The emergence of drug resistance, since the introduction of antibiotics, has driven humans to continually search for new antibiotics that can defeat evolving pathogens. This has paved the way for the development of various synthetic and semi-synthetic antibiotics with improved efficacy and expanded target coverage. Among different synthetic antibiotics like sulfonamides, quinolones and oxazolidinones, quinolones have gained popularity due to their wider application, broader spectrum of activity and drug safety (Walker, 1999, Saravanos and Duff 1992, Brown, 1996). Thus, in this section, the focus would be on the quinolone antibiotic class and the mechanism of bacterial resistance to these widely used synthetic antibiotics. Quinolones are the class of antibiotics that specifically kill bacteria by inhibiting nucleic acid synthesis. Quinonlones are exceptional antibiotics, unlike others not isolated from living organisms but obtained by chemical synthesis. The parent compound of quinolones, nalidixic acid, was derived from the antimalarial drug chloroquine in 1962 (Bolon, 2011, Andriole, 2005). Nalidixic acid is composed of a naphthyridine ring having an ethyl and methyl group attached to its N1 and C7 positions respectively as well as a keto and carboxyl group attached to its C4 and C3 positions respectively. Although it has narrow-spectrum antibacterial activity, it was widely used for urinary tract infections and diarrhea until the introduction of broad-spectrum fluroquinolones (Bambeke et al 2005, Drilca and Zhao, 1997). Fluroquinolones were derived from nalidixic acid by the introduction of a fluorine atom at the C6 position of the naphthyridine ring and also by replacing the N8 with a carbon atom (Ball, 2000).All available quinolones... ... middle of paper... ...ivate quinolones (ciprofloxacin and norfloxacin) by N-acetylating the amino nitrogen on its piperazinyl group. Two amino acid changes (Trp102Arg and Asp179Tyr) allowed the enzyme to additionally inactivate quinolones apart from aminoglycosides. The effect on the MIC of AAC (6')-Ib-cr is lower than that conferred by the Qnr protein and the drug spectrum covered by this enzyme is also restricted (ciprofloxacin and norfloxacin only). It is reasonably well documented that quinolone resistance in pathogenic bacteria, through their intrinsic and acquired traits, poses a major health problem. The synergistic action of all these chromosomal and plasmid factors helps the pathogen to confer a higher level of resistance to quinolones, as described by many researchers (Baranwal et al. 2002, Rushdy et al. 2013, Srinivasan et al. 2006, Zhu et al. al. 2013).Works citedshfrjfrtj