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      The mechanisms of granulation of activated sludge in wastewater treatment, its optimization, and impact on effluent quality

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          Granular activated sludge has gained increasing interest due to its potential in treating wastewater in a compact and efficient way. It is well-established that activated sludge can form granules under certain environmental conditions such as batch-wise operation with feast-famine feeding, high hydrodynamic shear forces, and short settling time which select for dense microbial aggregates. Aerobic granules with stable structure and functionality have been obtained with a range of different wastewaters seeded with different sources of sludge at different operational conditions, but the microbial communities developed differed substantially. In spite of this, granule instability occurs. In this review, the available literature on the mechanisms involved in granulation and how it affects the effluent quality is assessed with special attention given to the microbial interactions involved. To be able to optimize the process further, more knowledge is needed regarding the influence of microbial communities and their metabolism on granule stability and functionality. Studies performed at conditions similar to full-scale such as fluctuation in organic loading rate, hydrodynamic conditions, temperature, incoming particles, and feed water microorganisms need further investigations.

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          The biofilm matrix.

          The microorganisms in biofilms live in a self-produced matrix of hydrated extracellular polymeric substances (EPS) that form their immediate environment. EPS are mainly polysaccharides, proteins, nucleic acids and lipids; they provide the mechanical stability of biofilms, mediate their adhesion to surfaces and form a cohesive, three-dimensional polymer network that interconnects and transiently immobilizes biofilm cells. In addition, the biofilm matrix acts as an external digestive system by keeping extracellular enzymes close to the cells, enabling them to metabolize dissolved, colloidal and solid biopolymers. Here we describe the functions, properties and constituents of the EPS matrix that make biofilms the most successful forms of life on earth.
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            Natural Antibiotic Resistance and Contamination by Antibiotic Resistance Determinants: The Two Ages in the Evolution of Resistance to Antimicrobials

            The study of antibiotic resistance has been historically concentrated on the analysis of bacterial pathogens and on the consequences of acquiring resistance for human health. The development of antibiotic resistance is of course extremely relevant from the clinical point of view, because it can compromise the treatment of infectious diseases as well as other advanced therapeutic procedures as transplantation or anticancer therapy that involve immunosuppression and thus require robust anti-infective preventive therapies. Nevertheless, the studies on antibiotic resistance should not be confined to clinical-associated ecosystems. It was evident soon after introducing antibiotics for human therapy, that bacteria were able to develop resistance, not just as the consequence of mutations in the targets of antibiotics, but by acquiring genes conferring resistance to antimicrobials (Abraham and Chain, 1940). Since those genes were not present before in the human bacterial pathogens, the only suitable source for them was the environmental microbiota, and indeed the presence of R-factors (resistance plasmids) in pristine environments without any record of contact with antibiotics was described in the first studies of antibiotic resistance in the field (Gardner et al., 1969). Given that the origin of antibiotic resistance is the environmental microbiota, it would be necessary to study resistance in natural, non-clinical habitats in order to fully understand the cycle of acquisition of resistance by human pathogens. However, until recently the studies on antibiotic resistance in natural ecosystems have been fragmentary. The availability of metagenomic tools as well as high-throughput sequencing techniques is allowing describing in depth the presence of resistance genes in different ecosystems. Indeed, the use of functional genomic and metagenomic techniques has served to show that natural ecosystems, including not just soils but human gut as well, contain a large number of elements that, upon transfer to a new host, can confer resistance to any type of antimicrobial (D'Costa et al., 2006; Sommer et al., 2009). These include natural antibiotics, which are produced by the environmental microbiota, and synthetic antimicrobials, as quinolones. One important question from an evolutionary point of view is the function of these resistance genes in their natural environmental hosts (Davies and Davies, 2010). Whereas for naturally produced antibiotics a protective role for resistance genes in the producers organisms (or those coexisting with producers Laskaris et al., 2010) might be foreseen (Benveniste and Davies, 1973), this explanation is not suitable for synthetic antibiotics as quinolones. Indeed, it has been described that the origin of the quinolone resistance gene QnrA, which is now widespread in plasmids present in human pathogens is the environmental non-antibiotic producer Shewanella algae (Poirel et al., 2005). This means that a gene that confers resistance in a human pathogen does not necessary play the same role in its original host (Martinez et al., 2009a). The finding that several proteins, involved in basic processes of the bacterial physiology, contribute to intrinsic resistance to antibiotics (Fajardo et al., 2008; Laskaris et al., 2010; Linares et al., 2010), further supports the concept that resistance genes, acquired through horizontal gene transfer by human pathogens, might have evolved in their original host to play a different role than resisting the activity of antimicrobials in natural ecosystems. We can thus distinguish two ages in the evolution of antibiotic resistance genes. For billions of years (until the use of antibiotics by humans), these genes have been usually chromosomally encoded and had evolved for different purposes. Some of them, as those found in antibiotic producers, likely evolved for detoxifying the original host from the antibiotic it produces, although a role in the biosynthesis of the antibiotic itself has been proposed as well for some of them (Benveniste and Davies, 1973; Doyle et al., 1991). Others, as beta-lactamases might be involved in the biosynthesis of the cell wall (Jacobs et al., 1994; Massova and Mobashery, 1998), whereas others as multidrug efflux pumps might serve for different purposes including the trafficking of signaling molecules, detoxification of metabolic intermediates, or extrusion of plant-produced compounds among others (Martinez et al., 2009b). Like in the case of antibiotics, which do not necessarily have an inhibitory function at the concentrations in which they are present in natural ecosystems (Linares et al., 2006; Yim et al., 2007; Fajardo and Martinez, 2008), the fact that a plasmid-encoded gene produces resistance to antibiotics upon its expression in a new host, is not an unequivocal prove that it confers resistance as well in its original host. This reflection serves to show the relevance of the second age in the evolution of antibiotic resistance determinants. Once a gene is introduced in a new host in which it lacks its original biochemical and genetic context, its function is limited to antibiotic resistance (Baquero et al., 2009). This change of function without changing the sequence of the gene itself, has been named as exaptation (Gould and Vrba, 1982), and is the consequence of the strong selective pressure exerted by antibiotics in the last decades from the time they were introduced for therapy. Two important aspects are emerging from the studies of natural resistome. First, the environmental microbiota contains a much larger number of resistance genes than those seen to be acquired by bacterial pathogens (Wright, 2007; Davies and Davies, 2010). Furthermore, different ecosystems contain different resistance genes, which means that we are still far away to have a consistent estimation on the number of potential resistance genes present in natural ecosystems. Finally, the origin of most resistance genes currently found in transferrable elements is still ignored, despite genes (and genetic structures) belonging to the same families are regularly found in different ecosystems, including deep terrestrial subsurface (Brown and Balkwill, 2009), ice (Miteva et al., 2004), and even the permafrost (D'Costa et al., 2011), which have not been in contact with human contaminants. Second, those genes present in mobile elements in human bacterial pathogens can be found nearly everywhere, including pristine ecosystems or wild animals not supposed to be in contact with antibiotics (Martinez, 2009). This indicates that pollution with antibiotic resistance genes is widely spread and that resistance genes can persist even in the absence of a positive selection pressure. The analysis of historical soil archives has shown a consistent increase on the presence of antibiotic resistance genes since 1940 (Knapp et al., 2010), which is a clear prove of the contamination by antibiotic resistance elements of natural ecosystems and the resilience of those elements for their elimination. In this situation, which type of studies are needed to analyze in depth the role that natural ecosystems may have on the development of resistance in human bacterial pathogens? In my opinion, these studies have two faces (Martinez, 2008). One consists on the analysis of the genes already present in bacterial pathogens. In other words, we will study mainly contamination by antibiotic resistance determinants and how this contamination might increase the risks for the dissemination of those elements (Martinez, 2009). These studies might serve to define reservoirs, elements for enrichment and dissemination of resistance (as wild birds Simoes et al., 2010) or hotspots for the transfer of resistance as waste-water treatment plants (Baquero et al., 2008). For instance, a recent study has shown that soil composition and in particular the presence of heavy metals might enrich for the presence of antibiotic resistance genes in natural ecosystems (Knapp et al., 2011). The other type of studies consists on the analysis, using functional assays, of novel resistance genes in different ecosystems (D'Costa et al., 2006, 2011; Sommer et al., 2009). These studies are useful for defining novel mechanisms of resistance, but making risks assessments on whether those novel antibiotic resistance genes will be transferred to new hosts is likely unsuitable (Martinez et al., 2007). On the other hand tracking the source of currently known resistance gene has demonstrated to be a very difficult task. We have to be extremely careful for assigning the origin of resistance determinants. Only when the genes are nearly identical (as QnrA) and the gene is present in several strains of the original host, with the same synteny and without any sign of a recent acquisition event, we can firmly establish this host being the origin. The report of genes that are highly similar (even above 90%) to antibiotic resistance genes demonstrate their belonging to the same phylogenetic group, not that one is the origin of the other. Does it mean that we will be unable of tracking the source of resistance genes and to propose from this information valuable strategies for reducing antibiotic resistance? I do not believe that. It has been already determined that QnrA was originated in S. algae (Poirel et al., 2005) and that chromosomally encoded qnr genes are mainly present in water-dwelling bacteria (Sanchez et al., 2008). This suggests that the source of transferrable quinolone resistance is the water microbiota and puts a focus on the effect that the use of quinolones in aquaculture might have had for the emergence and dissemination of these resistance elements (Cabello, 2006). The study on antibiotic resistance in natural ecosystems and its role on the maintenance and spread of clinically relevant resistance determinants is still in its infancy. It is surprising that large efforts have been used to study the risks for the dissemination of resistance that may have the release of genetic modified organisms containing resistance genes in their chromosomes, whereas the study of the effect of the discharge of human wastes, which contain bacterial pathogens harboring the resistance genes that have demonstrated to be really relevant, in the elements that are important for their dissemination has received few attention if any. Studies in this new field are needed in order to understand the mechanisms involved in the emergence, spread, maintenance, and evolution of antibiotic resistance.
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              The sociobiology of biofilms.

              Biofilms are densely packed communities of microbial cells that grow on surfaces and surround themselves with secreted polymers. Many bacterial species form biofilms, and their study has revealed them to be complex and diverse. The structural and physiological complexity of biofilms has led to the idea that they are coordinated and cooperative groups, analogous to multicellular organisms. We evaluate this idea by addressing the findings of microbiologists from the perspective of sociobiology, including theories of collective behavior (self-organization) and social evolution. This yields two main conclusions. First, the appearance of organization in biofilms can emerge without active coordination. That is, biofilm properties such as phenotypic differentiation, species stratification and channel formation do not necessarily require that cells communicate with one another using specialized signaling molecules. Second, while local cooperation among bacteria may often occur, the evolution of cooperation among all cells is unlikely for most biofilms. Strong conflict can arise among multiple species and strains in a biofilm, and spontaneous mutation can generate conflict even within biofilms initiated by genetically identical cells. Biofilms will typically result from a balance between competition and cooperation, and we argue that understanding this balance is central to building a complete and predictive model of biofilm formation.

                Author and article information

                Appl Microbiol Biotechnol
                Appl. Microbiol. Biotechnol
                Applied Microbiology and Biotechnology
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                28 April 2018
                28 April 2018
                : 102
                : 12
                : 5005-5020
                [1 ]ISNI 0000 0001 0775 6028, GRID grid.5371.0, Division of Water Environment Technology, Department of Architecture and Civil and Engineering, , Chalmers University of Technology, ; SE-412 96 Gothenburg, Sweden
                [2 ]ISNI 0000 0000 9919 9582, GRID grid.8761.8, Department of Chemistry and Molecular Biology, , University of Gothenburg, ; SE-405 30 Gothenburg, Sweden
                © The Author(s) 2018

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                Funded by: Formas, The Swedish Research Council for Environment, Agricultural Sciences and Spatial Planning
                Award ID: 245-2013-627
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                © Springer-Verlag GmbH Germany, part of Springer Nature 2018


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