Botulism Clinical Presentation

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


Following the onset of symptoms, botulism quickly progresses over several days. The magnitude of the neuromuscular impairment can advance hourly. Persons who survive this phase eventually stabilize and then recover over a period of days to months. The mechanism of recovery is not fully understood but requires the generation of new presynaptic axons and the formation of new synapses, as the original synapses are permanently affected. As with tetanus, recovery from botulism does not confer long-term immunity. Rare reports have described a second episode in the same patient.

Foodborne botulism

Foodborne botulism should be suspected in patients who present with an acute gastrointestinal illness associated with neurologic symptoms. Symptoms usually appear within 12-36 hours following consumption of contaminated food products. The severity of the illness varies from mild to severe, but death can occur within 24 hours.

The incubation period is usually 18-36 hours. Depending on toxin dose, the incubation period ranges from 2 hours to 8 days. The onset of symptoms can be abrupt or can evolve over several days.

Wound botulism

Patients with wound botulism typically have a history of traumatic injury with wounds that are contaminated with soil.

Since 1994, the number of patients with wound botulism who have a history of chronic intravenous drug abuse has increased dramatically. In most cases, black-tar heroin has been the implicated vehicle. A study by Yuan et al followed 17 heroin users who had recurrent botulism after using black-tar heroin. Physicians need to be alert to recognize botulism, especially in patients who use black-tar heroin or in those with a history of injection drug–associated botulism. [8]

Rare cases of wound botulism after cesarean delivery have been documented.

Aside from a longer incubation period, wound botulism is similar to foodborne botulism. The incubation period of wound botulism ranges from 4-14 days, with a mean of 10 days. Unlike foodborne botulism, wound botulism causes no gastrointestinal symptoms. Patients may be febrile, but this is more likely due to the wound infection rather than the wound botulism. In many cases, the wound appears benign.

Adult intestinal toxemia

Adult intestinal toxemia results from enteric colonization with C botulinum that progresses to toxin production. The pathophysiology of the changes in the gastrointestinal flora that facilitate colonization is unclear. [9]

Iatrogenic botulism due to accidental overdose of botulinum toxin (Botox)

Cases of botulism due to Botox overdosage have been reported. Symptoms vary and can include dysphagia, ptosis, and diplopia, as well as more severe presentations of systemic weakness or muscle paralysis. [9]



More than 90% of patients with botulism have 3-5 of the following signs or symptoms: nausea, vomiting, dysphagia, diplopia, dilated/fixed pupils, and an 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. Except for nerves I and II, the cranial nerves are affected first.

  • 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 symmetric descending paralysis or weakness of motor and autonomic nerves.

  • Respiratory muscle weakness may be subtle or progressive, advancing rapidly to respiratory failure. Progressive muscle weakness occurs and often involves the muscles of the head and neck, as well as intercostal diaphragmatic muscles and those of the extremities.

The autonomic nervous system is also involved. Manifestations of this 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

Many patients with foodborne botulism and wound botulism are afebrile.



Wound botulism

Causes of wound botulism have been associated with traumatic injury involving contamination with soil, chronic abuse of intravenous drugs (eg, black-tar heroin), and cesarean delivery. Wound botulism illness can occur even after antibiotics are administered to prevent wound infection.

Foodborne botulism

Foodborne botulism results from the ingestion of preformed neurotoxins; A, B, and E are the most common. On average, 24 cases of foodborne botulism are reported annually.

High-risk foods include home-canned or home-processed low-acid fruits and vegetables; fish and fish products; and condiments, such as relish and chili peppers.

Commercially processed foods and improperly handled fresh foods are occasionally associated with botulism outbreaks.

Outbreaks of foodborne botulism in restaurants, schools, and private homes have been traced to uncommon sources, such as commercial pot-pies, baked potatoes, [10] beef stew, turkey loaf, sautéed onions, chopped garlic in oil, [11] and cheese sauce.