Biofilm-dispersal patterns in ESKAPE pathogens.

Abstract

Biofilm formation is now universal behavior of microbes to protect themselves from harsh environment. For ESKAPE (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumonia, Acinetobacter baumanii, Pseudomonas aeruginosa and Enterobacter) pathogens it is one of the strategies to deal with antibiotic tolerance. Biofilms formation involves following major steps initial adhesion of planktonic cells, microcolony formation, biofilm maturation, and finally dispersal. In recent, interest of researchers to understand biofilm dispersal is considered important as it can make us to recognize infection dynamics, antibiofilm strategies, bacterial ecology and antibiotic resistance. A widely supported strategy for combating biofilms involves promoting their dispersal followed by the application of antibiotic therapy to enhance treatment efficacy. But different molecular studies regarding transition of bacteria to biofilms and back to dispersal have highlighted unique physiology and phenotype which might impact treatment strategies. For example, enzymatic degradation using Dispersin B or DNase I have been shown to decrease biofilm mass by over 70% in S. aureus and P. aeruginosa models, significantly increasing antibiotic susceptibility. Similarly, in E. faecalis, combining proteases with antibiotics has demonstrated up to 3-log reductions in viable biofilm cells. Thus, we discuss how native dispersal cues helps the cells in biofilms to decide for dispersal, while how matrix degradation-based dispersal can develop antibiofilm strategies. Considering ESKAPE as priority pathogens and known for biofilm formation hence we discuss patterns of dispersal focused on them only. We believe dispersing biofilms by targeting biofilm matrix components have much potential for future treatments as signaling cues may generate virulent phenotype.