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Regarding reactions to common plant sources of allergy and injury, prevention is generally key. Because media reports sometimes exaggerate or embellish the impact of insect and plant exposures, dermatologists should stand ready to provide accurate information.
Denver - Regarding reactions to common plant sources of allergy and injury, prevention is generally key.
Because media reports sometimes exaggerate or embellish the impact of insect and plant exposures, says Julian Trevino, M.D., “It’s important for dermatologists to be knowledgeable about the facts relating to these exposures so we can provide our patients and colleagues with accurate information.” He is professor of dermatology at Boonshoft School of Medicine at Wright State University, Dayton, Ohio. Dr. Trevino spoke recently at the annual meeting of the American Academy of Dermatology.
Plant-induced skin reactions can present as urticaria, irritant dermatitis, contact dermatitis or phytophotodermatitis, he says.
“Toxin-mediated contact urticaria is the most common form of plant-induced urticaria and does not have an immunological basis,” Dr. Trevino says. The most common culprits are Urticaceae plants such as the stinging nettle. When people rub against the sharp hairs (trichomes) on the stems and leaves of such plants, he says, a bulb within these hairs discharges irritant chemicals such as histamine, acetylcholine and serotonin into the skin.
“Wheals appear within three to five minutes, with erythema, burning and tingling typically lasting for several hours,” he says. Moreover, Australian stinging trees of the Dendrocnide species have caused severe urticaria lasting for weeks, at least one human death and many equine fatalities.
Conversely, he adds, immunologic contact urticaria usually affects atopics and food handlers. A variety of fresh vegetables, fruits and nuts can be responsible for such reactions. Within 30 minutes of contact, susceptible individuals experience pruritus, urticaria, erythema and perhaps even dyshidrotic-like vesicles, Dr. Trevino says. Rarely, he says, a “contact urticaria syndrome,” which includes wheals with systemic symptoms (of the nose, throat, lungs, gastrointestinal tract and cardiovascular system) can occur.
Treatment for anaphylactic reactions can include epinephrine and antihistamines.
“Prevention is the preferred treatment,” Dr. Trevino says. For example, cooking, deep-freezing, processing or crushing the offending plant parts reduces allergenicity. “Tests of choice for immunologic contact urticaria are the prick test and scratch test,” versus the open application test for toxin-mediated contact urticaria.
Mechanical irritant dermatitis represents the most common form of plant-related dermatosis, Dr. Trevino says. Its symptoms range from mild erythema to hemorrhagic bullae and necrosis. Common causes include cacti and prickly pear bushes, as well as other plants containing thorns, spines or small emergences (glochids) that can lodge within the skin, sometimes causing foreign body granulomas and inoculating microorganisms such as Clostridium tetani, Staphylococcus aureus or Sporothrix schenkii. Treatment involves removing spines, thorns and larger glochids with forceps, Dr. Trevino says. To remove many smaller glochids, “Apply glue and gauze to the site. Let it dry, then peel off the gauze.”
Chemical irritant dermatitis commonly stems from contact with calcium oxalate, which is found in plants ranging from Dieffenbachia (“dumb cane”) to daffodil bulbs. In the former case, contact of Dieffenbachia leaves with a wet surface such as the oral mucosa releases the chemical, which causes increased salivation, mucosal edema and blistering, Dr. Trevino says. This can result in hoarseness or aphonia and require treatment with parenteral steroids. Calcium oxalate in the sap and bulbs of hyacinths and tulips also proves very irritating, he says.
“Additionally, pineapple plants contain calcium oxalate crystals and the cutaneous irritant enzyme bromelain, which can result in fissures and fingerprint loss in workers in the pineapple industry,” he says.
Other potentially perilous plants include buttercups (Ranunculaceae).
“They contain the glycoside ranunculin, which is converted to proteoanemonin after plant injury,” Dr. Trevino says. “This exposure can cause linear vesiculation resembling phytophotodermatitis.”
Somewhat similarly, he says, capsaicin, a component of chili peppers, can cause burns. Additionally, plants of the Euphorbiaceae family (which includes poinsettias and rubber trees) contain a milky sap which can cause skin irritation and, if leaves or fruits are swallowed, can result in vomiting and bloody diarrhea.
To prevent irritant chemical dermatitis from plant exposures, Dr. Trevino recommends wearing gloves over moisturizers or barrier creams applied to the hands. One also can apply vegetable fats high in linoleic acid (e.g., palm plant fats) before handling irritating plants, he says, and it never hurts to educate those who handle plants to recognize potential irritants.
Several plants - most commonly the genus Toxicodendron, which includes poison ivy, poison oak and poison sumac - can cause allergic contact dermatitis, according to Dr. Trevino.
“The allergens responsible for poison ivy/oak allergic contact dermatitis are a mixture of penta- or heptadecylcatechols contained in the oleoresin urushiol,” he says.
Intact plants are generally innocuous.
“Toxicodendron dermatitis is produced by exposure to some portion of the bruised plant, allowing the oleoresin to contact the skin,” Dr. Trevino says. In late fall, however, plants spontaneously release urushiol, and non-leaf portions of plants can induce dermatitis even in winter.
“At least 50 percent of the adult population in North America is allergic to poison ivy/oak,” and the sensitivity appears to be hereditary. The rash of poison ivy presents four to 96 hours after exposure, with pruritic, erythematous patches, often with vesicles arranged in streaks (corresponding to areas where the resin contacted the skin), he says. The fluid within the vesicles and bullae is not antigenic, he notes. As the blisters break, the eruption becomes “weepy,” and areas of crust form.
“Urushiol is water-soluble, so time is of the essence in removing the resin from the skin. Fifty percent of the resin can be removed if rinsed off within 10 minutes; by 30 minutes only 10 percent of the resin can be removed,” he says. Rinsing the skin with water is sufficient to remove urushiol; avoid use of soap as this can potentially expand the area of resin on the skin, he says.
Localized poison ivy rash can be effectively treated with steroid creams, lotions, ointments or foams. Conversely, “A severe, extensive poison ivy rash may require treatment with systemic steroids - prednisone 1 to 2 mg/kg/day tapered over two to three weeks,” Dr. Trevino says. Tepid baths, bland shake lotions (such as calamine), and wet-to-dry soaks (such as aluminum acetate) may provide additional relief. Oral antihistamines also may decrease pruritus, he says.
Patients allergic to poison ivy/oak should be advised that reaction to related plants can occur, he adds. Oil from cashew nut shells, skin of mangoes, and the sap of the Japanese lacquer tree are examples of plants containing substances which cross-react with urushiol.
Phytophotodermatitis is a phototoxic reaction to furocoumarins that produces erythema and delayed hyperpigmentation, Dr. Trevino says. The plant species most often responsible include the following:
Phytophotodermatitis initially presents as an erythematous, vesicular reaction in bizarre configurations 24 to 72 hours after UVA exposure, he says. The reaction impacts sun-exposed areas that also were exposed to the phototoxin. Hyperpigmentation follows one to two weeks later and can last months to years, Dr. Trevino adds. To prevent phytophotodermatitis, he says, avoid planting furocoumarin-containing plants near play areas, cover exposed skin when trimming weeds and promptly wash exposed skin with water (e.g., after squeezing limes for guacamole or margaritas).
Disclosures: Dr. Trevino reports no relevant financial interests.