Urushiol-induced contact dermatitis

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Urushiol-induced contact dermatitis
Classification and external resources
Poison ivy contact dermatitis.jpg
ICD-10 L23.7
ICD-9 692.6
DiseasesDB 32755
eMedicine emerg/452
MeSH D011040

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), other plants in the sumac Anacardiaceae family (mango, pistachio, Rengas tree, Burmese lacquer tree, India marking nut tree, and the shell of the cashew nut), and unrelated plants such as Ginkgo biloba.[1]

Symptoms of the rash include itching, inflammation, oozing, and in severe cases, a burning sensation. The American Academy of Dermatology estimates 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 United States, while poison ivy is most rampant in the eastern United States. Dermatitis from poison sumac is less common.

Exposure[edit]

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
Poison ivy rash with swelling about 3 days after direct contact.

Urushiol-induced contact dermatitis is contracted by contact with a plant or any other object containing urushiol oil. The oil adheres to almost anything with which it comes in contact, such as towels, blankets and 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 cannot be transferred once the urushiol has been washed away.

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.[2] 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.[3]

Mechanism[edit]

Urushiols are oxidized in-vivo, generating a quinone form of the moleules.[4]

The toxic effects of the oxidized urushiols is indirect, mediated by an induced immune response. The oxidized urushiols acts as haptens, chemically reacting with, binding to, and changing the shape of integral membrane proteins on exposed skin cells. One protein recognized in this process is CD28.[5]

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.[6] This immune response is directed towards the complex of urushiol derivatives (namely, pentadecacatechol) bound in the skin proteins, attacking the cells as if they were foreign bodies.

Rash[edit]

The result is an allergic eczematous contact dermatitis characterized by redness, swelling, papules, vesicles, blisters, and streaking.[7] People vary greatly in their sensitivity to urushiol. In approximately 15%[8] to 30%[9] 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, it only takes a trace of urushiol (two micrograms or less than one ten-millionth of an ounce) on the skin to initiate an allergic reaction (Epstein et al., 1974).[10]

The rash takes one to two weeks to run its course and may cause scars depending on severity of exposure. 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.

Treatments[edit]

Potential treatments are in two phases: stopping the urushiol contact causing a reaction with the skin (this must be done within minutes), and later in reducing the pain or pruritus (itching) of any blistering that has formed.[11][12]

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 an 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.

The U.S. Food and Drug Administration has recommended "using wet compresses or soaking in cool water", "applying OTC topical corticosteroid preparations or taking prescription oral corticosteroids", "applying topical OTC skin protectants, such as zinc acetate, zinc carbonate, zinc oxide, and calamine [to] dry the oozing and weeping of [urushiol-induced sores]. Protectants such as baking soda or colloidal oatmeal relieve minor irritation and itching. Aluminum acetate also known as Burow's solution is an astringent that relieves rash."[13]

Showers or compresses using very hot water (but not scalding) can offer relief of itching for up to several hours, with the caveats that this "also taxes the skin's integrity, opening pores and generally making it more vulnerable", and is only for secondary treatment (not while cleaning urushiol from the skin, which should be done with cold water).[14] Those who have had a prior systemic reaction may be able to prevent subsequent exposure from turning systemic by avoiding heat and excitation of the circulatory system, and by applying moderate cold to any infected skin with biting pain.

Antihistamines and hydrocortisone creams or antihistamines by mouth in severe cases can be used to alleviate the symptoms of a developed rash. Nonprescription oral diphenhydramine (US tradename Benadryl) is the most commonly suggested antihistamine. Topical formulations containing diphenhydramine are available, but may further irritate the affected skin areas.

In cases of extreme symptoms, steroids such as prednisone or triamcinolone 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.[15] 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 prevent urushiol rashes after the exposure. A study that compared Tecnu, Goop Hand Cleaner, and Dial Ultra Dishwashing Soap found protection levels of 70%, 62%, and 56% and costs per ounce of $1.25, $0.07, and $0.07 respectively. The study compared four 2.5 cm exposed squares on the inner aspect of the forearm, three of which were treated and one untreated.[16] 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.[17]
  • Ordinary laundering with laundry detergent will remove urushiol from most clothing,[18] but not from leather or suede.[citation needed] One home remedy includes laundering clothes with Fels-Naptha
  • The fluid from the resulting blisters does not spread poison ivy to others.[19][20]
  • Blisters should be left unbroken during healing.[21]
  • 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.[17]
  • Ice, cold water, cooling lotions, or cold air do not help cure poison ivy rashes, but cooling can reduce inflammation and soothe the itch.[18]

Jewelweed[22][23][24][25] are ineffective or of questionable effectiveness against itching.

See also[edit]

References[edit]

  1. ^ Lepoittevin, J.-P., Benezra, C., Asakawa, Y. 1989. Allergic contact dermatitis to Ginkgo biloba L.: retationship with urushiol. Arch. Dermatol. Res., 281: 227-230.
  2. ^ http://www.fireengineering.com/articles/2005/07/firefighters-battle-hidden-dangers-this-wildfire-season-poison-oak-ivy-and-sumac-plants-top-cause-of-disability-sick-time.html
  3. ^ 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. 
  4. ^ "Modulation of fatty acid oxidation alters contact hypersensitivity to urushiols: role of aliphatic chain beta-oxidation in processing and activation of urushiols". J Invest Dermatol 108 (1): 57–61. Jan 1997. 
  5. ^ Kalish, RS; Wood, JA. "Induction of hapten-specific tolerance of human CD8+ urushiol (poison ivy)-reactive T lymphocytes". J Invest Dermatol.date= 1997 Mar 108 (3): 253–7. 
  6. ^ C.Michael Hogan (2008) Western poison-oak: Toxicodendron diversilobum, GlobalTwitcher, ed. Nicklas Stromberg [1]
  7. ^ DermAtlas -1892628434
  8. ^ Wilson, Stephanie. "Howstuffworks "How Poison Ivy Works"". Science.howstuffworks.com. Retrieved 2010-06-04. 
  9. ^ Michael Rohde. "Contact-Poisonous Plants of the World". Mic-ro.com. Retrieved 2010-06-04. 
  10. ^ Herbalgram (American Botanical Council) Volume 34: 36-42, 1995 by W.P. Armstrong and W.L. Epstein, M.D. cited in http://waynesword.palomar.edu/ww0802.htm
  11. ^ "Soothing Remedies for Poison Ivy and Poison Oak". Googobits.com. 2005-08-04. Retrieved 2010-06-04. 
  12. ^ "Poison Oak". Wayne's Word. 
  13. ^ September 2, 2008 FDA Document
  14. ^ Hauser, Susan Carol; William L. Epstein (2008). A Field Guide to Poison Ivy, Poison Oak, and Poison Sumac. Globe Pequot. p. 60. ISBN 978-0-7627-4741-2. Retrieved 2010-11-21. 
  15. ^ "Poison Ivy, Oak, and Sumac". Surviveoutdoors.com. Retrieved 2010-06-04. 
  16. ^ Stibich, A. S., Yagan, M., Sharma, V., Herndon, B. and Montgomery, C. (25 Dec 2001). "Cost-effective post-exposure prevention of poison ivy dermatitis". International Journal of Dermatology (John Wiley & Sons) 39 (7): 515–8. doi:10.1046/j.1365-4362.2000.00003.x. PMID 10940115. 
  17. ^ a b "Poison Ivy Myths". PennState Integrated Pest Management project. 
  18. ^ a b "Poison Ivy: Prevention and Treatment". 
  19. ^ "Poison ivy, oak, and sumac". American Academy of Dermatology. 
  20. ^ "Outsmarting Poison Ivy and Other Poisonous Plants". U.S. Food and Drug Administration. 
  21. ^ "Poison Ivy, Oak and Sumac". OutDoorPlaces.com. Retrieved 22 September 2010. 
  22. ^ 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
  23. ^ Gibson, MR; Maher, FT (1950). "Activity of jewelweed and its enzymes in the treatment of Rhus dermatitis.". Journal of the American Pharmaceutical Association. American Pharmaceutical Association 39 (5): 294–6. PMID 15421925. 
  24. ^ 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
  25. ^ Zink, B. J.; Otten, E. J.; Rosenthal, M.; Singal, B. (1991). "The effect of jewel weed in preventing poison ivy dermatitis.". Journal of Wilderness Medicine 2 (3): 178–182. doi:10.1580/0953-9859-2.3.178.