Distribution of Conjugative-Plasmid-Mediated 16S rRNA Methylase Genes among Amikacin-Resistant Enterobacteriaceae Isolates Collected in 1995 to 1998 and 2001 to 2006 at a University Hospital in South Korea and Identification of Conjugative Plasmids Mediating Dissemination of 16S rRNA Methylase

Abstract

The distribution of conjugative-plasmid-mediated 16S rRNA methylase genes among amikacin-resistant Enterobacteriaceae collected between 1995 and 1998 and between 2001 and 2006 at a university hospital in South Korea was examined, and conjugative plasmids carrying the 16S rRNA methylase genes were characterized by PCR-based replicon typing and by determination of their antimicrobial resistance pattern. Among the 7,127 isolates, 463 isolates showed a high level of resistance to amikacin, and 218 of the 463 isolates transferred amikacin resistance by conjugation. Among the 218 isolates, armA was detected in 153 isolates (88 Klebsiella pneumoniae, 28 Escherichia coli, 19 Enterobacter cloacae, and 6 Serratia marcescens isolates and 12 isolates of other organisms), and rmtB was detected in 51 isolates (32 K. pneumoniae isolates, 18 E. coli isolates, and 1 Citrobacter freundii isolate). The first appearance of armA was in 1997. The armA gene was carried by conjugative plasmids of replicon groups IncL/M, IncFIIAs, IncF, IncA/C, IncHI2, and Inc(unidentified) in 38, 20, 7, 9, 4, and 75 strains, respectively. The rmtB gene was carried by conjugative plasmids of groups IncA/C, IncF, and IncI1-I␥ in 43 strains, 7 strains, and 1 strain, respectively. Transconjugants that received the IncL/M plasmid carrying armA or the IncA/C plasmid carrying rmtB showed an additional resistance to cefotaxime. Transconjugants that received the IncFIIA plasmid or Inc(unidentified) plasmid carrying the armA gene showed an additional resistance to cefoxitin and a high MIC 50 (0.25 mg/liter) of ciprofloxacin. In conclusion, this study demonstrated that the dissemination of 16S rRNA methylase genes among the Enterobacteriaceae is mediated by conjugative plasmids of various incompatibility groups that confer resistance to multiple drugs, including aminoglycosides, extended-spectrum ␤-lactams, and/or quinolones.Aminoglycosides have a high affinity for the 16S rRNA of the bacterial 30S ribosome, and they block protein synthesis (14,20). Over the past few decades, there have been many studies conducted regarding the mechanisms of resistance to aminoglycosides. One of the most common mechanisms of resistance to aminoglycosides is the production of aminoglycoside-modifying enzymes, such as 1-N-aminoglycoside acetyltransferase (AAC), adenyltransferase, and phosphotransferase (14,20). Amikacin was developed to suppress a variety of aminoglycoside-modifying enzymes from their accessing target sites (12), and therefore rare, amikacin-resistant bacteria could be expected. Recently, a series of special methylases that protect microbial 16S rRNA, however, were identified in several nosocomial pathogens, and these enzymes are capable of conferring extraordinarily high levels of resistance (MIC Ͼ 512 mg/liter) to most clinically important aminoglycosides, including amikacin, isepamicin, arbekacin, kanamycin, tobramycin, and gentamicin (5)(6)(7)(8)(21)(22)(23)(24). Since the first identification of a gene encoding 16S rRNA methylase, rmtA, from a Pseudomonas aeru...

Characterization of an rmtB-carrying IncI1 ST136 plasmid in avian Escherichia coli isolates from chickens

“…This indicated that both horizontal gene transfer and clonal spread were responsible for the dissemination of the rmtB gene in the E. coli strains in this study. The prevalence of plasmids carrying rmtB has frequently been observed to be associated with the incompatibility group F (IncF) in humans and other animals in China (Yu et al, 2010;Hou et al, 2012), and with IncA/ C in humans and IncF in companion animals in Korea (Kang et al, 2008;So et al, 2012). However, all rmtB-carrying plasmids in the present study belonged to IncI1.…”

“…Recently, the rmtB gene has often been found to coexist with bla CTX-M and fosA3 (Hou et al, 2012;Lee et al, 2012;Sun et al, 2012;Pan et al, 2014), which could pose a threat to animal husbandry and public health. The dissemination of plasmids carrying rmtB has frequently been observed to be associated with the IncF and IncA/C incompatibility groups (Kang et al, 2008;Yu et al, 2010;Hou et al, 2012), whereas IncI1 plasmids harbouring rmtB are scarce. The aim of this study was to characterize the IncI1 plasmid carrying rmtB from avian Escherichia coli strains.…”

Comparative Genomics of the IncA/C Multidrug Resistance Plasmid Family

“…This group of plasmids is regarded as a considerable public health threat due to its ability to spread across taxonomic borders (8,20,29,34,44,45). In this study, we present the complete plasmid sequence of pRA1 and provide new insights into the evolution of MDR IncA/C plasmids that allow for a better understanding of the underlying principles of plasmid propagation.…”

Serratia Infections: from Military Experiments to Current Practice

“…Six of the S. marcescens strains carried both ArmA and AAC(6Ј)-1b on plasmids. In this study, there were only four other Serratia species recovered from clinical specimens, and none were resistant to amikacin (210).…”

“…This enzyme is plasmid mediated and provides high-level resistance to several aminoglycosides, including kanamycin, tobramycin, amikacin, gentamicin, streptomycin, and arbekacin (110). Other plasmid-mediated 16S rRNA methylases have been identified in S. marcescens, including ArmA, RmtA, and RmtC (210).…”