ABSTRACT
Background: Pseudomonas aeruginosa is one of the leading opportunistic pathogen and its ability to acquire resistance against series of antimicrobial agents confi ne treatment option for nosocomial infections. Increasing resistance to fl uroquinolone (FQ) agents has further worsened the scenario. The major mechanism of resistance to FQs includes mutation in FQs target genes in bacteria (DNA gyrase and/or topoisomerases) and overexpression of antibiotic effl ux pumps. Objective: We have investigated the role of effl ux pump mediated FQ resistance in nosocomial isolates of P. aeruginosa from a tertiary referral hospital in north eastern part of India. Materials and Methods: A total of 234 non-duplicate, consecutive clinical isolates of P. aeruginosa were obtained from a tertiary referral hospital of north-east India. An effl ux pump inhibitor (EPI), carbonyl cyanide m-chlorophenylhydrazone (CCCP) based method was used for determination of effl ux pump activity and multiplex polymerase chain reaction (PCR) was performed for molecular characterisation of effl ux pump. Minimum inhibitory concentration (MIC) reduction assay was also performed for all the isolates. Results and Conclusion: A total number of 56 (23%) have shown effl ux mediated FQ resistance. MexAB-OprM effl ux system was predominant type. This is the fi rst report of effl ux pump mediated FQ resistance from this part of the world and the continued emergence of these mutants with such high MIC range from this part of the world demands serious awareness, diagnostic intervention, and proper therapeutic option.
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.