In recent years, multidrug resistance ofEscherichia colihas become a serious problem. However, resistance to fosfomycin (FOM) has been low. We screenedE. coliclinical 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 (fosgenes) and mutations inmurAthat underlie high resistance to FOM were not observed. We examined ability of FOM incorporation via glucose-6-phosphate (G6P) transporter andsn-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 ofuhpTthat encodes G6P transporter expression. Nucleotide sequences of theuhpT,uhpA, glpT,ptsI, andcyaAshared several deletions and amino acid mutations in the nine strains with lack of growth on G6P-supplemented M9 agar. In conclusion, reduction ofuhpTfunction is largely responsible for the reduced sensitivity to FOM in clinical isolates that have not acquired FOM-modifying genes or mutations inmurA. However, there are a few strains whose mechanisms of reduced susceptibility to FOM are still unclear.
Candida auris: A Quick Review on Identification, Current Treatments, and Challenges