Genetic basis of enzymatic resistance of E. coli to aminoglycosides

Over the past years, an increase in resistance to aminoglycosides has been observed among Enterobacteriaceae rods. This resistance development reduces therapeutic options for infections caused by multidrug-resistance organisms. Because of the changing epidemiology of extended-spectrum β-lactamases (ESBLs) and resistance to aminoglycosides, we investigated the prevalence of the aac(3)-Ia, aac(6')-Ib, ant(4')-IIa, ant(2")-Ia, and aph(3")-Ib genes encoding aminoglycoside-modifying enzymes (AMEs) in ESBL-producing Escherichia coli as well as ESBL-non-producing isolates. To understand bacterial resistance to aminoglycoside antibiotics, we estimated resistance phenotypes and the presence of genes responsible for this resistance.

The study was conducted on 44 E.coli strains originated from patients hospitalized at University Hospital of Bialystok. MIC values were obtained for gentamicin, amikacin, netilmicin, and tobramycin. Isolates were tested for the presence of the aac(3)-Ia, aac(6')-Ib, ant(4')-IIa, ant(2")-Ia, and aph(3")-Ib genes with the use of the PCR technique.

Resistance to aminoglycosides was found in 79.5% of the isolates. The highest percentages of resistance were observed for tobramycin (70,5%) and gentamicin (59%), followed by netilmicin (43.2%) and amikacin (11.4%). PCR assays revealed the presence of aac(6')-Ib among 26 (59.2%) strains, aph(3")-Ib among 16 (36.2%), aac(3)-Ia among 7 (15.9%), and ant(2")-Ia among 2 (4.6%) strains.

The enzymatic resistance against aminoglycosides in northeastern Poland among clinical isolates of E. coli is predominantly caused by aac(6')-Ib and aph(3")-Ib. Amikacin may be used for therapy of infections caused by ESBL-producing E. coli, because of the low rates of resistance.