eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Botulism

Author: Robert W Tolan Jr, MD, Chief, Division 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
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
Contributor Information and Disclosures

Updated: Jan 21, 2009

Introduction

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. Most countries have not yet reported a case of infant botulism, likely because of underrecognition, underreporting, or both.

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

Gender 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.

Clinical

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

More on Botulism

Overview: Botulism
Differential Diagnoses & Workup: Botulism
Treatment & Medication: Botulism
Follow-up: Botulism
Multimedia: Botulism
References
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Further Reading

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Keywords

botulism, constipation, food poisoning, dry mouth, autonomic dysfunction, Bacillus botulinus, blurred vision, botulinum toxin, botulinus, botulism, Clostridium argentinense, C argentinense, Clostridium baratii, C baratii, Clostridium botulinum, C botulinum, Clostridium butyricum, C butyricum, decreased ocular motility, diplopia, dysarthria, dysphagia, food-borne botulism, hyporeflexia, hypotonia, infant botulism, muscle weakness, mydriasis, orthostatic hypotension, paralysis, ptosis, urinary retention, wound botulism, abdominal cramps

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Contributor Information and Disclosures

Author

Robert W Tolan Jr, MD, Chief, Division 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, MD 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
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Coauthor(s)

Daniel AC Frattarelli, MD, FAAP, Senior Staff, Departments of Pediatrics and Emergency Medicine, Henry Ford Hospital
Daniel AC Frattarelli, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Clinical Pharmacology, and American Society for Clinical Pharmacology and Therapeutics
Disclosure: Nothing to disclose.

Nahed M Abdel-Haq, MD, Assistant Professor, Department of Pediatrics, Wayne State University School of Medicine
Nahed M Abdel-Haq, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Medical Editor

Itzhak Brook, MD, MSc, Professor, Department of Pediatrics, Georgetown University School of Medicine
Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Ear, Nose and Throat Advances in Children, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, and Surgical Infection Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School of Medicine
Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting; Pfizer Honoraria Consulting

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
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