Dear Colleagues,

Antibiotic resistance (AR) is a major form of antimicrobial resistance (AMR) which is known to be caused mainly by overuse (or misuse) of antibiotics. Currently, AR of strictly or opportunistic pathogens is one of the biggest challenges. The burden of resistant and multidrug-resistant bacterial strains is felt not only in the medical field, but also in the natural environment, because antibiotics are also used in agriculture and animal husbandry, and thus reach the water bodies. 

AMR is caused by both inherited and acquired genes, as well as phenotypical or behavioral resistance of microbial biofilms, both of which contribute to bacterial virulence. Virulence is a driving force in host–pathogen interaction and evolution of the infectious process, as it leads to a high rate of pathogen multiplication/ reproductive fitness, colonization and evolution of infection. However, the mobile genetic elements of virulence genes are often recombined with AR genes; in this way, the microbial fitness is increased and these superbug-resistant/multi-resistant and virulent pathogens represent a huge challenge for the medical field.

The biofilm-embedded cells manifest tolerance towards high concentrations of antimicrobials, as well as towards host defense mechanisms. This is great cause for concern within the medical field, as biofilm-associated infections are predominant (~80% of total infections) and develop on intact or damaged tissues, as well as medical devices. Moreover, resistance genes are easily exchanged among biofilm cells by horizontal transfer, due to their proximity. 

Biofilm formation caused by pathogens is correlated with the colonization step of the infectious process. Inside these dense populations, the cells communicate with one another or with their host. Quorum sensing (QS) is a communication mechanism mediated by chemical signals synthesized by bacteria/microorganisms, which accumulates inside cells but secretes extracellularly. These QS molecules modulate the expression of some target genes when they reach a critical concentration, and consequently induce changes in cell population behavior or phenotype, with a greater adaptive value. The QS mechanism controls different physiological processes such as biofilm formation, motility, cellular division, as well as expression of virulence factors (adhesins, enzymes, exotoxins, siderophores), etc. Thus, QS circuits are intensely studied as a potential target for fighting microbial infections, including those produced by genetically resistant or tolerant cells.

It has been shown that QS inhibitors and QS quenching molecules, which are produced by many organisms as innate defense mechanisms, including the normal microbiota members or eukaryotic hosts, can represent anti-pathogenic strategies, interfering with virulence/resistance gene expression. Use of these molecules as alternative or complementary antimicrobial treatments will slow down the selection of resistant and virulent strains, because they inhibit the expression of virulence genes without killing pathogens or selecting for AR genes.

For this special issue, both original research and review articles are welcomed. Potential topics include, but are not limited to:

• MDR pathogens;
• Virulence factors, fitness and their influence on bacterial and fungal pathogenesis;
• Biofilms and their tolerance to antimicrobials—means of recovering cell sensitivity;
• Anti-pathogenic strategies;
• In vitro and in vivo evaluation of novel antibacterial and anti-biofilm agents.

Prof. Dr. Veronica Lazar
Dr. Lia Mara Diţu
Guest Editors

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