Streptococcus pneumoniae serotype 3, isolated from a penicillin-allergic patient and initially susceptible to fluoroquinolones, macrolides, lincosamides, quinupristin-dalfopristin, and telithromycin, became resistant to all these drugs during treatment. Mutations in the parC and gyrA and in the 23S rRNA and the ribosomal protein L22 genes were detected in the resistant isolates.

Two real-time polymerase chain reaction assays were developed to detect mutations in codons 83 and 87 in gyrA and in codons 80 and 91 in parC, the main sites that causes quinolone resistance in pathogenic Escherichia coli and Shigella spp. isolates. These assays can be employed as a useful method for controlling infections caused by quinolone-resistant E coli and Shigella isolates.

Mutations in the quinolone resistance-determining regions of gyrA, gyrB, parC, and parE were studied in 30 fluoroquinolone-resistant clinical isolates of Escherichia coli producing extended-spectrum beta-lactamases. Ten isolates showed a mutation in parE that was significantly associated with an increase in the MIC for fluoroquinolones.

Of 1,994 group B streptococcal isolates collected, 26 (1.3%) of the isolates were resistant to levofloxacin, and cross-resistance to other fluoroquinolones was observed. The emergence and prevalence of high-level fluoroquinolone resistance in genetically unrelated isolates were linked to the presence of gyrA, parC, and parE triple mutations in each isolate.

Surveillance of antibiotic resistance in Neisseria gonorrhoeae showed a decrease in the percentage of beta-lactamase-producing isolates but an increase in intermediately penicillin-resistant strains and strains resistant to a high level of tetracycline. MICs for the ciprofloxacin-resistant isolates that emerged increased, and these isolates had mutations in gyrA and parC similar to those observ...

Human isolates of Salmonella enterica serovars Hadar, Kentucky, Virchow, Schwarzengrund, and the monophasic variant of S. Typhimurium, Salmonella enterica subsp. enterica serovar 4,5,12:i:- were examined for mutations within the quinolone resistance target genes gyrA, gyrB, parC, and parE and for plasmid-mediated resistance genes. Differences were observed among the serovars. A novel variant of...

We characterized 44 Salmonella enterica serotype Typhimurium isolates from Tongji Hospital outpatients in Wuhan, China, May 2002-October 2005. All 31 ciprofloxacin-resistant isolates were also resistant to > or = 8 other antimicrobial drugs and carried > or = 2 mutations in GyrA and 1 mutation in ParC. Class 1 integrons were identified in 37 isolates.

Antimicrobial susceptibility was determined in 15 epidemiologically unrelated clinical isolates of Acinetobacter genospecies 3. Moreover, the mechanisms of resistance to some beta-lactam antibiotics may be associated with the presence of a chromosomal cephalosporinase, AmpC, and the resistance to quinolones related to mutations in the gyrA and parC genes.

To investigate the mechanism of resistance in the isolates, fragments of gyrA (847 bp) and parC (822 bp) genes were amplifi ed by using primers gyrA1F (5′-gttttcccagtcacgacgttgtaATGA CCGACGCAACCATCCGCCAC-3′) and gyrA-1R (5′-ttgtgagcggataacaattt cCCAGCTTGGCTTTGTTGACCTG ATAG-3′), and parC-1F (5′-gttttcccag tcacgacgttgtaATGAATACGCAAGC GCACGCCCCA-3′) and parC-1R (5′ttgtgagcggataacaatttcGGAATTGGC GT...