Combination of a cell wall-active antibiotic with an aminoglycoside confers a synergistic effect in the treatment of some severe enterococcal infections. Unfortunately, with the emergence of enterococci with high-level resistance to aminoglycosides, particularly to gentamicin, the efficacy of the synergistic combinations has decreased. In this study, high-level gentamicin-resistant (HLGR) isolates of enterococci and the diversity of the genes encoding aminoglycoside-modifying enzymes (AMEs) as well as putative clonal dissemination of HLGR isolates were investigated in a university hospital in southeastern Iran.
The minimum inhibitory concentration of gentamicin was determined and HLGR isolates were investigated for AME genes. Genetic similarity between isolates was analyzed using repetitive extragenic palindromic (rep)-Polymerase Chain Reaction (PCR) assay.
Of 150 Enterococcus isolates, 62 isolates including Enterococcus faecalis (n = 46) and E. faecium (n = 16) were identified as HLGR. The most prevalent AME genes in both species were as follows: aph(3′)-IIIa (n = 44), aac(6′)-Ie-aph(2′)-Ia (n = 36), and ant(4′)-Ia (n = 15). The rep-PCR analysis showed clonality among E. faecalis isolates, so that 27 isolates were grouped in seven clusters representing similarity greater than 95%.
No link between AME determinants and clusters was found. Clonal spread of HLGR isolates of E. faecalis was found within our hospital. More rigorous recommendations are required to avoid dissemination of such resistant microorganisms in the hospital setting.