Surveillance of murA and the plasmid-mediated fosfomycin resistance fosA gene in uropathogenic E. coli isolates from UTI patients

Abstract

BackgroundUrinary tract infection, is a common nosocomial infection which became difficult to treat recently as multidrug-resistant strains have increased. The goal of this review was to determine phenotypic and molecular pattern of fosfomycin resistance represented in modifying enzyme FosA in Iraqi Escherichia coli isolates from patients hospitalised with UTI. MethodsUrine samples were got from 50 patients in the hospitals of Baghdad/Iraq. After isolation diagnosis was done using 16sDNA and murA genes. Minimum inhibitory concentrations (MICs) of isolates to fosfomycin were determined using the agar dilution method over a concentration range of 0.5–1024 μg/mL. Also, the presence of chromosomal and plasmid extracted modifying enzyme (fosA gene) investigated using polymerase chain reaction with specific primers. ResultsGenotypic identification of E. coli by using 16sDNA revealed that all the isolated 100% were gave appositive results with amplified size of 544 bp and 984 bp for murA as genes detection. The gene sequencing for murA showed a mutation (conversion in base 503 T→G), thus only one amino acid alteration when Histiden (H) residue change to Glutamine. The highest rate of MIC was 256mg/ml regarding fosfomycin as compared with break point 128 μg/mL. In this study, PCR assays for glpT and uhpT genes in 100% of uropathogenic E. coli. The high frequency of fosfomycin modifying-enzyme fosA is associated with its origin on chromosome or transferred by mobile elements like plasmid. ConclusionOur results indicated the bactericidal activity of fosfomycin against uropathogenic E. coli isolates. In agreement with similar studies, we concluded that the presence of murA is significantly associated with the development of resistance to fosfomycin. This type of resistance is in correlation with co-resistant by other classes of antimicrobial. Moreover, fosA gene on chromosomal genome and mediated-plasmid being the most prevalent fosfomycin-resistant determinant in UPEC. Therefore the results indicate that both fosA is contributed in genetic fosfomycin resistance.