Molecular Detection Of Efflux Pump and Virulence Factors Genes in Pseudomonas Aeruginosa

The pathogenesis of PA infections is multifactorial, and it is frequently complicated by the bacteria's intrinsic resistance to some antimicrobial agents such as sulfonamides, tetracyclines, and trimethoprim, as well as its ability to acquire or quickly develop resistance to major classes of antibiotics such as aminoglycosides, quinolones, B-lactams, and polymyxins (Bassetti et al., 2018).

The efflux systems, which mediate the expulsion of antibiotics out of the cell shortly after entry, the production of enzymes to inactivate antibiotics, and the decrease in permeability across the cell wall are some mechanisms used by PA to develop antimicrobial resistance (Meletis & Bagkeri, 2013).

PA possesses a large number of virulence factors that play a significant role in pathogenesis and the determination of infection severity. These virulence factors act alone or in synergy with each other to cause tissue damage, necrosis, and cell death. Among the virulence factors of PA, the major determinants of virulence are the type III secretion system (T3SS) and quorum sensing (cell-to-cell signaling system). The T3SS is a needle-like complex, also known as the injectisome, that enables a bacterium to deliver different effector proteins such as ExoS, ExoT, ExoU, and ExoY across the membrane into a host cell, altering host cell functions and increasing bacterial survival rates ( Horna G and, Ruiz J, 2021). In this study, we aimed to evaluate the prevalence of antibiotic resistance caused by the presence of Efflux genes and some virulence factors in Pseudomonas aeruginosa from clinical isolates.