Case report: A 23-year-old female presents to the emergency department due to the development of a perioral rash that has developed over the past few days that is intensely pleuritic, she reports the rash looks like “little bubbles” and when she looked up pictures online “it looks like herpes”. She reports she has not been recently sexually active with past sexual history of one, long term partner since she was sixteen. Which she has broken up with 6 months ago. The patient reports that the rash looks like an itchy rash she had on her legs last year when she was gardening. Patient ROS negative for cardiac, pulmonary, urinary, MSK, GI, and neurological complaints, no fever, chills, or sick contacts. No eye pain nor vision complaints. Patient has no significant PMH, PSH, is not on any medications, and reports only environmental allergies. No reported family history of auto-immune diseases. Patient reports that she grew up in a small town and only typically eats “American foods” but has recently started branching out and eating more “exotic foods” including quinoa, mangos, kiwi, and fancy cheeses” that she has been getting from a local store.

Physical exam: HR: 68, RR:14, SPO2: 99%, BP: 118/76. Temp: 36.8. Unremarkable cardiopulmonary, abdominal, musculoskeletal, and neurologic exam. Skin exam significant for a pleuritic, vesicular, mild ulcerated B/L perioral rash with signs of crusting and mild yellow transudative appearing fluid. Similar to the picture below (figure 1) (1):

Urushiol oil:

What it is: Urushiol oil is a mixture of 1-(alkyl)- )-2,3-dihydroxybenzene, and 1-(alkenyl)-2,3-dihydroxybenzene along with other phenolic lipid arrangements, which are lipid soluble organic compounds that are manufactured by a variety of different plant species for defense (8). They have the ability in humans to cause a type-4 lymphocyte mediated hypersensitivity reaction in humans. Leading to contact dermatitis on the skin (4). The substance is more dangerous when present near the eyes and/or when inhaled. It is estimated that 50-75% of the population can have a reaction to the urushiol oil and that race/ethnicity, gender, and age do not confer an increased degree of risk (9).

Where it is found: In the United States contact with urushiol oil is most common with skin contact with the following three plants: poison ivy, poison oak, and poison sumac. Poison ivy consists of 3 species: Toxicodendron radicans, Toxicodendron rydbergii, and Toxicodendron orientale. It is primarily found Throughout eastern Canada extending southward through the eastern United States into Mexico, the Bahamas and Bermuda. T. orientale is found in eastern Asia. Plant description: Plant can be a vein, shrub, or a small ground dwelling plant with different leaf patterns and varieties, general consistencies are white berries during summer, and the leaflets are in pairs of three and alternate on the stem. Refer to figure 2 below (3).

Poison oak includes two species; Toxicodendron diversilobum, which occurs along the pacific coast of the United States and Toxicodendron pubescens (Atlantic poison oak), which occurs in the southeastern portion of the United States. Plant description: deciduous ground dwelling plant that can be as large as a shrub. A set of three leaflets, like poison ivy. Leaves can have a tri-lobed appearance and resemble an oak, Refer to figure 3 below (5).

Poison sumac (Toxicodendron vernix) is found on the eastern coast of the United States primarily in the southern US and mid-Atlantic region. Plant description: It can appear as a shrub or small tree, at maximum of 9 meters in height. It has white berries and pinnate style leaves, each containing 7-13 leaflets in an oblong oval shape. Refer to figure 4 below (6).

Urushiol oil can also be found in Toxicodendron vernicifluum, and similar species due to it being a key ingredient in natural lacquers for home and manufacturing purposes. In addition, it is also found on the surface of the casings of unwashed/non-prepped edible nuts including cashews and pistachios. Urushiol is also present in mangos, more specifically on the skin, and concentrated near the stem. It is also present in the sap from a mango tree (2).

Pathophysiology: Exposure to the lipid soluble phenolic compounds with the skin and mucosal membranes, where it is readily absorbed can cause a delayed, T-cell mediated type 4 hypersensitivity reaction. Which in turn causes contact dermatitis. After the oil is absorbed, it is oxidized to quinone intermediates which can bind to antigen presenting cells in the epidermis. The antigen presenting cells (APCs) then travel to the lymph nodes and present it to the T-cells, which in term causes sensitization to the compounds (4). After sensitization, upon re-exposure of the compounds, clonal lymphocytes can elicit a cell meditated cytotoxic cascade that tends to lead to the production of the vesicles and erythema by irritating the underlying vasculature and causing destruction of epidermal cells (4).

The keratinocytes present in the epidermal tissue can also produce a variety of cytokines including TNF-alpha, Interleukins 8,6,1, along with granulocyte macrophage colony stimulating factor, which in turn contribute to a more pronounced immune response (13). Production of leukotrienes as well as prostaglandin by monocytes can also occur and can be one of the main causes of the delayed inflammatory response seen in the rash. This portion of the inflammatory cascade also tends to be responsive to corticosteroids.

For smoke inhalation exposure, the heat of the fire is enough to destroy the compound. It is not aerosolized in that manner, instead the urushiol oil is attached to dust and ash suspended in the air from the fire and inhaled (12).

Duration: The typical delay between exposure to urushiol oil and eruption of a rash is 1-2 days but can be as little as 5 hours up to 15 days (4). Without any form of intervention/treatment, the symptomatic course of the reaction usually runs from 2 to 3 weeks. In more severe cases it can be up to 6 weeks in duration.

Severity: The degree of reaction is depending on a number of factors including the degree/area of exposure, length of exposure, sensitization, and time since exposure without intervention. Higher concern should be given to patients with a reaction on their face, especially involving or close to their eyes as well as a smoke inhalation exposure. Very mild skin reactions may have slight erythema and lack vesicles. More severe reactions can develop vesicles that progress to bullae, notable edema and notable pruritis and discomfort. Erythema multiforme is a known, but very rare complication of severe reactions. Smoke mediated exposure tends to cause respiratory irritation and diffuse contact dermatitis.

Treatment: Treatment options are highly dependent on both the length of time since initial exposure, the severity of the exposure, and the location of the reaction. Urushiol oil is easily degraded in water and due to its lipophilic nature can be removed by saponification. It is important to note that removal of the oil will only likely have a clinically significant effect if it is removed very shortly after the exposure. At 10 minutes post exposure, 50% can be removed; at 15 minutes, only 25% can be removed. At the 30-minute mark, only 10%. After 30 minutes post exposure almost all of it has been absorbed (4).

Best initial method is gentle scrubbing with soap and cool water. Avoid vigorous scrubbing as it may spread the oil to other unaffected regions. A study performed by Adam S. Stibich MD et al. demonstrated that Tecnu®, Dial® ultra dishwashing soap, and Goop®, all had good efficacy vs no treatment with 2 hours post exposure, with a more cost affordable price point for Dial® and Goop® (8).

Topical antihistamines and topical antibiotics do not have a role in treatment as they do not have a positive impact in both length of clinical course and symptomatic outcomes. Some have the ability to sensitize the skin and worsen lesions (9). Jewel weed, a traditional remedy in the United States has not been shown to show increased efficacy compared to distilled water in the literature at this time (10).

Over the counter symptomatic management agents include: Zanfel cream and oral antihistamines which have been studied and have some efficacy (11). Calamine lotion, oatmeal, baking soda baths, hot tub treatments and vinegar have also been used. Which are unlikely to cause harm but have not been consistently studied for efficacy.

Topical corticosteroids can have a role in smaller reactions, and early on in the reactions when erythema and pruritis is present but before vesicles and large bullae form. These have less limited efficacy in more severe, more widespread reactions due to the amount of topical corticosteroids that would be used. Which would increase their risk if thinning the skin and causing adrenal suppression due to their rapid absorption (4). Using moderate strength creams 2-3 times daily such as 0.1% triamcinolone or 0.1% betamethasone may help with symptom management. These creams however should not be used on the face or genitalia. Instead, lower dose creams such as 1% hydrocortisone or 0.2% hydrocortisone valerate should be considered.

Systemic corticosteroids: Can be given either IV, IM or orally and are the mainstay of treatment for moderate to severe reactions with higher efficacy if given earlier in the course of the reaction. Dosing recommendations are to 2 mg/kg per day (0.5 mg/kg per day in children) once daily for 7-10 days (4). This is followed by 7–10-day taper.

In severe cases of urushiol oil smoke inhalation, systemic steroid and airway management may be needed as well as antibiotics prophylactically to help protect against opportunistic lung infections.

Primary prevention and mitigation techniques: When gardening, landscaping, handling brush and/or doing outside recreational activities it is advisable to wear long sleeve shirts, gloves and long pants, and safety glasses. Urushiol oil can penetrate “wet” clothing easier than dry clothing and can penetrate through latex gloves but not vinyl gloves (4).

Taking a moment and properly identifying the plants around you to ensure that there is no poison ivy, oak, or sumac is the best way to prevent contact. It is important to note that the plant does not have to be actively growing for you to get exposed. If the plant is dormant during fall-winter, damage to the plant can still release the oil. Wash the handles of all tools with soapy water after use to avoid cross contamination. Wash all clothes in hot, soapy water that may have been contaminated. The oils and their effects are destroyed by heat. Avoid rubbing your eyes with your hands.

If you are performing a brush pile burn, please identify what you are burning to avoid accidentally burning Toxicodendron plants that can lead to widespread dermatitis, eye irritation, lung irritation and mucosal membrane damage. If you are highly sensitive to these compounds please avoid gingko trees, mangos with the skins on them and improperly prepared cashews, pistachios. As well as “natural” lacquer finishing products for wood working.

Case conclusion: HSV-1 and HSV-2 PCR testing were negative. CMP, CBC unremarkable, patient does not have any other lesions, no rash present near eyes, no fever, and no history of auto-immune disease.  Diagnosis of urushiol induced contact dermatitis is made. Patient was given the precautions to avoid mangos at this time and the plan was a scheduled follow-up with ENT for allergy testing and with primary care as needed. Due to concerns about the rash being present on the face, the patient was given a 7-day dose of oral corticosteroids, followed by a 7-day taper, in addition to an antihistamine. Patient was advised she could use 1% hydrocortisone cream or 0.2% hydrocortisone valerate (4) but not to use a stronger topical steroid cream due to potential side effects. Advised she could use Zanfel and/or calamine lotion for additional symptomatic management. Patient education: about urushiol contact dermatitis and the likely length and progression of symptoms, discharged.

Literature discussion: Although corticosteroids have highly regarded efficacy; more research studies are necessary to help either support and/or disprove the efficacy claims of many post-exposure topical over the counter and home remedy products. The study produced by Adam S. Stibich MD et al for example did show the efficacy of Tecnu®, Dial® ultra dishwashing soap, and Goop® compared to a control, but not compared to each other, and used a very small sample size of participants n=20, which was non-randomized. (8,4).

A randomized, double-blinded comparison study produced by Long et al., was able to show that jewelweed, a traditional remedy did not have increased efficacy, compared to the control, distilled water (10). But more follow-up studies are likely needed.

Davila A. et al., (11) performed a randomized, double-blind, placebo-controlled study showing a statistically significant improvement in erythema, induration, and vesiculation at 48, 96, and 144 hours post exposure using Zanfel compared to control. The N value was only 24 in the study, and it contained confounding variables including the degree of sensitization of participants as well as the amount of urushiol oil used for exposure (which may have varied). More research is needed, especially considering how widespread this product is in the marketplace and its high price point relative to other options.

Written By: Michael DeCarolis, DO

Peer Reviewed and Edited by: Stevely Koshy, DO

References:

1.- Shubhavinyasa et al., Contact Dermatitis due to Mango Sap – A Case Report, IJHSR, ISSN: 2249-9571, Vol.3; Issue: 5; May 2013, https://www.ijhsr.org/IJHSR_Vol.3_Issue.5_May2013/15.pdf

2.- Yoo MJ, Carius BM. Mango Dermatitis After Urushiol Sensitization. Clin Pract Cases Emerg Med. 2019;3(4):361-363. Published 2019 Sep 30. doi:10.5811/cpcem.2019.6.43196, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861053/

3.- ©2020 Carnegie Institute, https://carnegiemnh.org/collected-on-this-day-poison-ivy/

4.- Aaron C.Gladman MD, Toxicodendron Dermatitis: Poison Ivy, Oak, and Sumac, Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance, CA, Wilderness & Environmental Medicine, Volume 17, Issue 2, June 2006, Pages 120-128, https://www.sciencedirect.com/science/article/pii/S108060320670299X

5.- Office of Public Affairs, Jul 01, 2014 11:45 PM, Copyright © 2022 University of Utah Health, https://healthcare.utah.edu/healthfeed/postings/2014/07/070214_poisonous-plants.php

6.- Toxicodendron vernix, North Carolina Extension Gardener Plant Toolbox, NC State University and N.C. A&T State University, https://plants.ces.ncsu.edu/plants/toxicodendron-vernix/#poison

7.- Charles Farber et al., Confirmatory non-invasive and non-destructive identification of poison ivy using a hand-held Raman spectrometer, Department of Biochemistry and Biophysics, Texas A&M University, College Station, Texas 77843, USA., Royal Society of Chemistry, DOI: 10.1039/D0RA03697H (Paper) RSC Adv., 2020, 10, 21530-21534, https://pubs.rsc.org/en/content/articlehtml/2020/ra/d0ra03697h

8.- Adam S. Stibich MD et al., Cost-effective post-exposure prevention of poison ivy dermatitis, International journal of dermatology, Volume39, Issue7, July 2000, Pages 515-518, https://doi.org/10.1046/j.1365-4362.2000.00003.x

9.- Williford PM, Sherertz EF. Poison ivy dermatitis—nuances in treatment. Arch Fam Med. 1994;3:184–188., https://www.ncbi.nlm.nih.gov/books/NBK557866/

10.- Long D, Ballentine NH, Marks JG. Treatment of poison ivy/oak allergic contact dermatitis with an extract of jewelweed. Am J Contact Dermatitis. 1997;8(3):150–153, https://pubmed.ncbi.nlm.nih.gov/9249283/

11.- Davila A, Lucas J, Laurora M, Jacoby J, Reed J, Heller M. A new topical agent, Zanfel, ameliorates urushiol-induced Toxicodendron allergic contact dermatitis [abstract 364]. Annals Emerg Med. 2003;42(suppl 4):s98.

12.- Burrill et al., Poison oak and poison ivy, weeds, Pacific northwest extension paper, 108, May 1994., https://www.kcgov.us/DocumentCenter/View/4083/Poison-Oak-and-Ivy-PDF

13.- Kupper TS. Production of cytokines by epithelial tissues. A new model for cutaneous inflammation. Am J Dermatopathol. 1989;11(1):69–73., https://pubmed.ncbi.nlm.nih.gov/2644870/