What Is the Cause of This Man’s Rash?

A 28-year-old man presented for evaluation of a new-onset rash on his back. The patient noted mild pruritus and a burning sensation. He denied any additional symptoms. His past medical history was insignificant, and he was not taking any current medications. The rash began 3 days following the return from a hunting trip in central California, during which he wore the same shirt for 3 days consecutively. Figure 1 shows when the rash was first recognized, displaying clusters of well-demarcated, smooth, erythematous papules and plaques along the midline of his back. The rash continued to grow at a surprising rate, and he eventually developed overlying weeping vesicles. Six days after onset, additional linear lesions were noted on the lower extremities that were not evident during the initial presentation (Figure 2).

What Is Your Diagnosis?

Diagnosis: Toxicodendron dermatitis

Toxicodendron (formerly Rhus) dermatitis is the most common cause of allergic contact dermatitis in North America.¹ It arises from members of the Anacardiaceae family and the Toxicodendron genus, most notably poison oak, poison ivy, and poison sumac. The stems, roots, leaves, and fruits contain an oily resin, called urushiol, which is responsible for the dermatitis.² The plant must undergo trauma to release this resin, so innocuous contact is not sufficient.

Clinical Presentation

Although the onset and duration can be variable, in sensitized individuals, symptoms typically develop 24 to 48 hours after exposure and resolve in 1 to 3 weeks.^3,4 Patients experience marked pruritus, erythema, and, in severe cases, vesicles and bullae (Figure 1). The classic presentation of Toxicodendron dermatitis consists of linear lesions on the extremities (Figure 2). A peculiar sign that sometimes precedes the dermatitis is known as the “black-spot.” It occurs due to oxidation of the resin in the stratum corneum.⁵

The most notable piece of the clinical presentation is the patient’s history. A detailed history of recent exposures is crucial to identifying the source of the lesions. Recent contact with vegetation supports the diagnosis. Urushiol can transfer to clothing, objects, pets, and notoriously harbor under the fingernails.⁶ Secondary exposure from such sources can cause dermatitis that lacks the typical linearity and distribution. Delayed lesions can develop from secondary exposures or if the initial contact was in a region with a thicker stratum corneum. A commonly mistaken factor that does not contribute to further lesions is the fluid in the vesicles and bullae, as it does not contain antigen.²

Geography

Urushiol-containing plants can be found all over the United States. According to the US Department of Agriculture’s PLANTS Database,⁷ Eastern poison ivy (Toxicodendron radicans) and poison sumac (Toxicodendron vernix) inhabit the eastern United States, while Western poison ivy (Toxicodendron rydbergii) inhabits the northern and western halves, except for California (Figure 3).² As their names suggest, Pacific poison oak (Toxicodendron diversilobum) grows along the Pacific coast while Atlantic poison oak can be found in southeastern states. These plants are uncommon above 4000 feet and in dry climates, and they seem to spare Washington and Oregon rain forests.⁶

Differential Diagnosis

Differential diagnoses for this rash included herpes zoster, viral exanthem, prurigo pigmentosa, dermatitis herpetiformis, phytophotodermatitis, irritant contact dermatitis, and urticaria. If this lesion were confined to a dermatomal distribution, there would be a high suspicion for herpes zoster. However, its distribution across midline lessens the suspicion. The initial presentation appeared as a morbilliform viral exanthem, but the patient denied any systemic symptoms, making this diagnosis unfavorable. Prurigo pigmentosa is an inflammatory skin disorder in which pruritic, erythematous papulovesicles erupt on the neck, back, and chest.⁸ Although the rash characteristics may appear similar, it is uncommon, forms a unique reticular pattern, and typically affects young Japanese women.⁸ Rather than the back, dermatitis herpetiformis usually localizes along the extensor surfaces of joints, scalp, buttocks, and proximal forearms.⁹ The region of the rash was not exposed to sunlight, so phytophotodermatitis was ruled out. Irritant contact dermatitis produces a rash soon after exposure and generally lacks vesicles and bullae. The initial presentation could be mistaken for urticaria, but the progression of the rash to a weeping vesicular stage makes urticaria unlikely. For these reasons, combined with the patient’s recent hunting trip and the delayed linear lesions on his lower extremities, the diagnosis of Toxicodendron dermatitis was favored.

Pathophysiology

Like other allergic contact dermatoses, the reaction is mediated by a delayed T-cell response.¹⁰ In this type-IV hypersensitivity reaction, Langerhans cells present components of urushiol to T cells in nearby lymph nodes. In response, the CD4 helper T cells undergo clonal expansion and are primed for re-exposure. Additionally, keratinocytes contribute to the immune response by releasing cytokines.¹¹ Of note, urushiol remains stable at high temperatures, so brush fires can lead to respiratory inflammation.²

Management

Immediately following exposure, a gentle wash with a mild soap should be done. It has been shown that after 10 minutes, 50% can be removed; after 30 minutes, 10% can be removed; and after 60 minutes, the urushiol has been fully absorbed.³ Fingernails and all contaminated clothing, pets, and objects should be cleansed thoroughly. A study compared the effectiveness of an organic solvent marketed as a poison ivy inactivator to that of dishwashing soap, and concluded that both provide significant benefit if used within 2 hours.¹

Many products provide symptomatic relief, such as oatmeal baths, cool compresses, and calamine lotion. Oral antihistamines are often used, but these seem to be beneficial solely for their sedative effects because the pruritus is not histamine-mediated. Topical steroids are helpful prior to vesicular eruption, but the amount required leaves the patient at risk for side effects that may outweigh the potential benefit, especially on the face or genitals.² Another topical immunosuppressive, pimecrolimus, has shown to be ineffective in Toxicodendron dermatitis.¹² For severe cases, systemic corticosteroids for 10 to 21 days have been valuable, but rebound flares can occur if the duration is too short.¹³ Secondary infection can be a complication of Toxicodendron dermatitis. The most common microbes in these infected lesions include Staphylococcus aureus and Streptococcus pyogenes often mixed with anaerobes.¹⁴

Prevention

The key preventative strategy is avoidance, which requires knowledge of morphologic features. As seen in Figure 3, the leaves of poison oak are smooth and lobulated; poison ivy can be smooth or notched; and poison sumac are smooth and oval. Both poison oak and poison ivy can grow as vines. Poison oak can also be found as a bush, while poison ivy can take the form of a shrub with thicker foliage.⁶ Poison sumac grows in boggy areas. Like the adage, “Leaves of three, let them be,” eludes to, poison ivy commonly has its leaves in groups of three; however; in poison oak and sumac, leaves can be found in larger groups.⁶ The plants’ appearances can be variable depending on the season and location. In Autumn, all three species produce green or off-white berries that arise from the leaf axils (the angle between the leaf and the associated twig).⁶ After the leaves fall off in the winter, the remaining stems are still toxic but not as recognizable.² For people with occupational exposure in which avoidance is not feasible, many barrier creams have shown to be effective at preventing or reducing the rash severity.^15,16

Our Patient

Due to the recent exposure to Californian vegetation, Western poison oak was most likely the culprit. Urushiol likely contaminated the patient’s shirt as he navigated through the foliage. The delayed linear demarcations on his lower extremities could have been from a thicker stratum corneum or resin in his fingernails that transferred to his legs upon scratching. An id reaction producing the secondary lesions cannot be excluded. Throughout the course of his dermatitis, the patient experienced minimal pruritus. Self-medicating with calamine lotion and an oral antihistamine before bed was sufficient to control his symptoms. Figure 4 shows the rash at 6 days after the onset. At this point, the rash had completed its vesicular stage and displayed slight post-inflammatory hyperpigmentation along the periphery. By 2 weeks after onset, the patient was completely asymptomatic.

Conclusion

Correct diagnosis of poison oak, ivy, and sumac relies on a comprehensive history of recent exposures. Urushiol can contaminate objects, clothing, and pets, causing secondary reactions in atypical distributions; however, vesicular fluid cannot spread the allergen. Avoidance is the best preventive measure. If affected, one should rinse the exposed region as soon as possible with a gentle soap. Symptomatic treatment can be sufficient in mild cases, but oral corticosteroids may be necessary for severe cases. For everything in between, clinical judgement should be used to determine if the benefit of topical steroids would outweigh the potential harm.  

Ms Brahs is a medical student at Western University of Health Sciences, Pomona, CA, OMS III. Ms Smith is an instructor in the physician assistant program at Western University of Health Sciences, Pomona, CA, and currently practices Internal Medicine in Irvine, CA.

Disclosure: The authors report no relevant financial relationships.  

References for this article can be found at the-dermatologist.com.

References

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16. Marks JG, Fowler JF, Sherertz EF, Rietschel RL. Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite. J Am Acad Dermatol. 1995;33(2 Pt 1):212-216.