PrefaceMost natural environments harbor a stunningly diverse collection of microbial species. Within these communities, bacteria compete with their neighbors for space and resources. Laboratory experiments with pure and mixed cultures have revealed many active mechanisms by which bacteria can impair or kill other microbes. Additionally, a growing body of theoretical and experimental population studies indicate that the interactions within and between bacterial species can profoundly impact the outcome of competition in nature. The next challenge is to integrate the findings of these laboratory and theoretical studies, and to evaluate the predictions they generate in more natural settings. IntroductionExamples of true charity and altruism in human societies are highly lauded, and rightfully so, but are far from the norm. Competition is a fact of modern life, with individuals and institutions vying to gain advantage in terms of finances, material resources, and status. In capitalist societies, competition is thought to continually hone the attributes of competing entities, improving their efficiency and defining their activities and structure. The high level of competition in human society in many ways mirrors the comparatively ancient and complex interactions observed at virtually every level in the natural world. The battle for resources through which organisms survive and pass on genes to the next generation can often be fierce and unforgiving. This leads to natural selection, which provides the driving force for innovation and diversification between competing organisms 1 .In animals and plants, there are a large number of well studied examples of populations which are held in balance, or driven to transition, by competitive forces. Connell's barnacles provide a classic example 2 . He found that in intertidal zones in Scotland, Balanus barnacles were always found closest to the shore, while Chthamalus barnacles grew further up the rocks. If he experimentally removed the Balanus barnacles from the lower areas, Chthamalus could grow there, but upon reintroduction of Balanus, Chthamalus would eventually be crowded out by the more competitive Balanus. However, Balanus could not grow further up the rocks, due to desiccation sensitivity. Thus, the habitat of Chthamalus was limited to areas where it could escape from competition with Balanus, an example of competitive exclusion.Similarly, most microorganisms face a constant battle for resources. Vast numbers of microbes are present in all but the most rarified environments. Tremendous microbial diversity has been revealed by new molecular methodologies such as metagenomic sequencing and deep microbial tag sequencing 3,4 . These approaches and others have begun to reveal that underlying the numerically dominant microbial populations is a highly diverse, low-abundance population (described as the rare biosphere, see 3 ). Members of the rare biosphere that are amplified under favorable conditions to which they are pre-adapted can give rise to discrete, abundant NIH Publ...

Pectobacterium and Dickeya spp. are related broad-host-range entero-bacterial pathogens of angiosperms. A review of the literature shows that these genera each cause disease in species from at least 35% of angiosperm plant orders. The known host ranges of these pathogens partially overlap and, together, these two genera are pathogens of species from 50% of angiosperm plant orders. Notably, there are no reported hosts for either genus in the eudicots clade and no reported Dickeya hosts in the magnoliids or eurosids II clades, although Pectobacterium spp. are pathogens of at least one plant species in the magnoliids and at least one in each of the three eurosids II plant orders. In addition, Dickeya but not Pectobacterium spp. have been reported on a host in the rosids clade and, unlike Pectobacterium spp., have been reported on many Poales species. Natural disease among nonangiosperms has not been reported for either genus. Phylogenetic analyses of sequences concatenated from regions of seven housekeeping genes (acnA, gapA, icdA, mdh, mtlD, pgi, and proA) from representatives of these genera demonstrated that Dickeya spp. and the related tree pathogens, the genus Brenneria, are more diverse than Pectobacterium spp. and that the Pectobacterium strains can be divided into at least five distinct clades, three of which contain strains from multiple host plants.

Urinary tract infections (UTIs) are caused by uropathogenic Escherichia coli (UPEC) strains. In contrast to many enteric E. coli pathogroups, no genetic signature has been identified for UPEC strains. We conducted a high-resolution comparative genomic study using E. coli isolates collected from the urine of women suffering from frequent recurrent UTIs. These isolates were genetically diverse and varied in urovirulence, or the ability to infect the bladder of a mouse model of cystitis. Importantly, we found no set of genes, including previously defined putative urovirulence factors (PUFs), that were predictive of urovirulence. In addition, in some patients, the E. coli strain causing a recurrent UTI had fewer PUFs than the supplanted strain. In competitive experimental infections in mice, the supplanting strain was more efficient at colonizing the mouse bladder than the supplanted strain. Despite the lack of a clear genomic signature for urovirulence, comparative transcriptomic and phenotypic analyses revealed that the expression of key conserved functions during culture, such as motility and sugar metabolism, could be used to predict subsequent mouse bladder colonization. Taken together, our findings suggest that UTI risk and outcome may be determined by complex interactions between host susceptibility and the urovirulence potential of diverse bacterial strains.

Multidrug resistant (MDR) Acinetobacter baumannii poses a growing threat to global health. Research on Acinetobacter pathogenesis has primarily focused on pneumonia and bloodstream infections, even though one in five A. baumannii strains are isolated from urinary sites. In this study, we highlight the role of A. baumannii as a uropathogen. We develop the first A. baumannii catheter-associated urinary tract infection (CAUTI) murine model using UPAB1, a recent MDR urinary isolate. UPAB1 carries the plasmid pAB5, a member of the family of large conjugative plasmids that represses the type VI secretion system (T6SS) in multiple Acinetobacter strains. pAB5 confers niche specificity, as its carriage improves UPAB1 survival in a CAUTI model and decreases virulence in a pneumonia model. Comparative proteomic and transcriptomic analyses show that pAB5 regulates the expression of multiple chromosomally-encoded virulence factors besides T6SS. Our results demonstrate that plasmids can impact bacterial infections by controlling the expression of chromosomal genes.

Urinary tract infections (UTIs) are common in women and recurrence is a major clinical problem. Most UTIs are caused by uropathogenic Escherichia coli (UPEC). UPEC are generally thought to migrate from the gut to the bladder to cause UTI. UPEC strains form specialized intracellular bacterial communities (IBCs) in the bladder urothelium as part of a pathogenic mechanism to establish a foothold during acute stages of infection. Evolutionarily, such a specific adaptation to the bladder environment would be predicted to result in decreased fitness in other habitats, such as the gut. To examine this concept, we characterized 45 E. coli strains isolated from the feces and urine of four otherwise healthy women with recurrent UTIs. Multi-locus sequence typing revealed that two of the patients maintained a clonal population in both of these body habitats throughout their recurrent UTIs, whereas the other two manifested a wholesale shift in the dominant UPEC strain colonizing their urinary tract and gut between UTIs. These results were confirmed when we subjected 26 isolates from two patients, one representing the persistent clonal pattern and the other representing the dynamic population shift, to whole genome sequencing. In vivo competition studies conducted in mouse models of bladder and gut colonization, using isolates taken from one of the patients with a wholesale population shift, and a newly developed SNP-based method for quantifying strains, revealed that the strain that dominated in her last UTI episode had increased fitness in both body habitats relative to the one that dominated in the preceding episodes. Furthermore, increased fitness was correlated with differences in the strains’ gene repertoires and their in vitro carbohydrate and amino acid utilization profiles. Thus, UPEC appear capable of persisting in both the gut and urinary tract without a fitness tradeoff. Determination of all of the potential reservoirs for UPEC strains that cause recurrent UTI will require additional longitudinal studies of the type described in this report, with sampling of multiple body habitats during and between episodes.