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The role of intra- and extragenic compensatory mutations in the suppression of fluoroquinolone resistance in a Salmonella Typhimurium gyrA mutant (D87G)
Author(s) -
Antje Preisler,
Peter Heisig
Publication year - 2008
Publication title -
journal of antimicrobial chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.124
H-Index - 194
eISSN - 1460-2091
pISSN - 0305-7453
DOI - 10.1093/jac/dkn480
Subject(s) - complementation , dna gyrase , efflux , biology , nalidixic acid , mutant , genetics , quinolone , mutation , dna supercoil , antibacterial agent , microbiology and biotechnology , topoisomerase iv , gene , escherichia coli , bacteria , antibiotics , dna replication
The live vaccine strain TAD Salmonella vacT (vacT) carrying gyrA mutations W59R, G75A, D87G and A866S shows resistance to nalidixic acid and rifampicin, but increased susceptibility to macrolides, fluoroquinolones and phenylalanyl-arginyl-beta-naphthylamide. This phenotype contrasts with the presence of the gyrA mutation D87G usually associated with reduced susceptibility to fluoroquinolones. Thus, a possible compensatory effect on the suppression of gyrA-mediated resistance by gyrA mutations within the quinolone resistance-determining region alone or in combination (intragenic) or by a mutation affecting AcrAB-TolC (extragenic), the major multidrug resistance efflux pump in Salmonella, was investigated.

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