Search Results

You are looking at 1 - 4 of 4 items for :

  • "AME genes" x
  • Refine by Access: All Content x
Clear All

The aim of the present study was to investigate, for the first time, the diversity of the genes encoding aminoglycoside-modifying enzymes (AME) and their association with class 1 integrons in Iranian Acinetobacter baumannii strains.A total of 100 multidrug resistant A. baumannii, isolated from eight distinct hospitals in Tehran, were enrolled in this study. Susceptibility of these isolates to antimicrobial agents including gentamicin and amikacin was determined by E-test. Aminoglycoside resistant isolates were then tested by PCR for AME genes, including aphA6, aacC1, aacC2, aacA4, aadB, aadA1, classes 1 integron, 5′-CS-3′ and typed by RAPD PCR.The rate of resistance to imipenem, meropenem, gentamicin and amikacin were 39%, 39%, 38% and 32%, respectively. Intermediate resistance phenotype to gentamicin and amikacin was observed in 2% and 5% of all the isolates, respectively. After aph6 with 90% (n = 36/40), aadA1, aacC1 and aadB with 82.5% (n = 33/40), 65% (n = 26/40) and 20% (n = 8/40) were the most prevalent AME genes among aminoglycosides resistant A. baumannii isolates. A combination of two to four different resistance genes was observed in 39 of 40 strains (97.5%), with a total of 7 different combinations. PCR of integrase genes revealed that AME gene was associated with 67% of class 1 integrons. RAPD analysis showed three predominant genotypes A (n = 20), B (n = 10) and 10 unrelated genotypes.The occurrence of identical resistance genes, gene combinations and class 1 integrons associated with these genes in clonally distinct strains indicates that horizontal gene transfer plays a major role in the dissemination of aminoglycoside resistance in A. baumannii.

Restricted access

Aminoglycosides are widely recommended for treatment of Acinetobacter baumannii infections in combination with β-lactams or quinolones. This cross-sectional study was aimed to investigate the coexistence of aminoglycoside modifying enzyme (AME) genes among A. baumannii isolates from clinical samples in Ahvaz, Iran. A total of 85 clinical A. baumannii isolates typed by ERIC-PCR were investigated for the presence of AME genes, including ant(3″)-Ia, aac(6′)-Ib, aac(3′)-Ia, ant(2″)-Ia, and aph(3′)-VIa by PCR. The resistance rates to aminoglycoside agents were evaluated by disk diffusion. In this study, 84 out of 85 A. baumannii isolates were resistant to at least one of the aminoglycosides and harbored at least one AME gene. The most common gene encoding AMEs was aph (3′)VIa, followed by aac(3′)-Ia, ant(3″)-Ia, ant (2″)-Ia, and aac(6′)-Ib. The aminoglycoside-resistant genotypes were completely matched to resistant phenotypes to each one of the aminoglycoside agents. There was a clear association between AME gene types and the phenotype of resistance to aminoglycosides with their ERIC-PCR types. Our findings highlight the coexistence of AME genes and clonal dissemination of multiresistant A. baumannii in hospital setting.

Restricted access
Acta Microbiologica et Immunologica Hungarica
Authors:
Mohsen Heidary
,
Alireza Salimi Chirani
,
Saeed Khoshnood
,
Gita Eslami
,
Seyyed Mohammad Atyabi
,
Habibollah Nazem
,
Mohammad Fazilati
,
Ali Hashemi
, and
Saleh Soleimani

Acinetobacter baumannii is a major opportunistic pathogen in healthcare settings worldwide. In Iran, there are only few reports on the prevalence of aminoglycoside resistance genes among A. baumannii isolates. The aim of this study was to investigate the existence of aminoglycoside-modifying enzyme (AME) genes from A. baumannii strains collected at a university teaching hospital in Iran. One hundred A. baumannii strains were collected between 2014 and 2015 from hospitalized patients at Loghman Hakim Hospital, Tehran, Iran. Antimicrobial susceptibility was determined by disk diffusion method according to the Clinical and Laboratory Standards Institute recommendations. The DNA was extracted using a kit obtained from Bioneer Co. (Korea) and was used as a template for polymerase chain reaction. The most active antimicrobial agent against these strains was colistin. The rate of extended-spectrum cephalosporin resistance was 97%. The aadA1, aadB, aac(6′)-Ib, and aac(3)-IIa genes were found in 85%, 77%, 72%, and 68% of A. baumannii isolates, respectively. This study showed a high prevalence rate of AME genes in A. baumannii. This prevalence rate has explained that further aminoglycoside resistance genes may have role in the resistance of clinical isolates of A. baumannii. Therefore, control and treatment of serious infections caused by this opportunistic pathogen should be given more consideration.

Restricted access

Escherichia coli and Klebsiella pneumoniae are frequently found resistance to aminoglycosides in Turkey. The aim of this study was to investigate aminoglycoside resistance in clinical isolates of E. coli and K. pneumoniae from Turkey using both phenotypic and genotypic methods and screening for the prevalence of gene coding for common aminoglycoside-modifying enzymes (AMEs) and 16S rRNA methylase genes. A total of 88 consecutive, non-duplicated E. coli (n = 65) and K. pneumoniae (n = 23) isolates showing resistance or intermediate resistance to amikacin and/or gentamicin were collected between October 2013 and May 2015 from clinical samples received at Gaziantep Dr. Ersin Arslan Training and Research Hospital. Seventeen isolates were obtained from Syrian patients. Isolates resistant to any of the two aminoglycosides were tested by PCR for seven AME genes, and 22 isolates with amikacin MIC ≥16 mg/L were also tested for 16S rRNA methylase genes. In E. coli isolates, the most frequent genes were aac(6′)-Ib (50 strains; 76.9%) and aac(3)-IIa (40 strains; 70.7%), followed by aph(3′)-Ia (5 strains; 7.6%) and ant(2″)-Ia (2 strains; 3.1%). Among the 23 resistant K. pneumoniae isolates, the most prevalent gene was aac(3′)-IIa (87.0%) followed by aac(6′)-Ib (73.9%) and aph(3′)-Ia (8.6%). The rmtC gene was detected in one K. pneumoniae isolate. Resistance to aminoglycosides in clinical isolates of E. coli and K. pneumoniae from our center is predominantly caused by AAC(6′)-Ib and AAC(3)-II enzymes, while the occurrence of 16S rRNA methylases is so far limited.

Restricted access