Original article / research
Biofilm Formation and Colistin Susceptibility of Clinical Isolates of Acinetobacter Species in a Tertiary Care Hospital of Nepal
Dr. Birendra Raj Tiwari,
Saint James School of Medicine, Albert Lake Drive, The Quarter, Anguilla.
E-mail: tiwari.birendra58@g mail.com
Introduction: Acinetobacter species are a major cause of hospital acquired infections worldwide with remarkable level of resistance to various classes of antibiotics.
Aim: To evaluate the MIC of colistin against biofilm forming, Multi Drug Resistant (MDR) Acinetobacter species by E-test in a tertiary care hospital of Kathmandu.
Materials and Methods: Isolation and identification of Acinetobacter species was done by standard methods. Biofilms were developed using 96-well microtiter plates in Tryptic Soy Broth (TSB). Optical Density (OD) was measured at 570 nm after washing, fixation and staining. Antibiotic susceptibility test was performed by Kirby-Bauer disk diffusion method. Carbapenem resistance and Metallo B-Lactamase (MBL) production were tested by Modified Hodge Test (MHT) and Imipenem-EDTA combined disk method respectively. MIC was determined by E-test against colistin.
Results: Out of 573 bacterial isolates the number of Acinetobacter species was 73 (12.7%) and among them 72 (99%) were biofilm producers having significant relationship to multi drug resistance (p=0.01). All isolates were resistant to cephalosporins; 65 isolates (89%) were carbapenem resistant, 61 isolates (93.8%) gave positive MHT, 36 (56%) of total carbapenem resistant Acinetobacter isolates revealed positive for MBL, 72 (99%) of isolates were found sensitive to colistin by disc diffusion method whereas only 68 (93.1%) by MIC testing.
Conclusion: Acinetobacter clinical isolates have a strong ability to produce biofilm. Carbapenemases and MBL were also observed in this study. Only colistin and polymyxin B were effective against higher numbers of isolates, however, 5 (6.9%) of the isolates were found resistant as detected by MIC testing and indicated reduced susceptibility to colistin.
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