Plant-Associated Dermatitis

Allergic contact dermatitis (ACD) is an important disease that notably affects 14.5 million Americans each year.¹ The economic impact of this disease is high in terms of both patient morbidity and loss of income, school and work, not to mention significant expenditures for visits to health care providers and for medicaments.¹ Once patch testing is performed and a culprit has been identified, education becomes the critical intervention to ensure adherence to an avoidance regimen. With allergen avoidance, remission of the dermatitis ensues. If patients are unable to comply with the avoidance regimen, they are at risk for recurrent or sustained dermatitis or progression to a systematized presentation.^2,3 In fact, education of the patient often begins before the diagnostic patch test is ever placed. This ensures that the patient has an appropriate understanding of potential outcomes, including his or her central role in both the disease and treatment.

At the initial consultation, patients are often taught about the pathophysiology of ACD: its delayed presentation, its relationship with the immune system (sensitization to a chemical and then elicitation of a dermatitis with re-exposure), and its occurrence at any point in time, even to something that the patient has been using regularly for a short period of time or even intermittently for years. In certain cases, the other key players, such as irritant contact dermatitis (ICD) and contact urticaria, may be explained by the patient history, as this information, not patch testing, can point to these as the correct diagnosis for the patient. It is important to note that ICD, the most prevalent form of contact dermatitis, can, at times, precede or be a concomitant diagnosis with ACD.^4,5 Unlike ACD, ICD is not immune mediated, occurring secondary to contact with an irritating or abrasive substance. Contact urticaria (wheal and flare reaction), on the other hand, represents the least prevalent form of ACD. It is important to note that it is an immune-mediated phenomenon whose hallmark is an IgE and mast cell-mediated, immediate-type hypersensitivity reaction. We acknowledge this form of hypersensitivity due to the severity of the potential deleterious anaphylactic type reactions and direct the reader to key sources.^6,7,8

In this section, we highlight plant ACD and explore top relevant allergens, regional-based dermatitis presentations, topic-based dermatitis presentations and clinical tips and pearls for diagnosis and treatment.

Plant-Associated Dermatitis

Plant-associated dermatitis is commonly seen in both primary care and dermatology clinics. Clinicians should be aware of the vast array of reactions that can occur following exposure to plants and that reactions differ based on the species as well as the route of exposure. Many of the plants noted for causing clinical symptoms are common species that patients can come in contact with on a daily basis, including hot peppers, daffodils and garlic. Generally, cutaneous manifestations can be classified into four basic reactions: urticarial, irritant, phototoxic (phytophotodermatitis) and allergic.^9-12 We will primarily focus on allergic contact dermatitis, but will first briefly discuss the clinical significance of the three other reactions.

Contact Urticaria

Urticaria after exposure to a plant can be secondary to either an immune response or a toxin-mediated response.¹³ Individuals who have frequent exposure to fresh fruits and vegetables have an increased chance of developing immunologic urticarial dermatitis. Chefs, florists and gardeners, for instance, are at a high risk.¹³ Apium graveolens, also known as celery, is a common culprit.¹⁴ The urticaria seen clinically is due to an IgE-mediated reaction that causes release of vasodilators from activated mast cells and basophils. The symptoms appear after repeated contact with an allergen.^12,13 Patients present with pruritus, erythema and swelling, usually within 30 to 60 minutes of exposure. Urticaria may also spread to areas beyond the site of contact and become generalized.¹³ These symptoms may resolve spontaneously or with the use of oral antihistamines.¹⁵

In contrast, toxin-mediated urticaria is due to the direct release of vasodilators, including histamine, acetylcholine, prostaglandins and serotonin, by the plants, when sharp hairs on their leaves come in contact with skin. It occurs without prior sensitization and is seen more frequently than immune-mediated contact urticaria. The skin lesions are limited to the site of contact and systemic symptoms are rare.¹³ A common plant to cause such a reaction is Urtica dioica, or the stinging nettle, found in moist wooded areas of the northern hemisphere. Clinically, patients may also experience paresthesias, secondary to the release of neurotoxic mediators.¹⁶

Irritant Dermatitis

Irritant dermatitis is further classified into mechanical dermatitis and chemical dermatitis.^9,10 Mechanical irritant dermatitis is caused by physical injury to the epidermis by the spines or glochids of plants. Parts of the plant get lodged in the skin, causing a local irritation by the foreign object. Contrary to the belief of most patients, the smaller the penetrating part, the more severe the clinical presentation may be, mainly because smaller penetrators will be present in larger numbers on a single plant. As a result, glochids can be easily transferred by clothing, making them more difficult to remove. The spines and glochids usually cause erythematous papules, nodules and, infrequently, a granulomatous response if retained within the skin. On occasion, a central black, pin point-size dot with surrounding erythema may be seen, indicating the entrance of a glochid or spine. Cacti are infamous for creating such a reaction due to their spines, although immunologic dermatitis can also ensue. Cacti are commonly found in North and South America, primarily in dry regions. Opuntia spp., or the prickly pear, is the largest genus of the cacti family, and contains multiple spines and glochids per plant.⁹

Chemical dermatitis is due to plants that contain irritants, which are released into the epidermis upon exposure. Many plants known to cause this type of reaction contain calcium oxalate, saponins and cyanogenic glycosides, among other irritants. Dieffenbachia spp., from the Araceae family, is a common decorative plant found in many homes. When the plant comes in contact with a moist surface, such as recently washed hands, the leaves are triggered to release calcium oxalate and histamine. These chemicals allow the penetration of other plant irritants — such as saponins, in the case of Dieffenbachia spp. — resulting in a spectrum of symptoms including salivation, edema and the appearance of bullae. Dermatitis secondary to Dieffenbachia spp. is common in children and pets, as they are more likely to accidently consume the leaves of the plant.¹⁰ Sansevieria trifasciata, also known as Mother-in-Law’s Tongue or snake plant, is another common house plant that contains saponins and calcium oxalate (see Figure 1, left). Though the risk of toxicity is low, it can cause a mild dermatitis.^17,18

Another common chemical plant dermatitis we see is “chili burn,” also known as “Hunan hand syndrome,” which occurs in individuals who handle chili peppers. Chili peppers, in addition to other spices and plants, are part of the Capsicum genus. The chemical irritant is the capsaicin, which causes a depolarization of nerves and vasodilation. Patients present with intense burning and erythema. Treatment includes washing the exposed areas with cold water and then immersing it in vegetable oil, which aids in removal of the fat-soluble capsaicin. Vinegar (5% acetic acid) may also be useful in reduction of the burning sensation.¹⁹

Phytophotodermatitis

Phytophotodermatitis is a phototoxic reaction elicited by exposure to a photo-sensitizing agent followed by exposure to ultraviolet (UV) radiation. Apiaceae and Rutaceae are the two most common plant families associated with this type of plant dermatitis. Plants of the Apiaceae family are easily identifiable due to their unique, distinguishing structure. They are composed of umbrels, which are long stalks that form an umbrella-like shape. Hogweed, carrot and celery are more well known members of the family.²⁰ Plants from the Rutaceae family include many citrus fruits such as lime, lemon, bergamot and grapefruit.²¹

Phytophotodermatitis is due to furocoumarins contained within the plant and are activated by UVA. Once activated, the furocoumarins form covalent linkages of DNA that result in damage to the epidermis and dermis. Erythema, edema, bullae and vesicles appear approximately 24 hours following the initial exposure and tend to be painful. Hyperpigmentation is a frequent sequelae of phytophotodermatitis and can take years to resolve.^20,21

Allergic Contact Dermatitis

Allergic contact dermatitis (ACD) is the most common type of plant dermatitis. ACD is due to a type IV- or delayed-type hypersensitivity reaction, which commonly occurs through outdoor exposures. The majority of cases of ACD are due to plants from the Anacardiaceae family, which includes members of the genus Toxicodendron: poison ivy, poison oak and poison sumac.^22,23,24 The species of poison oak are T. diversilobum and T. toxicarium. Poison ivy includes the species T. rybergii and T. radicans. Poison sumac is also known by the species T. vernix.¹⁹ This genus is easily identifiable because they contain a minimum of three leaflets. The most infamous culprit, poison ivy, always contains three leaflets per leaf.

Although the leaves are generally to blame for the vesicular, pruritic lesions of poison ivy, the non-leaf portions of the plant can cause a similar reaction.²² Urushiol, the main allergen of poison ivy, is found in the oleoresinous sap of a bruised plant.²⁵ Urushiol is a combination of catechols, penta- or heptadecylcatechols. It does not evaporate and can readily penetrate clothing, skin and shoes.^20,26,27

Catechols with longer side chains or larger number of double bonds are more allergenic and can result in a more pronounced clinical manifestation. It is thought that urushiol can sensitize 70% of patients who come in contact with a plant containing this allergen.²⁰ A plant is considered particularly toxic if its leaves have black spots (see Figure 2, left).²⁸ These black spots appear after urushiol, which is yellow, is oxidized following exposure to air.²⁶

Catechol gains its antigenicity when it binds to proteins in the skin after being oxidized to a quinone intermediate. Another mechanism of activation involves the oxidation of urushiol to free radical intermediates.²⁹ After penetrating the skin, the urushiol-protein complex attaches to Langerhans cells in the epidermis. The allergen is engulfed by the Langerhans cell via endocytosis and processed by partial degradation. The Langerhans cells migrate to regional lymph nodes and present the antigen to CD4 T cells. These T cells proliferate into T-memory and T-effector cells that are urushiol-specific and responsible for the allergic contact dermatitis.^23,29

Damage or injury must occur to the plant in order for urushiol to be released and make contact with the skin.²² If transferred to animals, clothing or other objects, urushiol can easily spread from person to person due to its adhesive character.³⁰ It can also be carried in smoke and inhaled, leading to inflammation of the respiratory tract. Sensitized individuals who come in contact with urushiol develop erythema and papules that develop into vesicles and bullae within two days of exposure.²² In unsensitized individuals, symptoms usually appear in 7 to 10 days. These lesions are generally distributed linearly on the skin.²⁵ The dermatitis can sometimes be prevented if the oleoresin is removed within 10 minutes of initial contact. These symptoms are self-limited and usually resolve within 2 to 3 weeks but it is also possible for new lesions to continue to appear for 1 to 2 weeks after initial contact.²² Each subsequent exposure is likely to be more severe in its clinical presentation and may have a shorter interval period following contact compared to the initial exposure.

There are many plants that cross-react with members of the Toxicodendron genus. The active moiety of poison ivy, poison oak and poison sumac, a 3-n-pentadecylcatechol, is similar to some of the allergens found in other plants. The mango tree, a member of the Anacardiaceae family, is one such plant. It contains urushiol and cardol, a resorcinol.²⁷ Cashew, also a member of the Anacardiaceae family, contains anacardic acid and cardol, both of which have a chemical structure similar to 3-n-pentadecylcatechol.^31,32,33 The Japanese lacquer, Indian marking nut and Rengas trees, all members of the Anacardiaceae family, contain urushiol and have shown to cross react in individuals who are sensitive to poison ivy, oak and sumac.^32,34,35 Smodingium argutum (African poison ivy), grevillea plant and the ginkgo biloba tree (see Figure 3, left), which are not members of Anacardiaceae, also exhibit cross sensitivity to members of the Toxicodendron genus.^34,36,37

Members of the Compositae (Asteraceae) family, or daisy family, are the second most likely plants to elicit ACD. They include sunflowers, dandelion, ragweed (see Figure 4, left) and the common house plant, chrysanthemums, in addition to edible plants such as lettuce and artichoke. Similar to the Anacardiaceae family, plants from the Asteraceae family are also easily identifiable by their appearance. They are generally composed of numerous small flowers or florets that cluster to form a head or capitulum. In these plants, the active sensitizer is sesquiterpene lactone (SQL), located within the leaves, flowers or stems of the plant. Dead plants will spread SQL by their hairs, which are easily carried by the wind; therefore, its presentation can be similar to that of an airborne dermatitis. Patients with a history of exposure to these plants will report flares during the summer months that may develop into a chronic pruritic condition following repeated exposure.³⁸ Dermatitis secondary to SQL is more common in adult men than it is in women or children. Liverworts, specifically the species Frullania dilatata and Frullania tamarisci of the Jubulaceae family, are known to cause ACD that has a similar clinical presentation as Asteraceae-induced dermatitis. This dermatitis usually occurs in forest workers during the wet winter months instead of the summer months, as seen with the Compositae family.^20,39

Allergy to Plant Extracts

Plant dermatitis can also occur after the use of certain cosmetics and topical medications that contain botanical extracts. For example, Arnica montana produces SQL and is often found as a component of ointments used to treat musculoskeletal pain and in pill form for the treatment of bruises. Anthemis nobilis and Matricaria chamomilla are chamomile plants that are brewed into teas and then used topically to relieve pain from burns and infections. These herbs have all been reported to cause contact dermatitis.^40-43 In the summer, plant-related dermatitis is a frequent cause of contact dermatitis. A careful history can help in determining the suspect plant, and patient education may reduce the risk and recurrence of contact dermatitis episodes.

Practicals of Patch Testing

As mentioned above, patch testing is often necessary to distinguish ACD from other causes of dermatitis and to identify the responsible allergen(s). Plant hypersensitivity can be determined by testing different parts of the plant: petals, pollen, leaf and stem. Prior to testing, the plant should be washed to remove potential fungal contamination. The stem, leaf and petals are cut into fine pieces, placed in individual plastic or aluminum chambers and applied to the upper back with hypoallergenic adhesive tape. The patches are removed after 48 hours and a preliminary reading of the test site is performed; another reading is performed 72-96 hours following the application of the patches. Unknown plants should not be tested. The test may need to be performed on controls to verify allergenicity and rule out irritancy. Screening patch test trays isolate the most common chemicals and offer the provider clues to potential sources. The North American Standard Series includes allergens from several different categories.⁴⁴ Supplemental plant trays containing common plant allergens are also available.

Pearls of Treatment: Every Dose Counts

It is possible to be exposed to, and subsequently sensitized to, a contact allergen in a plant for days to years before demonstrating the clinical picture of ACD. With some plants, however, such as poison ivy, the binding of the allergen to the skin and subsequent immune stimulation may result in a brisk cutaneous response at the next exposure.

Poison ivy dermatitis can be prevented by avoiding contact with the plant. Correct identification of this plant can be difficult because its appearance varies with the season and by geographical location. If an individual is exposed, washing the skin with soap and water within 5 minutes can potentially prevent an eruption. Protective barriers such as clothing and creams can be used if contact is anticipated. Bentoquatam, also known as Ivy Block, contains quaternium-18 bentonite, a compound that has been effective in preventing or reducing the severity of poison ivy, oak and sumac dermatitis. Other blocking agents include Ivy Off, Ivy–Shield, Stokogard Outdoor Cream, Hollister Moisture Barrier and Hydropel Moisture Barrier. They all work by preventing urushiol from penetrating the skin.

When personal care products contain plant extracts, avoidance can prove to be a tedious task. There are, however, programs to aid in this endeavor. Both the Contact Allergen Management Program (CAMP), a service offered through the American Contact Dermatitis Society (ACDS),⁴⁵ and the Contact Allergen Replacement Database (CARD), developed by Mayo Clinic,⁴⁶ allow a provider to enter a patient’s known contact allergens and produce a “shopping list” of products void of those particular chemicals. These programs also have the ability to exclude cross-reactors.

Dr. Jacob, the Section Editor of Allergen Focus, is Associate Clinical Professor of Medicine and Pediatrics WOS (Dermatology) at the University of California, San Diego. Disclosure: Dr. Jacob is the principal investigator for Smartchoice USA PREA-2 trial.

Allergic contact dermatitis (ACD) is an important disease that notably affects 14.5 million Americans each year.¹ The economic impact of this disease is high in terms of both patient morbidity and loss of income, school and work, not to mention significant expenditures for visits to health care providers and for medicaments.¹ Once patch testing is performed and a culprit has been identified, education becomes the critical intervention to ensure adherence to an avoidance regimen. With allergen avoidance, remission of the dermatitis ensues. If patients are unable to comply with the avoidance regimen, they are at risk for recurrent or sustained dermatitis or progression to a systematized presentation.^2,3 In fact, education of the patient often begins before the diagnostic patch test is ever placed. This ensures that the patient has an appropriate understanding of potential outcomes, including his or her central role in both the disease and treatment.

At the initial consultation, patients are often taught about the pathophysiology of ACD: its delayed presentation, its relationship with the immune system (sensitization to a chemical and then elicitation of a dermatitis with re-exposure), and its occurrence at any point in time, even to something that the patient has been using regularly for a short period of time or even intermittently for years. In certain cases, the other key players, such as irritant contact dermatitis (ICD) and contact urticaria, may be explained by the patient history, as this information, not patch testing, can point to these as the correct diagnosis for the patient. It is important to note that ICD, the most prevalent form of contact dermatitis, can, at times, precede or be a concomitant diagnosis with ACD.^4,5 Unlike ACD, ICD is not immune mediated, occurring secondary to contact with an irritating or abrasive substance. Contact urticaria (wheal and flare reaction), on the other hand, represents the least prevalent form of ACD. It is important to note that it is an immune-mediated phenomenon whose hallmark is an IgE and mast cell-mediated, immediate-type hypersensitivity reaction. We acknowledge this form of hypersensitivity due to the severity of the potential deleterious anaphylactic type reactions and direct the reader to key sources.^6,7,8

In this section, we highlight plant ACD and explore top relevant allergens, regional-based dermatitis presentations, topic-based dermatitis presentations and clinical tips and pearls for diagnosis and treatment.

Plant-Associated Dermatitis

Plant-associated dermatitis is commonly seen in both primary care and dermatology clinics. Clinicians should be aware of the vast array of reactions that can occur following exposure to plants and that reactions differ based on the species as well as the route of exposure. Many of the plants noted for causing clinical symptoms are common species that patients can come in contact with on a daily basis, including hot peppers, daffodils and garlic. Generally, cutaneous manifestations can be classified into four basic reactions: urticarial, irritant, phototoxic (phytophotodermatitis) and allergic.^9-12 We will primarily focus on allergic contact dermatitis, but will first briefly discuss the clinical significance of the three other reactions.

Contact Urticaria

Urticaria after exposure to a plant can be secondary to either an immune response or a toxin-mediated response.¹³ Individuals who have frequent exposure to fresh fruits and vegetables have an increased chance of developing immunologic urticarial dermatitis. Chefs, florists and gardeners, for instance, are at a high risk.¹³ Apium graveolens, also known as celery, is a common culprit.¹⁴ The urticaria seen clinically is due to an IgE-mediated reaction that causes release of vasodilators from activated mast cells and basophils. The symptoms appear after repeated contact with an allergen.^12,13 Patients present with pruritus, erythema and swelling, usually within 30 to 60 minutes of exposure. Urticaria may also spread to areas beyond the site of contact and become generalized.¹³ These symptoms may resolve spontaneously or with the use of oral antihistamines.¹⁵

In contrast, toxin-mediated urticaria is due to the direct release of vasodilators, including histamine, acetylcholine, prostaglandins and serotonin, by the plants, when sharp hairs on their leaves come in contact with skin. It occurs without prior sensitization and is seen more frequently than immune-mediated contact urticaria. The skin lesions are limited to the site of contact and systemic symptoms are rare.¹³ A common plant to cause such a reaction is Urtica dioica, or the stinging nettle, found in moist wooded areas of the northern hemisphere. Clinically, patients may also experience paresthesias, secondary to the release of neurotoxic mediators.¹⁶

Irritant Dermatitis

Irritant dermatitis is further classified into mechanical dermatitis and chemical dermatitis.^9,10 Mechanical irritant dermatitis is caused by physical injury to the epidermis by the spines or glochids of plants. Parts of the plant get lodged in the skin, causing a local irritation by the foreign object. Contrary to the belief of most patients, the smaller the penetrating part, the more severe the clinical presentation may be, mainly because smaller penetrators will be present in larger numbers on a single plant. As a result, glochids can be easily transferred by clothing, making them more difficult to remove. The spines and glochids usually cause erythematous papules, nodules and, infrequently, a granulomatous response if retained within the skin. On occasion, a central black, pin point-size dot with surrounding erythema may be seen, indicating the entrance of a glochid or spine. Cacti are infamous for creating such a reaction due to their spines, although immunologic dermatitis can also ensue. Cacti are commonly found in North and South America, primarily in dry regions. Opuntia spp., or the prickly pear, is the largest genus of the cacti family, and contains multiple spines and glochids per plant.⁹

Chemical dermatitis is due to plants that contain irritants, which are released into the epidermis upon exposure. Many plants known to cause this type of reaction contain calcium oxalate, saponins and cyanogenic glycosides, among other irritants. Dieffenbachia spp., from the Araceae family, is a common decorative plant found in many homes. When the plant comes in contact with a moist surface, such as recently washed hands, the leaves are triggered to release calcium oxalate and histamine. These chemicals allow the penetration of other plant irritants — such as saponins, in the case of Dieffenbachia spp. — resulting in a spectrum of symptoms including salivation, edema and the appearance of bullae. Dermatitis secondary to Dieffenbachia spp. is common in children and pets, as they are more likely to accidently consume the leaves of the plant.¹⁰ Sansevieria trifasciata, also known as Mother-in-Law’s Tongue or snake plant, is another common house plant that contains saponins and calcium oxalate (see Figure 1, left). Though the risk of toxicity is low, it can cause a mild dermatitis.^17,18

Another common chemical plant dermatitis we see is “chili burn,” also known as “Hunan hand syndrome,” which occurs in individuals who handle chili peppers. Chili peppers, in addition to other spices and plants, are part of the Capsicum genus. The chemical irritant is the capsaicin, which causes a depolarization of nerves and vasodilation. Patients present with intense burning and erythema. Treatment includes washing the exposed areas with cold water and then immersing it in vegetable oil, which aids in removal of the fat-soluble capsaicin. Vinegar (5% acetic acid) may also be useful in reduction of the burning sensation.¹⁹

Phytophotodermatitis

Phytophotodermatitis is a phototoxic reaction elicited by exposure to a photo-sensitizing agent followed by exposure to ultraviolet (UV) radiation. Apiaceae and Rutaceae are the two most common plant families associated with this type of plant dermatitis. Plants of the Apiaceae family are easily identifiable due to their unique, distinguishing structure. They are composed of umbrels, which are long stalks that form an umbrella-like shape. Hogweed, carrot and celery are more well known members of the family.²⁰ Plants from the Rutaceae family include many citrus fruits such as lime, lemon, bergamot and grapefruit.²¹

Phytophotodermatitis is due to furocoumarins contained within the plant and are activated by UVA. Once activated, the furocoumarins form covalent linkages of DNA that result in damage to the epidermis and dermis. Erythema, edema, bullae and vesicles appear approximately 24 hours following the initial exposure and tend to be painful. Hyperpigmentation is a frequent sequelae of phytophotodermatitis and can take years to resolve.^20,21

Allergic Contact Dermatitis

Allergic contact dermatitis (ACD) is the most common type of plant dermatitis. ACD is due to a type IV- or delayed-type hypersensitivity reaction, which commonly occurs through outdoor exposures. The majority of cases of ACD are due to plants from the Anacardiaceae family, which includes members of the genus Toxicodendron: poison ivy, poison oak and poison sumac.^22,23,24 The species of poison oak are T. diversilobum and T. toxicarium. Poison ivy includes the species T. rybergii and T. radicans. Poison sumac is also known by the species T. vernix.¹⁹ This genus is easily identifiable because they contain a minimum of three leaflets. The most infamous culprit, poison ivy, always contains three leaflets per leaf.

Although the leaves are generally to blame for the vesicular, pruritic lesions of poison ivy, the non-leaf portions of the plant can cause a similar reaction.²² Urushiol, the main allergen of poison ivy, is found in the oleoresinous sap of a bruised plant.²⁵ Urushiol is a combination of catechols, penta- or heptadecylcatechols. It does not evaporate and can readily penetrate clothing, skin and shoes.^20,26,27

Catechols with longer side chains or larger number of double bonds are more allergenic and can result in a more pronounced clinical manifestation. It is thought that urushiol can sensitize 70% of patients who come in contact with a plant containing this allergen.²⁰ A plant is considered particularly toxic if its leaves have black spots (see Figure 2, left).²⁸ These black spots appear after urushiol, which is yellow, is oxidized following exposure to air.²⁶

Catechol gains its antigenicity when it binds to proteins in the skin after being oxidized to a quinone intermediate. Another mechanism of activation involves the oxidation of urushiol to free radical intermediates.²⁹ After penetrating the skin, the urushiol-protein complex attaches to Langerhans cells in the epidermis. The allergen is engulfed by the Langerhans cell via endocytosis and processed by partial degradation. The Langerhans cells migrate to regional lymph nodes and present the antigen to CD4 T cells. These T cells proliferate into T-memory and T-effector cells that are urushiol-specific and responsible for the allergic contact dermatitis.^23,29

Damage or injury must occur to the plant in order for urushiol to be released and make contact with the skin.²² If transferred to animals, clothing or other objects, urushiol can easily spread from person to person due to its adhesive character.³⁰ It can also be carried in smoke and inhaled, leading to inflammation of the respiratory tract. Sensitized individuals who come in contact with urushiol develop erythema and papules that develop into vesicles and bullae within two days of exposure.²² In unsensitized individuals, symptoms usually appear in 7 to 10 days. These lesions are generally distributed linearly on the skin.²⁵ The dermatitis can sometimes be prevented if the oleoresin is removed within 10 minutes of initial contact. These symptoms are self-limited and usually resolve within 2 to 3 weeks but it is also possible for new lesions to continue to appear for 1 to 2 weeks after initial contact.²² Each subsequent exposure is likely to be more severe in its clinical presentation and may have a shorter interval period following contact compared to the initial exposure.

There are many plants that cross-react with members of the Toxicodendron genus. The active moiety of poison ivy, poison oak and poison sumac, a 3-n-pentadecylcatechol, is similar to some of the allergens found in other plants. The mango tree, a member of the Anacardiaceae family, is one such plant. It contains urushiol and cardol, a resorcinol.²⁷ Cashew, also a member of the Anacardiaceae family, contains anacardic acid and cardol, both of which have a chemical structure similar to 3-n-pentadecylcatechol.^31,32,33 The Japanese lacquer, Indian marking nut and Rengas trees, all members of the Anacardiaceae family, contain urushiol and have shown to cross react in individuals who are sensitive to poison ivy, oak and sumac.^32,34,35 Smodingium argutum (African poison ivy), grevillea plant and the ginkgo biloba tree (see Figure 3, left), which are not members of Anacardiaceae, also exhibit cross sensitivity to members of the Toxicodendron genus.^34,36,37

Members of the Compositae (Asteraceae) family, or daisy family, are the second most likely plants to elicit ACD. They include sunflowers, dandelion, ragweed (see Figure 4, left) and the common house plant, chrysanthemums, in addition to edible plants such as lettuce and artichoke. Similar to the Anacardiaceae family, plants from the Asteraceae family are also easily identifiable by their appearance. They are generally composed of numerous small flowers or florets that cluster to form a head or capitulum. In these plants, the active sensitizer is sesquiterpene lactone (SQL), located within the leaves, flowers or stems of the plant. Dead plants will spread SQL by their hairs, which are easily carried by the wind; therefore, its presentation can be similar to that of an airborne dermatitis. Patients with a history of exposure to these plants will report flares during the summer months that may develop into a chronic pruritic condition following repeated exposure.³⁸ Dermatitis secondary to SQL is more common in adult men than it is in women or children. Liverworts, specifically the species Frullania dilatata and Frullania tamarisci of the Jubulaceae family, are known to cause ACD that has a similar clinical presentation as Asteraceae-induced dermatitis. This dermatitis usually occurs in forest workers during the wet winter months instead of the summer months, as seen with the Compositae family.^20,39

Allergy to Plant Extracts

Plant dermatitis can also occur after the use of certain cosmetics and topical medications that contain botanical extracts. For example, Arnica montana produces SQL and is often found as a component of ointments used to treat musculoskeletal pain and in pill form for the treatment of bruises. Anthemis nobilis and Matricaria chamomilla are chamomile plants that are brewed into teas and then used topically to relieve pain from burns and infections. These herbs have all been reported to cause contact dermatitis.^40-43 In the summer, plant-related dermatitis is a frequent cause of contact dermatitis. A careful history can help in determining the suspect plant, and patient education may reduce the risk and recurrence of contact dermatitis episodes.

Practicals of Patch Testing

As mentioned above, patch testing is often necessary to distinguish ACD from other causes of dermatitis and to identify the responsible allergen(s). Plant hypersensitivity can be determined by testing different parts of the plant: petals, pollen, leaf and stem. Prior to testing, the plant should be washed to remove potential fungal contamination. The stem, leaf and petals are cut into fine pieces, placed in individual plastic or aluminum chambers and applied to the upper back with hypoallergenic adhesive tape. The patches are removed after 48 hours and a preliminary reading of the test site is performed; another reading is performed 72-96 hours following the application of the patches. Unknown plants should not be tested. The test may need to be performed on controls to verify allergenicity and rule out irritancy. Screening patch test trays isolate the most common chemicals and offer the provider clues to potential sources. The North American Standard Series includes allergens from several different categories.⁴⁴ Supplemental plant trays containing common plant allergens are also available.

Pearls of Treatment: Every Dose Counts

It is possible to be exposed to, and subsequently sensitized to, a contact allergen in a plant for days to years before demonstrating the clinical picture of ACD. With some plants, however, such as poison ivy, the binding of the allergen to the skin and subsequent immune stimulation may result in a brisk cutaneous response at the next exposure.

Poison ivy dermatitis can be prevented by avoiding contact with the plant. Correct identification of this plant can be difficult because its appearance varies with the season and by geographical location. If an individual is exposed, washing the skin with soap and water within 5 minutes can potentially prevent an eruption. Protective barriers such as clothing and creams can be used if contact is anticipated. Bentoquatam, also known as Ivy Block, contains quaternium-18 bentonite, a compound that has been effective in preventing or reducing the severity of poison ivy, oak and sumac dermatitis. Other blocking agents include Ivy Off, Ivy–Shield, Stokogard Outdoor Cream, Hollister Moisture Barrier and Hydropel Moisture Barrier. They all work by preventing urushiol from penetrating the skin.

When personal care products contain plant extracts, avoidance can prove to be a tedious task. There are, however, programs to aid in this endeavor. Both the Contact Allergen Management Program (CAMP), a service offered through the American Contact Dermatitis Society (ACDS),⁴⁵ and the Contact Allergen Replacement Database (CARD), developed by Mayo Clinic,⁴⁶ allow a provider to enter a patient’s known contact allergens and produce a “shopping list” of products void of those particular chemicals. These programs also have the ability to exclude cross-reactors.

Dr. Jacob, the Section Editor of Allergen Focus, is Associate Clinical Professor of Medicine and Pediatrics WOS (Dermatology) at the University of California, San Diego. Disclosure: Dr. Jacob is the principal investigator for Smartchoice USA PREA-2 trial.