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Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis and Rhus dermatitis) is the medical name given to allergic rashes produced by urushiol oil contained in various plants. This includes the genus Toxicodendron (including poison ivy, poison oak, and poison sumac), as well as other plants in the family Anacardiaceae (mango, Rengas tree, Burmese lacquer tree, India marking nut tree, and the shell of the cashew nut), and even unrelated plants such as Ginkgo biloba. Toxicodendron species are very resistant to many herbicides.
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 U.S., while poison-ivy is most rampant in the eastern U.S.. Dermatitis from poison sumac is less common, but just as problematic.
Mechanism
Urushiol-induced contact dermatitis is contracted by contact with a plant or any other object containing urushiol oil. Chemically, urushiol is harmless to humans, but when it bonds to skin cells it initiates a T-cell mediated immune response. This immune response is directed towards the complex of urushiol derivatives which are bound up in the skin proteins. 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. It is thought that about 20 to 40% of individuals are not significantly affected by it, although at least 25% of the CPE have strong reactions to poison ivy. Since the skin reaction is an allergic one, people may develop an increasingly strong reaction after repeated exposures, or show no immune response on their first exposure, but show definite sensitivity on following exposures.
Normally, it takes about twenty-four hours for the rash to first appear. Although it may worsen during the next few days and may appear to spread, in fact what is happening is that areas that received a lesser dose are latently reacting. The rash takes one to two weeks to run its course, but normally does not leave scars. 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.
The causative agent, urushiol, does not spread once it has bound with a cell membrane, and it is not found in weeping blisters. Thus, once the oil and resin has been thoroughly washed from the skin, the rash is usually not contagious.
Treatments
Immediate treatment involves washing exposed skin thoroughly with soap and water. Soap is necessary as urushiol is a hydrophobic oil, and is not washed off by plain water. Once an outbreak has occurred, cold compresses, calamine lotion, antihistamines, and hydrocortisone ointment are commonly used to abate the symptoms.
No vaccine has been developed to counter urushiol symptoms, so "cures" are generally held to be those products that physically remove the urushiol. After about 15 minutes of exposure, the urushiol is chemically bonded to the skin and can only be removed with pharmaceutical products, which vary by person in effectiveness. Two of these products are:
- Tecnu - Originally developed as a treatment for radiation exposure, it was discovered later that Tecnu provided some relief for poison ivy exposure. It is a milky liquid and the main active ingredient is octylphenoxy-polyethoxyethanol. The four octyl groups of this chemical are too large to surround the non-polar molecules in the urushiol, which remains partially active and requires multiple applications. Also, the chemical makeup of the product requires that it be applied no later than eight hours after exposure to urushiol.
- Zanfel - Developed in 1999, this paste uses an ethoxylate molecule with the large octyl groups removed. This allows the molecule to "wrap" around the non-polar molecules of the urushiol and inactivate it. The other ingredient, sodium lauryl sarcosinate, allows the ethoxylate to form a micelle around the urushiol molecule. This creates a large molecule that contains flexible non-polar groups and soluble polar groups, allowing it to be rinsed away with water.
There are many myths that deal with treating toxicodendrons such as poison ivy. Most have been discredited, but some persist, despite being proven false:
- The fluid from the resulting blisters spreads poison ivy to others.
- Poison ivy is harmless when the leaves have fallen off.
- Ice, water, soap, lotions, dry cold air, can help cure poison ivy rash faster. In reality, skin cells react to the urushiol even after the urushiol has been washed off, and the methods listed are for soothing the rash.
See also
External links
"Urushiol-induced contact dermatitis"