A 9-year-old boy is brought to the office due to oozing skin lesions on his legs. The patient developed the rash yesterday and has been uncomfortable due to pain and pruritus. He and his father returned 4 days ago from their annual camping excursion; they had applied sunscreen and insect repellants during the trip. The patient takes no medications and has no known allergies. Skin examination shows a well-demarcated tan line starting just above the knee as well as scattered erythema with overlying vesicles in a linear arrangement below the knees. Some lesions appear wet and others have a thin, crusted coating. Which of the following mechanisms is most likely responsible for this patient's skin findings?
Hypersensitivity reactions | ||
Immunology | Examples | |
Type I (immediate) | IgE-mediated |
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Type II (cytotoxic) | IgG & IgM autoantibody-mediated |
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Type III (immune complex) | Antibody-antigen complex deposition |
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Type IV (delayed type) | T cell- & macrophage-mediated |
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Allergic contact dermatitis (ACD) is a T cell-mediated, type IV hypersensitivity reaction. This type of reaction requires prior exposure to the allergen, allowing antigen-specific T cells to proliferate and, on reexposure, create a delayed inflammatory response. Classic antigens include urushiol (Toxicodendron plants [poison ivy, oak, sumac]), nickel (jewelry, belt buckles), and neomycin (a topical antibiotic).
ACD due to poison ivy exposure often causes linear lesions due to allergen inoculation into the skin by the branches and leaves of the plant. Starting 12 hours after exposure, severe pruritus and erythematous streaks develop with edema and vesicles, often leading to weeping drainage and crusting. Diagnosis is clinical, and lesions typically resolve within 1-3 weeks. Prevention is achieved by allergen avoidance (eg, wearing pants and long-sleeved shirts), and treatment includes reduction of post-exposure spread (eg, removing exposed clothing, washing fingernails) and topical/oral corticosteroids.
(Choice A) Antibodies can form complexes with antigens and activate the complement cascade in type III hypersensitivity reactions. Poststreptococcal glomerulonephritis is a condition in which streptococcal antibody-antigen complexes deposit in the glomerulus, leading to edema, hypertension, and hematuria.
(Choice B) Cytotoxic reactions result from antibody (IgM or IgG) binding to an already cell-bound self-antigen (autoantibody-antigen binding), leading to complement activation and cell damage. In autoimmune hemolytic anemia, an antibody directed toward red blood cell surface antigens leads to cell lysis.
(Choice C) Exposure to ultraviolet radiation can cause DNA damage to epidermal cells, causing local inflammation. A resulting sunburn presents with pain, erythema, and blistering if severe. The linear arrangement and use of sunscreen in this patient make this diagnosis unlikely.
(Choice D) IgE-mediated hypersensitivity reactions occur when an allergen binds to and cross-links IgE molecules attached to mast cells. In turn, mast cell activation results in the immediate release of histamine and other inflammatory mediators. This process is seen in anaphylaxis as well as urticaria (raised, erythematous, pruritic plaques without vesicles).
Educational objective:
Allergic contact dermatitis is caused by T cell-mediated (delayed, type IV) hypersensitivity and presents with erythema, edema, and vesicles >12 hours after contact with the allergen (eg, poison ivy, nickel).