Botanical Briefs: Contact Dermatitis Induced by Western Poison Ivy (Toxicodendron rydbergii)
“Leaves of three, leave it be” serves as an apt caution for avoiding poison ivy (Toxicodendron species) and its dermatitis-inducing sap. Toxicodendron contact dermatitis (TCD) poses a notable burden to the American health care system by accounting for half a million reported cases of allergic contact dermatitis (ACD) annually. Identifying and avoiding physical contact with the western poison ivy (Toxicodendron rydbergii) plant prevails as the chief method of preventing TCD. This article discusses common features of T rydbergii as well as clinical manifestations and treatment options following exposure to this allergenic plant.
PRACTICE POINTS
- Western poison ivy (Toxicodendron rydbergii) accounts for many of the cases of Toxicodendron contact dermatitis (TCD) in the western and northern United States. Individuals in these regions should be educated on how to identify T rydbergii to avoid TCD.
- Dermatologists should include TCD in the differential diagnosis when a patient presents with an erythematous pruritic rash in a linear pattern with sharp borders.
- Most patients who experience intense itching and pain from TCD benefit greatly from prompt treatment with an oral or intramuscular corticosteroid. Topical steroids rarely provide relief; oral antihistamines provide no benefit.
Identifying Features
Toxicodendron rydbergii turns red earlier than most plants; early red summer leaves should serve as a warning sign to hikers from a distance (Figure 1). It displays trifoliate ovate leaves (ie, each leaf contains 3 leaflets) on a dwarf nonclimbing shrub (Figure 2). Although the plant shares common features with its cousin T radicans (eastern poison ivy), T rydbergii is easily distinguished by its thicker stems, absence of aerial rootlets (abundant in T radicans), and short (approximately 1 meter) height.4
Curly hairs occupy the underside of T rydbergii leaflets and along the midrib; leaflet margins appear lobed or rounded. Lenticels appear as small holes in the bark that turn gray in the cold and become brighter come spring.13
The plant bears glabrous long petioles (leaf stems) and densely grouped clusters of yellow flowers. In autumn, the globose fruit—formed in clusters between each twig and leaf petiole (known as an axillary position)—change from yellow-green to tan (Figure 3). When urushiol exudes from damaged leaflets or other plant parts, it oxidizes on exposure to air and creates hardened black deposits on the plant. Even when grown in garden pots, T rydbergii maintains its distinguishing features.11
Dermatitis-Inducing Plant Parts
All parts of T rydbergii including leaves, stems, roots, and fruit contain the allergenic sap throughout the year.14 A person must damage or bruise the plant for urushiol to be released and produce its allergenic effects; softly brushing against undamaged plants typically does not induce dermatitis.4
Pathophysiology of Urushiol
Urushiol, a pale yellow, oily mixture of organic compounds conserved throughout all Toxicodendron species, contains highly allergenic alkyl catechols. These catechols possess hydroxyl groups at positions 1 and 2 on a benzene ring; the hydrocarbon side chain of poison ivies (typically 15–carbon atoms long) attaches at position 3.15 The catechols and the aliphatic side chain contribute to the plant’s antigenic and dermatitis-inducing properties.16
The high lipophilicity of urushiol allows for rapid and unforgiving absorption into the skin, notwithstanding attempts to wash it off. Upon direct contact, catechols of urushiol penetrate the epidermis and become oxidized to quinone intermediates that bind to antigen-presenting cells in the epidermis and dermis. Epidermal Langerhans cells and dermal macrophages internalize and present the antigen to CD4+ T cells in nearby lymph nodes. This sequence results in production of inflammatory mediators, clonal expansion of T-effector and T-memory cells specific to the allergenic catechols, and an ensuing cytotoxic response against epidermal cells and the dermal vasculature. Keratinocytes and monocytes mediate the inflammatory response by releasing other cytokines.4,17
Sensitization to urushiol generally occurs at 8 to 14 years of age; therefore, infants have lower susceptibility to dermatitis upon contact with T rydbergii.18 Most animals do not experience sensitization upon contact; in fact, birds and forest animals consume the urushiol-rich fruit of T rydbergii without harm.3
