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A 59-year-old man presents to the emergency department complaining of a diffuse, painful rash. The rash first arose 3 months ago and resolved after a course of oral prednisone. However, the rash recurred a month ago, manifesting in its current state and affecting most of the surface of his upper and lower extremities. No new drugs were added when the initial rash started, and he received only tapered prednisone therapy before his most recent presentation. At that time, he began applying an antibiotic ointment (Neosporin) on affected areas, with subsequent worsening of his rash. A short course of fluocinonide cream resulted in mild improvement. He is now taking only hydroxyzine for symptomatic relief of severe pruritus. He denies having other complaints.

The patient's medical history is significant for allergic contact dermatitis and hypertension. On physical examination, fissuring is present on the creases of his palms and heels, and his nails are thin. An erythematous, macular, scaly rash is observed on the patient's forearms and on the lateral aspects of both thighs, with multiple excoriations and pale, superficial ulcerations. His vital signs and the rest of the physical findings are unremarkable. A KOH preparation of a sample obtained from a thigh lesion yielded negative results.

What is the diagnosis?


Allergic contact dermatitis due to neomycin allergy, also known as neomycin sulphate allergy: Allergic contact dermatitis is a T cell–mediated, delayed skin hypersensitivity reaction to a specific antigen, such as common metals, dyes, rubber products, or cosmetics. Women are more commonly affected than men, and nickel is the most common allergen. The risk of neomycin allergy is directly related to the extent of use in a population. Neomycin is widely included as an ingredient in topical creams, and it is a component of Neosporin, an antibiotic product used to treat minor skin infections. The risk of contact dermatitis is higher when this agent is used to treat chronic stasis dermatitis than when it is used as a topical antibiotic, eg, applied to cuts in children. Chemically related aminoglycoside antibiotics include gentamicin and tobramycin; these should be avoided in individuals allergic to neomycin. Other cross-reactions involve framycetin, kanamycin, puromycin, spectinomycin, and streptomycin. Neomycin also co-reacts with bacitracin.

On physical examination, acute allergic contact dermatitis is characterized by pruritic papules and vesicles on an erythematous base. The lesions are sharply delineated. The reaction develops over 48 hours at the site of contact with the allergen. The skin initially becomes pruritic, red, and swollen. Tiny blisters develop and may rupture and leave ulcers, crusted vesicles, and scales. An inflamed, weepy ulcerated rash can result. The skin thickens with repeated exposure and can become increasingly erythematous and scaly. The skin may darken and become leathery and cracked. Chronic allergic contact dermatitis can manifest as lichenified, pruritic plaques.

Allergic contact dermatitis is a type IV or cell-mediated immune reaction. The reaction is mediated by lymphocytes and not antibodies. First, an induction phase occurs in which naïve lymphocytes are sensitized to an allergen. Allergens can be chemicals or haptens and are typically weak allergens that require several exposures for sensitization to occur. Langerhans cells and dermal dendritic cells, the antigen-presenting cells of the skin, first recognize the antigens. These cells then migrate through the lymph system to lymph nodes, where they interact with naïve T cells. Production of memory T cells results, and these T cells pass into general circulation by means of the lymphatic system. The T cells are now considered sensitized.

Once sensitized, T lymphocytes react when they subsequently encounter the antigen. On further exposure, the dendritic cells and Langerhans cells re-express the antigen. The T cells then recognize the antigen and release cytokines, interferon (IFN)-gamma, interleukin (IL)-8, and IL-2, which activate and recruit lymphocytes. Inflammatory cells accumulate in the dermis and epidermis, resulting in the elicitation phase of allergic contact dermatitis reaction.

The ability of allergens to sensitize varies. Poison ivy, for example, sensitizes after one exposure, whereas bricklayers who are exposed to chrome become allergic to it after a mean of 10 years. Localized contact dermatitis can develop into a generalized, symmetric reaction remote from the initial contact area. This is also known as the id reaction.

Treatment involves prompt removal of the causative agent, in this case neomycin. The allergic reaction is limited to the site of exposure and improves within weeks after the allergen is removed. Management of acute dermatitis includes the application of topical corticosteroids and emollients.

To diagnose neomycin allergy, a patch test is performed by using 20% neomycin in petrolatum. A positive result is an indurated papule that appears after 48 hours. If the result is negative, testing with an intradermal injection of neomycin 1:1000 can be considered; a positive result is a papule appearing in 24-48 hours.


  • Hogan D. Contact Dermatitis, Allergic. eMedicine Journal [serial online]. January 12, 2005. Available at:
  • Hunter J, Savin J, Dahl M. Clinical Dermatology. 3rd ed. Malden, Ma: Blackwell Publishing; 2002.
  • Leyden JJ, Kligman AM. Contact dermatitis to neomycin sulfate. JAMA 1979 Sep 21;242(12):1276-8.
  • Rietschel RL, Fowler JF, eds. Fisher's Contact Dermatitis. Philadelphia, Pa: Lippincott Williams and Wilkins; 2001.

Link to further Information on:

For more information on neomycin allergy, see the eMedicine articles Contact Dermatitis, Allergic and Drug Eruptions (within the Dermatology specialty).