2019
DOI: 10.9734/ajrimps/2018/45728
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Antimicrobial Resistance Profile of Escherichia coli Isolated from Urine of Patients in Nagari Allah Magani Hospital, Keffi, Nigeria

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Cited by 2 publications
(5 citation statements)
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“…The isolation of E. coli from urine of suspected UTIs patients in the study centre was expected and this agree with the study earlier reported by Rami'rez-Castillo et al [14] and El-Boumri et al [15], that E. coli is one of the is the most common agent of UTIs. The percentage occurrence of the isolates in the study centre was similar with the studies earlier reported by El-Boumri et al [15] in India, Eko et al [16] in Keffi, Nigeria, Eghieye et al [2] and Rami'rez-Castillo et al [14] in Mexico. The occurrence of the isolates was higher than 12.1 % reported by Eghieye et al [2] but less than 54.0 % reported by El-Boumri et al [15].…”
Section: Discussionsupporting
confidence: 89%
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“…The isolation of E. coli from urine of suspected UTIs patients in the study centre was expected and this agree with the study earlier reported by Rami'rez-Castillo et al [14] and El-Boumri et al [15], that E. coli is one of the is the most common agent of UTIs. The percentage occurrence of the isolates in the study centre was similar with the studies earlier reported by El-Boumri et al [15] in India, Eko et al [16] in Keffi, Nigeria, Eghieye et al [2] and Rami'rez-Castillo et al [14] in Mexico. The occurrence of the isolates was higher than 12.1 % reported by Eghieye et al [2] but less than 54.0 % reported by El-Boumri et al [15].…”
Section: Discussionsupporting
confidence: 89%
“…Our findings in this study shows that isolates were more resistance to ampicillin, ceftazidime, cefotaxime, cefoxitin, streptomycin and sulphamethoxazole/trimethoprim and this is not different from the study earlier described by Eko et al [16] and Eghieye et al [2]. The percentage resistance of the isolates to the antibiotics mentioned was less than 93.0 %, 60.5 %, 53.7 %, 72.1 %, 56.0 % and 86.0 % resistance to ampicillin, ceftazidime, cefotaxime, cefoxitin, streptomycin and sulphamethoxazole/trimethoprim as earlier reported by Eko et al (2018). The resistance of the isolates to antibiotic mentioned may be due to inappropriate use of the antibiotics during therapy of the infection caused by the isolates.…”
Section: Discussionsupporting
confidence: 53%
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“…Escherichia coli (E. coli) are Gram negative rod-shape facultative anaerobic bacteria belonging to the family Enterobacteriaceae. This organism is widely known as the most common etiological agent of Urinary tract infections (UTIs) causing about 75-80% of the UTIs in both hospital and community setting [1,2,3] .The treatment and control of UTIs are accomplished through therapy with different classes of antibiotics namely; β-lactam, fluoroquinolones, aminoglycosides and sulfamethoxazole/trimethoprim [4] and among the antibiotics mentioned, fluoroquinolones is widely used as empirical treatment of complicated and non-complicated UTIs [5,6] . Fluoroquinolones are synthetic, targeting enzymes involved in bacterial DNA replication [7,8] .…”
Section: Introductionmentioning
confidence: 99%
“…The preliminary mechanism of fluoroquinolones resistance in bacteria is traditionally mediated by the mutation of chromosomal genes encoding DNA gyrase, topoisomerase IV, regulatory efflux pumps, and/or porins giving rise to new strains of the same species [8] . Recent reports indicate that quinolone resistance in Enterobacteriaceae may be due to plasmid resistance genes namely: oqxAB, qnrA, qnrB, qnrS, aac(6′)-Ib-cr, and qepA [1,10] .The plasmid-mediated quinolone resistance (PMQR) genes namely: qnrA, qnrB, and qnrS code for proteins belonging to the pentapeptide repeat family interacting with DNA gyrase and topoisomerase IV enzymes to prevent the interaction of the quinolone with the enzymes [11] . The PMQR gene; aac(6′)-Ib-cr captured as a variant of aminoglycoside acetyltransferase, diminishes the fluoroquinolone activity by adding an acetyl group to this antimicrobial agent [12] .The quinolone efflux pump gene (qepA), is a proton-dependent transporter, which causes hydrophilic quinolone resistance, especially to norfloxacin, ciprofloxacin, and enrofloxacin [13] .…”
Section: Introductionmentioning
confidence: 99%