Aminoglycoside resistance in clinical Escherichia coli and Klebsiella pneumoniae isolates from Western Norway

Abstract

Resistance to gentamicin in Escherichia coli from blood culture has shown an increase over the past decade in Norway. This study was done to investigate aminoglycoside resistance in Escherichia coli and Klebsiella pneumoniae in Western Norway. The material included 49 blood culture isolates which had shown aminoglycoside resistance collected during 2000-2009. To investigate co-resistance to alternative antibiotics and dynamics involved in aminoglycoside resistance 67 isolates (mostly from urine) exhibiting resistance to both aminoglycosides and extended spectrum beta-lactam antibiotics were also included. MIC values were obtained for amikacin, gentamicin, kanamycin, netilmicin, streptomycin and tobramycin and all isolates were screened using PCR for aac(3)-II and aac(6')-Ib, encoding aminoglycoside modifying enzymes. Resistance to ≥3 aminoglycosides was found in 92% of the isolates and 60.3% showed resistance to gentamicin, netilmicin, tobramycin and kanamycin. Amikacin resistance was low. Co-resistance to ciprofloxacin was found in 88% of the isolates with gentamicin resistance. aac(3)-IIa/c was found in 79.3% and aac(6')-Ib in 37.9% of the isolates and 28.4% harboured both genes. aac(6')-Ib-cr, possibly contributing to ciprofloxacin resistance was found mostly in extended spectrum beta-lactamase producers. The aminoglycoside resistance patterns indicate co-existence of multiple resistance mechanisms. The use of ciprofloxacin and third generation cephalosporins is likely to have contributed to the increase in aminoglycoside resistance in Norway.

Molecular identification of aminoglycoside-modifying enzymes in clinical isolates of Escherichia coli resistant to amoxicillin/clavulanic acid isolated in Spain

“…In 20 European university hospitals participating in the European SENTRY Antimicrobial Surveillance Programme, the percentages of resistance to gentamicin, tobramycin and amikacin in E. coli obtained from three Spanish hospitals were 9.2%, 4.4% and 0.7%, respectively [23]. However, in ESBL-producing E. coli, the resistance rates were higher than those obtained in the current study; resistance to tobramycin, gentamicin and amikacin in a study in Norway were 94%, 73% and 6%, respectively [12].…”

“…There is little information on the production of AMEs in Enterobacteriaceae strains resistant to other antimicrobial groups [12][13][14].…”

Association between the Presence of Aminoglycoside-Modifying Enzymes and In Vitro Activity of Gentamicin, Tobramycin, Amikacin, and Plazomicin against Klebsiella pneumoniae Carbapenemase- and Extended-Spectrum-β-Lactamase-Producing Enterobacter Species

“…These low rates were observed despite that fact that 73% (16/22) of AMEϩ isolates possessed AAC(6=)-Ib, which is reported to confer AMK resistance. In fact, AMK MICs below the susceptibility breakpoints are commonly observed among Enterobacter and other Enterobacteriaceae that possess AAC(6=)-Ib (8,17,45,46). The clinical significance of susceptible MICs against bacteria carrying AMEs that are known to cause resistance is not established, and it is unclear if MICs or molecular markers are more relevant to treatment responses (47).…”

Detección y caracterización microbiológica de enterobacterias multidrogorresistentes transportadoras del gen modificador de aminoglicósidos durante tres décadas en un hospital universitario de Río de Janeiro

“…Ethidium bromide-stained agarose gel electrophoresis containing E. coli and K. pneumoniae plasmid DNA extracts isolated from different materials for plasmid detection according to the Kado and Liu protocol (13). Running conditions: 6.0 V/cm in 0.8% agarose; 861-molecular weight marker; R23-E. coli K 12 negative control; K-K. pneumoniae; E-E.coli (3)-II (Gen/Tob/Net) in most of the strains (8). Small changes in DNA sequences in genes throughout the replication processes, and/ or acquired genes, may have resulted in these phenotypical differences.…”

“…Resistance to these drugs occurs through several mechanisms that can coexist in the same cell; nevertheless, these resistance is often due to enzymatic inactivation by acetyltransferases, nucleotidyltransferases (adenylyltransferases), and phosphotransferases. The accC2 gene is among the most frequently detected in strains of Enterobacteriaceae isolated from clinical samples (8). Many of these genes are associated with transposons, which help to the rapid dissemination of drug resistance across species boundaries (9).…”