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The prokaryotic topoisomerase II that uses ATP to generate negative supercoils of DNA.
[L. gyro, to turn in a circle, fr. gyrus, G. gyros, circle + -ase, enzyme suff.]
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References in periodicals archive ?
ITS, internal transcribed spacer; gyrB, gyrase B Table 2.
([dagger]) hspSO, heat shock protein 60; gyrB, DNA gyrase subunit B.
Because identical mutations were found even in many uncommon strains, gyrase mutations and associated fluoroquinolone resistance alone cannot explain the high prevalence of ribotypes 001 and 027.
Around 0.3 million people die annually because of burn wounds around the globe with nosocomial infections contributing in 50% of these deaths.1 Gram negative, non-spore forming organism, Pseudomonas aeruginosa is responsible for 10-20% hospital acquired infections and causes 40-75% mortality in burn patients.2 Broad spectrum antimicrobial drugs, fluoroquinolones (FQn), are commonly suggested against pseudomonal infections.3 Misuse of FQn has led to an increase in bacterial resistance due to chromosomal mutation in DNA gyrase (gyr A and gyr B genes) and topoisomerase IV or changes in expression of genes controlling transport of FQns.4 Another important acquired mechanism of FQn resistance is Qnr genes.
Real time PCR was performed for cueO along with a gene Gyrase subunit A, a constitutively expressing gene used as internal control.
* Epidemiology of Neisseria gonorrhoeae Gyrase A Genotype, Los Angeles, California, USA
QRDR analysis revealed the S83L substitution in the predicted DNA gyrase (GyrA) amino acid sequence of all genome sequencing isolates, in addition to S80L (Ab112 and Ab124) and S80Y (Ab107) substitutions in topoisomerase IV subunit (ParC).
perfringens can develop quinolone resistance by altering the sites of drug action in the genes encoding DNA gyrase and topoisomerase IV.
Ciprofloxacin cured 100 percent of Gyrase A wild-type Neisseria gonorrhoeae infections, and physicians prescribed it significantly more frequently when they received electronic reminders of test results and recommendations, in a single-center study.
Reduced susceptibility to the fluoroquinolone group of antibiotics is usually linked with point mutations in the bacterial target genes gyrA, gyrB encoding DNA gyrase and parC, parE encoding DNA topoisomerase IV.