What to Do When Poison Ivy Allergy Presents

April 1st 2016

Toxicodendron, a term that means “poisonous tree,” is the genus that includes the most common culprits in allergic plant contact dermatitis, such as poison ivy.

Toxicodendronis 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.1Toxicodendrondermatitis can result from a variety of plants, including western and eastern poison ivy (Toxicodendron rydbergiiandToxicodendron toxicarium, respectively).2Patients’ reactions to these plants can vary as much as the plants themselves, rendering the common phrase “leaves of 3, leave them be” oversimplified.3Nevertheless, 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.4There is a natural tendency for outdoor workers to have plant dermatitis.5Unlike 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.6By 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.9,10Patients 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 withStaphylococcus aureusor beta-hemolytic group AStreptococcus.Depending on the affected site, the bacteria can also be polymicrobial.11Poison 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.

Prevention and Treatment

Prevention and treatment go hand-in-hand as the most effective treatment in the identification and avoidance of poisonous plants.

Preventive Measures

Patients need to be made aware that the plant allergens can have an effect year-round and that allergenicity can persist even after plant death. Patients should be counseled about protective barriers against poison ivy. The allergenic sap can be kept at bay by wearing heavy-duty vinyl gloves; it can seep through rubber and latex gloves and penetrate some clothing. Still, physical barriers afford some form of protection and are wise to use.

Patient education is paramount to appropriate self-management of poison ivy dermatitis. Educational handouts with colored photos of the various plants are helpful. Patients should be advised to remove any contaminated clothing and to wash the skin with soap and water as soon as possible. Removing debris and residual plant resin from beneath the fingernails is also beneficial, though harsh scrubbing can intensify the ensuing dermatitis and is not advised.

In a volunteer study involving approaches to postcontact prevention of poison ivy dermatitis, Tecnu, Goop, and Dial were compared with a positive control. Results showed 70%, 61.8%, and 56.4% protection, respectively, which is an insignificant difference among the 3 products. However, the results also showed that each product does help prevent the development of dermatitis after exposure.13

Bentoquatam (Ivy Block) is a barrier cream with the best evidence for prevention of poison ivy dermatitis. Results of a small, controlled trial showed that only 32% of subjects developed dermatitis at the site treated with the cream. Bentoquatam seems also to lessen the severity of the dermatitis. To be effective, however, it needs to be reapplied every 4 hours.14

Unlike with other allergens, desensitization programs have not been found to be effective in the management of poison ivy dermatitis.15

Treatment Tactics

Although few clinical trials have examined poison ivy dermatitis, clinical experience is vast and the measures recommended herein are generally effective. Symptomatic relief is a starting point for treatment and consists of cool compresses and oatmeal baths. Calamine lotion has also been helpful against the pruritus.16The itching related to poison ivy dermatitis is not histamine-mediated, although antihistamines have been used to combat the pruritus in common practice. Specifically, sedating antihistamines are beneficial in relieving nocturnal itching that causes insomnia.

Either alone or in combination, topical and systemic steroids have become a mainstay of therapy for poison ivy dermatitis. Topically, the high-potency corticosteroids are most helpful in symptom management. Clobetasol propionate 0.05% ointment has proven to be the only topical steroid that can modify the disease course. Use of super-potent topical corticosteroids for less than a week will likely not cause significant atrophy in that time frame. Once the characteristic bullae have formed, topical steroids do little to help.17

Systemic corticosteroids may be indicated with facial or genital involvement, or in cases of severe dermatitis. Despite a lack of evidence-based studies defining the exact amount of steroids needed, clinical experience dictates that too short a course may cause rebound dermatitis because of continued cytokine activation from T lymphocytes.18

One small, randomized, controlled trial compared a long versus short course of oral prednisone in patients with severe poison ivy. One group received 40 mg of prednisone for 5 days and the other group received the same regimen, plus a 10-day taper, for a total treatment time of 15 days. Nonadherence rates, rash return, medication side effects, time to improvement, and complete healing of the rash were not significantly different between the 2 groups. In addition, patients receiving the long-course regimen were significantly less likely to use other medications for symptom relief (22.7% vs. 55.6%), reducing the need for excess nonprescription medications.19

With the easy-to-remember 1 mg/kg/day dosing, up to 60 mg a day, oral prednisone has been suggested with a long taper (eg, 14 to 21 days). Intramuscular administration of steroids is useful in patients who cannot tolerate parenteral dosing. Again, published data are lacking on the ideal steroid dose for patients with poison ivy dermatitis.4,20

Secondary bacterial infection must be considered if painful erythema, induration, or pus develops. Antimicrobial coverage should be directed against gram-positive organisms.S aureusor group AStreptococcusmust be considered first, along with methicillin-resistantS aureus.

Michele Brannan, MPAS, PA-C,earned her bachelor’s degree in health science and her masters of physician assistant studies degree from Gannon University. She started her career working in cardiology at St. Louis University before joining Alton Internal Medicine in Alton, Illinois, where she has practiced for more than 10 years.

References

  1. Usatine RP, Riojas M. Diagnosis and management of contact dermatitis.Am Fam Physician.2010;82(3):249-255.
  2. McGovern TW, Barkley TM. Botanical dermatology.Int J Dermatol.1998 May;37(5):321-334.
  3. Parkinson G. Images in clinical medicine. The many faces of poison ivy.N Engl J Med.2002;347(1):35.
  4. Baer RL. Poison ivy dermatitis.Cutis. 1990 Jul;46(1):34-36.
  5. Epstein WL. Occupational poison ivy and oak dermatitis.Dermatol Clin.1994;12(3):511-516.
  6. Fisher AA. Poison ivy/oak/sumac. Part II: Specific features.Cutis.1996;58(1):22-24.
  7. Hershko K, Weinberg I, Ingber A. Exploring the mango-poison ivy connection: the riddle of discriminative plant dermatitis.Contact Derm.2005;52(1):3-5.
  8. McGovern TW. Dermatoses due to plants. In: Bolognia JL, Jorizzo JL, Rapini RP, et al, eds.Dermatology,New York, NY: Mosby; 2003:274.
  9. Cohen LM, Cohen JL. Erythema multiforme associated with contact dermatitis to poison ivy: three cases and a review of the literature.Cutis.1998;62(3):139-142.
  10. Shankar DS. Contact urticaria induced bySemecarpus anacardium. Contact Derm.1992;26(3):200.
  11. Brook I, Frazier EH, Yeager JK. Microbiology of infected poison ivy dermatitis.Br J Dermatol.2000;142(5):943-946.
  12. Fisher AA. Poison ivy/oak/sumac. Part II: Specific features.Cutis.1996;58(1):22-24.
  13. Stibich AS, Yagan M, Sharma V, Herndon B, Montgomery C. Cost-effective post-exposure prevention of poison ivy dermatitis.Int J Dermatol.2000;39(7):515-518.
  14. Marks JG Jr, Fowler JF Jr, Sheretz EF, Rietschel RL. Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite.J Am Acad Dermatol.1995;33(2 pt 1):212-216.
  15. Marks JG Jr, Trautlein JJ, Epstein WL, Laws DM, Sicard GR. Oral hyposensitization to poison ivy and poison oak.Arch Dermatol. 1987;123(4):476-478.
  16. Williford PM, Sheretz EF. Poison ivy dermatitis. Nuances in treatment.Arch Fam Med.1994;3(2):184-188.
  17. Vernon HJ, Olsen EA. A controlled trial of clobetasol propionate ointment 0.05% in the treatment of experimentally inducedRhusdermatitis.J Am Acad Dermatol.1990;23(5 pt 1):829-832.
  18. Goodall J. Oral corticosteroids for poison ivy dermatitis [letter].Can Med Assoc J.2002;166(3):300.
  19. Curtis G, Lewis AC. Treatment of severe poison ivy: a randomized, controlled trial of long versus short course oral prednisone.J Clin Med Res. 2014;6(6)429-434. doi: 10.14740/jocmr1855w.
  20. Dickey RF. Parenteral short-term corticosteroid therapy in moderate to severe dermatoses. A comparative multiclinic study.Cutis. 1976;17(1):179-183.

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