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There are many myths that deal with treating toxicodendrons such as poison ivy. Most have been discredited, but some persist despite their falsehood:
There are many myths that deal with treating toxicodendrons such as poison ivy. Most have been discredited, but some persist despite their falsehood:
*The fluid from the resulting blisters spreads poison ivy to others.
* '''Myth:''' The fluid from the resulting blisters spreads poison ivy to others.
*Poison ivy is harmless when the leaves have fallen off.
* '''Myth:''' 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.
* '''Myth:''' 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.
*Urinating on the infected areas will cure most rashes.
* '''Myth:''' Urinating on the infected areas will cure most rashes.


== See also ==
== See also ==

Revision as of 23:51, 1 July 2007

Urushiol-induced contact dermatitis
SpecialtyDermatology Edit this on Wikidata
Toxicodendron pubescens ("Atlantic Poison-oak"), one of a large number of species containing urushiol irritants.

Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis and Rhus dermatitis) is the medical name given to allergic rashes produced by oil urushiol, which is contained in various plants, including the plants of 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.

Symptoms of the rash 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 U.S., while poison-ivy is most rampant in the eastern U.S. Dermatitis from poison sumac is less common, but just as problematic.

Exposure

Blistering 48 hours after urushiol contact

Urushiol-induced contact dermatitis is contracted by contact with a plant or any other object containing urushiol oil. Clothing or other materials that contact the plant and then, before being washed, contact the skin are common causes of exposure. Normally, it takes about 24 hours for the rash to first appear, though it may worsen during the next few days and may appear to spread, when in fact what is happening is that areas that received a lesser dose are reacting. The rash can take one to two weeks to run its course, and in some cases up to five weeks.

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 has been thoroughly washed from the skin, the rash is usually not contagious. Urushiol does not spread once it has bound with the skin, and it is not found in weeping blisters. Although the rash may worsen during the first few days and may appear to spread to new areas, this is usually simply latent reaction.

Although simple skin exposure is most common, ingestion can also 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. However, some sources dispute the danger of burning urushiol-containing plant material.[1]

Mechanism

Poison ivy rash after 2 days.

Chemically, urushiol is harmless to humans, but when it bonds to skin cell membranes, it changes the cells configuration initiating a T-cell mediated immune response. The body's immune system no longer recognizes these cells as belonging to the body, this immune response is directed towards the complex of urushiol derivatives which are bound up in the skin proteins and attacks the cells as if they were a foreign agent. 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. Around 15%[1] to 30%[2] of people are immune to the effects, although at least 25% of people 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.

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.

Treatments

Primary 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, Burow's solution, 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.

In cases of extreme symptoms, steroids such as cortisone are sometimes administered, either by injection or through prescription oral medication. If bacterial secondary infection of affected areas occurs, antibiotics may also be necessary.

There are many myths that deal with treating toxicodendrons such as poison ivy. Most have been discredited, but some persist despite their falsehood:

  • Myth: The fluid from the resulting blisters spreads poison ivy to others.
  • Myth: Poison ivy is harmless when the leaves have fallen off.
  • Myth: 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.
  • Myth: Urinating on the infected areas will cure most rashes.

See also

References

  1. ^ Dietrich Frohne and Hans Jurgen Pfander (1984). A Colour Atlas of Poisonous Plants: A Handbook for Pharmacists, Doctors, Toxicologists, and Biologists. Wolfe Publishing Ltd. pp. 291 pp. ISBN 0-7234-0839-4.