Information About Poison-lvy Contact Dermatitis

Diagnostic Hallmarks

Distribution: exposed areas, asymmetrical locations

Angular and linear lesions

History of exposure

Clinical Presentation

The antigens responsible for the development of allergic contact dermatitis resulting from poison ivy, poison oak, or poison sumac are, for all practical purposes, identical. In a sensitized patient, direct skin contact with the resin from any of these plants results in an inflammatory, blistering eruption that develops 24-48 hours later.

The eruption consists of bright-red, edematous papules and plaques. Weeping and crusting are usually observed. Vesicles and bullae of widely varying size are surmounted on some of the inflammatory lesions. As a reflection of external causation, there is usually a unilateral or asymmetrical distribution pattern. Linear-and angular-shaped lesions, which occur as a result of antigen deposition in scratch marks, are highly distinctive for this disease.

Lesions can also occur on nonexposed areas as a result of antigen having been carried on the hands and transferred elsewhere. The antigen penetrates wet, sweaty clothing surprisingly well, in which case edematous, nonvesicular plaques may be found in areas such as the buttocks and knees. Palms and soles are usually spared because of the protective effect of the thick stratum corneum normally present in these locations. Pruritus is intense, and some evidence of excoriation is often present.

Allergic contact dermatitis to substances other than poison ivy rarely results in vesiculobullous reactions. The more common patterns of allergic contact dermatitis are covered with the eczematous diseases .

Poison Ivy Variants

When the leaves of poison ivy are burned, small particles of resin are carried with the smoke. Sensitized individuals will develop marked erythema and edema of the face, but there is little or no evidence of vesiculation. Poison ivy contact dermatitis is occasionally seen in circumstances where there has been no recent exposure to the plants. Such cases may be due to contact with contaminated firewood or with clothing that was previously contaminated and was then stored without washing.

Course and Prognosis

People previously sensitized to poison ivy develop lesions only after a latent period of 24-48 hours. Lesions appear first at the site of heaviest antigen deposition, but new lesions can continue to develop for an additional 3 or 4 days at sites where antigen concentration was less intense. Spontaneous healing begins within a week and is usually complete by the end of 2 weeks. Allergy to poison ivy is maintained for long periods of time, and thus subsequent exposure, even years later, regularly leads to redevelopment of the eruption.

Pathogenesis

The specific antigen responsible for the reaction is found in the resin of poison ivy, poison oak, and poison sumac. Its chemical structure is that of a pentadecylcatechol. Substances chemically related to this compound can be found in cashew oil and in some oils used for lacquers. The antigen is extraordinarily potent; nearly every person given sufficient exposure will become sensitized.

Probably 30-50% of the American population has developed allergy as the result of sporadic natural contact. The resin is not found on the exterior surface of the plants, and thus development of a chemical reaction requires breakage of leaves or stems. Within 30 minutes of contact, the resin binds so well to the skin that washing will not remove it, nor will washing at that point prevent the appearance of the rash. Unbound resin does remain on the fingernails and clothing, however, and can cause additional lesions when it is transferred elsewhere. Washing with soap and water does remove and inactivate this resin. Of special note is the fact that the fluid within the bullae does not contain resin, and thus contact of blister fluid with normal skin does not result in the development of new lesions.

The immunologic aspects of poison ivy contact dermatitis are similar to those of other types of allergic contact dermatitis.

Therapy

Mild attacks of poison ivy contact dermatitis can be treated with high-potency topical steroids. Patients with more severe involvement and those with lesions on the face or genitalia are better treated with a "burst" of prednisone in a dosage of 60-80 mg/ day. Itching, redness, and swelling are much improved by the second day, but treatment must be continued for 7-10 days, lest the lesions rapidly reappear when the steroids are stopped. The steroid dose does not need to be tapered prior to discontinuation. Soaks and antihistamines, as needed, can be added to this program. All exposed clothing, including shoes, should be washed with soap and water to remove any remaining resin. Pets who have been exposed to the plants should likewise be shampooed. There is no practical way of using poison ivy antigen to "vaccinate" or hyposensitize patients.