Botulism is poisoning due to Clostridium botulinum toxin that affects the peripheral nerves. Botulism may occur without infection if toxin is ingested, injected, or inhaled. Symptoms are symmetric cranial nerve palsies accompanied by a symmetric descending weakness and flaccid paralysis without sensory deficits. Diagnosis is clinical and by laboratory identification of toxin. Treatment is with support and antitoxin.
(See also Overview of Anaerobic Bacteria and Overview of Clostridial Infections.)
C. botulinum is one of several species of clostridia that cause human disease. Botulism is a rare, life-threatening disorder that occurs when botulinum toxin spreads hematogenously. The toxin interferes irreversibly with release of acetylcholine at peripheral nerve endings in the neuromuscular junctions, manifesting as weakness. Botulism is a medical emergency and sometimes a public health emergency. C. botulinum is also categorized as a category A agent on the Centers for Disease Control and Prevention's (CDC)/U.S. Department of Agriculture's list of potential agents of bioterrorism.
C. botulinum elaborates 8 types of antigenically distinct neurotoxins (types A through G and F/A Hybrid). Five of the toxins affect humans: types A, B, E, and rarely F and F/A Hybrid (formerly labeled H). Botulinum toxins are highly poisonous proteins resistant to degradation by gastric acidity and proteolytic enzymes. Type F/A Hybrid is the most potent known toxin. Approximately 50% of foodborne outbreaks in the United States are caused by type A toxin, followed by types B and E (1).
In the United States, type A toxin occurs predominantly west of the Mississippi River, type B in the eastern states, and type E in Alaska and the Great Lakes area (type E is frequently associated with ingestion of fish and fish products).
Botulism can occur when neurotoxin is elaborated in vivo by C. botulinum or when preformed neurotoxin is acquired in an external source.
In vivo elaboration causes the following forms:
Infant botulism (the most common form)
Wound botulism
Adult enteric botulism (rare)
In wound botulism, neurotoxin is elaborated in infected tissue.
In infant botulism and in adult enteric botulism, spores are ingested, and neurotoxin is elaborated in situ in the gastrointestinal tract. Predisposing factors for enteric botulism in adults and in children > 12 months of age include previous bowel or gastric surgery, anatomic bowel abnormalities, inflammatory bowel disease, antimicrobial therapy, and immunosuppressive medications.
Acquisition of preformed neurotoxin causes the following forms:
Foodborne botulism
Iatrogenic botulism
Inhalation botulism
In foodborne botulism, neurotoxin is produced in contaminated food and ingested.
In iatrogenic botulism, type A or B toxin is injected therapeutically to relieve excess muscle activity (onabotulinumtoxinA); rarely, botulism has occurred after cosmetic injections of a specific, modified formulation of botulinum type A toxin (onabotulinumtoxinA).type A or B toxin is injected therapeutically to relieve excess muscle activity (onabotulinumtoxinA); rarely, botulism has occurred after cosmetic injections of a specific, modified formulation of botulinum type A toxin (onabotulinumtoxinA).
In inhalation botulism, toxins becomes aerosolized either accidentally (eg, via intranasal use of contaminated cocaine) (2) or intentionally when used as a bioweapon; aerosolized toxins do not occur in nature.
C. botulinum spores are highly heat-resistant and may survive boiling for several hours at 100° C. However, exposure to moist heat at 120° C for 30 minutes kills the spores. Toxins, on the other hand, are readily destroyed by heat, and cooking food at 80° C for 30 minutes safeguards against botulism. C. botulinum can produce type E toxin at temperatures as low as 3° C (ie, inside a refrigerator—for example, in vacuum-packed smoked fish).
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Sources of toxin
Home-canned foods, particularly low-acid foods (ie, pH > 4.5), are the most common sources of ingested toxin, but commercially prepared foods have been implicated in a small number of outbreaks (3). Vegetables (but usually not tomatoes), fish, fruits, and condiments are the most common vehicles, but beef, milk products, pork, poultry, and other foods have been involved. Type E causes approximately 50% of outbreaks resulting from contaminated seafood; types A and B cause the rest. In recent years, foods that are not canned (eg, foil-wrapped baked potatoes, chopped garlic in oil, patty melt sandwiches) have caused restaurant-associated outbreaks.
Sometimes the toxin is absorbed through the eyes or a break in the skin and, in such cases, may cause serious disease.
C. botulinum spores are common in the environment; most cases of infant botulism are caused by ingestion of spores, typically when honey is ingested.
Spores can also enter the body when drugs are injected with unsterilized needles; wound botulism may result. Injecting contaminated black tar heroin into a muscle or under the skin (skin popping) is riskiest; it can cause gas gangrene as well as botulism.
If botulinum toxins enter the bloodstream, botulism results, regardless of how the toxins are acquired.
General references
1. Rawson AM, Dempster AW, Humphreys CM, Minton NP. Pathogenicity and virulence of Clostridium botulinum. Virulence. 2023;14(1):2205251. doi:10.1080/21505594.2023.2205251
2. Roblot F, Popoff M, Carlier JP, et al. Botulism in patients who inhale cocaine: the first cases in France. . Botulism in patients who inhale cocaine: the first cases in France.Clin Infect Dis. 2006;43(5):e51-e52. doi:10.1086/506567
3. Sobel J, Tucker N, Sulka A, McLaughlin J, Maslanka S. Foodborne botulism in the United States, 1990-2000. Emerg Infect Dis. 2004;10(9):1606-1611. doi:10.3201/eid1009.030745
Symptoms and Signs of Botulism
Common botulism symptoms and signs include:
Dry mouth
Blurred or double vision
Drooping eyelids
Slurred speech
Dysphagia
Pupillary light reflex is diminished or totally lost. Dysphagia can lead to aspiration pneumonia. Neurologic symptoms are characteristically bilateral and symmetric, beginning with the cranial nerves and followed by descending weakness or paralysis.
There are no sensory disturbances, and the sensorium usually remains clear.
Muscles of respiration and of the extremities and trunk progressively weaken in a descending pattern. Fever is absent, and the pulse remains normal or slow unless intercurrent infection develops. Constipation is common after neurologic impairment appears.
Major complications of botulism include:
Respiratory failure caused by diaphragmatic paralysis
Pulmonary and other nosocomial infections
Foodborne botulism
Symptoms begin abruptly, usually 18 to 36 hours after toxin ingestion, although the incubation period may vary from 4 hours to 8 days.
Nausea, vomiting, abdominal cramps, and diarrhea frequently precede neurologic symptoms.
Wound botulism
Neurologic symptoms appear, as in foodborne botulism, but there are no gastrointestinal symptoms or evidence implicating food as a cause.
Diagnosis of Botulism
Toxin assays
Sometimes electromyogram
Botulism may be confused with Guillain-Barré syndrome (Miller-Fisher variant), poliomyelitis, stroke, myasthenia gravis, tick paralysis, and poisoning caused by heavy metals, curare, or belladonna alkaloids.
Electromyogram shows characteristic augmented response to rapid repetitive stimulation in most cases.
In foodborne botulism, the pattern of neuromuscular disturbances and ingestion of a likely food source are important diagnostic clues. The simultaneous presentation of at least 2 patients who ate the same food simplifies diagnosis, which is confirmed by finding C. botulinum toxin in serum, gastric secretions, or stool. Finding C. botulinum toxin in suspect food identifies the source.
In wound botulism, a history of a traumatic injury or a deep puncture wound (particularly injection of illicit drugs) in the preceding 2 weeks may suggest the diagnosis. A thorough search should be made for breaks in the skin and for skin abscesses caused by self-injection of illicit drugs.
Finding toxin in serum or isolating C. botulinum organisms on anaerobic culture of the wound confirms the diagnosis of botulism.
Toxin assays are done only by certain laboratories, which may be located through local health authorities or, in the United States, the Centers for Disease Control and Prevention (CDC) (1). Details regarding specimen collection and handling can be obtained from state health departments or the CDC.
Diagnosis reference
1. CDC: Clinician Resources for Botulism. April 30, 2024. Accessed August 15, 2025.
Treatment of Botulism
Supportive care
Equine heptavalent antitoxin
Anyone known or thought to have been exposed to contaminated food must be carefully observed. Administration of activated charcoal or purgatives may be helpful. Patients with significant symptoms often have impaired airway reflexes, so charcoal, if used, should be given via gastric tube, and the airway should be protected by a cuffed Anyone known or thought to have been exposed to contaminated food must be carefully observed. Administration of activated charcoal or purgatives may be helpful. Patients with significant symptoms often have impaired airway reflexes, so charcoal, if used, should be given via gastric tube, and the airway should be protected by a cuffedendotracheal tube.
The greatest threat to life is:
Respiratory impairment and its complications
Patients with botulism should be hospitalized and closely monitored with serial measurements of vital capacity. Progressive paralysis prevents patients from showing signs of respiratory distress as their vital capacity decreases. Respiratory impairment requires management in an intensive care unit, where intubation and mechanical ventilation are readily available. Improvements in supportive care have reduced mortality to approximately 5 to 8% (1).
Nasogastric intubation is the preferred method of alimentation because it:
Simplifies management of calories and fluids
Stimulates intestinal peristalsis (which eliminates C. botulinum from the gut)
Allows the use of human milk in infants
Avoids the potential infectious and vascular complications inherent in IV alimentation
Patients with wound botulism require wound debridement and parenteral antibiotics such as penicillin or metronidazole.Patients with wound botulism require wound debridement and parenteral antibiotics such as penicillin or metronidazole.
Antitoxin
A heptavalent equine botulinum antitoxin (HBAT [A to G]) is available in the United States; it replaces the older trivalent antitoxin (2). Antitoxin does not inactivate toxin that is already bound at the neuromuscular junction; therefore, preexisting neurologic impairment cannot be reversed rapidly. (Ultimate recovery depends on regeneration of nerve endings, which may take weeks or months.) However, antitoxin may slow or halt further progression. In patients with wound botulism, antitoxin can reduce complications and mortality rate.
Antitoxin should be given as soon as possible after clinical diagnosis and not delayed to await culture or toxicology results. Antitoxin is less likely to be of benefit if given > 72 hours after symptom onset.
One 20- or 50-mL vial of the heptavalent antitoxin, diluted 1:10, is administered to adults as a slow infusion; dose and infusion rate are adjusted for children. For infants < 1 year of age, HBAT is administered at 10% of the adult dose (2). In the United States, all patients who require the antitoxin must be reported to state health authorities, who then request the antitoxin from the CDC, which is the only source; clinicians cannot obtain antitoxin directly from the CDC.
Because antitoxin is derived from horse serum, there is a risk of anaphylaxis or serum sickness. (For precautions, see Drug Hypersensitivity; for treatment, see Anaphylaxis.)
Human botulinum immune globulin (BabyBIG) is available for the treatment of infant botulism types A and B; in the United States, it is available from the Infant Botulism Treatment and Prevention Program (IBTPP—call 510-231-7600 or see the IBTPP web site).
Treatment references
1. Wilcox PG, Morrison NJ, Pardy RL. Recovery of the ventilatory and upper airway muscles and exercise performance after type A botulism. Chest. 1990;98(3):620-626. doi:10.1378/chest.98.3.620
2. Rao AK, Sobel J, Chatham-Stephens K, Luquez C. Clinical Guidelines for Diagnosis and Treatment of Botulism, 2021. MMWR Recomm Rep. 2021;70(2):1-30. Published 2021 May 7. doi:10.15585/mmwr.rr7002a1
Prevention of Botulism
Because even minute amounts of C. botulinum toxin can cause serious illness, all materials suspected of containing toxin require special handling. Correct canning and adequate heating of home-canned food before serving are essential. Canned foods showing evidence of spoilage and swollen or leaking cans should be discarded.
Toxoids once available for active immunization of people working with C. botulinum or its toxins are no longer manufactured because of frequent local reactions and lack of prolonged immunogenicity.
Immunity to C. botulinum toxin does not develop after infection.
Key Points
Botulism may develop from ingestion of foodborne toxin, from elaboration of toxin from a clostridial wound infection, or, in infants, from ingestion and enteric colonization by C. botulinum spores.
Botulism may result from man-made botulism toxin that is injected therapeutically or for cosmetic reasons or is inhaled (in an aerosolized form).
Botulinum toxins block release of acetylcholine at peripheral nerve endings and cause bilateral, symmetric, descending weakness, beginning with the cranial nerves.
Sensation and mental status are unaffected.
Cooking destroys botulinum toxin but not the spores.
For diagnosis, use toxin assays.
Give heptavalent equine botulinum antitoxin (HBAT) to adults and children; for infants < 1 year of age, give HBAT at 10% of the adult dose.
Drugs Mentioned In This Article
