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Poison Ivy dermatitis is the most common allergic contact dermatitis in the US.

Belongs to the genius Toxicodendron and the family Anacardiaceae.

Eastern poison ivy known as T radicans is a small shrub or climbing vine that grows mainly east of the Rocky Mountains.

Western poison ivy T rydhergii is a non-climbing shrub that grows mainly in the northern US and in southern Canada.

The leaves are usually notched and in groups of three.

Flowering branches arise from axillary positions on the single stem.

Approximately 50-75% of adults are sensitive.

Peak frequency occurs between the ages of eight and 14, and in Eastern states and usually occurs in the spring and summer whereas in southwestern states occurs the whole year round.

It’s very slightly more common in males, and is of increased frequency in individuals who engage in outdoor activities.

Approximate half to 3/4 of US adult population will develop contact dermatitis after contact with poison ivy, poison oak, and poison sumac.

Approximately 10 to 50,000,000 people in US develop a rash from exposure to these plants annually.

Individuals at highest risk for such contact dermatitis are those who work outdoors.

Caused by a type IV T-cell mediated, delayed hypersensitivity reaction to urushiol, which is found in the sap from damaged leaves or plants.

Poison ivy, poison oak, and poison sumac plants contain sap oil (utrishiol) in their leaves, stems and roots, which is released on contact and penetrates the skin to cause an itchy, red rash or allergic contact dermatitis.

Dermatitis results from direct contact with urushiol or indirect contact with contaminated clothing or smoke from poison ivy.

Urushiol can remain stable in high temperatures and can be carried by smoke when the plants are burned.

Urushiol is naturally amber or colorless and may turn black when exposed to air in a warm humid environment due to the enzyme laccase found in the oleoresin.

Urshiol on the skin can be spread to other areas by touch.

People can come in contact with urshiol by petting an animal that has sap on its fur.

Urshiol can spread rarely to other people who contact with clothing or objects such as garden tools that has urushiol on it.

Damage to the plant is required for release of the chemical, and slight contact with the plant is usually innocuous in does not lead to dermatitis.

Urushiol is a mixture of 3 catechols, which penetrate the outer layer of the skin within minutes and become activated to quinone intermediates which can bind to antigen-presenting cells.

Antigen-presenting cells present the processed antigen to CD4 T-helper lymphocytes which form a clone of urushiol-specific T effector and T- memory lymphocytes.

Re-exposure to urushiol activates clonal lymphocytes eliciting a cell-mediated cytotoxic immune response.

Following contact sensitized individuals usually develop an intensely pruritic erption within 48 hours of exposure.

Skin eruption may appear as early as five hours or as late as 14 days after exposure.

Intense itching is the most common presenting symptom and may precede eruption.

Erythema and papules in a linear arrangement in the area of involvement may follow the pruritus.

Vesicles may develop hours later and evolve into large bullae.

Mild cases lack vesicles where as more severe cases may present with bullae and edema.

Fluid exudation does not contain urushiol and will not spread the process.

The severity of the rash depends on the level of sensitization, individual susceptibility, skin thickness at the site of involvement, the degree of exposure, and the amount of urushiol that binds with the skin.

The arms, legs, and face or sites of involvement.

The genitals may become involved when contact with urushiol contaminated hands.

Black spot poison ivy can develop if the patient has a large exposure to urushiol left on the skin and it becomes oxidized.

Diagnosis is a clinical one, with a history of exposure to a plant with three leaflets and familiarity with the clinical appearance of the rash.

Must be differentiated from phytophotodermatitis which results from an interaction of solar radiation and photosensitizing compounds in plants.

Differential diagnosis includes phytophotodermatitis, allergic contact dermatitis, chemical irritants dermatitis, arthropod bites, dyshidrotic eczema, toxic epidermal necrolysis, bullous pemphigoid, bullous tinea, bullous impetigo, Steven-Johnson syndrome, neurotic excoriations, and nummulite eczema.

The rash can take up to three weeks to develop an individuals with the first exposure to one of these plants.

The rash typically resolves within one to three weeks.

Complications include secondary bacterial infection with Staphylococcal aureus and group A beta hemolytic streptococci, and transient post inflammatory hyperpigmentation.

Post inflammatory pigmentation more pronounced in dark skinned individuals.

Hyper pigmentation usually resolves within months without treatment.

Rare complications including urticaria, erythema multiforme and nephropathy due to immune complex deposition in the kidney.

Prognosis is usually good being a self-limited process of approximately three weeks.

The first step in the management of poison ivy is decontamination.

The involved site should be washed thoroughly with hot water and patted dry.

Decontamination of all clothing or other materials that may have come into contact with the plant is required.

Topical corticosteroids and anti-pruritic compounds should be applied to the skin.

In the majority of cases an ultra potency topical corticosteroid is the cornerstone of therapy.

Mid potency topical corticosteroids are utilized when the dermatitis involves the face, genitalia or intertriginous areas.

With refractury or severe and widespread disease involving the face, genitalia, and intertriginous areas a short course of oral corticosteroids or cyclosporine is indicated.

Topical antihistamines are generally not helpful.

In widespread cases or if patient remains symptomatic after a few days, systemic steroids are an option.