Journal Article

Genes and Spectrum: The Theoretical Limits

Sebastian G. B. Amyes

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 27, issue Supplement_1, pages S21-S28
Published in print August 1998 | ISSN: 1058-4838
Published online August 1998 | e-ISSN: 1537-6591 | DOI: https://dx.doi.org/10.1086/514918
Genes and Spectrum: The Theoretical Limits

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Antibiotic resistance can result either from mutations within a chromosomal gene or from mobile genes imported from outside. In the last 15 years, some of these mobile genes have shown a propensity to adapt to successive antibiotic challenges, the most versatile being the class A β-lactamases. The TEM and SHV β-lactamase nuclei, usually after one initial critical mutation, allow a series of successive mutations that increase the spectrum to hydrolyze most cephalosporins. The class C β-lactamases also show some versatility; while it migrates from the chromosome, subtle changes can occur in the gene to broaden the spectrum. Trimethoprim resistance has shown less adaptability in gram-negative bacteria, but in gram-positive organisms the plasmid has captured the chromosomal dihydrofolate reductase of Staphylococcus epidermidis, and a minimal number of changes have occurred that decrease the binding of trimethroprim. Other resistance mechanisms appear less adaptable, relying rather on the importation of new genes to cope with new challenges.

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

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