Plasmid-mediated quinolone resistance determinants in fluoroquinolone-nonsusceptible Escherichia coli isolated from patients with urinary tract infections in a university hospital, 2009–2010 and 2020

Kuo, Pei-Yun; Lo, Yueh-Hsin; Chiou, Yu-Jing; Chen, Chao-An; Hidrosollo, Jazon Harl; Thuy, Tran Thi Dieu; Zhang, Yen-Zhen; Wang, Mingcheng; Lin, Tzu Chen; Lin, Wen Chang; Kao, Cheng Yen

doi:10.1016/j.jgar.2022.06.004

Cited by 5 publications

(2 citation statements)

References 32 publications

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“…Another study found qnrS in 21 of 43 isolates, qnrB in 6 of 45 isolates and qnrA in 2 of 43 isolates [ 221 ]. They are highly transmissible and are transferred in tandem with additional β-lactams, gentamicin, and tetracycline resistance genes [ 222 ].…”

Section: Antibiotic Resistance Mechanismsmentioning

confidence: 99%

“…Plasmids carry genes encoding resistance to nitrofurantoin [ 185 ] β-lactams [ 240 ], fluoroquinolones [ 222 ], aminoglycosides [ 241 ], trimethoprim [ 209 ], sulfamethoxazole [ 242 ], tetracyclines [ 243 ], and fosfomycin [ 195 ] among others. These genes are often distributed within plasmids in different combinations, allowing for the spread of multidrug resistance during horizontal transfer events [ 66 ].…”

Section: The Mobilomementioning

confidence: 99%

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Uropathogenic Escherichia coli (UPEC)-Associated Urinary Tract Infections: The Molecular Basis for Challenges to Effective Treatment

Whelan,

Lucey,

Finn

2023

Microorganisms

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Urinary tract infections (UTIs) are among the most common bacterial infections, especially among women and older adults, leading to a significant global healthcare cost burden. Uropathogenic Escherichia coli (UPEC) are the most common cause and accounts for the majority of community-acquired UTIs. Infection by UPEC can cause discomfort, polyuria, and fever. More serious clinical consequences can result in urosepsis, kidney damage, and death. UPEC is a highly adaptive pathogen which presents significant treatment challenges rooted in a complex interplay of molecular factors that allow UPEC to evade host defences, persist within the urinary tract, and resist antibiotic therapy. This review discusses these factors, which include the key genes responsible for adhesion, toxin production, and iron acquisition. Additionally, it addresses antibiotic resistance mechanisms, including chromosomal gene mutations, antibiotic deactivating enzymes, drug efflux, and the role of mobile genetic elements in their dissemination. Furthermore, we provide a forward-looking analysis of emerging alternative therapies, such as phage therapy, nano-formulations, and interventions based on nanomaterials, as well as vaccines and strategies for immunomodulation. This review underscores the continued need for research into the molecular basis of pathogenesis and antimicrobial resistance in the treatment of UPEC, as well as the need for clinically guided treatment of UTIs, particularly in light of the rapid spread of multidrug resistance.

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Section: Antibiotic Resistance Mechanismsmentioning

confidence: 99%