RESUMO
Background: Fluoroquinolones are the drugs extensively employed for the treatment of Salmonella infections. Over the couple of decades that have elapsed since the introduction of fl uoroquinolones, resistance to these agents by Enterobacteriaceae family members has become common and widespread. Although fl uoroquinolone resistance is mediated by genomic DNA (deoxyribonucleic acid) as well as plasmid DNA, the plasmid-mediated quinolone resistance (PMQR) facilitates higher level resistance by interacting with genomic mechanism and is capable of horizontal spread. Materials and Methods: During a period of 1-year, 63 typhoidal Salmonellae were isolated from 14,050 blood cultures and one parietal wall abscess. 36 (56.25%) were Salmonella Typhi and 27 (42%) were Salmonella Paratyphi A. They were all screened for resistance by the disc diffusion method and their minimum inhibitory concentrations were determined using agar dilution, broth dilution and E-strip method. Ciprofl oxacin resistant isolates were screened for PMQR determinants by polymerase chain reaction assay. Results: All the 63 isolates were resistant to nalidixic acid. Among the 36 S. Typhi isolates 20 were resistant to ciprofl oxacin, of which 14 carried the plasmid gene qnrB and one carried the aac(6’)-Ib-cr gene. qnrA and qnrS genes were not detected. Ciprofl oxacin resistance was not seen in any of the S. Paratyphi A isolates. Conclusion: The antibiotic sensitivity pattern of typhoidal Salmonellae shows an increasing trend of PMQR. The allele B of qnr gene was found to be the predominant cause of PMQR in this study.
RESUMO
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.