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. 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, as do unrelated plants such as Ginkgo biloba. 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. Additionally, smoke from burning plant matter may be toxic. 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 U.S. 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.
Signs and symptoms 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 have a very strong immune response resulting in severe symptoms. 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 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
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. Common causes of exposure are clothing or other materials that touch the plant and then, before being washed, touch the skin. For people who have never been exposed or are not yet allergic to urushiol, it may take 10 to 20 days for a reaction to occur the first time. Once allergic to urushiol, 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. The rash typically persists one to two weeks, but in some cases may last up to five weeks. Urushiol primarily is found in the spaces between cells beneath the outer skin of the plant, so exposure increases when plant tissue is crushed or damaged. 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 danger of burning urushiol-containing plant material.
Species Species that cause urushiol-induced contact dermatitis include all members of Toxicodendron, such as:
T. radicans (poison ivy) T. pubescens (poison oak – eastern) T. diversilobum (poison oak – western) T. vernix (poison sumac) T. vernicifluum (Japanese lacquer tree) Other members of the Anacardiaceae can produce a similar effect. People who are sensitive to urushiol also can experience a similar rash from mangoes, with the tree's sap and fruit's skin containing a similar chemical compound. A related allergenic compound is present in the raw shells of cashews. Similar reactions have been reported occasionally from contact with the related fragrant sumac (Rhus aromatica). Other similar taxa include:
Gluta spp (rengas tree) Lithraea molleoides (aruera – South America) Smodingium argutum (African poison ivy)
Mechanism
Urushiol is fat-soluble, penetrating the stratum corneum of the skin, then binding to Langerhans cells in the epidermis. 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. 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. Urushiols are oxidized in vivo, generating a quinone form of the molecules. 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 complex of urushiol derivatives (namely, pentadecacatechol) bound in the skin proteins, attacking the cells as if they were foreign bodies.
… excerpt ends here. Continue reading the full article.
