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Urushiol-induced contact dermatitis
Classification and external resources
ICD-10 L23.7
ICD-9 692.6
DiseasesDB 32755
eMedicine emerg/452
MeSH D011040
Toxicodendron pubescens ("Atlantic Poison-oak"), one of a large number of species containing urushiol irritants.
Blistering 48 hours after urushiol contact
Poison ivy rash after 2 days.

Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis and Rhus dermatitis) is the medical name given to allergic rashes produced by the oil urushiol, which is contained in various plants, including the plants of the genus Toxicodendron (including poison ivy, poison oak, and poison Sumac), as well as other plants in the family Anacardiaceae (mango, Rengas tree, Burmese lacquer tree, India marking nut tree, and the shell of the cashew nut), and also unrelated plants such as Ginkgo biloba.

Symptoms of the rash include itching, inflammation, oozing, and in severe cases a burning sensation. The American Academy of Dermatology estimates that there are up to 50 million cases of urushiol-induced dermatitis annually in the United States alone, accounting for 10% of all lost-time injuries in the United States Forest Service. Poison oak is a significant problem in the rural western and southern U.S., while poison-ivy is most rampant in the eastern U.S. Dermatitis from poison sumac is less common but also problematic.



Urushiol-induced contact dermatitis is contracted by contact with a plant or any other object containing urushiol oil. The oil adheres to almost anything it comes in contact with, such as towels, blankets, even clothing. Clothing or other materials that contact the plant and then, before being washed, contact the skin are common causes of exposure. Normally, it takes about 24 hours for the rash to first appear; for those with severe reactions it will worsen during the next few days. For severe reactions a prednisone prescription is necessary to stop skin damage especially if the eyes are involved. The rash persists typically one to two weeks and in some cases up to five weeks. At least 25% of people have very strong responses resulting in severe symptoms. Since the skin reaction is an allergic one, people may develop progressively stronger reactions after repeated exposures.

Urushiol is primarily found in the spaces between plant cells beneath the outer skin of the plant, so the effects of urushiol rash are less severe if the plant tissue remains undamaged on contact. Once the oil and resin are thoroughly washed from the skin, the rash is not contagious. Urushiol does not always spread once it has bonded with the skin, and it is not often transferred from weeping blisters. However, those with severe reactions can spread it by these means.

Although simple skin exposure is most common, ingestion can lead to serious, more systemic reactions. Burning plant material is commonly said to create urushiol-laden smoke that causes systemic reaction as well as rash inside the throat and on the eyes. Firefighters often get rashes and eye inflammation from smoke-related contact. A high-temperature fully inflamed bonfire may incinerate the urushiol before it can cause harm, while a smoldering fire could vaporize the volatile oil and spread it as white smoke. However, some sources dispute the danger of burning urushiol-containing plant material.[1]


The toxic effects of urushiol are indirect, mediated by an induced autoimmune response. Urushiol acts as a hapten, chemically reacting with, binding to, and changing the shape of integral membrane proteins on exposed skin cells. Affected proteins interfere with the immune system's ability to recognize these cells as normal parts of the body, causing a T-cell mediated immune response.[2] This immune response is directed towards the complex of urushiol derivatives bound in the skin proteins, attacking the cells as if they were foreign bodies.


The result is an allergic eczematous contact dermatitis characterized by redness, swelling, papules, vesicles, blisters, and streaking.[3] People vary greatly in their sensitivity to urushiol. In approximately 15%[4] to 30%[5] of people urushiol does not initiate an immune system response, while at least 25% of people have very strong immune responses resulting in severe symptoms. Since the skin reaction is an allergic one, people may develop progressively stronger reactions after repeated exposures, or show no immune response on their first exposure, but show sensitivity on following exposures.

Approximately 80% to 90% of adults will get a rash if they are exposed to 50 micrograms of purified urushiol. Some people are so sensitive that it only takes a molecular trace of urushiol (two micrograms or less than one millionth of an ounce) on the skin to initiate an allergic reaction (Epstein et al., 1974).[6]

The rash takes one to two weeks to run its course and normally does not leave scars. Severe cases will have small (1–2 mm) clear fluid-filled blisters on the skin. Pus-filled vesicles, containing a whitish fluid, may indicate a secondary infection. Most poison ivy rashes, without infections, will self-resolve within 14 days without treatment. Excessive scratching may result in secondary infection, commonly by staphylococcal and streptococcal species; these may require the use of antibiotics.


Potential treatments are in two phases: stopping the urushiol contact causing a reaction with the skin (this must be done within minutes), or later in reducing the pain of any blistering that has formed.[7][8]

Primary treatment involves washing exposed skin thoroughly with soap and water as soon as possible after exposure is discovered. Soap or detergent is necessary, as urushiol is a hydrophobic (not water-soluble) oil. Commercial removing preparations, which are available in areas where poison-ivy grows, usually contain surfactants, such as the nonionic detergent Triton X-100 to solubilize urushiol; some preparations also contain abrasives.

Antihistamines and hydrocortisone creams or antihistamines by mouth in severe cases can be used to alleviate the symptoms of a developed rash. Non-prescription oral diphenhydramine is the most commonly suggested antihistamine. Topical formulations containing diphenhydramine are available but may further irritate the affected skin areas. No vaccine has been developed to counter urushiol symptoms, so the most effective "cures" are generally held to be those products that physically remove the urushiol. After about 15 minutes of exposure, the urushiol is chemically bonded to the skin and can only be removed with pharmaceutical products, which vary by person in effectiveness.

In cases of extreme symptoms, steroids such as prednisone are sometimes administered to attenuate the immune response. Prednisone is the most commonly prescribed systemic treatment, but can cause serious adrenal suppression changes, so it must be taken carefully, tapering off slowly.[9] If bacterial secondary infection of affected areas occurs, antibiotics may also be necessary.

Many home remedies and even commercial products (e.g., Zanfel and Tecnu) claim to treat urushiol rashes or remove bonded urushiol from the skin. However, a study of Tecnu, Goop, and Dial soap found 70%, 62%, and 56% protection relative to the possible maximum response, at costs per ounce of $1.25, $0.07, and $0.07. The study compared four 2.5 cm exposed squares on the inner aspect of the forearm, three of which were treated and one untreated. The relatively high cost of Dial indicates very thorough washing.[10]

Some clarifications:

  • Scrubbing with plain soap and cold water will remove the urushiol from skin if it is done within a few minutes of exposure, before it bonds.[11]
  • Ordinary laundering with laundry detergent will remove urushiol from most clothing[12], but not from leather or suede.
  • The fluid from the resulting blisters does not spread poison ivy to others.[11]
  • Poison ivy is not harmless when the leaves have fallen off as the toxic resin is very persistent. Every part of the plant contains urushiol, and can cause a rash with exposure at any time of the year.[11]
  • Ice, cold water, cooling lotions, or cold air do not help cure poison-ivy rashes, but cooling can reduce inflammation and soothe the itch.[12]
  • Burow's solution, calamine lotion[13] and Jewelweed[14][15][16][17] are ineffective or of questionable effectiveness against itching.

See also


  1. ^ Dietrich Frohne and Hans Jurgen Pfander (1984). A Colour Atlas of Poisonous Plants: A Handbook for Pharmacists, Doctors, Toxicologists, and Biologists. Wolfe Publishing Ltd. p. 291 pp.. ISBN 0-7234-0839-4.  
  2. ^ C.Michael Hogan (2008) Western poison-oak: Toxicodendron diversilobum, GlobalTwitcher, ed. Nicklas Stromberg [1]
  3. ^ DermAtlas -1892628434
  4. ^ Howstuffworks "How Poison Ivy Works"
  5. ^ Contact-Poisonous Plants of the World
  6. ^ Herbalgram (American Botanical Council) Volume 34: 36-42, 1995 by W.P. Armstrong and W.L. Epstein, M.D. cited in
  7. ^ Soothing Remedies for Poison Ivy and Poison Oak
  8. ^ "Poison Oak". Wayne's Word.  
  9. ^
  10. ^ "Cost-effective post-exposure prevention of poison ivy dermatitis".;jsessionid=KyvXjvnwSXZXQHDpG6hgytBwGvGG7hTY4GCF215g18cMgvc9PHpK!1032775582!181195628!8091!-1.  
  11. ^ a b c "Poison Ivy Myths". PennState Integrated Pest Management project.  
  12. ^ a b "Poison Ivy: Prevention and Treatment".  
  13. ^ Arthur Higbee (1992-09-09). "An Outdated Notion, That Calamine Lotion". International Herald Tribune. Retrieved 2008-04-15.  
  14. ^ D. Long, N. H. Ballentine, J. G. Marks. Treatment of poison ivy/oak allergic contact dermatitis with an extract of jewelweed. Am. J. Contact. Dermat. 8(3):150-3 1997 PMID 9249283
  15. ^ M. R. Gibson, F. T. Maher. Activity of jewelweed and its enzymes in the treatment of Rhus dermatitis. J. Am. Pharm. Assoc. Am. Pharm. Assoc. 39(5):294-6 1950 PMID 15421925
  16. ^ J. D. Guin, R. Reynolds. Jewelweed treatment of poison ivy dermatitis. Contact Dermatitis 6(4):287-8 1980 PMID 6447037, doi:10.1111/j.1600-0536.1980.tb04935.x
  17. ^ B. J. Zink, E. J. Otten, M. Rosenthal, B. Singal. The effect of jewel weed in preventing poison ivy dermatitis. Journal of Wilderness Medicine 2(3):178–182 1991, abstract

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