Journal Article

Mechanisms of Resistance to Quinolones

George A. Jacoby

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 41, issue Supplement_2, pages S120-S126
Published in print July 2005 | ISSN: 1058-4838
Published online July 2005 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/428052
Mechanisms of Resistance to Quinolones

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The increased use of fluoroquinolones has led to increasing resistance to these antimicrobials, with rates of resistance that vary by both organism and geographic region. Resistance to fluoroquinolones typically arises as a result of alterations in the target enzymes (DNA gyrase and topoisomerase IV) and of changes in drug entry and efflux. Mutations are selected first in the more susceptible target: DNA gyrase, in gram-negative bacteria, or topoisomerase IV, in gram-positive bacteria. Additional mutations in the next most susceptible target, as well as in genes controlling drug accumulation, augment resistance further, so that the most-resistant isolates have mutations in several genes. Resistance to quinolones can also be mediated by plasmids that produce the Qnr protein, which protects the quinolone targets from inhibition. Qnr plasmids have been found in the United States, Europe, and East Asia. Although Qnr by itself produces only low-level resistance, its presence facilitates the selection of higher-level resistance mutations, thus contributing to the alarming increase in resistance to quinolones.

Journal Article.  4914 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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