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This article describes the clinical presentation, differential diagnosis, and treatment of 2 unrelated cases with different presentations of black-spot Toxicodendron dermatitis. In the first case, a healthy 7-y-old male presented with a rash consisting of black dots with localized surrounding erythema on the left arm. The rash then progressed to a vesicular, pinpoint, raised rash spreading to the face, arms, and neck. In the second case, a 4-y-old male presented with non-pruritic, black, flat, non-erythematous lesions that did not progress. This patient's older sibling had been diagnosed with poison ivy 1 wk prior, and they attended the same child care where the poison ivy was thought to be acquired. In both cases, diagnosis of black-spot Toxicodendron dermatitis was made. The black spot of Toxicodendron dermatitis is caused by urushiol oxidation on exposure to air. The subject may or may not go on to develop allergic contact dermatitis after the exposure. Diagnosis of this dermatitis is made on clinical presentation, with careful consideration of history, distribution, and lesion morphology. When allergic dermatitis does develop as in the first case, systemic treatment with oral steroids is recommended. In both of these cases the black dots completely resolved in 2 to 3 wk. Dermatologic referral for dermoscopy and biopsy may be necessary if the dermatosis does not resolve as anticipated.

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Rhus chicken is a common traditional remedy used to cure gastrointestinal diseases and as a health food in Korea. Unfortunately, systemic contact dermatitis (SCD) due to the ingestion of Rhus occasionally occurs. In this study, the clinical and laboratory findings were reviewed and analysed for 30 Korean patients with SCD developing after ingestion of Rhus chicken. Summer was found to be the commonest period for hospital visits because of this condition. The mean period of incubation for SCD, was 4 ± 1.5 days. The commonest skin features were generalized maculopapular eruptions. Of the 30 patients, 10 had a known history of allergy to Rhus chicken. Many of the patients developed neutrophilia and leucocytosis. All the patients responded well to standard treatments. The commonest reason for their ingestion of Rhus chicken was indigestion. We conclude that SCD often occurs in Koreans after ingestion of Rhus chicken. Patients should be educated about the harmful effects of Rhus chicken and advised not to ingest it.

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In black-spot poison ivy dermatitis, a black lacquerlike substance forms on the skin when poison ivy resin is exposed to air. Although the Toxicodendron group of plants is estimated to be the most common cause of allergic contact dermatitis in the United States, black-spot poison ivy dermatitis is relatively rare.

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BACKGROUND: We present two cases of Toxicodendron dermatitis, one acquired in the United States but presenting in the United Kingdom (UK), the other a recurrent dermatitis following importation of the plant to the UK. Poison ivy, poison oak and poison sumac are native to North America and belong to the genus Toxicodendron. This group of plants is of interest to the dermatologist because they contain a mixture of potent sensitisers which cause a severe allergic contact dermatitis. CONCLUSIONS: The dermatitis can present to the dermatologist in Europe after an individual has been in contact with the plant whilst visiting an endemic area. The plants have the potential to grow in Europe and it is therefore possible for an individual to be sensitised and subsequently to develop the rash without leaving the continent.

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Allergic contact dermatitis caused by the Toxicodendron (formerly Rhus) species-poison ivy, poison oak, and poison sumac-affects millions of North Americans every year. In certain outdoor occupations, for example, agriculture and forestry, as well as among many outdoor enthusiasts, Toxicodendron dermatitis presents a significant hazard. This review considers the epidemiology, identification, immunochemistry, pathophysiology, clinical features, treatment, and prevention of this common dermatologic problem. Recent research in prevention is emphasized, and resources to help in the identification of plants are provided in the bibliography. The literature was searched using a MEDLINE query for "Toxicodendron dermatitis", and the identified article bibliographies were searched as well.

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We report three paediatric cases of severe allergic contact dermatitis caused by a Japanese lacquer tree (Rhus verniciflua), which is a rare specimen plant in the UK. The diagnosis of allergic contact dermatitis produced by plants that are not indigenous to a particular country is more likely to be delayed, as well as mistaken for cellulitis.

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In successive years, three members of the same family (a man and woman aged 46 years and their son, aged 20) constantly developed severe pruritic, erythematous, vesicular and bullous dermatitis in the spring and summer after working in the garden. Although the findings were consistent with a photophytotoxic dermatitis, the causative plant remained unclear. Oral therapy with high doses ofprednisolone was necessary. When the man travelled to the USA and visited a doctor there, he recognised the symptoms as those of contact dermatitis caused by poison ivy (Toxicodendron radicans), a plant that is found sporadically in the wild state in Europe. Their grandparents had brought the plant back from a trip to the USA and planted it in the garden because of the beautiful fall colours. The family identified the plant via a search on Internet and eliminated it from the garden completely. Since then, the family has no longer suffered from contact-allergy dermatitis.

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Oral or parenteral exposure to certain contact allergens may elicit an eczematous skin reaction in sensitized individuals. This phenomenon has been called systemic contact dermatitis (SCD) and is relatively rare when compared with classical contact dermatitis. We reviewed and analysed the clinical and immunologic features of 42 patients with SCD caused by ingestion of Rhus (Toxicodendron), 24 males and 18 females, average age 44 years (range 24-72). Several of such patients (33%) had a known history of allergy to lacquer. The patients developed skin lesions such as generalized maculopapular eruptions (50%), erythroderma (29%), vesiculobullous lesions (14%) and erythema multiform (EM)-like lesions (7%). Many patients (57%) developed leucocytosis with neutrophilia (74%). In some patients (5%), abnormalities of liver function developed. We also analysed lymphocyte subsets in the peripheral blood of 12 patients. The lymphocyte subsets studied were T cells (CD3), B cells (CD19), natural killer (NK) cells (CD3-CD16+/CD56+), helper/inducer cells (CD4), cytotoxic/suppressor cells (CD8) and helper/suppressor ratio (CD4/CD8). The lymphocyte subsets of all 12 patients studied were within the normal range. Moreover, there were no differences between patients with a history of allergy to lacquer and those without a history of allergy to lacquer. Therefore, rather than an immunologic response, the skin eruption seems to be caused by a toxic reaction because of Rhus.

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Black-spot poison ivy dermatitis is a rare manifestation of a common condition. It occurs on exposure to the resins of the plants of the Rhus family also known as Toxicodendron. We describe 5 patients with black deposits on their skin and clothing after contact with poison ivy and review the literature reflecting different aspects of this phenomenon including clinical presentation, histologic findings, and historical background.

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Within 3 days two female patients presented with an eruption featuring erythema, edema, vesicles and bullae. We suspected poison ivy allergy which was subsequently proven by history and positive patch tests. In Germany the risk of specific hypersensitivity to Toxicodendron species is low, since the distribution of such plants is confined to botanical gardens. Other species belonging to the family of Anacardiaceae contain urushiols as well (e.g., mango, cashew) and may cause allergic contact dermatitis.

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In Korea, Rhus has been used as a folk medicine to cure gastrointestinal diseases and as a health food. We review the clinicopathological and laboratory findings in patients with systemic contact dermatitis caused by intake of Rhus. We reviewed medical records and histopathological sections from 31 patients during a 10-year period. The male/female ratio was 1.4: 1 and the average age was 43.8 years (range 22-70). Ten patients (32%) had a known history of allergy to lacquer. Rhus was ingested to treat gastrointestinal problems including indigestion and gastritis (45%), and as a health food (39%), in cooked meat, in herbal medicine, or taken by inhalation. The patients developed skin lesions such as a maculopapular eruption (65%), erythema multiforme (EM, 32%), erythroderma (19%), pustules, purpura, weals and blisters. Erythroderma was very frequent in patients with a known history of allergy to lacquer, but maculopapular and EM-type eruptions were more frequently observed in those without a history of allergy. All patients experienced generalized or localized pruritus. Other symptoms included gastrointestinal problems (32%), fever (26%), chills and headache; many developed leucocytosis (70%) with neutrophilia (88%), while some showed toxic effects on liver and kidney. Fifty-nine per cent of patients observed cutaneous or general symptoms within a day after ingestion of Rhus. There was no difference in the time lag for symptoms to develop between patients allergic and not allergic to Rhus. All patients responded well to treatment with systemic steroids and antihistamines. Common histopathological findings were vascular dilatation, perivascular lymphohistiocytic infiltration, and extravasation of red blood cells in the upper dermis. Rhus lacquer should not be ingested in view of its highly allergic and toxic effects.

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Abstract: Epidermal keratinocytes in culture have been shown to produce many cytokines, and their proteins have been identified in skin tissue samples. It has therefore been assumed that these cytokines are transcribed in vivo by the epidermis in response to contact allergens. In this report, in situ hybridization was used to detect the messenger RNAs for interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) in samples of human skin prior to and at various times after application of urushiol, the immunogenic component of poison ivy/oak. In sensitive subjects, IL-1 alpha and TNF-alpha mRNAs showed a progressive increase in transcript levels that paralleled the clinical and histological features of the inflammatory process. The time-course of the IL-1 beta response differed from that of IL-1 alpha and TNF-alpha, in that there was an early (by 6 h after urushiol administration) elevation in IL-1 beta mRNA that occurred before there was evidence of inflammation and had returned to background levels by 72 h when the reaction had reached its peak. In contrast to urushiol-sensitive subjects, urushiol-anergic individuals did not exhibit an increase in IL-1 alpha, IL-1 beta or TNF-alpha mRNA levels. The data provide evidence for an in vivo role for epidermal IL-1 alpha, IL-1 beta and TNF-alpha transcription in the regulation of IL-1 beta and TNF-alpha polypeptide levels in the epidermis in response to this common contact allergen.

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