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Poison Oak Allergic Contact Dermatitis

Paul Auerbach, M.D.
Case Reviews in Clinical Dermatology, Volume 1 Issue 3, had an interesting discussion about certain aspects of poison oak/ivy dermatitis. The following are some of the points made by the authors, with additional comments by me:

"Contact dermatitis" (CD) is a broad term used to describe inflammation of the skin caused by direct contact with an irritating substance or allergen (a substance that induces an allergic reaction/response). Allergic contact dermatitis is a hypersensitivity reaction to a substance exposed to the skin to which a person has become allergic.

Sensitization to a substance can develop at any time, including adulthood. It may develop for substances that have been used repeatedly without any difficulty by an individual in the past. Poison oak/ivy allergic contact dermatitis is quite common. It is most likely to occur in persons with significant outdoor exposure, such as forest firefighters and backpackers. Sometimes a person may unknowingly encounter the allergen. For instance, urushiol in poison oak can persist on items such as clothes and gardening tools for years, and may be transmitted to a person from the fur of a pet, in the smoke of a campfire, or from a casual brush with plant that intrudes on a hiking path.

In general, a contact dermatitis eruption due to poison oak appears as itchy blisters, both large and small, on a reddened base in a linear (patterned in lines) distribution. Despite common belief, the fluid contained in the blisters does not spread the rash; only the urushiol resin itself can spread the rash. The resin in the is composed of a mixture of catechols and causes the hypersensitivity reaction when it comes in direct contact with the skin.

Urushiol is a water-soluble substance that can only be removed in significant amounts if washed immediately. Only 50% can be removed after ten minutes of contact, 25% after 15 minutes, and no resin can be removed after one hour of contact with the skin. Prevention of exposure to these plants is the most sensible, but not always the most practical solution. Many attempts have been made to prevent contact with the resin by applying topical skin protectants.

To make some treatment recommendations, the authors of the article offered a clinical case:

A 28-year-old, otherwise healthy man presented with a one-week history of a rash that began as small, itchy blisters on his inner arms a few days after camping in the Sierra Nevada Mountains. A few days later, he started to develop new large, red areas on his back. He felt somewhat fatigued but denied having fever or other symptoms. On physical examination, small blisters and black streaks were apparent in a cluster on his inner arm. There were other large reddened areas on his back. Based on his presentation, the diagnosis was "black spot poison oak contact dermatitis with systematization (spread to other parts of the body)."

The patient was treated with oral prednisone, starting at 60 mg per day and tapered by 10 mg per oral dose every 3 days. His symptoms resolved completely within two weeks.

According to the authors, this case illustrated an unusual presentation of poison oak contact dermatitis and the importance of rapid diagnosis and treatment. "Rhus dermatitis," commonly known as "poison ivy, poison oak, or poison sumac," and currently referred to as "toxicodendron dermatitis," is one of the most common forms of contact dermatitis (CD) in the U.S. It is characterized by itchy blisters on a reddened base in the setting of a history of exposure to an offending plant or some other vehicle (such as a dog's fur) that is carrying the resin.

Poison ivy grows in all states in North America with the exception of Alaska. Poison oak is separated into two categories: Western Poison Oak, which only grows on the Pacific coast of North America, and Atlantic Poison Oak, which is found mostly in sandy soils in the eastern part of the U.S. Poison ivy and poison oak are grouped with other toxicodendron dermatitis agents, including Japanese lacquer tree, cashew nut tree, poison sumac, and other members of the Anacardiaceae family of plants. Marked pruritus is typically the first symptom of toxicodendron dermatitis, beginning between the fingers, and on the eyelids, wrists, and top (opposite the palm) aspects of the fingers within 48 hours of exposure.

Itching is generally followed by inflammation and the characteristic appearance of a linear bumpy (raised) rash with blisters. As long as the plant oil remains on the skin, it can be transferred from the hands to other body parts. However, once the offending agent has been washed off, there is generally no further expansion of the rash, except in areas that have come in contact with the resin. In some cases, CD can become severe, covering over 20% of the body in adults and 10% of the body in children or manifesting systemically with fevers, fatigue (tiredness), and other symptoms.

The offending urushiol is an oleoresin that is both an allergen (causes an allergic response) and a primary irritant. It is a very resilient substance, and can persist for weeks to months on clothes, furniture, and animal fur. Typically, the allergic reaction to urushiol occurs within 24 to 72 hours, but it can be seen as quickly as six hours after exposure, particularly in highly sensitive individuals.

Black spot contact dermatitis is usually caused by poison ivy and poison oak, but can also be caused by sap from the Japanese lacquer tree, because the chemical structures of the oils in both plants are quite similar. When the resin from the Japanese lacquer tree comes into contact with skin, it turns black and attains a shiny appearance that becomes especially noticeable within the first 72 hours after exposure.

Black spot poison oak as a diagnosis can be challenging when the presentation consists of only asymptomatic black spots. Patients become concerned when these black spots, appearing as marker or ink spots, do not wipe off, and they sometimes confuse the lesions with melanoma. The ability of the resin to persist on clothes, fur, and tools for years can also complicate the picture since patients may deny a history of exposure because they are unaware of their contact with the resin. This pigment develops not only on the skin but on clothing as well. The black lesions cannot be washed off the skin and are followed by itchy blisters. They eventually peel off, and the skin heals without scarring.

This presentation is not commonly observed, probably because for the black lesions to occur, the skin needs to come into contact with a much higher concentration of plant sap. In most cases, persons experience only brief contact with the offending plant and then further dilute the concentration of oleoresin via perspiration or bathing so the appearance of black spots does not occur.

Regardless of whether or not black coloration occurs, after suspected exposure to the resin, the first step should be to wash the skin with soap to remove the urushiol and prevent further spread of the agent. This is most effective if done within 15 minutes of exposure. All clothes and any other items that came into contact with the offending plant should also be washed. Many patients find cool tub baths helpful in relieving the itching and edema associated with the rash, and oral antihistamines provide nighttime relief from itching. During the acute blistering stage, cool, wet dressings applied for approximately 20 minutes several times a day may help with swelling, especially around the eyes and on the face.

The decision to use topical or oral steroid medication(s) depends on a number of factors, including but not limited to age of the patient, severity of symptoms, amount of body surface area involved, and presence or history of a medical condition in which administration of an oral steroid could cause an adverse reaction.

The American Academy of Dermatology recommends topical steroid treatment only for mild cases. Typically, medium potency topical steroids are used, except on (delicate) skin around the eyes, which requires a less potent steroid. In general, the steroid preparations are liberally applied to the affected areas twice daily for 7 days. Oral steroids are used in more severe cases and in sufferers who have systemic involvement.

In severe cases, oral steroid courses (typically prednisone) are given at 0.75 to 1 mg/kg/day every morning, and this dose is tapered over a three-week period. Generally, oral steroids are tapered by approximately 10 mg every 2 to 3 days. For these severe, generalized cases, short (e.g., a few days) courses of low-dose oral corticosteroids have proven inadequate.

image of black spot reaction courtesy of Professional Education Services Group

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