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Last update 08 May 2025

Bacterial efflux pump

Last update 08 May 2025

Basic Info

Synonyms-

Introduction-

Drugs associated with Bacterial efflux pump

SMJ-5

Target

Bacterial efflux pump

Mechanism

Bacterial efflux pump inhibitors

Active Org.

Academy of Scientific & Innovative Research [+1]

Originator Org.

Institute of Microbial Technology [+1]

Active Indication

Staphylococcus Aureus Infections

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BDM-91288

Target

ACRBP x Bacterial efflux pump

Mechanism

ACRBP inhibitors [+1]

Active Org.

Institut Pasteur de Lille [+1]

Originator Org.

Johann Wolfgang Goethe-Universität Frankfurt am Main

Active Indication

Klebsiella pneumoniae infection

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NUNL02

Target

Bacterial efflux pump

Mechanism

Bacterial efflux pump inhibitors

Active Org.

Universidade Federal do Rio Grande

Originator Org.

Universidade Federal do Rio Grande

Active Indication

Tuberculosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Bacterial efflux pump

100 Translational Medicine associated with Bacterial efflux pump

0 Patents (Medical) associated with Bacterial efflux pump

319

Literatures (Medical) associated with Bacterial efflux pump

01 May 2025·Journal of Hazardous Materials

Arsenic-induced modulation of virulence and drug resistance in Pseudomonas aeruginosa

Article

Author: Song, Yingjie ; Li, Ze ; Bao, Rui ; Li, Tao ; Zhao, Fang

Arsenic contamination of water sources, whether from natural or industrial origins, represents a significant risk to human health. However, its impact on waterborne pathogens remains understudied. This research explores the effects of arsenic exposure on the opportunistic pathogen Pseudomonas aeruginosa, a bacterium found in diverse environments. The arsenic exposure at concentrations of 0.12-20 mg/L As(III) resulted in rapid growth arrest of P. aeruginosa. Moreover, arsenic exposure significantly reduced the production of key virulence factors such as elastase (by 1.48- to 9.24-fold), pyocyanin, and flagella while increasing siderophore and extracellular polysaccharide production (by 1.44-1.75 and 1.36-2.59 times, respectively). Proteomic analysis revealed that both low (0.12 mg/L) and high (1.2 mg/L) As(III) levels activated an antioxidant defense response, with upregulation of Fnr-2, TrxB2, and Ohr. Furthermore, arsenic-induced the overexpression of multidrug resistance efflux proteins MexAB-OprM, MexCD-OprJ, and MexEF-OprN. At the same time, proteins associated with quorum sensing (QS), type III secretion system (T3SS), pyocyanin biosynthesis, and flagellar assembly were downregulated. In vitro assays confirmed that arsenic reduced bacterial virulence and significantly enhanced survival and proliferation under antibiotic treatment. These results indicate that arsenic exposure modulates the virulence and antibiotic resistance of P. aeruginosa, raising concerns about the public health risks posed by the convergence of arsenic-contaminated water and multidrug-resistant bacteria.

01 May 2025·Environmental Science and Ecotechnology

Biocides as drivers of antibiotic resistance: A critical review of environmental implications and public health risks

Review

Author: Machado, Idalina ; Sousa, Mariana ; Simões, Lúcia C ; Simões, Manuel

The widespread and indiscriminate use of biocides poses significant threats to global health, socioeconomic development, and environmental sustainability by accelerating antibiotic resistance. Bacterial resistance development is highly complex and influenced significantly by environmental factors. Increased biocide usage in households, agriculture, livestock farming, industrial settings, and hospitals produces persistent chemical residues that pollute soil and aquatic environments. Such contaminants contribute to the selection and proliferation of resistant bacteria and antimicrobial resistance genes (ARGs), facilitating their dissemination among humans, animals, and ecosystems. In this review, we conduct a critical assessment of four significant issues pertaining to this topic. Specifically, (i) the role of biocides in exerting selective pressure within the environmental resistome, thereby promoting the proliferation of resistant microbial populations and contributing to the global spread of antimicrobial resistance genes (ARGs); (ii) the role of biocides in triggering transient phenotypic adaptations in bacteria, including efflux pump overexpression, membrane alterations, and reduced porin expression, which often result in cross-resistance to multiple antibiotics; (iii) the capacity of biocides to disrupt bacteria and make the genetic content accessible, releasing DNA into the environment that remains intact under certain conditions, facilitating horizontal gene transfer and the spread of resistance determinants; (iv) the capacity of biocides to disrupt bacterial cells, releasing intact DNA into the environment and enhancing horizontal gene transfer of resistance determinants; and (iv) the selective interactions between biocides and bacterial biofilms in the environment, strengthening biofilm cohesion, inducing resistance mechanisms, and creating reservoirs for resistant microorganisms and ARG dissemination. Collectively, this review highlights the critical environmental and public health implications of biocide use, emphasizing an urgent need for strategic interventions to mitigate their role in antibiotic resistance proliferation.

04 Mar 2025·Microbiology Spectrum

Mutations leading to ceftolozane/tazobactam and imipenem/cilastatin/relebactam resistance during in vivo exposure to ceftazidime/avibactam in Pseudomonas aeruginosa

Article

Author: Rokes, Alecia B. ; Rapsinski, Glenn J. ; Cooper, Vaughn S. ; Van Tyne, Daria

ABSTRACT Identifying resistance mechanisms to novel antimicrobials informs treatment strategies during infection and antimicrobial development. Studying resistance that develops during the treatment of an infection can provide the most clinically relevant mutations conferring resistance, but cross-sectional studies frequently identify multiple candidate resistance mutations without resolving the driver mutation. We performed whole-genome sequencing of longitudinal Pseudomonas aeruginosa from a patient whose P. aeruginosa developed imipenem/cilastatin/relebactam and ceftolozane/tazobactam resistance during ceftazidime/avibactam treatment. This analysis determined new mutations that arose in isolates resistant to both imipenem/cilastatin/relebactam and ceftolozane/tazobactam. Mutations in penicillin-binding protein 3 ftsI, the MexAB-OprM repressor nalD , and a virulence regulator pvdS were found in resistant isolates. Importantly, drug efflux was not increased in the resistant isolate compared to the most closely related susceptible isolates. We conclude that mutations in peptidoglycan synthesis genes can alter the efficacy of multiple antimicrobials. IMPORTANCE Antibiotic resistance is a significant challenge for physicians trying to treat infections. The development of novel antibiotics to treat resistant infections has not been prioritized for decades, limiting treatment options for infections caused by many high-priority pathogens. Cross-resistance, when one mutation provides resistance to multiple antibiotics, is most problematic. Mutations that cause cross-resistance need to be considered when developing new antibiotics to guide developers toward drugs with different targets, and thus a better likelihood of efficacy. This work was undertaken to determine the mutation that caused resistance to three antibiotics for highly resistant Pseudomonas aeruginosa infection treatment while the bacteria were exposed to only one of these agents. The findings provide evidence that drug developers should endeavor to find effective antibiotics with new targets and that medical providers should utilize medications with different mechanisms of action in bacteria that have become resistant to even one of these three agents.

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Bacterial efflux pump

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