Diverse carbapenem-resistance mechanisms in 16S rRNA methylase-producing Acinetobacter baumannii

Yamada, Yoshiaki; Suwabe, Akira

doi:10.1099/jmm.0.048991-0

Cited by 13 publications

(8 citation statements)

References 28 publications

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“…rmtB or rmtC genes were not able to be detected in the current isolate group. These results were also in accordance with other reports which found armA to be the only 16S rRNA methylase gene detected in high level aminoglycoside resistant A. baumannii 13 , 14 , 21 , 22 .…”

Section: Resultssupporting

confidence: 93%

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

Nie

Yuan

et al. 2014

Acta Pharmaceutica Sinica B

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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.

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Section: Resultssupporting

confidence: 93%

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

Nie

Yuan

et al. 2014

Acta Pharmaceutica Sinica B

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“…ArmA and OXA-23-like producing Gram-negative pathogens have been reported in Bulgaria [21], France [22], India [23], Korea [24], Norway [25] and the United States of America [26], and ArmA and OXA-51-like producing strains have been reported in Japan [27]. Moreover, armA and rmtB have been linked to bla CTX-Ms [28,29], but almost all ArmA producing isolates in Vietnam did not harbor bla CTX-Ms.…”

Section: Discussionmentioning

confidence: 99%

Emergence of 16S rRNA methylase-producing Acinetobacter baumannii and Pseudomonas aeruginosa isolates in hospitals in Vietnam

et al. 2013

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Background16S rRNA methylase-producing Gram-negative bacteria are highly resistant to all clinically important aminoglycosides. We analyzed clinical strains of 16S rRNA methylase-producing Acinetobactor baumannii and Pseudomonas aeruginosa obtained from clinical isolates in medical settings in Vietnam.MethodsFrom 2008 to 2011, 101 clinical strains of A. baumannii and 15 of P. aeruginosa were isolated from patients in intensive care units (ICUs) in two medical settings in Vietnam. Antimicrobial susceptibilities were determined using the microdilution method and epidemiological analysis was performed by pulsed-field gel electrophoresis and MLST. Genes encoding the 16S rRNA methylases, OXAs and CTX-Ms were analyzed by PCR and sequence analysis.Results16S rRNA methylase-producing Gram-negative pathogens were detected in two hospitals in Vietnam. Of the 101 clinical isolates of A. baumannii and the 15 of P. aeruginosa isolated from two ICUs in these hospitals, 72 (71.3%) were highly resistant to amikacin, arbekacin and gentamicin, with MICs greater than 1,024 mg/L. The 16S rRNA methylases ArmA and RmtB were produced by 61 and 9 isolates of A. baumannii, respectively, and RmtB was produced by 2 isolates of P. aeruginosa. Moreover, 52 of the A. baumannii isolates producing 16S rRNA methylases harbored both blaOXA-23-like and blaOXA-51-like genes. Most A. baumannii isolates producing 16S rRNA methylase obtained in hospital A in Hanoi were ST91 and ST231, whereas most from hospital B in Ho Chi Minh City were ST136, ST195, and ST254.The two P. aeruginosa isolates harboring rmtB showed different patterns on PFGE, one each corresponding to ST217 and ST313.ConclusionsGram-negative bacteria producing the 16S rRNA methylases ArmA and RmtB are emerging in medical settings in Vietnam. A. baumannii isolates in northern and southern regions of Vietnam may be of different lineages.

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“…Such isolates have been identified in China [274], South Korea [275,276], Vietnam [277], Japan [278], North America [279], Norway [280], Italy [281], Bulgaria [282], Iran [283] and Algeria [136]. The armA gene was always found to be located on a functional composite transposon Tn1548 [279].…”

Section: Acinetobacter Baumanniimentioning

confidence: 99%

Emerging broad-spectrum resistance in Pseudomonas aeruginosa and Acinetobacter baumannii : Mechanisms and epidemiology

Potron

Poirel

Nordmann

2015

International Journal of Antimicrobial Agents

573

460

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Multidrug resistance is quite common among non-fermenting Gram-negative rods, in particular among clinically relevant species including Pseudomonas aeruginosa and Acinetobacter baumannii. These bacterial species, which are mainly nosocomial pathogens, possess a diversity of resistance mechanisms that may lead to multidrug or even pandrug resistance. Extended-spectrum ␤-lactamases (ESBLs) conferring resistance to broad-spectrum cephalosporins, carbapenemases conferring resistance to carbapenems, and 16S rRNA methylases conferring resistance to all clinically relevant aminoglycosides are the most important causes of concern. Concomitant resistance to fluoroquinolones, polymyxins (colistin) and tigecycline may lead to pandrug resistance. The most important mechanisms of resistance in P. aeruginosa and A. baumannii and their most recent dissemination worldwide are detailed here.

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Diverse carbapenem-resistance mechanisms in 16S rRNA methylase-producing Acinetobacter baumannii

Cited by 13 publications

References 28 publications

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

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

Emergence of 16S rRNA methylase-producing Acinetobacter baumannii and Pseudomonas aeruginosa isolates in hospitals in Vietnam

Emerging broad-spectrum resistance in Pseudomonas aeruginosa and Acinetobacter baumannii : Mechanisms and epidemiology

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