin, equine Consult the CDC.3 Treatment and prophylaxis of botulism. Available from the CDC.3 Ten to 20 percent incidence of serum reactions. [Pg.1410]

In 1991 the FDA approved the use of botulism toxin (BT) for the treatment of an "orphan" condition called blepharospasm. A victim of this syndrome will experience uncontrollable winking caused by spasms of the eyelid muscles. Use of botulism toxin will cause abatement of the symptoms in 90% of patients for 2 to 4 months. [Pg.74]

The history of the development of antitoxins in combating bacterial infection dates back to the early beginnings of organized bacteriology. Belrring was tile first to show that animals that were immune to diphtheria contained, in their serum, factors which were capable of neutralizing the poisonous effect of the toxins derived from the diphtheria bacillus. While this work was earned out in 1890, prior to many of the great discoveries of mass immunization, and much later the antibiotics, there yet remains a place for antitoxins in medical treatment or prophylaxis for some diseases, such as tetanus and botulism,... [Pg.141]

Botulism antitoxin, which binds and neutralizes toxin, is used in me treatment of botulism. [Pg.213]

The data about fields of application of Silics in clinics for treatment for infectious diseases are presented in Table 4. From Table 4 it is evident that the field of application of Silics is rather large and covers both intestinal infections and toxicoses which victimize infants, as well as viral hepatitis, and botulism. It is appropriate to mention here that inclusion of Silics into the complex treatment of patients suffering from salmonellosis, dysentery, and intestinal toxicoses accelerates normalization of clinic manifestations of these diseases by a factor of two and more. In the case of botulism the normalization of symptoms characteristic of lesions of the nervous system is shortened by almost 4 days. If intestinal infections are not severe, Silics can be recommended as a single therapeutic agent. In the case of a considerable diarrheal syndrome it is more expedient to use it together with rehydration substances. Inclusion of Silics into a complex of therapeutic agents for patients suffering from viral hepatitis substantially accelerates recovery rates of patients, so that their normal level of bilirubin and activity of alanine aminotranspherase are recovered within shorter periods of time. [Pg.197]

The mainstays of botulism therapy include ventilatory support as well as the administration of botulinum antitoxin. Botulinum antitoxin is a trivalent, equine antitoxin that provides antibodies to botulinum toxin Types A, B, and E. It acts only against unbound toxin and therefore its efficacy is greatest early in the patient s clinical course. Cathartics and enemas have also been recommended for elimination of botulinum toxin from the GI tract. Antibiotics are not recommended except for the treatment of secondary infectious complications... [Pg.410]

Sodinm nitrite is commonly utilized in food preservation. In spite of its known potential for metabolism to carcinogenic nitrosamines, nitrite snpplementation is still in widespread nse in nntrition because the addition of nitrite (plus a reducing agent such as ascorbate) has two desirable effects it imparts a red color to meats (primarily a result of the production of nitrosylheme from myoglobin ) and, perhaps more importantly, the organism responsible for botulism Clostridium botulinum) is exquisitely sensitive to this treatment. There is indeed a massive literature on the role of NO and its reactions in foods in the nutrition fields and is worthy of scrutiny by researchers in the biological effects of endogenously produced -NO in mammahan systems. [Pg.2993]

Gastrointestinal colonization in adults or children by clostridial bacteria does not typically take place except under circumstances where the normal flora has been altered by antibiotic treatment (Cheiington, 1998). Botulism results from in vivo production of toxin, analogous to the pathogenesis of infant botulism (McCroskey and Hatheway, 1988 Chia et al, 1986). Support for this form of botulism is provided by demonstration of prolonged excretion of toxin and C. botulinum in stool and/or by the demonstration of C. botulinum spores but not preformed toxin in suspected foods. [Pg.410]

The therapeutic indications for BoNTs are numerous. They are used in the treatment of ophthahnological disorders (strabismus, Duane s syndrome, esotropia/exotropia), movement disorders (focal dystonias, blepharospasm), spasticity, neiuomuscular disorders, pain (headache, myo-facial pain), disorders of the pelvic floor (anal fissures), ear/ nose/throat disorders, cosmetic applications (wrinkles), and hyperhidrosis. The recent explosion in new indications for BoNTs in the treatment of a wide range of medical conditions also brings the possibihty for medical errors in BoNT dosing. Systemic botulism may result from injection of excessive doses of the potent neurotoxin. The most infamous case of systemic botulism involved the paralysis of four Florida patients, including the doctor, treated with BoNTs for wrinkles. The physician used non-FDA approved formulations of type A from Toxin Research International,... [Pg.411]

The duration of muscle paralysis following intoxication by BoNT/A exceeds that resulting from exposure to other BoNT serotypes (Keller et ah, 1999 Robinson and Nahata, 2003 Femandez-Salas et ah, 2004). The remarkable persistence of BoNT/A action has led to its widespread use in the treatment of disorders of muscle tone and movement (Jankovic and Brin, 1997). Although a long duration is desirable in clinical use, the prolonged action of BoNT/A would also make intoxication by this serotype difficult to treat, particularly if used as a bioweapon (Franz, 1997). The duration of intoxication by BoNT/E is relatively brief (several weeks), whereas BoNT/B is of intermediate duration (Keller et ah, 1999 Blanes-Mira et ah, 2004). The basis for the differences in serotype persistence is currently unknown. In any case, a bioterrorist attack, involving the most lethal substance known to humankind, would overwhelm the limited resources (i.e. mechanical ventilators) available to treat botulism patients. [Pg.426]

The administration of heterologous antitoxin was one of the first therapeutic approaches developed for botuhsm patients and remains the most effective when initiated in the early stages of intoxication. The primary limitation of antitoxin treatment was established in some of the earhest published reports on experimental botuhsm. One of these reports evaluated the pathogenesis of oral intoxication and the efficacy of antitoxin therapy in monkeys (Back and Wood, 1928). Antitoxin treatment was not effective when administered after symptoms of botulism were already apparent, despite the fact that circulating toxin could still be detected in many of the animals. [Pg.426]

Lewis, G., Metzger, J. (1980). Studies on the prophylaxis and treatment of botulism. In Natural Toxins (D. Baker, T. Wad-strom, eds), pp. 601-6. Pergamon Press, New York. [Pg.430]

Bacteria are both harmful and beneficial. They degrade the waste-products produced by society. They are used in wastewater treatment plants— thus, they are beneficial. On the other hand, they can also be pathogenic. The bacteria. Salmonella typhosa, causes typhoid fever Shigella flexneri causes bacillary dysentery. Clostridium tetani excretes toxins producing tetanus. Clostridium botulinum excretes the toxin causing botulism. Corynebacterium diphtheriae is the agent for diphtheria. [Pg.167]

A pentavalent botulinum toxoid (botulinum toxin in different antigenic types) has been used for more than 30 years in some countries to prevent the disease in laboratory workers and to protect troops against attack. Pre-exposure immunization for the general population is neither feasible nor desirable the vaccine is ineffective for postexposure prophylaxis. Treatment of botulism consists of passive immunization and supportive care. Most licensed antitoxins contain antibodies against the most common toxin types A, B, and E. About 9% of recipients of equine antitoxin developed urticaria, serum sickness, or other hypersensitivity reactions. In 2% of recipients anaphylaxis occurred within 10 minutes of antitoxin... [Pg.3563]

Future important discoveries will be the identification of the neuron-specific receptors of CNTs and of the mode of internalization and membrane translocation of the neurotoxins. Another important line of research is aimed at finding specific inhibitors of these metallo-proteinases. Inhibitors which can cross the neuronal plasmalemma into the cytosol would be potential therapeutic agents in the treatment of tetanus and botulism. The modification of BoNTs to prolong their life time inside the NMJs would be an important research goal to improve the treatment of dystonias. The determination of the three-dimensional structure of these neurotoxins will greatly accelerate the research on these fronts. [Pg.186]

Chemical Abstracts Service Registry Number CAS 93384-43-1. Botulinum toxins comprise a series of seven related protein neurotoxins that prevent fusion of synaptic vesicles with the presynaptic membrane and thus prevent release of acetylcholine. Exposure in a battlefield or terrorist setting would most likely be to inhaled aerosolized toxin. The clinical presentation is that of classical botulism, with descending skeletal muscle weakness (with an intact sensorium) progressing to respiratory paralysis. A toxoid vaccine is available for prophylaxis, and a pentavalent toxoid can be used following exposure its effectiveness wanes rapidly, however, after the end of the clinically asymptomatic latent period. Because treatment is supportive and intensive (involving long-term ventilatory support), the use of botulinum toxin has the potential to overwhelm medical resources especially at forward echelons of care. [Pg.276]

Plague pneumonia is almost always fatal if treatment is not initiated within 24 hours of the onset of symptoms. A number of readily available, broad-spectrum antibiotics have shown efficacy. Specific broad-spectrum antibiotics are also recommended for post-exposure treatment against tularemia and Q fever. A licensed trivalent equine antitoxin available from CDC is the only approved therapy for airborne botulism. [Pg.116]


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