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AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Robert W Tolan Jr, MD, Chief of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan, Jr, is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Coauthor(s):
Daniel AC Frattarelli, MD, FAAP, Senior Staff, Departments of Pediatrics and Emergency Medicine, Henry Ford Hospital;
Nahed M Abdel-Haq, MD, Assistant Professor, Department of Pediatrics, Wayne State University School of Medicine
Editors: Itzhak Brook, MD, MSc, Professor, Department of Pediatrics, Georgetown University School of Medicine; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School of Medicine; Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine; Russell W Steele, MD, Professor and Vice Chairman, Department of Pediatrics, Head, Division of Infectious Diseases, Louisiana State University Health Sciences Center
Author and Editor Disclosure
Synonyms and related keywords:
Bacillus botulinus, botulinum toxin, botulinus, botulism, Clostridium botulinum, C botulinum, food-borne botulism, food poisoning, infant botulism, wound botulism, Clostridium baratii, C baratii, Clostridium butyricum, C butyricum, Clostridium argentinense, C argentinense, dry mouth, paralysis, autonomic dysfunction, orthostatic hypotension, urinary retention, constipation, blurred vision, ptosis, mydriasis, decreased ocular motility, dysphagia, dysarthria, muscle weakness, dysphagia, diplopia, hypotonia, hyporeflexia
Background
Botulism is a broad term encompassing 3 clinical entities caused by botulinum toxin. Propagation of this toxin under different circumstances can lead to food-borne, wound, or infant botulism. Food-borne botulism was the first of the 3 entities to be described. Byzantine Emperor Leo VI documented cases of fatal food poisoning in the ninth century. In the 1820s, Justinus Kerner, a German physician and romantic poet, scrutinized a number of food-poisoning cases and found that most were caused by improperly prepared sausages.1, 2 As a result, he named the disease botulism, after the Latin word for sausage, botulus. Kerner correctly deduced the presence of the culpable toxin in the sausages and extracted a compound he termed wurstgift (German for sausage poison). Kerner continued studying botulism. In an experiment that would surely cause controversy in any modern human investigations committee, Kerner injected himself with the wurstgift extract and demonstrated many of the signs and symptoms so convincingly that the causal relationship was proven. Lastly, Kerner presaged the therapeutic uses of this toxin in individuals with motor overactivity by some 150 years. Despite his contributions to the field, questions remained regarding how the toxin entered the sausages. In 1897, the microbiologist Emile-Pierre van Ermengen identified a gram-positive, spore-forming, anaerobic bacterium in a ham that caused 23 cases of botulism in a Belgian nightclub.3 He termed the bacterium Bacillus botulinus; it was later retermed Clostridium botulinum. Wound botulism was the next type to be described. C botulinum was cultured from the wounds of asymptomatic patients as early as 1942, but wound botulism was not described as it is known today until 1951. In 1973, Merson and Dowell reported the case of a girl who had open leg and ankle fractures.4 The girl demonstrated clear clinical signs of botulism without any history of food-borne illness or symptomatic family members. Infant botulism was described separately in 1976 by Midura and Arnon and by Pickett et al.5, 6 Currently, the infant form is the most common presentation of botulism in the United States. Although frequently mentioned, honey is the apparent cause in only 15% of cases; the origin of the spores is unknown in 85% of cases.
Pathophysiology
C botulinum is a gram-positive, spore-forming anaerobe that naturally inhabits soil, dust, and fresh and cooked agricultural products. Although classified as a single species, C botulinum is better described as a group of at least 3 (possibly 4) genetically unique organisms. All of the organisms share the ability to produce a type of botulinum toxin, although not all produce the same type. Clostridium baratii and Clostridium butyricum also produce botulinum toxin. These organisms produce type E and F toxins. Whether Clostridium argentinense is a subgroup of C botulinum or a separate species is currently under debate. Botulinum toxin is the most potent naturally occurring toxin known to humankind. Botulinum toxin is lethal at a femtomolar dose of 10–9 g/kg, making botulinum toxin 15,000-100,000 times more potent than sarin gas. Food-borne botulism is not seen after eating fresh foods. Some methods of food preparation, such as home canning, produce an anaerobic, low-acid (ie, pH >4.6), low-solute environment in which the toxin can be produced. A similar environment exists in wounds, thus providing an opportunity for wound botulism to develop. Infant botulism is unique. In persons older than 1 year, the spores are unable to germinate in the gut; therefore, food-borne disease is the result of ingesting a preformed toxin. C botulinum spores can germinate in the gut of infants younger than 1 year because of their relative lack of gastric acid, decreased levels of normal flora, and immature immune systems (ie, specifically lacking secretory immunoglobulin A). This environment is conducive to toxin production; therefore, infant botulism can arise from eating the spores present in unprepared foods. Once produced, several activating steps are required for the toxin to produce deleterious effects. The toxin precursor is produced as a 150-kd protein encoded by a single gene. The precursor is cleaved to a 100-kd heavy chain and a 50-kd light chain, joined by a disulfide bond. The bond is essential for membrane penetration, and reduction of the bond inactivates the toxicity of the polypeptides. The light chain is more toxic than the heavy chain, although both must be present to achieve the full toxic effect. All botulinum toxins are zinc metalloproteases that bind to different membrane proteins involved in fusion of the synaptic vesicle to the presynaptic membrane. This fusion allows release of acetylcholine into the synaptic junction. The toxins are classified as types A through G, although only types A, B, E, and F cause human disease. Types A and E bind to synaptosomal-associated protein 25, type C binds to syntaxin, and types B, D, and F bind to vesicle-associated membrane protein. Inhibition of the proteins effectively blocks acetylcholine transmission across the synapse and functionally denervates the muscle. The magnitude of the clinical effect depends on the proportion of synapses blocked and the effects can range from weakness to flaccid paralysis and atrophy.
Frequency
United States
From 1973-1996, 724 cases of food-borne botulism, 103 cases of wound botulism, and 1444 cases of infant botulism were reported; the type of botulism was undetermined in 39 cases.7 Type A accounts for 50% of food-borne cases; the other 50% of cases are evenly split between types B and F. Wound botulism is caused by type A in 80% of cases; type B causes most of the remaining cases. The cause of infant botulism is evenly split between types A and B.7 Geographically, type A predominates west of the Mississippi River, while type B predominates east of the river.8
International
In Europe, contaminated hams and sausages are the usual mode of transmission. Poland has the highest frequency by far, with 325 outbreaks and 448 cases in a 3-year period. China is a distant second with 38 outbreaks and 168 cases in a 25-year period.
Mortality/Morbidity
Around the year 1900, the mortality rate associated with botulism was 70%. Today, the mortality rate approaches 15%.
Race
Botulism has no racial predilection.
Sex
Sex is not a factor in botulism infection.
Age
Infant botulism usually occurs in children aged 2-6 months, although it can occur in infants aged 3-382 days.
History
- Food-borne botulism
- GI tract symptoms usually occur first, beginning 18-36 hours after ingestion (range, 2 h to 8 d) and consist of nausea, vomiting, and diarrhea followed by constipation.
- Motor function symptoms follow, with the cranial nerves usually affected first. As a result, many patients present with diplopia (eg, impaired lateral gaze secondary to sixth cranial nerve involvement) and blurred vision secondary to loss of accommodation.
- Many patients have dry mouth.
- Finally, a rapidly progressive descending weakness or paralysis occurs. Autonomic dysfunction may lead to orthostatic hypotension, urinary retention, or constipation.
- Since the toxin affects only motor and autonomic systems, sensation and mentation remain intact. Patients are usually afebrile.
- Wound botulism
- Except for the prerequisite history of a wound, this type of botulism presents in the same way as food-borne botulism.
- Wound botulism is the least common type of botulism and may follow a penetrating or blunt injury.
- The incubation period is 4-14 days.
- Infant botulism
- The incubation period is 2-4 weeks. The peak age of incidence is 2-4 months.
- Constipation is the usual presenting symptom, often preceding motor function symptoms by several days or weeks.
- Other signs of autonomic dysfunction usually present early as well, including those mentioned above. Gag reflexes are frequently impaired, which can lead to aspiration if the airway is unprotected.
- Infants with botulism are afebrile, suck poorly, and are lethargic and listless; they develop the same descending weakness and paralysis that occurs in those with food-borne disease.
- Breastfeeding may protect infants from lethal fulminant infant botulism, but exclusive breastfeeding is a risk factor for the disease, presumably because the relatively pristine bowel flora of the exclusively breastfed infant is more permissive for spore germination and toxin production.
Physical
Suspect botulism in patients with autonomic dysfunction (eg, dry mouth, blurred vision, orthostatic hypotension), cranial nerve involvement (eg, ptosis, mydriasis, decreased ocular motility, dysphagia, dysarthria), and muscle weakness or flaccid paralysis.
- Frequencies of the most common symptoms of food-borne and wound botulism are as follows:
- Dysphagia - 96%
- Dry mouth - 93%
- Diplopia - 91%
- Dysarthria - 84%
- Extremity weakness - 73%
- Constipation - 73%
- Blurred vision - 65%
- Nausea - 64%
- Dyspnea - 60%
- Vomiting - 59%
- Abdominal cramps - 42%
- Diarrhea - 19%
- Frequencies of the most common symptoms of infant botulism are as follows:
- Poor ability to suck - 96%
- Poor head control - 96%
- Hypotonia - 93%
- Weak crying - 84%
- Constipation - 83%
- Lethargy - 71%
- Facial weakness - 69%
- Irritability - 61%
- Hyporeflexia - 52%
- Sluggish pupils - 50%
- Respiratory difficulty - 43%
Causes
See Pathophysiology.
Dehydration
Hypermagnesemia
Hypothyroidism
Poliomyelitis
Toxicity, Carbon Monoxide
Toxicity, Organophosphates
Other Problems to be Considered
Guillain-Barré syndrome (especially Miller-Fisher variant)
Acute poliomyelitis
Myasthenia gravis
Lambert-Eaton syndrome
Tick paralysis
Stroke
Aminoglycoside toxicity
Atropine poisoning
Paralytic shellfish poisoning (saxitoxin)
Puffer fish ingestion (tetrodotoxin)
Sepsis
Meningitis/encephalitis
Congenital myopathy
Electrolyte imbalance
Genetic metabolic disorders
Lab Studies
Although clinical suspicion should be sufficient to prompt supportive therapy for botulism, other differential diagnoses must be excluded.
- Obtain stool cultures in all patients, adding wound cultures if wound botulism is suspected.
- Approximately 60% of food-borne cases yield positive culture results; a positive finding in the presence of flaccid paralysis is diagnostic. Currently, specific assays for the toxin, including enzyme-linked immunoassays and polymerase chain reaction, are under investigation.
- Currently, the mouse inoculation test is the best test available and can be performed by the Centers for Disease Control and Prevention (CDC) in Atlanta, GA. In the assay, mice are injected with a serum sample from the patient and test results are considered positive for toxin if the mice die of respiratory arrest within 24 hours. The exact type of toxin is determined through pretreating each mouse in a set of mice with a different type-specific antitoxin, then injecting the serum. The mouse left alive the next day is the one pretreated with the antitoxin to the toxin affecting the patient.
Imaging Studies
- Perform CT scanning or MRI as clinically indicated to exclude stroke.
Other Tests
- Perform an edrophonium chloride test to exclude myasthenia gravis, if indicated, although transient responses have been reported with botulism.
- Electromyelography (EMG) demonstrates a nonspecific, decreased amplitude of action potentials. Rapid repetitive EMG at frequencies of 20-50 Hz is more specific for botulism and useful in excluding Guillain-Barré syndrome, but this response does not distinguish botulism from Lambert-Eaton syndrome. Infant botulism is characterized by a pattern known as brief, small, abundant motor-unit action potential on EMG in clinically affected muscles.
Procedures
- Lumbar puncture findings can usually exclude Guillain-Barré syndrome, a condition that tends to elicit a higher protein level in cerebrospinal fluid (especially later in the course of the disease) than does botulism.
Medical Care
In patients with botulism, supportive care, especially ventilatory support, is essential.
- Promptly initiate ventilatory support promptly because respiratory muscle weakness rapidly progresses and the gag reflex is frequently impaired, which predisposes patients to aspiration. Patients need continued suctioning and may require intubation or tracheostomy.
- Antitoxin (see Medication) dramatically alters the course of the disease, especially if administered within the first 24 hours.
- In general, antibiotic therapy to clear clostridial GI infection in infant botulism is contraindicated, because the treatment increases toxin release and worsens the condition. Antibiotics may be considered to treat secondary bacterial infections.
- Aminoglycosides, such as gentamicin or tobramycin, may potentiate the neuromuscular blockade; therefore, they are contraindicated.
Surgical Care
In patients with wound botulism, surgical debridement of the wound is indicated to remove the source of toxin production.
Consultations
Consultations with an infectious diseases specialist and a neurologist are frequently beneficial.
Diet
Tube feeding may be useful if GI tract motility is intact. If motility is not intact, consider parenteral feeding.
In addition to the equine-derived botulinum antitoxin available from the CDC, a human-derived antitoxin is currently under an Investigational New Drug (IND) treatment protocol; the treatment IND protocol is only for infant botulism and only for infants aged 1 year or younger.9, 10 For infants who meet these criteria, the human-derived antitoxin may be obtained from the California Department of Health Services at (510) 231-7600.
Drug Category: Antitoxins
These agents are used for food-borne and wound botulism. They are produced from horse serum stimulated with specific antibodies directed against C botulinum and provide passive immunity.
| Drug Name | Botulism antitoxin trivalent (equine) types A, B, and E |
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| Description | Effective against serotypes A, B, and E. Only medication available and should be started immediately. Antitoxin binds only to the toxin that is circulating and has no effect on bound toxin inside the presynaptic nerve end (only halts progression of symptoms and does not reverse existing symptoms).
Available from the CDC in Atlanta, GA (404-639-2206 during business hours and 404-639-2888 after hours).
Administration within the first 24 h decreases mortality and shortens the average duration of hospital stays. |
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| Adult Dose | 2 vials of 10,000 IU IV (each vial contains approximately 100 times more antitoxin than needed to neutralize toxin) |
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| Pediatric Dose | Not established; physicians can inquire about dosing guidelines when obtaining antitoxin from CDC |
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| Contraindications | Documented hypersensitivity |
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| Interactions | None reported |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | Derived from horse serum; therefore, allergic reactions (eg, urticaria, serum sickness, anaphylaxis) may occur; perform allergy testing prior to administration; rapid 2- to 4-h desensitization protocol may be used in appropriate individuals |
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| Drug Name | Botulism immune globulin, human (BabyBIG) |
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| Description | Solvent-detergent–treated and viral-screened immune globulin. Derived from pooled adult plasma from persons immunized with botulinum toxoid who developed high neutralizing antibody titers against botulinum neurotoxins type A and B. Indicated to treat infant botulism caused by type A or B C botulinum. |
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| Adult Dose | Not indicated |
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| Pediatric Dose | <1 year: 50 mg/kg (1 mL/kg) IV infusion; 25 mg/kg/h IV (0.5 mL/kg/h) initial infusion rate (0-15 min), not to exceed infusion rate of 50 mg/kg/h (1 mL/kg/h)
>1 year: Not indicated |
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| Contraindications | Documented hypersensitivity to other human immunoglobulins; IgA deficiency |
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| Interactions | Antibodies may interfere with immune response to live virus vaccines (eg, MMR), defer live vaccine administration for 5 mo following botulism immune globulin administration; coadministration with nephrotoxic drugs (eg, gentamicin, furosemide) may increase nephrotoxicity risk |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | Caution if predisposed to acute renal failure or any degree of pre-existing renal impairment, diabetes mellitus, volume depletion, sepsis, paraproteinemia, or concurrent nephrotoxic drugs; like other plasma products, possibility for blood-borne virus transmission exists (eg, Creutzfeldt-Jakob disease); rarely causes aseptic meningitis syndrome; monitor blood pressure during infusion |
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Further Inpatient Care
- Avoid administration of sedatives or CNS depressants.
- Stool softeners and adequate hydration are useful in patients with constipation.
Further Outpatient Care
Transfer
- Transfer the patient to an institution able to provide antitoxin and adequate supportive care, if necessary.
Deterrence/Prevention
- Instruct patients to adhere to safe methods of food handling and preparation.
- Thoroughly cleanse and debride potentially contaminated wounds.
- Instruct parents to avoid feeding honey to infants in the first year of life.
Complications
- Aspiration pneumonia
- Secondary urinary and respiratory tract infections and sepsis
- Subglottic stenosis (following intubation)
Prognosis
- Timing of antitoxin administration greatly influences the prognosis. Retrospective analysis has shown that use of antitoxin within 24 hours is associated with a 10% mortality rate, antitoxin administered more than 24 hours later is associated with a 15% mortality rate, and failure to administer antitoxin carries a 46% mortality rate. Timing of administration also affects length of hospital stay, with a median stay of 10 days when antitoxin is administered within 24 hours, 41 days if administered after 24 hours, and 56 days if not used at all.
- After recovery from acute illness, late symptoms may remain, primarily muscle weakness including diplopia and fatigue with exertion. Although some patients have reported feeling breathless, pulmonary function test results demonstrate that results in lung volumes, forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC), maximum inspiratory and expiratory pressures, and ventilatory response to exercise fall within reference ranges.
Medical/Legal Pitfalls
- Failure to consider the diagnosis of botulism in the hypotonic infant
- Failure to administer antitoxin promptly
- Failure to provide ventilatory support early in the course of treatment
Special Concerns
- Physicians and staff members at the CDC are intensely interested in botulism. Epidemiologists in the Foodborne & Diarrheal Diseases Branch are available 24 hours a day, both to gather information for surveillance and to help physicians treat patients. To contact the CDC, call (404) 639-2206 during business hours and (404) 639-2888 at other times.
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Bioterrorist Agents. Signs and symptoms. Chart courtesy of North Carolina Statewide Program for Infection Control and Epidemiology (SPICE), copyright University of North Carolina at Chapel Hill. |
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Botulism excerpt Article Last Updated: Feb 7, 2008
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