Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

CBRNE - Botulism Clinical Presentation

  • Author: Peter P Taillac, MD; Chief Editor: Duane C Caneva, MD, MSc  more...
 
Updated: Apr 21, 2015
 

History

Although laboratory confirmation is necessary for a definitive diagnosis, clinical presentation, patient history, and physical examination (particularly neurologic exam) can be used as strong indicators for the presence of botulism. Due to the delay in laboratory confirmation and the necessity of treatment prior to the binding of the toxin to neurons, antitoxin should be empirically begun in patients with highly suggestive presentations.

Place special attention on eliciting a complete patient history, including the following:

  • History of foods eaten, and any ill contacts who ate the same foods.
  • History of intravenous drug abuse (especially "skin popping")
  • Recent surgery or trauma
  • Gastrointestinal problems or intestinal bypass surgery
  • Laparoscopic appendectomy [5] (one case report)
Next

Physical

Physical examination findings vary according to the form of botulism (ie, food borne, infant, wound).

Food-borne botulism

The Centers for Disease Control and Prevention (CDC) suggests attention to the following cardinal features:

  • Patient is afebrile unless another infection is present
  • Patient demonstrates symmetric neurologic symptoms
  • Patient remains responsive, with intact sensation (14% of patients report some paresthesias or decreased sensation)
  • Patient has a normal or slow heart rate in the absence of hypotension
  • Signs typically are not accompanied by sensory deficits, with the exception of blurred vision
  • The neurologic manifestations often have been described as a progressive, symmetric, descending weakness or paralysis that first affects muscles innervated by the cranial nerves, then progresses to involve muscles of the neck, arms, and legs; this occurs in an alert patient with intact sensorium and intact sensation
  • The typical progression of symptoms (in order of appearance) in a botulinum neurotoxin poisoning can be summarized by the Dozen D's: dry mouth, diplopia, dilated pupils, droopy eyes, droopy face, diminished gag reflex, dysphagia, dysarthria, dysphonia, difficulty lifting head, descending paralysis, and diaphragmatic paralysis.
  • Respiratory difficulty arises from airway obstruction and diaphragmatic weakness. Diplopia, dysarthria, dry mouth, and generalized weakness are among the most common presenting symptoms. Other symptoms that have been associated with botulism include ptosis, dysphagia, sore throat, dysphonia, nystagmus, ataxia, paresthesias, paralytic ileus, severe constipation, urinary retention, and orthostatic hypotension.
  • Pupils are dilated or unreactive (ophthalmoplegia) in 50% of patients. Unless secondary complications such as respiratory failure develop, patients are alert and mental function is unimpaired
  • Sensory deficits only have been reported in isolated cases; neurologic symptoms may appear from 6 hours to 10 days after ingestion of toxin, with a median incubation period of 1 day
  • Nausea, vomiting, and diarrhea often precede or accompany neurologic manifestations; constipation typically follows after neurologic signs have appeared. GI symptoms are more prominent in food-borne botulism and much less pronounced in cases of wound botulism.

Infant botulism

The degree of involvement in this form of the disease can vary from asymptomatic to paralysis to sudden death.

A prominent and common sign of the disease is constipation (defined as 3 or more days without defecation). Other clinical features include listlessness, lethargy, difficulty in sucking and swallowing, hypotonia, weak cry, poor feeding, pooled oral secretions, generalized muscle weakness, and poor head control, which gives the infant a characteristic floppy appearance.

Neurologic findings include the following:

  • Ptosis
  • Ophthalmoplegia
  • Sluggish pupillary reaction to light
  • Flaccid expression
  • Dysphagia
  • Weak gag reflex
  • Poor anal sphincter tone

Respiratory failure occurs in approximately 50% of diagnosed patients.

The incubation period (between the time of spore ingestion and onset of symptoms) associated with infant botulism varies from 3-30 days.

Wound botulism

Patients often present with much of the same symptomatology that is observed in the food-borne form, including acute blurred vision, dysphagia, dysarthria, generalized weakness (with or without absence of deep tendon reflexes), and pupillary abnormalities. Gastrointestinal manifestations are absent.

The Clostridium- infected wound generally appears benign, without typical signs of infection (unless also infected by other bacteria, in which case a fever also may be present). In some cases, the wound is not apparent.

The average incubation period is 10 days.

Previous
 
 
Contributor Information and Disclosures
Author

Peter P Taillac, MD Clinical Professor of Surgery, Division of Emergency Medicine, University of Utah Health Sciences Center

Peter P Taillac, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Joseph Kim, MD Chairman, Department of Emergency Medicine, Western Medical Center; Clinical Instructor, University of California, Irvine, School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Barry J Sheridan, DO Chief Warrior in Transition Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Duane C Caneva, MD, MSc Senior Medical Advisor to Customs and Border Protection, Department of Homeland Security (DHS) Office of Health Affairs; Federal Co-Chair, Health, Medical, Responder Safety Subgroup, Interagency Board (IAB)

Disclosure: Nothing to disclose.

Additional Contributors

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Sobel J, Tucker N, Sulka A, McLaughlin J, Maslanka S. Foodborne botulism in the United States, 1990-2000. Emerg Infect Dis. 2004 Sep. 10(9):1606-11. [Medline]. [Full Text].

  2. Centers for Disease Control and Preventions. CDC U.S.National Botulism Surveillance Summary. Available at http://www.cdc.gov/nationalsurveillance/botulism-surveillance.html. Accessed: December 22, 2014.

  3. McCroskey LM, Hatheway CL. Laboratory findings in four cases of adult botulism suggest colonization of the intestinal tract. J Clin Microbiol. 1988 May. 26(5):1052-4. [Medline].

  4. Mechem CC, Walter FG. Wound botulism. Vet Hum Toxicol. 1994 Jun. 36(3):233-7. [Medline].

  5. Nystrom SC, Wells EV, Pokharna HS, et al. Botulism toxemia following laparoscopic appendectomy. Clin Infect Dis. 2012 Feb 15. 54(4):e32-4. [Medline].

  6. Ching KH, Lin A, McGarvey JA, Stanker LH, Hnasko R. Rapid and selective detection of botulinum neurotoxin serotype-A and -B with a single immunochromatographic test strip. J Immunol Methods. 2012 Jun 29. 380(1-2):23-9. [Medline].

  7. Basavanna U, Muruvanda T, Brown EW, Sharma SK. Development of a Cell-Based Functional Assay for the Detection of Clostridium botulinum Neurotoxin Types A and E. Int J Microbiol. 2013. 2013:593219. [Medline]. [Full Text].

  8. Kiris E, Burnett JC, Kane CD, Bavari S. Recent advances in botulinum neurotoxin inhibitor development. Curr Top Med Chem. 2014. 14(18):2044-61. [Medline].

  9. Arnon SS, Schechter R, Inglesby TV. Botulinum toxin as a biological weapon: medical and public health management. JAMA. 2001 Feb 28. 285(8):1059-70. [Medline].

  10. Bigalke H, Rummel A. Medical aspects of toxin weapons. Toxicology. 2005 Oct 30. 214(3):210-20. [Medline].

  11. Centers for Disease Control and Prevention. Botulism associated with commercially canned chili sauce--Texas and Indiana, July 2007. MMWR. Aug 3, 2007. 56(30):767-9. [Medline].

  12. Dunbar EM. Botulism. J Infect. 1990 Jan. 20(1):1-3. [Medline].

  13. Fox CK, Keet CA, Strober JB. Recent advances in infant botulism. Pediatr Neurol. 2005 Mar. 32(3):149-54. [Medline].

  14. Freedman M, Armstrong RM, Killian JM. Botulism in a patient with jejunoileal bypass. Ann Neurol. 1986 Nov. 20(5):641-3. [Medline].

  15. Goonetilleke A, Harris JB. Clostridial neurotoxins. J Neurol Neurosurg Psychiatry. 2004 Sep. 75 Suppl 3:iii35-9. [Medline].

  16. Hatheway CL. Botulism: the present status of the disease. Curr Top Microbiol Immunol. 1995. 195:55-75. [Medline].

  17. Horowitz BZ. Botulinum toxin. Crit Care Clin. 2005 Oct. 21(4):825-39, viii. [Medline].

  18. Horowitz, B. Zane. The ripe olive scare and hotel Loch Maree tragedy: Botulism under glass in the 1920’s. Clinical Toxicology. 2011. 49:345-347.

  19. Mandell GL, Bennett JE, Dolin R. Clostridium botulinum. Principles and Practice of Infectious Diseases. 4th ed. 1995. 2178.

  20. Marks JD. Medical aspects of biologic toxins. Anesthesiol Clin North America. 2004 Sep. 22(3):509-32, vii. [Medline].

  21. Mcnally RE, Morrison MB, Berndt JE, et al. Effectiveness of medical defense interventions against predicted battlefield levels of botulinum toxin A. 1994.

  22. Park JB, Simpson LL. Progress toward development of an inhalation vaccine against botulinum toxin. Expert Rev Vaccines. 2004. 3(4):477-87. [Medline].

  23. Schmidt RD, Schmidt TW. Infant botulism: a case series and review of the literature. J Emerg Med. 1992 Nov-Dec. 10(6):713-8. [Medline].

  24. Shukla HD, Sharma SK. Clostridium botulinum: a bug with beauty and weapon. Crit Rev Microbiol. 2005. 31(1):11-8. [Medline].

  25. Smith, LA; Rusnak, JM. Botulinum neurotoxin vaccines: past, present, and future. Crit Rev Immunol. 2007. 27(4):303-18. [Medline].

  26. Ting PT, Freiman A. The story of Clostridium botulinum: from food poisoning to Botox. Clin Med. 2004 May-Jun. 4(3):258-61. [Medline].

  27. Underwood K, Rubin S, Deakers T, Neuth C. Infant botulism: a 30-year experience spanning the introduction of botulism immune globulin intravenous in the intensive care unit at Childrens Hospital Los Angeles. Pediatrics. Dec 2007. 120(6):e1380-5. [Medline].

  28. Weber JT, Hoeprich PD, et al. Botulism. Jordan MC, et al, eds. Infectious Diseases. 5th ed. 1994. 1185.

  29. Wenham TN. Botulism: a rare complication of injecting drug use. Emerg Med J. 2008 Jan. 25(1):55-6. [Medline].

  30. World Health Organization. Outbreak news. Botulism, Thailand. Wkly Epidemiol Rec. 2006 Mar 31. 81(13):118. [Medline].

 
Previous
Next
 
Courtesy of Arnon SS, et al. Botulinum toxin as a biological weapon: medical and public health management. JAMA 2001 Apr 25;285:1059.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.