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Larkin Community Hospital and Baystate Medical Center
Exposure to species in the genus Toxicodendron accounts for the most common cause of plant-induced allergic contact dermatitis in the United States and more plant-dermatitides than all of the other families of dermatitis-causing plants combined.[1,2] This exposure is a common complaint seen in the emergency department with an estimated 25-40 million people affected every year. Of note, Rhus dermatitis is an antiquated term for these dermatitides; members of the genus Rhus do not cause dermatitis.
The significant members of the Toxicodendron genus include poison ivy, poison oak, and poison sumac. While it is possible to find these in many areas of the United States, they are not found in deserts, rainforests, or at altitudes higher than 1500 meters.
Poison ivy can be identified by 10 to 30 cm long ovate leaflets in groups of three. The leaves can be either shiny, smooth, and hairless, or rough, hairy, and velvety. Their characteristic appearance has led to the adage, “leaves of three, let them be.” Poison oak is more of a shrub-type plant with clusters of yellow flowers and cream-colored berries. Poison sumac is a taller plant with an average height of 4.5 m but can grow as large as 12 m in height. Leaves of the sumac variety are different because they are smooth and oval-shaped and found in groups of 7 to 13 from a central stem with pale-colored fruit.
Dermatitis occurs by a type IV hypersensitivity immune reaction with two phases: an initial sensitization event and a re-exposure event (although sensitization can occur upon initial exposure). Both are triggered by the oleoresin called urushiol, which oxidizes to a black color when exposed to the air. The oleoresin is found in all parts of the plant, but interestingly returns from the leaves to the central plant during the winter months, devoiding dead leaves on the ground of urushiol. Other members of the Anacardiaceae family that may cause cross-reactivity with previous exposure to urushiol include the peel of the mango, cashew nut shell oil, pulp from the gingko biloba, Japanese lacquer tree, and India marker ink tree.[1,4]
The onset time of reaction formation ranges from 4 to 48 hours after exposure. Because of its antigenicity, symptoms can occur during the initial sensitization step, usually after 10 to 21 days.[1,4] Symptoms in cases of re-exposure occur faster, typically within 4 to 96 hours.[1,4,6] Spontaneous resolution occurs in 14 to 21 days in most individuals. Systemic symptoms may include fever, chills, fatigue, and lethargy. Presentations may demonstrate a characteristic linear patterning and progress through any of the following stages: acute eczematous reaction, pruritic, edematous and erythematous papules, urticarial-looking plaques, and vesicles and bullae. Other complications include erythema multiforme, black-spot staining of the skin, renal and genitourinary complications, subacute lichenoid neurodermatitis, and bacterial secondary infections.[1,3]
While there are various treatment options listed in the literature, prophylaxis via plant identification and protective clothing is best. Once contact occurs, only about 50% of urushiol can be removed within the first 10 minutes, 10% in 30 minutes, and none after 60 minutes. Topical symptomatic therapy, including the use of astringents, menthol- and phenol-containing compounds, cool wet compresses, and acetic acid wet dressings may provide anecdotal relief, but their efficacy not been proven.[3,8] As the dermatitis is not a histamine-releasing reaction, any benefits from antihistamines are most likely due to their sedating properties.
Traditionally, the cornerstone of therapy is corticosteroid use. Topical corticosteroids can be given for mild to moderate disease, while systemic steroid therapy is required for moderate to severe presentations. Topical clobetasol 0.05% twice daily can be used to affected areas for two weeks. Oral prednisone should be dosed at 1 mg/kg/day for three to four days, with a taper over 14 to 21 days. It is important to note that abrupt discontinuation or inadequate duration of treatment has a high likelihood of causing rebound inflammation.
1. Shofner JD, Kimball AB. Plant-induced dermatitis. In: Wilderness Medicine. 6th ed. Philadelphia, PA: Mosby; 2012:1238-1244.
2. Lee N, Arriola E. Poison ivy, oak, and sumac dermatitis. West J Med. 1999;171:354-5.
3. Baer RL. Poison Ivy Dermatitis. Cutis. 1990;46(1):34-6.
4. McGovern TW. Dermatoses Due to Plants. In: Dermatology. 3rd ed. Amsterdam, Netherlands: Elsevier; 2012:281-287.
5. Sasseville D. Clinical patterns of phytodermatitis. Dermatol Clin. 2009;27(3):299-308.
6. Williams J V, Light J, Marks JG. Individual variations in allergic contact dermatitis from urushiol. Arch Dermatol. 1999;135(8):1002-1003.
7. McGovern TW, Barkley TM. Botanical Dermatology. Int J Dermatology. 1998;37:321
8. Vaught CK, Mold JW. Poison ivy: How effective are available treatments? J Fam Pract. 2016;65(11):801-809.
9. Yosipovitch G, Fleischer A. Itch associated with skin disease: advanced in pathophysiology and emerging therapies. Am J Clin Dermatol. 2003; 4:617.
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