The first published records of poison ivy in North America date back to the early 1600s in the writings of Captain John Smith. In fact, Captain Smith included an illustration of the plant and originated the common name because of its superficial resemblance to English ivy (Hedera helix) or Boston ivy (Parthenocissus tricuspidata). The name ivy or "hiedra" was also used by early Mexican settlers in California who mistakenly thought poison oak was a kind of ivy. A little-known subspecies of poison ivy, T. radicans ssp. divaricatum, is native to southern Baja California and Sonora, Mexico. Our California poison oak was noted by another British explorer of the 19th century, Captain Frederick Beechey, who took samples back to England. Much to the chagrin of unwary gardeners, both poison oak and poison ivy were planted in English gardens for their graceful climbing habit and beautiful autumnal coloration.

North Americans and English gardeners are not the only ones exposed to Toxicodendron dermatitis. In his monograph of poison oak and poison ivy, Gillis (1971) lists four native species of Toxicodendron in North America, including seven subspecies of poison ivy. He also lists three species in Malaysia and China, including two subspecies of poison ivy, one in China and one in Japan.

Poison oak is a widespread deciduous shrub throughout mountains and valleys of California, generally below 5,000 feet elevation. In shady canyons and riparian habitats it commonly grows as a climbing vine with aerial (adventitious) roots that adhere to the trunks of oaks and sycamores. Poison oak also forms dense thickets in chaparral and coastal sage scrub, particularly in central and northern California. It regenerates readily after disturbances such as fire and the clearing of land. Rocky Mountain poison oak (Toxicodendron rydbergii) occurs in canyons throughout the western United States and Canada. Because the two species of western poison oak often exhibit a viny growth form, they are listed as subspecies of eastern poison ivy by some authors.

The pinnately trifoliate leaves typically have three leaflets (sometimes five), the terminal one on a slender rachis (also called a stalk or petiolule). Eastern poison ivy often has a longer rachis and the leaflet margins tend to be less lobed and serrated (less "oak-like"). In the similar-appearing squaw bush (Rhus trilobata) the terminal leaflet is sessile (without a stalk). Like many members of the Sumac Family (Anacardiaceae) new foliage and autumn leaves often turn brilliant shades of pink and red due to anthocyanin pigments. In the eastern states poison ivy is often mistaken for another common native called Virginia creeper (Parthenocissus quinquefolia). Virginia creeper has a similar growth habit and beautiful autumn foliage, but typically has five leaflets rather than three. It belongs to the Grape Family (Vitaceae) along with the common wild grape (Vitis girdiana).

During late spring loose clusters (panicles) of small greenish-white flowers are produced in the leaf axils of poison oak. Functional male and female flowers are typically produced on separate plants (dioecious) or, occasionally, unisexual and bisexual flowers may occur on the same plant (polygamous). Male flowers contain five stamens and a rudimentary pistil surrounded by five cream-colored petals and five sepals. Female flowers have a fertile pistil (gynoecium) and reduced, sterile stamens. During summer and fall, female plants produce small clusters of ivory-white fruits, each with a papery outer exocarp, a soft waxy mesocarp and a hard stony endocarp surrounding the seed. The fruits of related shrubs such as squaw bush, lemonadeberry (Rhus integrifolia) and sugar bush (Rhus ovata) are reddish with a sticky-pubescent exocarp. The old adage about poison oak and poison ivy is quite accurate: "Leaves of three, let it be; berries white, poisonous sight."

Freshly cut stems exude a sticky, terpene oleoresin that oxidizes and polymerizes into a shiny black lacquer resembling pruning sealer. The resinous sap is produced in resin canals of the stems, roots, leaves, and flowers. Cross sections of poison oak stems show distinct concentric annual rings (ring-porous wood). Numerous resin canals appear as tiny black dots and are confined to the phloem layer just inside the bark. [Caution: Cutting and sanding poison oak wood is extremely unwise and hazardous -- even if you think you are immune to its dermatitis. This is how one of the authors (WPA) was rudely initiated into the ranks of poison oak sufferers, after tramping through it for decades with impunity!] Dark resin canals (appearing as black striations)also occur in the waxy mesocarp of the fruits just beneath the papery skin. Abundant resin canals is one of the reasons poison oak is now placed in the genus Toxicodendron along with poison ivy, poison sumac (T. vernix) and the Japane se lacquer tree (T. vernicifluu -- the commercial source of natural lacquer). In fact, Pomo Indians of California used the natural lacquer of poison oak to dye their baskets. The resin canals also contain urushiol, the insidious allergen that gives poison oak its bad reputation. The name is derived from "kiurushi," Japanese for sap of the lacquer tree.

Urushiol is a general term applied to the toxic substance in the sap causing allergic contact dermatitis in people. It is actually a mixture of phenolic compounds called catechols, potent benzene ring compounds with a long side-chain of 15 or 17 carbon atoms (Figure 1). The side chain may be saturated or unsaturated with one, two, or three double bonds (Dawson, 1954, 1956). The remarkable immune reaction and specificity of the catechol molecule is determined by the long side-chain (Baer et al., 1967, 1968). Poison oak urushiol contains mostly catechols with 17 carbon side-chains (heptadecylcatechols), while poison ivy and poison sumac contain mostly 15 carbon side-chains (pentadeylcatechols). Urushiol is found in resin canals only -- it is on plant surfaces only if leaves and stems are bruised or attacked by chewing/ sucking insects. It does not occur in pollen or honey made from poison oak flowers. Although nonvolatile, it may be carried in ash and dust particles and as minute droplets in smoke from burning foliage.

Some people are so sensitive that it only takes a molecular trace of urushiol (two micrograms or less than one millionth of an ounce) on the skin to initiate an allergic reaction (Epstein et al., 1974). Even the amount on a pinhead is sufficient to cause rashes in 500 sensitive people. Approximately 80-90 percent of adult Americans will get a rash if they axe exposed to 50 micrograms of purified urushiol (Epstein et al., 1974). This is indeed a minute amount when you consider that one grain of table salt weighs about 60 micrograms. An urushiol residue on the skin is difficult to wash off and may be spread by scratching. Contrary to popular belief, it is not spread through blister fluids. It is a relatively stable compound and can retain its potency for years in the absence of oxidation. Herbarium specimens 100 years old have been known to cause dermatitis. It is readily transferred from contaminated clothing, objects and fur of animals. To make matters worse it readily penetrate s the epidermal layer of the skin where it binds to proteins of deeper skin cell membranes. Before the protein bond can occur, the catechol is oxidized to a more reactive quinone in which the two OH groups are replaced by double-bonded oxygens (Figure 2). In the conjugated state (bound to cell membranes) urushiol is virtually impossible to wash off. By itself the urushiol molecule (also called a hapten) probably would not initiate a full-blown immune response, but when attached to the cell membrane it becomes a "warning flag" that attracts patrolling T-cells.

In addition to poison oak, poison ivy, and poison sumac, a number of other species in the Sumac Family contain urushiol mixtures (Figure 3). In Japan, dermatitis reactions have been reported from contact with lacquered objects (from the Japanese lacquer tree) such as bar tops, rifle stocks, and toilet seats. Dermatitis has also been reported in people handling mangoes (Mangifera indica), shells of cashew nuts (Anacardium occidentale), the Rengas tree (Gluta renghas), Burmese lacquer tree (Melanorrhoea usitata), and two attractive Caribbean shrubs, Metopium toxiferum and Comocladia dodonaea. The name Rengas actually refers to several genera of large Malaysian trees with resinous sap that blackens when exposed to the air. The heartwood is dark red-brown with a beautiful grain, but it is dangerous to work. Were it not for this drawback, Rengas timber would be one of the finest decorative hardwoods. Imported Haitian voodoo dolls and swizzle sticks made from cashew nuts have produce d dermatitis reactions similar to poison oak. Laundry markings made from the India marking nut tree (Semecarpus anacardium) have caused neck irritation and rashes, even after the clothing was repeatedly washed. Urushiols also occur in the seeds of Ginkgo biloba (Ginkgoaceae) and in several genera of the Proteaceae.

Poison oak urushiol causes a complicated delayed allergic reaction with the body's immune system. It is technically classified as a cell-mediated immune response and the "peak misery" may not appear until days or weeks later. It is quite different from the primary irritants of nettle (Urtica spp.) and euphorbias (Euphorbia spp.), the effects of which are immediate. The following "two-phase" scenario for poison oak dermatitis is summarized from Epstein (1984). PHASE I (Induction): Initial contact with poison oak may result in urushiol penetrating the stratified squamous epithelial cells of the skin and binding to large dendritic (branched) white blood cells in the epidermis called Langerhans cells (Figure 4). The Langerhans cell (with urushiol on its membrane) migrates to a nearby lymph node where special white blood cells, called effector T-cells, are programmed to recognize urushiol. There are literally millions of effector T-cells roaming throughout the blood and lymphatic sy stem, each with special receptor molecules on their membranes for a particular allergenic chemical, such as the urushiol of poison oak. T-cells patrol our circulatory system looking for invading cells and viruses, inspecting surface membranes like security guards checking I.D. cards. PHASE II (Elicitation): If you get urushiol absorbed into the skin during a subsequent encounter with poison oak, an effector T-cell may encounter it bound to a Langerhans cell and attach to it by a complicated and specific recognition system. The effector T-cell then produces more clones of itself and releases special proteins called lymphokines which attract a legion of different white blood cells, including macrophages and cytotoxic ("killer") T-cells. The new army of white blood cells releases cytokines or proteins which destroy everything in the vicinity including bound urushiol and other skin cells, thus producing a blistering rash. Fluid oozes from the blood vessels and lymphatics (edema) and cell death and necrosis (breakdown) of skin tissue occurs. Milder effects range from redness (vasodilation) and itching (nerve injury) to small blisters (vesicles and bullae).

Explanations for natural immunity to poison oak are complicated by myths, conflicting reports and ongoing controversies among authorities. Sensitization depends on the chance meeting of a special effector T-cell (with correct receptor site) and the poison oak allergen -- a painful biochemical rendezvous. A person may not have effector T-cells with the special receptor for urushiol -- or perhaps your relatively few effector T-cells with precise poison oak receptor may never encounter the urushiol allergen. The allergen may be absorbed and degraded before the T-cells find it. Most people will probably experience some degree of dermatitis if a sufficient quantity of urushiol is thoroughly rubbed into their skin. Sensitizing may occur by a white blood cell transfusion from a sensitized person. Immunity to poison oak with age, exposure, and homeopathic remedies may involve suppressor T-cells which inhibit or block the action and reproduction of other T-cells. Circulating IgG immunog lobulin antibodies that block the T-cell receptor for urushiol may also be involved (Stampf et el., 1990).

Since the HIV virus attacks T-cells, persons afflicted with the deadly disease AIDS have a serious deficiency in cellular (T-cell) immunity. AIDS patients may not have problems with poison oak dermatitis and this likely reflects their decreased cellular immunity. In fact, one treatment for AIDS patients is to try to sensitize them to another allergenic chemical (dinitrochlorobenzene) in order to stimulate T-cell production (Striker et al., 1994).

During the last century scientists have tried all sorts of homeopathic remedies made from extracts of poison oak. Some products, such as poison oak tablets and droplets, have been withdrawn from the market because of severe allergic reactions in hypersensitive people. In fact, the side effects in some people, such as severe anal itching, is often unacceptable. One promising area of desensitization research involves oral pills and intramuscular injections of related or modified urushiol: a molecule similar enough to urushiol to have the same immunological effect, but different enough to avert its excruciating side effects. Several compounds have been used successfully with laboratory animals (Stampf et al., 1986). Future development currently under way may lead to a vaccine that blocks the specific urushiol T-cell receptor and immunizes "high risk" people against urushiol for periods of time (Stampf et al., 1990). In fact, Allergene, a small biotech company in San Mateo, Californ ia, has successfully produced a hybridoma (fused lymphocyte and carcinoma cell) that produces urushiol-binding monoclonal antibodies that prevented sensitized mice from reacting. These antibodies soon will undergo Phase I trials in people and eventually they will be available in a serum.

According to Albert M. Kligman's classic paper on poison oak (1958) there is no evidence of racial immunity to poison oak urushiol, not even among full-blooded Indians; however, skin of persons of African racial origin is slightly less susceptible. Native American Indians were much more "in tune" with nature and probably learned to recognize, respect, and avoid the plant at an early age. There is some evidence suggesting that native-born Hawaiians and Orientals may be less susceptible to poison oak, possibly due to early exposure to mangoes and Japanese lacquer (Epstein & Claiborne, 1957). Eskimos also are thought to be relatively immune, but the generics of poison oak/ivy susceptibility are very poorly understood on a population basis. On an individual basis, children of very sensitive parents are highly likely to become poison oak sufferers (Walker et al., 1989).

It is difficult to explain how California Indians utilized poison oak so extensively without suffering the ill effects of urushiol. Perhaps some may have acquired an immunity from early exposure to the plant, or perhaps they handled the plant very cautiously. In addition to using poison oak lacquer as a black dye, Pomo Indians reportedly used it to cure warts (Saunders, 1933). The wart was incised and then fresh resin was applied to the incision. Fresh resin was also used as a cure for ringworm and was applied to rattlesnake bites. Several tribes used the young flexible stems to weave baskets, although squaw bush (Rhus trilobata) branches were more commonly used. According to Balls (1970), Karok Indians of northwestern California covered the bulbs of soap lilies (Chlorogalum pomeridianum) with poison oak leaves and then baked them in earth ovens for food. Other northern California tribes wrapped acorn meal with poison oak leaves during baking.

The list of "treatments" for poison oak is bewildering and in some cases preposterous. Just about every conceivable substance has been tried for topical therapy, from morphine and kerosine to buttermilk and gunpowder! Most authorities agree that lotions, creams, and sprays containing anti-inflammatory corticosteroids (hydrocortisones) are the most effective agents to relieve painful, itching rashes. Serious outbreaks may require medical attention and hospitalization. Ideally the best therapy when exposed to poison oak is to wash the contaminated areas thoroughly. The problem is that most ordinary bath soaps have little effect on removing the resinous sap. In fact, added moisturizers and oils in the soap together with brisk rubbing may even spread the urushiol, increasing the area of allergic response. Strong laundry soaps, such as Fels Naptha(R), may also spread the allergen and be harsh on sensitive skin. Some books still recommend antipruritic (anti-itch) agents such as calami ne lotion for mild cases. A poultice made from the resinous flowers and leaves of gum plant (Grindelia robusta) was commonly used by Indians and early settlers in California to relieve inflammation and itching. Native Americans also made concentrated poultices from boiled leaves of the common shrubs yerba santa and manzanita (Eriodictyon and Arctostaphylos spp.), and from the thick roots of mule ears (Wyethia longicaulis), a resinous, balsam-scented sunflower with large basal leaves (Balls, 1970; Bean and Saubel, 1972). Other reported naturopathic remedies to relieve the inflammation and itching of poison oak rashes include salves made from the crushed leaves of Aloe vera and narrow-leaf plantain (Plantago lanceolata). A poultice made from juicy stems of the North American jewelweeds (Impatiens capensis and I. pallida), succulent wildflowers that grow with poison ivy in the eastern states, is also listed in herbal manuals (Schwartz, 1986); although its value as an effective therapy ha s been amply disproved (Zink et al., 1991).

A recent editorial in Mushroom, The Journal (Winter 1994-95) discussed a mycological cure for poison oak rash which consists of rubbing fungi such as Boletus and Polyporus on the affected skin. This treatment is based on the fact that freshly cut pieces of mushrooms, apples, and potatoes turn dark when exposed to the air. The actual mechanism for this blackening process involves the oxidation of phenolic compounds in the tissues of these pieces by the enzyme tyrosinase. The resulting quinones rapidly polymerize into a brown residue. Placing the pieces under water prevents this "unsightly" oxidation. In fact, chefs add lemon juice, which contains the strong reducing agent ascorbic acid; this keeps the phenolics reduced. Since urushiol is a phenolic compound, tyrosinase would probably also detoxify it. The enzymes might also reduce the spreading of urushiol to other parts of the body by deactivating it at the initial site of exposure. One of the authors (WLE) has studied an even m ore specific and potent oxidase for urushiol called catechol 2,3 oxidase. A bacterial gene was cloned and expressed to reduce this recombinant enzyme. In vitro, in a test tube, it oxidized urushiol within seconds. When applied to skin it sometimes prevented a rash, but only if the urushiol was inactivated before penetrating the epidermis. The efficacy of patented creams containing oxidase enzymes depends on the oxidation of urushiol at the initial site of contact before it has penetrated the skin. Once urushiol binds to the protein of skin cell membranes, these creams would have little effect on the subsequent immune response.

A product called TECNU OAK-N-IVY(R) Cleanser is now marketed through forestry supply catalogs. It contains a mixture of organic solvents and wood pulp by-products which remove terpene resins and urushiol from the skin. Thorough rinsing with water is recommended. Other organic solvents, such as rubbing alcohol, would probably also remove the urushiol residue. Of course, if the allergen has already penetrated the epidermal layer and bonded to deeper skin cells, it is too late. Interestingly enough, the original TECNU product was developed to remove radioactive fallout dust from the skin without water (Mermon, 1987). It was supposed to be stocked in fallout shelters across the United States. Later it was found to be highly effective in removing paint resins and, quite by accident, urushiol. (TECNU is a crude distillate of gasoline and is quite expensive compared to other solvents such as gasoline, paint thinner and acetone.)

Another product in development for the U.S. Forest Service is called IVY-BLOCK. It is an aerosol spray containing activated clay used in antiperspirants. IVY-BLOCK forms a barrier that both prevents urushiol from touching the skin and chemically binds with it so it becomes inactive. IVY-BLOCK is very effective but is not a panacea for extremely sensitive people. At the present time it is not available pending FDA approval. Another effective blocking agent called StokoGard Outdoor Cream(R), a fatty acid ester, is available through industrial supply houses and by asking your pharmacist to order it from Stockhausen, Inc. of Greensboro, North Carolina.

The evolutionary significance of poison oak resin containing urushiol is difficult to explain. The resinous sap probably helps to seal wounds and may retard the growth of infectious fungal and bacterial spores. A chemical defense strategy against "predatory pressure" seems unlikely since the foliage and fruits are eaten by deer, goats, horses, cattle and a variety of birds. In fact, wood rats even use the branches to construct their nests. Only humans appear to have painful encounters with the plant, although laboratory studies indicate sensitivity on exposed skin of guinea pigs, rabbits, mice, sheep, dogs, and rhesus monkeys.

Literature cited

Baer, H., Watkins, R. C., Kurtz, A. P., Byck, J. S. and C. R. Dawson. 1967. "Delayed Contact Sensitivity to Catechols." Journal of Immunology 99: 370-375.

Baer, H., Dawson, C. R., and A. P. Kurtz. 1968. "Delayed Contact Sensitivity to Catechols," Journal of Immunology 101: 1243-1247.

Balls, E. K. 1970. Early Uses of California Plants. University of California Press, Berkeley.

Bean, J. L. and K. S. Saubel. 1972. Temalpakh: Cahuilla Indian Knowledge and Usage of Plants, Malki Museum, Inc., Banning, California.

Dawson, C.R. 1954. "The Toxic Principle of Poison Ivy and Related Plants." Recent Chemical Progress 15: 39-53.

Dawson, C. R. 1956. "The Chemistry of Poison Ivy." Transactions of the New York Academy of Sciences 18: 427-443.

Epstein, E. and E. R. Claiborne. 1957. "Racial and environmental factors in susceptibility to Rhus." Archives of Dermatology, Vol. 75:197-201.

Epstein, W. L. 1984. "Allergic Contact Dermatitis." In: Current Perspectives in Immunodermatology, pp. 253-263. Churchill Livingstone.

Epstein, W. L. 1994. "Occupational Poison Ivy and Oak Dermatitis." Dermatologic Clinics 12 (3): 511-516.

Epstein, W. L., Baer, H., Dawson, C.R. and R.G. Khurana. 1974. "Poison Oak Hyposensitization: Evaluation of Purified Urushiol." Archives of Dermatology 109: 356-360.

Gillis, W.T. 1971. "The Systematics and Ecology of Poison-Ivy and the Poison-Oaks." Rhodora 73: 72-159, 161-237, 370-443, 465-540.

Kligman, A.M. 1958. "Poison Ivy (Rhus) Dermatitis." Archives of Dermatology 77: 149-180.

Mermon, D. 1987. "Life's an Itch." Outdoor Life October: 76-77, 119-120.

Saunders, C. F. 1933. Western Wildflowers and Their Stories. Doubleday Doran and Company, New York.

Schwartz, D.M. 1986. "Leaflets Three: The Sense and Nonsense of Poison Ivy and its Itchsome Kin." Blair & Ketchum's Country Journal 13: 42-50.

Stampf, J-L, et al., 1986. "Induction of Tolerance to Poison Ivy Urushiolin the Guinea Pig by Epicutaneous Application of the Structural Analog 5-Methyl-3-n-Pentadecylcatechol." Journal of Investigative Dermatology 86: 535-538.

Stampf, J-L., Castagnoli, N., Epstein, W., et al., 1990. "Suppression of Urushiol-Induced Delayed-Type Hypersensitivity Responses in Mice with Serum IgG Immunoglobulin from Human Hyposensitized Donors." Journal of Investigative Dermatology 95: 363-365.

Striker, R.B., et al., 1994. "Clinical and Immunologic Evaluation of HIV-Infected Patients Treated with Dinitroclorobenzene." Journal of American Academy of Dermatology 31: 462-466.

Walker, et al. 1989. Chapter 23:617-636. Management of Wilderness and Environmental Emergencies. Ed. P.S. Auerback, E. C. Geehr. C. V. Mosley Co., St. Louis)

Zink, B.J., et al., 1991. "The Effect of Jewel Weed in Preventing Poison Ivy Dermatitis." Journal of Wilderness Medicine 2:178-182.

Article copyright American Botanical Council.

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By W.P. Armstrong and W.L. Epstein