Botulism is a rare, life-threatening paralytic illness caused by neurotoxins produced by an anaerobic, gram-positive, spore-forming bacterium, Clostridium botulinum. Unlike Clostridium perfringens, which requires the ingestion of large numbers of viable cells to cause symptoms, the symptoms of botulism are caused by the ingestion of highly toxic, soluble exotoxins produced by C. botulinum while growing in foods.
The incidence of foodborne botulism is extremely low. Nonetheless, the extreme danger posed by the bacteria has required that “intensive surveillance is maintained for botulism cases in the United States, and every case is treated as a public health emergency.” This danger includes a mortality rate of up to 65% when victims are not treated immediately and properly. Most of the botulism events that are reported annually in the United States are associated with home-canned foods that have not been safely processed. Very occasionally, however, commercially- processed foods are implicated as the source of a botulism events, including sausages, beef stew, canned vegetables, and seafood products.
In foodborne botulism cases, symptoms usually begin anywhere between 12 and 72 hours after the ingestion of toxin-containing food. Longer incubation periods—up to 10 days—are not unknown, however. The duration of the illness is from 1 to 10 (or more) days, depending on host-resistance, the amount of toxin ingested, and other factors. Full recovery often takes from weeks to months.
After their ingestion, botulinum neurotoxins are absorbed primarily in the duodenum and jejunum and 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 starting with the eyes and face, and then 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, and 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.
Although a minority of botulism patients eventually recovers their pre-infection health, the majority does not. For those who fully recover, the greatest improvement in muscle strength occurs in the first three months after the acute phase of illness. The outside limit for such improvement appears, however, to be one year. Consequently, physical limitations that still exist beyond the one-year mark are more probably than not permanent. Recovery from acute botulism symptoms may also be followed by persistent psychological dysfunction that may require intervention.
Even several years after acute illness, patients who had botulism were more likely than control subjects to experience fatigue, generalized weakness, dizziness, dry mouth, difficulty lifting things, and difficulty breathing caused by moderate exertion.