Detection of quinolone resistance from nosocomial pathogens
INTRODUCTION
INTRODUCTION
Fluoroquinolones have been frequently prescribed as empirical therapy against mosthospital and community infections due to increased appearance of multiple drug resistantGram negative bacteria includingKlebsiella pneumoniaeand to the disease severity.Withextensive clinical use of quinolones. Fluoroquinolone resistance has been a problem inclinical medicine for its limiting of available agents in the treatment of many types ofinfection.Quinolone resistance in the family Enterobacteriaceae is mostly attributed to theaccumulation of mutations in the bacterial enzymes targeted by: DNA gyrase and DNAtopoisomerase IV. In addition Active efflux systems (acrAB-TolC) resulting in decreasedintracellular accumulation of fluoroquinolones inK.pneumoniae.Morever,Plasmid-mediated quinolone resistance (PMQR) with the potential for horizontal transfer has beendescribed along with three mechanisms: (i) a quinolone-protective mechanism encoded by theqnrgenes(3); (ii) a modifying enzyme, aac(60)-Ib-crand (iii) an efflux pump encoded by theqepAgene(5,6). Plasmid-encoded quinolone resistance determinants confer low-levelresistance, but their presence could potentially facilitate the evolution of the bacterial hosttoward higher levels of resistance by mutational alterations in type II topoisomerases.K.pneumoniaestrains represent an incredibly great epidemic potential and are one of the majorsources of horizontally spreading antimicrobial resistance(2).Fluoroquinolone resistantK.pneumoniaeconstitutes one of the most common Gram-negative bacteria showing multipleantibiotic resistance worldwide
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