EVOLUTION OF RESISTANCE IN Acinetobacter baumannii ISOLATES OF CLONAL COMPLEX 1

The increase in carbapenem resistance rates and the majority of antibiotics available in Acinetobacter baumannii isolates has been worrying. In Brazil, carbapenem resistant A. baumannii is considered endemic and the most important clonal complexes (CCs) disseminated in the country are CC1, CC15, CC25 and CC79. In our region, A. baumannii clones were susceptible to carbapenems in the 1990s, but today the majority is already multidrug resistant (MDR) and have spread very easily. The aim of this study was analyses the evolution of one clone in a period of fifteen years. Two isolates previously typed by the enterobacterial repetitive intergenic consensus-polymerase chain reaction (ERIC-PCR) were selected. Antimicrobial susceptibilities were determined by an automatized method and agar dilution (meropenem, imipenem and polymyxin). Multiplex PCR analyses were performed to detect KPC, metallo-beta-lactamases (blaIMP, blaVIM, blaGIM, blaSPM, blaSIM, and blaNDM) and oxacillinases genes (blaOXA-23, blaOXA-24, blaOXA-51, blaOXA-58, and blaOXA-143). ISAba1 was detected using the primers ISAba1F and ISAba1R in combination with the primers OXA-23 (R and F). To confirm the genetic similarity, the isolates were typed by multilocyus sequence typing (MLST). The strain A was isolate in 1996 in clinical sample (tracheal secretion) of one inpatient in unit care intensive (ICU) of a university hospital. This isolate showed antimicrobial susceptibility to carbapenems, polymyxins, tetraciclyne, tigeciclyne, ampicillin-sulbactam and levofloxacin. Only the OXA-51 carbapenemase was detected in this isolate. The strain B was isolate in 2011 in clinical sample (tracheal secretion) of one inpatient in the ICU of the same hospital. This isolate was resistant all antimicrobials tested, including polymyxin. The carbapenemases OXA-51 and OXA-23 and insertion sequence ISAba1 were detected in this isolate. The isolates belonged to the same sequence type (ST983) and same complex clonal (CC1). This ST differs from ST1 (founder genotype of CC1) by a single allelic mismatch. Despite of the dissemination of the CC1 worldwide, the ST983 was identified only one isolate belonged this ST, according to the MLST database. Our results suggest one possible acquisition of resistance mechanisms over the years by isolate ST983, which reinforces the importance of adequate use de antimicrobials and the importance of control measures to prevent the spread of MDR clones.