No abstract

Acinetobacter baumannii is an increasingly common pathogen in healthcare settings globally. It is frequently resistant to multiple antimicrobial agents and there are recent reports on strains that are pandrug resistant. The aim of the study was to characterize the mechanisms of carbapenem resistance of A. baumannii strains from a nursing home in Zagreb and to genotype the strains. Antimicrobial susceptibility testing was performed by the broth microdilution method according to the Clinical and Laboratory Standards Institute (CLSI). PCR was used to detect genes encoding carbapenemases of groups A, B, and D and extended-spectrum β-lactamases. Genotyping of the strains was performed by rep-PCR. All strains were found to be resistant to ceftazidime, cefotaxime, ceftriaxone, cefepime, piperacillin/tazobactam, imipenem, meropenem, and ciprofloxacin. All, but one strain, were resistant to gentamicin. PCR revealed blaOXA-23 genes in 14, blaOXA-24 in 5, and blaVIM in 11 strains. All strains positive for blaVIM genes coharbored blaOXA-23 genes. The 14 strains with OXA-23 belonged to ICL II, whereas the 5 strains positive for blaOXA-24 belonged to ICL I. In contrast to hospitals where OXA-24/40-like β-lactamases and OXA-58 were the most prevalent, OXA-23-like β-lactamases are the dominant group in the nursing home. OXA-58-like β-lactamase, which is the most widespread group, was not found. Acquisition of blaMBL genes in A. baumannii strains was observed. Rep-PCR identified two clones. Two strains A10 and A13 were alocated to a novel sequence type ST 637. Nursing homes can act as a source of dissemination of blaOXA and blaMBL genes in the environment and the possible influx to the hospital environment.

No abstract

Previous studies found short postantibiotic effect of colistin on Acinetobacter baumannii. Many studies have evaluated the potential for synergy between colistin and other antibiotics against A. baumannii. The aim of this study was to determine in vitro synergy and postantibiotic effect (PAE) of colistin alone and combined with other antibiotics (vancomycin or meropenem) against eight carbapenem-non-susceptible Acinetobacter spp. strains with defined resistance mechanisms. It was hypothesised that vancomycin or meropenem would prologue the PAE of colistin since it was previously found that they exert synergism with colistin in time-kill kinetics and chequerboard analysis. After exposure of 1 hour colistin alone exhibited the negative ( - 0.07 hour) (OXA-143), short (0.2-1.82 hours) (OXA-24, OXA-58, OXA-72, VIM-1+OXA-23, OXA-58+NDM-1, ISAba1/OXA-69) or moderate PAE (3.2 hours) for OXA-23 positive strain. When combined with vancomycin, the PAE was moderate (1.7-4 hours) with OXA-23, OXA-23+VIM-1, OXA-72 and OXA-24 positive strains while with OXA-58, OXA-143, OXA-58/NDM-1 and ISAba1/OXA-69 positive strains, it was not possible to calculate mean duration of PAE because there was no regrowth after exposure to antibiotics or it was longer than 5 hours. The combination with meropenem resulted in short (0.2 hours) (OXA-143), moderate (2.4-3.73 hours) (OXA-24, OXA-58, OXA-23, OXA-23+VIM-1), long PAE of 5 hours (OXA-23) or longer than 5 hours (OXA-58+VIM-1, ISAba1/OXA-69). From the clinical point of view, the prolongation of colistin PAE when combined with other antibiotics could provide a rationale for the modification of the dosing interval and could be important for the optimization of the treatment regimen and the minimization of drug-induced side effects.

No abstract