eMedicine Specialties > Emergency Medicine > Toxicology

Plant Poisoning, Toxicodendron

Author: Steven L Stephanides, MD, Attending Physician, Department of Emergency Medicine, Eisenhower Medical Center
Coauthor(s): Chris Moore, PhD, MD, Medical Director, Department of Emergency Medicine, Virginia Mason Medical Center
Contributor Information and Disclosures

Updated: Aug 18, 2009

Introduction

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.

Forearm approximately 10 days after exposure to p...

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

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Forearm approximately 10 days after exposure to p...

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

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. 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.

Frequency

United States

Toxicodendron species are abundant throughout the United States except in desert areas, elevations above 4000 ft, Alaska, or 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 US 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.1,2

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.

Race

No clear racial difference in susceptibility exists.

Sex

No difference in susceptibility between the sexes exists.

Age

Elderly people have reduced sensitivity.

Clinical

History

  • Known exposure to poison ivy, oak, or sumac
  • Outdoor activities in areas with Toxicodendron species within the previous 8 hours to 14 days
  • History of toxicodendron dermatitis
  • Contact with a pet who has been outside in an area with Toxicodendron species

Physical

The dermatitidis is highly variable and depends on the sensitivity of the patient and extent of exposure.

  • Mild cases
    • In mild cases, classic lesions on exposed skin are secondary to brushing against the plant or excoriations from scratching.
    • Characteristics of mild classic lesions are as follows:
      • Linear
      • Erythematous, possibly edematous
      • Pruritic or mildly painful
      • May have small vesicles
  • Moderate-to-severe cases
    • Diffuse areas of erythema and edema
    • Severe pruritus and/or pain
    • Bullae (Note that fluid from bullae does not contain urushiol.)
  • Erythema multiforme is an atypical presentation of toxicodendron dermatitis.

Causes

Exposure to urushiol-containing plants

  • Poison ivy (Toxicodendron rydbergii), poison oak (Toxicodendron diversilobum), and poison sumac (Toxicodendron vernix) are most common in North America.
  • Urushiol can also be found in mango plants and Japanese lacquer tree (Rhus verniciflua), although these are not Toxicodendron species.
    • Mango fruit skin can cause reaction in susceptible individuals.3
    • Exposure to unroasted cashew nut shells can cause a dermatitis often confused with toxicodendron dermatitis in susceptible individuals. Roasting inactivates the allergen.

More on Plant Poisoning, Toxicodendron

Overview: Plant Poisoning, Toxicodendron
Differential Diagnoses & Workup: Plant Poisoning, Toxicodendron
Treatment & Medication: Plant Poisoning, Toxicodendron
Follow-up: Plant Poisoning, Toxicodendron
Multimedia: Plant Poisoning, Toxicodendron
References
Further Reading
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References

  1. 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. Jul 23 2005;149(30):1697-700. [Medline].

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

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

  4. 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].

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

  6. Botanical dermatology: allergic contact dermatitis. Electronic Textbook of Dermatology. Available at http://telemedicine.org/botanica/bot6.htm. Accessed June 16, 2007.

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

  8. Chapel TA, Chapel J. Toxicodendron dermatitis. In: Emergency Medicine - A Comprehensive Study Guide. 4th ed. 1996:1111-1113.

  9. Davila A, Laurora M, Fulton J. 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. Epstein WL. The poison ivy picker of Pennypack Park: the continuing saga of poison ivy. J Invest Dermatol. Mar 1987;88(3 Suppl):7s-11s. [Medline].

  11. Epstein WL. Topical prevention of poison ivy/oak dermatitis. Arch Dermatol. Apr 1989;125(4):499-501. [Medline].

  12. Epstein WL, Epstein JH. Plant-induced dermatitis. In: Auerbach PS, ed. Wilderness Medicine. 4th ed. Mosby; 2001:1088-1107.

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

  14. Orchard SM, Fellman JH, Storrs FJ. Topical substances which prevent poison ivy allergic contact dermatitis. Acta Derm Venereol Suppl (Stockh). 1987;134:103-6. [Medline].

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

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

  17. Williford PM, Sheretz EF. Poison ivy dermatitis. Nuances in treatment. Arch Fam Med. Feb 1994;3(2):184-8. [Medline].

  18. Wooldridge WE. Acute allergic contact dermatitis. How to manage severe cases. Postgrad Med. Mar 1990;87(4):221-4. [Medline].

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Further Reading

Clinical guidelines

American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol 2006 Sep;97(3 Suppl 2):S1-38. 5

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Keywords

poison ivy, poison oak, poison sumac, toxicodendron plant poisoning, rhus dermatitis, urushiol-containing plants, poison ivy, Toxicodendron rydbergii, Toxicodendron diversilobum, Toxicodendron vernix, plant poisoning, toxicodendron exposure, toxicodendron dermatitis, allergic contact dermatitis, allergic phytodermatitis, contact dermatitis

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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, and 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 and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Miguel C Fernández, MD, FAAEM, FACEP, FACMT, Associate Clinical Professor; Medical and Managing Director, South Texas Poison Center, Department of Surgery/Emergency Medicine and Toxicology, University of Texas Health Science Center at San Antonio
Miguel C Fernández, MD, FAAEM, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, Society for Academic Emergency Medicine, and Texas Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & 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.

Managing Editor

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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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