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To the Editor: Colistin is a last-line drug for treatment of multidrug-resistant, gram-negative bacterial infections, including those caused by Escherichia coli. We report colistin-resistant E. coli isolates from Japan, including [...]

Background: Topical antimicrobial formulations containing neomycin are commonly used to prevent and treat burn infections. However, Pseudomonas aeruginosa shows rapid acquisition of adaptive resistance to neomycin. This study aimed to evaluate the survival of P. aeruginosa during exposure to neomycin at high concentrations comparable to those used in topical formulations, and to investigate the effect of adaptive resistance to neomycin on the susceptibility to other aminoglycosides. Methods: Strain IID1130 [neomycin minimal inhibitory concentration (MIC) = 4 μg/ml] was incubated on an agar medium containing neomycin at high concentrations (8-4,096 μg/ml), and growing colonies were macroscopically observed. Acquisition of adaptive resistance was examined for 5 P. aeruginosa strains. Cells were sequentially passaged on agar medium containing neomycin with step-wise increased concentrations (8-2,048 μg/ml). To assess reversion of antibiotic susceptibility, the resulting colonies were repeatedly subcultured on antibiotic-free agar plates. Results: Growing IID1130 colonies were macroscopically detected on a neomycin-containing (2,048 μg/ml) agar plate for 48 h. These cells showed increasing MIC for not only neomycin, but also gentamicin and amikacin; the MIC values were occasionally higher than the breakpoints. When the adapted cells were subcultured on antibiotic-free agar, several passages were required for reversion of susceptibility. Conclusions: Our findings suggest that P. aeruginosa can survive in the presence of neomycin with a concentration typically used in topical dosage forms, and that the acquired adaptive resistance is persistent and is accompanied by cross-resistance to other aminoglycosides. [ABSTRACT FROM AUTHOR]

In recent years, multidrug resistance of Escherichia coli has become a serious problem. However, resistance to fosfomycin (FOM) has been low. We screened E. coli clinical isolates with reduced susceptibility to FOM and characterized molecular mechanisms of resistance and reduced susceptibility of these strains. Ten strains showing reduced FOM susceptibility (MIC ≥ 8 μg/mL) in 211 clinical isolates were found and examined. Acquisition of genes encoding FOM-modifying enzyme genes (fos genes) and mutations in murA that underlie high resistance to FOM were not observed. We examined ability of FOM incorporation via glucose-6-phosphate (G6P) transporter and sn-glycerol-3-phosphate transporter. In ten strains, nine showed lack of growth on M9 minimum salt agar supplemented with G6P. Eight of the ten strains showed fluctuated induction by G6P of uhpT that encodes G6P transporter expression. Nucleotide sequences of the uhpT, uhpA, glpT, ptsI, and cyaA shared several deletions and amino acid mutations in the nine strains with lack of growth on G6P-supplemented M9 agar. In conclusion, reduction of uhpT function is largely responsible for the reduced sensitivity to FOM in clinical isolates that have not acquired FOM-modifying genes or mutations in murA. However, there are a few strains whose mechanisms of reduced susceptibility to FOM are still unclear. [ABSTRACT FROM AUTHOR]

The article discusses a reports about the colistin-resistant Escherichia coli isolates from Japan, including a global-spreading pathogenic lineage. E. coli isolates obtained from clinical specimens taken at Sapporo Clinical Laboratory Inc. and Sapporo Medical University Hospital in Japan were tested and four E. coli isolates exceeded the colistin resistance breakpoint. The colistin-resistant isolates reported were resistant to fluoroquinolones, and one (SME296) was resistant to cephalosporins.

Transmission of tigecycline-nonsusceptible pathogenic Enterobacteriaceae from companion animals to human should be a concern because tigecycline is a last-line drug for treating multidrug-resistant Enterobacteriaceae in human medicine. However, tigecycline susceptibility of Enterobacteriaceae isolated from companion animals has not been investigated. In this study, we investigated the tigecycline susceptibility of Klebsiella pneumoniae complex and Escherichia coli isolates from dogs and cats, and evaluated their human pathogenicity potential. Tigecycline susceptibility of K. pneumoniae , including Klebsiella quasipneumoniae ( n  = 86) and E. coli ( n  = 100) strains isolated from dogs and cats was investigated. The antimicrobial susceptibility, capsular serotype, multilocus sequence type, ompK36 group, presence of virulence genes, and serum resistance of tigecycline-nonsusceptible isolates were evaluated. All E. coli isolates were susceptible to tigecycline. Two K. pneumoniae (minimum inhibitory concentration [MIC], 4 mg/L) and one K. quasipneumoniae (MIC, 8 mg/L) isolates were tigecycline resistant. Sixteen K. pneumoniae and one K. quasipneumoniae isolates were tigecycline intermediate (2 mg/L). All tigecycline-nonsusceptible isolates ( n  = 20) were also ciprofloxacin nonsusceptible. These isolates harbored five to nine virulence genes; 16 isolates were resistant to the human serum. In addition, STs of 13 K. pneumoniae isolates were reported to be found in strains isolated from human; isolates considered high-risk clones in human (ST11, ST15, and ST147) were also identified. In conclusion, the isolation of tigecycline-nonsusceptible K. pneumoniae from companion animals is an impact from the viewpoint of One Health approach to antimicrobial resistance that companion animals are a reservoir of human pathogenic lineages. [ABSTRACT FROM AUTHOR]

Tigecycline (TGC) is a last-line drug for multidrug-resistant Enterobacteriaceae We investigated the mechanism(s) underlying TGC nonsusceptibility (TGC resistant/intermediate) in Escherichia coli clinical isolates. The MIC of TGC was determined for 277 fluoroquinolone-susceptible isolates (ciprofloxacin [CIP] MIC, <0.125 mg/liter) and 194 fluoroquinolone-resistant isolates (CIP MIC, >2 mg/liter). The MIC 50 and MIC 90 for TGC in fluoroquinolone-resistant isolates were 2-fold higher than those in fluoroquinolone-susceptible isolates (MIC 50 , 0.5 mg/liter versus 0.25 mg/liter; MIC 90 , 1 mg/liter versus 0.5 mg/liter, respectively). Two fluoroquinolone-resistant isolates (O25b:H4-ST131-H30R and O125:H37-ST48) were TGC resistant (MICs of 4 and 16 mg/liter, respectively), and four other isolates of O25b:H4-ST131-H30R and an isolate of O1-ST648 showed an intermediate interpretation (MIC, 2 mg/liter). No TGC-resistant/intermediate strains were found among the fluoroquinolone-susceptible isolates. The TGC-resistant/intermediate isolates expressed higher levels of acrA and acrB and had lower intracellular TGC concentrations than susceptible isolates, and they possessed mutations in acrR and/or marR The MICs of acrAB-deficient mutants were markedly lower (0.25 mg/liter) than those of the parental strain. After continuous stepwise exposure to CIP in vitro, six of eight TGC-susceptible isolates had reduced TGC susceptibility. Two of them acquired TGC resistance (TGC MIC, 4 mg/liter) and exhibited expression of acrA and acrB and mutations in acrR and/or marR In conclusion, a population of fluoroquinolone-resistant E. coli isolates, including major extraintestinal pathogenic lineages O25b:H4-ST131-H30R and O1-ST648, showed reduced susceptibility to TGC due to overexpression of the efflux pump AcrAB-TolC, leading to decreased intracellular concentrations of the antibiotics that may be associated with the development of fluoroquinolone resistance., (Copyright © 2017 American Society for Microbiology.)

We determined the chemical structure of lipoteichoic acid (LTA) from Lactobacillus gasseri JCM 1131(T). The repeating unit was comprised of glycerolphosphate and 2-alanylglycerolphosphate. The glycolipid anchor was tetrahexosylglycerol with two or three acyl groups. To our knowledge, this is the first demonstration of a tetrahexose structure in an LTA glycolipid anchor.