Foodborne Illnesses / Botulism /

Symptoms of Botulism

After their ingestion, botulinum neurotoxins are absorbed primarily in the duodenum and jejunum, pass into the bloodstream, and travel to synapses in the nervous system. There, the neurotoxins cause flaccid paralysis by preventing the release of acetylcholine (a neurotransmitter) at neuromuscular junctions, thereby preventing motor-fiber stimulation.

The flaccid paralysis progresses symmetrically downward, usually beginning with the eyes and face before moving to the throat, chest, and extremities. When the diaphragm and chest muscles become fully involved, respiration is inhibited and, unless the patient is ventilated, death from asphyxia results.

Classic symptoms of botulism include nausea, vomiting, fatigue, dizziness, double vision, drooping eyelids, slurred speech, difficulty swallowing, dryness of skin, mouth, and throat, lack of fever, muscle weakness, and paralysis. Infants with botulism appear lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone. Throughout all such symptoms, the victims are fully alert, and the results of sensory examination are normal.

In foodborne botulism cases, symptoms usually begin 12 to 72 hours after the ingestion of toxin-containing food. The incubation period is usually 12 to 36 hours but may range from a few hours to 10 days. The rapidity of disease onset and rate of progression depend on the dose of the neurotoxin, with a range of hours to several days. The duration of symptoms is a function of toxin dose, toxin elimination, and neurologic regeneration.

If diagnosed early, botulism can be treated with an antitoxin that blocks the action of toxin circulating in the blood. Botulinum antitoxin is produced from the serum of toxoid- and toxin-immunized horses. Infant botulism is treated with a human-derived antitoxin (BabyBIG). Few articles have been published on hypersensitivity to equine-source botulinum antitoxin formulations, yet the potential for antitoxin-induced anaphylaxis is an important concern. Clinical data support the effectiveness of antitoxin when it is used before all circulating toxin has been bound.