Allergic phytodermatitis is a type of allergic contact dermatitis that results from exposure to plants, most commonly poison ivy and poison oak. Poison ivy and oak belong to the genus Toxicodendron.1 These plants contain the chemical irritants oleoresins (collectively known as urushiol) that trigger a type IV delayed hypersensitivity reaction in susceptible individuals.2
The pathophysiology in this reaction involves urushiol from the plant contacting the skin and becoming linked to skin protein, forming an antigen complex that leads to sensitization. Re-exposure of the skin to the antigen, urushiol, leads to initiation of an inflammatory cascade by the sensitized T-cells, producing the resultant skin reaction.3 Toxicodendron dermatitis is the most common cause of allergic dermatitis in the United States, exceeding all other causes combined.4
Poison ivy and poison oak are common throughout the United States with poison ivy most common east of the Continental Divide and poison oak most common in the west. Researchers have estimated that 50 to 75 percent of the population is sensitive to poison ivy and oak.5 Sensitivity to poison oak and ivy increases significantly with repeat exposure.
Allergic phytodermatitis presents clinically as pruritic papules and vesicles on an erythematous skin base. The skin lesions often have a linear streak pattern where the plant came in contact with the skin. Skin lesions typically appear within 12 to 48 hours following exposure. New lesions can continue to occur for two to three weeks and can result from both a slow reaction to the oleoresins and due to repeat contact with contaminated surfaces, such a clothing and pet hair. It is a common misconception that fluid from the vesicles of a poison ivy or oak rash contains oleoresins and can produce new lesions.6
The severity of dermatitis secondary to poison ivy and oak depends both on the sensitivity of the individual as well as the degree of exposure. Symptoms can range from localized erythema and mild pruritus to profound erythema, edema, severe pain, severe pruritus and bulla formation. Phytodermatitis skin lesions can be complicated by secondary bacterial infections and rarely by erythema multiforme and urticarial.7
One typically diagnoses allergic phytodermatitis based upon the patient history and clinical exam findings. Clinicians can perform patch testing if the etiologic agent of the dermatitis is unclear. Skin biopsy can exclude other cutaneous disorders such as psoriasis and tinea pedis.
The first step in the management of allergic phytodermatitis is removal of the causative substance. Urushiol is an oily substance and can persist on skin, clothing, outdoor equipment and gardening tools. Wash exposed areas thoroughly with soap and water, preferably within 10 minutes of exposure, as immediate removal of the allergen can prevent the development of dermatitis.6 Patients should clean all contaminated clothing and equipment as well.
One can treat mild dermatitis with colloidal oatmeal baths, diluted aluminum acetate solution (Burow’s solution) or calamine lotion.6,8 Treat localized allergic phytodermatitis lesions with topical corticosteroids such as triamcinolone 0.1% (Fougera Pharmaceuticals) or clobetasol 0.05% (Clobex, Galderma Laboratories).8 Severe allergic phytodermatitis and dermatitis affecting extensive skin areas requires oral corticosteroid treatment. The recommended oral corticosteroid treatment regimen is prednisone, 0.5 to 1 mg per kg daily for five to seven days followed by 50 percent of the initial dose for another five to seven days.8 Authors have found that steroid dose packs have insufficient dosing and duration, and one should not use them in the management of allergic phytodermatitis.9
Allergic phytodermatitis is a very common condition with poison ivy and poison oak being the most common causes of allergic dermatitis. The pathophysiology of allergic phytodermatitis involves a type IV delayed hypersensitivity reaction to urushiol from the plant contacting the skin. Management of allergic phytodermatitis varies depending on severity and can include topical astringents, topical corticosteroids and oral corticosteroids.
1. Gladman AC. Toxicodendron dermatitis: poison ivy, oak, and sumac. Wilderness Environ Med. 2006;17(2):120-128.
2. Tadjimukhamedov FK, Huang G, Ouyang Z, Cooks RG. Rapid detection of urushiol allergens of Toxicodendron genus using leaf spray mass spectrometry. Analyst. 2012;137(5):1082-1084.
3. Usatine R. Contact dermatitis. In: Usatine RP SM, Mayeaux EJ, et al, (eds.). Color Atlas of Family Medicine. McGraw-Hill, New York, 2009.
4. Chapel TC, Chapel J. Toxicodendron dermatitis. Emergency Medicine - A Comprehensive Study Guide, Fourth Edition, McGraw-Hill, New York, 1996, pp. 1111-1113.
5. Wolff KJ, Johnson RA, eds. Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology, Sixth Edition. McGraw-Hill, 2009, p. 30.
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7. Sadovsky R. Poison ivy, oak and sumac contact dermatitis. Am Fam Physician. 2000;61(11):3408.
8. American Academy of Allergy AaIACoA, Asthma and Immunology. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol. 2006;97(3 suppl 2):S1-S38.
9. Usatine RR, Riojas M. Diagnosis and management of contact dermatitis. Am Fam Physician. 2010;82(3):249-255.