What to Do When Poison Ivy Allergy Presents

Michele Brannan, MPAS, PA-C
Friday April 01, 2016
Toxicodendron is a term that means “poisonous tree.” It is also the genus that includes the most common culprits in allergic plant contact dermatitis, such as poison ivy.1 Toxicodendron dermatitis can result from a variety of plants, including western and eastern poison ivy (Toxicodendron rydbergii and Toxicodendron toxicarium, respectively).2 Patients’ reactions to these plants can vary as much as the plants themselves, rendering the common phrase “leaves of 3, leave them be” oversimplified.3 Nevertheless, this adage is most applicable to poison ivy, as it has 3 leaflets with flowering branches.
An estimated 25 to 40 million Americans require medical treatment after plant exposure.4 There is a natural tendency for outdoor workers to have plant dermatitis.5 Unlike some types of dermatitis, the rash of poison ivy is not selective to any particular skin type, so individuals of any ethnicity can be affected.6 By the time they are 8 years old, most children are sensitized, and it appears that allergic reactions from the plant tend to wane with age, so the elderly are affected less often.5
Poison ivy dermatitis is a type IV hypersensitivity, cell-mediated, allergic reaction to the urushiol compound. Because urushiol is a potent antigen, a single exposure can cause clinical signs such as a pruritic rash. The allergen can be found on the leaves, stem, fruit, and even the root of the plant, and there is greater uptake when exposure occurs after the plant is broken or bruised, such as after a rainfall or cutting the plant. When the toxic plant oil makes contact with skin, clothing, pets, or other fomites, the allergen easily penetrates the epidermis and is taken up by the Langerhans cells. Now covered in antigen, these cells activate T lymphocytes in regional lymph nodes before circulating throughout the body. Once clonally-expanded T lymphocytes are present, re-exposure to the poisonous plant elicits cytokine release and subsequent symptoms in 12 to 48 hours. Interestingly, those with a history of poison ivy dermatitis may be at risk for cross-reaction with other urushiol-containing plants such as mango trees.7
Clinical Presentation
Patients typically present to their health care provider when the pruritus and dermatitis become overwhelming. The initial redness may transform into papules, plaques, and/or bullae. The characteristic linear configuration is often present where the plant made contact with the skin.
After exposure, initial symptoms usually develop within 4 to 96 hours and peak within 1 to 14 days. However, new lesions may present up to 21 days after exposure. The severity of the rash and when it develops in a certain area of the body are contingent upon the amount of urushiol present on exposure, the thickness of the stratum corneum of the area involved, and the patient's individual sensitivity. The longer the oils are on the skin, the more likely and more severe the allergic response tends to be. These factors can give the impression that the rash is spreading.8
In addition to pruritic erythema and papules/vesicles, poison ivy can yield edema in the exposed area. Urticaria and erythema multiforme have been known to occur with urushiol exposure in severe cases.9,10 Patients often believe that blister fluid causes spreading of the rash, yet the fluid is not known to be antigenic. Moreover, once the oils are washed off the skin, poison ivy cannot spread to others, which is another common misnomer among patients. Nevertheless, patients can continue to come in contact with contaminated items such as clothing, pets, and tools, thus perpetuating the dermatitis. Without treatment, poison ivy dermatitis is typically self-limiting within 1 to 3 weeks.
Because of a disruption in the skin barrier, the most common complication of poison ivy dermatitis is secondary bacterial infection with Staphylococcus aureus or beta-hemolytic group A Streptococcus. Depending on the affected site, the bacteria can also be polymicrobial.11 Poison ivy dermatitis sequelae can include postinflammatory hyperpigmentation, which is more common in darker-skinned patients and typically resolves with time.12
Differential Diagnosis
Although the diagnosis of poison ivy rash is largely clinical, the following diagnostic differentials should still be considered:
  • Allergic contact dermatitis: other allergens, such as gold or nickel, can cause a rash that resembles poison ivy.
  • Phytophotodermatitis: the lesions are present in only sun-exposed areas and may or may not blister.
  • Arthropod reactions: pruritic burrows from scabies can resemble poison ivy dermatitis, although scabies does not involve blisters or vesicles. Like plant dermatitis, bedbug rash can also be linear and pruritic.
  • Nummular dermatitis: this dermatitis of unknown etiology results in intensely pruritic patches of eczema and can include papules, scaling, and oozing.
  • Herpes zoster: both zoster rash and poison ivy dermatitis can result in vesicles, although the former has a characteristically unilateral and dermatomal distribution.

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