Eczematous reaction from skin contact with chemical irritants (ICD) or allergens triggering type IV hypersensitivity (ACD).
Also known as: contact dermatitis, allergic contact dermatitis, irritant contact dermatitis, ACD, ICD, poison ivy
Overview
Inflammatory dermatitis caused by direct contact with an exogenous agent. Two main forms: irritant contact dermatitis (ICD, non-immunologic toxic injury) and allergic contact dermatitis (ACD, T-cell mediated type IV delayed hypersensitivity).
Epidemiology
ICD accounts for ~80% of all contact dermatitis; most common occupational skin disease (hairdressers, healthcare, cleaning, construction, food handling). ACD prevalence ~20%; nickel is the most common allergen worldwide.
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Question 1DermatologyMedium
A 45-year-old female develops red itchy linear streaks on her arm 2 days after gardening. The pattern follows where leaves brushed her skin. Which of the following is the most likely diagnosis?
AAllergic contact dermatitis
BAtopic dermatitis
CContact urticaria
DIrritant contact dermatitis
ENummular dermatitis
Reveal answer & full explanation
Correct answer: A — Allergic contact dermatitis
AAllergic contact dermatitis✓
BAtopic dermatitis
CContact urticaria
DIrritant contact dermatitis
ENummular dermatitis
Why Allergic contact dermatitis is correct
Allergic contact dermatitis is a type IV (delayed) hypersensitivity reaction, T-cell mediated, requiring prior sensitization
Onset occurs 24–72 hours after re-exposure to the allergen
The linear streak pattern following where leaves brushed the skin is characteristic of Toxicodendron (poison ivy/oak/sumac) contact — the urushiol oil causes this linear distribution
Treatment: avoid the allergen, topical mid-to-high potency corticosteroids, oral corticosteroids if severe
Patch testing identifies the specific causative allergen
Why the others are wrong
Irritant contact dermatitis — more common than allergic; non-immunologic (no prior sensitization required); caused by direct cellular damage from soap, detergent, or solvent; typically presents with more burning/stinging rather than pruritus; an acute reaction to a strong irritant appears within minutes to hours of exposure, not 2 days later
Nummular dermatitis — chronic, intensely pruritic coin-shaped (discoid) eczematous plaques on the extremities, often in the setting of dry skin; not triggered by plant contact and does not form linear streaks
Atopic dermatitis — chronic pruritic eczema in flexural distributions; not caused by plant contact and does not produce linear streaks
Contact urticaria — plant contact during gardening can cause it, but contact urticaria (IgE-mediated, as with latex, or nonimmunologic, as with stinging nettle) produces wheals within minutes to an hour of contact that usually fade within hours; a rash appearing 2 days after exposure fits a delayed, T-cell-mediated reaction
Additional high-yield points
Most common cause of allergic contact dermatitis in adults: nickel (found in jewelry, snaps, watches)
Distinguishing allergic from irritant contact dermatitis: allergic is typically more pruritic and appears 1-3 days after exposure; irritant causes more burning/stinging and, after a single strong exposure, appears within minutes to hours
Question 2DermatologyMedium
A 40-year-old man who clears brush along utility lines has had two or three episodes of poison ivy dermatitis every summer for several years; one was extensive enough to require oral glucocorticoids. During past episodes, new itchy patches kept appearing over several days, on his face and wrists as well as the original streaks on his forearms. He already wears work gloves and long sleeves on the job. His skin is clear today. He asks what will most reduce his outbreaks, because he cannot avoid the plants at work. Which of the following is the most appropriate counseling?
AStart allergy shots to build tolerance to urushiol
BKeep blister fluid off unaffected skin during each flare
CWash skin, clothing, and tools promptly with soap and water
DApply hydrocortisone 1% to arms, neck, and face before work
ETake a non-sedating oral antihistamine before each shift
Reveal answer & full explanation
Correct answer: C — Wash skin, clothing, and tools promptly with soap and water
AStart allergy shots to build tolerance to urushiol
BKeep blister fluid off unaffected skin during each flare
CWash skin, clothing, and tools promptly with soap and water✓
DApply hydrocortisone 1% to arms, neck, and face before work
ETake a non-sedating oral antihistamine before each shift
Why Wash skin, clothing, and tools promptly with soap and water is correct
Poison ivy dermatitis is a type IV (delayed, T-cell-mediated) allergic contact dermatitis to urushiol, the oily resin in Toxicodendron plants. Once he is sensitized, the dose of urushiol that reaches his skin determines whether he reacts, and every re-contact counts.
Urushiol binds to skin within minutes. Washing exposed skin with soap and plenty of water as soon as possible after contact (ideally within minutes, and including under the fingernails) removes resin before it can bind. This is the core recommendation in AAD patient guidance and in CDC/NIOSH guidance for outdoor workers who are exposed to poisonous plants.
Urushiol also stays active on gloves, sleeves, boots, and tools for a long time (reportedly years). Gloves and long sleeves protect him only if they are washed, and tools only if they are cleaned, after exposure. Otherwise he touches the resin again every time he picks them up or pulls them off.
This also explains his history. The new patches on his face and wrists came from resin carried there by his hands and contaminated gear, plus the normal delay at sites that got less resin. They did not come from the rash itself, so removing the resin is what stops new patches from appearing.
Why the others are wrong
Take a non-sedating oral antihistamine before each shift - histamine does not drive a type IV T-cell reaction, so taking an antihistamine first does not stop sensitized skin from reacting to urushiol. Antihistamines barely relieve the itch of allergic contact dermatitis either, apart from a sedating dose at bedtime (the trap is treating poison ivy like a type I allergy).
Apply hydrocortisone 1% to arms, neck, and face before work - a topical steroid is not a barrier and does not keep urushiol off the skin, so putting it on beforehand does not prevent the reaction. Hydrocortisone 1% is also too weak to help much once poison ivy dermatitis starts (the trap is thinking a treatment also works as prevention).
Keep blister fluid off unaffected skin during each flare - blister fluid contains no urushiol, so it cannot spread the rash to him or anyone else. New lesions appearing over days reflect uneven resin doses and repeated contact with contaminated hands, clothing, and tools. This advice does nothing to reduce his future outbreaks (the trap is the common myth that the rash spreads through its fluid).
Start allergy shots to build tolerance to urushiol - desensitization works for some IgE-mediated allergies such as insect venom, and urushiol extracts were tried for poison ivy in the past, but they gave inconsistent protection with side effects, and no urushiol immunotherapy is approved or recommended today. Shots would also do nothing about the resin he keeps re-contacting on his skin and gear (the trap is assuming any allergy can be desensitized).
Additional high-yield points
Other accepted preventive measures work alongside prompt washing. They include protective clothing and appropriate gloves (washed after each exposure), and bentoquatam 5% lotion, a barrier applied about 15 minutes before possible exposure and reapplied every few hours.
Washing later is still worthwhile even when it is not prompt: it removes any resin that has not yet bound and stops further spread from contaminated gear and pets' fur. The sooner he washes, the better it works.
Never burn poison ivy, oak, or sumac. Urushiol carried in the smoke can cause severe reactions in the airway and lungs as well as on the skin.
Poison ivy, poison oak, and poison sumac all contain urushiol and cause the same dermatitis. Cross-reactions can also follow contact with mango skin and cashew shells.
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Antibiotic only if secondary bacterial infection — cephalexin, dicloxacillin
Topical antipruritic: pramoxine, menthol
Refer to occupational medicine for workers' compensation documentation
Complications
Secondary bacterial infection (S. aureus, S. pyogenes)
Post-inflammatory hyperpigmentation, especially Fitzpatrick IV-VI
Chronic occupational hand dermatitis → job loss, disability
Erythroderma in widespread severe cases
Steroid-induced atrophy with prolonged high-potency topical use
PANCE pearls
Linear streaky vesicles after hiking = poison ivy / oak / sumac (urushiol). The fluid in vesicles does NOT spread the rash; new lesions reflect different exposure doses absorbed at different rates.
Eyelid dermatitis from nail polish (tosylamide formaldehyde resin) is classic — patient touches eyes with allergen-coated nails.
Nickel patch testing is positive in ~15-20% of women and ~5% of men; the dimethylglyoxime spot test identifies nickel-releasing metal jewelry.
Topical neomycin and bacitracin are common ACD culprits — avoid prophylactic 'triple antibiotic' on clean wounds; petrolatum is sufficient.
Oral prednisone for poison ivy MUST be tapered ≥14-21 days; shorter courses cause rebound.
Toxicodendron prevention when exposure cannot be avoided: wash exposed skin (including under the nails) with soap and water as soon as possible, because urushiol binds within minutes; wash clothing, gloves and tools, where the resin stays active for a long time; bentoquatam 5% lotion applied before exposure is a barrier option; never burn the plants (smoke carries urushiol into the airway).
References
AAD/ACDS 2020 — American Contact Dermatitis Society Core Allergen Series (Schalock et al., Dermatitis 2020)
NACDG — North American Contact Dermatitis Group Patch-Test Results Periodic Reports (DeKoven et al., Dermatitis)
BAD 2017 — British Association of Dermatologists' Guidelines for the Management of Contact Dermatitis 2017 (Johnston GA, Exton LS, Mohd Mustapa MF, et al., Br J Dermatol 2017;176(2):317-329)
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