Dermatoses Due to Plants

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 ).

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 .

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 ).

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.