.A phenomenon when a client who exhibits hypersensitivity reaction to an antibiotic may develop a similar reaction with an agent in the same or related chemical class
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Antibiotics are commonly prescribed to treat a variety of bacterial infections. As with all medications, hypersensitivity reactions may occur and clinicians should be able to recognize them accurately and recommend appropriate management. Antibiotic related hypersensitivity reactions may be one of four different types: Type I reactions, which are IgE mediated and may lead to anaphylaxis; Type II reactions that are antibody-mediated and may result in thrombocytopenia, neutropenia, or hemolytic anemia; Type III reaction that involves an immune complex formation such as vasculitis; and Type IV reactions that consist of four subtypes and typically include a rash of varying level of severity with or without systemic signs and symptoms. Herein, we describe the mechanisms of different types of allergic reactions to commonly prescribed antibiotics and offer recommendations for management. Further, we briefly refer to antibiotic reactions that mimic hypersensitivity reactions but are not immune mediated, such as pseudoallergies and serum sickness-like reactions.
Keywords: antimicrobial, hypersensitivity, antibiotic, allergy, anaphylaxis, Type I, Type II, Type III, Type IV
The discovery of antibiotics to treat bacterial infections has been one of the greatest achievements in medicine. Such drugs may be used to treat a variety of diseases, from mild to life threatening. However, drug hypersensitivity reactions (DHR) can exclude some patients from receiving these medications. Patients with true DHR need to be promptly identified and managed as they may develop life-threatening complications from the offending drug. Understanding the underlying immunologic mechanisms of DHR can help clinicians distinguish between true hypersensitivity vs. inaccurate and potentially harmful antibiotic allergy diagnoses. If DHR is suspected, further work-up into classifying the immune-mediated process will be necessary to appropriately manage the patient both acutely and long-term.
Different classification systems have been developed to categorize DHR. The International Consensus on drug allergy (ICON) classifies DHR clinically by the onset of actions as either immediate or delayed [1]. Immediate reactions are usually IgE-mediated and occur within the first hour of drug administration, while delayed reactions are a heterogenous group of immune mediated reactions that typically take days to weeks to occur. The Gell and Coombs system classifies DHR by their immunologic mechanism into four categories (Type I–IV) [2]. Type I reactions are immediate and IgE-mediated, where IgE antibodies specific to the allergen bind to mast cells and trigger the release of mediators such as histamine and leukotrienes, among others, to cause vasodilation and increased capillary permeability [1,2,3,4,5,6]. Type II, III, and IV reactions are delayed in onset. Specifically, type II hypersensitivities are the result of antibodies binding to cell surface antigens, leading to an antibody-dependent cell-mediated cytotoxicity. Type III hypersensitivities are due to the development of an immune complex formation which deposits in vasculature and tissues, activating the complement that releases inflammatory mediators [1,2,3,4,5,6]. Lastly, type IV hypersensitivity is mediated by T cells and occurs when T cells are sensitized to an antigen. These antigens may be the drug itself or its metabolite. Such products may then bind to serum or cell bound proteins, creating an immunogenic molecule, which is subject to the antigen processing pathway and presentation to T cells. Type IV reactions are further subcategorized into four groups (IVa, IVb, IVc, IVd) depending on the specific T cell type involved [1,2,3,4,5,6,7].
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