High prevalence of vancomycin and high-level gentamicin resistance in Enterococcus faecalis isolates

Abstract

Multiple drug-resistant enterococci are major cause of healthcare-associated infections due to their antibiotic resistance traits. Among them, Enterococcus faecalis is an important opportunistic pathogen causing various hospital-acquired infections. A total of 53 E. faecalis isolates were obtained from various infections. They were identified by phenotypic and genotypic methods. Determination of antimicrobial resistance patterns was done according to CLSI guidelines. The isolates that were non-susceptible to at least one agent in ≥3 antimicrobial categories were defined as multidrug-resistant (MDR). Detection of antimicrobial resistance genes was performed using standard procedures. According to MDR definition, all of the isolates were MDR (100%). High-level gentamicin resistance was observed among 50.9% of them (MIC ≥ 500 μg/ml). The distributions of aac(6′)-Ie-aph(2′′)-Ia and aph(3′)-IIIa genes were 47.2% and 69.8%, respectively. The aph(2′′)-Ib, aph(2′′)-Ic, aph(2′′)-Id, and ant(4′)-Ia genes were not detected. Vancomycin resistance was found in 45.3% of strains. The vanA gene was detected in 37.7% of isolates, whereas vanB and vanC 1 genes were not observed in any strain. Erythromycin resistance rate was 79.2% and the frequencies of ermB and ermC genes were 88.6% and 69.8%, respectively. The ermA and msrA genes were not present in any of the isolates. Our data indicate a high rate of MDR E. faecalis strains. All of high-level gentamicin-resistant isolates carried at least one of aac(6′)-Ie-aph(2′′)-Ia or aph(3′)-IIIa genes. Distribution of vanA was notable among the isolates. In addition, ermB and ermC were accountable for resistance to erythromycin.

Next-Generation Sequencing and MALDI Mass Spectrometry in the Study of Multiresistant Processed Meat Vancomycin-Resistant Enterococci (VRE)

“…Infections with VRE are more difficult to treat than infection with vancomycin-susceptible enterococci (VSE) [8,9]. The resistance to vancomycin can be mediated by nine different types of van cluster genes (vanA -B, -C, -D, -E, -G, -L, -M, and -N) and we can distinguish them based on their physical location (encoded in the core genome or on a mobile genetic element); the level of resistance they confer; the specific glycopeptides to which they confer resistance (often distinguished operationally as providing resistance to both vancomycin and teicoplanin, or providing resistance to vancomycin but not teicoplanin); whether resistance is inducible or constitutively expressed; and the type of peptidoglycan precursor that is produced by their gene products.…”

“…However, high-level resistance to aminoglycosides (HLGR) is usually acquired on a mobile element that encodes an aminoglycoside-modifying enzyme. Such an enzyme is usually the bifunctional aminoglycoside-modifying enzyme, AAC(6 )-Ie-APH(2 )-Ia, which is encoded by the aac(6 )-Ie-aph(2 )-Ia gene, reducing the effect of aminoglycosides except for streptomycin [9,11]. Furthermore, among gentamicin-resistant strains, three aminoglycoside resistance genes, i.e., aph(2 )-Ib, aph(2 )-Ic, and aph(2 )-Id, have been reported.…”

“…Furthermore, among gentamicin-resistant strains, three aminoglycoside resistance genes, i.e., aph(2 )-Ib, aph(2 )-Ic, and aph(2 )-Id, have been reported. The ant(4 )-Ia and aph(3 )-IIIa genes encode resistance to various aminoglycosides as well [4,9,15]. Thus, in spite the intrinsic resistance, aminoglycosides are still used in the treatment of enterococcal infections but at high concentrations to prevent intrinsic resistance.…”

“…Moreover, enterococci also show resistance to macrolides, and their major determinants of resistance are ribosomal target modification by 23S rRNA methylases encoded by erm genes and efflux pump systems encoded by msr and mefA/E genes [9,16]. Enterococci that carry erm genes can result in inducible or constitutive resistance to all macrolide, lincosamide, and streptogramin B antibiotics.…”

“…Enterococci that carry erm genes can result in inducible or constitutive resistance to all macrolide, lincosamide, and streptogramin B antibiotics. Alternatively, resistance to streptogramin B and some macrolide antibiotics is induced by the msrA gene [9,17].…”