Toxicodendron Poisoning

Updated: Jun 13, 2022
  • Author: Steven L Stephanides, MD; Chief Editor: Michael A Miller, MD  more...
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Practice Essentials

Toxicodendron dermatitis is an allergic contact dermatitis (allergic phytodermatitis) that occurs from exposure to urushiol, a skin-irritating oil produced by 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, mangoes and Japanese lacquer trees also contain urushiol and can incite a similar clinical picture. [1] 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.

Treatment of toxicodendron dermatitis comprises the following (see Treatment):

  • Decontamination
  • Topical/symptomatic treatment
  • Immunomodulation


Toxicodendron species contain oleoresins known collectively as urushiol. In susceptible individuals, these compounds can 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. [2]

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.



Dermatitis from urushiol oleoresins follows exposure to members of the plant genus Toxicodendron.

Poison ivy (Toxicodendron rydbergii), poison oak (Toxicodendron diversilobum), and poison sumac (Toxicodendron vernix) are most common in North America. [3]

Urushiol can also be found in mango plants and the Japanese lacquer tree (Rhus verniciflua), although these are not Toxicodendron species; mango fruit skin can cause reactions in susceptible individuals. [4]

Exposure to unroasted cashew nut shells can cause a dermatitis often confused with toxicodendron dermatitis in susceptible individuals. Roasting inactivates the allergen.



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. According to the 2018 Annual Report of the American Association of Poison Control Centers' National Poison Data System, skin irritation from Toxicodendron was the 6th most common plant exposure, accounting for 1015 cases. [5]

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. [6, 7]

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



Complete resolution is expected within 7-21 days. 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.

Potential complications include the following:

  • Superinfection of skin lesions
  • Hyperpigmentation of healing lesions (usually resolves spontaneously within a few weeks)

Patient Education

Instruct the patient that the fluid from the bullae is not an irritant and cannot extend the rash.

If steroids have been given, caution the patient on the risks of rebound flare if steroid therapy is stopped prematurely.

For patient education information, see the Allergies Center, as well as Poison Ivy, Oak, and Sumac.