Toxicodendron Poisoning

Updated: Jun 13, 2022
Author: Steven L Stephanides, MD; Chief Editor: Michael A Miller, MD 


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.




The history in cases of possible Toxicodendron toxicity should include questions about the following:

  • 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 that has been outside in an area with Toxicodendron species

Physical Examination

The dermatitis 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

Characteristics of moderate-to-severe cases are as follows:

  • Diffuse areas of erythema and edema
  • Severe pruritus and/or pain
  • Bullae (note that fluid from bullae does not contain urushiol)

Uncommonly, dermatitis from exposure to poison ivy may include black spots. The spots consist of urushiol oleoresins, which harden within minutes of exposure to air to form a black resin.[8, 9]

Erythema multiforme is an atypical presentation of toxicodendron dermatitis reported after sumac ingestion.



Diagnostic Considerations

Other problems to be considered include the following:

  • Inverse psoriasis

  • Nontoxicodendron contact dermatitis

  • Palmoplantar psoriasis

  • Photosensitivity

  • Cellulitis

Differential Diagnoses



Approach Considerations

Toxicodendron dermatitis is a clinical diagnosis. Laboratory testing is usually not necessary as part of the emergency department evaluation.

Patch testing is discouraged for toxicodendron dermatitis because it might sensitize an unsensitized individual. However, if contact dermatitis is being considered, patch testing for other allergens might be considered.

Leaf spray mass spectrometry, which is a new ambient ionization method, can detect allergenic urushiols directly from poison ivy with no sample preparation; the results show all the urushiols reported using liquid chromatography mass spectrometry methods. The identifications were confirmed with tandem mass spectrometry analysis of the leaf spray ions. Enhanced detection of some urushiols was achieved in the negative mode if chloride anions were added to the spray solvent.[10] This technique, although not yet readily available, has been used to confirm the diagnosis of black-spot poison ivy, which may clinically resemble melanoma.[8]



Prehospital Care

Preventive measures for toxicodendron dermatitis includes using barriers. Classic preventive strategies include wearing long sleeves, long pants, and gloves. Vinyl gloves are preferred because they will not absorb the urushiol as readily as leather or fabric gloves. Rubber gloves can be permeable to urushiol.

A number of commercially available creams are marketed to prevent penetration of urushiol into the skin. The published data on these remedies are limited and conflicting. Although some protective effect is suggested, the degree of protection and the cost-to-benefit ratio are unclear.

The initial treatment of toxicodendron dermatitis is to wash the affected area as soon as possible after exposure. Washing exposed areas with copious amounts of water within 20 minutes of exposure has been shown to reduce reactivity.[11] The efficacy of washing appears to decrease over time.

Emergency Department Care

Treatment can be considered in the following three categories:

  • Decontamination
  • Topical/symptomatic treatment
  • Immunomodulation


Immediate decontamination: Urushiol penetrates the skin and binds to membrane lipids within 10-20 minutes of contact. If the toxin can be removed before this occurs, reaction can be avoided.

Although multiple products are marketed for skin decontamination, they are only slightly more efficacious than soap and water.[12] Copious water is recommended because soaps can spread the urushiol oil around the skin.

It is important to instruct patients to clean their clothes and any other objects that might have been in contact with the oils.

Topical or symptomatic care

Topical preparations for symptomatic relief are the standard care for poison ivy exposure. Calamine (a combination of zinc oxide and ferric oxide), oatmeal baths, and Burow solution (an aqueous solution of aluminium triacetate, Domeboro®), all have been recommended. To prevent ground oatmeal from caking in pipes, it can be placed in a tied sock before being dropped in the bathtub.

Zanfel®, a soap mixture of ethoxylate and sodium lauroyl sarcosinate surfactants, is a product that is claimed to bind the urushiol resin for a number of days after exposure. It has been aggressively marketed. Limited data on this product show a mild benefit of up to 6 days after experimental exposure.[13]

A number of herbally based folk remedies (eg, jewelweed[14] ) have been proposed over the years and are receiving some new attention, although none can be particularly endorsed at this time.[15] A study by Abrams Motz and colleagues confirmed that jewelweed mash is effective for preventing development of dermatitis after poison ivy contact, but is less effective than soap.[16] These researchers subsequently confirmed that saponins in jewelweed are responsible for this effect.[17]

Oral antihistamines can be of some benefit for the relief of pruritus, especially in severe cases with urticarial lesions accompanying the bullae.

Low-potency topical steroids and topical antihistamines have not been shown to have any beneficial effect.

Oral analgesics (eg, acetaminophen, nonsteroidal anti-inflammatory drugs [NSAIDs]) occasionally are required for very severe cases, especially as an aid to sleep.


Systemic steroids are the standard treatment for severe toxicodendron dermatitis. These generally are given orally, although some authors prefer high-potency steroid creams (fluocinonide or clobetasol propionate applied topically twice a day for a week and then once a day for a week) if started early in the course.

Orally, various bursts of prednisone or methylprednisolone are used. These medications should be tapered off for at least 10-14 days (up to 3 wks). A study by Curtis and Lewis in 49 patients with severe poison ivy dermatitis found that patients who received a 5-day burst followed by a 10-day taper were significantly less likely to utilize other medications, compared with patients who received a burst regimen only (22.7% vs. 55.6%, P = 0.02). The longer regimen consisted of 5 days of 40 mg oral prednisone daily followed by the following taper[18] :

  • 30 mg daily for 2 days
  • 20 mg daily for 2 days
  • 10 mg daily for 2 days
  • 5 mg daily for 4 days

Early withdrawal of steroid therapy can lead to a recrudescence of the lesions. Therefore, avoid premade dose packs, and emphasize to the patient the importance of finishing his or her course of medication.


Avoid exposure. Protective clothing, such as gloves (nonlatex), should be worn if handling the plants or contaminated objects or animals. A number of barrier creams and lotions are available. Although they cannot completely eliminate the reaction, they can diminish the exposure.

Long-Term Monitoring

Patients should follow up with their primary care physician. All contaminated clothing and articles should be washed. Pets that have been exposed should be bathed well to remove the oil from their fur. Precautions include watching for secondary bacterial infection of skin lesions.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Oral antihistamines can be of some benefit for the relief of pruritus. Systemic steroids are the standard for severe toxicodendron dermatitis.


Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.

Prednisone (Deltasone)

Immunosuppressant that may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. DOC used in moderate-to-severe cases. Blocks type IV hypersensitivity reaction.

Methylprednisolone (Solu-Medrol)

Steroids ameliorate delayed effects of anaphylactoid reactions and may limit biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may be beneficial to reduce inflammatory effects of this immune complex–mediated disease. Available as PO/IV preparations.


Class Summary

These agents provide symptomatic relief of pruritus.

Diphenhydramine (Benadryl)

For symptomatic relief of symptoms caused by release of histamine in allergic reactions.

Hydroxyzine (Vistaril, Atarax)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Sedating, alternative to diphenhydramine.

Cimetidine (Tagamet)

If no response to H1 antagonist alone, coadministration with this H2 antagonist treats itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis.


Questions & Answers


What is toxicodendron dermatitis?

How is toxicodendron dermatitis treated?

What is the pathophysiology of toxicodendron dermatitis?

What causes toxicodendron dermatitis?

What is the prevalence of toxicodendron dermatitis?

What is the prognosis for toxicodendron dermatitis?

What are the possible complications of toxicodendron dermatitis?

What is included in patient education about toxicodendron dermatitis?


Which clinical history findings are characteristic of toxicodendron dermatitis?

Which factors affect the severity of toxicodendron dermatitis?

What are the signs and symptoms of mild toxicodendron dermatitis?

What are the signs and symptoms of moderate-to-severe toxicodendron dermatitis?


Which conditions are included in the differential diagnoses of toxicodendron dermatitis?

What are the differential diagnoses for Toxicodendron Poisoning?


How is toxicodendron dermatitis diagnosed?

What is the role of leaf spray mass spectrometry in the workup for toxicodendron dermatitis?


What are the barrier methods of prevention for toxicodendron dermatitis?

What is the efficacy of topical creams for the prevention for toxicodendron dermatitis?

What is included in prehospital care for toxicodendron dermatitis?

What are the treatment options for toxicodendron dermatitis?

What is the role of decontamination in the treatment of toxicodendron dermatitis?

What is included in symptomatic care for toxicodendron dermatitis?

What is the role of steroids in the treatment of toxicodendron dermatitis?

How is toxicodendron dermatitis prevented?

What is included in long-term monitoring following treatment of toxicodendron dermatitis?


What is the role of medications in the treatment of toxicodendron dermatitis?

Which medications in the drug class Antihistamines are used in the treatment of Toxicodendron Poisoning?

Which medications in the drug class Corticosteroids are used in the treatment of Toxicodendron Poisoning?