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Chapter 4 : Fluoroquinolone Resistance

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Abstract:

Fluoroquinolones are an important class of widespectrum antibacterial agents. The DNA gyrase is known to play an important role in both the transcription and replication of DNA. Topoisomerase IV has also been found to be a protein target for quinolones. The major role of this enzyme seems to be in decatenating daughter replicons following DNA replication. The chromosomal mutations can be distributed into two groups: (i) mutations in topoisomerases genes (gyrA, gyrB, parC, and parE), and (ii) mutations causing reduced drug accumulation, either by a decreased uptake or by increased efflux. The high level of fluoroquinolone resistance observed in some countries is probably due to two factors. First, lacks topoisomerase IV; therefore a mutation in the gyrA gene is sufficient to increase the MIC of ciprofloxacin and levofloxacin above 32 mg/liter, whereas two mutations are necessary in the gyrA gene to generate a high level (32 mg/liter) of resistance to moxifloxacin. Second, the constitutive expression of the CmeABC pump contributes to the intrinsic resistance. NorA is one of the efflux systems related to fluoroquinolone resistance, and it seems that the increase in the level of resistance provided by NorA is due to the overexpression of the gene associated with a mutation in the promoter region. The molecular bases of fluoroquinolone resistance are similar in all microorganisms mainly due to mutations in the gyrA and parC genes, encoding the A subunits of the DNA gyrase and topoisomerase IV, the protein targets for quinolones.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4

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First Generation Quinolones
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Figures

Image of Figure 1.
Figure 1.

Chemical structure of the main commercialized quinolones.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4
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Image of Figure 2.
Figure 2.

Process of DNA replication and DNA transcription involving DNA gyrase and topoisomerase IV.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4
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Image of Figure 3.
Figure 3.

Functional domains of the quinolone molecule according to Palumbo’s and Shen’s models.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4
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Image of Figure 4.
Figure 4.

(A) Distance between Ser-83 and Asp-87 of the GyrA protein. (B) Distance between substituents at positions 1 and 7 of the quinolone molecule.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4
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Tables

Generic image for table
Table 1

Classification of main commercialized quinolones

Levofloxacin has been included in the third generation because it is more active than ofloxacin against gram-positive cocci and also because the serum peak allows a good therapeutic index against these microorganisms.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4
Generic image for table
Table 2

Mechanisms of resistance to fluoroquinolones in different microorganisms

These are the most frequently found substitutions.

The main efflux pumps for each microorganism are mentioned but are not related to the MIC in the table.

Can be extrapolated to the remaining .

This microorganism does not have topoisomerase IV.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4
Generic image for table
Table 3

Factors favoring emergence of quinolone resistance Factors dependent on the quinolone

These factors generate a transitory resistance.

Citation: Vila J. 2005. Fluoroquinolone Resistance, p 41-52. In White D, Alekshun M, McDermott P (ed), Frontiers in Antimicrobial Resistance. ASM Press, Washington, DC. doi: 10.1128/9781555817572.ch4

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