Close
New

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

 

Toxicodendron Poisoning

  • Author: Steven L Stephanides, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Apr 12, 2016
 

Background

Toxicodendron dermatitis is an allergic contact dermatitis (allergic phytodermatitis) that occurs from exposure to members of the plant genus Toxicodendron. In North America, this includes poison ivy, poison oak, and, much less frequently, poison sumac. Although technically not Toxicodendron species, the irritant chemical (urushiol) is also found in mangoes and Japanese lacquer trees and can incite a similar clinical picture. A large number of other botanicals that produce a similar reaction mediated by different irritant chemicals also exist. See the image below.

Forearm approximately 10 days after exposure to po Forearm approximately 10 days after exposure to poison ivy in a garden. Note vesicles and linear areas of the rash.

See 11 Common Plants That Can Cause Dangerous Poisonings, a Critical Images slideshow, to help identify plant reactions and poisonings.

Next

Pathophysiology

Toxicodendron species contain oleoresins known collectively as urushiol. In susceptible individuals, these compounds trigger a type IV delayed hypersensitivity reaction. Usually, the skin is involved; however, the eyes, airway, and lungs may be involved if exposed to smoke from burning plants. Reactions from gastrointestinal exposure in the form of urushiol-containing homeopathic remedies have also been reported.[1]

In susceptible individuals, lesions generally appear within 12-48 hours, although they have been noted to appear earlier. New lesions may continue to appear for up to 2-3 weeks. Initially, these lesions tend to occur from the slow reaction to adsorbed urushiol; however, lesions that appear later are often secondary to contact with contaminated surfaces (eg, clothing, pet hair, gardening tools, camping equipment). Although a common misconception, fluid from the vesicles of a poison ivy rash does not contain urushiol and is not an irritant source for new lesions.

Previous
Next

Epidemiology

Frequency

United States

Toxicodendron species are abundant throughout the United States except in desert areas, elevations above 4000 ft, Alaska, and Hawaii. Poison oak is most common west of the Rockies, poison ivy to the east, and poison sumac in the southeast.

Approximately 50-70% of the United States population is susceptible if exposed casually; however, this percentage increases with significant exposure. Approximately 10-15% of the population is extremely sensitive. Toxicodendron dermatitis is the most common cause of contact dermatitis in the United States, exceeding all other causes combined.

International

Toxicodendron dermatitis occurs outside North America. However, the most prevalent form of plant dermatitis worldwide occurs from exposure to the numerous members of the family Compositae and varied sesquiterpene lactone allergens from these plants. With increasing global travel and transport of plants, true toxicodendron dermatitis is being increasingly reported in Europe, although it is still case reportable.[2, 3]

Mortality/Morbidity

Morbidity is related to sensitivity of the individual exposed as well as the degree and route of exposure. Morbidity ranges from localized mild erythema and pruritus to diffuse erythema, edema, severe pain, and pruritus with bullous lesions. Secondary infection can complicate the dermatitis.

Previous
Next

Race-, Sex-, and Age-related Demographics

No clear racial difference in susceptibility exists. No difference in susceptibility between the sexes exists. Elderly people have reduced sensitivity.

Previous
 
 
Contributor Information and Disclosures
Author

Steven L Stephanides, MD Attending Physician, Department of Emergency Medicine, Eisenhower Medical Center

Steven L Stephanides, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Chris Moore, PhD, MD Medical Director, Department of Emergency Medicine, Virginia Mason Medical Center

Chris Moore, PhD, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Texas Medical Association, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Michael Hodgman, MD Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare

Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society

Disclosure: Nothing to disclose.

References
  1. Cardinali C, Francalanci S, Giomi B, et al. Contact dermatitis from Rhus toxicodendron in a homeopathic remedy. J Am Acad Dermatol. 2004 Jan. 50(1):150-1. [Medline].

  2. Leclercq RM. [Severe contact-allergy dermatitis due to poison ivy--a plant that is rarely encountered in The Netherlands; a family history]. Ned Tijdschr Geneeskd. 2005 Jul 23. 149(30):1697-700. [Medline].

  3. Gach JE, Tucker W, Hill VA. Three cases of severe Rhus dermatitis in an English primary school. J Eur Acad Dermatol Venereol. 2006 Feb. 20(2):212-3. [Medline].

  4. Rader RK, Mu R, Shi H, Stoecker WV, Hinton KA. Dermoscopy of black-spot poison ivy. Dermatol Online J. 2012 Oct 15. 18(10):8. [Medline]. [Full Text].

  5. Botanical dermatology: allergic contact dermatitis. Electronic Textbook of Dermatology. Available at http://telemedicine.org/botanica/bot6.htm. Accessed: April 11, 2016.

  6. Thoo CH, Freeman S. Hypersensitivity reaction to the ingestion of mango flesh. Australas J Dermatol. 2008 May. 49(2):116-9. [Medline].

  7. Tadjimukhamedov FK, Huang G, Ouyang Z, Cooks RG. Rapid detection of urushiol allergens of Toxicodendron genus using leaf spray mass spectrometry. Analyst. 2012 Mar 7. 137(5):1082-4. [Medline].

  8. Stibich AS, Yagan M, Sharma V, Herndon B, Montgomery C. Cost-effective post-exposure prevention of poison ivy dermatitis. Int J Dermatol. 2000 Jul. 39(7):515-8. [Medline].

  9. Davila A, Laurora M, Fulton J, Jacoby J, Reed J, Heller M. A new topical agent, Zanfel, ameliorates urushiol-induced Toxicodendron allergic contact dermatitis. Ann Emerg Med. 2003. 42(4 supp 1):Abstract no 364; s98.

  10. Abrams Motz V, Bowers CP, Mull Young L, Kinder DH. The effectiveness of jewelweed, Impatiens capensis, the related cultivar I. balsamina and the component, lawsone in preventing post poison ivy exposure contact dermatitis. J Ethnopharmacol. 2012 Aug 30. 143(1):314-8. [Medline].

  11. Canavan D, Yarnell E. Successful treatment of poison oak dermatitis treated with Grindelia spp. (Gumweed). J Altern Complement Med. Aug 2005. 11(4):709-11. [Medline].

  12. Abrams Motz V, Bowers CP, Mull Young L, Kinder DH. The effectiveness of jewelweed, Impatiens capensis, the related cultivar I. balsamina and the component, lawsone in preventing post poison ivy exposure contact dermatitis. J Ethnopharmacol. 2012 Aug 30. 143 (1):314-8. [Medline].

  13. Motz VA, Bowers CP, Kneubehl AR, Lendrum EC, Young LM, Kinder DH. Efficacy of the saponin component of Impatiens capensis Meerb.in preventing urushiol-induced contact dermatitis. J Ethnopharmacol. 2015 Mar 13. 162:163-7. [Medline].

  14. Curtis G, Lewis AC. Treatment of severe poison ivy: a randomized, controlled trial of long versus short course oral prednisone. J Clin Med Res. 2014 Dec. 6 (6):429-34. [Medline]. [Full Text].

  15. [Guideline] Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol. 2006 Sep. 97(3 Suppl 2):S1-38. [Medline].

  16. Shofner JD, Kimball AB. Plant-induced dermatitis. Auerbach PS, Ed. Wilderness Medicine. 6th ed. Philadelphia PA: Elsevier Mosby; 2012. 1232-50.

  17. Oh SH, Haw CR, Lee MH. Clinical and immunologic features of systemic contact dermatitis from ingestion of Rhus (Toxicodendron). Contact Dermatitis. 2003 May. 48(5):251-4. [Medline].

  18. Sasseville D. Clinical patterns of phytodermatitis. Dermatol Clin. 2009 Jul. 27(3):299-308, vi. [Medline].

  19. Tanner TL. Rhus (Toxicodendron) dermatitis. Prim Care. 2000 Jun. 27(2):493-502. [Medline].

 
Previous
Next
 
Forearm approximately 10 days after exposure to poison ivy in a garden. Note vesicles and linear areas of the rash.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.