Phenotypic and genotypic evaluation of aminoglycoside resistance in Escherichia coli isolated from patients with blood stream infections in Tehran, Iran

is a significant causative agent of bloodstream infections (BSIs). Aminoglycoside antibiotics play a crucial role in treating severe infections such as sepsis and pneumonia. However, resistance to these antibiotics often occurs due to the production of aminoglycoside-modifying enzymes (AMEs). This s...

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Veröffentlicht in:Iranian journal of microbiology 2024-04, Vol.16 (2), p.187-192
Hauptverfasser: Ghamari, Mahsa, Emaneini, Mohammad, Hemmati, Saeed, Jabalameli, Fereshteh, Beigverdi, Reza
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Sprache:eng
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Zusammenfassung:is a significant causative agent of bloodstream infections (BSIs). Aminoglycoside antibiotics play a crucial role in treating severe infections such as sepsis and pneumonia. However, resistance to these antibiotics often occurs due to the production of aminoglycoside-modifying enzymes (AMEs). This study was conducted to assess antimicrobial susceptibility patterns against various aminoglycosides and to determine the prevalence of common AME genes in strains isolated from BSIs. Sixty-five isolates were obtained from blood samples in a referral hospital in Tehran, Iran. The susceptibility patterns of aminoglycosides were determined using disk diffusion method and AMEs genes were investigated using PCR assay. Resistance to aminoglycosides was observed in 64.6% (42/65) of the isolates. The most frequent resistance rate was found for kanamycin (44.6%) and gentamicin (38.5%), followed by tobramycin (29.2%) and amikacin (4.6%). The most frequent AME gene was , which detected in 49.2% isolates, followed by (40%), (32.3%), and (30.8%), respectively. Athough the findings of this survey are based on specimens collected from a single hospital, our study shows that the high prevalence of aminoglycoside resistance is primarily attributed to the presence of the and genes. The low rate of resistance to amikacin makes this antibiotic a good candidate for treatment of BSIs due to
ISSN:2008-3289
2008-4447
DOI:10.18502/ijm.v16i2.15351