Description of compensatorygyrAmutations restoring fluoroquinolone susceptibility inMycobacterium tuberculosis | Zendy

Alix Pantel | Zendy; S. Petrella | Zendy; Nicolas Véziris | Zendy; Stéphanie Matrat | Zendy; A Bouige | Zendy; Hélène Ferrand | Zendy; Wladimir Sougakoff | Zendy; Claudine Mayer | Zendy; Alexandra Aubry | Zendy

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Description of compensatorygyrAmutations restoring fluoroquinolone susceptibility inMycobacterium tuberculosis

Author(s) -

Alix Pantel,

S. Petrella,

Nicolas Véziris,

Stéphanie Matrat,

A Bouige,

Hélène Ferrand,

Wladimir Sougakoff,

Claudine Mayer,

Alexandra Aubry

Publication year - 2016

Publication title -

journal of antimicrobial chemotherapy

Language(s) - Uncategorized

Resource type - Journals

SCImago Journal Rank - 2.124

H-Index - 194

eISSN - 1460-2091

pISSN - 0305-7453

DOI - 10.1093/jac/dkw169

Subject(s) - dna gyrase , mycobacterium tuberculosis , ofloxacin , quinolone , mutant , dna supercoil , biology , microbiology and biotechnology , escherichia coli , tuberculosis , antibacterial agent , dna , genetics , ciprofloxacin , antibiotics , medicine , gene , dna replication , pathology

Resistance to fluoroquinolones (FQs) in Mycobacterium tuberculosis (Mtb) is mainly due to mutations in DNA gyrase (GyrA2B2), with the most common substitutions located at positions 90 and 94 in GyrA. Two clinical MDR Mtb (MDR-TB) strains harbouring an A90E or D94N substitution in GyrA were found to be surprisingly susceptible to FQs (ofloxacin MIC ≤2 mg/L). We studied the impact of the additional GyrA substitutions found in these strains (T80A and T80A + A90G, respectively) on FQ susceptibility.

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