Abstract
Multidrug resistant strains of Staphylococcus aureus cause serious problems worldwide. We have characterized the quinolone resistant mechanisms in clinical isolates of S. aureus and tested their susceptibilities to other classes of antibiotics. Results of this study showed high level of resistance to quinolone in the selected isolates and suggested that resistance is due to mutations in gyrA and parC genes in addition to efflux mechanism. The selected strains were not only resistant to quinolones but also found resistant to a number of other antibiotics. This study also shed some light on the possibility of using Clove as an efflux pump inhibitor. The minimum inhibitory concentration of ciprofloxacin against multidrug resistant isolates was reduced from 256 to 64 µg/ml when used in combination with Clove extract. This result indicated that Clove is a potential efflux pump inhibitor. In addition, the effect of different efflux pump inhibitors on the resistance of these isolates was determined. Key words: Staphylococcus aureus, fluoroquinolone antibiotics, ciprofloxacin, efflux pump inhibitor, clove. .
Highlights
Staphylococcus aureus is a Gram positive human pathogen that causes a wide range of infections, some of which can be life-threatening such as septicemia, pneumonia, osteomyelitis and endocarditis (Pan et al, 2002)
The susceptibility of all S. aureus isolates were tested against fluoroquinolone antibiotics (Cibrofloxacin, Norfloxacin and Levofloxacin) in a concentration of 5 μg/ml
Four of these isolates were resistant to the three tested fluoroquinolone antibiotics
Summary
Staphylococcus aureus is a Gram positive human pathogen that causes a wide range of infections, some of which can be life-threatening such as septicemia, pneumonia, osteomyelitis and endocarditis (Pan et al, 2002). Fluoroquinolones are broad-spectrum antibacterial agents that act on bacteria by inhibiting their DNA synthesis They are known to have two enzyme targets, DNA gyrase and topoisomerase IV, in the bacterial cell. Resistance to fluoroquinolones in bacteria may result from point mutations within DNA gyrase (encoded by gyrA and gyrB genes). This causes a reduction in the affinity of the enzyme for fluoroquinolones and thereby decreases the susceptibility of the organisms to these antibiotics (Everett et al, 1996; Ruiz, 2003). In S. aureus, several studies have shown that a combination of mutations in genes for both enzymes can cause high-level of fluoroquinolone resistance (Hooper, 2002; Horii et al, 2003; Iihara et al, 2006; Wang et al, 1998)
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