Quinolone resistance of Salmonella enterica serovar Virchow isolates from humans and poultry in Israel: evidence for clonal expansion

Abstract

Salmonella enterica serovar Virchow is highly prevalent in humans and farm animals in Israel. In addition to high rates of resistance to multiple antibiotics, this serovar exhibits a high incidence of resistance to nalidixic acid. More than 90% of Salmonella serovar Virchow isolates of human and poultry origin obtained from 1997 to 2004 were resistant to nalidixic acid (MIC > or = 128 microg/ml), with reduced susceptibility to ciprofloxacin (MIC between 0.125 and 0.250 microg/ml). Most isolates belonged to two predominant, closely related pulsed-field gel electrophoresis image types. Investigation of the mechanisms of quinolone resistance revealed that this pathogen probably emerged from a parental clone that overproduced the AcrAB efflux pump and had a single point mutation in gyrA leading to the Asp87Tyr substitution. The close resemblance between human and poultry isolates points to poultry as a likely source of Salmonella serovar Virchow in the food chain.

FIG. 1.

Transcription of acrAB, marA, and soxS in E. coli K-12 strains AG100 and AG102, Salmonella serovar Typhimurium ATCC 14028 (ST), and representative isolates of Salmonella serovar Virchow (V1-V19). Numbers represent the means of normalized GFP fluorescence intensities of cultures with the following promoter-gfp fusions: acrAp::gfp (dark gray), soxSp::gfp (black), and marAp::gfp (light gray). The bars represent the standard errors of the means of the results of three experiments; each experiment was conducted in triplicate. SV10 and SV11 are cyclohexane-resistant isolates.