Revamping the role of biofilm regulating operons in device-associated Staphylococci and Pseudomonas aeruginosa

Abstract

Extensive use of indwelling devices in modern medicine has revoked higher incidence of device associated infections and most of these devices provide an ideal surface for microbial attachment to form strong biofilms. These obnoxious biofilms are responsible for persistent infections, longer hospitalization and high mortality rate. Gene regulations in bacteria play a significant role in survival, colonization and pathogenesis. Operons being a part of gene regulatory network favour cell colonization and biofilm formation in various pathogens. This review explains the functional role of various operons in biofilm expression and regulation observed in device-associated pathogens such as Staphylococcus aureus, Staphylococcus epidermidis and Pseudomonas aeruginosa.

General Overview on Nontuberculous Mycobacteria, Biofilms, and Human Infection

“…One of them is horizontal gene exchanges favored by the maximum proximity experienced by bacteria within biofilms [ 96 ]. This gene transmission is a major cause for bacteria survival [ 97 ] and can account for a high frequency of mutations responsible for antimicrobial resistance [ 98 ] mediated by triggering enzymatic production, modification of antibiotic target, or expression of efflux pumps [ 99 – 101 ]. Another mechanism is the appearance of persisters defined as phenotypically different bacteria exhibiting slower growth rate [ 102 ].…”

Novel Strategies for the Treatment ofPseudomonas aeruginosaInfections

“…In a similar fashion, other indwelling healthcare items like coronary stents or endotracheal tubes also bear the risk for medical-device-associated infections by P. aeruginosa. , …”

“…10 In a similar fashion, other indwelling healthcare items like coronary stents or endotracheal tubes also bear the risk for medical-deviceassociated infections by P. aeruginosa. 11,12 In immunocompromised patients, any of these infections by the title pathogen can be severe and result in serious complications associated with rates of high morbidity and possible mortality. 3 1.1.…”

Repeated exposure of nosocomial pathogens to silver does not select for silver resistance but does impact ciprofloxacin susceptibility

“…DltA is part of the dltABCD operon which is in charge of incorporating d-alanine to teichoic acids. Mutations on this gene can lead to a lack of d-alanine in these highly charged cell wall polymers, resulting in a stronger negative charge on the cell surface and affecting resistance to cationic antimicrobial peptides, vancomycin, autolysins activity and a reduction in biofilm formation [102][103][104][105]. This, coupled with the variant observed on MexT, which can confer quinolone resistance [106], may have influenced the response of this P. aeruginosa strain to both antimicrobials studied, although it must be said that the ligands and mechanism of activation of MexT are still poorly understood [107].…”