Genetic basis of high level aminoglycoside resistance in Acinetobacter baumannii from Beijing, China

Abstract

The objective of this study was to investigate the genetic basis of high level aminoglycoside resistance in Acinetobacter baumannii clinical isolates from Beijing, China. 173 A. baumannii clinical isolates from hospitals in Beijing from 2006 to 2009 were first subjected to high level aminoglycoside resistance (HLAR, MIC to gentamicin and amikacin>512 µg/mL) phenotype selection by broth microdilution method. The strains were then subjected to genetic basis analysis by PCR detection of the aminoglycoside modifying enzyme genes (aac(3)-I, aac(3)-IIc, aac(6′)-Ib, aac(6′)-II, aph(4)-Ia, aph(3′)-I, aph(3′)-IIb, aph(3′)-IIIa, aph(3′)-VIa, aph(2″)-Ib, aph(2″)-Ic, aph(2″)-Id, ant(2″)-Ia, ant(3″)-I and ant(4′)-Ia) and the 16S rRNA methylase genes (armA, rmtB and rmtC). Correlation analysis between the presence of aminoglycoside resistance gene and HLAR phenotype were performed by SPSS. Totally 102 (58.96%) HLAR isolates were selected. The HLAR rates for year 2006, 2007, 2008 and 2009 were 52.63%, 65.22%, 51.11% and 70.83%, respectively. Five modifying enzyme genes (aac(3)-I, detection rate of 65.69%; aac(6′)-Ib, detection rate of 45.10%; aph(3′)-I, detection rate of 47.06%; aph(3′)-IIb, detection rate of 0.98%; ant(3″)-I, detection rate of 95.10%) and one methylase gene (armA, detection rate of 98.04%) were detected in the 102 A. baumannii with aac(3)-I+aac(6′)-Ib+ant(3″)-I+armA (detection rate of 25.49%), aac(3)-I+aph(3′)-I+ant(3″)-I+armA (detection rate of 21.57%) and ant(3″)-I+armA (detection rate of 12.75%) being the most prevalent gene profiles. The values of chi-square tests showed correlation of armA, ant(3″)-I, aac(3)-I, aph(3′)-I and aac(6′)-Ib with HLAR. armA had significant correlation (contingency coefficient 0.685) and good contingency with HLAR (kappa 0.940). The high rates of HLAR may cause a serious problem for combination therapy of aminoglycoside with β-lactams against A. baumannii infections. As armA was reported to be able to cause high level aminoglycoside resistance to most of the clinical important aminoglycosides (gentamicin, amikacin, tobramycin, etc), the function of aminoglycoside modifying enzyme gene(s) in A. baumannii carrying armA deserves further investigation.

Prevalence of carbapenemases among high-level aminoglycoside-resistant Acinetobacter baumannii isolates in a university hospital in China

“…The prevalence of armA genes in A. baumannii isolates has been described in several studies that showed 50% (52/104) in strains isolated in Lishui, eastern China (10), 60.4% (61/101) in clinical strains in Vietnam (53), and 59.54% (103/173) in hospitals in Beijing, China (54). In the present study, 45.76% (54/118, Table IV) of isolates harbored the armA gene, which is similar to the above cases reported in China.…”

Whole-genome sequence of multi-drug resistant Pseudomonas aeruginosa strains UY1PSABAL and UY1PSABAL2 isolated from human broncho-alveolar lavage, Yaoundé, Cameroon

“…Additionally, rmtB is a 16S rRNA methylase which confers resistance to almost all aminoglycosides except streptomycin [48]. This ability was verified in UY1PSABAL and was confirmed harbouring the rmtB gene and consequently displayed resistance to all tested aminoglycosides (amikacin, gentamicin, gentamicin and tobramycin) represented by AMK R GEN R NET R TOB R .…”

Prevalence of Aminoglycoside Resistance and Aminoglycoside Modifying Enzymes in Acinetobacter baumannii Among Intensive Care Unit Patients, Ismailia, Egypt

“…Nie et al proposed that increased aminoglycoside resistance in A. baumannii is related to acc (6ʹ). 29 Another study reported the presence of acetyltransferase genes (aacC1) in 63.3% of Acinetobacter isolates and other genes including aphA6, aadA1 and aadB were detected in 65%, 41.7% and 3.3%, of the isolates, respectively. 30 In our study the prevalence of aphA6 and aadA1 genes was less prevalent than reported previously.…”