JAC Advance Access originally published online on February 25, 2004
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Journal of Antimicrobial Chemotherapy (2004) 53, 657-659
© 2004 The British Society for Antimicrobial Chemotherapy
Role of TolC and parC mutation in high-level fluoroquinolone resistance in Salmonella enterica serotype Typhimurium DT204
Unité BioAgresseurs, Santé et Environnement, Institut National de la Recherche Agronomique, 37380 Nouzilly, France
Received 27 November 2003; returned 13 December 2003; revised 18 December 2003; accepted 19 December 2003
Objectives: To study the role of TolC and of parC mutation in high-level fluoroquinolone resistance in clonal clinical strains of Salmonella enterica serotype Typhimurium phage type DT204 (S. Typhimurium DT204).
Methods: Deletion of the tolC gene (
tolC) was first performed in a susceptible S. Typhimurium DT104 strain lacking target gene mutations involved in fluoroquinolone resistance. P22 transduction was further used to transduce tolC from this strain to a high-level fluoroquinolone-resistant S. Typhimurium DT204 strain carrying several target gene mutations, including one in parC (ciprofloxacin MIC of 32 mg/L).
Results: Deletion of tolC in the high-level fluoroquinolone-resistant S. Typhimurium DT204 strain resulted in the same decrease in resistance levels (16- to 32-fold) as shown previously for an acrB mutant of the same strain, suggesting that AcrAB-TolC is the main efflux system involved in high-level fluoroquinolone resistance of S. Typhimurium DT204 strains. In some S. Typhimurium DT204 tolC transductants, concomitant loss of the parC (Ser-80
Ile) mutation, located 
9.3 kb upstream of tolC, resulted in a further 16- to 32-fold decrease in resistance levels to fluoroquinolones and thus a hypersusceptible phenotype (ciprofloxacin MIC of 0.063 mg/L).
Conclusion: The AcrAB-TolC efflux system, together with multiple target gene mutations, including the parC mutation, appear essential to confer high-level fluoroquinolone resistance in S. Typhimurium DT204.
Keywords: salmonellosis, multidrug resistance, AcrAB-TolC efflux system, multidrug transporter AcrB, outer membrane component TolC, target gene
* Corresponding author. Tel: +33-2-47-42-77-50; Fax: +33-2-47-42-77-74; E-mail: cloeckae{at}tours.inra.fr
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