Toxicodendron radicans dermatitis with black lacquer deposit on the skin

Four patients with clinical Toxicodendron dermatitis (poison ivy) presented with dramatic black lacquer-like deposits on several lesions. This black deposit was also observed at sites of injury on poison ivy plants and was reproduced on volunteers by the application of plant sap on the skin. Histologically, the observed material was identified in the stratum corneum. This little-recognized phenomenon has been mentioned in past dermatologic literature.     

Black spot poison ivy: A report of 5 cases and a review of the literature.

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.     

Exploring the mango-poison ivy connection: the riddle of discriminative plant dermatitis

A relationship between sensitivity to poison oak or poison ivy and mango dermatitis has been suggested by previous publications. The observation that acute allergic contact dermatitis can arise on first exposure to mango in patients who have been sensitized beforehand by contact with other urushiol-containing plants has been documented previously. We report 17 American patients employed in mango picking at a summer camp in Israel, who developed a rash of varying severity. All patients were either in contact with poison ivy/oak in the past or lived in areas where these plants are endemic. None recalled previous contact with mango. In contrast, none of their Israeli companions who had never been exposed to poison ivy/oak developed mango dermatitis. These observations suggest that individuals with known history of poison ivy/oak allergy, or those residing in area where these plants are common, may develop allergic contact dermatitis from mango on first exposure. We hypothesize that previous oral exposure to urushiol in the local Israeli population might establish immune tolerance to these plants.     

Systemic contact dermatitis to raw cashew nuts in a pesto sauce

Systemic contact dermatitis from the cashew nut shell oil resorcinol allergens cardol and anacardic acid is recognized clinically as a dermatitis with flexural accentuation, typically distributed on the extremities, groin, and buttocks, and occurring generally 1 to 3 days after ingestion of raw cashew nuts contaminated with allergenic oil. We report a case of systemic contact dermatitis to raw cashew nuts, an atypical and unexpected ingredient flavoring an imported pesto sauce. Plants with allergens that potentially cross-react with poison ivy and other Toxicodendrons, and the concepts of systemic contact dermatitis and hyposensitization are reviewed.     

Toxicodendron dermatitis in the UK

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.     

Erythema multiforme‐like eruption associated with plant‐induced allergic contact dermatitis in a pediatric patient: A case report

An 11‐year‐old boy presented to the emergency department 5 days after playing in the forest. His initial eruption, consistent with allergic contact dermatitis to poison ivy, progressed into target lesions involving his extremities, palms, upper trunk, and face, consistent with an erythema multiforme‐like eruption. This report details the case and reviews the literature concerning this atypical and potentially underreported complication of plant‐induced allergic contact dermatitis.     

FS11.5Toxicodendron dermatitis in the United Kingdom

We describe two cases of Toxicodendron dermatitis, one acquired in the United States but presenting in the United Kingdom, the other a recurrent dermatitis following importation 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. 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 the UK and it is therefore possible for an individual to be sensitised and subsequently to develop the rash without leaving the UK. A 35‐year‐old American man who lived in the UK visited his family in Marietta, Georgia USA. Shortly before his return to the UK he cut some plants back in his mother’s garden. Two days following his arrival back in the UK he developed a widespread pruritic and painful vesicobullous eruption. He required admission for intensive potent topical corticosteroid therapy and the eruption settled over the next two weeks. The plant he had been pruning was subsequently identified as poison sumac (Toxicodendron vernix). A 54‐year‐old woman living in Wales was referred to the Contact Dermatitis Investigation Unit because during the summer months for the previous four years she had experienced an intermittent, intensely pruritic, vesicular and in parts linear eruption affecting her face, arms and legs. This responded slowly to potent topical corticosteroids. She is a keen gardener and suspected that it was related to a plant in her garden. She was patch tested to our Standard Series, Plant Series and all the plants in her garden. She showed ++ allergic reactions to sodium metabisulphite, propolis and a strong vesicular reaction to the leaf of one of the plants from her garden Inspection of the plant revealed that it had three leaflets per stem. She had taken a cutting whilst visiting friends in Pennsylvania in 1996 and on returning to the UK had planted it in her garden. It grew but had never flowered or produced seeds. Once the cause of her dermatitis had been confirmed our patient took the necessary protective measures and removed the plant including its roots from her garden. She has not experienced any further problems with her skin. She contacted her friends in the USA who knew precisely where she had picked the plant. A further specimen was taken to the local Conservation Office where it was confirmed to be poisonivy. Poison ivy and poison sumac belong to the genus Toxicodendron which is native to North America and Mexico. They cause an allergic contact dermatitis when there is exposure to a bruised portion of the plant. This leads to the oleoresin, urushiol coming into contact with the skin. 25–60% of North Americans are reported be allergic to poison ivy and its relatives. The importation of plants into the UK is restricted by law. It is clear that this plant grew in its new habitat but did not extend beyond the confines of the garden. With frequent and more extensive air travel it seems reasonable to speculate that similar occurrences have taken place and that plants not endemic to Europe should be considered in those with suspected plant dermatitis.     

Recent developments in the pathogenesis of allergic contact dermatitis

Allergic contact dermatitis is both an important clinical problem and a model system for lymphocyte-mediated pathologic changes. Elicitation of allergic contact dermatitis requires interaction of antigen with epidermal Langerhans cells, followed by migration of the Langerhans cells to the lymph nodes to present antigen to T lymphocytes. These activated T lymphocytes must then home to the antigen-exposed skin. Adhesion molecules such as LFA-1 and ICAM-1 have a role in this homing. Only a small proportion of the T lymphocytes in the skin lesion are specific for the inducing antigen. Studies of poison ivy (urushiol dermatitis) have determined this fraction to be less than one per 100 infiltrating lymphocytes. By a variety of amplification mechanisms, it is possible for this small number of antigen-specific T lymphocytes to induce the pathologic changes of allergic contact dermatitis. Improved understanding of this condition should result in increased knowledge of the pathogenesis of a variety of T lymphocyte-mediated skin conditions.     

Irritant contact dermatitis: a review

Irritant contact dermatitis is the most common form of contact dermatitis, and yet is often overlooked. Recent progress in understanding the pathogenesis has reignited the interest of clinicians in this area of dermatology. Irritant contact dermatitis is not a homogenous entity, but rather a number of subtypes contributing to different clinical presentations. The diagnosis of irritant contact dermatitis is often clinical, and may only be possible after the exclusion of allergic contact dermatitis with patch testing. There is no readily available diagnostic test. There is an incomplete understanding of the factors which lead to the development of cumulative irritant contact dermatitis and persistent postoccupational dermatitis. We have used the experience from our tertiary referral occupational dermatology clinic to illustrate various aspects of irritant contact dermatitis, and to highlight the difficulty sometimes encountered in making this diagnosis. We believe that increased awareness of the often pivotal role of irritant contact dermatitis, as well as all the other factors contributing to occupational dermatitis, will lead to improvement in outcomes for patients.     

Toxische Kontaktdermatitis auf Poison Ivy in einem Privatgarten in Deutschland

A couple suffered for 5 years from recurrent eruptions with vesicles and bullae after contact with an unknown "climbing weed" in their private garden in Germany. After this plant was identified as poison ivy and eradicated, their skin problems were solved. This is the first report of poison ivy in this setting. Urushiols in poison ivy are not only strong allergens but also potent irritants. Negative patch tests in the husband suggest that the bullous dermatitis was a toxic reaction.     

Neuropeptides enhance irritant and allergic contact dermatitis.

It is supposed that neuropeptides participate in the regulation of delayed-type hypersensitivity (DTH) reactions. However, their function in this kind of immune response is not known presently. Therefore, in vivo studies were initiated to test the effect on allergic (ACD) and irritant contact dermatitis (ICD) of the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), and somatostatin (SOM), which are released from afferent neurons in the skin. Each neuropeptide was applied topically at the site of contact with the allergen (oxazolone) or irritant (croton oil) during the challenge and sensitization phase of contact dermatitis. The intensity of the inflammation was measured as an increase of ear-swelling response, which represents the degree of plasma extravasation in the early phase of inflammation. Neuropeptides alone led only to a distinct vasodilation. All three neuropeptides were equally able to increase allergic and irritant inflammation. Even minor irritant stimuli were enhanced. Beyond that, CGRP was able to boost sensitization, whereas SOM and SP did not show any effects on the sensitization process. The results presented demonstrate that neuropeptides increase plasma extravasation independent of the pathogenesis of inflammation and may act as priming substances for other mediators of increased vascular permeability. In addition, CGRP enhances the sensitization process.     

Is it,or isn't it? Poison ivy look-a-likes

Poison ivy causes more allergic contact dermatitis (ACD) than any other cause. Although physicians rightfully focus on the treatment of the dermatitis, prevention will be aided by recognition of the foreboding plant. Likewise, many other plants can masquerade as poison ivy and cause one to needlessly curtail his or her activities because of fear of a bad reaction. The most common poison ivy pretenders in the United States are discussed, and distinguishing plant characteristics are highlighted.     

Hyposensitization to poison ivy after working in a cashew nut shell oil processing factory

19 adults were patch tested to urushiol, the allergen in poison ivy/oak, to determine their sensitivity to this allergen after working in a cashew nut shell oil (CNSO) processing plant. The cashew nut tree and poison ivy/oak are in the same botanical family. Anacardiaceae, and they share similar chemicals which cause allergic contact dermatitis. 13 of the 19 workers had a preemployment history of poison ivy sensitivity, with 10 developing CNSO dermatitis. After working in this factory for several months, 9 of the 13 noticed a decreased sensitivity or no sensitivity to poison ivy/oak. When tested to urushiol extract, only 3 reacted positively, 2 minimally. These results imply that hyposensitization to poison ivy/oak occurred in these employees after development of hardening to cashew nut shell oil.     

Skin irritant reactivity following experimental cumulative irritant contact dermatitis

Despite the frequency of irritant contact dermatitis, very little is known about the duration of barrier function impairment following cumulative irritant contact dermatitis. We studied post-irritation irritant reactivity by assessing the response to SLS irritation in previously irritated sites. Cumulative irritant contact dermatitis was induced on the forearms of 15 volunteers aged 18 to 50 years by repeated occluded application of 0.5% SLS I h per day over 3 weeks. 3, 6 and 9 weeks later, previously irritated and unirritated control sites were challenged with 2% SLS under occlusion for 23 h. Irritation was assessed by visual scoring, transepidermal water loss (TEWL) as an indicator of epidermal barrier function, and capacitance as a parameter of epidermal water content. While no difference in irritant reactivity between pre-irritated and unirritated sites was observed 3 weeks following irritant contact dermatitis, there was a significant hyporeactivity of previously irritated skin as expressed by clinical scores, TEWL and capacitance at 6 and 9 weeks. Our results indicate that epidermal barrier function remains altered even 9 weeks after cumulative irritant contact dermatitis. With regard to patch testing, post-irritation hyporeactivity might be a cause of false-negative tests on previously irritated sites.     

Do‐it‐yourself cement work: the main cause of severe irritant contact dermatitis requiring hospitalization

Background. There are myriads of potentially irritant agents causing acute irritant contact dermatitis. In the large majority of cases, dermatitis is mild to moderate, and patients do not need hospitalization. However, some agents or special circumstances may cause severe dermatitis requiring more intensive therapy. Objectives. The aim of this study was to evaluate causative agents of severe acute irritant contact dermatitis requiring hospitalization. Methods. In this single‐centre observational cohort study, we included 54 consecutive patients presenting with signs and symptoms of acute irritant contact dermatitis for which hospitalization was necessary. The severity of dermatitis was graded (grade I–IV) according to intensity, and details related to the skin irritation (irritant agent, area of exposure, time interval to onset of symptoms, and duration of hospitalization) were determined. Results. All cases with severe ulcerative dermatitis (grade IV) were caused by wet cement, owing to prolonged skin contact. These cement burns are clearly associated with amateur work, younger age, male preponderance, and leg localization. Conclusions. The study data provide clear‐cut evidence that wet cement is a severely irritant substance that regularly causes the most severe form of acute irritant contact dermatitis. The main causative prerequisite for these cement burns is do‐it‐yourself work with poor protective measures.     

Leaves of three, let them be: if it were only that easy!

Humans of all races and skin color are susceptible and uniquely sensitive to poison ivy, oak, and sumac. Contact with the plant oil, urushiol, found not only in the leaves but in the stems and roots, results in an allergic contact dermatitis in 50% to 60% of people. Clinical manifestations, differential diagnosis, complications, and treatments are discussed, with a special emphasis on the pediatric population.     

Studies on contact dermatitis in stomatological staff

84 patients with contact dermatitis (38 dentists, 18 dental nurses and 28 dental technicians) were studied. All were patch tested with standard patch test series of the CMEA countries and with some professional allergens. 31 (36.9%) of them had allergic occupational contact dermatitis and 39 (46.2%) had irrtiant contact dermatitis. The highest prevalence of irritant contact dermatitis was found among dental surgeons. The percentage of atopics in the group of patients with irritant contact dermatitis was twice greater compared to that in the group of patients with allergic contact dermatitis. The contact allergens most frequently encountered were acrylic compounds, disinfectants (eugenol, thymol, trioxymethylene) mercury compunds and anesthetics.     

Confocal histopathology of irritant contact dermatitis in vivo and the impact of skin color (black vs white)

BACKGROUND: The pathogenesis of irritant contact dermatitis and its modulation according to skin color is not well understood. Reflectance confocal microscopy (RCM) enables high-resolution, real-time, in-vivo imaging of human skin. OBJECTIVE: The goal of our study was to use RCM to determine whether susceptibility to irritant contact dermatitis differs between black and white skin. METHODS: Participants were placed in groups on the basis of skin color and the volar aspects of their forearms exposed to 1% and 4% sodium lauryl sulfate using Finn Chambers (Allerderm Laboratories Inc, Petaluma, Calif). They were evaluated at 6, 24, and 48 hours by RCM, transepidermal water loss, laser Doppler velocimetry, and routine histology. RESULTS: Participants with white skin had more severe clinical reactions than those with black skin. RCM revealed microscopic changes even without clinical evidence of irritation. Confocal features included parakeratosis, spongiosis, perivascular inflammatory infiltrate, and microvesicle formation, and these features were confirmed by routine histology. Also, participants with white skin had greater mean increases in transepidermal water loss after exposure to 4% sodium lauryl sulfate than did participants with black skin. CONCLUSION: In-vivo RCM can track early pathophysiologic events revealing differences between black and white skin during the development of irritant contact dermatitis, and may support the theory that those with black skin are more resistant to irritants.     

Allergic contact dermatitis

Contact dermatitis is an inflammatory skin condition induced by exposure to an environmental agent. Eczema and dermatitis are used synonymously to denote a polymorphous pattern of skin inflammation characterized at least in its acute phase by erythema, vesiculation and pruritus. Substances responsible for contact dermatitis after single or multiple exposures are non protein chemicals, i.e. haptens, that induce skin inflammation through activation of innate skin immunity (irritant contact dermatitis) or both innate and acquired specific immunity (allergic contact dermatitis). The present review will focus on allergic contact dermatitis, a delayed-type hypersensitivity reaction, which is mediated by hapten-specific T cells. Recent advances in the pathophysiology of ACD have shown that the occurrence of ACD, as well as its magnitude and duration, is controlled by the opposite functions of CD8 effector T cells and CD4 regulatory T cells. From these studies ACD can be considered as a breakdown of cutaneous immune tolerance to haptens.     

Irritant contact dermatitis to glyceryl monothioglycolate

Glyceryl monothioglycolate has recently been implicated as an allergen. A case of a hairdresser who used this material is presented. He appeared to have an irritant contact dermatitis on his fingertips. Patch testing the patient and extensive patch testing in a group of fifty-four volunteers showed a very high incidence of irritant positive patch tests. No instance of allergy could be demonstrated in the reading of the patch tests or in biopsies of several individuals. Differentiation between allergens and irritants is difficult at times, but is necessary to avoid mislabeling of chemicals.