Botanical Aspects

Becoming familiar with basic botanical nomenclature will help clinicians to better understand the literature that addresses plant-related dermatoses .

Patch Testing

Details of patch testing are beyond the scope of this chapter (see Ch. 14 ). The reader is also referred to the paper by Mitchell . The most common allergenic plants and a proposed botanical screening tray are found in Table 17.3 .

Epidemiology

Immunologic contact urticaria is rather uncommon. Approximately 95% of cases are work-related – long-time food handlers with under­lying dermatitis are at greatest risk. However, fully half of patients with “protein contact dermatitis” (a type IV eczematous eruption arising from repeated type I urticarial reactions) are not atopic.

Examples of reported urticants include common vegetables (e.g. celery, onions, potatoes, lettuce), fruits (e.g. tomatoes, bananas, lemons), herbs (e.g. parsley, dill), nuts, shrubs, algae, lichens, trees and grasses.

Pathogenesis (see Ch. 18 )

IgE-mediated release of vasoactive mediators from mast cells leads to local urticaria and, rarely, a “contact urticaria syndrome” that includes local wheals plus systemic symptoms involving the nose, throat, lungs, gastrointestinal tract or cardiovascular system. The main cause seems to be histamine release, but prostaglandins, kinins and leukotrienes probably augment the inflammatory response.

Clinical Features

Within 30 minutes of contact with certain fresh foods, affected individuals experience pruritus, erythema, urticarial swelling, and even dyshidrotic-like vesicles. Sometimes, individuals only develop symptoms of pruritus, burning or tingling without objective findings . Theoretically, any plant can cause contact urticaria, especially with repeated exposures on the wet, macerated skin of food handlers. Cooking, processing, deep-freezing or crushing fruits and vegetables generally reduces their allergenicity.

Some individuals become cross-sensitized to pollen and similar allergens in fruits or vegetables . Upon eating a cross-reacting food, they experience sudden, IgE-mediated, oral cavity itching, stinging and pain. Edema of the lips, tongue, palate and pharynx typically ensue as the “oral allergy syndrome” (OAS) progresses. Gastrointestinal symptoms and anaphylaxis are possible if enough allergens are ingested. As an example, 70% of European patients with immediate hypersensitivity to birch pollen develop OAS while eating apples, pears, cherries, peaches, plums, apricots, almonds, celery, carrots, potatoes, kiwis, hazelnuts or mangoes. Pollen-associated foods are often, but not always, edible when heated.

The term “protein contact dermatitis” is used to describe a chronic dermatitis in which patch tests are typically negative but prick tests to large protein allergens are positive . Patients develop a chronic dermatitis that acutely urticates within minutes of contact with the offending allergen. This is one of multiple mechanisms by which plants can cause chronic hand and fingertip eczema ( Fig. 17.1 ).

Causes and types of chronic hand or finger dermatitis caused by plants.

Differential Diagnosis and Pathology

See Toxin-Mediated (Non-immunologic) Contact Urticaria and Chs 16 & 18 .

Treatment

Prevention is the preferred form of “treatment”, but oral antihistamines are sometimes helpful. Parenterally administered epinephrine (adrenaline) is required for anaphylactic reactions.

History

Plants causing toxin-mediated urticaria have been used since antiquity as counterirritants in folk medicine, and Native Americans used stinging nettles to treat rheumatism, stomach upset, postpartum hemorrhage, paralysis, fevers, colds and tuberculosis. Stinging nettle is used to produce homemade diuretics, and stem fibers were even used to make cloth until the early twentieth century.

Epidemiology

Urticaceae family members cause the majority of plant-induced contact urticaria. Because all persons exposed to the toxins develop urticaria, toxin-mediated urticaria is far more common than immunologic urticaria. Since very few affected people seek medical attention, the true incidence of toxin-mediated urticaria is unknown. The most common culprit in the US is the stinging nettle ( Urtica dioica ; Fig. 17.2A ) , which is widely scattered throughout the northern hemisphere (except in lowland tropical areas), especially in moist woods, roadsides and on waste land. Other common urticating plants are listed in Table 17.4 .

Stinging nettle ( Urtica dioica ).

A Note the trichomes on both the stem and the leaf surfaces. B Broken trichome from the stinging nettle ( Urtica dioica ). A bubble is visible where urticating chemicals are found.

B with permission from McGovern TW, Barkley TM. Botanical briefs: stinging nettle – Urtica dioica L. Cutis. 1998;62:63–4; © Quadrant Health Com Inc.

Pathogenesis (see Ch. 18 )

Inciting plants possess sharp hairs (trichomes) on leaves and stems (see Fig. 17.2A ). The proximal silicaceous hair is attached to a distal calcified portion that possesses a terminal bulb. When rubbed against, the bulb dislodges to reveal a beveled, hypodermic needle-like, hollow hair ( Fig. 17.2B ). The latter releases an irritant chemical cocktail (histamine, acetylcholine, serotonin) that supposedly serves as a defense mechanism against herbivores.

Clinical Features

Wheals achieve maximal size 3 to 5 minutes after contact, and erythema, burning and pruritus last 1–2 hours. Paresthesias may last 12 hours or more. Although histamine, acetylcholine and serotonin explain the early cutaneous reaction, they do not account for the persistent paresthesias.

Reactions to stinging nettle pale in comparison to those elicited by members of the Dendrocnide genus of the Urticaceae family. These trees grow up to 40 meters tall in eastern Australian rainforests. Young shoots are covered with stiff stinging hairs. Severe urticaria from these may last for weeks, and contact with water or cold objects reactivates the urticaria. Severe, intermittent, stabbing pains may follow the course of lymphatics. Human and animal deaths due to Dendrocnide contact have been documented.

Pathology (see Ch. 18 )

Five minutes after contact with Urtica dioica , dermal edema and telan­giectasias with or without mild spongiosis are seen. At 12 hours, the edema resolves but vasodilation persists. Some patients develop spongiosis in conjunction with a neutrophilic and/or lymphocytic infiltrate. Mast cells are observed within the papillary dermis at 12 hours, but not at 5 minutes.

Differential Diagnosis (see Ch. 18 )

Although the evaluation of such patients is difficult, office testing of suspected allergens or toxin-containing plants may involve one of several methods . The most sensitive tests for immunologic contact urticaria are the prick and scratch-chamber tests. For the scratch-chamber test, a 5-mm scratch is made on the back or forearm. Test material is applied and occluded with a Finn chamber for 15 minutes. The site is examined following Finn chamber removal and every 15 minutes for an hour. After reading, the chamber can be replaced for 48 hours to test for delayed hypersensitivity.

The open application test provides the most reliable way to test for toxin-mediated urticaria. Samples (0.1 ml) from a series of dilutions are each spread onto discrete 3 × 3 cm areas of skin. Sites are observed every 10–15 minutes for an hour. Maximal erythema and edema typically occur 30–40 minutes after application.

Treatment

Most stings are benign, self-limited, and require no treatment. Trichomes may be removed with glue and gauze as described in the next section. Topical pramoxine or oral analgesics may provide some symptomatic relief.

Epidemiology

Mechanical irritant dermatitis can affect anyone. Many plants, including most cacti, can inflict mechanical injury via small or large emergences. Generally, the amount of damage to the skin is inversely proportional to the size of the emergence. Many of the plant families that can cause mechanical irritant dermatitis are listed in Table 17.5 .

Pathogenesis

Whereas cacti possess large spines, their smaller glochids cause more notorious dermatologic problems. The glochids – tufts of hundreds of short, barbed or hooked hairs – arise from pincushion-like structures called “areoles”, from which larger spines may also arise. The minute, barbed glochids ( Fig. 17.3A ) often point outward and backward like a fishhook and produce considerable irritation and pruritus after penetrating the skin. For example, Opuntia microdasys (“polka dot cactus”, “bunny ears cactus”), a house and garden favorite, bears disarming-appearing “fluffy” clusters of 100–200 glochids on its pads (see Fig. 17.12 ).

Prickly pears ( Opuntia spp.) and their glochids.

A Microscopic appearance of glochids from Opuntia microdasys . B Prickly pear ( Opuntia ficus-indica ) habit. C Prickly pear ( Opuntia ficus-indica ) fruit. Fine spines and glochids are visible.

Courtesy, Dirk Elston, MD.

Clinical Features

One form of glochid dermatitis from prickly pears ( Opuntia spp.) is “Sabra dermatitis”, a pruritic, papular eruption that occurs among prickly-pear pickers and those who unwarily stumble into burglar-proof hedges of this native Mexican plant ( Fig. 17.3B ). The fruit contains the highest concentration of glochids ( Fig. 17.3C ) and the ensuing eruption can resemble fiberglass dermatitis or scabies. Prickly pears should be picked only when wetted, and harvesting should cease when it is windy, since the glochids can become airborne.

All 200 or so species of Opuntia are native to the New World, ranging from New England and British Columbia southward to the Straits of Magellan. Numerous species have become established in the Mediterranean basin, South Africa, South Asia and Australia.

Spine and thorn injuries can be complicated by the inoculation of microorganisms such as Clostridium tetani and Staphylococcus aureus into the skin. Grasses, sphagnum moss and rose thorns can transmit Sporothrix schenckii . Atypical mycobacteria such as Mycobacterium kansasii (blackberries), M. marinum (cactus spines), and M. ulcerans (spiky tropical vegetation) have also added infectious insult to mechanical injury.

Treatment

In a controlled study in rabbits, Opuntia glochids were most effectively removed by first detaching the larger clumps with tweezers and then applying glue and gauze to the affected area. After the glue dried, the gauze was grasped and peeled off, resulting in the removal of 95% of implanted glochids .

History

Plant-derived irritant chemicals have been recognized for centuries. Native Mexican Indians once used smoke from burning peppers ( Capsicum [Solanaceae]) as a weapon against enemies, and latex from the manchineel tree ( Hippomane mancinella [Euphorbiaceae]) was used by Caribbean people as poison for arrow tips.

Epidemiology

Several major plant families found throughout the world contain chemical irritants ( Table 17.6 ).

Pathogenesis, Clinical Features and Treatment (see Ch. 15 )

Calcium oxalate, one of the most common chemical irritants, is found in Dieffenbachia picta (Araceae), a plant that decorates millions of homes and public places. Upon contact with a moist surface, the leaves release water-insoluble calcium oxalate. When leaves are chewed, salivation, burning, mucosal edema, and blistering ensue. This causes hoarseness or aphonia (hence the common name “dumb cane”). Treatment includes parenteral corticosteroids, antacid mouthwashes, and analgesics; antihistamines are of no benefit. The pain and edema wane over 4–12 days.

Calcium oxalate enhances the irritancy of other chemicals, including the proteolytic enzyme bromelain (bromelin) found in pineapples. Pineapple workers often develop cracks, fissures, fingerprint loss, and microhemorrhages on their hands. Calcium oxalate-induced microabrasions allow bromelain to exert its proteolytic effect on dermal blood vessels. Nitrile gloves can be worn for protection.

Bulb dermatitis, though less dramatic, is more common . Daffodil sap, found not only in bulbs but also in stems and leaves, contains calcium oxalate and causes “daffodil itch”, probably the most common dermatitis in florists. Dryness, scaling, fissures and erythema develop on the fingertips, hands and forearms. Bulbs of several other plants (e.g. tulips, hyacinths) also commonly cause dermatitis. Allergens found in garlic bulbs act as irritants at high concentrations leading to second- and third-degree burns as well as subungual hyperkeratosis and hemorrhage that can mimic nail psoriasis.

While spurges are notorious for their irritant latex, they derive their common name from the purgative properties of their seeds. The milky latex contains irritant phorbol esters, diterpenes, and daphnane esters that may cause a painful, blistering dermatitis and even temporary blindness if the latex contacts the eye. Sitting under a manchineel tree in the Caribbean during a rainstorm will lead to intense cutaneous burning, erythema and bullae, often accompanied by periocular swelling through transfer of the latex by rain. The fruit of this tree is known locally as the “apple of death”. The latex of the best-known family member, the poinsettia ( Euphorbia pulcherrima ), is only mildly irritating.

Buttercups (Ranunculaceae) contain the glycoside ranunculin that is converted to protoanemonin after plant injury. Protoanemonin causes severe, linear vesiculation that may resemble early phytophotodermatitis, but no hyperpigmentation ensues. Because protoanemonin rapidly polymerizes to the non-irritant anemonin, only freshly damaged plants cause reactions.

“Chili burns” commonly occur among those who remove skins from large batches of roasted chili peppers ( Capsicum annuum ). When applied to skin, the active principle, capsaicin, depolarizes nerves causing vasodilation, smooth muscle stimulation, glandular secretion, and sensory nerve activation. Because only nerves are affected, there is erythema but no vesicles or bullae. Symptoms may be delayed and last hours to days. The best home remedy for chili burns is handwashing with soap and water followed immediately by 1 hour of immersion in vegetable oil to remove the fat-soluble capsaicin.

The “century plant” ( Agave americana ) grows in temperate, subtropical and tropical climates and forms rosettes of tough, sword-shaped leaves with spiny margins. The marked pruritus and stinging that follows within five minutes of contact with the agave leaf is thought to be caused by latex-derived calcium oxalate crystals and saponins. Purpura may appear subsequently. Soldiers have been known to try to “earn” sick leave by rubbing broken leaves on their skin to induce a severe vesiculopustular irritant dermatitis, often accompanied by systemic symptoms .