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BotulismDiagnosisThe occurrence of an epidemic of afebrile patients with progressive symmetrical descending flaccid paralysis strongly suggests botulinum intoxication. Foodborne outbreaks tend to occur in small clusters and have never occurred in soldiers on military rations such as MREs (Meals, Ready to Eat). Higher numbers of cases in a theater of operations should raise at least the consideration of a BW` attack with aerosolized botulinum toxin. Individual cases might be confused clinically with other neuromuscular disorders such as Guillain-Barre syndrome, myasthenia gravis, or tick paralysis. The edrophonium or Tensilon® test may be transiently positive in botulism, so it may not distinguish botulinum intoxication from myasthenia. The cerebrospinal fluid in botulism is normal and the paralysis is generally symmetrical, which distinguishes it from enteroviral myelitis. Mental status changes generally seen in viral encephalitis should not occur with botulinum intoxication. It may become necessary to distinguish nerve agent and/or atropine poisoning from botulinum intoxication. Nerve agent poisoning produces copious respiratory secretions, miotic pupils, convulsions, and muscle twitching, whereas normal secretions, mydriasis, difficulty swallowing, and progressive muscle paralysis is more likely in botulinum intoxication. Atropine overdose is distinguished from botulism by its central nervous system excitation (hallucinations and delirium) even though the mucous membranes are dry and mydriasis is present. The clinical differences between botulinum intoxication and nerve agent poisoning are depicted in Appendix H. Laboratory testing is generally not critical to the diagnosis of botulism. Mouse neutralization (bioassay) remains the most sensitive test, and serum samples should be drawn and sent to a laboratory capable performing of this test. PCR might detect C. botulinum genes in an environmental sample. Detecting toxin in clinical or environmental samples is sometimes possible by ELISA or ECL. Clinical samples can include serum, gastric aspirates, stool, and respiratory secretions. Survivors do not usually develop an antibody response due to the very small amount of toxin necessary to produce clinical symptoms. Exposure does not confer immunity.
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