Biofilm Formation among Enterococcus Species from Milk and Raw Milk Cheese

Abstract

Nosocomial bacteria called enterococci have the ability to create biofilms, which increase their pathogenicity and drug resistance. While several genes involved in biofilm formation have been discovered, little is known about how these genes are distributed among enterococci at the genomic level or how they might be used to diagnose biofilm morphologies. Gram-positive bacteria called enterococci cause dangerous nosocomial infections such as endocarditis, bloodstream infections, and urinary tract infections [1]. The potential of enterococci to create biofilms—populations of cells that are permanently adhered to and encased in a variety of biotic agents and abiotic surfaces—is well documented. Biofilms, which seem to be populations of cells that are permanently attached to and enclosed in a range of biological agents and abiotic substrates in a hydrated matrix of exopolysaccharide components, proteins, polysaccharides, and nucleic acids [2]. Bacterial pathogenicity is increased by biofilms in a number of ways. Due to Enterococcus spp.’s high rate of survival, the food preparation procedure does not completely eliminate all microbial cells from the raw material, allowing bacteria to adhere to the catheter by adhesion, an early stage of biofilm development. These bacteria thus constitute a component of the residual microflora in final goods [3].

One of the most crucial characteristics of Enterococcus spp. pathogenicity is their capacity to create biofilms [4, 5]. A population of cells is encased in a hydrated matrix called biofilms, which are made up of exopolymeric materials, proteins, polysaccharides, and nucleic acids and linked to diverse biotic and abiotic surfaces. The biofilm structure fosters the transmission of mobile genetic elements across various bacterial species and provides an ideal environment for bacterial development [6]. The production of biofilms involves several proteins. One of Enterococcus spp.’s most important virulence traits is its capacity to produce biofilms. By defending against antimicrobial agents and facilitating host cell attachment, this capacity permits colonization of inert and biological surfaces. The capacity of enterococci to create biofilms is well documented. A hydrated matrix of exopolysaccharides, materials, enzymes, polymers, and nucleic acids surrounds these populations of cells, which are permanently bound to numerous biotic and abiotic surfaces [7]. The biofilm structure promotes the transfer of mobile genetic components between bacteria and offers an ideal habitat for development [6].

On stents and other artificial devices, enterococci frequently build biofilms that call for long-term antibiotic treatment if removal of the device is not an option. Nonetheless, there is debate concerning the processes behind the pathogenicity and biofilm development of urinary enterococci. The oral pathogen E. faecalis that forms biofilms has been linked to conditions such caries, endodontic infections, periodontitis, and peri-implantitis. Consequently, in individuals with enterococcal infection, biofilm elimination with antibiotic treatment is crucial. Bacterial biofilms exhibit a phenotype of antibiotic resistance and are challenging to remove. In order to cure infections brought on by bacterial biofilms, combined therapy is advised. Surprisingly, vancomycin reduces biofilm formation in robust biofilm-forming isolates when given at subminimal inhibitory doses the faecal streptococcal regulatory operon, which consists of the three genes fsrA, fsrB, and fsrC, regulates biofilm formation, which is crucial for quorum sensing quorum sensing, which controls microbial gene expression in reaction to increased cell population densities, is generally linked to biofilm development. The genetic variables discussed above that are involved in biofilm production and control in enterocytes as well as proteins known as autoinducers often drive this regulation, and no conclusive genotype-phenotype link has been demonstrated for these determinants. These genes interact via Fsr quorum signaling as well as communicate via peptide pheromones secreted by recipient cells to trigger a donor cell conjugation mechanism that facilitates the transfer of pheromone-responsive plasmids. Connections among certain of these genes and biofilm formation have also been discovered. Several of these plasmids include genes, such as plasmid-encoded aggregate agent genes, that control or encourage the production of biofilms.