Camper with a rash

By Lewis Nelson MD
Yale University School of Medicine

A twenty five year old presents to the Emergency Department on Monday morning complaining of diffuse pruritic rash most prominent on his arms and legs. He knows of no allergies, and has never had a rash similar to this before. The rash began earlier in the day and he cannot associate it with any new medications, soaps, foods, or colognes. He did, however, just return from a two day family camping trip. On exam the rash is erythematous, mildly edematous, with linear vesiculation and marked excoriation. It is most prominent on his arms and legs, but is also present on his left neck and left buttock.

What is the differential diagnosis of this patient's rash?

Fortunately it is rarely critical to pinpoint the cause of a patients rash since it generally does not dramatically alter emergency care. Assuming we can rule out an allergic response to the aforementioned items, the camping trip plays high on our list of etiologies for the rash. Exposure to arthropods such as caterpillars or insects may result in vesicular lesions but rarely are they linear or diffuse. The patient went swimming in a lake, not the ocean, which rules out seabather's eruption, caused by larvae of "thimble jellyfish" and localized to areas covered by a bathing suit. With close contact with foliage in the forest exposure to plant toxins seem likely. While there are multiple dermatologic reactions to plant resins, the most common are allergic contact dermatitis and phototoxicity.

Phototoxic reactions require not only exposure of moist skin to plant parts, but sun exposure as well. They are due to the presence of furocoumarin, notably psoralen, in flowers and leaves. Psoralen is used clinically in the treatment of psoriasis (PUVA therapy), but uncontrolled exposure may result in severe bullous dermatitis, analogous to a severe sunburn. When exposure is to windborne toxin, the dermatitis affects any sun-exposed body area, but when due to direct contact the lesion are typically streaky (known as dermatitis bullosa striata pratensis). The Umbilliferae family consists of several psoralen containing plants such as Queen Anne's lace, wild parsnip and celery. Dermatitis commonly occurs in gardeners using a hand-held nylon fiber weed cutter, as plant fragments containing psoralen are thrown towards the patient's skin ("weed wacker dermatitis"). Finding the lesions in this patient in presumably covered areas (buttocks) rules out photodermatitis.

What is phytodermatitis?

Allergic contact dermatitis due to plants (phytodermatitis) is a very common occupational disorder, but is also seen frequently in campers, home gardeners, flower recipients, and perfume wearers. By far the most common type of allergic contact phytodermatitis is rhus dermatitis, caused by the various species of the family Anacardiaceae. Rhus, also known as Toxicodendron, dermatitis appears as an edematous, vesicular eruption, in a telltale streaky pattern. The streaks result because the resin, lodged beneath the fingernail, is applied to various body regions by scratching.

The agent responsible for the eruption is urushiol, which is actually a collection of several different catechol derivatives with long and variably saturated hydrocarbon side chains (poison ivy is predominantly pentadecylcatechol). This agent is metabolized to a quinone which attacks a skin protein, probably keratin. Acting as a hapten, the urushiol alters the protein in such a way the immune system no longer recognizes it, and initiates an immune response with the first exposure, and an amnestic response with subsequent exposures. Reaction to the urushiol containing resin occurs in over half the people in the US, and many of the rest are capable of being sensitized with the first exposure.

How should poison ivy dermatitis be treated?

Obviously, a good offense is the best defense. However, most barrier creams perform poorly, although Fisher's experience seems better than most. Clothing is most effective, but patients must be cautious when removing and washing them to avoid transfer of the resin to their skin. If washed off the skin within 10 minutes of exposure, it may be possible to avoid dermatitis. Soap and water seems to work best, but others have had success with organic solvents such as ethanol or isopropanol.

Treatment of mild dermatitis can include a soothing agent such as Domeboro (aluminum acetate) solution or a lubricating agent such as petrolatum. It is probably best to avoid drying antipruritic lotions such as calamine except for weeping lesions. Potent topical corticosteroids can be tried for moderate lesions or for severe pruritis, but only mild agents such as hydrocortisone 1% should be used on the face or genitals. Systemic steroids can be used for severe dermatitis, but should be continued for at least two weeks to avoid rebound dermatitis. A typical dose of oral prednisone is 40-60 mg daily. Others have found that triamcinolone acetonide 40 mg given intramuscularly is sufficient to suppress a bout of dermatitis without rebound. Systemic antipruritics such as diphenhydramine can be used but topical versions of the same medications are sensitizing and should be avoided.

Although beyond the scope of the ED, hyposensitization has been suggested as a means of suppressing a dermatologic response in those likely to be continually exposed such as park rangers or gardeners. Success has been limited by side effects and the need for maintenance therapy.

What other plants cause dermatitis that looks like poison ivy?

Poison ivy is a catch-all term for several agents in the family Anacardiaceae that produce contact dermatitis related to urushiol. Toxicodendron radicans (eastern US) and T. rydbergii (midwest) are the real poison ivies, recognized by their "leaves of three" and sap that turns block on exposure to air. Other similar species, all containing urushiol include T. toxicarium (eastern poison oak), T. diversilobum (western poison oak) and T. vernix (poison sumac). Several cross reacting plants that contain either urushiol or similar substances exist and cause a rash indistinguishable from rhus dermatitis. Mango fruit (Mangifera indica) contains urushiol and cardol, and causes disease in those eating intact fruit or peeling the skin. The flesh of the fruit is safe to eat. Cashew nut shell contains cardanol, which is destroyed during roasting. Eating improperly roasted cashews or handling raw cashew nuts or shells has caused dermatitis. The resin in ginkgo tree resembles urushiol and can produce a poison ivy like syndrome.

Finally, allergic contact phytodermatitis is produced by other haptenic substances, notably the sesquiterpene lactones found in the Compositae family. This family includes chrysanthemum, feverfew and dandelions, all of which are a source of dermatitis. The contact dermatitis is similar, although not generally linear, and treatment is similar.

Recommended reading

Epstein WL. Occupational poison ivy and oak dermatitis. Dermatology Clinics 1994;12:511-516.

Fisher AA. Efficiency of topical barrier creams in prevention of poison ivy dermatitis. Am J Contact Dermatitis. 1990;1:208

Guin JD. The black spot test for recognizing poison ivy and related species. J Am Acad Dermatol 1980;2:332-333

Hjorth N, Roed-Petersen J, Thomsen K. Airborne contact dermatitis from Compositae oleoresins simulating photodermatitis. Br J Derm 1976;95:613-619

Marks JG, Trautlein JJ, Epstein WL, Laws DM, Sicard GR. Oral hyposensitization to poison ivy and poison oak. Arch Dermatol 1987;123:476-478.

Reynolds NJ, Burton JL, Bradfield JWB, Matthews CNA. Weed wacker dermatitis. Arch Dermatol 1991;127:1419-1420.