Abstract
INTRODUCTION: This study aimed to determine the role of genes encoding aminoglycoside-modifying enzymes (AMEs) and 16S rRNA methylase (ArmA) in Acinetobacter baumannii clinical isolates. METHODS: We collected 100 clinical isolates of A. baumannii and identified and confirmed them using microbiological tests and assessment of the OXA-51 gene. Antibiotic susceptibility testing was carried out using disk agar diffusion and micro-broth dilution methods. The presence of AME genes and ArmA was detected by PCR and multiplex PCR. RESULTS: The most and least effective antibiotics in this study were netilmicin and ciprofloxacin with 68% and 100% resistance rates, respectively. According to the minimum inhibitory concentration test, 94% of the isolates were resistant to gentamicin, tobramycin, and streptomycin, while the highest susceptibility (20%) was observed against netilmicin. The proportion of strains harboring the aminoglycoside resistance genes was as follows: APH(3′)-VIa (aphA6) (77%), ANT(2”)-Ia (aadB) (73%), ANT(3”)-Ia (aadA1) (33%), AAC(6′)-Ib (aacA4) (33%), ArmA (22%), and AAC(3)-IIa (aacC2) (19%). Among the 22 gene profiles detected in this study, the most prevalent profiles included APH(3′)-VIa + ANT(2”)-Ia (39 isolates, 100% of which were kanamycin-resistant), and AAC(3)-IIa + AAC(6′)-Ib + ANT(3”)-Ia + APH(3′)-VIa + ANT(2”)-Ia (14 isolates, all of which were resistant to gentamicin, kanamycin, and streptomycin). CONCLUSIONS: High minimum inhibitory concentration of aminoglycosides in isolates with the simultaneous presence of AME- and ArmA-encoding genes indicated the importance of these genes in resistance to aminoglycosides. However, control of their spread could be effective in the treatment of infections caused by A. baumannii.
Highlights
This study aimed to determine the role of genes encoding aminoglycoside-modifying enzymes (AMEs) and 16S rRNA methylase (ArmA) in Acinetobacter baumannii clinical isolates
Among the 22 gene profiles detected in this study, the most prevalent profiles included aminoglycoside phosphotransferase (APH)(3′)-VIa + aminoglycoside nucleotidyltransferase (ANT)(2”)-Ia (39 isolates, 100% of which were kanamycin-resistant), and aminoglycoside acetyltransferase (AAC)(3)-IIa + AAC(6′)-Ib + ANT(3”)-Ia + APH(3′)-VIa + ANT(2”)-Ia (14 isolates, all of which were resistant to gentamicin, kanamycin, and streptomycin)
High minimum inhibitory concentration of aminoglycosides in isolates with the simultaneous presence of AME- and ArmA-encoding genes indicated the importance of these genes in resistance to aminoglycosides
Summary
This study aimed to determine the role of genes encoding aminoglycoside-modifying enzymes (AMEs) and 16S rRNA methylase (ArmA) in Acinetobacter baumannii clinical isolates. Conclusions: High minimum inhibitory concentration of aminoglycosides in isolates with the simultaneous presence of AME- and ArmA-encoding genes indicated the importance of these genes in resistance to aminoglycosides Control of their spread could be effective in the treatment of infections caused by A. baumannii. Acinetobacter baumannii, living in the soil, the water, and different hospital environments, is an important opportunistic pathogen that causes nosocomial infections such as pneumonia, urinary tract infections, intravenous catheter-associated infections, and ventilation-associated infections, in intensive care units[1,2,3,4] The ability of this microorganism to remain in the hospital environment and to spread among the patients, along with their resistance to several antibiotics, are the main driving forces behind large-scale recurrent events in different countries[5]. The enzymatic alteration of the aminoglycoside molecule at -OH or -NH2 groups by www.scielo.br/rsbmt I www.rsbmt.org.br
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