The influence of microorganisms growing as sessile communities in a large number of human infections has been extensively studied and recognized for 30–40 years, therefore warranting intense scientific and medical research. Nonetheless, mimicking the biofilm-life style of bacteria and biofilm-related infections has been an arduous task. Models used to study biofilms range from simple in vitro to complex in vivo models of tissues or device-related infections. These different models have progressively contributed to the current knowledge of biofilm physiology within the host context. While far from a complete understanding of the multiple elements controlling the dynamic interactions between the host and biofilms, we are nowadays witnessing the emergence of promising preventive or curative strategies to fight biofilm-related infections. This review undertakes a comprehensive analysis of the literature from a historic perspective commenting on the contribution of the different models and discussing future venues and new approaches that can be merged with more traditional techniques in order to model biofilm-infections and efficiently fight them.

This review describes how nonbiocidal competitive interactions can profoundly impact on microbial behavior in biofilm environments and discusses the potential b

Summary: Bacterial extracellular polysaccharides have been shown to mediate many of the cell‐to‐cell and cell‐to‐surface interactions that are required for the formation, cohesion and stabilization of bacterial biofilms. However, recent studies have identified several bacterial polysaccharides that inhibit biofilm formation by a wide spectrum of bacteria and fungi both in vitro and in vivo . This review discusses the composition, modes of action and potential biological roles of antibiofilm polysaccharides recently identified in bacteria and eukarya. Some of these molecules may have technological applications as antibiofilm agents in industry and medicine.

An atypically large outbreak of Elizabethkingia anophelis infections occurred in Wisconsin. Here we show that it was caused by a single strain with thirteen characteristic genomic regions. Strikingly, the outbreak isolates show an accelerated evolutionary rate and an atypical mutational spectrum. Six phylogenetic sub-clusters with distinctive temporal and geographic dynamics are revealed, and their last common ancestor existed approximately one year before the first recognized human infection. Unlike other E. anophelis, the outbreak strain had a disrupted DNA repair mutY gene caused by insertion of an integrative and conjugative element. This genomic change probably contributed to the high evolutionary rate of the outbreak strain and may have increased its adaptability, as many mutations in protein-coding genes occurred during the outbreak. This unique discovery of an outbreak caused by a naturally occurring mutator bacterial pathogen provides a dramatic example of the potential impact of pathogen evolutionary dynamics on infectious disease epidemiology.

The beneficial contribution of commensal bacteria to host health and homeostasis led to the concept that exogenous non-pathogenic bacteria called probiotics could be used to limit disease caused by pathogens. However, despite recent progress using gnotobiotic mammal and invertebrate models, mechanisms underlying protection afforded by commensal and probiotic bacteria against pathogens remain poorly understood. Here we developed a zebrafish model of controlled co-infection in which germ-free zebrafish raised on axenic living protozoa enabled the study of interactions between host and commensal and pathogenic bacteria. We screened enteric fish pathogens and identified Edwardsiella ictaluri as a virulent strain inducing a strong inflammatory response and rapid mortality in zebrafish larvae infected by the natural oro-intestinal route. Using mortality induced by infection as a phenotypic read-out, we pre-colonized zebrafish larvae with 37 potential probiotic bacterial strains and screened for survival upon E. ictaluri infection. We identified 3 robustly protective strains, including Vibrio parahaemolyticus and 2 Escherichia coli strains. We showed that the observed protective effect of E. coli was not correlated with a reduced host inflammatory response, nor with the release of biocidal molecules by protective bacteria, but rather with the presence of specific adhesion factors such as F pili that promote the emergence of probiotic bacteria in zebrafish larvae. Our study therefore provides new insights into the molecular events underlying the probiotic effect and constitutes a potentially high-throughput in vivo approach to the study of the molecular basis of pathogen exclusion in a relevant model of vertebrate oro-intestinal infection. The beneficial contribution of commensal bacteria to host health led to the concept that exogenous and non-pathogenic bacteria (probiotics) could be used to prevent infectious disease. However, the absence of relevant experimentally tractable in vivo models severely limits our understanding of the molecular processes behind probiotic effects, therefore hampering prophylactic and therapeutic use of probiotics against infections. Here we developed a protocol to raise microbe-free zebrafish larvae fed on microbe-free live food. We placed this microbiologically controlled model in contact with known pathogens and potential probiotics to investigate molecular events underlying pathogen exclusion by probiotic bacteria. We showed that Edwardsiella ictaluri, the causative agent of catfish enteric septicemia, causes rapid death of infected larvae following exposure via the natural immersion route. We used this mortality to screen potential probiotic bacteria able to extend zebrafish survival to E. ictaluri infection and thereby identified 3 protective strains. While host immune response modulation did not contribute to protection against E. ictaluri infection, comparison of protective and non-protective strains demonstrated a key role for their adhesion factors. Our in vivo approach constitutes a relevant new model of vertebrate oro-intestinal infection and provides new insight into molecular events underlying probiotic effects against incoming pathogens.

Bacterial biofilms are dense and often mixed-species surface-attached communities in which bacteria coexist and compete for limited space and nutrients. Here we present the different antagonistic interactions described in biofilm environments and their underlying molecular mechanisms, along with ecological and evolutionary insights as to how competitive interactions arise and are maintained within biofilms.