Bacteria form colonies and secrete extracellular polymeric substances that surround the individual cells. These spatial structures are often associated with collaboration and quorum sensing between the bacteria. Here we investigate the mutual protection provided by spherical growth of a monoclonal colony during exposure to phages that proliferate on its surface. As a proof of concept we exposed growing colonies of to a virulent mutant of phage P1. When the colony consists of less than [Formula: see text]50,000 members it is eliminated, while larger initial colonies allow long-term survival of both phage-resistant mutants and, importantly, colonies of mostly phage-sensitive members. A mathematical model predicts that colonies formed solely by phage-sensitive bacteria can survive because the growth of bacteria throughout the colony exceeds the killing of bacteria on the surface and pinpoints how the critical colony size depends on key parameters in the phage infection cycle.

Virulent phages can expose their bacterial hosts to devastating epidemics, in principle leading to complete elimination of their hosts. Although experiments indeed confirm a large reduction of susceptible bacteria, there are no reports of complete extinctions. We here address this phenomenon from the perspective of spatial organization of bacteria and how this can influence the final survival of them. By modelling the transient dynamics of bacteria and phages when they are introduced into an environment with finite resources, we quantify how time delayed lysis, the spatial separation of initial bacterial positions, and the self-protection of bacteria growing in spherical colonies favour bacterial survival. our results suggest that spatial structures on the millimetre and submillimetre scale play an important role in maintaining microbial diversity. open Scientific RepoRtS | (2020) 10:3154 | https://doi.org/10.1038/s41598-020-59635-7www.nature.com/scientificreports www.nature.com/scientificreports/ been shown that a microcolony can grow exponentially in volume for a substantial period of time 8,9 , demonstrating the importance of exponential growth even in a spatially structured environment.With our model, we bridge the gap between the zero-dimensional mass action models and the spatial cellular automata models, and thereby incorporate both spatial structure and exponential growth of bacteria. This allows us to resolve length scales ranging from micrometres to more than centimetres while retaining (some of) the submillimetre behaviour of the cellular automata models. In particular, we are interested in systems where the bacteria form microcolonies, as is seen when bacteria grow in semisolid medium. We approximate the submillimetre structure of the colonies and retain exponential growth by making modifications to the traditional Lotka-Volterra models. It is worth noting that a similar approach of coupling mass-action growth and lattice model was taken in ref. 32 to simulate the phage attack on a biofilm with the spacial resolution of ~ 4 μm. We here consider length scales which are orders of magnitude larger where one lattice site can contain several of microcolonies. This allows for faster and larger-scale simulations while including the effects of colony structure in the phage-bacteria interaction as described below.We partition space into a three-dimensional lattice, which allows for spatial variation in the densities of phage and bacteria (see Fig. 1(a)). Each box in the lattice is well-mixed, meaning that bacterial colonies within each box are identical, i.e. they have the same size and composition as each other, but they are typically different from colonies in other boxes. Due to their small size, phages and nutrients diffuse readily around in the system, while the much larger bacteria remain fixed in space. Consequently, the phages and the nutrients need to propagate before interacting with distant areas, and we include diffusion to couple the dynamics in one box with its neighbouring boxes (see Fig. 1(b))....

Bacteria form colonies and secrete extracellular polymeric substances that surround the individual cells. These spatial structures are often associated with collaboration and quorum sensing between the bacteria. Here we investigate the mutual protection provided by spherical growth of a monoclonal colony during exposure to phages that proliferate on its surface. As a proof of concept we exposed growing colonies of Escherichia coli to a virulent mutant of phage P1. When the colony consists of less than ∼50000 members it is eliminated, while larger initial colonies allow long-term survival because the growth of bacteria throughout the spherical colony exceeds the killing of bacteria on the surface. A mathematical model pinpoints how this critical colony size depends on key parameters in the phage infection cycle. Surprisingly, we predict that a higher phage adsorption rate would allow substantially smaller colonies to survive a virulent phage.Virulent phage | Bacteria | Microcolony | Spatial structure

Limited evidence exists on the level and longevity of protection afforded by current COVID-19 vaccines against infection and hospitalisation with the Omicron variant. SARS-CoV-2 PCR testing rates in Denmark are exceptionally high. In this nationwide cohort analysis, from December 28, 2021 to February 15, 2022 during which Omicron was the predominant variant, PCR testing data are combined with other national register data with near-complete information on all vaccinations, hospitalisations and comorbidities in the population. Trends over time in vaccine effectiveness after two and three doses with BNT162b2 (Pfizer-BioNTech) and mRNA-1273 (Moderna) are estimated using Cox regression. Despite relatively poor protection against infection (symptomatic or asymptomatic), vaccine effectiveness against COVID-19-associated hospitalisation was high after the third dose declining from 88.8% (95% CI: 87.3 to 90.1%) to 79.0% (76.5 to 81.3%) for BNT162b2 and 90.2% (87.3 to 92.5%) to 83.6% (77.7 to 88.0%) for mRNA-1273 over the first four months after vaccination.

Bacteria often arrange themselves in various spatial configurations, which changes how they interact with their surroundings. In this work, we investigate how the structure of the bacterial arrangements influences the adsorption of bacteriophages. We quantify how the adsorption rate scales with the number of bacteria in the arrangement and show that the adsorption rates for microcolonies (increasing with exponent $1/3) and bacterial chains (increasing with exponent $0.5-0.8) are substantially lower than for well-mixed bacteria (increasing with exponent 1). We further show that, after infection, the spatially clustered arrangements reduce the effective burst size by more than 50% and cause substantial superinfections in a very short time interval after phage lysis.