Chapter 63 Plant-Induced Dermatitis
Cutaneous exposure to plants may cause a wide array of skin problems. Plant-induced dermatitis can manifest in multiple fashions, including weeping eczematous patches and plaques, vesicles and bullae, fine scaly patches, or any combination of the above. Because the end result may be a generic response to injury, dermatitis is often an easy clinical diagnosis to make. However, determining the type of dermatitis with which the patient is afflicted can be difficult and frustrating. Acute care providers are often the first individuals to encounter and treat severe plant-induced dermatitis, so the ability to make a rapid and accurate diagnosis is crucial.
There are numerous subtypes of dermatitis: contact (irritant or allergic), photoallergic, nummular, asteatotic, stasis, seborrheic, atopic, and dyshidrotic. Dermatitis can manifest acutely with vesicles and bullae or can manifest in a chronic form with lichenification and hyperpigmentation. The acute nature of dermatitis is often itchy and uncomfortable, leading patients to seek emergency care. The history and physical examination are of the utmost importance in determining causality. A morphologic approach to the physical examination is a high-yield method for generating the appropriate differential diagnosis. Is the rash linear in nature? This often implies an external contactant. Is the rash in sun-exposed areas? This implies a photosensitive dermatitis.
In addition, the symptoms of the rash are important. Irritant reactions tend to decrescendo in severity, being the worst at presentation and gradually improving over time, whereas those that are allergic tend to crescendo, then decrescendo. They gradually build over 1 to 21 days to peak intensity, then slowly improve.
There are many clinical mimics of plant-induced dermatitis, including drug hypersensitivity reactions, connective tissue disease, superficial fungal infections, urticaria, and cutaneous T-cell lymphoma. If a patient has persistent dermatitis that lasts longer than a month, a biopsy is often indicated to help differentiate possible mimickers. A pathologic review of the biopsy specimen will help rule out other conditions and lead to appropriate therapy.
The subset of dermatitis discussed in this chapter is plant-induced dermatitis. Plant-induced dermatitis can be caused by contact with a wide variety of plants. Thousands of species of plants have been reported to cause dermatitis. The specific effects that each of these plants has on the skin have not been fully determined or described. The majority of medical literature regarding plant-induced dermatitis is anecdotal and has not been confirmed by independent observers. Few large-scale studies of the effects of plants have been performed. The exception to that is the Toxicodendron (poison ivy/oak/sumac) species of plants, owing to their ubiquitous nature.
The most common injury to skin caused by plants is a simple scratch, laceration, or puncture wound. This can lead to either bacterial or fungal infection. Plant-induced dermatitis reactions can be further subclassified into numerous groups. These include irritant contact dermatitis, allergic contact dermatitis, phototoxic dermatitis, and photoallergic dermatitis. Plants can also cause contact urticaria and foreign-body reactions.
A wide variety of plants cause irritant contact dermatitis, or nonallergic inflammation of the skin caused by direct contact with the offending plant. Most of these rashes are mild and self-limited, typically involving 1% to 2% body surface area. Irritant contact dermatitis causes transient redness and pruritus of the contacted skin. The spectrum of reactions ranges from linear scratch marks to weeping ulcerated red scaly plaques, the latter of which may be difficult to link to the originating plant.
The most common cause of plant-induced contact dermatitis is irritant in nature. Irritant contact dermatitis can be further subdivided into traumatic (mechanical) and chemical causes. Most plants have the potential to cause traumatic skin injury. Whether it is a thorn from a hawthorn tree, a cut from a sharp leaf edge, or scratches from briars, human skin is ill prepared to protect itself from such insults (Figure 63-1).
FIGURE 63-1 The spiny thorns of the rose bush.
(Courtesy USDA-NRCS PLANTS Database; Herman DE, et al: North Dakota tree handbook, USDA NRCS ND State Soil Conservation Committee, Bismarck, ND, 1996, NDSU Extension and Western Area Power Administration.)
Any foreign body embedded in the skin can cause a granulomatous reaction pattern. Some plants are more prone to causing this type of inflammatory reaction. Plants with thorns and barbs (Figure 63-2) are the most likely culprits. Rose thorns and cactus spines are common offenders. Cacti are indigenous to the southwestern United States. They are popular as houseplants and can be grown indoors with proper care. Therefore, cactus injuries can be seen in a wide variety of locales.109 The initial contact and acute injury may lead to chronic granulomatous inflammatory eruption, which typically takes 4 to 8 weeks to develop. It is the lag time that may make the diagnosis difficult. Clinically, the rash consists of erythematous and indurated papules, plaques, and nodules. The lesions are often grouped and localized, which is a clue to the diagnosis. Cactus spines may also penetrate so deeply into the skin that they cause pseudotumors of bone.101
(Courtesy Paul S. Auerbach.)
The prickly pear (Opuntia ficus-indica) is found in North and Central America, as well as around the Mediterranean Sea. It is a member of the Cactaceae family. The fruit is covered with glochids. A unique example of mechanical trauma is from a glochid. Glochids are modified leaves that appear as tufts of barbed spines or hairs found on Opuntia species of cacti (Figure 63-3). They have sharp tips that penetrate skin and cause irritation by disrupting the epidermis. They are very loosely held to the cactus, release with the slightest touch, are quite irritating to skin, and cause variable amounts of discomfort and itching. They have a tendency to break off from the cactus and work their way onto the skin, causing a granulomatous reaction that may resemble scabetic nodules.101 They can also implant into the conjunctiva.125 Glochids are present year-round and cause dermatitis in all seasons.
Similarly, penetrating injuries from a variety of cactus species, including the Echinopsis, have been reported throughout the southwestern United States. Typical injuries manifest on the extremities as inflammatory papules. In rare cases, the cactus spines can penetrate into bone and soft tissue spaces and cause an inflammatory arthritis. Appropriate footwear and clothing, including gloves, are of utmost importance when encountering plants that can cause mechanical skin trauma. Treatment is to remove the spines from the skin. This is best done mechanically with a forceps under bright illumination and magnification if necessary (Figure 63-4).91,125
(From O’Neill PJ, Sinha M, McArthur RA, et al: Penetrating cactus spine injury to the mediastinum of a child, J Pediatr Surg 43:e33, 2008.)
When biopsies are performed of the chronic (4 weeks after initial injury) inflammatory papules that are caused by cacti glochid implantation, a granulomatous reaction pattern is found.75 Multiple multinucleated giant cells, histiocytes, granulomas, and organic plant material can be seen histologically under polarized light sources. Occasionally, a traumatic injury may implant one or more microbes. When performing a biopsy, one should also perform a tissue culture for bacteria, mycobacterium, and fungal species. This is especially true in cases with pustular morphologies.
Initial treatment should be prompt extraction of the cactus spines. The smaller the spine, the more difficult the removal.75 This is a particular problem when encountering injuries from the beaver tail cactus (Figure 63-5), which has very small glochids that can be quite difficult to remove. Many methods of removal have been employed to remove the spines. Tweezers are often the first line of removal, and various gels, glue, tape, and facial masks have been tried.81 The best method is mechanical removal with a small forceps or fine needle. Once removal is accomplished, a topical corticosteroid can be employed. A midpotency topical corticosteroid, such as triamcinolone acetonide (Aristocort, Kenalog) 0.1% cream or ointment, is often all that is needed. Most granulomatous reactions resolve within 2 to 4 months.35 Often, the removal is unsuccessful, and the glochids work their way to the surface over a period of months to years. Supportive care with cool compresses with aluminum acetate solution 1 : 40 in water used as soak, compress, or wet dressing is very helpful. Administering pain medication and initiating prompt therapy for any co-infection are integral parts of the overall treatment plan.
Infections may also be inoculated into the skin from mechanical plant injury. The most well known is Sporothrix schenckii fungal infection occurring after a prick or puncture from a rose thorn. S. schenckii is a common dimorphic fungus found in organic material. The characteristic lymphangitic spread is easily recognized (Figure 63-6). Typically, an ulcerating nodule develops at the site of inoculation; then over the next 3 weeks, on average (3 days to 12 weeks), nodules develop along the draining lymphatic channels. The nodules eventually ulcerate, and patients develop chronic lymphangitis. First-line therapy is either saturated solution of potassium iodide or itraconazole.85 There are many other infections caused by traumatic implantation of bacteria, fungus, and algae into skin or underlying subcutaneous tissues (Box 63-1).
Infections Associated with Mechanical Plant Injury
Another common problem, is direct implantation of plant organic material into the skin, causing a foreign-body reaction, such as that seen with a splinter. The goals in treatment are to remove the foreign material promptly and treat infections with the appropriate antimicrobial agent.
Wood dust can also cause an eczematous dermatitis of either the irritant or allergic type. The victims are nearly always woodworkers who have been exposed repeatedly. Allergic contact dermatitis occasionally develops. Rarely, an erythema multiforme-like configuration is noted.48 Respiratory hypersensitivity, including asthma, to wood dusts is well documented.111 Solid wood has very rarely been reported to cause dermatitis.116 Table 63-1 lists the most commonly reported woods to cause contact dermatitis. Dermatitis from woods is almost entirely seen in an occupational setting. Treatment includes avoidance of the offending agents and use of ultra-potent topical steroids such as clobetasol 0.05% ointment twice daily to the affected areas for up to 2 weeks.
|Common Name||Botanical Name|
|African black walnut||Mansonia altissima|
|African blackwood||Dalbergia melanoxylon|
|Bolivian rosewood||Machaerium acutifolium|
|Brazilian box tree||Aspidosperma species|
|East Indian rosewood||Dalbergia latifolia|
|Honduran mahogany||Swietenia macrophylla|
|Macassar ebony||Diospyros celebica|
|Milo wood||Thespesia populnea|
|Pao ferro||Machaerium scleroxylum|
|Sapele wood||Entandrophragma cylindricum|
|Silky oak||Grevillea robusta|
|Tali wood||Erythrophleum guineense|
|White ash||Fraxinus americanus|
The most common form of plant-induced irritant contact dermatitis is from plant-derived chemicals. Acids, enzymes, isothiocyanates, phorbol esters, calcium oxalate, and alcohols cause these reactions. The chemicals are directly toxic to the skin, and work by altering the inherent pH balance, dissolving the protective lipids of the stratum corneum, and denaturing skin proteins. They require direct contact of the plant material with the epidermis. Many factors can modify irritant reactions. The most important variables are duration of skin contact, concentration of the irritant, and underlying skin integrity and thickness.8 Concentration of the irritant chemical in the plant will be at different levels in the stem, petals, roots, and leaves. Levels of the irritant also fluctuate at different times of the year, so it would not be uncommon for someone to have a reaction in the summer months from contacting the leaves of an irritating plant and not have the same reaction when touching the stem in winter.
Plants in the spurge (Euphorbiaceae) family exude a milky sap when traumatized. This sap contains a chemical mixture of irritating diterpenes and phorbol esters.42 After skin contact, the reactions can vary from mild stinging and burning to erythema, vesiculation, and bulla formation. Blister formation occurs typically within 24 hours. Eczematous weeping plaques can also be seen in the first 24 hours. Reactions can last for 2 to 3 weeks. The spurge family is a large family of plants with more than 7000 described members. These plants are found predominantly in tropical climates; in the United States, they can be found mainly in Florida and the southwestern states. Some well-known members of the Euphorbiaceae family include the croton plant, wolfsmilk, manchineel tree, and snow-on-the-mountain. Figure 63-7 demonstrates three of these commonly irritating plants. Table 63-2 is a list of the most common Euphorbiaceae.
(C courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)
|Common Name||Botanical Name|
|Candelabra cactus||Euphorbia lactea|
|Caper spurge||Euphorbia lathyrus|
|Chinese tallow||Sapium sebiferum|
|Cypress spurge||Euphorbia cyparissias|
|Manchineel tree||Hippomane mancinella|
|Pencil tree||Euphorbia tirucalli|
|Petty spurge||Euphorbia peplus|
|Sandbox tree||Hura crepitans|
|Sun spurge||Euphorbia helioscopia|
Data from Asilian A, Faghihi G: Severe irritant contact dermatitis from cypress spurge, Contact Dermatitis 51:37, 2004; and Lovell CR: Irritant plants. In Lovell CR, editor: Plants and the skin, Oxford, 1993, Blackwell Scientific Publications, pp 42-95.
Plants of the genus Croton are also members of the spurge family. These tropical plants are the source of croton oil. This oil had been used in the past as a purgative and for many medicinal remedies. The plants contain a mixture of phorbol esters and diterpenes in their leaves, stems, and seeds.18 These esters can cause immediate blistering of the skin, as well as a weeping eczematous eruption. These plants are found mostly in Central and South America, but about 40 species live in the southern United States. They typically appear as low-lying shrubs.
Some plants, such as those listed in Table 63-3, contain proteolytic enzymes, which cause skin irritation when contacted in sufficiently high concentrations. Plants such as Mucuna pruriens (cowhage) contain a proteolytic enzyme—mucunain—that causes intense itching immediately on contact. Its seed pods are covered with tiny stinging hairs called trichomes. Trichomes contain high concentrations of mucunain. This enzyme has been used for decades by practical jokers in its dried form as itch powder. Recently, medical researchers have made use of the irritant enzyme found in papaya. Papain is a proteolytic enzyme that is used in a number of commercial wound dressings to aid in degradation of necrotic tissue and aid in wound healing.98
|Common Name||Botanical Name||Proteolytic Enzyme|
|Fig tree||Ficus carica||Ficin|
Calcium oxalate is a common skin irritant. Calcium oxalate in plants is found in a crystalline needle-like form called raphides. It is present in many plants, including dumb cane, rhubarb, agave, daffodils, and hyacinths, in irritating concentrations. Dumb cane (Dieffenbachia species) is a common houseplant well known to cause irritant skin and mucous membrane reactions (Figure 63-8).29 The common name arises from the effect it has on those unlucky enough to chew its leaves, which release calcium oxalate. Calcium oxalate causes irritation, swelling, salivation, pain, and blistering of mucous membranes. In an extreme case, the afflicted person is unable to speak normally, owing to involvement of the mucous membranes.126 When the sap of this plant contacts the eye, conjunctival swelling and corneal ulcers may occur.82 Raphides are also found in Agave species. Irritant contact dermatitis has been reported in tequila distillery workers, who are in frequent contact with Agave tequilana.104 Purpuric and irritant reactions have been reported to occur after exposure to the sap of Agave americana.25,100 Immediate burning on exposure is characteristic of calcium oxalate toxicity.
Daffodils and hyacinths are among the many other species containing calcium oxalate, which is found in its highest concentration in the bulb.114 Agricultural workers who gather these bulbs and flowers are at highest risk for irritant dermatitis, typically on the distal extremities where they came into contact with the plant.59
The family Solanaceae contains the peppers. These plant species contain several capsaicinoids, the most common of which is capsaicin. Capsaicin is a chemical compound that can cause skin and mucous membrane burning, itching, and in severe cases, vesiculation and bulla formation. Specialized cells of the plant’s placenta produce capsaicin. Capsaicin binds to receptors on neurons and causes release of substance P from primary sensory neurons. With repeated applications, capsaicin causes depletion of substance P and desensitizes the neuron. This effect is used in clinical practice with topical application of capsaicin-containing compounds to skin in areas of chronic pain, such as for postherpetic neuralgia.
Brassicaceae (Cruciferae) is a large family of plants that causes irritant contact dermatitis. More than 3500 species live in temperate regions of the world.31 Its members include horseradish (Armoracia rusticana), black mustard (Brassica nigra), and white mustard (Sinapis alba) (Figure 63-9). These plants contain glucosinolates, which are converted to isothiocyanate, which causes irritant dermatitis.78 This reaction is catalyzed by the enzyme myrosinase. Substrate interacts with the enzyme after the plant is crushed, as in chewing.31 Contact with these plants can cause a wide range of cutaneous reactions, including burning sensation, pain, red patches, and blister formation.
FIGURE 63-9 White mustard plant.
(Courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)
The Ranunculaceae family includes buttercups and Old Man’s Beard (Figure 63-10). Table 63-4 lists a small sampling of plants in this family reported to cause irritant contact dermatitis. Protoanemonin is considered the primary irritant toxin in this group of plants. Reactions from these plants tend to be mild and rarely cause people to seek medical care. Table 63-5 includes plants and plant families that cause irritant phytocontact dermatitis and lists their primary irritant substance.70,114
(B courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)
|Common Name||Botanical Name|
|American prairie crocus||Pulsatilla patens|
|Christmas rose||Helleborus niger|
|Meadow rue||Thalictrum foliosum|
|Pasque flower||Pulsatilla vulgaris|
|Traveler’s joy||Clematis vitalba|
|Common Name||Botanical Name||Irritant Chemical|
|Agave||Agave americana||Calcium oxalate|
|Black mustard||Brassica nigra||Isothiocyanates|
|Cowhage||Mucuna pruriens||Proteolytic enzymes|
|Croton||Croton tiglium||Phorbol esters|
|Daffodils||Amaryllidaceae family||Calcium oxalate|
|Dumb cane||Dieffenbachia species||Calcium oxalate|
|Hyacinths||Liliaceae family||Calcium oxalate|
|Manchineel tree||Hippomane mancinella||Phorbol esters|
|May apple||Podophyllium peltatum||Podophyllin resin|
|Pencil tree||Euphorbia tirucalli||Triterpene alcohols|
|Prickly pear||Opuntia species||Spines|
|Spurges||Euphorbiaceae family||Shorbol and diterpene esters|
|Mustard, radish, etc.||Cruciferae (Brassicaceae) family||Isothiocyanates|
|Common caper||Capparidaceae family (e.g., Capparis spinosa)||Isothiocyanates|
|Spider plant||Cleomaceae family (e.g., Cleome species)||Isiothiocyanates|
Data from High WA: Agave contact dermatitis, Am J Contact Dermat 14:213, 2003; and Ricks MR, Vogel PS, Elston DM, et al: Purpuric agave dermatitis, J Am Acad Dermatol 40:356, 1999.
It is currently believed that both irritation and contact sensitization are mediated by epidermally derived cytokines. Tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), macrophage inflammatory protein-2 (MIP-2), and granulocyte-macrophage colony-stimulating factor (GM-CSF) are produced and secreted into tissue in response to both allergens and irritants. However, a number of other proteins are released only by allergenic stimulation.
In irritant contact dermatitis, the chemical irritant (which is usually an acid, alkali, surfactant, solvent, oxidant, enzyme or toxin) damages the keratinocyte. This damage is highly dependent on the concentration of the irritant. No sensitization or elicitation phase occurs, as is seen in allergic contact dermatitis, which is a key discerning feature between the two types of plant-induced contact dermatitis. The damaged keratinocyte activates phospholipase A2. This in turn cleaves arachidonic acid and diacylglyceride (DAG) from the cell membrane. The arachidonic acid is converted into various prostaglandins and leukotrienes. Prostaglandins and leukotrienes cause endothelial cells to dilate and become leaky, resulting in edema. They also act on mast cells to release histamine and are chemoattractants for lymphocytes and neutrophils. Further recruitment of lymphocytes and neutrophils is facilitated by expression of intercellular adhesion molecule-1 (ICAM-1) by keratinocytes.79 The DAG causes upregulation of genes for cytokines such as interleukin-1 (IL-1) and GM-CSF. These proteins then act to stimulate T cells and neutrophils. All these inflammatory cells and release of various cytokines and vasoactive substances lead to the clinical findings in irritant contact dermatitis. This is a continuing area of investigation.102,127
Treatment of primary irritant dermatitis requires multiple steps. The victim must be removed from exposure to the irritant chemicals. Gentle cleansing of the wound with antibacterial soap, applying cool compresses, and watching for infection are essential. Antihistamines, such as hydroxyzine, 10 to 25 mg administered orally 4 times daily, or diphenhydramine, 25 mg orally 2 to 4 times daily, can help with itching. The sedating antihistamines tend to work better than the newer nonsedating types (fexofenadine, loratadine, and desloratadine), although some patients respond well to the nonsedating forms. Topical medium-strength steroids, such as triamcinolone 0.1% cream, may be applied twice a day to the affected areas for up to 2 weeks without risk for atrophy. Clobetasol 0.05% cream or ointment (an ultrapotent topical steroid) can also be used in severe cases. In the case of topical medium-strength and ultrapotent topical steroids, care should be taken to avoid application in the groin, axillae, and face. Typical application regimens are twice daily for 1 to 2 weeks. Cool compresses with aluminum acetate solution (Domeboro, Burow’s solution) diluted 1 : 40 in water are very helpful in soothing pruritus and exudative skin irritation. Dermatitis generally heals in less than 7 days if no complications develop and if tissue damage is minimal. If the patient is unable to be removed from the source of irritation, no medicine, cream, or soak will alleviate the problem. People are sometimes forced to change occupations or hobbies, or at the very least modify their environment.
Allergic contact dermatitis is a type IV delayed hypersensitivity reaction. This form of contact allergy is far more common than is contact urticaria. The most common acute presentation is linearly arranged eczematous, edematous patches and plaques with varying amounts of vesiculation and bulla eruption. Occasionally, the eruption is widespread. If the face is involved, there can be severe eyelid swelling. Patients are quite distressed by their appearance. In severe cases, they can have systemic symptoms of fever, chills, fatigue, and lethargy. In its more chronic form, as is seen with the Compositae family, allergic contact dermatitis presents with lichenified eczematous plaques in exposed areas.
The most common cause of acute allergic contact dermatitis in the United States is from exposure to poison ivy, oak, and sumac plants (Table 63-6). In the past, allergic contact dermatitis caused by poison ivy, oak, or sumac was referred to as Rhus dermatitis. Recent botanical nomenclature places the poison ivy, oak, and sumac plants in the Anacardiaceae family in the genus Toxicodendron. The Rhus genus contains plants that are not known to cause allergic contact dermatitis. Therefore the term “Rhus dermatitis” should be abandoned.
|Common Name||Botanical Name|
|Western poison oak||Toxicodendron diversilobum|
|Eastern poison oak||Toxicodendron quercifolium|
|Poison ivy||Toxicodendron radicans|
|Rydberg’s poison ivy||Toxicodendron rydbergii|
|Poison sumac||Toxicodendron vernix|
Toxicodendron weeds are fastidious. They do not grow in Alaska or Hawaii and do not survive well above 1500 m (5000 feet), in deserts, or in rainforests. They grow best along cool streams and lakes and luxuriate if it is also sunny and hot. They are found in every state of the continental United States. The plants have different configurations in different regions, but generally, poison ivy grows east of the Rockies, poison oak grows west of the Rockies, and poison sumac grows best in the southeastern United States. Because avoidance is the best prevention, it is important to learn what the plants look like in a given area (Figure 63-11). Once contaminated with the oil (resin), an average person has 1 to 4 hours to wash it off with soap and water to prevent dermatitis.
(C courtesy Paul S. Auerbach.)
Poison ivy (T. radicans) grows in moist shady regions east of the Rockies. The plants thrive at sea level and do very poorly above 1500 m (5000 feet). Poison ivy is never found on the west coast of the United States. The leaflets are 10 to 30 cm (4 to 12 inches) long and are found in groups of three. The shape of the leaves is often ovate or obtuse. The leaves can be shiny, smooth, and hairless, or they can be rough, hairy, and velvety (Figure 63-12).12,31 Its characteristic shape has lead to the adage, “Leaves of three, let them be” (Figure 63-13). It is a climbing shrub commonly found growing up the trunks of large trees, with aerial roots that are quite prominent.
(Courtesy Peter Schalock, Massachusetts General Hospital, Boston, Mass.)
Poison oak (T. diversilobum) is found in the west coastal states of North America and is given the designation western poison oak. It is a common shrub with multiple stems that form three leaflets. The leaves are larger on plants that grow in shade than on those grown in full or partial sunny conditions. It has many brown aerial roots and clusters of yellow flowers that bloom in the spring.31 The flowers bear cream-colored berries. In the California hills, poison oak grows like a forest, but in cooler, dry climates, it remains isolated in small patches.
Poison sumac (T. vernix) is a fast-growing small tree or shrub. Some plants grow as tall as 12 m (40 feet), but the average height is about 4.5 m (15 feet). The plants are found in wet marshy regions of the United States. Its leaves are unique among Toxicodendron species. They are configured as 7 to 13 smooth oval leaflets attached along a central stem.31 The plant forms pale-colored fruit. Nonpoisonous sumacs can be recognized by their jagged leaf margins and red berries.
All Toxicodendron plants have many interconnected channels that contain sap. When the plant is traumatized and a channel is broken open, the sap is extruded and hardens as a black resin to seal off the damage. This sap is the material that contains the allergen urushiol.31
All parts of the plant contain the urushiol resin (Figure 63-14, online), which is a heavy, nonvolatile oil. In its natural state, the oil is colorless or slightly yellow. Because the oil is virtually invisible, many people fail to understand how they acquired the rash. It is not a vapor, because at 315° C (600° F) in a fire or oven, urushiol splatters like butter. In a camp or forest fire, it attaches to smoke particles and can be carried downwind. The oil also readily coats the fur of animals, which explains why people often get the dermatitis from their outdoor pets. On exposure to air, the oil oxidizes, polymerizes, and turns black. This is a way to recognize the weeds, especially in autumn when the leaves fall off.
The amount of urushiol present in poison ivy and poison oak is roughly equal year-round, even when the plants are only sticks without leaves in the winter. As the leaves turn red and start to dry up in the fall, important nutrients, including urushiol, return to the stem and roots through subepidermal resin canals.50 Thus dead leaves that fall to the ground are virtually devoid of urushiol.
Urushiol is exposed to skin when a plant that has been injured or bruised releases it to the surface of the leaf, petal, stem, or root. Clinical effects are usually manifested 24 to 48 hours after contact in a previously sensitized individual; 10 to 14 days after contact in a patient on first exposure. Typically, linear streaking of papulovesicles occurs; edema, weeping, and crusting are also commonly seen (Figure 63-15). A distinct linear nature is often a clue to the diagnosis of allergic contact dermatitis. On occasion, the eruption can appear to be urticarial in nature or can mimic cellulitis. Appearance of black dots on the skin in areas of involvement can be helpful in determining the etiology.65 The black dots represent dried urushiol that has been oxidized by air (Figure 63-16). Severe itching leading to excoriations nearly always accompanies the rash. This can lead to secondary infection.
FIGURE 63-16 Poison ivy–induced allergic contact dermatitis after a young woman accidentally pinched some poison ivy leaves behind her knee. Note the central black dots, which represent the dried urushiol.
The antigen is found in the milky sap, which is quickly absorbed into the skin. Thus it is nearly impossible to wash off the sap quickly enough to prevent dermatitis. Once the sap touches the body, it is often spread by inadvertent transfer. This explains why patients often develop eruptions in sites distant from the initial contact with the plant. There are many unique urushiol chemicals. Collectively, they can be called urushioids. Each plant has a different urushioid concentration and composition. Urushioids have a structure that contains a benzene ring with a varying-length carbon side chain. The concentrations of the various urushioids of each plant depend on growing conditions and season, which also affect their antigenic properties. If the side chain is desaturated and longer, this increases the catechols’ antigenicity. Conversely, if there is a substitution on the catechol ring, this reduces antigenicity.79 Addition of an aliphatic side chain and presence of free phenolic groups also increase antigenicity.114 Poison ivy contains predominantly urushiol III, poison oak contains mostly urushiol I, and poison sumac contains predominantly urushiol II.31,79
If the patient avoids re-exposure, dermatitis resolves within 14 to 21 days in most cases. It is important to diagnose secondary impetiginization because this can lead to cellulitis if not treated with appropriate antibiotics. The most likely pathogens are Staphylococcus aureus and streptococcal species. Hyposensitization therapy has not proved practical or particularly effective and is rarely performed. Patients need to be informed to thoroughly clean clothing, through at least one complete automated hot water wash and rinse cycle with detergent, and to clean any object that may have come in contact with the plant in order to avoid repeat exposure.
It is estimated that 50% to 70% of the population is sensitive to the causative antigen, urushiol. The amount of purified urushiol required to elicit a reaction is 2 to 2.5 mg.45 Some people (about 35%) are considered subclinically sensitive because they have negative skin test reactions to 2.5 mg urushiol, but react to higher concentrations, such as 5, 10, and 50 mg.40,45 Clinically, this group is interesting because they invariably did not have poison ivy dermatitis as teenagers and often plucked the weeds with apparent impunity. However, usually in midlife after a bout of weed pulling, a rash spreads explosively. For unknown reasons, they have crossed the line into clinical sensitivity. If patch-tested with dilutions of urushiol, these individuals are often exquisitely sensitive and do not appear to lose their reactivity. The flare-up may last for several weeks, probably because of prior contamination of the home and workplace with urushiol oil. Treatment must be aggressive and more prolonged than usual.
A smaller group (10% to 15%) does not react to higher concentrations and cannot be sensitized by 1000 mg. This group was first detected and studied in passive transfer experiments in the 1950s.46 These individuals are considered to be naturally tolerant, but it remains unclear whether they achieved that state by early antigenic exposure or by genetic luck. They have no inherent resistance to contact sensitization with other chemicals and otherwise appear healthy.47 They may hold a clue to the molecular basis for immunologic tolerance.
From a practical standpoint, only 10% to 15% of Americans (up to 40 million people) can be categorized as exquisitely sensitive. Generally, these persons seek and need emergency medical care (Figure 63-17). They typically have had prior unpleasant experiences. Within 2 to 6 hours after exposure, swelling is accompanied by an erythematous, intensely pruritic, edematous, vesicular, and ultimately bullous eruption that can be associated with fever, malaise, and prostration (Figure 63-18). This true dermatologic emergency should be treated immediately and vigorously.