ABSTRACT
Purpose: There are increasing reports on failure of clinical response to ciprofl oxacin in typhoid fever despite the strain being sensitive to drug in in-vitro using standard guidelines and showing mutations in DNA gyrase. But this increased MIC and clinical failures with ciprofl oxacin are not always co-related with mutations presently identifi ed in gyrA and parC genes. This shows that there may be other mechanisms such as an active drug effl ux pump responsible as has been shown in other Enterobacteriaceae. This study was carried out to determine the role of effl ux pump in Salmonella Typhi isolates. Materials and Methods: Total 25 already characterized nalidixic acid sensitive and nalidixic acid resistant S. Typhi strains with different range of ciprofl oxacin MIC were included to study the role of effl ux pump in the presence of CCCP (effl ux pump inhibitor). For genotypic characterization, the entire acrR gene was sequenced to confi rm the presence of any mutation in the gene. Results: The MIC of ciprofl oxacin remained same in the presence and absence of CCCP in the studied strains and no signifi cant mutations were found in the acrR gene in any of the isolates studied. Conclusions: No role of effl ux pump in ciprofl oxacin resistance was found in strains studied. There is a need to explore further mechanism of ciprofl oxacin resistance in Salmonella Typhi.