Poison Ivy
Tocicodendron diversilobum (Torr. & A. Gray) Greene, T. quercifolium Michx. Greene, T. radicans (L.) Kuntze, T. vernix (L.) Kuntze. Family: Anacardiaceae
Poison ivy , poison oak , poison sumac , markweed , poison elder , poison dogwood
 
Clinical Overview
Uses
There are unsubstantiated claims of usefulness in the treatment of conditions such as osteoarthritis.

Dosing
Poison ivy has been used primarily to desensitize patients with urushiol allergy. Its internal use is strongly contraindicated.

Contraindications
No longer considered safe.

Pregnancy/Lactation
Information regarding safety and efficacy in pregnancy and lactation is lacking.

Interactions
None well documented.

Adverse Reactions
Dermatitis in severity ranging from mild to fatal, depending upon point of contact and individual resistance.

Toxicology
Allergic reactions and dermatitis, which may be severe or even fatal.

 
Botany
The contact sensitivities induced by poison ivy and several closely related species present a persistent public health problem. These dermatites affect from 50% to 70% of the general population. 1
Poison ivy is a member of the sumac family (Anacardiaceae). Although originally classified as a member of the genus Rhus , it is now included in the genus Toxicodendron . Four related species are responsible for the majority of plant dermatites. These perennials are identified as: T. diversilobum (Torr. & A. Gray) Greene - Western poison oak, T. quercifolium (Michx.) Greene - Eastern poison oak, T. radicans (L.) Kuntze - Poison ivy, markweed, three-leaved ivy, T. vernix (L.) Kuntze - poison sumac, poison elder, poison dogwood.
The nonpoisonous shrubby sumacs ( Rhus spp.) also have long, pinnately divided leaves, but the flowers and fruits are in dense, terminal and erect clusters. 2
T. diversilobum - The western poison oak is found along the Pacific coast from British Columbia to Mexico. It thrives in low places, thickets, and wooded slopes, usually below 5000 feet elevation. The 3-leaflet clusters are irregularly lobed and resemble oak leaves.
T. quercifolium - Eastern poison oak grows in the eastern and southern states from New Jersey to Missouri and North Florida. This erect, low, woody shrub is most frequently restricted to sandy soil, dry barrens and pine woods.
T. radicans - Poison ivy grows throughout the United States and Canada, with the exception of parts of the West Coast. The habit of this weed is extremely variable; it may grow as a nonclimbing woody shrub or as a vine along the ground, on low plants, or on high trees or poles. Only the presence of a cluster of 3 leaflets is a constant characteristic. The adage of “leaflets three, let it be; berries white, poison sight” remains a good rule of thumb. The plant is odorless but has an acrid, slightly astringent taste. 3 The leaflets vary in color from green in spring to yellow and red in autumn. The waxy white to yellowish fruits may remain on the plant throughout the winter.
T. vernix - Poison sumac is native to bogs of the north (as a shrub) and to swamps and river bottoms of the south (as a small tree). Its distribution is widespread but is predominantly found east of the Mississippi river. The 7- to 13-leaflet clusters are arranged in alternate pairs, with a single leaflet at the end of the midrib.
A major factor in poison plant dermatitis is the failure to recognize the plant. In general, all of the plants discussed here have 3-leaflet clusters, with the exception of poison sumac. They also have U- or V-shaped leaf scars (the scar remaining at the point that the leaf breaks from the stem), and flowers and fruits arising in the axillary position (in the angle between the leaf and the branch). Another helpful finding is a black deposit often present when Toxicodendron has been injured. Following trauma, the oleoresin exudes, darkens on exposure to air, and hardens. One source suggests crushing a few leaves of a suspected plant on a piece of white paper, releasing the sap from the petioles; the resulting stain will darken markedly within 10 minutes if it is from Toxicodendron . Although the test is not conclusive, it provides supportive evidence in making a positive identification. 4
Other members of the family anacardiaceae include the tropical cashew nut tree ( Anacardium occidentale ), the tropical mango tree ( Mangifera indica ), the Indian marking nut tree ( Semecarpus anacardium ) and Japanese lacquer tree ( Rhus vernicifera ). Because of their chemically similar allergens, these also may cause allergic contact dermatitis in sensitive individuals. 5,  For example, cashew ingestion has been associated with mouth blistering and perianal itching, if the antigens cardol and anacardic acid have not been properly removed. 6 Contact dermatitis can also result from mango ingestion without first removing the fruit skin, or from lacquer tree sap (from Rhus spp.) in furniture. 5
 
Chemistry
An oily phenolic resin called toxicodendrol (lobinol) is present in all poisonous Toxicodendron species and contains a complex active principle known as urushiol. The name “urushiol” is derived from the Japanese term “sap.” 5,  It is a mixture of antigenic catechols. 7,  These antigens are closely related to 3-n-pentadecylcatechol (3- PDC, hydrourushiol) but differ in the degree of unsaturation at the 3n-alkyl side chains, 3,  , 8,  and in their side chain lengths sumac has 13 carbons, poison ivy 15 carbons and oak 17 carbons. 5,  In general, the more unsaturated or longer the side chain is, the more antigenically reactive the catechol. 9 Urushiol is carried by resin canals found in the bark, stem, leaflets, and certain flower parts. The relative percentages of 3-PDC and related catechols varies among the species and may also be related to environmental conditions. The danger of toxicity is greatest in spring and summer, when the sap is abundant, the urushiol content is high, and the plant is bruised easily.
Chromatographic procedures have been developed for use in separation and characterization of urushiol in poison ivy and poison oak. 10,  , 11
 
Uses and Pharmacology
Extracts of poison oak have been used in homeopathic medicine to treat conditions such as osteoarthritis. Controlled studies have failed to substantiate the efficacy of such treatments, 12,  but the methodology of these studies has been questioned. 13,  , 14
Urushiols are haptens that must bind with skin proteins to form complete antigens. This is thought to occur on the surface of Langerhans cells, where the urushiols are irreversibly bound. 3,  , 5,  Sensitization appears to require bonding of quinones derived from urushiol components with nucleophilic groups on the proteins. 15,  A later report suggests free radicals, and not quinones, to be the haptenic species derived from urushiol. 16,  Blocking the C5-position on the catechol ring seems to suppress sensitivity. 15,  Mouse data suggest that contact sensitivity to urushiol is mediated by serum factors. 17,  In vitro studies with human lymphocytes, however, indicate that urushiol reacts initially with T cells. Interaction with a non-T accessory lymphocyte is necessary for reactivity. 18,  A recent report describes processing or urushiol hapten by both endogenous and exogenous pathways for presentation to T-cells. 19,  After the previously sensitized T-lymphocytes have been activated, the allergy cascade is locally initiated. 5
Many more recent immunological studies continue, including isolation of urushiol triggered T-cells; 20,  T-cell clone generation from blood; 20,  , 21,  , 22,  enrichment and function of urushiol-specific T-lymphocytes; 23,  role of keratinocytes in allergic contact dermatitis; 24,  , 25,  increased levels of telomerase activity in poison ivy dermatitis; 26,  UL-8 enhanced expression; 27,  and modulation; 28,  and poison ivy analog sensitization. 29,  , 30,  , 31,  , 32
 
Administration & Dosage
Poison ivy has been used primarily to desensitize patients with urushiol allergy. Its internal use is strongly contraindicated.
 
Pregnancy/Lactation
Information regarding safety and efficacy in pregnancy and lactation is lacking. Avoid use.
 
Interactions
None well documented.
 
Adverse Reactions
Mild to severe dermatitis, which may also be fatal (see toxicology), depending upon point of contact and individual resistance.
 
Toxicology
Toxicodendrol does not enter the blood. Minute quantities (0.001 mg) applied to the skin can cause dermatitis. The sensitivity may persist for years. Infants are not as readily sensitized as adults, and with intermittent exposure, the sensitivity decreases with age. After contact, the first symptoms of itching, burning and redness may appear in a few hours or may take up to 5 days, depending on the sensitivity of the individual. The rash is characterized by linear streaks of erythematous lesions where the plant has “brushed” the skin. 5,  Urticarial plaques and bullae may develop, filled with fluid. Contrary to popular belief, this blister fluid does not contain urushiol, and therefore, cannot spread infection by fluid contact. Continued spreading of infection actually results from variation in time of onset of clinical reaction (“delayed reaction”), antigen load and individual sensitivity. 1,  Secondary changes include the blisters oozing until a crust is formed. Intense itching may last for up to 7 days. Rare complications include hematologic changes, renal damage and psychological reactions. Barring complications, the dermatitis is self-limiting, lasting from 1 to 3 weeks. The skin usually recovers unblemished, because only the epidermal layer is involved; however, excessive scratching and infection may result in permanent scarring. 3
Other means of exposure from the plant include inhaling resin droplets carried in smoke from burning poison ivy, which can cause fever, major lung infection and even death from the throat swelling shut. 32 ,  Exposure to urushiol can also come about by contact through animal fur, contaminated clothing, garden tools and sports equipment. Urushiol is so long-lasting, if not properly washed away, that dermatitis can occur years later if these still contaminated items are touched again. 3,  , 32 Soaking contaminated clothing in a 1% solution of hypochlorite for 15 minutes, followed by laundering, should remove the resin (caution: may discolor clothing). Avoidance, however, remains the best approach to preventing Toxicodendron dermatitis.
If ingested, poison ivy can produce severe gastrointestinal effects. 3,  Some individuals, however, can consume poison ivy without effect, apparently because of a lack of reactivity in the digestive mucosa. 33
The choice of an appropriate treatment is dependent upon the severity of the episode. Treatment objectives include protecting the damaged skin until the acute reaction has subsided, preventing accumulation of epidermal debris, relieving the intense itching, and avoiding excoriation. Affected areas should be cleaned immediately with soapy water, however, oils from certain soaps may spread the sap. According to the American Academy of Dermatology in a recent report, water alone is best to use when contact with the plant is known. Urushiol is neutralized by water, and if the exposed area is washed with water within 5 to 10 minutes after contact, the reaction may be avoided. 34,  Swabbing with alcohol may not halt the allergic reaction but may limit its spread. Wet compresses (Burow's solution, normal saline, potassium permanganate, 10% tannic solution), cornstarch, or oatmeal baths may provide symptomatic relief. Astringent soaks should not be used on the skin of the face or genitals. Other over-the-counter therapies include local anesthetics, antipruritics, antiseptics and counterirritants (eg, menthol). 5,  , 35,  , 36,  , 37,  , 38,  , 39,  , 40
Calamine lotion has long been the drug of choice in poison ivy dermatitis. Its astringent action may also provide relief of itching, pain and discomfort of poison ivy. 41,  , 42 ,  Oral antihistamines can provide transient symptomatic improvement of pruritis (eg, hydroxyzine 10 to 25 mg 4 times/day as needed). 1,  , 5,  Topical antihistamines should be discouraged, because their use has been associated with skin sensitization; further, their use here is irrational, because these dermatites are not dependent on the release of histamine. 43 Two to three times per day application of topical corticosteroids such as betamethasone valerate 0.1% (   Valisone ), betamethasone dipropionate 0.05% (   Diprolene ), flucinolone acetonide 0.01% to 0.25% (   Synelar ) and triamcinolone acetonide 0.1% (   Aristocort ,   Kenalog ) are all frequently prescribed and may slightly reduce erythema and pruritis, but they hardly alter the natural overall course of the lesions, unless applied early in the course. 1,  , 44,  Some systemic absorption may occur so application to the sensitive areas (eg, face), pregnant/nursing mothers, diabetics, etc, should be avoided. Occlusive dressings should not be placed over these creams because increased absorption will occur as well. 38,  Low-dose otc topical steroids haven't been proven effective, except in the most mild cases. 1,  In cases of extensive dermatitis, systemic steroids (for adult patients) are indicated. Oral prednisone 1 mg/kg/day tapered over 14 to 21 days is standard, and can dramatically improve the condition. 1,  A common mistake is to taper the steroid dosages too quickly, resulting in rebound flares. Complications can result from prepackaged “dosepaks,” because initial dosage here is approximately ½ the recommended dosage. Other problems with this treatment include rapid tapering and too short a course of therapy. The manufacturer of this methylprednisolone dosepak does, however, include such a warning on its product. 1,  A case report describes an example of this type of treatment failure and how it was resolved. 45
Other treatment options include use of poultices prepared from narrow and broad leaf plantain to control the itching 46,  and acupuncture, both with clinically unsubstantiated but variable results. A report of four cases has noted success with acupuncture in relieving the itching of the dermatites within a few hours to 2 days and promoting healing of skin lesions within 2 to 4 days. 47
Desensitization by the administration of plant extracts is not regularly attained. In general, hyposensitization procedures require large doses and months of treatment, and the sensitivity is regained rapidly upon cessation of therapy. 48,  Oral ingestion of antigens (bypassing Langerhans cells) may allow suppressor T-cell populations to develop, that can inhibit the response to skin contacting the plant. 1,  Oral administration in inducing tolerance and desensitization to poison ivy dermatitis in Guinea pigs has been reported. 1,  , 49,  The three most widely used agents for hyposensitization are crude plant extract, alum-precipitated pyridine extracts, and synthetic 3-PDC. Commercial products vary in antigen content. The preparations are taken in gradually increasing daily doses for at least 4 weeks with maintenance doses several times a week during the growing season. Intramuscular preparations are usually given at weekly or biweekly intervals. 50,  No well-controlled studies have established the efficacy of these preparations, although studies with a purified urushiol extract have demonstrated good hyposensitization compared with placebo. 51,  A double-blind, placebo-controlled study of a 1:1 oral mixture of 3-PDC and heptadecylcatechol failed to demonstrate any decrease in sensitivity to poison ivy or poison oak in 44 subjects. 52,  Animal studies, however, suggest that topical application of 5-methyl-3-n-pentadecylcathechol or a related compound could be effective in inducing tolerance to 3-PDC. 53,  At best, hyposensitization reduces the duration and severity of the dermatitis, while inducing numerous side effects, including gastrointestinal disturbances, itching, and inflammation. There still remains no US Food and Drug Administration (FDA)-approved or reliable oral regimen for desensitization. 1
Topical application may provide an alternative to systemic administration of agents to protect against poison-plant dermatitis. Clinical patch tests have identified several polyamide salts of a linoleic acid dimer that prevented dermatitis in 70% of subjects tested. The salts were particularly effective when both the preparation and the plant antigen were washed off the skin within 8 to 12 hours of antigen exposure. 54 The effectiveness of this, and other barrier preparations to prevent dermatitis has been evaluated in another report. The percent reductions in dermatitis severity per day in order of effectiveness were:   Stokogard ( Stockhausen , Greensboro, NC) which contains PPG-3 diamine dilinoleate;   Hollister Moisture Barrier ( Hollister , Inc., Libertyville, IL) containing a propylparaben, BHA mixture;   Hydropel ( C & M Pharmacal, Inc. , Hazel Park, MI) with 30% silicone;   Ivy Shield ( Interpro, Inc. , Haverhill, MA) a tea stearate mixture;   Shield Skin ( Mentor Corp. , Minneapolis, MN) with plasticized ethyl cellulose;   Dermofilm ( Innovetec , Brussels, Belgium); and   Uniderm ( Smith & Nephew, Inc. , Largo, FL) with lanolin, benzethonium chloride, quaternium-15 and others. 55
Organoclay, an ingredient of antiperspirants, is the most recent, effective barrier cream studied thus far. This agent has reduced or totally prevented experimental dermatitis. 56 The oranoclay, quaternium-18 bentonite, has the ability to “bind” with urushiol. This product contains 5% quaternium-18 bentonite in the form of a lotion, called   Ivyblock ( Enviroderm Pharmaceuticals, Inc. ). When applied, the product lays down an active barrier on skin, blocking potential contact with the allergan, thus, offering protection from poison ivy, poison oak and poison sumac rash. 57   Ivyblock should be of great help in “high risk” individuals, including firefighters, utility and lumber workers, armed forces and certain medical professionals.
 
References
 

1. Williford P, et al. Arch Fam Med . 1994;3:184–188.  PubMed

 

2. Hardin JW, Arena JM. Human Poisoning from Native and Cultivated Plants , 2nd Ed. Durham: Duke Univ. Press, 1975.

 

3. DerMarderosian AH. Drug Therapy . 1977;7:57.

 

4. Guin JD. J Am Acad Dermatol . 1980;2:332–333  PubMed

 

5. Guay D. J Prac Nurs . 1993;43:24–31.  PubMed

 

6. MMWR . 1983;32:129.

 

7. Dawson CR. Recent Chem Prog . 1954;15:39.

 

8. Corbett M, Billets D. J Pharm Sci . 1975;64:1715.  PubMed

 

9. El Sohly MA, et al. J Med Chem . 1986;29:606.  PubMed

 

10. El Sohly MA, et al. J Pharm Sci . 1980;69:587–589.

 

11. El Sohly MA, et al. J Nat Prod . 1982;45:532–538.

 

12. Shipley M, et al. Lancet . 1983;8316:97.  PubMed

 

13. Kennedy CO. Lancet . 1983;8332:482.

 

14. Ghosh A. Lancet . 1983;8319:304.

 

15. Dunn IS, et al. Cell Immunol . 1986;97:189.  PubMed

 

16. Schmidt R, et al. Arch Dermatol Res . 1990;282:56–64.

 

17. Dunn IS, et al. J Invest Dermatol . 1987;89:296.  PubMed

 

18. Byers VS, et al. J Clin Invest . 1979;64:1437.  PubMed

 

19. Kalish R, et al. J Clin Invest . 1994;93:2039-2047.  PubMed

 

20. Kalish R, et al. J Invest Dermatol . 1989;92:46–52  PubMed

 

21. Kalish R, et al. J Invest Dermatol . 1990;94(6–Suppl):108S-111S  PubMed

 

22. Kalish R, et al. J Clin Invest . 1988;82:825–832.  PubMed

 

23. Kalish R, et al. J Immunol . 1990;145:3706–3713.  PubMed

 

24. Griffiths C, et al. Am J Pathol . 1989;135:1045–1053.  PubMed

 

25. Barker J. Contact Dermatitis . 1992;26:145–148.  PubMed

 

26. Taylor R, et al. J Invest Dermatol . 1996;106:759–765  PubMed

 

27. Mohamadzadeh M, et al. Exp Dermatol . 1994;3:298–303.  PubMed

 

28. Griffiths C, et al. J Dermatol . 1991;124:519–526  PubMed

 

29. Roberts D, et al. Contact Dermatitis . 1993;29:78–83.

 

30. Haas J, et al. Exp Dermatol . 1992;1:76–83.

 

31. Fraginals R, et al. J Med Chem . 1991;34:1024–1027.  PubMed

 

32. Vietmeyer N. Smithsonian Magazine . 1995.

 

33. Heald P, et al. N Carolina Med J . 1983;44:437.  PubMed

 

34. Lane L. Austin American Statesman . 1995;;F1–2.

 

35. Witkowski J, et al. Drug Ther . 1984;14:81–83, 87–88.

 

36. Bagley J. Am Druggist . 1986;193:114, 116.

 

37. Levine H. Am Druggist . 1988;197:47–48.  PubMed

 

38. Praw W. US Pharmacist . 1991;16:16, 19, 20, 24.

 

39. Anonymous. Drug Store News for Pharmacists . 1994;4:55–61.

 

40. Praw W. US Pharmacist . 1994;19:99–100.

 

41. Desimone E. Am Pharm . 1983;NS23:8–13.  PubMed

 

42. Olin B, ed. Drug Facts and Comparisons . St. Louis, MO: Facts and Comparisons, Inc. May 1992 Update: 564.

 

43. Reynolds H. Poison Ivy Dermatitis, Current Therapy. Philadelphia: W.B. Saunders, 1972.

 

44. Beyea S. RN . 1989;52:23–25.  PubMed

 

45. Ives T, et al. JAMA . 1991;266:1362.  PubMed

 

46. Duckett S. N Engl J Med . 1980;303:583.  PubMed

 

47. Liao SJ. Electrother Res . 1988;13:31.  PubMed

 

48. Watson ES, et al. J Pharm Sci . 1981;70:785.  PubMed

 

49. El Sohly M, et al. J Pharm Sci . 1983;72:792–795.

 

50. Medical Letter . 1981;23:40.

 

51. Epstein WL, et al. Arch Dermatol . 1974;109:356.  PubMed

 

52. Marks JG, et al. Arch Dermatol . 1987;123:476.  PubMed

 

53. Stampf JL, et al. J Invest Dermatol . 1986;86:535.  PubMed

 

54. Orchard S, et al. Arch Dermatol . 1986;122:783.  PubMed

 

55. Grevelink S, et al. J Am Acad Dermatol . 1992;27:182–188.  PubMed

 

56. Marks J, et al. J Am Acad Dermatol . 1995;33:212–216

 

57. Anonymous. Fact Sheet from Product Info. Packet, EnviroDerm Pharmaceuticals, 929 S. 3rd St., Louisville, KY 40203 (502) 634–7700.