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Title: Toxicodendron Dermatitis: Identification, Immunologic Mechanisms, Diagnosis, and Treatment Author:
Thomas W. McGovern, MD
Accreditation Information
Introduction
Figure 2: Types of Basic Skin Lesions
EPIDEMIOLOGY According to Dr. Alexander Fisher, perhaps the grandfather of contact dermatitis as a subspecialty of dermatology, the Toxicodendron group of plants probably causes more cases of ACD than all other causes combined.4 Ten to 50 million Americans develop contact dermatitis to a Toxicodendron each year.5 Up to 73% of individuals react to undiluted Toxicodendron oleoresin during patch testing,6 while 50-65% react to brushing up against plants in nature.1, 2, 7, 8 Therefore, if there is only one type of plant a physician or other health care provider should recognize in nature and know how to describe to patients, poison ivy (and its close relatives) is the one. Workers in certain occupations are at highest risk for developing ACD to urushiol. Forestry workers, particularly in the Pacific Northwest where western poison oak is abundant, frequently contact poison oak while performing their regular tasks.9 Throughout the United States, Toxicodendron dermatitis accounts for more than 10% of all USDA Forestry Service lost-time injuries.10 This problem is most severe in California, Oregon, and Washington for poison oak and in Illinois, Kentucky, West Virginia, and Mississippi for poison ivy.10 In California, 1% of the Worker's Compensation state budget goes for poison oak reactions. Even more importantly, as many as 1/3 of forestry workers and firefighters are completely disabled by poison oak exposure when they are working to control forest fires in California, leading to severe personnel shortages.10, 11 In one study, 10% of all occupational illnesses and injuries among seasonal farm workers in New York and Pennsylvania were due to poison ivy contact.12 Construction and utility maintenance workers, park rangers, groundskeepers, and lawn care workers are also at high risk for contact with Toxicodendrons.13, 14 Outdoor enthusiasts including hikers, campers, spelunkers, and mountain climbers, frequently contact Toxicodendrons and are at a higher risk for developing ACD.14 Routes of Exposure Individuals may be exposed to the allergenic urushiol via direct plant contact, including the dried stems and roots, smoke from burning brush, resin on animal fur, and contaminated clothing.8 Effect of Race, Age, Heredity, and Atopic status In a review, Williford and Sheretz state that the historical notion that blacks are less sensitive to urushiol than whites has not been borne out by published investigations.8 Yet, 50 years ago, Kligman found that in California 53% of whites, 32% of blacks, 28% of Puerto Ricans, and 42% of Hawaiians were sensitive to poison ivy leaves.1 In Philadelphia, he found 54% (223/416) of whites and 42% (383/921) of blacks positive to leaf pressed on the forearm of adults. However, another study in California found no difference between the sensitivity of whites (62%) and non-whites (57%) to urushiol.6 In 1958, Kligman presented information supporting a decrease in responsiveness of individuals by age patch-tested with poison oak leaves.1
Another study comparing a group of 18-25 year-olds with 65-84 year-olds showed delayed onset, diminished peak and prolonged duration in the older group.15 The peak frequency of reactions to urushiol is in the 8-14 year-old age range, and this may reflect both increased sensitivity and increased exposure.7 Maximal sensitivity to urushiol appears to occur between 5-30 years of age, individuals over age 60 years definitely demonstrate a reduced response to urushiol compared to younger individuals.1, 16 Sensitivity does seem to run in families, so that if both parents are sensitive, chances are 80% that their children will be sensitive.17 Atopic individuals are less sensitive than non-atopic subjects. Only 15% of atopic individuals compared to 61% of non-atopic subjects were sensitive to urushiol in one study (p<0.01).6 When trying to sensitize adults who were negative on an initial patch test to urushiol, only 1/16 (6.3%) atopic subjects but 8/26 (31%) of non-atopic subjects became sensitized. The authors concluded that adult American atopic dermatitis patients are less susceptible both to natural and experimental sensitization with Toxicodendron antigens.6 Interestingly, a European study demonstrated no difference in ability to primarily sensitize atopic vs. non-atopic patients (43% vs. 45%).18 However, Toxicodendrons do not grow in Europe, and the difference in responses in different countries may be due to atopic dermatitis patients in USA developing a form of tolerance through environmental exposure to urushiol.6 TOXICODENDRONS The naming of poison ivy and its relatives has gone through many changes over the years as a greater understanding of these plants has developed. Currently, poison ivy and its close relatives are almost universally accepted as members of the genus Toxicodendron. Toxicodendron, a name predating Linnaeus himself, the father of binomial nomenclature, means 'poison tree.' This genus includes two species each of poison ivy and poison oak, one species of poison sumac, and the Japanese lacquer tree. Common poison ivy was traditionally included in the genus Rhus as Rhus radicans or even Rhus toxicodendron.19 Research in the 1950's and 1960's showed that poison ivy and its immediate cohorts represented a distinct developmental lineage and should be grouped not within Rhus but as a distinct genus.11, 20 The correct generic name for the poison ivies and their relatives was Toxicodendron, and thus we now call common poison ivy Toxicodendron radicans. The family Anacardiaceae (the cashew family) includes the genus Toxicodendron (and other genera with cross-reactive allergenic plants). Rhus is the largest genus in the family Anacardiaceae and was once thought to be a cohesive, widespread genus of many species including the current members of the genus Toxicodendron. However, Toxicodendrons produces smooth, white fruits that arise in small clusters in the axils of the upper leaves, while in Rhus the fruits are hairy and reddish-brown, and they arise in large clusters at the ends of branches. Moreover, Toxicodendrons contains allergenic dihydroxybenzene compounds, while Rhus does not.20 Important members of the Anacardiaceae and allergenically-related families are listed below.
(Allergenically but not botonically related)
Identification of Toxicodendrons One of the best articles in the dermatology literature teaching the identification of these notorious plants was published in 1986 by Guin and Beaman, and stresses that to become truly proficient, one must identify and observe several plants in a location where they can be observed throughout the year.21 
Figure 3: Identification of Poison Ivy, Oak, and SumacThese renditions of various Toxicodendrons demonstrate some of the variability in leaflet morphology, the odd-pinnate nature of the leaves (trifoliate in poison ivy and oak, and 7-13 leaflets in poison sumac), and the axillary position of the fruiting structures where the leaf stem (petiole) meets the branch. On poison ivy (T. radicans only), the aerial rootlets are demonstrated that allow the vine to cling to objects. Toxicodendron leaves have three (ternate) or more leaflets. (See Figure 4) (The old saying about Poison Ivy "Leaves of three; leave them be" refers to each leaf having three leaflets.) Flowers and fruit (which do not grow until a plant is at least three years old) arise in an axillary position, that is, in the angle between the leaf and the twig from which the leaf is borne. (See Figure 5) All Toxicodendrons grow as male and female plants. While flowers fall off the male plants, the flowers on female plants are pollinated and bear fruit. The leaf stalk is enlarged at its origin from the supporting twig and has a groove on its distal surface. (See Figure 5). Therefore, even in the winter, when the leaf has fallen off, a 'U' or 'V'-shaped scar remains. (See Figure 6) In contrast, the flower and fruiting structures of true Rhus arise at the end of the branch (not in an axillary position). (See Figure 7) 
Figure 4: Toxicodendron radicans demonstrating trifoliate leaves with three leaflets each. Brown aerial rootlets can also be seen emanating from the branches. These are clinging to the bark of the tree.
Figure 5: T. radicans demonstrating axillary fruit (green and immature). Note the "U" or "V" shaped end of the leaf stalk (petiole) attaching to the branch.
Figure 6: V-shaped scars where poison ivy leaves have fallen off.
Figure 7: Non-allergenic Rhus glabra (common sumac). Note the terminal, red fruiting structure (inset).The fruit of Toxicodendrons are green while growing (See Figure 5) and off-white when mature (See Figure 8). When the outer exocarp peels away, a chalk-white mesocarp can be seen. Longitudinal black lines from the toxic oleoresin in the mesocarp often embellish the surface. Toxic Anacardiaceae sap is self-melanizing; sites of prior plant injury demonstrate areas resembling black enamel paint. (See Figure 9) Few other plants, such as apples, bananas, and catalpa, can self-melanize; however, not to the extent of toxic Toxicodendrons (personal communication, Jere Guin, April 23, 2004). This phenomenon results from the enzymatic oxidation of sap constituents and is an additional helpful aid to the identification of toxic Anacardiaceae, as sap from poison oak, poison ivy, and poison sumac turns dark brown within 10 minutes of exposure to the air and black in 24 hours. 
Figure 8: White fruit on poison ivy in the winter.
Figure 9: Urushiol on leaf, oxidized to black. Urushiol self-melanizes on exposure to oxygen.As noted in the list of Anacardiaceae above, there are two species each of poison ivy and poison oak and one species of poison sumac listed that are common to the United States. Some of these have multiple subspecies. Poison oak and poison ivy are weeds that grow along roads, trails, or streams; they possess three leaflets (sometimes five) per leaf (compound leaves). Poison sumac contains 7-13 leaflets per leaf. Young leaves are frequently red in color, and the mature fruit (drupes) are tan or cream colored and have no hairs (the young drupes will have hairs; 'pubescence' that will fall off). Classically, poison ivy leaves have pointed tips and are ovate (widest point below the center). Poison oak leaves usually have rounded ends. Western poison oak has oval leaves, while Eastern poison oak has variable leaf appearances that can mimic white oak leaves. (See Figure 3) The "winter" shape of poison ivy on fence posts resembles 'Medusa heads' that are said to be identifiable while driving down the highway! (See Figure 10) In snow, T. rydbergii grows so low to the ground, that the upward, tine-like branches may be the only clue to its identification. 
Figure 10: Medusa head of T. radicans negundo on a fence post of an Indiana farm.Poison Ivy Poison Ivy and Poison oak probably originated in North America, which explains why the United States sees the greatest frequency of reactions to these plants.12 The distribution of the various Toxicodendrons may be found in Figures 11 and 12. 
Figure 11: Distribution of common poison ivy (T. radicans) subspecies in the United States.
Figure 12: Distribution of non-poison ivy Toxicodendrons in the United States.T. radicans (Eastern of common poison ivy) grows as either a shrub (See Figure 13) or climbing vine. Very noticeable, hair-like, adventitious (in an unusual place, here, in the air) roots anchor the plant to various structures so that they may grow over 100 feet high on trees (See Figure 14). These distinctive roots also gave rise to the species name (radicans is from the Latin 'radix' = 'root'). The plants propagate predominantly via underground rhizomes. The leaves are trifoliate (three leaflets per leaf, rarely 5-7), pinnately compound (leaflets on each side of a common rachis or leaf stem), and arranged opposite each other on the stems. Leaves are glabrous (possess no hair or 'pubescence'). The polymorphic leaflet margins can be smooth or serrated. The deciduous leaves turn yellow and deep red in the fall, often before most other leaves change color. The leaf stalk is wide at the base and forms a 'U' or 'V' shape where it connects to the stem. Even after the leaves fall off, this 'U' or 'V'-shaped scar on the stem will help one recognize plants in the winter. 
Figure 13: Early shrub version of T. radicans.
Figure 14: T. radicans ssp radicans growing at least 20 feet up an Alanthus tree. All the leaves on the lower half of the tree are poison ivy. Note the rear end of a trunk in the lower left hand corner for comparison.The subspecies T. radicans ssp. radicans grows along the Eastern seaboard, climbs trees and other tall objects, and possesses aerial rootlets. (See Figure 15) T. radicans ssp. negundo grows in the Midwestern United States. Its leaves resemble those of the box elder (Acer negundo, Family Aceraceae, the maple family). Four other subspecies of T. radicans inhabit much smaller geographic areas of the United States. It prefers to live in heavy, moist, fertile soil that does not drain excessively. 
T. rydbergii (Northern and Western poison ivy) grows as a small shrub without aerial rootlets and does not climb trees. It is found in most of the continental U.S. except California and the Southeast. The leaf, fruit, and sap characteristics are the same as for T. radicans except that leaflets may have pubescence (hairs) on their undersurface. Black spots may be seen on any part of the plant. Branches sometimes grow upright, like tines of a fork, but often these short plants have thick, drooping leaves. (See Figure 16) Plants only 8-10 inches tall may produce fruit. In the Pacific Northwest, it hybridizes with western poison oak. T. rydbergii, like T. radicans will grow in a variety of soils but prefers moist, fertile soil that is well-drained.
Figure 16: Western poison ivy (T. rydbergii ) growing just west of Denver in the foothills of the Rocky mountains. Contrary to what many sources say, poison ivy can grow above an altitude of 4000 feet. The lowest elevation in the park is 7600 feet. If you look closely, you can see black dots of self-melanizing sap on the leaflets.Poison Oak Western or Pacific poison oak (T. diversilobum) grows along the entire Pacific coast and in Nevada. It grows as a shrub or climbing vine with adventitious roots in a wide variety of soils and locations, especially in canyons, where it can find abundant water. The pinnate leaves are generally trifoliate, but they have five or more leaflets more often than poison ivy. Again, polymorphic leaflet margins vary from smooth to undulate, crenate, or dentate. (See Figure 17) Some of the leaflets resemble leaves of California live oak (Quercus agrifolia, Fagaceae). It has the largest drupes (7.5 mm) of all the domestic toxicodendrons; these may hang like ripe cherries. It develops aerial rootlets and climbs, but it mostly grows as a shrub. In fact, it is the most abundant shrub in California! 
Figure 17: Western poison oak (T. diversilobum).Eastern or Atlantic poison oak (T. pubescens, a.k.a. T. toxicarium) like T. rydbergii, is a small subshrub that never climbs trees, does not produce aerial rootlets, and can produce fruit when only 12 inches tall (See Figure 18). It prefers sandy soil of ridge and valley areas amidst oak and pine trees of the Southeastern United States north to Illinois and west to Texas where there are oak and pine trees growing nearby. The leaflets often resemble those of white oak (Quercus alba, Fagaceae), and can even fool an experienced botanist, but Eastern poison oak's leaflets can also be smooth. Major features separating this from poison ivy include rounded lobes on leaves, absence of aerial rootlets (v. T. radicans), and preference for nutritionally poor soil. 
Figure 18: Eastern poison oak (T. toxicarium).Poison Sumac T. vernix (poison sumac) grows as a large shrub or small tree up to three meters tall in isolated areas. It favors the standing water of boggy areas, swamps, and peat bogs, especially in the southeast, but also in the northeast and some Midwestern areas.5 It has also been found on dry land. Construction workers at Disney World in Orlando, FL were plagued by it.11 It does not form colonies and dies in the presence of minimal disturbance (it is not a weed and does not grow where human activity is common). Large, unlobed compound leaves of 7-13 leaflets per stem, usually in odd numbers, angle up from the stem like rabbit ears. Each leaflet is oval, smooth-edged, and about 10 cm long. (See Figure 19) Because of its isolation, few people are affected by it. Poison sumac has white flowers and white fruit that grow from an axillary position (between the compound leaf and branch). 
Figure 19: Poison sumac (T. vernix). Note flowers growing from an axillary position.Other Allergenic Anacardiaceae Japanese Lacquer Tree (Toxicodendron verniciflua) While Toxicodendron dermatitis is most common in North America, the greatest number of species of Toxicodendrons is found in Asia. Only six species are found in the Western Hemisphere, while 15 are found in China and another seven distinct species in the Malay archipelago.22 Perhaps the Japanese lacquer tree is the best known of these species among Westerners. The 15-20 meter tall Japanese lacquer tree (Toxicodendron verniciflua) is cultivated in SW Japan19 and provides a thick, self-melanizing, viscous bark sap or oleoresin used (See Figure 20) throughout Japan, China, and Korea for varnishing furniture, floors, canes, wooden toilet seats, and ornaments. Lacquering a single piece of wood may require several years and 300-400 coats! Like poison sumac, it has leaves composed of 7-13 oblong or oval leaflets.22 Lacquer is obtained by tapping the bark of lacquer trees by making an incision in the bark. 
Figure 20: Branch from the Japanese lacquer tree (T. verniciflua).T. verniciflua has been recognized as a cause of dermatitis since at least 453 BC.23 Because polymerized urushiol remains in the lacquer, it has been known to maintain its allergenicity for over a thousand years! Patients allergic to poison ivy usually react to Japanese lacquer tree allergens. American soldiers in Japan came in contact with toilet seats and bars beautifully finished with Japanese lacquer!1 The Cashew Tree (Anacardium occidentale) The cashew nut tree (Anacardium occidentale) is a northeast Brazil native that was introduced into the West Indies centuries ago 24 and was taken to Asia by the Portuguese where it has also naturalized.22 It now grows worldwide in the tropics, especially in Brazil and India.25 The nut grows 2.5-4.0 cm long at the apex of a 5-10 cm fruit known as the cashew apple (See Figure 21)26, and it contains an oily, brown juice between the two layers of its shell. The concentration of phenols in the nutshell and bark is so high, that contact with them causes an immediate vesicant reaction. Africans used this in ritual scarification and keloid formation while others used the nutshell oil for wart removal. In fact, dermatitis can be caused by contact with any part of the tree, except the roasted nut.24 
Figure 21: Cashew apples and cashew nuts.The cashew nut shell (pericarp) is three-layered. The outer, leathery exocarp and thin, hard, inner endocarp envelop a honeycombed mesocarp filled with an oily fluid. The cashew nutshell liquid (CNSL) is used to produce friction dust in brake linings and clutch facings, to make epoxy resins, paints, varnishes, and foundry core oil, and to control mosquito larvae and schistosomiasis vectors.27 This juice contains two active allergens: cardol (the primary allergen) and anacardic acid (primarily an irritant).25, 26 The nuts are processed by heating them in a bath. The heating accomplishes three functions: 1) the shell is more easily removed, 2) the time removing the shells is decreased for workers, and 3) the risk of contact dermatitis among workers is reduced.25 The epicarp bursts, the CNSL is released (simultaneously decarboxylating the anacardic acids into less allergenic cardanols), and the nuts are centrifuged in sawdust to remove residual phenols. The endocarp is then removed to yield an edible and hypoallergenic nut.24 Mango Tree (Mangifera indica) The mango tree (Mangifera indica) is the most popular fruit tree in tropical and subtropical America and grows throughout the Caribbean (See Figure 22).24 Some 35 species of mango grow in Southeast Asia.22 Unlike the cashew nut tree, it does grow in the continental United States in southern portions of Florida, Texas, and California. The leaves, bark, stems, and skin of the mango contain several different resorcinols, but no catechols (which are found in Toxicodendrons).28 Two resorcinols have been described in the skin of the fruit (See Figure 23), and one in the latex of the tree.28 Peeling the fruit before eating it prevents allergic contact dermatitis that occurs most commonly on the hands, around the mouth, and on the lips when eating unpeeled fruit.24 Hawaiian natives rarely react to mango. Likewise, Latin Americans who frequently mush up the fruit, make a hole through the rind, and suck out the fruit, rarely, if ever, report dermatitis. In fact, no cases of mango dermatitis were detected in and around Caracas, Venezuela (an area with numerous cultivated mango trees) during a plant dermatitis survey lasting 20 years.29 It is thought that early, oral exposure to mango results in immunologic tolerance.2, 24 
Figure 22: The mango tree (Mangifera indica). Photo courtesy of Richard Gentry, MD.
Figure 23: Mango fruit with sap. Photo courtesy of Richard Gentry, MD.Non-Anacardiaceae with Urushiol-like Resin Ginkgo Tree (Ginkgo biloba, Family Ginkgoaceae) Ginkgolic acid in the seed of the Ginkgo tree (Ginkgo biloba L.), the only living member of the family Ginkgoaceae, cross-reacts with allergens in poison ivy and poison oak. Fossils of this genus have been dated to be 200 million years old.19, 30 The popularity of this tree, also known as the maidenhair tree, has spread into many urban and suburban areas having become popular in Massachusetts, Michigan, Washington, DC, Canada (along the St. Lawrence River), and France (in Paris and Strasbourg) (See Figure 24).31 These beautiful trees grow to be 40 meters tall and are resistant to high levels of air pollution.30, 31 The male trees are much preferred to the female trees. Only female trees make seeds, and in the fall, the seed pulp disintegrates causing a rancid-butter-like odor.19, 30 Therefore, only the non-fruiting male trees are generally grown in cultivation. The tree produces a plum-like fruit with a raisin-like surface. The ivory-colored, seed kernel resembles a dried almond (See Figure 25). This white seed kernel is regarded as a delicacy in the Orient and is sold in markets.30 
Figure 24: Branch of Ginkgo tree. Note the accordion-like nodes on the branches and bilobed leaves.
Figure 25: Leaves of Gingko biloba with the seed kernel and a dime for comparison.Allergic and irritant reactions mainly occur to the seed pulp, but positive patch-test reactions have also occurred to both leaves and seed kernel (known colloquially as the ginkgo nut).30, 31 Its irritant ability has been known since ancient times.30 The unique leaf morphology, resembling a fan, makes ginkgo trees easy to recognize.19, 30 (See Figure 24 Poison Ivy Impostors32 There are several North American plants that may resemble poison ivy. These plants are listed in Figure 26.
Figure 26. North American plants that may superficially resemble poison ivy. PATHOGENESIS OF TOXICODENDRON DERMATITIS Urushiol, Allergen and Irritant A Few Definitions The 'sap' contained in resin canals of Toxicodendrons and related species is an oleoresin, a compound of an essential oil and resin, present in certain plants. This thick, grayish fluid turns black in air and dries to form a lustrous translucent varnish. A resin is any one of a class of yellowish brown solid inflammable substances, of vegetable origin, which are nonconductors of electricity and are soluble in ether, alcohol, and essential oils, but not in water. Urushiol refers to the component of the oleoresin that contains the allergenic and irritant chemicals that also form a lacquer when painted onto wood. Urushiol derives its name from the Japanese word 'urushi' referring to lacquer.33 Urushiol purportedly serves as a defense system against herbivorous insects and vertebrates.27 Distribution of Urushiol All portions of Toxicodendrons and allergenic Anacardiaceae containing resin canals contain urushiol.34 These canals are located in the roots, stems, leave roots, bark, petiole, leaf blade, stem cortex, pith pedicels, calyx, corolla, exocarp and mesocarp of the drupe (fruit).1, 2, 7 The leaves are the most common parts of the plant contacted that lead to dermatitis.35 It is even carried in the tiny aerial rootlets of T. radicans that attach the vine to the tree, pole, wall, or other structure on which it is climbing.35 Resin canals, however, are not present in stamens, pollen grains, anthers, pollen, xylem, and epidermis,1, 27 nor connect to the surface of the plant. Therefore, the leaf (or other plant part) must be bruised to produce dermatitis. Composition of Urushiol The composition of urushiol in common poison ivy (T. radicans) and the Japanese lacquer tree are similar. Both contain at least 70% of di-olefin and tri-olefin, which are apparently the most allergenic forms of allergenic catechols. Dihydroxybenzenes The majority of sensitizing chemicals in the Toxicodendrons are dihydroxybenzenes. There are three naturally occurring types: catechols (1,2 dihydroxybenzenes), resorcinols (1,3 dihydroxybenzenes), and hydroquinones (1,4, dihydroxybenzenes). While catechols and resorcinols have been found in Anacardiaceae, hydroquinones have not.36 All long-chain alkyldihydroxybenzenes appear to be sensitizers.36 Catechol is a poor sensitizer, and the aliphatic side chains are non-sensitizing, yet the combination of the two is both irritant and sensitizing!28 Alkylresorcinols have not only been isolated from members of the Anacardiaceae, but also from other plant families: Araceae (philodendron), Cystoseiraceae, Ginkgoaceae, Poaceae, Proteaceae, and Sargassaceae.28 In general, Toxicodendrons contain catechols and allergenic non->Toxicodendron Anacardiaceae contain resorcinols or anacardic acids (similar to a catechol, except the position two hydroxyl group is substituted by a carboxyl group). Effect of Side Chain Double Bonds Unsaturated side chains (pentadecylcatechol [PDC], pentadecylresorcinol [PDR]) are less sensitizing than saturated chains. Pentadecylcatechol only causes 37% of urushiol-sensitive individuals to react, yet this has often been used to test for allergy to poison ivy.a href="#37">37 In natural urushiol, PDC is often undetectable, and has not been found in concentrations >20%.38 Allergenicity and skin reactivity increases with degree of unsaturation (increasing double bonds increase reaction), however, two-double bonds seems to be the strongest irritant and allergen.37 Poison ivy and poison oak urushiols are mainly composed of diolefins.38 Stability of Urushiol in Nature Urushiol has the propensity to oxidize, polymerize, and form a black lacquer. Glass slides blackened with sap and kept dry in a dessicator caused allergic reactions six months later. In a moist chamber, urushiol completely lost its allergenic capability within a week. Extracts containing as little as 5% water deteriorated rapidly.1 When contaminated fomites are dry, the antigenic principles contained in the sap may last indefinitely, but after 3-5 days under warm, moist conditions, antigens rapidly deteriorate.1 Even though urushiol has very limited water solubility, application to skin results in very rapid distribution throughout the body, and it could be found in every organ and tissue examined.39 Excision of a urushiol application site 60 minutes following application resulted in a reduction in percent of guinea pigs sensitized, but it did not completely eliminate sensitization.39 This explains why relatively early washing of the skin following exposure frequently fails to prevent sensitization or induction of a reaction. Urushiol antigenicity remains up to three days on someone's skin, if the urushiol was not washed off. In one study, Kligman rubbed poison ivy leaves on the back of non-allergic individuals. Each day, he touched his thumb to these spots and then touched the forearm of a highly-sensitive individual. For the first three days, those sensitive individuals developed dermatitis.1 Even dead plant material contains the oleoresin.1 Therefore, midwinter outbreaks are entirely possible.2 Allergenic Characteristics To test for sensitivity in an individual, extracts should not be used. For example alcoholic extracts are less active than ether extracts, and these are less sensitive than plant oleoresin.(1) Kligman did not find changes in allergenicity of leaves at different times of the year based on clinical response of sensitized individuals.(1) Even after dry leaves fall to the ground, they maintain sensitizing abilities, but probably at a much reduced ability than when they were alive.(1) Urushiol dried on objects such as tools or shoes can cause reactions years later.(15) Lacquer maintains allergenicity, but not irritancy. Cross-reactivity of Catechols and Resorcinols Few studies have compared cross-reactivity between catechols and resorcinols. No cross-reactivity has been found between resorcinol (from philodendrons, family Araceae) and catechols (from poison ivy). The bottom line on cross-reactivity: Toxicodendron-sensitive patients will not necessarily develop an allergic contact dermatitis (ACD) from contact with resorcinol-containing plants (including mangoes which contain no catechols).28 IMMUNOPATHOGENESIS The alkylcatechols in Toxicodendrons are small (<500 Dalton),40 lipid soluble molecules with an affinity for protein, and as such, they serve as haptens (incomplete antigens) that can bind to carrier proteins. This hapten-protein complex forms a complete antigen capable of initiating a delayed type hypersensitivity (DTH) reaction. The DTH (a.k.a., Type IV hypersensitivity) reaction can be broken down into three phases: an afferent phase (when the antigen is presented to and recognized by a T-cell), an efferent phase (stimulation of the clinical response, in this case, dermatitis), and a resolution phase. Afferent Phase The first step of the afferent phase requires the antigen to traverse the stratum corneum barrier and enter the viable epidermis.41 The lipophilic nature of alk[en]ylcatechols allows them to accomplish this. The antigen must next be processed in the skin by an antigen-presenting cell (APC); the Langerhans cell (LC). There are two main pathways by which haptens can become complete antigens. The first route is known as the exogenous pathway. In this pathway, antigens found external to cells, such as bacteria, bacterial toxins, fungal antigens, vaccines, and allergens such as dust mites and pollens are endocytosed by LCs. These antigens are broken down to smaller particles by a variety of enzymes and attached to major histocompatibility complex (MHC) class II molecules, which are then transported to the cell surface for presentation to T-cells. MHC class II molecules are found only on the surface of antigen presenting cells, such as LCs.41, 42 The second route of antigen processing is known as the endogenous pathway. Antigens found inside the cell, such as transplantation antigens, viral antigens, and tumor-associated antigens, are processed into small peptides and complexed to MHC class I molecules. These complexes may be expressed on the surface of all nucleated cells.42 Urushiol antigens are found external to cells and can be processed through the exogenous pathway. However, because of their lipid solubility, they are able to enter epidermal cells and also processed through the endogenous pathway. In fact, the endogenous pathway is the more common pathway taken by urushiol antigens.42, 43 In a person who is not yet sensitive (allergic) to urushiol, LCs bearing antigen travel to a regional lymph node where they present themselves to na&#iuml;ve T-cells. Some individuals will have na&#iuml;ve T-cells (TH0 cells) to recognize the antigen, and thus, they will not develop a DTH reaction. However, most individuals (in the case of urushiol) will have a TH0 cell that recognizes the complete antigen (portion of hapten complexed to MHC I or II molecule). Through interaction of the LC and the TH0 cell (which may be either a CD4+ or CD8+ cell), the TH0 cell matures to become a memory/effector cell that then releases cytokines. If the effector cell is CD4+, it is called a TH1 cell, and if it is CD8+, it is called a TC1 cell. Both cells release similar cytokines that will stimulate DTH in the skin. In the case of urushiol antigens, the main effector cell is the CD8+ T-cell, although CD4+ T-cells can also serve this role.42, 43 This dominant role of CD8+ cells, unlike with most other causes of allergic contact dermatitis, explains why HIV-positive patients with very low CD4+ cell counts still have brisk reactions to urushiol.44 In the lymph node, these antigen-specific cells proliferate. For simplicity, only CD8+ cells will be discussed below, although CD4+ cells can follow the same steps. This same antigen presentation by LCs to T-cells also occurs in the skin of someone already allergic to urushiol antigens. In such a person, memory CD8+ cells that recognize a component of urushiol will proliferate before T-cells can be recruited from the draining lymph node. Efferent Phase Typically, 48-96 hours after antigenic challenge, the antigen-specific CD8+ cells reach the epidermis.43 These cells again encounter antigen-presenting LCs in the skin, and this interaction stimulates the antigen-specific CD8+ cells to release cytokines that attract other TC1 cells and TH1 cells. In fact, in the skin of an active Toxicodendron dermatitis, less than 1 T-cell per 1000 is an antigen-specific T-cell that recognizes urushiol antigen. Most of the T-cells in the infiltrate are non-antigen-specific CD4+ cells that are assisting the antigen-specific T-cells by releasing cytokines that cause the clinical dermatitis.43 Resolution Phase In allergic contact dermatitis, keratinocytes, macrophages, and T-cells release cytokines that turn off the immune response. The very cells that cause the pathologic response also, downregulate this response that negatively feeds back on the dermatitis-causing processes.41 As noted above, this clinical process occurs over the course of approximately three weeks. CLINICAL CHARACTERISTICS OF TOXICODENDRON DERMATITIS Diagnosis In an area where Toxicodendrons grow, Toxicodendron dermatitis should be suspected in anyone with acute, severe, allergic contact dermatitis. And in the summer, any contact dermatitis of unknown cause is Toxicodendron dermatitis until proven otherwise.35 History When evaluating a patient suspected of having a Toxicodendron-induced dermatitis, one should take a history, but only after examining the patient. Dermatologists often follow the motto "look first, ask questions later" when diagnosing most skin disease. While the history may or may not help determine the diagnosis of poison ivy dermatitis, you may be able to help the patient determine how they contacted the offending plant. The patient should be asked about recent travel and activities, hobbies, pets, and occupation. Has the patient been working in the yard, garden, or farm? Were they working with topsoil or potting soil or handling firewood? Did they borrow and wear others' clothing?35 Ask where the eruption first appeared and whether it was related to sun exposure (possible phytophotodermatitis). Does the patient know if he has been exposed or is sensitive to poison ivy/oak/sumac? What other skin diseases (especially atopic dermatitis) does the patient have? And what is the temporal relationship of potential exposure to the onset of the eruption?45, 46 Poison ivy dermatitis can be acquired at any time of the year, so you cannot exclude the diagnosis based on the month of presentation. Physical Examination The reaction to poison ivy is an acute dermatitis (eczema) followed by a subacute dermatitis. Clinically, dermatitis presents with pruritic, erythematous lesions with or without distinct margins. Such lesions pass through acute (vesicular), subacute (scaling and crusting), and chronic (acanthotic with thick epidermis) phases. Primary lesions include macules, papules, vesicles, edematous patches (that may appear urticarial without being urticaria), or plaques (See Figure 2). Secondary lesions with oozing, crusting, scaling, fissuring, and lichenification frequently follow. The primary histologic event is spongiosis (intercellular epidermal edema) with lymphocytic and/or eosinophilic infiltrates in the epidermis and dermis.47 Allergic contact dermatitis and irritant contact dermatitis are two potential causes. Others include seborrheic dermatitis and atopic dermatitis. Toxicodendron dermatitis usually starts with pruritus followed by erythema (See Figure 27).2 Linear arrays of juicy, red papules and vesicles generally follow.4, 8 This may be accompanied by edema and weeping, oozing lesions.48 (See Figures 28, 29, and 30) Edematous urticaria-like plaques (See Figure 31) and bullae may develop (See Figure 32). Edema on the face, neck, extremities, and genitalia can be extreme (See Figure 33).8 Lesions localize to areas that the hands can easily reach while sparing hard-to-reach areas, such as the mid-back.35 Broad areas of erythema and dermatitis are generally due to rubbing.35 After a week or so, a subacute stage with dry scale, dry papules, excoriations, crusts, and fissures may ensue.48 Finally, if lesions are scratched enough, lichenification and post-inflammatory hyperpigmentation may remain after antigenic stimulation has passed.48 
Figure 27: Curvilinear erythematous, edematous streaks of poison ivy dermatitis where patient was struck by a branch.
Figure 28: Example of an acute, weeping allergic contact dermatitis. This patient had a reaction to a topical medication that she was applying.
Figure 29: Acute reaction to poison ivy from hand transfer of allergen to face. Note significant periorbital edema.
Figure 30: Example of acute vesicular dermatitis on an erythematous base due to poison ivy.
Figure 31: Acute allergic contact dermatitis with edematous plaques due to mangoes.
Figure 32: Acute poison ivy dermatitis with vesicles and bullae.
Figure 33: Significant penile edema from poison ivy dermatitis.The distribution of lesions varies based on the method and site of contact with urushiol. Most commonly, the arms, legs, and face are involved.46 In men, the genitalia become secondarily involved from hand contact while urinating.49 Meanwhile, the palms usually remain uninvolved because of the great thickness of the stratum corneum. However, if there are fissures or breaks in the skin, or if the amount of allergen exposure is high, dermatitis can then occur on the palms.35 The clinical pattern of the eruption gives no clues as to whether poison ivy, poison oak, or some other plant caused the eruption.1 Mild cases of dermatitis may lack vesicles and only cause erythema and pruritus.46 Moderate cases may demonstrate erythematous, sometime edematous, pruritic papules and plaques with small vesicles.3 Severe cases may exhibit diffuse erythema and edema, severe, disabling pruritus and/or pain, and large bullae.3 The extent of the dermatitis depends on three factors 1) the degree of sensitization of the individual, 2) the site of exposure (sun-exposed or not, thickness of the epidermis), and 3) quantity of antigen deposited.8 The duration of the eruption is the most variable aspect of poison ivy dermatitis.1 One study of 40 subjects (ages 26-57) determined the timing of symptom onset after placing urushiol extract (1:100 in ethanol) on a Finn chamber and allowing it to dry for 5-10 minutes. The Finn chamber was then applied to the forearm of known allergic individuals for four hours.50 The reaction onset ranged from 4 hours to 4 days with a mean of 1 day. The peak reaction ranged from day 1 to 14 with a mean of 7 days. However, 35% of individuals didn't have their peak reaction until after day 8. By day 21, 60% of reactions had completely resolved. Of the 16 patients with an eruption remaining on day 21, only two demonstrated more than macular erythema. More severe reactions took longer to resolve.50 After initial exposure to urushiol, a clinical reaction is uncommon, but if lesions occur, they typically appear 9-14 days after allergen contact.2 In a previously sensitized individual, though, 12-72 hours is all that it takes for erythema, inflammation, pruritus and vesicles to form.8, 14 If allergen exposure occurs on sun-exposed skin, however, a delayed response may occur because of ultraviolet radiation-induced suppression of epidermal Langerhans cells.8 Clinical experience corroborates the above patch-test study in that lesions usually last 14-20 days if untreated.14 New lesions may appear up to 14 days after exposure.8 Scarring only occurs if scratching leads to fissuring into the dermis. As long as the basement membrane separating the epidermis from the dermis is not breached, scarring does not occur. While post-inflammatory hyperpigmentation may occur and be confused with 'scarring', true scarring refers to a permanent change in the elevation or texture of the skin, and not a temporary color change. Various Presentations Following Toxicodendron Exposure Patients may present with hand print (See Figure 34) or finger-mark (See Figure 35) patterns due to transfer of urushiol from the palms. Finger-mark patterns are broad streaks spread by finger tips, and a hand-print pattern may look like mittens.35 
Figure 34: Note the pattern of transfer in these photos in a young woman with poison ivy dermatitis. Wiping with hands led to this "mitten" pattern on the neck (right hand dominant person with left side neck lesions).
Figure 35: Acute dermatitis lesions in a "finger-mark" pattern after hand transfer of urushiol.Black spot poison ivy dermatitis refers to the dramatic appearance that some patients develop when high concentrations of urushiol are deposited on the skin and polymerize to form black, lacquer-like spots (See Figure 36). These areas do not wash off of the skin and must slough off on their own.51 Patients present with black spots atop edematous plaques and bullae. Stains of polymerized urushiol do not come out of clothes despite repeated washings. In fact, washing or boiling of stained clothing does not make it "harmless"; it can cause dermatitis indefinitely.52 Because urushiol is a primary irritant and allergen, the histologic picture reveals an acute, primary irritant contact dermatitis superimposed upon an acute allergic contact dermatitis.51 Sometimes post-inflammatory hyperpigmentation follows, especially in dark-skinned persons.51 
Figure 36: Black spot reaction 30 minutes after urushiol contact.A variant of both vesicular and black spot dermatitis known as weed-whacker dermatitis occurs when individuals trim weeds and scatter poison ivy debris on their skin in a 'buckshot' pattern (See Figure 37). This does not fit the typical appearance of linear vesicles or a few focal areas of black, lacquer-like reactions.52 
Figure 37: Examples of "weed-whacker" dermatitis.Systemic Reactions Cutaneous contact with Toxicodendrons can lead to various types of systemic reactions. Weeks after a severe dermatitis, particularly if it is recurrent, signs of kidney damage may emerge. Renal tubular damage and nephritic syndrome have been reported, but this is probably not caused by the urushiol, but by glomerulonephritis from secondarily infected dermatitis.1 Autoeczematization reactions have been reported, and these reactions appear with dozens or hundreds of symmetrical 2-4 mm juicy, red papules on the trunk and extremities.1 Urinary retention can occur due to edema of the prepuce.4 Eruptions resembling measles, scarlatina, and erythema multiforme are likely due to systemic absorption of antigen.4 Poison ivy dermatitis has led to the development of targeted palmoplantar lesions of erythema multiforme (EM).53 As in other cases of allergic contact dermatitis associated EM, the lesions appear during the resolution of the dermatitis. This reaction is thought to be due to circulating antigen-antibody complexes and/or activated CD8+ T-cells, so that a combination of Type III and Type IV hypersensitivity reactions may cause the EM.53 Post-inflammatory pigmentation changes may occur, particularly in dark skin. While leukoderma occasionally develops, hyperpigmentation is much more common and rarely occurs in fair-skinned individuals.4 The hyperpigmentation may last a few weeks after resolution of the dermatitis,1, 12 whereas the hyperpigmentation from phytophotodermatitis lasts months to years.54 Primary Toxicodendron dermatitis lesions may develop oozing, vesiculopustular lesions with frank pus due to secondary bacterial infections. In one study of 33 patients with infected lesions, 18 patients (55%) had aerobic bacteria, 7 (21%) had anaerobic, and the other 8 (24%) had both aerobes and anaerobes in their wounds.55 Staphylococcus aureus was the most common organism, found in 13 (39%) patients. Polymicrobial colonization/infection was found in 15 (45%) patients, and 48% of isolates produced beta-lactamase.55 Systemic exposure to urushiol can cause cutaneous and potentially serious internal health concerns. Systemic symptoms include gastrointestinal upset, fever, chills, and headache.33 Hypotension, shock, and syncope have also been reported following ingestion of urushiol.33 Differential Diagnosis Other Plant-induced Allergic Contact Dermatitis The differential diagnosis of an acute eczematous eruption with any combination of erythema, pruritus, juicy red papules, vesicles, bullae, and edematous plaques includes anything that can cause an acute dermatitis. Non-Toxicodendron members of the Anacardiaceae and other plant allergens, particularly of the family Asteraceae (formerly Compositae), the sunflower family, should be considered based on exposure history.56 Non-plant Induced Allergic Contact Dermatitis Non-plant allergens may cause similar dermatitis, however, they do not usually present with the hand-print pattern or streaky vesicles of poison ivy dermatitis. The top 10 non-plant contact allergens in the United States are nickel (14%), neomycin (13%), balsam of Peru and fragrance (12%), thimerosal (11%), gold (10%), formaldehyde, quaternium-15 (a formaldehyde releaser), cobalt, and bacitracin (9%).57 Irritant Contact Dermatitis Irritant contact dermatitis describes a non-allergic inflammatory reaction of the skin. These can be due to alkalis, acids, metal salts, fiberglass, dusts, hydrocarbons, and solvents. In the winter, excessive soap, water, and scrubbing are common causes of irritant dermatitis. Irritant dermatitis typically present with features of chronic dermatitis and not acute dermatitis. Nummular Eczema Nummular eczema presents with discrete, coin-shaped, erythematous, plaques of aggregated juicy papules and vesicles and crusted patches measuring 5-40 mm in diameter. The legs, thighs, back, and extensor surfaces of the hands and arms are the most commonly involved areas. The disease has been associated with low humidity, and it sometimes worsens during periods of moderate to severe emotional stress. Men in their 50's and 60's are most frequently affected. Clinically, the lesions appear as subacute dermatitis, not acute dermatitis with vesicles and edema. Phytophotodermatitis Phytophotodermatitis is a phototoxic reaction consisting of erythema (with or without blistering) followed by delayed hyperpigmentation that can last for months or years. Anyone can develop a phototoxic reaction if they get enough ultraviolet radiation (UVR), as in the case of sunburn. Phototoxic reactions may occur with less UVR if a photosensitizing agent has been applied or ingested.45, 58 It is therefore not an immunologic reaction, and no prior sensitizing exposure is necessary for any potential victim. Phototoxic reactions can occur from UVR exposure only 15 minutes after contact with topical furocoumarins (found in a variety of plants).59 Striate or bizarre configurations of erythema, edema, and bullae appear after a latent period of roughly 12-24 hours (See Figure 38).4 The inflammatory reaction peaks at 72 hours. These painful, non-pruritic reactions are more often seen in middle to late summer when psoralen concentrations are highest in the offending plants and more skin is exposed to direct sunlight. Wet skin, sweating, and heat enhance the phototoxic response.54 Hyperpigmentation follows one to two weeks after UVR exposure and lasts months to years.4, 5154 (See Figure 39). 
Figure 38: Acute linear edema and vesicles in phytophotodermatitis.
Figure 39: Residual hyperpigmentation that is the hallmark of phytophotodermatitis. This case is due to lime juice.Patients can be exposed to furocoumarins in many settings. Plants of the Apiaceae (parsley, formerly Umbelliferae) and Rutaceae (citrus) families are the most common instigators. Celery and limes are the two most commonly reported sensitizers. Patients may present with 'weed-whacker' dermatitis, streaks of blisters or hyperpigmentation from lime juice running down a part of the body, or pendant-like streaks of pigmentation on the neck, face, arms, or trunk from colognes containing oil of the bergamot orange. Key differentiating features from Toxicodendron dermatitis include the presence of lesions only on sun-exposed areas, lack of pruritus, and prolonged, intense hyperpigmentation seen in all patients with phytophotodermatitis. Arthropod Reactions Scabies is an intensely pruritic infestation caused by Sarcoptes scabiei, also known as the "itch mite". Patients develop tiny burrows, 2-5 mm juicy red papules, and excoriations, particularly affecting the finger webs, wrists, flexures, axillae, lower abdomen, genitalia, buttocks, and ankles. The mite is typically contracted by close personal contact or by the common use of contaminated towels, bedding, or clothing. Linear papules or vesicles, large patches of erythema, and edematous skin, as seen in Toxicodendron dermatitis, are not typically seen in scabies. The bedbug (Cimex lectularius) may cause a linear group of pruritic, erythematous papules or nodules during their nocturnal escapades. Lesions develop because of a hypersensitivity reaction to a protein in the bug's saliva. Reactions may be either urticarial (IgE-mediated hypersensitivity) or papular (DTH). Vesicles and widespread reactions are uncommonly seen. Figure 40. Demystifying Poison Ivy. POISON IVY MYTHS
PREVENTION Plant Recognition and Avoidance Poison ivy dermatitis is better prevented than treated, and plant recognition is key.34 Patients need to learn to recognize their local Toxicodendrons in all seasons of the year, and they should pick a known plant and observe it regularly for changes.12, 34 If a patient has contaminated objects such as pet hair, garden tools, and even clothing, they should be washed with water or soap and water to prevent antigen transfer.34 Garments that have been exposed and have not developed black spots may be washed and safely worn again.34 Systemic Hyposensitization Basis for Hyposensitization The idea of desensitizing, or at least, hyposensitizing individuals to Toxicodendrons was stimulated by rumors that American Indians used to chew poison ivy leaves to achieve hyposensitivity to poison ivy. Infrequent allergy to mango, cashew nutshell liquid, and the Brazilian pepper tree in Central and South America suggests that early exposure to these allergenic resorcinol-containing-plants may lead to tolerance to urushiol. From pre-Columbian times, Chileans have fed their infants fruits and tender leaves of litre, a toxic tree (Lithraea caustica) of the family Anacardiaceae.29 The active principles of toxicodendrons are catechols and those of other Anacardiaceae are resorcinols and phenols. Ample skin exposure to catechols prepares North Americans to be sensitive to resorcinols, but Latin Americans are made tolerant to less-allergenic resorcinols through early, oral exposure.29 Three criteria have to be met to prove that someone has been desensitized to an allergen.60 First, the subject has had ACD due to a specific chemical that caused a strongly positive patch test reaction. Second, the ACD produced by the chemical clears and remains clear in spite of exposure to the chemical that caused the positive reaction. And third, previous strong patch test reaction to the chemical becomes negative or weakly positive. Japanese lacquer craftsmen who use urushiol from the Japanese lacquer tree have been investigated. In a survey of 232 lacquer craftsmen, 189 had developed dermatitis from the lacquer (81%). Fully 83% (158/189) of these reactions resolved with continued lacquer exposure! To fulfill the criteria listed above, a sequential patch test study of students learning the art of applying lacquer was performed on 8 apprentices. Before training, only 1/8 of apprentices reacted to the lacquer. During training, two apprentices never became allergic, but the other five developed positive patch test reactions that became negative (3/5) or milder (2/5) over a 9-10 month period of working with lacquer.60 Results of Hyposensitization Attempts Throughout the 20th century, numerous oral and injectable methods have been attempted.34 Patients, however, often said that "the treatment was worse than the disease."7, 61 In 1986, all intramuscular hyposensitization methods were banned by the Food and Drug Administration (FDA).61 The FDA forced all remaining hyposensitization products off the market in 1993.14 It appears that hyposensitization after becoming sensitized to the potent allergens in poison ivy and poison oak is difficult if not impossible. Topical Prevention Clothing Protective clothing is the primary method of preventing dermatitis if contact with Toxicodendrons is unavoidable.34 Remember that vinyl (polyvinyl chloride) gloves are protective, but rubber gloves allow penetration of the antigen.13 Barrier Creams Because so many workers (soldiers, loggers, farmers, fire fighters, construction workers, and utility maintenance workers) are at risk for contact with poison ivy, many attempts have been made to develop effective barrier creams, leading to the testing of over 150 different preparations.13 In 1995, Marks and co-workers published encouraging results with an organoclay barrier compound, 5% quaternium-18 bentonite lotion (IvyBlock, Enviroderm Pharmaceuticals). IvyBlock is the only barrier cream FDA-approved for the prevention of Toxicodendron dermatitis. TREATMENT Immediate Post-exposure Soap and Water Based on the positive results seen in studies performed by both Kligman and Fisher, immediately after suspecting contact with a Toxicodendron, individuals should wash with water (and soap, if available).1, 13, 26 Studies show that the sooner the exposed areas are washed, the lesser the reactions. The potentially contaminated hand that can spread antigen must be washed first.34 While urushiol is not water soluble, it probably physically forces the urushiol off the skin. Additionally, high concentrations of water seem to inactivate urushiol.1 Strong soap and scrubbing merely irritate the skin and are not more effective than mild soap and gentle washing.13 While various authors have warned against using soap with water,3, 8 the concern of spreading urushiol over greater surface areas seems to be theoretical only. The fingernails need to be thoroughly washed, also, as urushiol can remain under them for long periods and remain allergenic.52 Decontamination New outbreaks of Toxicodendron dermatitis from contaminated articles must be prevented. As mentioned, clothes will be rendered harmless (as long as they have no black lacquer deposits) after one cycle of washing with an ordinary detergent.1 Various fomites, such as shoes, tools, sports equipment, should be at least rinsed with copious amounts of water.2 Pets suspected of harboring urushiol should be bathed.3 Topical Treatment of Dermatitis The goal of topical therapy is to decrease pruritus, redness, and heat.2 Kligman stated that effective treatment of the pruritus (the main reason patients come in for treatment) requires successful treatment of the dermatitis that causes it.1 The old dermatology dictum, "If it's dry, wet it; if it's wet, dry it" holds for Toxicodendron dermatitis. In the acute stages, the eruption is moist and weepy. Wet-to-dry dressings ameliorate pruritus, erythema, and even vesicles.848 Aluminum subacetate (Burow's solution, Domeboro™) comes as a 5% solution that must be diluted to 1:40 concentration, or it comes as a powder or tablets that can be dissolved in water. Patients should apply cotton-soaked wet dressings 3-4 times daily for 15-30 minutes each application to dry out the weeping, bullous lesions. Aseptic drainage of bullae reduces itching.3 Patients can first bathe in warm water with colloidal oatmeal or cornstarch for their soothing, antipruritic properties. To prevent ground oatmeal from caking in pipes, place it in a tied sock before dropping it in the bathtub.3 Application of bland shake lotions such as calamine (not Caladryl™, a topical antihistamine), can also dry moist skin lesions. A recently-introduced, OTC product has been demonstrated to reduce both itching and objective signs of dermatitis. Zanfel™ is a soap mixture of ethoxylate and sodium lauroyl sarcosinate surfactants. It has been demonstrated that this soap forms a complex that surrounds alk[en]ylcatechols and removes them from the skin.(Zanfel laboratories, Data on file). A randomized, double-blinded, bilateral-controlled study of 24 urushiol-sensitive adults demonstrated that an objective score combining erythema, induration, and vesiculation was reduced (p<0.05) at times 48, 96, and 144 hours post-exposure to urushiol in patients who washed with the soap or placebo.62 In another study, urushiol was placed on the arms of 16 Toxicodendron-sensitive adults (Zanfel Laboratories, Data on file). The patients returned at day 4 for evaluation of pruritus (using the 10-centimeter visual analog scale) and for evaluation of objective signs of dermatitis (5-point scale). Before application of the soap on day 4, the average itch score was 6.7/10 and the dermatitis score was 2.5/5 (moderate-to-marked erythema, mild edema, initial vesicle formation). Immediately after washing for 2-3 minutes with the soap, the average itch score had dropped to 4.3/10 (p<0.001) and dermatitis score was statistically unchanged at 2.3/5. Two hours later, the itch score had dropped to 2.0/10 (p<0.001) and the dermatitis score had dropped to 1.7/5 (mild to moderate erythema with no or minimal edema) (p=0.001). While late application of even super potent (Class I) topical steroids does little to help poison ivy dermatitis, early application, particularly under occlusion, can alter the natural course of disease and significantly reduce pruritus, which is what really bothers the patient in the first place.35 To be effective, they need to be applied before the presentation of vesicles and bullae.7 They must be continued for 2-3 weeks, or the dermatitis will rebound.8 Using ointments (no water in the base, and therefore, no preservatives either) reduces the likelihood of sensitization to another allergen.34 The new topical calcineurin inhibitor pimecrolimus (Elidel™) was tested in a double-blind, placebo-controlled study in 12 subjects exposed to 'poison ivy tincture'. While quite effective in atopic dermatitis, it was shown to be ineffective for allergic contact dermatitis due to urushiol.63 For subacute, scaly red dermatitic lesions, high-potency (Class II-IV) corticosteroid creams will be useful, and for chronic lichenified dermatitis, ointments or flurandrenolide tape will help the active ingredient to penetrate the lesion.48 Topical Agents to Avoid A number of other topical products have been recommended for use in Toxicodendron dermatitis. Jewelweed (Impatiens biflora) has been used for centuries to treat poison ivy and oak ACD. Numerous claims for its effectiveness have appeared in the lay press, and it is used as an ingredient in over-the-counter (OTC) medications. Ten volunteers were exposed to urushiol on two sites. One site was treated with jewelweed extract from fresh stems, and the other site was exposed to distilled water. Patients were examined on days 2, 3 7, and 9. All subjects developed an allergic reaction, and there was no difference in objective dermatitis scores between jewelweed-treated and control sites.64 The use of topical antihistamines, topical anesthetics with benzocaine (an ester anesthetic), and antibiotics with neomycin or bacitracin should be avoided because of their potential to stimulate their own allergic contact dermatitis when absorbed through large breaks in the epidermal barrier.2, 8 Topical amide anesthetics should be safe, as they have a low potential to sensitize. Topical antihistamines do not work to reduce dermatitic itching,3 although topical doxepin may make patients sleepy. OTC hydrocortisone 1% is far too weak to have any helpful effect, regardless of the frequency of application.1, 8 Systemic Treatment of Dermatitis Systemic Agents to Use Systemic steroids are the standard treatment for severe Toxicodendron dermatitis. The typical dose of oral prednisone is 0.5-2.0 mg/kg/day (usually 1.0 mg/kg/day) tapered over a 14-21 day period.2, 6, 8, 34 Based on the results of one study,50 three-weeks is a reasonable duration, although this aspect of treatment is debated. If steroids are stopped earlier than 14 days after onset of dermatitis, the eruption will "break through".3 Alternatively, intramuscular triamcinolone acetonide, 1.0 mg/kg, naturally tapers over 3-4 weeks and, in the author's experience, compliance is 100%,35 and there are less acute side effects such as emotional lability, water retention, hyperactivity, and increased appetite. Rare side effects of corticosteroid use include exacerbation of gastric ulcers, diabetes, hypertension, and rarely, avascular necrosis of the hip.49 Corticosteroids decrease inflammation by reversing increased capillary permeability and by suppressing neutrophil activity. Corticosteroids reduce itching by inhibiting a delayed type hypersensitivity response. When should systemic corticosteroids be used? Typically, patients with widespread dermatitis (>25% body surface area), limited, but disabling involvement (hands, face, periocular, perioral, or genital lesions), or if a patient has a history of severe reactions in the past.2, 49 Reasons to avoid systemic steroids may include hypersensitivity, viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, fungal or tubercular skin infection, and diabetes.3 One option for patients with diabetes or peptic ulcer disease is cyclosporine. While its used for Toxicodendron dermatitis has not been reported in peer-reviewed medical publications, its use has been reported by individual dermatologists (http://dermatology.cdlib.org/rxderm-archives/cyclosporin-for-contact-derm). Adult dosing of cyclosporine is suggested at 200 mg twice daily for 10 days and 100 mg twice daily for 10 more days resulting in clear skin within 2-4 days. Cyclosporine is much more expensive than prednisone. Systemic Treatments to Avoid Oral ibuprofen (400 mg orally three times daily) did not affect patch test reactivity or pruritus to urushiol extract.65 There is little evidence that sedating or nonsedating antihistamines are effective in the treatment of AD. In studies by Kligman,1 diphenhydramine (Benadryl™) 100 mg daily, tripelennamine (Pyribenzamine™) 200 mg daily, and chlorpheniramine (Chlor-Trimeton™) 16 mg daily had no effect on Toxicodendron dermatitis. For sedating antihistamines, it can be difficult to distinguish antipruritic or other clinical effects from the sedative or soporific effect.8 Reported improvements in disease severity and quality of life may be due primarily to promotion of restful sleep rather than a reduction in symptoms. Anti-histamines have been more widely used in another form of dermatitis, atopic dermatitis. Atopic dermatitis is also considered a delayed type hypersensitivity reaction.44 Even with atopic dermatitis, there is a paucity of proper clinical trials and no evidence to support the efficacy of non-sedating antihistamines.66 While systemic steroids are extremely effective when indicated, it is common for patients to seek further treatment for Toxicodendron dermatitis after receiving a dosepak of methylprednisolone. This 6-day treatment regimen contains the equivalent of 30-25-20-15-10-5 mg of prednisone on each of the six days. This is a lower and shorter dose than will effectively treat Toxicodendron reactions.8, 49 The dermatitis 'recurs' because it requires at least 3 weeks to run its course,50 and stopping the steroids merely allows the natural disease to "come out of hiding." Bibliography 1Kligman AM. Poison ivy (Rhus) dermatitis. Arch Dermatol. 1958;77:149-180. 2Resnick SD. Poison-ivy and poison-oak dermatitis. Clin Dermatol. 1986;4:208-212. 3Stephanides SL, Moore C. 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