Abstract
In considerations of the mechanisms of antibiotic resistance in bacteria that contain plasmids, four mechanisms are generally possible. In one, the plasmid encodes an enzyme (or enzymes) that alters the target site for the antibiotic such that the binding of the antibiotic is greatly reduced. There are very few examples of this mechanism but such is known to be the case with macrolide-lincosaminide resistance in Staphylococcus aureus; plasmids mediate specific methylation of the 23S ribosomal RNA and destroy the binding site for the drug (1). In a second mechanism, plasmids encode a replacement function that is insensitive to the drug, allowing the inhibited form of the enzyme to be bypassed. For example, in sulfonamide resistance where the resistant cell contains two dihydropteroate synthetases, one chromosomally determined and inhibited by sulfa drugs, the other plasmid determined and refractory to this inhibition (2). A similar situation exists for trimethoprim resistance (3).
This work was supported by grants from the National Institutes of Health and Cell and Molecular Biology Training Grant, University of Wisconsin.
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Davies, J., Kagan, S.A. (1977). What Is the Mechanism of Plasmid-Determined Resistance to Aminoglycoside Antibiotics?. In: Drews, J., Högenauer, G. (eds) R-Factors: Their Properties and Possible Control. Topics in Infectious Diseases, vol 2. Springer, Vienna. https://doi.org/10.1007/978-3-7091-8501-8_13
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DOI: https://doi.org/10.1007/978-3-7091-8501-8_13
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