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Increasing antibiotic resistance is a global health problem. In recent years, due to the indiscriminate use of antibacterial compounds, many bacterial pathogens, including staphylococci, members of the Enterobacteriaceae family including Klebsiella pneumoniae and bacteria such as Pseudomonas aeruginosa and Acinetobacter baumannii have become multi-drug resistant. Consequently, it is important to explore alternative approaches for eliminating resistant strains. Bacteria synthesize low-weight molecules called siderophores to chelate iron from the environment as a vital element for their growth and survival. One way to deal with resistant bacterial strains is to utilize siderophore-mediated iron uptake pathways as entrance routes for drug delivery. Therefore, the production of drugs with Trojan horse strategy in the form of conjugated siderophore-antibiotic complexes has recently received much attention for dealing with resistant isolates. In this review, we discuss the efficacy of siderophore-antibiotic conjugates as a Trojan horse strategy for eliminating drug-resistant pathogens.

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Background and objectives: Antibiotic resistance in Helicobacter pylori is a significant cause of failure in the treatment of this infection. This study aimed to evaluate the antibiotic resistance to metronidazole, clarithromycin and fluoroquinolone in Helicobacter pylori strains isolated from biopsy specimens of patients.
methods: This study was carried out in (2016 to 2017) on 80 biopsy specimens of the Golestan province. Resistance to metronidazole (rdxA), fluoroquinolones (gyrA) was determined by PCR. Mutations at the A2143G and A2142G loci in the 23srRNA gene associated with clarithromycin resistance in strains were performed by PCR-RFLP with BsaI and BbsI enzymes.
Results: In this study, 25% of Helicobacter pylori strains were resistant to clarithromycin. A mutation in the A2143G locus (65%) and the A2142G locus (35%) were detected in these strains. Resistance to fluoroquinolones (27.5%) was observed, among which mutations in the 91 amino acid position of aspartate (63.63%) and mutations in the 87 amino acid position of asparagine (36.36%) were observed in the samples. Resistance to metronidazole was not observed in any of the strains of this study, and concomitant resistance to clarithromycin and fluoroquinolones was observed in (13.75%) of Helicobacter pylori strains.
Conclusions: According to our study, the resistance of Helicobacter pylori to clarithromycin, is increasing, which is a factor in treatment failure. The mechanism of clarithromycin resistance is related to mutations in the A2143G and A2142G positions, and resistance to fluoroquinolones is by a mutation in the gyrA gene and more in the 91 amino acid position.