Author/Authors :
Salimizand، Himen نويسنده Department of Microbiology, Besat Hospital, Medical University of Kurdistan, Kurdistan, Iran Salimizand, Himen , Modarresi، Farzan نويسنده Department of Microbiology, Kerman Medical Students Research Committee, Kerman University of Medical Sciences, Kerman, IR Iran Modarresi, Farzan , Azizi، Omid نويسنده Department of Microbiology, Kerman Medical Students Research Committee, Kerman University of Medical Sciences, Kerman, IR Iran Azizi, Omid , Mansouri، Shahla نويسنده , , Rahmati، Mehdi نويسنده Department of Microbiology and Immunology, Kerman University of Medical Sciences, Kerman, IR Iran Rahmati, Mehdi
Abstract :
Background: One of the most challenging isolates in nosocomial infections is Acinetobacter baumannii which is rapidly changing towards multi-drug resistant. Resistance to the last resort antibiotics, carbapenems, is reported around the world. In particular, metallo-B-lactamases (MBL) are responsible and detection of MBLs is of interest.
Objectives: In this study we have evaluated the prevalence of MBLs in A. baumannii isolated during 2012 by two feasible described methods.
Materials and Methods: In this cross sectional study, during 2012, 40 A. baumannii non-replicate isolates gathered from clinical and environmental specimens from Afzalipur hospital of Kerman. Isolates were characterized by conventional biochemical tests as A. baumannii-calcoaceticus complex (ABC). For antimicrobial susceptibility testing, 17 different antibiotics were sought by agar diffusion method. Phenotypic MBL detection was assessed by double disk test and Modified Hodge test for carbapenem resistant isolates.
Results: During the study 40 isolates of ABC were collected. Of which, 23 (57%) isolates were resistant to carbapenems. Phenotypic MBLs detection was negative by two methods.
Conclusions: The rates of resistance of the isolated ABCs in our clinical setting were at high level. Though, carbapenems were the most efficient antibiotic, but, there was a pronounced rate of resistant. MBL genes were not responsible for carbapenem resistance in under study clinical setting.