Abstract
Objectives:
Outbreak and endemic isolates of Acinetobacter baumannii are known to be polyclonal. In an ongoing study, we hypothesized that the patient gut was the source of the polyclonality where genetic exchanges take place. To test the hypothesis, we collected 270 serial rectal isolates from 32 adult intensive care unit patients over 16 months and investigated their drug resistance profiles.
Methods:
Antimicrobial susceptibility was determined according to recommended methods. The blaIMP, blaVIM, blaSIM, blaOXA-23, blaOXA-24/40, blaOXA-51, blaOXA-48, blaKPC, blaGES, blaNDM and blaOXA-58 were sought by PCR. A subset of 42 isolates were studied for plasmid-mediated resistance.
Results:
Most of the 270 isolates were multidrug resistant (MDR; with resistances to meropenem of 85.18% and imipenem of 87.04%), but susceptible to colistin and trimethoprim/sulfamethoxazole. There was no correlation between the pattern of resistance and antibiotics administered to treat infections. There was no consistent pattern of resistance or content of carbapenemase genes in serial rectal isolates suggesting polyclonality of the isolates. Genes mediating production of OXA-23, OXA-24/40, IMP, and GES enzymes were carried on plasmids and they mediated resistance to all carbapenems in conjugation studies.
Conclusion:
A. baumannii colonizing the rectum were polyclonal, MDR, and carbapenem resistance genes were found on plasmids and some plasmids were transferable.
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