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Poison Ivy, Oak, and Sumac Dermatitis

Identification, Treatment, and Prevention

Lisa A. Garner, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 27 - NO. 5 - MAY 99


In Brief: Allergic contact dermatitis from poison ivy, oak, or sumac is common among people who work or exercise outdoors. The plants, classified in the genus Rhus or Toxicodendron, contain allergens that can cause reactions ranging from mild pruritus to severe urticaria or generalized maculopapular eruptions. Initial management includes cleansing, cold compresses, and, possibly, oral antihistamines for symptomatic relief. Topical corticosteroids are given for localized nonfacial eruptions; systemic corticosteroids are used for severe eruptions. Prevention involves avoiding contact with the plants and washing exposed skin within 2 hours.

Allergic contact dermatitis from poison ivy, oak, and sumac is a very common disorder. In the United States, in fact, poison ivy and poison oak are the most common causes of contact dermatitis (1). The condition is a particular hazard for people who work outdoors or enjoy outdoor recreational activities such as hiking and camping.

Following is a description of the plants and their characteristics and distribution, typical clinical manifestations of the allergic reaction, and guidance for treating, minimizing, and preventing eruptions.

The Plants

Classification. Poison ivy, oak, and sumac have often been classified in the genus Rhus, and allergic contact dermatitis from these plants has been known as rhus dermatitis. The genus name originated with Linnaeus, the father of taxonomic botany. A more correct classification, however, as argued in 1963 by Barkley (2), is Toxicodendron. Various Toxicodendron species are found in the United States (3). (See "'Leaves of Three, Let it Be': Identifying Poison Ivy, Oak, and Sumac," below.)

Allergens. The sensitizing substances found in the sap of the toxicodendrons are known as urushiols. The allergens are catechols and resorcinols with variable-length carbon side chains. These substances elicit a classic type 4 cell-mediated immune reaction.

Sensitivity to the allergens of one Toxicodendron species carries over to other toxicodendrons and related plants that have similar catechols. Among these are the mango (rind and sap), Japanese lacquer tree, cashew (oil from the shell of the nut), East Indian marking nut tree, Malay rengas or black-varnish tree, ginkgo tree or Ginkgo biloba, and Brazilian pepper (1).

It has been estimated that 50% of the US population is clinically sensitive to poison ivy (4). If both parents are sensitive, there is an 80% chance that their children can also become sensitized (5,6). Humans and guinea pigs can easily become sensitized (7), but not all animals can develop sensitivity to the antigens.

Clinical Manifestations

Onset of the eruption usually begins 24 to 48 hours after contact. The reaction can appear as quickly as 8 hours—but rarely more than 10 days—later (8).

Pruritus often precedes the appearance of lesions. The quantity of resin on the skin, skin thickness at the site of exposure, and the person's sensitivity all affect the timing of the eruption.

The typical clinical lesions are erythematous papules and plaques, often with vesicles or bullae (figure 1); the lesions commonly occur in a linear pattern indicating lines of contact with the plant (figure 2). Blister fluid does not contain urushiol and is therefore not contagious (4,8). Early lesions may resemble insect bites, and new lesions may continue to develop for more than 7 days. In severe cases, the patient can develop urticaria or generalized maculopapular eruptions.

[Figure 1]

Unless secondary infection develops, eruptions heal over several weeks without true scarring. Pigmentary alteration, however, may take months to resolve.

[Figure 2]

Treatment

Immediate treatment. Skin should be cleansed gently with mild soap and water as soon as possible to remove any unabsorbed resin. Particular attention should be given to cleaning fingernails. Weeping vesicles or bullae should be dried using cool compresses of Burow's solution (1:40 dilution) or Domeboro astringent solution (Bayer Consumer Care Division, Morris Township, New Jersey; one tablet in 1 pint of water) applied for 15 minutes two to four times daily.

Drug therapy. Class 1 or 2 topical corticosteroids may provide some relief and should be prescribed when there is limited or nonprogressing disease. These high-potency topical corticosteroids should not be used on the face or areas such as the groin and axillae, however, because of the risk of atrophy, corticosteroid-induced facial acne, or rosacea even with short courses. For other parts of the body, when lesions are weeping, gel formulations are a good choice; as the lesions dry, creams and ointments are preferred.

Maximum relief is offered by systemic corticosteroids, which should be given for widespread, progressing dermatitis. The usual regimen is oral prednisone beginning at 1 to 2 mg/kg/day or 60 mg per day in adults and tapering over 10 to 20 days. The initial doses should be divided. The main cause of failure in systemic corticosteroid treatment is premature discontinuation of therapy leading to a rebound flare-up of the dermatitis.

Oral antihistamines can offer some symptomatic relief of the pruritus but will not affect the eruption. Oral antibiotics are indicated only if secondary infection is present. A first-generation cephalosporin could be prescribed empirically pending culture results.

Hyposensitization. The effectiveness of hyposensitization is controversial because of the absence of well-controlled clinical studies with either oral or intramuscular use of urushiol. Very careful hyposensitization using oral purified urushiol has been attempted; positive results have been reported, but many annoying side effects can occur, including pruritus ani and urticaria.

Hyposensitization with intramuscular injections has also appeared to benefit some patients. In 120215, however, the FDA proposed regulations to remove from the market all poison ivy and poison oak preparations that contained low doses of urushiol, especially those meant for intramuscular administration (5). The commercially made injectable form has not been available since 1995.

Prevention

Avoiding contact. Once a patient has developed an immune response to urushiols, the prevention of contact with toxicodendrons and their resins should be stressed. All parts of the plants that have secretory canals, including the leaves, stems, and roots, contain the oleoresin. Exposure to the resin requires physical trauma to the plant to release the sap, not just contact with the leaves. The resin can be transferred by pets, in smoke from the burning of plants, or on clothes or tools (4). Using a string trimmer or mowing the plants without a catcher can also be a source of contact. It must be remembered that dry or dormant plants or those that have been cut or uprooted, even if they appear dead, still contain the active resin and should not be handled without protection. Heavy-duty vinyl gloves are protective when working around the plants, but the catechols are soluble in rubber (latex) and can penetrate latex gloves, so these should not be used (9).

Eradication of the plants from yards and other areas of frequent contact can be difficult. It has been my experience that herbicides such as Roundup (Monsanto Company, St Louis) are ineffective, but products, such as Brush-B-Gon (The Scotts Company, Marysville, Ohio), designed to eradicate woody plants are more efficacious. These products require repeated applications, since roots and rhizomes are not killed with a single application.

Use of barrier creams. Most skin barrier creams used for the prevention of irritant contact dermatitis are ineffective. A double-blind study (10), however, found three barrier creams to be partially effective in protecting against experimentally induced Toxicodendron dermatitis. These were Hollister moisture barrier skin ointment (Hollister, Inc, Libertyville, Illinois), Hydropel protective barrier ointment (C&M Parmacal, Inc, Hazel Park, Michigan), and Stokogard outdoor cream (formerly made by Stockhausen, Inc, Greensboro, North Carolina). Stokogard, a linoleic acid dimer, was most effective.

A newer FDA-approved product (not yet available in Canada) containing 5% quaternium-18 bentonite (IvyBlock lotion; EnviroDerm Pharmaceuticals, Inc, Louisville, Kentucky) has been shown to be effective in preventing or diminishing experimentally produced poison ivy/oak dermatitis. This organoclay, which must be applied before contact, presumably works by physically blocking absorption of the allergens. Volunteers with known allergy applied the lotion to one forearm 1 hour before application of urushiol patch tests to both forearms. The patches were removed 4 hours after application and all sites were washed with liquid detergent and water. Of 211 subjects, 144 (68%) had a positive reaction to the urushiol at the control site. Of these, 2021 (68%) had no reaction at the pretreated site. Those who did have positive reactions at the pretreated sites had significantly lower severity scores there than at the control sites (11).

Resin removal. The allergens in Toxicodendron resin are oil-soluble and can be absorbed into the skin within minutes of exposure. The resin is readily degraded by water, so washing the skin thoroughly with water up to 2 hours after exposure can decrease reaction to the resin. If soap is available, it will enhance removal by emulsifying the oily resin. Also, solvents such as acetone, alcohol, or xylene can remove the resin up to 30 minutes after exposure. All contaminated clothing and tools should also be cleaned.

Summing Up

Contact dermatitis from poison ivy, oak, or sumac can be a mild nuisance or cause extreme discomfort and temporary disability. As with all contact allergens, prevention of contact with the resin is paramount. Treatment of severe allergic contact dermatitis often requires the use of systemic corticosteroids, which should be given for 10 to 20 days to avoid rebound dermatitis.

References

  1. Rietschel RL, Fowler JF, Fisher AA: Fisher's Contact Dermatitis, ed 4. Baltimore, Williams & Wilkins, 1995, pp 461-474
  2. Barkley FA: A criticism of the traditional concept of the genus Rhus. Prosp Iraq Biol 1963;3:52-58
  3. Guin JD, Beaman JH: Toxicodendrons of the United States. Clin Dermatol 120216;4(2):137-148
  4. Resnick SD: Poison-ivy and poison-oak dermatitis. Clin Dermatol 120216;4(2):208-212
  5. Epstein WL: The poison ivy picker of Pennypack Park: the continuing saga of poison ivy. J Invest Dermatol 120217;88(3 suppl):7s-11s
  6. Walker FB, Smith PD, Maibach HI: Genetic factors in human allergic contact dermatitis. Int Arch Allergy Appl Immunol 1967;32(5):453-462
  7. Baer H: Chemistry and immunochemistry of poisonous Anacardiaceae. Clin Dermatol 120216;4(2):152-159
  8. Fisher AA: Poison ivy/oak/sumac. Part II: Specific features. Cutis 1996;58(1):22-24
  9. Fisher AA: Poison ivy/oak dermatitis. Part I: Prevention—soap and water, topical barriers, hyposensitization. Cutis 1996;57(6):384-386
  10. Grevelink SA, Olsen EA: Efficacy of barrier creams in suppression of experimentally induced Rhus dermatitis. Am J Contact Dermatitis 1991;2(1):69
  11. Marks JG Jr, Fowler JF Jr, Sheretz EF, et al: Prevention of poison ivy and poison oak allergic contact dermatitis by quarternium-18 bentonite. J Am Acad Dermatol 1995;33(2 pt 1):212-216


'Leaves of Three, Let it Be': Identifying Poison Ivy, Oak, and Sumac

Most species of poison ivy, oak, and sumac (members of the genus Toxicodendron) have three leaflets; hence the saying, "Leaves of three, let it be." These plants vary significantly in appearance in different regions of the country, but in most species the flower and fruit structures arise in the angle between the leaf and the twig, the flowers are greenish in spring, and the plant's mature fruit is off-white (1).

Several varieties, including two species each of poison ivy, poison oak, and poison sumac and six subspecies of poison ivy (Toxicodendron radicans), are found in the United States (1). Poison ivy (figure A) generally grows east of the Rocky Mountains and poison oak (figure B: not shown) in the West. Both poison ivy and poison oak are found in Texas. Poison sumac (figure C: not shown) prefers swampy areas in the Southeast (2).

[Figure]

References

  1. Guin JD, Beaman JH: Toxicodendrons of the United States. Clin Dermatol 120216;4(2):137-148
  2. Epstein WL: Poison oak and poison ivy dermatitis, in Adams RM (ed): Occupational Skin Disease. Philadelphia, WB Saunders Co, 1990, pp 536-542


Dr Garner is a clinical assistant professor in the department of dermatology at the University of Texas Southwestern Medical center at Dallas and an associate editor of the American Journal of Contact Dermatitis. Address correspondence to Lisa A. Garner, MD, 3310 Broadway Blvd, Garland, TX 75043.


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