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Poison ivy (Toxicodendron) dermatitis

Poison ivy (Toxicodendron) dermatitis
Authors:
Lori Prok, MD
Thomas McGovern, MD
Section Editors:
Robert P Dellavalle, MD, PhD, MSPH
Daniel F Danzl, MD
Joseph Fowler, MD
Deputy Editor:
Rosamaria Corona, MD, DSc
Literature review current through: Sep 2022. | This topic last updated: Feb 11, 2022.

INTRODUCTION — Exposure to plants of the Anacardiaceae family accounts for more cases of allergic contact dermatitis than all other plant families combined. Anacardiaceae are ubiquitous in many environments throughout the world. In North America, the most common members of this family are those of the genus Toxicodendron, which includes poison ivy, poison oak, and poison sumac [1,2]. Toxicodendron dermatitis is caused by the highly allergenic oleoresin urushiol, a light, colorless oil present in the fruit, leaves, stem, and root of the plant.

This topic reviews the epidemiology, prevention, and treatment of allergic contact dermatitis due to Toxicodendron species. Throughout the text, we refer to Toxicodendron dermatitis by the common name "poison ivy dermatitis."

The evaluation and management of contact dermatitis from other causes is discussed separately. (See "Overview of dermatitis (eczematous dermatoses)", section on 'Contact dermatitis'.)

EPIDEMIOLOGY — Approximately 50 to 75 percent of the United States adult population is sensitized to poison ivy, oak, and sumac [1]. Annually, an estimated 10 to 50 million Americans require medical treatment for poison ivy dermatitis [2]. Firefighters, forestry workers, and farmers constitute a large proportion of the victims affected through occupational exposure [3,4].

Poison ivy dermatitis affects all ethnicities and skin types, and most geographical regions in the United States are at risk [5] (see 'Geographic distribution' below). Children are also affected; most children over the age of eight years are sensitized [3]. Allergic responsiveness to poison ivy appears to wane with age, especially in those with mild reactions and limited sensitizing exposures [6].

GEOGRAPHIC DISTRIBUTION — Toxicodendron species and other Anacardiaceae allergenic plants are ubiquitous in many environments throughout the world. In the United States (except Alaska and Hawaii), Canada, and northern Mexico, common Toxicodendron species include [1,2]:

Eastern or common poison ivy (Toxicodendron radicans)

Western or northern poison ivy (Toxicodendron rydbergii)

Eastern poison oak (Toxicodendron toxicarium)

Western poison oak (Toxicodendron diversilobum)

Poison sumac (Toxicodendron vernix)

Eastern poison ivy is more common east of the Rocky Mountains, often growing as climbing vines. Poison ivy in and west of the Rocky Mountains is found as a low-growing shrub. Poison oak is primarily found west of the Rocky Mountains, and poison sumac is found in boggy, uninhabited areas of the southeastern part of the United States. It is less common to find Toxicodendron species above 5000 feet of elevation or in arid, desert climates (figure 1A-C) [1].

Anacardiaceae members common in other parts of the world that can cause allergic contact dermatitis and contain chemicals cross-reacting with urushiol include [1]:

South African poison ivy (Smodingium argutum; South Africa)

Cashew nut tree (Anacardium occidentale; tropical Americas)

Japanese lacquer tree (Toxicodendron vernicifluum; Japan and China)

Indian marking nut tree (Semecarpus anacardium; Southeast Asia, Pacific Islands, Australia)

Mango tree (Mangifera indica; tropical countries)

Brazilian pepper tree or Florida holly (Schinus terebinthifolia; South America, Florida, Hawaii)

IDENTIFYING THE PLANT — Poison ivy and poison oak are often identified by three leaflets with flowering branches arising from axillary positions on a single stem (figure 2). While the common phrase "leaves of three, let them be" is a helpful reminder to avoid poison ivy and related plants, members of the Toxicodendron genus have varied presentations based on the season, growth cycle, region, and climate (picture 1A-C) [7].

Poison sumac more often forms leaflets of five, seven, or more that angle upward toward the top of the stem. One may also find characteristic black dots on Toxicodendron species; this black lacquer is oxidized urushiol (due to the enzyme laccase found in the oleoresin) and can be found on plant leaves within 10 minutes of its exposure to oxygen. Toxicodendron species also produce a green or off-white fruit in the autumn months [8]. Two species of Rhus possess trifoliate leaves; however, the fruiting structures are red and terminal, not off-white and axillary (figure 2).

PATHOGENESIS

Allergenic compounds — The plant oleoresin urushiol is the antigenic substance in poison ivy and related plants. It is a light, colorless oil present in the fruit, leaves, stem, and root of the plant. Urushiol is a mixture of 3-n-pentadecylcatechols, which contain a catechol ring moiety substituted with different aliphatic side chains at position 3 or 4 with zero, one, two, or three double bonds [1]. The diolefin (two double bonds) is the most allergenic.

Poison ivy dermatitis is a classic type IV hypersensitivity (cell-mediated) allergic reaction. Catechols are low molecular weight haptens that easily and quickly penetrate the epidermis, where they are oxidized to quinone intermediates that bind to surface proteins on antigen-presenting cells in the epidermis and dermis, such as Langerhans cells and dendritic cells. These antigen-presenting cells then travel to regional lymph nodes where effector T lymphocytes are activated, expand, and circulate throughout the body. (See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)

Because urushiol is a powerful antigen, a single exposure can be adequate to cause sensitization. Once clonally expanded T lymphocytes exist, re-exposure to poison ivy causes cytokine release and clinical symptoms in 12 to 48 hours.

Usually, damage is required for plants to release the oleoresin. Of note, when exposed to the air, the oil dries quickly and retains its allergenic potential in the dry state indefinitely. Contact with bruised, broken, or dead plant parts allows the toxic oil to contaminate the skin, fingernails, clothing, pets, tools, or other objects. Intact plant parts generally do not cause dermatitis. However, plants are easily damaged by rubbing, rain, or dry fall weather.

Of note, contact with the dried, black, antigenic resin on contaminated clothing, pet fur or claws, gardening tools, or in crevices under the fingernails may cause continued exposure to the allergen, prolonging or disseminating the eruption. (See 'Avoidance' below.)

Cross-reacting substances — The urushiol in poison ivy, poison oak, and poison sumac differs only slightly in structure; thus, they cross-react. Other members of Anacardiaceae and related families contain allergenic catechols or noncatechol phenols that cross-react with components of urushiol found in Toxicodendron species. Mango rind, cashew nutshell, Japanese lacquer tree, Indian marking nut tree (used for laundry marking in India), Brazilian pepper tree, and Ginkgo biloba tree can all cause dermatitis in individuals with a history of poison ivy dermatitis.

CLINICAL PRESENTATION — Poison ivy dermatitis typically presents as an acute, intensely pruritic eruption characterized by erythematous papules or plaques, vesicles, and bullae, often arranged in characteristic, linear or streak-like configurations where a portion of a plant has made contact with the skin (picture 2A-D). Involvement of the face and genitals may cause significant edema. Severe facial dermatitis can result from airborne exposure, such as when burning plants containing urushiol resin.

The so-called "black spot" poison ivy dermatitis occurs when urushiol is left on the skin and oxidizes, appearing as black spots that cannot be washed off (picture 3 and picture 4) [9]. The concentrated resin causes both an irritant dermatitis and an allergic dermatitis.

Symptoms of poison ivy dermatitis in sensitized individuals generally develop within 4 to 96 hours after exposure and peak between 1 and 14 days after exposure [2]. Lesions may present in different locations at different times after exposure, depending on the amount of urushiol present on the skin and the stratum corneum thickness of the involved areas. This can give the impression that the eruption is spreading from one region to another. Blister fluid is not antigenic, however.

Left untreated, the dermatitis usually resolves in one to three weeks.

Complications are uncommon and include postinflammatory hyperpigmentation and secondary bacterial infection. Postinflammatory hyperpigmentation is more common in darker skin types (picture 5) and, while it can persist for several months, usually resolves without treatment [5].

DIAGNOSIS — The diagnosis of poison ivy dermatitis is typically made based on a history of exposure and a characteristic clinical finding of erythematous papules or plaques, vesicles, and bullae, often arranged in characteristic, linear or streak-like configurations in areas of skin that could have come in contact with plant parts (picture 2A-D). Atypical presentations may occur when patients are exposed secondarily, such as when a pet gets urushiol on its fur and then brushes against the patient.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of poison ivy dermatitis includes:

A different plant-induced allergic contact dermatitis – Many plant families other than Toxicodendron can cause allergic contact dermatitis in sensitized individuals. Examples include Asteraceae or Compositae (Achillea millefolium, Chrysanthemum, Matricaria chamomilla, Taraxacum officinale), Alliaceae (Allium sativum [garlic], Allium cepa [onion]), and Myrtaceae (Melaleuca alternifolia [tea tree]).

Allergic contact dermatitis not from plants – Important allergens include nickel and topical antibacterials (picture 6A-B). (See "Common allergens in allergic contact dermatitis".)

Irritant contact dermatitis – Many substances, including plant toxins and chemicals, can induce a nonallergic, inflammatory skin reaction (picture 7). Examples of plant irritants include calcium oxalate (agave, daffodil, daisy, hyacinth), thiocyanates (radish, wasabi, horseradish), and diterpene esters (castor bean plant, croton, poinsettia) [10]. (See "Irritant contact dermatitis in adults" and "Contact dermatitis in children", section on 'Allergic contact dermatitis'.)

Nummular dermatitis – Nummular dermatitis typically presents with intensely pruritic, coin-shaped, eczematous plaques (picture 8A-B). Scale, crusting, or serous drainage may be evident. Patients can present with as few as 1 lesion or as many as 20 to 50 lesions. Lesions tend to be circular and usually measure between 2 and 10 cm in diameter. (See "Nummular eczema".)

Phytophotodermatitis – Phytophotodermatitis is a phototoxic reaction with erythema with or without blistering in response to ultraviolet exposure in patients exposed to photosensitizing plant compounds (picture 9A-B). Unlike poison ivy dermatitis, lesions will only be seen on sun-exposed skin. Lesions often resolve with significant hyperpigmentation. (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Phytophotodermatitis'.)

Reactions to insect and arthropod bites. (See "Insect and other arthropod bites".)

PREVENTION

Avoidance — Identification and avoidance of toxic plants and related allergens are key to prevent poison ivy dermatitis. Because urushiol retains its allergenic potential in the dry state indefinitely, dormant or dead plant parts should be handled with caution. Allergenicity can also persist for years after the plant dies. Burning poison ivy is not a safe way to dispose of the vegetation. Urushiol is stable at high temperatures, and the plant particles dispersed in the smoke are allergenic and irritant.

Protective clothing is useful, but patients should be reminded that clothing, pets, and fingernails can harbor the allergenic resin for many days. The oleoresin can seep through clothing and can penetrate rubber or latex gloves (but not heavy-duty vinyl gloves or leather gloves) [11].

Washing — After a known exposure, patients should remove any contaminated clothing and wash the whole body with mild soap or dish soap on a damp washcloth under very warm or hot running water as soon as possible. One study found that after approximately 10 minutes on the skin, 50 percent of the urushiol can be removed. This number falls to 10 percent after 30 minutes and 0 percent after 1 hour [8].

Despite this, washing even two hours after exposure significantly reduces the likelihood and severity of dermatitis [12,13]. Some clinicians suggest washing the entire body three times while always wiping in one direction, not back and forth; this seems to reduce irritation and help remove the oils [13]. If there is no rapid access to dishwashing liquid, plain water can be used to wipe the skin in the same fashion. This will at least remove some of the resin.

Comparison of dishwashing liquid with more expensive products made for removing poison ivy oils did not show a difference in effectiveness [12]. Clothing, tools, or other items that may be contaminated with the oleoresin should also be washed with warm, soapy water prior to reuse.

Barrier creams — The use of barrier creams to prevent contact dermatitis is controversial. Barrier creams are topical preparations that are applied prior to exposure to a contact allergen in attempt to prevent the development of dermatitis. (See "Management of allergic contact dermatitis", section on 'Skin protection'.)

Bentoquatam (5% quaternium-18 bentonite lotion), an organoclay compound that showed efficacy for the prevention of poison ivy dermatitis, is no longer available [14]. Other preparations that have been studied but are not proven to be effective include [15]:

Linoleic acid dimers. These do not prevent urushiol penetration of the skin and, thus, must be rinsed off and reapplied after four to eight hours.

Occlusive barrier ointments.

Other topical barrier creams may emerge as research continues for preparations effective in preventing dermatitis from chemical warfare agents [16,17].

Desensitization — Reports of Native Americans achieving hyposensitivity to poison ivy dermatitis by chewing the leaves, the lower prevalence of mango dermatitis in Native Hawaiians compared with immigrants, and decreased poison ivy sensitivity in cashew nut shell oil processing factory workers have all prompted research into oral hyposensitization [18-20]. However, in a small, randomized trial, oral ingestion of very small doses of a mixture of urushiol components (pentadecylcatechol and heptadecylcatechol) over five weeks was not more effective than placebo in reducing hypersensitivity to poison ivy and poison oak [19].

TREATMENT — Despite the high prevalence of allergic sensitization to Toxicodendron, very few well-designed studies of poison ivy dermatitis prevention and treatment have been performed [2]. Therefore, the approach to management is largely based on clinical experience.

In a survey involving 36 clinicians, poison ivy dermatitis was treated with oral or parenteral corticosteroids 80 percent of the time, less frequently in combination with high-potency topical corticosteroids or oral sedating antihistamines (25 and 30 percent of the time, respectively) [21].

A study demonstrated that treatment of poison ivy dermatitis in emergency departments costs more than in clinician offices [22]. It also revealed that the cost of treatment with superpotent topical steroids is more expensive than with oral or injected systemic medications.

Symptomatic therapy — Symptomatic treatment of poison ivy dermatitis may include:

General measures – Soothing measures, such as oatmeal baths and cool, wet compresses, may be helpful to alleviate skin discomfort. Topical treatment with compounds containing menthol and phenol (calamine lotion) may also provide symptomatic relief. Topical astringents such as aluminum acetate (Burow's solution) or aluminum sulfate calcium acetate used under occlusion may be useful to dry weeping lesions [23,24]. A wash containing a surfactant mixture of ethoxylate and sodium lauroyl sarcosinate has been reported as beneficial [25].

Topical agents with known allergenic potential, including topical anesthetics containing benzocaine, topical antihistamines, and topical antibiotics containing neomycin or bacitracin, should be avoided.

Oral antihistamines – Oral antihistamines are commonly used for the symptomatic treatment of pruritus associated with allergic contact dermatitis and atopic dermatitis, despite that the evidence to support their efficacy in these disorders is limited [26,27]. We do not routinely use antihistamines to treat poison ivy dermatitis, since pruritus in poison ivy dermatitis is not caused by histamine. However, first-generation, sedating H1 antihistamines given at bedtime may be beneficial for patients who experience exacerbations of pruritus at night. Sedating antihistamines may increase daytime sleepiness and should be used with caution, particularly in older adults. (See "Pruritus: Therapies for generalized pruritus", section on 'Role of antihistamines'.)

Limited mild dermatitis — We suggest super high-potency topical corticosteroids (table 1) for mild poison ivy dermatitis that involves a limited area of the body. Superpotent corticosteroids, such as clobetasol propionate 0.05% cream, are applied twice daily until improvement. Of note, topical corticosteroids are most helpful for early-stage poison ivy dermatitis. Once vesicles and blisters are established, they do little to alter the natural course of the disease [28].

The use of superpotent corticosteroids, even under occlusion, for up to one week on involved areas poses little threat for permanent atrophy. More prolonged use on thin skin, such as the face, genitals, or intertriginous areas, should be avoided due to the potential for these agents to cause skin atrophy and other adverse effects. (See "Topical corticosteroids: Use and adverse effects".)

Severe dermatitis — We suggest systemic glucocorticoids for adults and children with severe poison ivy dermatitis that is too extensive and severe for topical treatment alone, particularly if involving the face or genital region [29,30]. Oral prednisone is started at a dose of approximately 1 mg/kg/day (maximum initial dose 60 mg/day) and then tapered over two to three weeks. As an example, prednisone is given at a dose of 40 mg for five days, 20 mg for five days, 10 mg for five days, and then discontinued. In the authors' experience, 15-day courses only rarely result in rebound dermatitis and may be appropriate if there are concerns about steroid toxicity. (See "Major side effects of systemic glucocorticoids".)

Although oral administration of glucocorticoids offers flexibility in daily dosing, intramuscular injection of glucocorticoids is a treatment option for patients who cannot tolerate or comply with administration of oral glucocorticoids [31]. In our clinical experience, we have found intramuscular injection with a mixture of triamcinolone acetonide (1 mg/kg), a long-acting glucocorticoid, and betamethasone (0.1 mg/kg), a short- to intermediate-acting glucocorticoid, beneficial and associated with fewer side effects than oral prednisone. Wet to dry dressings, with or without a topical corticosteroid, may provide immediate relief for patients with weeping lesions, while waiting for the systemic corticosteroids to take effect.

Intralesional injection of triamcinolone acetonide (4 to 5 mg/mL) may occasionally be useful for treatment of severe disease confined to small areas.

There are no well-designed studies examining the proper dose and course of systemic corticosteroids for poison ivy dermatitis. However, extensive clinical experience suggests that rebound dermatitis commonly occurs if too short of a course is used (eg, the six-day course in a methylprednisolone dose pack) [32]. As in other forms of allergic contact dermatitis, circulating T lymphocytes directed toward urushiol are able to expand and activate cytokines for a significant time after exposure to antigen, leading to rebound dermatitis when corticosteroids are stopped too early.

Secondary bacterial infection — If secondary bacterial infection is suspected, appropriate systemic antibiotics (typically directed at gram-positive organisms) should be administered. Most patients with secondary impetigo will be infected with Staphylococcus aureus or group A Streptococcus. However, given increasing rates of community-acquired methicillin-resistant Staphylococcus aureus (MRSA), performing a skin culture is reasonable if pus is present. (See "Impetigo" and "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Prevention and control" and "Acute cellulitis and erysipelas in adults: Treatment".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Contact dermatitis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Contact dermatitis (The Basics)" and "Patient education: Poison ivy (The Basics)")

Beyond the Basics topics (see "Patient education: Contact dermatitis (including latex dermatitis) (Beyond the Basics)" and "Patient education: Poison ivy (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

EpidemiologyToxicodendron dermatitis is the most common cause of allergic contact dermatitis in North America, with an estimated 10 to 50 million Americans requiring medical treatment for poison ivy dermatitis. Occupational exposure is prominent for firefighters, forestry workers, and farmers.

Geographic distributionToxicodendron species and other allergenic plants of the Anacardiaceae family (eg, cashew nut tree, Japanese lacquer tree, Indian marking nut tree, mango tree) are ubiquitous in many environments throughout the world. They account for more cases of allergic contact dermatitis than all other plant families combined. (See 'Geographic distribution' above.)

Plant identification – In North America, the most common members of this family are those of the genus Toxicodendron, which includes poison ivy, poison oak, and poison sumac. While the common phrase "leaves of three, let them be" is a helpful reminder to avoid poison ivy and related plants, members of the Toxicodendron genus have varied presentations based on the season, growth cycle, region, and climate (figure 2 and picture 1A-C). (See 'Identifying the plant' above.)

Pathogenesis – Poison ivy dermatitis is a classic type IV hypersensitivity (cell-mediated) allergic reaction. The oleoresin urushiol is the allergenic substance in Toxicodendron. Exposure to urushiol can occur through contact with damaged or dead parts of the plant (eg, roots, sap, leaves, or stems) or via contact with objects that have been contaminated by the plant oleoresin. Of note, allergenicity can also persist for years after the plant dies. (See 'Pathogenesis' above.)

Clinical presentation – Intense pruritus and erythema are the most common presenting signs of poison ivy dermatitis. Patients then develop papules, vesicles, and/or bullae, often arranged in characteristic, linear or streak-like configurations where a portion of a plant has made contact with the skin (picture 2A-D). (See 'Clinical presentation' above.)

Diagnosis – The diagnosis of poison ivy dermatitis is typically made based on a history of exposure and a characteristic pattern of a well-demarcated contact dermatitis in areas of skin that could have come in contact with plant parts, particularly when linear streaks are present. Atypical presentations may occur when patients are exposed secondarily, such as when a pet gets urushiol on its fur and then brushes against the patient. (See 'Diagnosis' above.)

Prevention – Poison ivy dermatitis is best prevented by avoiding exposure through the use of protective clothing, such as heavy-duty vinyl gloves. Washing with a detergent soap (or with special preparations designed for poison ivy) as soon as possible after exposure can reduce the risk of dermatitis, but washing even two hours after exposure can be beneficial. (See 'Washing' above and 'Prevention' above.)

Treatment – Symptomatic treatment of poison ivy dermatitis includes soothing measures, such as oatmeal baths; cool, wet compresses; and topical astringents. Oral antihistamines are of limited efficacy for reducing pruritus associated with poison ivy dermatitis (see 'Symptomatic therapy' above):

Mild/limited dermatitis – For mild poison ivy dermatitis that involves a limited area of the body, we suggest super high-potency topical corticosteroids (table 1) (Grade 2C). Of note, topical corticosteroids are most helpful for early-stage poison ivy dermatitis. Once vesicles and blisters are established, they do little to alter the natural course of the disease. (See 'Limited mild dermatitis' above.)

Severe/extensive dermatitis – For severe or extensive dermatitis and dermatitis involving the face or genitals, we suggest systemic glucocorticoids (Grade 2C). Oral prednisone is started at a dose of approximately 1 mg/kg/day (maximum initial dose 60 mg/day) and then tapered over two to three weeks. Shorter courses of systemic corticosteroids (eg, a six-day methylprednisolone dose pack) can result in rebound dermatitis and should be avoided. (See 'Severe dermatitis' above.)

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