• Investigation of phenotypic and genotypic resistance to aminoglycosides in clinical isolates of Staphylococcus aureus.
  • Fatemeh Norouzalinia,1 Leila Asadpour,2,*
    1. Department of Biology, Rasht Branch, Islamic Azad University, Rasht, Iran
    2. Department of Biology, Rasht Branch, Islamic Azad University, Rasht, Iran


  • Introduction: Staphylococcus aureus is known as a nosocomial pathogen capable of causing a wide range of infections, from a simple skin infection to fatal necrotizing pneumonia, osteomyelitis, food poisoning, urinary tract infections, scaly skin syndrome, and toxic shock syndrome. This bacterium has a high ability to gain resistance to various antimicrobial agents. This has caused the spread of infections caused by this bacterium and also the occurrence of problems such as increased mortality, increased length of hospitalization of patients in hospitals, and increased treatment costs, which makes doctors treat infections caused by Staphylococcus aureus limited have faced many.
  • Methods: Bacterial sampling and isolation Clinical isolates of Staphylococcus aureus were collected from blood, urine, joint fluid, sputum, wound, and abscess samples of patients referred to Rasht medical diagnostic laboratories and confirmed by culture and biochemical tests to identify the bacteria. To determine the antibiotic sensitivity of clinical isolates of Staphylococcus aureus to aminoglycosides, an antibiogram test was performed by diffusion method . Molecular identification and frequency of resistance genes Genomic DNA extraction of Staphylococcus isolates was done using a Cinagen DNA extraction kit (Cat. No. PR881614). To confirm the diagnosis of Staphylococcus aureus isolates, a pair of specific 23SrRNA primers and to identify resistance genes were used using the specific primers of the aac(6')-Ie-aph(2") and aph(3')-IIIa genes.
  • Results: Determination of antibiotic resistance of isolates In this study, 50 isolates of Staphylococcus aureus were identified. 89.38% of samples were resistant to kanamycin and 70.28% of samples were resistant to gentamicin. In examining the MIC of gentamicin in 20 isolates, 5% of the samples had an MIC of 250 μg/ml, 35% of the samples had an MIC of 1000 μg/ml, and 60% of the samples had an MIC of 2000 μg/ml. Frequency of aac(6')-Ie-aph(2") and aph(3')-IIIa genes In the genotypic study, the frequency of aac(6')-Ie-aph(2") gene was 70%, and the frequency of aph(3')-IIIa gene was 93%. Except for 11 isolates, both genes were the same in the rest.
  • Conclusion: Aminoglycosides are powerful bactericidal agents that are often used in combination with beta-lactams or glycopeptides in the treatment of staphylococcal infections. In this study, out of 50 drug-resistant isolates, 87.2% were resistant to kanamycin, 74.5% were resistant to gentamicin, and the MIC of gentamicin was high in resistant isolates. In the present study, the frequency of aminoglycoside modifying genes including aph(3)-IIIa and aac(6)-le-aph(2)-l in 31 resistant strains was investigated by PCR. In this study, in 31 isolates with resistant phenotype, the frequency of aac(6)-le-aph(2)-l gene was 70% and the frequency of aph(3)-IIIa gene was 93%. In the study of Rayos et al., 2016 in Madrid, Spain, in 55 isolates of Staphylococcus aureus resistant to methicillin, the most common aminoglycoside modifying genes were aac(6')le-aph(2")la (87.3%) and followed by It was ant(4')la (52.7%) and aph(3")IIIa (52.7%) .(36) During the study of Ghaznavi Rad et al. (2012) in Arak, out of 98 cases of Staphylococcus aureus isolated from clinical samples, 77.3% of the isolates had the acc(6')/aph(2") gene and 16.9% The samples had aph(3')-IIIa gene and 1.8% of isolates had ant(4')-Ia gene. Also, 16.9% of isolates had both aac(6')/aph(2') genes. and aph(3')-IIIa and 1.8% of the isolates had all three genes . The results show high resistance to aminoglycosides in Staphylococcus aureus strains, and high presence of aminoglycoside modifying genes aac(6')/aph(2') and aph(3')-IIIa.
  • Keywords: S. aureus, aminoglycosides, aac(6’)-Ie-aph(2”) and aph(3’)-IIIa genes