What does poison oak allergy look like
Urushiol causes an 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 trigger an immune system response, while at least 25% of people own a extremely strong immune response resulting in severe symptoms. Since the skin reaction is an allergic one, people may develop progressively stronger reactions after repeated exposures, or own no immune response on their first exposure but show sensitivity on subsequent 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 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 the severity of the exposure. Severe cases involve little (1–2 mm), clear, fluid-filled blisters on the skin. Pus-filled vesicles containing a whitish fluid may indicate an infection.
Most poison ivy rashes, without infections, will resolve within 14 days without treatment. Excessive scratching may result in infection, commonly by staphylococcal and streptococcal species; these may require antibiotics.
Poison ivy rash after 2 days.
Severe allergic reaction to urushiol (poison oak) 4 days after exposure.
Blistering 48 hours after urushiol contact.
Poison ivy rash with swelling about 3 days after direct contact.
- ^ ab«Aetna InteliHealth: Featuring Harvard Medical School’s Consumer Health Information».
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- ^Wilson, Stephanie (2005-09-23). «Howstuffworks «How Poison Ivy Works»». Science.howstuffworks.com. Retrieved 2010-06-04.
- ^Stibich, A. S.; Yagan, M.; Sharma, V.; Herndon, B. & 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.
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- ^«Outsmarting Poison Ivy and Other Poisonous Plants».
U.S. Food and Drug istration.
- ^«How to never own a serious poison ivy rash again» on YouTube
- ^ abcBill 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.
- ^Motz; Bowers; Young; Kinder (2012). «The effectiveness of jewelweed, Impatiens capensis, the related cultivar I.
balsamina and the component, lawsone in preventing post poison ivy exposure contact dermatitis». Journal of Ethnopharmacology. 143 (1): 314–318. doi:10.1016/j.jep.2012.06.038. PMID 22766473.
- ^Lepoittevin, J.-P., Benezra, C., Asakawa, Y. 1989. Allergic contact dermatitis to Ginkgo biloba L.: relationship with urushiol. Arch. Dermatol. Res., 281: 227-230.
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Boca Raton, Florida, USA: CRC Press. ISBN . Retrieved October 5, 2015.
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- ^Ray, Thomas MD, Professor Emeritus of Dermatology. «Poison Ivy: The Most Common of Allergens». University of Iowa Health Care.
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Urushiols are oxidized in-vivo, generating a quinone form of the molecules.[non-primary source needed] The toxic effect is indirect, mediated by an induced immune response.
The oxidized urushiols act as haptens, 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. This response is directed at the complicated of urushiol derivatives (namely, pentadecacatechol) bound in the skin proteins, attacking the cells as if they were foreign bodies.
A rarely cited double-blind study in 1982 reported that a course of oral urushiol generally hyposensitized subjects.
Urushiol-induced contact dermatitis is caused 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 touch the plant and then, before being washed, touch the skin are common causes of exposure.
For people who own never been exposed or are not yet allergic to urushiol, it may take 10 to 21 days for a reaction to happen the first time. Once allergic to urushiol, however, most people break out 48 to 72 hours after contact with the oil. Typically, individuals own been exposed at least once, if not several times, before they develop a rash. The rash typically persists one to two weeks, but in some cases may final up to five weeks.
Urushiol is primarily found in the spaces between cells beneath the outer skin of the plant, so the effects 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 of urushiol can lead to serious, systemic reactions. Burning plant material is commonly said to create urushiol-laden smoke that causes a systemic reaction, as well as a rash in the throat and eyes. Firefighters often get rashes and eye inflammation from smoke-related contact. A high-temperature bonfire may incinerate urushiol before it can cause harm, while a smoldering fire may vaporize the volatile oil and spread it as white smoke.
However, some sources dispute the harm of burning urushiol-containing plant material.
Further information on poison ivy.
See Case studies in immunology — a clinical companion by Fred S. Rosen and Raif S. Geha, Garland Publishing Inc., 1996 (Case 6, contact hypersensitivity). Further information on allergy and hypersensitivity, and the underlying mechanisms, can be found in any textbook of immunology.
For a discussion of corticosteroids, see a physiology book, such as the current edition of the Review of Medical Physiology by William F. Ganong, Appleton and Lange.
Godfrey, H. P., H. Baer, and R. C. Watkins. 1971. Delayed hypersensitivity to catechols. V. Absorption and distribution of substances related to poison ivy extracts and their relation to the induction of sensitization and tolerance. J. Immunol. 106(1):91-102.
Here are some relevant web sites:
- Poison ivy, sumac, and oak by the American Academy of Dermatology.
Includes what to do and common myths.
- An excellent series of photos in diverse seasons is at the Poison Ivy, Western Poison Oak, Poison Sumac site by Gerald A. Mulligan of Agriculture and Agri-Food Canada.
- Poison Ivy and Poison Oak Products at Wayne State U.
There’s a excellent list of links here!
- Excellent photo at the PLANTS TOXIC TO ANIMALS site of the U Illinois, Urbana-Champaign.
- Camper with a rash by Lewis Nelson, M.D., Yale University School of Medicine. Clinical case study with list of plant species and discussion of alternative treatments.
- Contact dermatitis home sheet by A. P. Truett, III, M.D. at Vanderbilt University. 4-tertiary-butylcatechol is an industrial chemical which causes contact dermatitis for some workers exposed to it.
- There is a excellent common-sense discussion of the medical side of poison ivy at the Famil-e-docs physicians’ website.
- An excellent photo of the red-leafed stage is provided at the Cornell University Poisonous Plants Sheet.
- Poisonous Plant Database by D. Jesse Wagstaff, DVM (US Food and Drug istration). An extensive bibliography.
This sheet is maintained by Eric Martz.
I would love to add more graphics to this sheet. If you own some to contribute, please contact me.
Final updated March 31, 1997.
Scientists own finally scratched the surface about why, exactly, poison ivy makes people so itchy.
About 10 million Americans suffer from an allergic reaction to poison ivy every year.
It’s a serious threat to firefighters, farmers, and others who work outdoors; poison ivy is to blame for 10 percent of the US Forest Service’s lost-time injuries. Now, researchers looking for clues about how poison ivy causes allergic reactions own stumbled upon a key chemical that offers some answers — and points to a potential treatment.
“It’s the most common cause of environmental contact allergy,” said Sven-Eric Jordt, an inflammation researcher at Duke University and the lead author of the new research, published Monday in the Proceedings of the National Academy of Sciences.
The major allergen found in poison ivy is a chemical called urushiol, which is found in the sap of poison ivy plants and its cousins, poison oak and poison sumac.
Between 50 and 75 percent of people are allergic to urushiol.
But it’s been hard for scientists to study, in part because animal models haven’t been useful. So Jordt and his colleagues developed a new mouse model of poison ivy allergy that focused on immune mediators, which are responsible for detecting when the skin comes into contact with an allergen.
“The immune system has a memory of being in contact with this before and then fiercely defends against it,” he explained. “It produces this extremely exaggerated response.”
For poison ivy, that means an irritating, persistent itch, rashes, and swelling of the skin.
That can cause an uncontrollable urge to scratch, which in turn worsens the rash. A run-in with poison ivy can quickly devolve into a painful, scratchy cycle that can final for weeks and, in some cases, cause skin infections that require antibiotics.
Minuscule proteins are triggering that immune response — and, it turns out, one of them is driving the sensation to itch, too.
“One of these proteins, IL-33, acts on the extremely fine nerve endings in the skin that make us sense itch,” Jordt explained.
When an allergic person comes into contact with urushiol, that protein fires off a signal to the brain in much the same way it would signal temperature or pressure.
IL-33 has previously been investigated for its role in food allergies, anaphylaxis, and other inflammatory responses. Two companies, AnaptysBio and Genentech, are currently conducting clinical trials for IL-33 blockers as potential asthma treatments.
That finding gives Jordt and his colleagues a jumping-off point to investigate potential treatments that clamp below on IL-33’s response in poison ivy allergies.
“We used an antibody that blocks that signaling response,” Jordt said.
“And when we interfere with this signal, then the itch is alleviated.”
They also discovered a binding protein that’s present in the nerves that trigger itch. Another antibody that blocked that receptor seemed to shut off the itch response, too.
There’s still much more work to be done — it’s not yet clear whether IL-33 works in the same way in human skin cells that it does in mice. Jordt is currently working with dermatologists to collect skin samples of poison ivy patients to confirm IL-33 is present.
“If we can confirm that, it would be a excellent sign that these treatments might work,” he said.
Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis or Rhus dermatitis) is a type of allergic contact dermatitis caused by the oil urushiol found in various plants, most notably species of the genus Toxicodendron: poison ivy, poison oak, poison sumac, and the Chinese lacquer tree.
The name is derived from the Japanese expression for the sap of the Chinese lacquer tree, urushi. Other plants in the sumac family (including mango, pistachio, the Burmese lacquer tree, the India marking nut tree, and the shell of the cashew) also contain urushiol, as do unrelated plants such as Ginkgo biloba.
As is the case with every contact dermatitis, urushiol-induced allergicrashes are a Type IV hypersensitivity reaction, also known as delayed-type hypersensitivity. Symptoms 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 every 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.
Treatment consists of two phases: stopping the urushiol contact that is causing the reaction (this must be done within minutes) and, later, reducing the pain and/or itching.
Primary treatment involves washing exposed skin thoroughly with soap, cool water, and friction as soon as possible after exposure is discovered.
Soap or detergent is necessary because urushiol is an oil; friction, with a washcloth or something similar, is necessary because urushiol adheres strongly to the skin. Commercial removal preparations, which are available in areas where poison ivy grows, generally contain surfactants, such as the nonionic detergent Triton X-100, to solubilize urushiol; some products also contain abrasives.
The U.S. Food and Drug istration recommends applying a wet compress or soaking the affected area in cool water; topical corticosteroids (available over-the-counter) or oral corticosteroids (available by prescription); and topical skin protectants, such as zinc acetate, zinc carbonate, zinc oxide, and calamine.
Baking soda or colloidal oatmeal can relieve minor irritation and itching. Aluminium acetate, sometimes known as Burow’s solution, can also ease the rash.
Showers or compresses using boiling (but not scalding) water can relieve itching for up to several hours, though this «also taxes the skin’s integrity, opening pores and generally making it more vulnerable», and is only useful for secondary treatment (not for cleaning urushiol from the skin, which should be done with freezing water). People who own had a prior systemic reaction may be capable to prevent subsequent exposure from turning systemic by avoiding heat and excitation of the circulatory system and applying moderate freezing to any infected skin with biting pain.
Antihistamine and hydrocortisone creams, or oral antihistamines in severe cases, can alleviate the symptoms of a developed rash. Nonprescription oral diphenhydramine (U.S. trade name Benadryl) is the most commonly suggested antihistamine. Topical formulations containing diphenhydramine are also available but may further irritate the skin.
In cases of extreme symptoms, steroids such as prednisone, triamcinolone, or dexamethasone are sometimes istered to attenuate the immune response and prevent long-term skin damage, especially if the eyes are involved. Prednisone is the most commonly prescribed systemic treatment but can cause serious adrenal suppression, so it must be taken carefully and tapered off slowly. If bacterial secondary infection of affected areas occurs, antibiotics may also be necessary.
Scrubbing with plain soap and freezing water will remove urushiol from skin if it is done within a few minutes of exposure. Numerous home remedies and commercial products (e.g., Tecnu, Zanfel) also claim to prevent urushiol rashes after exposure. A study that compared Tecnu ($1.25/oz.) with Goop Hand Cleaner or Dial Ultra Dishwashing Soap ($0.07/oz.) found that differences among the three—in the range of 56–70% improvement over no treatment—were nonsignificant (P > 0.05), but that improvement over no treatment was significant at the same level of confidence.
- Poison ivy and poison oak are still harmful when the leaves own fallen off, as the toxic residue is persistent, and exposure to any parts of plants containing urushiol can cause a rash at any time of the year.
- Ordinary laundering with laundry detergent will remove urushiol from most clothing but not from leather or suede.
- Ice, freezing water, cooling lotions, and freezing air do not assist cure poison ivy rashes, but cooling can reduce inflammation and soothe the itch.[dead link]
- Blisters should be left unbroken during healing.
- The fluid from the resulting blisters does not spread urushiol to others.
- Results for jewelweed as a natural agent for treatment are conflicting.
Some studies indicate that it «failed to decrease symptoms of poison ivy dermatitis»  and had «no prophylactic effect» . The juice of the leaves and stems of Impatiens capensis is a traditional Native American remedy for skin rashes, including poison ivy and such use has been supported by at least one peer-reviewed study, as recently as 2012.