Updated: Feb 15, 2019
  • Author: Kirk M Chan-Tack, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Practice Essentials

Botulism is an acute neurologic disorder that causes potentially life-threatening neuroparalysis due to a neurotoxin produced by Clostridium botulinum. The 3 main clinical presentations of botulism are as follows:

  • Infant botulism

  • Foodborne botulism

  • Wound botulism

Signs and symptoms

More than 90% of patients with botulism have 3-5 of the following signs or symptoms:

  • Nausea

  • Vomiting

  • Dysphagia

  • Diplopia

  • Dilated/fixed pupils

  • Extremely dry mouth unrelieved by drinking fluids

Generally, botulism progresses as follows:

  • Preceding or following the onset of paralysis are nonspecific findings such as nausea, vomiting, abdominal pain, malaise, dizziness, dry mouth, dry throat, and, occasionally, sore throat

  • Cranial nerve paralysis manifests as blurred vision, diplopia, ptosis, extraocular muscle weakness or paresis, fixed/dilated pupils, dysarthria, dysphagia, and/or suppressed gag reflex

  • Additional neurologic manifestations include symmetrical descending paralysis or weakness of motor and autonomic nerves

  • Respiratory muscle weakness may be subtle or progressive, advancing rapidly to respiratory failure

The autonomic nervous system is also involved in botulism, with manifestations that include the following:

  • Paralytic ileus advancing to severe constipation

  • Gastric dilatation

  • Bladder distention advancing to urinary retention

  • Orthostatic hypotension

  • Reduced salivation

  • Reduced lacrimation

Other neurologic findings include the following:

  • Changes in deep tendon reflexes, which may be either intact or diminished

  • Incoordination due to muscle weakness

  • Absence of pathologic reflexes and normal findings on sensory and gait examinations

  • Normal results on mental status examination

Ophthalmic manifestations may reflect the anticholinergic effects of the neurotoxins. [1, 2]

  • Accommodation paresis, with blurred vision
  • Pupil dysfunction with mydriasis and poorly reactive pupils
  • Dry eye symptoms with impairment of lacrimation

Ophthalmic manifestations may reflect a deficit at the neuromuscular junction. [1, 2, 3, 4]

  • Oculoparesis or ophthalmoplegia manifests as diplopia.
  • Blepharoptosis is common.
  • Nystagmus may be noted.

Ocular manifestations may be the manifesting features of botulism. However, their absence does not exclude this disease, since the various toxins appear to involve the ocular system to various degrees. Neurotoxin A may have no specific ophthalmic manifestations.


A mouse neutralization bioassay confirms botulism by isolating the botulinum toxin. Toxin may be identified in the following:

  • Serum

  • Stool

  • Vomitus

  • Gastric aspirate

  • Suspected foods

C botulinum may be grown on selective media from samples of stool or foods. Note that the specimens for toxin analysis should be refrigerated, but culture samples of C botulinum should not be refrigerated. Wound cultures that grow C botulinum suggest the presence of wound botulism.


Characteristic electromyographic findings in patients with botulism include the following:

  • Brief, low-voltage compound motor-units

  • Small M-wave amplitudes

  • Overly abundant action potentials

An incremental increase in M-wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction.

See Workup for more detail.


Rigorous and supportive care, including use of the following, is essential in patients with botulism:

  • Meticulous airway management - Of paramount importance, since respiratory failure is the most important threat to survival in patients with botulism

  • Cathartics and enemas - Administered to patients with bowel sounds to remove unabsorbed botulinum toxin from the intestine

  • Stress ulcer prophylaxis - A standard component of intensive care management

  • Nasogastric suction and intravenous hyperalimentation - Helpful if an ileus is present; if no ileus is present, tube feeding can be used for nutritional supplementation

  • Foley catheter - Often used to treat bladder incontinence; the catheter must be monitored conscientiously and changed regularly

  • Antibiotic therapy - Useful in wound botulism, but has no role in foodborne botulism

Magnesium salts, citrate, and sulfate should not be administered, because magnesium can potentiate the toxin-induced neuromuscular blockade.

Wound botulism requires the following:

  • Incision and thorough debridement of the infected wound

  • Antitoxin therapy

  • High-dose intravenous penicillin therapy

Prevention of nosocomial infections

Measures to reduce the risk of nosocomial infections include the following:

  • Close observation for hospital-acquired infections - Especially pneumonia (particularly aspiration pneumonia); precaution against aspiration is also necessary

  • Close observation for urinary tract infection

  • Meticulous skin care - To prevent decubital ulcers and skin breakdown

Careful attention to peripheral and central intravenous catheters with regular site rotation to reduce the risks of thrombophlebitis, cellulitis, and line infections should be part of the patient’s supportive care.

See Treatment and Medication for more detail.



Botulism is an acute neurologic disorder that causes potentially life-threatening neuroparalysis due to a neurotoxin produced by Clostridium botulinum. The toxin binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions. Toxin binding blocks acetylcholine release, resulting in weakness, flaccid paralysis, and, often, respiratory arrest. Cure occurs following sprouting of new nerve terminals.

The 3 main clinical presentations of botulism include infant botulism (IB), foodborne botulism (FBB), and wound botulism (WB). Additionally, because of the potency of the toxin, the possibility of botulism as a bioterrorism agent or biological weapon is a great concern. [5] For more information, see CBRNE – Botulism.

Infant botulism is caused by ingested C botulinum spores that germinate in the intestine and produce toxin. These spores typically come from bee honey or the environment. Most infants fully recover with supportive treatment; the attributed infant mortality rate is less than 1%. Improperly canned or home-prepared foods are common sources of the toxin that can result in foodborne botulism. Wound botulism results from contamination of a wound with toxin-producing C botulinum. Foodborne botulism and wound botulism occur predominantly in adults and are the focus of this article.

C botulinum is an anaerobic gram-positive rod that survives in soil and marine sediment by forming spores. Under anaerobic conditions that permit germination, it synthesizes and releases a potent exotoxin. Microbiologically, the organism stains gram-positive in cultures less than 18 hours old. The organism may stain gram-negative after 18 hours of incubation, potentially complicating attempts at diagnosis. On a molecular weight basis, botulinum toxins are the most potent toxins known.

Eight antigenically distinct C botulinum toxins are known, including A, B, C (alpha), C (beta), D, E, F, and G. Each strain of C botulinum can produce only a single toxin type. Types A, B, E, and, rarely, F cause human disease. Toxins A and B are the most potent, and the consumption of small amounts of food contaminated with these types has resulted in full-blown disease. During the last 20 years, toxin A has been the most common cause of foodborne outbreaks; toxins B and E follow in frequency. In 15% of C botulinum infection outbreaks, the toxin type is not determined. Toxins C and D cause disease in various animals. Type G toxin has been associated with sudden death but not with neuroparalytic illness. It was isolated from autopsy material from 5 patients in Switzerland in 1977.



The mechanism of action involves toxin-mediated blockade of neuromuscular transmission in cholinergic nerve fibers. This is accomplished by either inhibiting acetylcholine release at the presynaptic clefts of the myoneural junctions or by binding acetylcholine itself. Toxins are absorbed from the stomach and small intestine, where they are not denatured by digestive enzymes. Subsequently, they are hematogenously disseminated and block neuromuscular transmission in cholinergic nerve fibers. The nervous, gastrointestinal, endocrine, and metabolic systems are predominantly affected.

Because the motor end plate responds to acetylcholine, botulinum toxin ingestion results in hypotonia that manifests as descending symmetric flaccid paralysis and is usually associated with gastrointestinal symptoms of nausea, vomiting, and diarrhea. Cranial nerves are affected early in the disease course. Later complications include paralytic ileus, severe constipation, and urinary retention.

Wound botulism results when wounds are contaminated with C botulinum spores. Wound botulism has developed following traumatic injury that involved soil contamination, among injection drug users (particularly those who use black-tar heroin [6] ), and after cesarean delivery. The wound may appear deceptively benign. Traumatized and devitalized tissue provides an anaerobic medium for the spores to germinate into vegetative organisms and to produce neurotoxin, which then disseminates hematogenously. The nervous, endocrine, and metabolic systems are predominantly affected. Symptoms develop after an incubation period of 4-14 days, with a mean of 10 days. The clinical symptoms of wound botulism are similar to those of foodborne botulism except that gastrointestinal symptoms (including nausea, vomiting, diarrhea) are uncommon.



United States

In the United States, approximately 154 cases of botulism are reported annually to the Centers for Disease Control and Prevention (CDC). Infant botulism accounts for nearly 75% of all botulism cases.

The incidence of foodborne botulism is approximately 24 cases per year. The incidence of wound botulism is 3 cases per year. The incidence of infant botulism is 71 cases per year, with a mean age of 3 months.

Toxin A is found predominantly west of the Mississippi River. Toxin B is found most commonly in the eastern United States. Toxin E is found in northern latitudes, such as the Pacific Northwest, the Great Lakes region, and Alaska. The frequency of botulism in native Alaskans is among the highest in the world. [7] Toxin E outbreaks are frequently associated with fish products.


Human botulism is found worldwide. Spores from C botulinum strains that produce type A or B toxins are distributed widely in the soil and have been found throughout the world. Toxin type B is commonly found in Europe. Toxin G was originally isolated in Switzerland.



Mortality rates vary based on the age of the patient and the type of botulism. Foodborne botulism carries an overall mortality rate of 5-10%. Wound botulism carries a mortality rate that ranges from 15-17%. The risk of death due to infant botulism is usually less than 1%.

The recovery period from botulism is often prolonged (30-100 d). Some patients demonstrate residual weakness or autonomic dysfunction for 1 year after the onset of the illness. However, most patients achieve full neurologic recovery. Permanent deficits may occur in those who sustain significant hypoxic insults.


Wound botulism is more common in males. Foodborne botulism has no sexual predilection.


Foodborne botulism and wound botulism predominately occur in adults. The mean age of infant botulism is 3 months.