Poison Ivy (Rhus) Dermatitis
In the United States, poison ivy, poison oak, and poison sumac produce more cases of ACD than all other contactants combined.327 The plants causing poison ivy dermatitis are included under the botanical term Rhus and are Toxicodendron species. Poison ivy and poison oak are the principal causes of Rhus dermatitis in the United States. Regardless of the specific Rhus plant, the clinical appearance of the dermatitis may be identical. The Rhus group belongs to the family of plants known as Anacardiaceae, and cross reactions may occur. These include furniture lacquer derived from the Japanese lacquer tree, oil from the shell of the cashew or Brazil nut, the fruit pulp of the gingko tree, and the marking nut tree of India, from which a black “ink” used to mark wearing apparel is produced. The ACD to this ink is termed dhobi itch. The rind of the mango also cross reacts, and the possibility of contact dermatitis to Rhus should be considered in children with perioral dermatitis after eating mango or on the hands of mango pickers328 (Fig. 3-55).
The poison ivy plant (Fig. 3-56) characteristically shows three leaflets notched at the edge. It grows luxuriantly as a tall shrub or woody rope-like vine in vacant lots, among grasses, and on trees or fences throughout all sections of the United States except the extreme southwest. Poison sumac grows as a shrub or tree, never as a vine. It has 7 to 13 leaflets (arranged in pairs along a central stem), with a single leaflet at the end, is relatively uncommon, grows less abundantly, and is found only in woody or swampy areas primarily east of the Mississippi River. Poison oak, conversely, grows as an upright shrub, is most prominent on the West Coast, and is not a problem in the eastern United States. Although Rhus dermatitis is more common in the summer, the eruption may occur at any time of year by direct contact with the sensitizing allergen from the leaves, roots, or twigs of the plants.
The eruption produced by poison ivy and related plants is a delayed contact hypersensitivity reaction to an oleoresin (urushiol) of which the active sensitizing ingredient is a pentadecylcatechol. It is characterized by itching, redness, papules, vesicles, and bullae (Fig. 3-57). Although often irregular and spotty, a linear distribution is highly characteristic because of scratching and transfer of the urushiol oleoresin (Koebner phenomenon). When contact is indirect, such as from a pet that has the oleoresin on its fur, the dermatitis is often diffuse, thus making the diagnosis more difficult unless the true nature of exposure is suspected. In the fall, when brush and leaves are burned, it must be remembered that the sensitizing oil may be vaporized and transmitted by smoke to exposed cutaneous surfaces, often presenting as a diffuse facial dermatitis with periorbital swelling (Fig. 3-58).
Rhus dermatitis usually first appears in susceptible, sensitized individuals within 1 to 3 days after contact with the sensitizing oleoresin; in highly sensitive individuals it may occur within 8 hours of exposure. Such temporal differences are probably the result of the degree of exposure, individual susceptibility, and variation in cutaneous reactivity of different body regions.
About 70% of the population of the United States would acquire Rhus dermatitis if exposed to the plants or the sensitizing oleoresin contained in its leaves, stems, and roots. The result is an acute eczematous eruption that, barring complications or reexposure to the offending allergen, persists for 1 to 3 weeks. Since the undiluted sap from plants of the Toxicodendron species turns black when exposed to dry surfaces and skin, dramatic black lacquer- or enamel-like deposits on the skin (“black spot poison ivy”) and clothing of individuals exposed to poison ivy or other urushiol-containing plants may rarely be seen.329,330 These spots typically cannot be removed with soap and water and may precede the development of typical dermatitis.
The best prophylaxis, as with any type of ACD, is complete avoidance of the offending allergen. Patients should be instructed in how to recognize and avoid members of the poison Rhus group. When poison ivy is present in the garden or in children's play areas, chemical destruction or physical removal is indicated. Heavy-duty vinyl gloves should be used if the plants are uprooted, because the urushiol is soluble in rubber and can penetrate latex gloves.331 No topical measure is totally effective in the prevention of poison ivy dermatitis, but certain commercially available barrier preparations with quaternium-18 bentonite (organoclay) have been shown to diminish reactivity significantly (IvyBlock, StokoGard, Hollister Moisture Barrier, Hydropel).332 Desensitization to the oleoresin of poison ivy by systemic administration of Rhus antigen is unreliable and should be reserved only for extremely sensitive individuals who cannot avoid repeated exposure to the antigen. Systemic reactions are not uncommon with the use of hyposensitization procedures.
In an effort to minimize the degree of dermatitis, individuals with known exposure should wash thoroughly with soap and water as rapidly as possible so that removal of the oil is accomplished, preferably within 5 to 10 minutes of exposure. If the oleoresin is not carefully removed shortly after exposure, the allergen may be transmitted by the fingers to other parts of the body (particularly the face, forearms, or male genitalia) (Fig. 3-59). However, the fluid content of vesicles and bullae is not contagious and does not produce new lesions. Thus unless the sensitizing antigen is still on the skin, the disorder is neither able to be spread on an individual nor contagious from one person to another.
Complete change of clothing is advisable, and whenever possible, contaminated shoes and clothing should be washed with soap and water or cold water mixed with alcohol to remove the urushiol. Harsh soaps and vigorous scrubbing offer no advantage over simple soaking and cool water. Thorough washing may not prevent a severe dermatitis in highly sensitive persons. It may, however, reduce the reaction and prevent spread of the oleoresin. When early washing is not feasible, it is worthwhile to wash at the first opportunity in an effort to remove any oleoresin remaining on the skin or clothing and thus prevent its transfer to other parts of the body.
In the management of mild Rhus dermatitis, treatment with an antipruritic “shake” lotion such as calamine lotion is helpful. Topical preparations containing potential sensitizers such as diphenhydramine or benzocaine should be avoided. As in other acute eczematous eruptions, cool compresses with plain tap water or Burow solution are soothing, help remove crusts, and relieve pruritus. Administration of potent topical corticosteroids and systemic use of antihistamines and antipruritic agents are helpful. Because the acutely involved areas tend to be vesicular and weeping, creams and lotion forms of topical steroids are more commonly used than occlusive ointments.
In severe, more generalized cases of Rhus dermatitis, short-term systemic corticosteroid treatment may be indicated. Systemic corticosteroid therapy may be initiated with dosages of 1 mg/kg per day of prednisone or its equivalent. Steroids should be tapered gradually over 2 to 3 weeks. Premature termination of systemic corticosteroids may result in a rapid rebound, with return of the dermatitis to its original intensity.