These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Resistance to fluoroquinolones by the combination of target site mutations and enhanced expression of genes for efflux pumps in Shigella flexneri and Shigella sonnei strains isolated in Korea. Author: Kim JY, Kim SH, Jeon SM, Park MS, Rhie HG, Lee BK. Journal: Clin Microbiol Infect; 2008 Aug; 14(8):760-5. PubMed ID: 18727800. Abstract: Among 5938 clinical Shigella spp. isolates, two S. flexneri strains were isolated as those resistant to fluoroquinolones based on the MICs of the following antibiotics: ciprofloxacin, norfloxacin, ofloxacin, sparfloxacin and levofloxacin. S. flexneri 021787 had three substitutions, one in GyrA (Ser83Leu) and two in ParC (Ser80Ile and Arg91Gln). S. flexneri 021895 had four substitutions, two in GyrA (Ser83Leu and Asp87Gly) and two in ParC (Ser80Ile and Arg91Gln). The increased susceptibility of S. flexneri 021787 and S. flexneri 021895 to ciprofloxacin, norfloxacin and ofloxacin in the presence of the uncoupler carbonyl cyamide-m-chlorophenyldrazone implied that energy-dependent active efflux pumps contributed to the resistance against fluoroquinolones. Both S. flexneri 021787 and S. flexneri 021895 were also induced to express tolC (encoding a resistance-nodulation-division transporter), mdfA (encoding a major facilitator superfamily transporter), and ydhE (encoding a multidrug and toxic compound extrusion transporter) in the presence of ciprofloxacin. Thus, these results indicated that chromosome-mediated fluoroquinolone resistance of S. flexneri 021787 and S. flexneri 021895 resulted from the combination of target site mutations and enhanced expression of genes encoding efflux pumps.[Abstract] [Full Text] [Related] [New Search]