Escherichia coli klinik izolatlarında plazmid aracılı florokinolon direnci
Loading...
Date
2014-12-18
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Selçuk Üniversitesi Sağlık Bilimleri Enstitüsü
Access Rights
info:eu-repo/semantics/openAccess
Abstract
Arkaplan: Escherichia coli insanların normal bağırsak florasında bulunan ve birçok doku ve organda çeşitli enfeksiyonlara neden olabilen fırsatçı bir patojendir. Kinolonların son yıllarda yaygın olarak kullanılmaları nedeniyle bu türler arasında bu antibiyotiğe karşı direnç giderek artmaktadır. Kinolonlara karşı direnç gelişimi, genellikle kromozomlarla kodlanan topoizomeraz ve efflux pump genlerindeki mutasyonlara, porin kaybına ve plasmid aracılı qnr, aac (6')-Ib-cr ve qepA gen transferine bağlı olarak gelişmektedir. Bu çalışmanın amacı, kinolon dirençli E.coli klinik izolatlarında plazmid aracılı kinolon direnç genlerinin varlığını araştırmaktır. Yöntem: Çalışmaya, Selçuk Üniversitesi Tıp Fakültesi Mikrobiyoloji Laboratuvarında çeşitli klinik örneklerden izole edilen toplam 115 kinolon dirençli E. coli suşları alındı. qnrA, qnB, qnrC, qnrS, qepA, and aac (6')-1b-cr genleri polimeraz zincir reaksiyonu (PZR) ile araştırıldı. Tüm aac (6')-1b-cr varyantını tanımlamak için aac (6')-1b pozitif amplikonlar BseGI restriksiyon enzimiyle kesilerek araştırılmıştır. Bulgular: 115 kinolon dirençli E.coli suşları arasında, qnrA, qnrC ve qepA genleri tespit edilmedi, bu suşların üçünde (% 2.6) qnrB, dokuzunda (% 7.8) qnrS ve ellisinde (% 43.5) aac (6')-1b-cr genleri pozitif bulundu. Sonuç olarak tez projemizde, Konya şehrinde izole edilen E. coli klinik suşlarında yüksek kinolon direncinden, aac (6 ')-1b-cr geninin sorumlu olduğu belirlendi. Bunun yanında, QnrB ve qnrS gen sıklığı düşük olarak tespit edildi ancak qnrA, qneC ve qepA genleri tespit edilemedi.
Background: Escherichia coli is found in the normal intestinal flora of humans and cause various infectionsin many tissues and organs. Because quinolones are widely used in recent years, the resistance has been increasing among this species. Bacterial resistance to quinolones usually results from mutations in the topoisomerase genes encoded chromosomally and also the expression of efflux pumps, loss of porines and the transfer of plasmid-mediated genes namely qnr, aac (6')-Ib-cr, and qepA.The aim of this study was to investigate the presence of plasmid-mediated quinolone resistance genes in E.coli clinical isolates. Methods: A total of 115 quinolone-resistant E. coli strainsisolated from various clinical specimens in Selcuk University, Microbiology Laboratory of Medical Faculty were included in the study. qnrA, qnrB, qnrC, qnrS, qepA, and aac (6')-1b-cr genes were investigated by polymerase chain reaction (PZR). All aac (6')-1b positive amplicons were analyzed by digestion with BseGI restriction enzyme to identify aac (6')-1b-cr variant. Results: Among 115 quinolone-resistant E. coli strains, none of themharboured qnrA, qnrC and qepA genes, however qnrB, qnrS and aac (6')-1b-cr were positive in three (2.6%), nine (7.8%) and 50 (43.5%) strains, respectively. Conclusion: In conclusion, we determined that aac (6')-1b-crgene was responsible for high quinolone resistance in clinical strains of E. coli from Konya, Turkey. The prevalence of qnrB and qnrS genes were low and qnrA, qnrC and qepA genes were not detected.
Background: Escherichia coli is found in the normal intestinal flora of humans and cause various infectionsin many tissues and organs. Because quinolones are widely used in recent years, the resistance has been increasing among this species. Bacterial resistance to quinolones usually results from mutations in the topoisomerase genes encoded chromosomally and also the expression of efflux pumps, loss of porines and the transfer of plasmid-mediated genes namely qnr, aac (6')-Ib-cr, and qepA.The aim of this study was to investigate the presence of plasmid-mediated quinolone resistance genes in E.coli clinical isolates. Methods: A total of 115 quinolone-resistant E. coli strainsisolated from various clinical specimens in Selcuk University, Microbiology Laboratory of Medical Faculty were included in the study. qnrA, qnrB, qnrC, qnrS, qepA, and aac (6')-1b-cr genes were investigated by polymerase chain reaction (PZR). All aac (6')-1b positive amplicons were analyzed by digestion with BseGI restriction enzyme to identify aac (6')-1b-cr variant. Results: Among 115 quinolone-resistant E. coli strains, none of themharboured qnrA, qnrC and qepA genes, however qnrB, qnrS and aac (6')-1b-cr were positive in three (2.6%), nine (7.8%) and 50 (43.5%) strains, respectively. Conclusion: In conclusion, we determined that aac (6')-1b-crgene was responsible for high quinolone resistance in clinical strains of E. coli from Konya, Turkey. The prevalence of qnrB and qnrS genes were low and qnrA, qnrC and qepA genes were not detected.
Description
Keywords
Drug hypersensitivity, İlaçlara duyarlılık, Drug resistance, İlaçlara direnç, Drugs, İlaçlar, Plasmids, Plazmitler, Escherichia coli infections, Escherichia coli enfeksiyonları, Escherichia coli, Anti infective agents, Antienfektif ajanlar, Antibiotics, Antibiyotikler
Journal or Series
WoS Q Value
Scopus Q Value
Volume
Issue
Citation
Al-Dulaimi, D. A. A. (2014). Escherichia coli klinik izolatlarında plazmid aracılı florokinolon direnci. Selçuk Üniversitesi, Yayımlanmış yüksek lisans tezi, Konya.
