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The Truth About Poison Ivy

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Picture it: It’s 1948. You’re 12, and you’re itching. Then a rash develops. Your mother says you probably have poison ivy—and sure enough, you’ve been thrashing about in the woods where they told you not to go (but you didn’t listen). It never hurt you before, but now the blisters are coming, in long streaks, on your legs and arms. There’s no sleeping and no holding still, not even in church. The itching is so bad, and vinegar and the pink stuff they put on you don’t help at all; they only call more attention to your rash. Everyone, even your own family, is giving you a wide berth, because they all believe poison ivy is contagious.

Six weeks later, the rash and itching are finally gone—but not the memory of this common condition, for which no effective treatment will exist until topical corticosteroids are introduced in 1951.

All these years later, many myths about poison ivy persist. Some are such powerful misconceptions that many people cannot be swayed from them, even by facts. For example, poison ivy is not in the least contagious. Nor is it caused by any kind of “poison.”

The culprit is an oleoresin known as urushiol. This oily resin is contained in the stems, leaves, and flowers of plants from the Toxicodendron genus, which includes poison ivy (by far the most common source), poison oak (found almost exclusively west of the Rockies) and poison sumac (found in limited areas of the southeastern United States). Similar reactions can be caused by exposure to other botanicals, including ficus, fern, fig, mango, and Japanese lacquer trees. (Another member of the Toxicodendron family is the Rhus tree, found mostly in Australia, where it is notorious for causing rashes.)

A history of recent exposure to the great outdoors can therefore usually be obtained, although exposure can also occur through contact with pets or with the clothing of family members who have been exposed. A live plant is not necessary. Many a victim has acquired poison ivy from clearing brush or handling firewood in the dead of winter. (The antigen can also be acquired through an airborne route, such as from the smoke generated by burning brush—even at a considerable distance.) Repeated exposure to poison ivy over several years’ time is required, which explains why children and city-dwelling adults may appear to be immune.

Typically, the blisters begin to appear within 12 to 48 hours of exposure (with some notable exceptions). Much to the consternation of the patient and family, new lesions can continue to manifest for up to two weeks after initial exposure, which is probably why so many people think poison ivy is contagious. The truth is, there is no urushiol in the fluid from the blisters, nor is the antigen “poison” in any way. In short, poison ivy cannot be transmitted from one person to another.

Poison ivy rashes manifest in several different ways. The most common is a type IV delayed hypersensitivity reaction, with pathognomic linear streaks of erythematous patches of edematous, blistery skin. Figure 1 shows a classic linear lesion on the face of a 69-year-old woman who had cleaned out her fence line a few days previously. This particular patient had a similar rash on her chest.

Figure 2 shows a more atypical form of poison ivy, entirely lacking linear lesions or even blisters. The patient’s rash was widespread, but concentrated on popliteal and antecubital areas and medial thighs. It comprised large sheets of highly erythematous skin, in the centers of which were targetoid reddish blue patches. This is a variant of erythema multiforme, which is by definition a secondary condition usually triggered by bugs (strep, herpes simplex virus) or drugs (sulfa, tetracycline, aspirin, penicillin) but occasionally by an exaggerated reaction to antigens such as poison ivy. In this case, this 185-pound 47-year-old woman and her family acquired poison ivy while picking wildflowers in wet weeds—bringing a rapid end to the family vacation.

The most effective treatment for severe, symptomatic poison ivy is the use of systemic glucocorticoids (eg, prednisone) and/or intramuscular injection of a corticosteroid (eg, triamcinolone). Patient 2’s condition was so severe that she couldn’t sleep, eat, or even drive a car. (Interestingly enough, she was the only one who sought medical evaluation. The rest of her family was content to clean out the local pharmacy’s supply of calamine lotion and diphenhydramine capsules.) Severity of this nature demands serious medication—in this case, a two-week taper of prednisone (from 60 mg down to 20 mg) plus an IM injection of triamcinolone (60 mg).

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