·        Caused by toxin from Clostridium botulinum, a spore-forming, obligate anaerobic bacillus.

·        Botulinum toxins are a group of seven related neurotoxins, A through G.

·        Botulinum toxins are considered one of the most potent lethal substances known.

·        The toxins inhibit the release of acetylcholine from the presynaptic nerve endings causing flaccid paralysis.

·        May result in extensive respiratory muscle paralysis leading to ventilatory failure and death unless supportive care is provided.

·        There are three naturally occurring forms of botulism – foodborne, wound, infant and child or adult intestinal colonization botulism.

·        Intentional exposure could occur through contamination of food or water or via aerosol.

·        Person-to-person transmission does NOT occur with botulism.  


Incubation: 12-36 hours (may be as long as several days, depending on the size of the inoculum)

Clinical Signs and Symptoms: The hallmarks of foodborne botulism are:

·        Acute bilateral cranial nerve impairment, visual difficulty (blurred or double vision), ptosis, dysphagia, dry mouth and slurred speech in an afebrile patient.

o       Cranial nerve palsies almost always occur in botulism. 

·        Progression to descending weakness or paralysis.

o       Symptoms may extend to a symmetrical flaccid paralysis in which sensation is completely preserved and result in respiratory failure. 

·        Symptoms of inhalational botulism would most likely be similar to those seen in foodborne botulism.

Ancillary testing:

·         Tensilon test may be slightly positive

·         Brain imaging (CT or MRI) normal

·         Lumbar puncture normal

·         Electromyography may show decreased amplitude of action potentials in involved muscle groups

·         Rapid repetitive electromyography (20-50 Hz) will result in facilitation (increasing pattern of action potential amplitude

·         Edrophonium chloride test negative  

Bilateral cranial nerve impairment and descending paralysis 

Differential Diagnosis:

  • The Guillain-Barre syndrome (especially the Miller-Fisher variant)

  • Myasthenia gravis

  • Stroke

  • Intoxication with organophosphates, atropine, carbon monoxide, or aminoglycosides

  • Tick paralysis

  • Paralytic shellfish poisoning

  • Puffer fish ingestion

  • The Eaton-Lambert syndrome  




Laboratory Confirmation of Diagnosis

  • Testing should be performed by the DOH Public Health Laboratories.

  • Appropriate clinical samples for botulinum toxin testing at DOH include serum and stool.

  • Transport and packaging of clinical specimens must be coordinated with local and state health departments.

  • DPH has capacity to report preliminary results within 18-24 hours.


·        Intravenous administration of 1 vial of polyvalent (AB or ABE) botulinum antitoxin as soon as possible.

·        Patients with a clinical diagnosis of botulism should be treated as soon as possible. 

-         Confirmation by laboratory testing should always be done, but testing may require up to two days.

-         Administration of antitoxin should not be withheld pending results.

·        Prior to treatment with antitoxin, serum should be collected to identify specific toxin.

·        Antitoxin must be procured from CDC via the State Department of Health (see below).

·        Careful monitoring of respiratory vital capacity and aggressive respiratory care for those with ventilatory insufficiency is necessary.

·        Meticulous and intensive care must be provided for the duration of the often prolonged paralytic illness.


·        May prevent progression or shorten duration of illness. 

·        Most effective when administered early in the course of illness.

·        Before administration of antitoxin, skin testing should be performed to test for sensitivity to serum or antitoxin (see package insert).

·        Administration of one 10-ml vial of trivalent botulism antitoxin by the intravenous route results in serum antibody levels of type A, B, and E antibodies capable of neutralizing serum toxin concentrations manyfold in excess of those reported for botulism patients.

·        Antitoxin need not be repeated since the circulating antitoxins have a half-life of 5 to 8 days.

·        For exposed infants, the risk of inducing lifelong sensitivity to horse serum should be weighed against the benefits of administering botulism antitoxin.  A human-derived antitoxin product is available solely for the treatment of infant botulism under a Treatment Investigational New Drug protocol and may be procured through the California DOH.

·        Physicians may be asked to get an informed consent signed for administration of the antitoxin supplied by the National Pharmaceutical Stockpile (NPS).


  • Individuals potentially exposed, but not yet showing signs of intoxication should be closely monitored for the development of symptoms.


  • A pentavalent toxoid of Clostridium botulinum toxins A through E is currently under IND status but is not widely available.  Currently there is no botulism vaccine licensed.  

Infection Control

  • Botulinum toxin is NOT absorbed through intact skin.  Person-to person transmission does not occur.

  • Isolation of patients is NOT necessary.

  • Standard (Universal) Precautions for care and transport of patients and during post-mortem care.