A paralytic illness, botulism results from an exotoxin produced by the gram-positive, anaerobic bacillus Clostridium botulinum. It occurs as botulism food poisoning, wound botulism, and infant botulism. Mortality from botulism is about 25%, with death usually caused by respiratory failure during the first week of illness.
Botulism is usually the result of ingesting inadequately cooked contaminated foods, especially those with low acid content, such as home-canned fruits and vegetables, sausages, and smoked or preserved fish or meat. Honey and corn syrup may contain C. botulinum spores and shouldn’t be fed to infants. Rarely, botulism results from wound infection with C. botulinum.
Botulism occurs worldwide and affects more adults than children. Recently, findings have shown that an infant’s GI tract can become colonized with C. botulinum from some unknown source, and then the exotoxin is produced within the infant’s intestine. Incidence had been declining, but the current trend toward home canning has resulted in an upswing in recent years. Wound botulism occurs when open areas are infected with C. botulinum that secretes the toxin.
The disease usually manifests within 12 to 36 hours (range is 6 hours to 8 days) after the ingestion of contaminated food. The severity varies with the amount of toxin ingested and the patient’s degree of immunocompetence. Generally, early onset (within 24 hours) signals critical and potentially fatal illness. Initial signs and symptoms include dry mouth, sore throat, weakness, vomiting, and diarrhea.
The cardinal sign of botulism, though, is acute symmetrical cranial nerve impairment (characterized by ptosis, diplopia, and dysarthria), followed by descending weakness or paralysis of muscles in the extremities or trunk and dyspnea from respiratory muscle paralysis. Such impairment doesn’t affect mental or sensory processes and isn’t associated with fever.
Usually afflicting infants ages 3 to 20 weeks, infant botulism can produce hypotonic (floppy) infant syndrome, which is characterized by constipation, feeble cry, depressed gag reflex, and inability to suck. Cranial nerve deficits also occur in infants and are manifested by a flaccid facial expression, ptosis, and ophthalmoplegia. Infants also develop generalized muscle weakness, hypotonia, and areflexia. Loss of head control may be striking. Respiratory arrest is likely.
Identification of the offending toxin in the patient’s serum, stool, or gastric content or in the suspected food confirms the diagnosis. An electromyogram showing diminished muscle action potential after a single supramaximal nerve stimulus is also diagnostic.
Diagnosis also must rule out other diseases often confused with botulism, such as Guillain-Barré syndrome, myasthenia gravis, cerebrovascular accident, staphylococcal food poisoning, tick paralysis, chemical intoxication, carbon monoxide poisoning, fish poisoning, trichinosis, and diphtheria.
With food-borne illness, administration of botulinum antitoxin (available through the Centers for Disease Control and Prevention) is the treatment of choice. Infant botulism requires supportive care because neither antitoxin nor antibiotics are beneficial; human botulism immune globulin is experimental.
Clinical tip Antibiotics and aminoglycosides shouldn’t be administered because they increase the risk of neuromuscular blockade. They should be used only to treat secondary infections.
If you suspect ingestion of contaminated food, perform the following:
❑ Obtain a careful history of the patient’s food intake for the past several days. Check to see if other family members exhibit similar symptoms and share a common food history.
❑ Observe the patient carefully for abnormal neurologic signs. If he returns home, tell his family to watch for signs of weakness, blurred vision, and slurred speech and to return the patient to the facility immediately if such signs appear.
❑ If ingestion occurred within the past several hours, induce vomiting, begin gastric lavage, and give a high enema to purge any unabsorbed toxin from the bowel.
If signs and symptoms of botulism appear, perform the following:
❑ Bring the patient to the intensive care unit, and monitor cardiac and respiratory function carefully.
❑ Administer botulinum antitoxin, as required, to neutralize any circulating toxin. Before giving antitoxin, obtain an accurate patient history of allergies, especially to horses, and perform a skin test.
Clinical tip Serum samples should be collected to identify the toxin before antitoxin is administered.
❑ After administration of antitoxin, watch for anaphylaxis or other hypersensitivity and serum sickness. Keep epinephrine 1:1,000 (for subcutaneous administration) and emergency airway equipment available.
❑ Closely observe and accurately record neurologic function, including bilateral motor status (including reflexes and ability to move arms and legs).
❑ Give I.V. fluids as needed. Turn the patient often, and encourage deep-breathing exercises. Assisted respiration may be required.
❑ The patient needn’t be isolated.
❑ Because botulism is sometimes fatal, keep the patient and his family informed about the course of the disease.
❑ Immediately notify local public health authorities of all cases of botulism.
To help prevent botulism, encourage patients to observe proper techniques in processing and preserving foods. Warn them to avoid even tasting food from a bulging can or one with a peculiar odor and to sterilize by boiling any utensil that comes in contact with food that may be contaminated with botulism toxin. Remember: Ingestion of even a small amount of the food can prove fatal.
Review other book chapters online related to Ptomaine food poisoning:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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