Delayed Hypersensitivity Reactions Clinical Presentation

Updated: May 07, 2018
  • Author: Stuart L Abramson, MD, PhD; Chief Editor: Michael A Kaliner, MD  more...
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Presentation

History

The clinical history of delayed hypersensitivity reactions differs depending on the etiology. Some of the more common examples are as follows:

Contact hypersensitivity (ie, allergic contact dermatitis)

Patients often report being in wooded areas or having made contact with poison ivy or poison oak, which caused a rash, itching, or both.

The exposure occurs 48-72 hours before the development of symptoms.

Tuberculin hypersensitivity reactions

Many times during a routine health screening, patients have a positive Mantoux test result and are asymptomatic. In these cases, patients may recall being exposed to someone with TB or with a chronic cough. In many cases, patients do not recall a possible exposure.

The Mantoux test itself is a delayed hypersensitivity reaction. [2, 3] Thus, 48-72 hours following the intradermal administration of purified M tuberculosis protein derivative, patients who have been exposed to the bacteria develop a delayed hypersensitivity reaction manifested by inflammation and edema in the dermis. [4]  A positive Mantoux test is the result of the recruitment of several types of mononuclear leukocytes and the release of several cytokines that promote the DTH inflammatory reaction (see Pathophysiology section).  Measurement by the QuantiFERON test of interferon production by peripheral blood mononuclear cells has been used as an in vitro surrogate for the Mantoux test.

Granulomatous hypersensitivity reactions

Diseases in which delayed hypersensitivity is the major pathophysiological response include tuberculous leprosy, TB, sarcoidosis, and schistosomiasis. The inability to mount an adequate delayed hypersensitivity response results in a poor outcome in diseases such as leprosy and tuberculosis. 

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Physical

The physical examination findings can be normal, or they can reveal the signs and symptoms of the specific disease.

  • Contact hypersensitivity: Examination usually reveals edematous and erythematous epidermal tissue with microvesicles. If the offending antigen is from the Rhus genus of plants, the involved area usually appears in a linear fashion. If the offending antigen is nickel (eg, jewelry), then the involved area is oriented in a fashion consistent with the area of contact. Long-term nickel exposure results in an eczematous dermatitis with lichenification of the skin.

  • Tuberculin hypersensitivity reactions: Approximately 48-72 hours following the intradermal administration of purified M tuberculosis protein, patients who have been sensitized to M tuberculosis by previous exposure develop an area of erythema and induration.

  • Granulomatous hypersensitivity reactions: The physical examination findings differ depending on the underlying disease. For example, if the patient has active TB, then a chronic cough, malaise, night sweats, weight loss, and pyrexia are present.

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Causes

Delayed hypersensitivity reactions are normal physiological events. Anything that alters these normal events can lead to multiple opportunistic infections. Immune deficiencies (congenital or acquired) and immunosuppressive agents can alter this normal response.

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