Poison-ivy and poison-oak dermatitis

Poison ivy (Toxicodendron radicans), poison oak (T. diversilobum), and poison sumac (T. vernix) are the primary causes of contact dermatitis in the United States, affecting 10–50 million Americans every year. The prevalence of sensitivity to poison ivy and poison oak in the general adult population ranges from 50% to 70% with peak frequency for sensitization occurring between the ages of 8 and 14. Outdoor activities as well as outdoor occupations which relate to firefighting, forestry and agriculture are at high risk, costing significant medical expenses and worker's disability. During our ongoing studies aimed at the discovery of an effective prophylactic treatment for toxicodendron dermatitis, we have developed a series of novel agents and tested the efficacy of these agents in an in vivo animal model. Here, we present the protective effect of our pro-drug ELI-21C-76C in our guinea pig experimental model.

Cross-Sensitization in Diverse Poisonous Members of the Sumac Family (Anacardiaceae)

Computational Biology

Allergic contact dermatitis from poison ivy, oak, or sumac is common among people who work or exercise outdoors. The plants, classified in the genus Rhus or Toxicodendron, contain allergens that can cause reactions ranging from mild pruritus to severe urticaria or generalized maculopapular eruptions. Initial management includes cleansing, cold compresses, and, possibly, oral antihistamines for symptomatic relief. Topical corticosteroids are given for localized nonfacial eruptions; systemic corticosteroids are used for severe eruptions. Prevention involves avoiding contact with the plants and washing exposed skin within 2 hours.

When the itching won’t stop: Counseling on exposure to poison ivy and other poisonous plants

Commonly encountered plants that produce an oil called urushiol, which triggers allergic contact der…

The black spot test for recognizing poison ivy and related species

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While it is true that poison oak and its sister plants have rarely, if ever, caused a death, it is also true that a large majority of people living in the temperate zones find their enjoyment of the country seriously curtailed by the menace of these noxious plants. And besides this restriction of healthful pleasures, there is an unestimated monetary loss to laborers and construction companies operating in infested regions, which I am sure is not inconsiderable. Yet in spite of these well-known facts, very little has been attempted, and still less accomplished, to abate this wide-spread evil. SKETCH OF PLANT The plants specially referred to are poison oak (Rhus diversiloba), poison ivy (R. toxicodendron) and poison sumach (R. venenata), which form a widely distributed group. The poison ivy1is found in abundance throughout the United States as far west as eastern Texas, eastern Kansas and Minnesota, and in

Contact dermatitis is an infl ammatory condition caused by direct skin exposure to an offending chemical with or without a requirement for ultraviolet light. There are two distinct types of contact dermatitis: irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD). ACD, an eczematous disease mediated through immune mechanisms, is an acquired skin disorder that occurs at sites of contact with small chemical haptens in only those individuals who have been previously exposed to, and immunologically sensitized to a particular chemical. In contrast to ICD typically only a small percentage of the population develops an eruption when exposed to chemicals causing ACD. The most common chemical allergens causing the condition in North America include nickel sulfate (NiSO4), as well as the pentadecylcatechols, the active moiety in plants of the genus Rhus, which include poison ivy, poison oak, and poison sumac (1).

Captain Smith’s ‘‘Ivie’’ was well known to his Powhatan Indian neighbors. For centuries, they and other Native Americans had used it for medicine. Navajos made arrow poison from this native plant, and California’s Miwoks made the Western version, it-tum in their language, into black dye for baskets (Balls, 1962). They were very aware of its harmful character—in Mexico, it was called mala mujer, the wicked woman—but to unwary European settlers, the attractive weeds became familiar as ‘‘poison ivy’’ and ‘‘poison oak.’’

Poison oak and poison ivy: 1. Dermatitant units as a standard measure of potency for extracts from these plants

Toxic shock syndrome commonly occurs in menstruating women, but it is known to be associated with a variety of staphylococcal infections. We report a case of nonmenstrual toxic shock syndrome in an 11-year-old male who presented with altered consciousness and infected poison oak dermatitis of the feet. This is the first reported case of toxic shock syndrome associated with poison oak dermatitis. The signs and symptoms, laboratory findings, and treatment of toxic shock syndrome are reviewed.

Poison ivy-induced allergic contact dermatitis (ACD) is the most common environmental allergic condition in the United States. Case numbers of poison ivy ACD are increasing due to growing biomass and geographical expansion of poison ivy and increasing content of the allergen, urushiol, likely attributable to rising atmospheric CO2 Severe and treatment-resistant itch is the major complaint of affected patients. However, because of limited clinical data and poorly characterized models, the pruritic mechanisms in poison ivy ACD remain unknown. Here, we aim to identify the mechanisms of itch in a mouse model of poison ivy ACD by transcriptomics, neuronal imaging, and behavioral analysis. Using transcriptome microarray analysis, we identified IL-33 as a key cytokine up-regulated in the inflamed skin of urushiol-challenged mice. We further found that the IL-33 receptor, ST2, is expressed in small to medium-sized dorsal root ganglion (DRG) neurons, including neurons that innervate the skin. IL-33 induces Ca2+ influx into a subset of DRG neurons through neuronal ST2. Neutralizing antibodies against IL-33 or ST2 reduced scratching behavior and skin inflammation in urushiol-challenged mice. Injection of IL-33 into urushiol-challenged skin rapidly exacerbated itch-related scratching via ST2, in a histamine-independent manner. Targeted silencing of neuronal ST2 expression by intrathecal ST2 siRNA delivery significantly attenuated pruritic responses caused by urushiol-induced ACD. These results indicate that IL-33/ST2 signaling is functionally present in primary sensory neurons and contributes to pruritus in poison ivy ACD. Blocking IL-33/ST2 signaling may represent a therapeutic approach to ameliorate itch and skin inflammation related to poison ivy ACD.

HISTORY A 9-year old male presented to the office complaining of bilateral wrist pain. It was reported that he was playing on a rope swing and let go landing on both outstretched arms, wrists dorsiflexed. No clicks or pops were heard or felt. He was immediately evaluated at a local emergency department, where x-rays were obtained of both arms and he was diagnosed with a left distal radius fracture. He was experiencing bilateral wrist pain, swelling, and weakness with left wrist deformity and clicking. Baseline pain was rated as 4–5 out of 10 and was intensified to 9 out of 10 with wrist flexion bilaterally. He was then referred to our office for casting. PHYSICAL EXAMINATION The patient is a 4 '10″,80 pound, pleasant, cooperative, well-nourished 9-year old, appearing healthy and in no acute distress. Inspection of the wrists bilaterally reveals swelling, left greater than right. He was able to move all digits bilaterally and wrist range of motion was decreased bilaterally, left more than right. Grip strength was 3 out of 5 bilaterally. Range of motion at the elbow and shoulder joints was full. Both upper extremities were neurovascularly intact and there were no fracture associated breaks in the skin noted. The exam was affected significantly by the patient's level of pain. Of note, he had been previously diagnosed with poison ivy by his primary care physician and had characteristic dermatitis with excoriations confined to the dorsum of his forearms and hands bilaterally. DIFFERENTIAL DIAGNOSIS Unilateral fracture (e.g.left radius, ulna, navicular, lunate) with contralateral sprain. Salter-Harris fracture Metabolic bone disorder with pathologic fracture Triangular.fibrocartilage complex (TFCC) injury Injury secondary to child abuse (multiple injuries) Skin rash consistent with poison ivy TEST AND RESULTS The x-rays from the initial emergency department visit were consistent with a torus fracture of the left distal diaphyseal metaphyseal junction of the left radius and a subtle right distal radius torus fracture that was revealed during our re-evaluation of the films. FINAL WORKING DIAGNOSIS Bilateral torus fractures of the distal radius Contact dermatitis (poison ivy) TREATMENT AND OUTCOMES Due to the complication of contact dermatitis, sugar tong splints were utilized rather than circumferential casting. He was referred to hand therapy to have ventral orthoplast splints made for extended wear. Splints were to be removed daily for dermatologic checks and application of topical steroids. Follow-up x-rays were taken at 4 and 8 weeks with reasonable interval healing. He was placed in velcro type wrist braces at 4 weeks and was essentially pain free at 8 weeks.