Urushiol-induced contact dermatitis
|This article relies too much on references to primary sources. (October 2015) (Learn how and when to remove this template message)|
|Urushiol-induced contact dermatitis|
|Classification and external resources|
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, most notably the plants of the genus Toxicodendron, which includes the Chinese laquer tree, poison ivy, poison oak, and poison sumac, with the name derived from the Japanese name for the sap of the Chinese laquer tree, urushi. Other plants in the sumac family Anacardiaceae also contain urushiol (including 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 also contain this oil.[non-primary source needed] As is the case with all contact dermatitis, urushiol-induced rashes are a type-IV hypersensitivity reaction, also known as delayed-type hypersensitivity.
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.
Signs and symptoms
The result is an allergic eczematous contact dermatitis characterized by redness, swelling, papules, vesicles, blisters, and streaking. People vary greatly in their sensitivity to urushiol. In approximately 15% to 30% 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.
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.
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, clothing and landscaping tools. Clothing or other materials that contact the plant and then, before being washed, contact the skin are common causes of exposure. For people who have never been exposed, or are not yet allergic to urushiol, it may take 10 to 21 days for a reaction to occur the first time, once allergic to urushiol, however, most people break out 48 to 72 hours after contact with the plant. Typically, individuals have been exposed at least once, if not several times, before they break out with a rash. For individuals already allergic to urushiol, it normally 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. 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.
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.[non-primary source needed]
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. 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.
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.
Primary treatment involves washing exposed skin thoroughly with soap, water and friction as soon as possible after exposure is discovered. Soap or detergent is necessary, as urushiol is an oil, friction applied with a washcloth or something similar, is necessary as urushiol strongly adheres to the skin. 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. A solution of aluminum acetate known as Burow's solution is an astringent that relieves rash."
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). 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 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. If bacterial secondary infection of affected areas occurs, antibiotics may also be necessary.
Scrubbing with plain soap and cold water will remove urushiol from skin if it is done within a few minutes of exposure. Many home remedies and commercial products (e.g., Tecnu, Zanfel) have also claimed to prevent urushiol rashes after the exposure. A study that compared Tecnu ($1.25/oz.), versus Goop Hand Cleaner or Dial Ultra Dishwashing Soap ($0.07/oz.) found that differences between the three—in the range of 56-70% improvement over the no treatment control[clarification needed]—were nonsignificant (P>0.05), but that improvement over no treatment was significant at the same level of confidence.[non-primary source needed]
- Ordinary laundering with laundry detergent will remove urushiol from most clothing but not from leather or suede.
- The fluid from the resulting blisters does not spread urushiol to others.
- Blisters should be left unbroken during healing.
- Poison ivy and poison oak are still harmful when the leaves have fallen off, as the toxic residue is persistent, and exposure to any parts of plants containing urushiol and can cause a rash at any time of the year.
- Ice, cold water, cooling lotions, or cold air do not help cure poison ivy rashes, but cooling can reduce inflammation and soothe the itch.[dead link]
- Results for jewelweed as a natural agent for treatment are conflicting, but the latest studies offer results indicating it as having "failed to decrease symptoms of poison ivy dermatitis"  and as having "no prophylactic effect" .
A rarely cited double-blind study in 1982 reported a course of oral urushiol usually hyposensitized subjects.
|Wikimedia Commons has media related to Urushiol-induced contact dermatitis.|
- Lepoittevin, J.-P., Benezra, C., Asakawa, Y. 1989. Allergic contact dermatitis to Ginkgo biloba L.: retationship with urushiol. Arch. Dermatol. Res., 281: 227-230.[non-primary source needed]
- DermAtlas -1892628434
- Wilson, Stephanie. "Howstuffworks "How Poison Ivy Works"". Science.howstuffworks.com. Retrieved 2010-06-04.
- Michael Rohde. "Contact-Poisonous Plants of the World". Mic-ro.com. Retrieved 2010-06-04.
- "Poison Oak". Waynesword.palomar.edu. 2011-01-16. Retrieved 2015-10-06.
- Ray, Thomas MD, Professor Emeritus of Dermatology. "Poison Ivy: The Most Common of Allergens". University of Iowa Health Care. Retrieved 30 October 2015.
- "FIREFIGHTERS BATTLE HIDDEN DANGERS THIS WILDFIRE SEASON: POISON OAK, IVY AND SUMAC PLANTS TOP CAUSE OF DISABILITY, SICK TIME". Fireengineering.com. Retrieved 2015-10-06.
- Dietrich Frohne; 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.
- "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. doi:10.1111/1523-1747.ep12285632.
- Kalish, RS; Wood, JA (Mar 1997). "Induction of hapten-specific tolerance of human CD8+ urushiol (poison ivy)-reactive T lymphocytes". J Invest Dermatol. 108 (3): 253–7. doi:10.1111/1523-1747.ep12286447.
- C.Michael Hogan (2008) Western poison-oak: Toxicodendron diversilobum, GlobalTwitcher, ed. Nicklas Stromberg 
- "Soothing Remedies for Poison Ivy and Poison Oak". Googobits.com. 2005-08-04. Retrieved 2010-06-04.
- on YouTube
-  Archived July 16, 2010, at the Wayback Machine.
- 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.
- "Poison Ivy, Oak, and Sumac". Surviveoutdoors.com. Retrieved 2010-06-04.
- Bill Einsig, Bill (2002), Poison Ivy Myth: Science, Environment and Ecology Flash for Educators (No. 341), in Keystone Outdoors Magazine (May 11), excerpted by the Penn State Integrated Pest Management, accessed 7 October 2015.
- Stibich, A. S., Yagan, M., Sharma, V., Herndon, B. and Montgomery, C. (2001). "Cost-effective post-exposure prevention of poison ivy dermatitis". International Journal of Dermatology. 39 (7): 515–518. doi:10.1046/j.1365-4362.2000.00003.x. PMID 10940115.
- "Aetna InteliHealth: Featuring Harvard Medical School's Consumer Health Information". Intelihealth.com. Archived from the original on February 11, 2012. Retrieved 6 October 2015.
- "Poison ivy, oak, and sumac". American Academy of Dermatology.
- "Outsmarting Poison Ivy and Other Poisonous Plants". U.S. Food and Drug Administration.
- "Poison Ivy, Oak and Sumac". OutDoorPlaces.com. Retrieved 22 September 2010.
- Shenefelt, Philip D. (2011). "Herbal Treatment for Dermatologic Disorders". Herbal Medicine: Biomolecular and Clinical Aspects (2nd ed.). Boca Raton, Florida, USA: CRC Press. Retrieved October 5, 2015.
- Epstein, W. L.; Byers, V. S.; Frankart, W. (1982-09-01). "Induction of antigen specific hyposensitization to poison oak in sensitized adults". Archives of Dermatology. 118 (9): 630–633. doi:10.1001/archderm.118.9.630. ISSN 0003-987X. PMID 6180687.