Friday, 7 January 2022

Determination of Molecular Characterization of Extended Spectrum -Lactamase Genes in Clinical E. coli Isolates | Chapter 08 | New Visions in Science and Technology Vol. 11

 This study demonstrates that molecular characterisation and analytical approaches have a strong relationship. The genes that encode Extended Spectrum Beta-Lactamases (ESBLs) (TEM, SHV, and OXA) were amplified from multidrug-resistant E. coli. The plasmid encoded multidrug resistance E. coli isolates from various clinical sources were confirmed to be resistant to -lactam and cephalosporin. Seventy percent (70%) of the selected multi-drug resistant clinical isolates tested positive for ESBLs, with a 5 mm increase in zone diameter for either antibiotic relative to its zone when tested alone, according to conventional laboratory analysis. The antibiotic susceptibility test revealed that 100% of the isolates were resistant to amoxicillin-clavulanic acid, amoxicillin, cefuroxime, and ampicillin-sulbactam, while 90% were resistant to ceftazidine and tetracycline, 80% to ofloxacin, 70% to ceftriazon, nalidixic acid, cefalexin, 60% to ciprofloxacin, 50% to nitrofuranto The multiplex PCR with primers TEM (931bp), SHV (868), OXA-2 (478), aac(3)-IIa (900), and rmtA (634), which are genes responsible for extended spectrum -lactamase and aminoglycoside resistance in E. coli, shows that isolate W15 contains three (3) resistant genes, which correspond to TEM resolving as a 931 base pair, SHV 868 base pair, and a 4 Isolate B2 has a single resistant gene (478 base pair) that is interpreted as OXA-2, whereas isolates URO2, U64, and S45 have two resistance genes that resolve as 868 and 478 base pair, respectively, indicating SHV and OXA-2. Despite the varying degrees of antibiotic susceptibility profile test produced with traditional detection analysis, isolates S57, U58, and B7 revealed no gene amplification. Because these isolates are likely to contain other resistant genes that are also expressed at a molecular level, we assume that the primers utilised in this work do not code for their resistant genes.

 
Author(S) Details

James Chibueze Igwe
Department of Medical Biotechnology, National Biotechnology Development Agency, Abuja, Nigeria.

Josiah Ademola Onaolapo
Department of Pharmaceutics and Pharmaceutical Microbiology, Ahmadu Bello University, Zaria, Nigeria.

Mohammed Kachallah
Department of Pharmaceutics and Pharmaceutical Microbiology, University of Maiduguri, Maiduguri, Nigeria.

Amose Nworie
Department of Medical Laboratory Science, Ebonyi State University, Abakaliki, Nigeria.

Hannah Oluwakemi Oladipo
Department of Medical Biotechnology, National Biotechnology Development Agency, Abuja, Nigeria.

Beatrice Onyiye Ojiego
Department of Medical Biotechnology, National Biotechnology Development Agency, Abuja, Nigeria.

Obadiah Dauda Enose
Department of Medical Biotechnology, National Biotechnology Development Agency, Abuja, Nigeria.

Seyi Ebun Adeboye
Department of Medical Biotechnology, National Biotechnology Development Agency, Abuja, Nigeria.

Mojirayo Titilayo Durowaiye
Department of Pharmaceutical Microbiology, University of Ibadan, Ibadan, Nigeria.

Alex Uwadiegwu Akpa
Department of Medical Biotechnology, National Biotechnology Development Agency, Abuja, Nigeria.

Inimfon Akaninyene Ibanga
Department of Pharmaceutics and Pharmaceutical Microbiology, Ahmadu Bello University, Zaria, Nigeria.

View Book:- https://stm.bookpi.org/NVST-V11/article/view/5246

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