Viewing Study NCT05828550


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Study NCT ID: NCT05828550
Status: COMPLETED
Last Update Posted: 2025-07-11
First Post: 2023-04-13
Is NOT Gene Therapy: False
Has Adverse Events: False

Brief Title: Detection of Efflux Pump Genes Mediating Ciprofloxacin Resistance in Staphylococcus Aureus Isolates in Sohag University Hospitals
Sponsor: Sohag University
Organization:

Study Overview

Official Title: Detection of Efflux Pump Genes Mediating Ciprofloxacin Resistance in Staphylococcus Aureus Isolates in Sohag University Hospitals
Status: COMPLETED
Status Verified Date: 2025-07
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: Among multidrug-resistant bacteria, Methicillin-resistant Staphylococcus aureus (MRSA) isolates were recognized to be an important mortality factor in hospital infections and a major concern in health-care and community settings . The antibiotic-resistant of S. aureus is extended by various bacterial strategies, including limiting uptake of the drug, alteration of the drugtargets, production of druginactivating enzymes and the activation of efflux pumps that effectively remove antibiotics . Relying on the type of antibiotics, bacteria can apply one or more strategies. Specifically, localization of resistance genes in transferable genetic elements, such as plasmid and transposons , causing Horizontal transfer of resistance genes between bacterial strains . MRSA strains are resistant to nearly all beta-lactam antibiotics by producing an alternative penicillin-binding protein known as PBP2a . This protein is encoded by the mecA gene and has a low affinity to manybeta-lactam antibiotics. Furthermore, these strains often show resistance to a wide range of antibiotics . The use of fluoroquinolone for the effective infectious therapy is limited by presence of fluoroquinolone resistance . There are two mechanisms causing resistance to fluoroquinolone. The first one is attributed to mutations occurring in the quinolone-resistance determining region (QRDR) of topoisomerase IV encoded by grlA/grlB and DNA gyrase encoded by gyrA/gyrB; these mutations decrease the affinity ofthe drug. The other mechanism is mediated by efflux pumps which is less recognized . Recently, several efflux pumps have been identified for S. aureus including efflux pumps encoded by chromosome or plasmids. The efflux pumps norA, norB, norC, mdeA, sepA, mepA, sdrM and lmrS are encoded by chromosome while qacA/B, qacG, qacH, qacJ and smr are plasmid-encoded . Efflux pumps could be specialized for specific substrate or mobilized a wide varieties of different antibiotic classes . Despite, efflux pumps can potentially increase resistance to antibiotics in clinical isolates of S. aureus, few studies have been evaluated the individual and collective participation of the efflux system in resistant isolates . Therefore the aim of the study is to detect ciprofloxacin resistant strains of staphylococcus aureus isolates and to detect efflux pump genes ( norA , norB and norC ) mediating resistance in such strains.
Detailed Description: None

Study Oversight

Has Oversight DMC: False
Is a FDA Regulated Drug?: False
Is a FDA Regulated Device?: False
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: False
Is an FDA AA801 Violation?: