β-Lactam Antibiotic Induces the Expression of blaOXA-51-like and blaOXA-23 in Clinically Isolated Acinetobacter baumannii and Acinetobacter lowffii

Al-Haideri, Halah H. (2020) β-Lactam Antibiotic Induces the Expression of blaOXA-51-like and blaOXA-23 in Clinically Isolated Acinetobacter baumannii and Acinetobacter lowffii. In: Recent Progress in Microbiology and Biotechnology Vol. 4. B P International, pp. 13-31. ISBN 978-93-90516-11-7

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Abstract

Acinetobacter is opportunistic pathogens responsible of nosocomial infections worldwide. It belongs to
gamma protoebacteria, Gram-negative bacteria, aerobic and well known for their ability to resist a
spectrum of antibiotics. In this study, two isolates A. lowffii, and A. baumannii were obtained clinically,
and genomically identified by 16S rRNA assessment with high percent similarity with the
corresponding strains in the NCBI server, with the accession number MH685113 and MH685112 for
A. baumannii and A. lowffii respectively. The sensitivity profile of the isolates was variable, and A.
baumannii was the most resistant strain towards a wide range of antibiotics, and it did not show any
growth defect in the presence of β-lactam antibiotic, in comparison with A. lowffii. We identified that
the blaOXA-23 variant gene was responsible for imipenem resistance in A. baumannii, whereas, blaOXA-
51-like was moderately confer resistance towards A. lowffii which lack of blaOXA-23. This was determined
when the isolates were subjected to qRT-PCR. We identified that the blaOXA-23 variant gene was
increased about 1-fold in the presence of imipenem, whereas, blaOXA-51-like did not increased in
comparison to the control. Bioinformatic analyses revealed that blaOXA-23 is located in the cytoplasm,
and blaOXA-like 51 is located in the periplasm, and this pattern may contribute in the outbreak of
multidrug resistance Acinetobacter species.

Item Type: Book Section
Subjects: Journal Eprints > Biological Science
Depositing User: Managing Editor
Date Deposited: 08 Dec 2023 04:25
Last Modified: 08 Dec 2023 04:25
URI: http://repository.journal4submission.com/id/eprint/3331

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