RÉSUMÉ
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.
Sujet(s)
Acinetobacter baumannii , Acinetobacter baumannii/génétique , Aminosides/pharmacologie , Antibactériens/pharmacologie , Protéines bactériennes , Résistance bactérienne aux médicaments/génétique , Methyltransferases , Tests de sensibilité microbienne , ARN ribosomique 16S/génétiqueRÉSUMÉ
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.
Sujet(s)
Acinetobacter baumannii/génétique , Protéines bactériennes , ARN ribosomique 16S/génétique , Tests de sensibilité microbienne , Résistance bactérienne aux médicaments/génétique , Aminosides/pharmacologie , Methyltransferases , Antibactériens/pharmacologieRÉSUMÉ
Twenty seven isolates of vancomycin resistant Enterococci based on the disk diffusion and E- test have been screened; being found eight (0.3%) clinical isolates of vanA & vanB through Taq Man Real Time PCR assay. This study shows the presence of both vanA & vanB genotypes in vanA phenotypes clinical isolates in the three hospitals in Iran.
Sujet(s)
Protéines bactériennes/génétique , Carbon-oxygen ligases/génétique , Entérocoques résistants à la vancomycine/effets des médicaments et des substances chimiques , Entérocoques résistants à la vancomycine/génétique , Antibactériens/pharmacologie , Tests d'agents antimicrobiens par diffusion à partir de disques , Humains , Iran , Réaction de polymérisation en chaine en temps réelRÉSUMÉ
Twenty seven isolates of vancomycin resistant Enterococci based on the disk diffusion and E- test have been screened; being found eight (0.3%) clinical isolates of vanA & vanB through Taq Man Real Time PCR assay. This study shows the presence of both vanA & vanB genotypes in vanA phenotypes clinical isolates in the three hospitals in Iran.
Sujet(s)
Humains , Protéines bactériennes/génétique , Carbon-oxygen ligases/génétique , Entérocoques résistants à la vancomycine/effets des médicaments et des substances chimiques , Entérocoques résistants à la vancomycine/génétique , Antibactériens/pharmacologie , Tests d'agents antimicrobiens par diffusion à partir de disques , Iran , Réaction de polymérisation en chaine en temps réelRÉSUMÉ
Twenty seven isolates of vancomycin resistant Enterococci based on the disk diffusion and E- test have been screened; being found eight (0.3%) clinical isolates of vanA & vanB through Taq Man Real Time PCR assay. This study shows the presence of both vanA & vanB genotypes in vanA phenotypes clinical isolates in the three hospitals in Iran.(AU)