TMSS Medical College Journal

Background: Antimicrobials of different structural classes including the fluoroquinolones have shown resistance in a multitude of bacterial species in the hospitals and in the community. Decreased susceptibility to fluoroquinolones arises mainly by single step mutations in the gyrA and parc genes, which encode the fluoroquinolones targets, the topisomerase enzymes conferring cross resistance to all fluoroquinolones. Accumulation to multiple mutations in several genes confers increasing level of resistance associated with clinical failure. However, even low level of resistance can generate therapeutic failure. In 1998, some mobile elements with a potential for the horizontal transfer of the quinolone resistance genes were described. The loci which are responsible for this plasmid-mediated quinolone resistance, which have been designated as qar A, qur B and qor S. have been identified in the Enterobacteriaceae species. Aim: To evaluate the susceptibility pattern of the isolates to various antibiotics and to know the prevalence rate of Ciprofloxacin resistance in King Saud Medical Complex. Materials and Methods: A total of 510 gram- negative bacilli (GNB) were isolated from specimens of clinically diagnosed UTI patients over a period of six months (from January 2009 to June 2009) were subjected to antibiotic susceptibility testing. Isolates with resistance or with a decreased susceptibility to Ciprofloxacin (Zone of inhibition of bacterial growth around 20 mm of the E-strip) were then screened for their minimum inhibitory concentration (MIC) by using the E-strip test. Results: Out of 510 GNB, 97 (196) isolates were resistant to Ciprofloxacin. The MIC of these isolates ranged from 4 to 32 pg/ml. Conclusion: The resistance rate of Ciprofloxacin was 19% in our study. The Ciprofloxacin resistance was also closely associated with multi-drug resistance, thus limiting the treatment options. Ciprofloxacin resistance can be used as a general surrogate marker of multi-drug resistance, thus limiting the already restricted treatment options. Key words: Gram-negative bacilli, MIC, Fluoroquinolone, Ciprofloxacin.

There were major therapeutic advance of fluoroquinolone antimicrobials in 1980, because they have 100 fold greater activities than their parent compound, Nalidixic acid. Unlike Nalidixic acid, which is used only for urinary infections and occasionally for shigellosis, the fluoroquinolones have a broad range of therapeutic indications and are given as prophylaxis, eg, in veterinary medicine fluoroquinolones are used as treatment and metaphylaxis but not as growth promoters. Early researchers thought that fluoroquinolones resistance was unlikely to evolve, largely because resistant Esch.coli mutants are exceptionally difficult to select in vitro and because plasmid-mediated quinolone resistance remained unknown even after 30 years of Nalidixic acid usage. Nevertheless multi-national quinolone resistance emerges 25 in Staphylococci and Pseudomonads, which are inherently less susceptible than Esch.coli. More recently, fluoroquinolone resistance has emerged in Esch.coli and other Enterobactericeae, contingent on multiple mutations that diminish the affinity of its topisomerase II and IV targets in varying ways reduce permeability and up regulate efflux. Plasmid-mediated quinolone resistance has been reported but it is exceptional.