The poison ivy plant and its relatives are common throughout the United States. Poison ivy leaves are coated with a mixture of chemicals called urushiol. When people get urushiol on their skin, it causes an allergic contact dermatitis. This is a T cell-mediated immune response, also called delayed hypersensitivity, in which the body's immune system recognizes as foreign, and attacks, the complex of urushiol-derivatives with skin proteins. The irony is that urushiol, in the absence of the immune attack, would be harmless. The most common treatment for severe contact dermatitis is with corticosteroids, which diminish the immune attack and resulting inflammation. A recent recommendation for mild cases is to use manganese sulfate solution to reduce the itching. Jewel weed is also recommended.
Dermatitis is an inflammation of the skin. If the allergy which causes the dermatitis is a response to something which came into contact with the skin, it is called allergic contact dermatitis. In addition to poison ivy, other things which contact the skin such as clothing, shampoo, jewelry, make-up, and deodorants can also cause allergic contact dermatitis. Allergic dermatitis can also be caused from within, as when a skin rash develops because of something we ate.
An extensive list of substances causing allergic contact dermatitis
has been provided by Truett.
Allergic inflammations, also called hypersensitivities, are caused by three
underlying mechanisms. The one which is responsible for the reaction
to poison ivy is called delayed hypersensitivity.
Cortosteroids are natural hormones in the body. They are immunosuppressive
and antiinflammatory. They work by affecting gene expression in a complex
manner, and the ways they reduce immune inflammation are not fully understood.
They reduce the production of inflammatory cytokines and arachadonic acid and
its derivatives (prostaglandins, prostacyclin, thromboxanes, and
leukotrienes). The major natural antiinflammatory corticosteroid in the body
is hydrocortisone (also called cortisol). Longer-lasting and more potent
synthetic analogs of hydrocortisone are often used in the clinic, such
as prednisolone, prednisone, or dexamethasone.
Poison Ivy Plant
The poison ivy plant is Toxicodendron radicans in the eastern US,
and T. rydbergii in the midwestern US. T. radicans
is also called Rhus
toxicodendron or Rhus radicans.
See Truett and
Nelson for more
information. Western poison oak is Rhus diversiloba, and
poison sumac is Rhus vernix.
Urushiol is a mixture of catchol derivatives. The major catechol on poison
ivy leaves is pentadecylcatechol. If urushiol is washed off the skin within
an hour or so, the reaction can be largely prevented. However, if left on the
skin, some diffuses through the skin, where it is metabolized to
derivatives. These form covalent complexes with skin proteins such as
keratin. These complexes appear foreign to the immune system, which therefore
Further information on poison ivy.
See Case studies in immunology - a clinical companion by Fred S. Rosen
and Raif S. Geha, Garland Publishing Inc., 1996 (Case 6, contact
hypersensitivity). Further information on allergy and hypersensitivity, and
the underlying mechanisms, can be found in any textbook
of immunology. For a discussion of corticosteroids, see a physiology
book, such as the current edition of the Review of Medical Physiology
by William F. Ganong, Appleton and Lange.
Allergic inflammations, also called hypersensitivities, are caused by three underlying mechanisms. The one which is responsible for the reaction to poison ivy is called delayed hypersensitivity.
Godfrey, H. P., H. Baer, and R. C. Watkins. 1971. Delayed hypersensitivity to catechols. V. Absorption and distribution of substances related to poison ivy extracts and their relation to the induction of sensitization and tolerance. J. Immunol. 106(1):91-102.
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Last updated March 31, 1997.