Abstract
The purpose of the current study was to evaluate the phenotypic and genotypic patterns of aminoglycoside resistance among the Gram-negative bacteria (GNB) isolates collected from pediatric and general hospitals in Iran. A total of 836 clinical isolates of GNB were collected from pediatric and general hospitals from January 2018 to the end of December 2019. The identification of bacterial isolates was performed by conventional biochemical tests. Susceptibility to aminoglycosides was evaluated by the disk diffusion method (DDM). The frequency of genes encoding aminoglycoside-modifying enzymes (AMEs) was screened by the PCR method via specific primers. Among all pediatric and general hospitals, the predominant GNB isolates were Acinetobacter spp. (n = 327) and Escherichia coli (n = 144). However, E. coli (n = 20/144; 13.9%) had the highest frequency in clinical samples collected from pediatrics. The DDM results showed that 64.3% of all GNB were resistant to all of the tested aminoglycoside agents. Acinetobacter spp. and Klebsiella pneumoniae with 93.6%, Pseudomonas aeruginosa with 93.4%, and Enterobacter spp. with 86.5% exhibited very high levels of resistance to gentamicin. Amikacin was the most effective antibiotic against E. coli isolates. In total, the results showed that the aac (6')-Ib gene with 59% had the highest frequency among genes encoding AMEs in GNB. The frequency of the surveyed aminoglycoside-modifying enzyme genes among all GNB was found as follows: aph (3')-VIe (48.7%), aadA15 (38.6%), aph (3')-Ia (31.3%), aph (3')-II (14.4%), and aph (6) (2.6%). The obtained data demonstrated that the phenotypic and genotypic aminoglycoside resistance among GNB was quite high and it is possible that the resistance genes may frequently spread among clinical isolates of GNB.
Highlights
Antimicrobial resistance is being increasingly recognized as a serious public health threat worldwide [1,2,3,4]
The aminoglycosides including tobramycin, gentamicin, and amikacin play a bactericidal role against a wide range of Gram-negative bacteria (GNB) such as Acinetobacter baumannii (A. baumannii), Pseudomonas aeruginosa (P. aeruginosa), Escherichia coli (E. coli), and Klebsiella pneumoniae (K. pneumoniae) [10, 11]
The resistance mechanisms against aminoglycosides in GNB mainly result from the (1) production of aminoglycoside-modifying enzymes (AMEs), inactivating antibiotics classified in several families such as aminoglycoside nucleotidyltransferases (ANTs), aminoglycoside acetyltransferases (AACs), and aminoglycoside phosphoryltransferases (APHs); (2) methylation of 16S rRNA by a family of ribosomal methyltransferase enzymes; (3) mutation in the 30S ribosomal subunit; (4) active expulsion of antibiotics from the bacterial cells by efflux pumps; and (5) alteration of cell membrane permeability and reduction in intracellular concentration of aminoglycosides [13,14,15]
Summary
Antimicrobial resistance is being increasingly recognized as a serious public health threat worldwide [1,2,3,4]. The resistance mechanisms against aminoglycosides in GNB mainly result from the (1) production of aminoglycoside-modifying enzymes (AMEs), inactivating antibiotics classified in several families such as aminoglycoside nucleotidyltransferases (ANTs), aminoglycoside acetyltransferases (AACs), and aminoglycoside phosphoryltransferases (APHs); (2) methylation of 16S rRNA by a family of ribosomal methyltransferase enzymes; (3) mutation in the 30S ribosomal subunit; (4) active expulsion of antibiotics from the bacterial cells by efflux pumps; and (5) alteration of cell membrane permeability and reduction in intracellular concentration of aminoglycosides [13,14,15] Among these factors, AMEs represent the most common mechanism by which clinical isolates of GNB and Gram-positive bacteria (GPB) can enzymatically modify the hydroxyl or amino groups of the drug, inhibiting their binding to ribosomes and allowing the bacteria to survive [16, 17]. Antibiotic-resistant GNB can cause severe infections in neonates and children and are considered the main concern for physicians [18]
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