Urushiol-induced contact dermatitis

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Urushiol-induced contact dermatitis
Poison ivy contact dermatitis.jpg
Specialty Dermatology   OOjs UI icon edit-ltr-progressive.svg
Symptoms rashes, itching, inflammation, oozing, and, in severe cases, a burning sensation.
Causes urushiol contact

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 sumac family species of the genus Toxicodendron : poison ivy, poison oak, poison sumac, and the Chinese lacquer tree. [1] The name is derived from the Japanese word 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 cashew) also contain urushiol, [2] as do unrelated plants such as Ginkgo biloba. [3]

Contents

As is the case with all contact dermatitis, urushiol-induced allergic rashes 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 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

Urushiol causes an eczematous contact dermatitis characterized by redness, swelling, papules, vesicles, blisters, and streaking. [4] [5] People vary greatly in their sensitivity to urushiol. In approximately 15% [6] to 30% [7] of people, urushiol does not trigger an immune system response, while at least 25% of people have a very strong immune response resulting in severe symptoms.[ citation needed ]

The rash takes one to two weeks to run its course and may cause scars, depending on the severity of the exposure. [4] Severe cases involve small (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.

Cause

Toxicodendron pubescens (Atlantic poison oak), one of a large number of species containing urushiol irritants. Poisonoak.jpg
Toxicodendron pubescens (Atlantic poison oak), one of a large number of species containing urushiol irritants.

Urushiol-induced contact dermatitis is caused by contact with a plant or any other object containing urushiol oil. [1] The oil adheres to almost anything with which it comes in contact, such as towels, blankets, clothing, and landscaping tools. [4] Clothing or other materials that touch the plant and then, before being washed, touch the skin are common causes of exposure. [4]

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 oil. Typically, individuals have been exposed at least once, if not several times, before they develop a rash. [8] The rash typically persists one to two weeks, but in some cases may last 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. [9] 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 danger of burning urushiol-containing plant material. [10]

Mechanism

A video describing the mechanism of action for poison ivy and other plants containing urushiol.

Urushiol is fat-soluble, penetrating the stratum corneum of the skin, then binding to Langerhans cells in the epidermis. [1] The affected cells then migrate to lymph nodes, where T cells become activated, then return to the skin where they stimulate an urushiol-activated dermatitis. [1] The toxic effect is indirect, mediated by an induced immune response. [1] The oxidized urushiols act as haptens, chemically reacting with, binding to, and changing the shape of integral membrane proteins on exposed skin cells. [1] Urushiols are oxidized in vivo, generating a quinone form of the molecules. [11]

Affected proteins interfere with immune system ability to recognize these cells as normal parts of the body, causing a T-cell-mediated immune response. [12] This response is directed at the complex of urushiol derivatives (namely, pentadecacatechol) bound in the skin proteins, attacking the cells as if they were foreign bodies.

Treatments

Treatment consists of two phases: stopping the urushiol contact that is causing the reaction (this must be done within minutes) [13] and, later, reducing the pain and itching. [4]

Primary treatment involves washing exposed skin thoroughly with soap, cool water, and friction as soon as possible after exposure is discovered. [4] 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. [4] Commercial removal 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 products also contain abrasives.

The U.S. Food and Drug Administration 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 triacetate, sometimes known as Burow's solution, can also ease the rash. [14]

Showers or compresses using hot (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 cold water). [15] People 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.

In cases of extreme symptoms, steroids such as prednisone, triamcinolone, or dexamethasone are sometimes administered 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. [16] 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. [4] [13]

Further observations

Prevention

A rarely cited double-blind study in 1982 reported that a course of oral urushiol usually hyposensitized subjects, with the principal side effect, pruritus ani, being reported by 85% of the participants who ingested the urushiol. [22]

Research conducted on urushiol by Mahmoud ElSohly led to the development of PDC-APB, a candidate for a vaccine against skin irritation from poison ivy. [23]

See also

Related Research Articles

<span class="mw-page-title-main">Allergy</span> Immune system response to a substance that most people tolerate well

Allergies, also known as allergic diseases, are various conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment. These diseases include hay fever, food allergies, atopic dermatitis, allergic asthma, and anaphylaxis. Symptoms may include red eyes, an itchy rash, sneezing, coughing, a runny nose, shortness of breath, or swelling. Note that food intolerances and food poisoning are separate conditions.

<span class="mw-page-title-main">Dermatitis</span> Inflammatory disease of the skin

Dermatitis is a term used for different types of skin inflammation, typically characterized by itchiness, redness and a rash. In cases of short duration, there may be small blisters, while in long-term cases the skin may become thickened. The area of skin involved can vary from small to covering the entire body. Dermatitis is also called eczema but the same term is often used for the most common type of skin inflammation, atopic dermatitis.

<i>Toxicodendron</i> Genus of plants

Toxicodendron is a genus of flowering plants in the sumac family, Anacardiaceae. It contains trees, shrubs and woody vines, including poison ivy, poison oak, and the lacquer tree. All members of the genus produce the skin-irritating oil urushiol, which can cause a severe allergic reaction. The generic name is derived from the Greek words τοξικός (toxikos), meaning "poison," and δένδρον (dendron), meaning "tree". The best known members of the genus in North America are poison ivy (T. radicans), practically ubiquitous throughout most of eastern North America, and western poison oak, similarly ubiquitous throughout much of the western part of the continent.

<i>Toxicodendron radicans</i> Species of plant

Toxicodendron radicans, commonly known as eastern poison ivy or poison ivy, is an allergenic flowering plant that occurs in Asia and eastern North America. The species is well known for causing urushiol-induced contact dermatitis, an itchy, irritating, and sometimes painful rash, in most people who touch it. The rash is caused by urushiol, a clear liquid compound in the plant's sap. The species is variable in its appearance and habit, and despite its common name, it is not a true ivy (Hedera), but rather a member of the cashew and pistachio family (Anacardiaceae). T. radicans is commonly eaten by many animals and the seeds are consumed by birds, but poison ivy is most often thought of as an unwelcome weed. It is a different species from western poison ivy, T. rydbergii, which has similar effects.

<span class="mw-page-title-main">Blister</span> Small pocket of fluid within the upper layers of the skin

A blister is a small pocket of body fluid within the upper layers of the skin, usually caused by forceful rubbing (friction), burning, freezing, chemical exposure or infection. Most blisters are filled with a clear fluid, either serum or plasma. However, blisters can be filled with blood or with pus.

<span class="mw-page-title-main">Urushiol</span> Oily mixture of organic compounds

Urushiol is an oily mixture of organic compounds with allergenic properties found in plants of the family Anacardiaceae, especially Toxicodendronspp., Comocladia spp. (maidenplums), Metopium spp. (poisonwood), and also in parts of the mango tree as well as the fruit of the cashew tree.

<span class="mw-page-title-main">Itch</span> Uncomfortable skin sensation

An itch is a sensation that causes a strong desire or reflex to scratch. Itches have resisted many attempts to be classified as any one type of sensory experience. Itches have many similarities to pain, and while both are unpleasant sensory experiences, their behavioral response patterns are different. Pain creates a withdrawal reflex, whereas itches leads to a scratch reflex.

<span class="mw-page-title-main">Contact dermatitis</span> Inflammation from allergen or irritant exposure

Contact dermatitis is a type of acute or chronic inflammation of the skin caused by exposure to chemical or physical agents. Symptoms of contact dermatitis can include itchy or dry skin, a red rash, bumps, blisters, or swelling. These rashes are not contagious or life-threatening, but can be very uncomfortable.

<i>Toxicodendron diversilobum</i> Species of plant

Toxicodendron diversilobum, commonly named Pacific poison oak or western poison oak, is a woody vine or shrub in the sumac family, Anacardiaceae.

<span class="mw-page-title-main">Photodermatitis</span> Skin condition

Photodermatitis, sometimes referred to as sun poisoning or photoallergy, is a form of allergic contact dermatitis in which the allergen must be activated by light to sensitize the allergic response, and to cause a rash or other systemic effects on subsequent exposure. The second and subsequent exposures produce photoallergic skin conditions which are often eczematous. It is distinct from sunburn.

<span class="mw-page-title-main">Hives</span> Skin disease characterized by red, raised, and itchy bumps

Hives, also known as urticaria, is a kind of skin rash with red, raised, itchy bumps. Hives may burn or sting. The patches of rash may appear on different body parts, with variable duration from minutes to days, and does not leave any long-lasting skin change. Fewer than 5% of cases last for more than six weeks. The condition frequently recurs.

Antipruritics, abirritants, or anti-itch drugs, are medications that inhibit the itching often associated with sunburns, allergic reactions, eczema, psoriasis, chickenpox, fungal infections, insect bites and stings like those from mosquitoes, fleas, and mites, and contact dermatitis and urticaria caused by plants such as poison ivy or stinging nettle. It can also be caused by chronic kidney disease and related conditions.

<i>Toxicodendron vernix</i> Species of plant

Toxicodendron vernix, commonly known as poison sumac, or swamp-sumach, is a woody shrub or small tree growing to 9 metres (30 feet) tall. It was previously known as Rhus vernix. This plant is also known as thunderwood, particularly where it occurs in the southern United States.

Burow's solution is an aqueous solution of aluminium triacetate. It is available in the U.S. as an over-the-counter drug for topical administration, with brand names including Domeboro, Domeboro Otic, Star-Otic, and Borofair. The preparation has astringent and antibacterial properties and may be used to treat a number of skin conditions, including insect bites and stings, rashes caused by poison ivy and poison sumac, swelling, allergies, and bruises. However, its main use is for treatment of otitis, including otomycosis.

<span class="mw-page-title-main">Allergic contact dermatitis</span> Inflammation of the skin due to contact with an allergen

Allergic contact dermatitis (ACD) is a form of contact dermatitis that is the manifestation of an allergic response caused by contact with a substance; the other type being irritant contact dermatitis (ICD).

<i>Toxicodendron pubescens</i> Eastern poison oak

Toxicodendron pubescens, commonly known as Atlantic poison oak, or eastern poison oak, is an upright shrub which can cause contact dermatitis for most people.

<span class="mw-page-title-main">Tecnu</span> Over-the-counter skin cleanser

Tecnu is an over-the-counter skin cleanser manufactured by Tec Laboratories, a pharmaceutical company based in Albany, Oregon. It is intended for use by humans and furry pets after topical exposure to urushiol, the active ingredient in poison oak, poison ivy, and poison sumac. Tecnu is made from deodorized mineral spirits, water, propylene glycol, octylphenoxy-polythoxethanol, mixed fatty acid soap, and fragrance.

<span class="mw-page-title-main">Poison ivy</span> Allergenic plant of Asia and North America

Poison ivy, aka ‘3 leaves’, is a type of allergenic plant in the genus Toxicodendron native to Asia and North America. Formerly considered a single species, Toxicodendron radicans, poison ivies are now generally treated as a complex of three separate species: Toxicodendron radicans, Toxicodendron rydbergii, and Toxicodendron orientale. They are well known for causing urushiol-induced contact dermatitis, an itchy, irritating, and sometimes painful rash, in most people who touch them. The rash is caused by urushiol, a clear liquid compound in the plant's sap. They are variable in appearance and habit, and despite its common name, it is not a "true" ivy (Hedera), but rather a member of the cashew and pistachio family (Anacardiaceae). T. radicans is commonly eaten by many animals, and the seeds are consumed by birds, but poison ivy is most often thought of as an unwelcome weed.

<span class="mw-page-title-main">Aluminium diacetate</span> Chemical compound

Aluminium diacetate, also known as basic aluminium acetate, is a white powder with the chemical formula C4H7AlO5. It is one of a number of aluminium acetates and can be prepared in a reaction of sodium aluminate (NaAlO2) with acetic acid.

<span class="mw-page-title-main">Nickel allergy</span> Medical condition

Nickel allergy is any of several allergic conditions provoked by exposure to the chemical element nickel. Nickel allergy often takes the form of nickel allergic contact dermatitis (Ni-ACD), a form of allergic contact dermatitis (ACD). Ni-ACD typically causes a rash that is red and itchy and that may be bumpy or scaly. The main treatment for it is avoiding contact with nickel-releasing metals, such as inexpensive jewelry. Another form of nickel allergy is a systemic form: systemic nickel allergy syndrome (SNAS) can mimic some of the symptoms of irritable bowel syndrome (IBS) and also has a dermatologic component.

References

  1. 1 2 3 4 5 6 "Urushiol". PubChem. US National Library of Medicine. 1 January 2022. Retrieved 4 January 2022.
  2. Gross M, Baer H, Fales HM (1975). "Urushiols of poisonous anacardiaceae". Phytochemistry. 14 (10): 2263–2266. doi:10.1016/S0031-9422(00)91113-0.
  3. Lepoittevin JP, Benezra C, Asakawa Y (1989). "Allergic contact dermatitis to Ginkgo biloba L.: relationship with urushiol". Archives of Dermatological Research. 281 (4): 227–30. doi:10.1007/BF00431055. PMID   2774654. S2CID   24855206.
  4. 1 2 3 4 5 6 7 8 9 10 "Poison ivy rash". Mayo Clinic. 17 October 2020. Retrieved 4 January 2022.
  5. DermAtlas -1892628434
  6. Wilson S (2005-09-23). "Howstuffworks "How Poison Ivy Works"". Science.howstuffworks.com. Retrieved 2010-06-04.
  7. Rohde M. "Contact-Poisonous Plants of the World". Mic-ro.com. Archived from the original on 2010-07-02. Retrieved 2010-06-04.
  8. Ray T. "Poison Ivy: The Most Common of Allergens". University of Iowa Health Care. Archived from the original on 12 January 2016. Retrieved 30 October 2015.
  9. "Firefighters Battle Hidden Dangers This Wildfire Season: Poison Oak, Ivy And Sumac Plants Top Cause Of Disability, Sick Time". FireEngineering. Fireengineering.com. 26 July 2005. Archived from the original on 2021-10-20. Retrieved 2015-10-06.
  10. Frohne D, Pfander HJ (1984). A Colour Atlas of Poisonous Plants: A Handbook for Pharmacists, Doctors, Toxicologists, and Biologists. Wolfe Publishing Ltd. p. 291 pp. ISBN   978-0-7234-0839-0.
  11. Kalergis AM, López CB, Becker MI, Díaz MI, Sein J, Garbarino JA, De Ioannes AE (January 1997). "Modulation of fatty acid oxidation alters contact hypersensitivity to urushiols: role of aliphatic chain beta-oxidation in processing and activation of urushiols". The Journal of Investigative Dermatology. 108 (1): 57–61. doi: 10.1111/1523-1747.ep12285632 . PMID   8980288.
  12. Hogan CM (2008). "Western poison-oak: Toxicodendron diversilobum". GlobalTwitcher. Archived from the original on 2009-07-21. Retrieved 2010-04-21.
  13. 1 2 3 Einsig B (May 2002). "Poison Ivy Myth: Science, Environment and Ecology Flash for Educators". Keystone Outdoors Magazine (341). Penn State Integrated Pest Management. Archived from the original on 25 July 2017. Retrieved 7 October 2015.
  14. 1 2 "Outsmarting Poison Ivy and Other Poisonous Plants". Food and Drug Administration . Archived from the original on July 16, 2010. Retrieved December 16, 2019.
  15. Hauser SC, Epstein WL (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.[ permanent dead link ]
  16. "Poison Ivy, Oak, and Sumac". Surviveoutdoors.com. Archived from the original on 2010-06-12. Retrieved 2010-06-04.
  17. Chastant LR, Davis T, Libow L (March 2018). "Black-spot poison ivy, a report of 3 cases with clinicopathologic correlation". JAAD Case Reports. 4 (2): 140–142. doi:10.1016/j.jdcr.2017.09.035. PMC   5789763 . PMID   29387766.
  18. "Poison ivy, oak, and sumac". American Academy of Dermatology. Archived from the original on 9 March 2012.
  19. "Poison Ivy, Oak and Sumac". OutDoorPlaces.com. Archived from the original on 18 October 2010. Retrieved 22 September 2010.
  20. Shenefelt PD (2011). "Herbal Treatment for Dermatologic Disorders". Herbal Medicine. Oxidative Stress and Disease. Vol. 20115386 (2nd ed.). Boca Raton, Florida, USA: CRC Press. pp. 383–403. doi:10.1201/b10787-19. ISBN   978-1-4398-0713-2. PMID   22593930 . Retrieved October 5, 2015.{{cite book}}: |journal= ignored (help)
  21. Smith HH (1933). "Ethnobotany of the Forest Potawatomi Indians". Bulletin of the Public Museum of the City of Milwaukee. 7: 1-230 (42).
  22. Epstein WL, Byers VS, Frankart W (September 1982). "Induction of antigen specific hyposensitization to poison oak in sensitized adults". Archives of Dermatology. 118 (9): 630–633. doi:10.1001/archderm.1982.01650210010008. PMID   06180687.
  23. Niemeyer, Kenneth (10 July 2019). "Poison ivy vaccine making progress, still years away". The Daily Mississippian. Retrieved 27 July 2022.