Gastrointestinal botulism

Botulism. Clinical features include symmetric cranial neuropathies (i.e., drooping eyelids, weakened jaw clench, and difficulty swallowing or speaking), blurred vision or diplopia, symmetric descending weakness in a proximal to distal pattern, and respiratory dysfunction from respiratory muscle paralysis or upper airway obstruction without sensory deficits. Inhalational botulism would have a similar clinical presentation as food-borne botulism however, the gastrointestinal symptoms that accompany foodborne botulism may be absent. 

All botulin neurotoxins act in a similar way. They only differ in the amino-acid sequence of some protein parts (Prabakaran et al., 2001). Botulism symptoms are provoked both by oral ingestion and parenteral injection. Botulin toxin is not inactivated by enzymes present in the gastrointestinal tracts. Foodborne BoNT penetrates the intestinal barrier, presumably due to transcytosis. It is then transported to neuromuscular junctions within the bloodstream and blocks the secretion of the neurotransmitter acetylcholine. This results in muscle limpness and palsy caused by selective hydrolysis of soluble A-ethylmalemide-sensitive factor activating (SNARE) proteins which participate in fusion of synaptic vesicles with presynaptic plasma membrane. SNARE proteins include vesicle-associated membrane protein (VAMP), synaptobrevin, syntaxin, and synaptosomal associated protein of 25 kDa (SNAP-25). Their degradation is responsible for neuromuscular palsy due to blocks in acetylcholine transmission from synaptic terminals. In humans, palsy caused by BoNT/A lasts four to six months. 

Pulmonary Dyspnea CNS Cranial nerve deficits are universal Descending symmetric paralysis Gastrointestinal Constipation (later in course) OTHER FORMS OF BOTULISM ISOLATION/DECON PRECAUTIONS Droplet precautions Extensive precautions for laboratory personnel VACCINE Botulinum toxoid vaccine available but restricted in use to military and laboratory personnel. POSTEXPOSURE PROPHYLAXIS None... 

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. 

Amon, S. (1995). Botulism as an intestinal toxemia. In Infections of the Gastrointestinal Tract (M. Blaser, P. Smith, J. Ravdin, H. Greenberg, R. Guerrant, eds), pp. 257-71. Raven Press, New York. 

Amon, S.S. (1998). Infant botulism. In Textbook of Pediatric Infections of the Gastrointestinal Tract (R.D. Feigen, J.D. Cherry, eds). W.B. Saunders, Philadelphia. 

Ingestion is the primary exposure pathway for botulism. Wound botulism occurs when the bacterium encounters devitalized human tissue, synthesizes toxin, and thus causes disease. Intestinal (adult and infant types) botulism involves ingestion of spores or the live bacterium and, due to impaired intrinsic defenses, the gastrointestinal tract becomes colonized with Clostridium botulinum. In infant type, the mucosal surface of the intestines is susceptible to colonization due to multiple factors including decreased acidity of the stomach and lack of bile of acids, which are natural barriers. In adult-type intestinal botulism, patients have had surgical vagotomy/... 

Natural human botnlism, a relatively rare disease, occurs in four epidemiologic forms food-borne, infantile, wound, and adult botulism from intestinal colonization (38). None of these is transmissible person to person. All four forms result from absorption of the toxin into the bloodstream through the mucosa, such as the gastrointestinal tract or a wonnd. The toxin cannot penetrate intact skin, hi the United States, fewer than 200 cases of human botuhsm occur each year (36). 

The least common form of human botulism, botulism from intestinal colonization, includes cases in patients greater than 1 year of age not associated with ingestion of contaminated food or wound infection with the only possibility being intestinal colonization (38). Stool in these patients will contain toxin and C. botulinum, and the suspected food may contain spores without preformed toxin. Some cases occur in patients with a history of gastrointestinal surgery or inflammatory bowel disease, conditions that could support enteric colonization of B. botulinum (38). In 2001, in the United States, one case of adult colonization botulism occurred in a 45 year old who survived (39). 

Amon, S.S. 1995. Botulism as an intestinal toxaemia. In Infections ofthe Gastrointestinal Tract, eds. M.J. Blaser, P.D. Smith, J.L Ravdin, H.B. Greenberg, and R.L. Guerrant, 257-271 New York, NY Raven Press. 

Contact precautions are used to prevent contact with bacteria in wounds or infected gastrointestinal secretions. Botulism is not transmitted from human to human. 

Arnon, S., Schecter, R., Inglesby, T., et al., 2001. Botulinum toxin as a biological weapon. Medical and Public Health Management. JAMA 285, 1059-1070. Arnon, S.S., 1998. Infant botulism. In Feigen, R.D., Cherry, J.D. (Eds.), Textbook of Pediatric Infections of the Gastrointestinal Tract W.B. Saunders, Philadelphia. Bakry, N., Kamata, Y., Simpson, L., 1997. Expression of botulinum toxin binding sites in Xenopus oocytes. Infect. Immun. 65, 2225-2232. 

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