OPHEPR; Botulism - Profile for Healthcare Workers

Causative Agent: A group of seven related toxins produced by the bacillus, Clostridium botulinum. The seven distinct toxins (A through G) are produced by different strains of the bacillus.

Routes of Exposure: Inhalation, oral (infant botulism and wound botulism are not included in the discussion below)

Toxic Dose: 1 ng/kg (for type A toxin)

Incubation Period: Neurologic symptoms of foodborne botulism generally begin 12-36 hours after ingestion. Neurologic symptoms of inhalational botulism generally begin 24-72 hours after aerosol exposure. However, the incubation period for both can range from 6 hours to 10 days.

Clinical Effects: Acute, afebrile, symmetric descending paralysis. Botulinum toxins are neurotoxins that act to prevent the release of acetylcholine presynaptically and thus block neurotransmission. Multiple cranial nerve palsies are often the first symptoms seen. Bulbar palsies are prominent early, with eye symptoms such as blurred vision due to mydriasis, diplopia, ptosis and photophobia, in addition to other bulbar signs such as dysarthria, dysphonia, and dysphagia. Skeletal muscle paralysis follows with a symmetrical descending and progressive weakness, which may culminate abruptly in respiratory failure. Deep tendon reflexes may be present or absent.

Lethality: The mortality rate from botulism is 60% if the patient goes untreated and less than 5% if the patient receives appropriate treatment. All the botulinum toxins are slightly less toxic when exposure is by the pulmonary route.

Transmissibility: Botulinum toxin cannot be transmitted person-to-person.

Primary Contaminations & Methods of Dissemination: The use of botulinum toxin as a biological weapon would likely be by aerosolization, or by intentional contamination of food or water supplies.

Secondary Contamination & Persistence of Organism: The toxin does not penetrate intact skin. C. botulinum spores can persist in the environment, and wound botulism can result when an open wound is contaminated.

Decontamination & Isolation:

Patients – Patients can be managed using standard precautions. No decontamination is necessary following foodborne exposure. Following aerosol exposure to botulinum toxin, skin should be rinsed with soap and water.
Equipment, clothing & other objects – A 0.5% hypochlorite solution (1 part household bleach + 9 parts water = 0.5% solution) applied for 10 to 15 minutes and/or soap and water should be used for environmental decontamination. Clothing should be washed with soap and water.

Laboratory Testing: For detection of inhaled aerosolized botulinum toxin, gastric aspirate and possibly stool may contain the toxin. In suspected food borne disease the appropriate specimens for toxin assay are serum, stool, gastric aspirate, vomitus, and the implicated food (if available). The confirmatory test is based on a mouse bioassay demonstrating the toxin. Diagnostic services are available only through the CDC via the state health department.

Therapeutic Treatment: Treatment is the same for inhalation (aerosolized) exposure as for ingestion (foodborne). Care is supportive. Long term mechanical ventilation may be needed for several weeks to months. A trivalent equine antitoxin for food-borne botulism is available from the CDC through the Arizona Department of Health Services. Use of the antitoxin requires skin testing for horse serum sensitivity prior to administration. Providers should refer to the information sheet that comes with the antitoxin.

Prophylactic Treatment: Currently, there is no commercially available vaccine.

Differential Diagnosis: Single cases may be confused with various neuromuscular disorders such as atypical Guillain-Barré syndrome, myasthenia gravis, or tick paralysis. Botulism could also be confused with enteroviral infections, but in these patients, fever is present, paralysis is often asymmetrical, and the CSF is abnormal. It may be necessary to distinguish nerve agent and atropine poisoning from botulinum intoxication. In organophosphate nerve agent poisoning pupils are miotic and copious secretions are present. In atropine poisoning, the pupils are dilated and mucous membranes are dry, but central nervous system excitation with hallucinations and delirium is present.

References:

Arnon SA, Schecter R, Inglesby TV, et al. Botulinum toxin as a biological weapon: medical and public health management. JAMA. 2001; 285: 1059-1070.
Chin J. Control of Communicable Diseases Manual, Seventeenth Edition, American Public Health Association; 2000.
Kortepeter M, Christopher G, Cieslak T, et al. Medical Management of Biological Casualties Handbook, U.S. Army Medical Research Institute of Infectious Diseases, U.S. Department of Defense; 2001:63-69
Middlebrook JL, Franz DR. Botulinum Toxins. In: Zajtchuk R, Bellamy RF, eds. Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General, U.S. Department of the Army; 1997: 643-654.

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