Abstract
BackgroundEnterococci are intrinsically resistant to clinically achievable concentrations of aminoglycosides. However, high-level resistance to aminoglycosides (HLAR) is primarily due to the acquisition of genes encoding aminoglycoside-modifying enzymes (AMEs). Aminoglycosides along with cell wall inhibitors are given clinically for treating enterococcal infections. The current study was conducted to investigate the rate of HLAR and to determine aminoglycoside resistance encoding genes profile in enterococcal isolates from different clinical specimens.ResultsFrom 120 Enterococcus species, 50 (41.7%) enterococcal isolates were proven to have HLAR, 78% (39/50) have high-level gentamicin resistance (HLGR), and 74% (37/50) were high-level streptomycin-resistant (HLSR). HLGR isolates carried aminoglycoside modifying gene aac (6′)-Ie-aph (2′)-Ia in 26/39 (66.7%) of isolates, whereas 32/37 (86.5%) of HLSR carried aph (3′)-IIIa gene and were observed in E. faecalis, E. faecium, E. gallinarum, and E. casseliflavus. The aph (2′)-Ib, aph (2′)-Ic, and aph (2′)-Id that encode HLGR could not be detected.ConclusionsThe high detection rate of HLAR among the studied Enterococcus species and the coexistence of HLGR and HLSR strains provide crucial insights to the necessity of routine testing for HLAR in the microbiology lab. The main AME genes among HLGR and HLSR enterococci were aac (6′)-Ie-aph (2″)-Ia and aph (3′)-IIIa, respectively.
Highlights
Enterococci are intrinsically resistant to clinically achievable concentrations of aminoglycosides
High-level gentamicin resistance (HLGR) in enterococci is predominantly mediated by aac (6′)-Ie-aph(2′)-Ia gene, which encodes the bifunctional aminoglycoside modifying enzyme AAC (6′)-APH (2′)
Detection of High-level resistance to aminoglycosides (HLAR) in enterococcal isolates Enterococcus species isolates were screened for HLAR by Kirby-Bauer disc diffusion method using streptomycin (300 μg) and gentamicin (120 μg) discs (Bio-Rad, France), and results were interpreted according to the Clinical and Laboratory Standards Institute [7]
Summary
Enterococci are intrinsically resistant to clinically achievable concentrations of aminoglycosides. Enterococci acquire resistance to a wider range of antimicrobial agents aminoglycosides, glycopeptides, and beta-lactams. This poses a therapeutic challenge to clinicians as they are left with very few treatment options [3, 4]. High-level gentamicin resistance (HLGR) in enterococci is predominantly mediated by aac (6′)-Ie-aph(2′)-Ia gene, which encodes the bifunctional aminoglycoside modifying enzyme AAC (6′)-APH (2′). The action of such enzyme in enterococci eliminates the synergistic activity of gentamicin when combined with a cell wall active agent, such as ampicillin or vancomycin. Highlevel streptomycin and kanamycin resistance in enterococci are mediated by aph (3′)-IIIa [6]
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