Author: Mike Sharland, Karina Butler, Andrew Cant, Ron Dagan, Graham Davies, Ronald de Groot, David Elliman, Susanna Esposito, Adam Finn, Manolis Galanakis, Carlo Giaquinto, Jim Gray, Paul Heath, Terho Heikkinen, Ulrich Heininger, Philipp Henneke, Irja Lutsar, Hermione Lyall, Federico Martinon Torres, Andrew Pollard, Mary Ramsay, Andrew Riordan, Fernanda Rodrigues, Emmanuel Roilides, Pablo Rojo, Delane Shingadia, Steve Tomlin, and Maria Tsolia
Format: Webpage Publisher: Oxford University Press
Published: 2016
Print ISBN-13: 9780198729228
DOI: 10.1093/med/9780198729228.001.0001
Antimicrobial agents either kill (bactericidal) or inhibit (bacteriostatic) the growth of a microorganism by targeting specific unique bacterial sites or metabolic pathways. Common antibiotic adverse effects and toxicities include allergic reactions, numerous possible toxicities, alteration of human flora, drug interactions, and promoting of antibiotic resistance. Presumptive and empirical therapy relies on the clinical syndrome and anatomical site of infection. Factors to consider when choosing empirical therapy include identification of the organism, the estimated benefit to the patient, the probable susceptibility of the isolated (or suspected) pathogen based on laboratory results or local epidemiological parameters, and pharmacokinetic/pharmacodynamic considerations. Host factors, including age, immune deficiency status, and other underlying conditions, should always be considered when choosing an antibiotic. There are few absolute indications for the prophylactic use of antimicrobials, and this is one area where misuse is common. The susceptibility of common pathogens is often predictable, allowing adequate empirical treatment. The main driver for the development of antibiotic resistance is the inappropriate use of antibiotics. Bacteria may be naturally resistant or may acquire resistance by means of DNA mutation or acquisition of resistance-conferring DNA from another source (e.g. plasmids). Mechanisms of antibiotic resistance include chemical modification of antibiotics, reduced uptake into cells, active efflux from cells, target site modification, overproduction of antibiotic target, and metabolic bypass of inhibited reaction. Control of resistance may be achieved through adherence to prescribing guidelines, restriction policies that reduce the use of certain antibiotics, and antimicrobial stewardship programmes