The primary habitat of Escherichia coli is the vertebrate gut, where it is the predominant aerobic organism, living in symbiosis with its host. Despite the occurrence of recombination events, the population structure is predominantly clonal, allowing the delineation of major phylogenetic groups. The genetic structure of commensal E. coli is shaped by multiple host and environmental factors, and the determinants involved in the virulence of the bacteria may in fact reflect adaptation to commensal habitats. A better characterization of the commensal niche is necessary to understand how a useful commensal can become a harmful pathogen. In this Review we describe the population structure of commensal E. coli, the factors involved in the spread of different strains, how the bacteria can adapt to different niches and how a commensal lifestyle can evolve into a pathogenic one.

The population genetics of commensal Escherichia coli.

https://www.cell.com/trends/microbiology/pdf/0966-842X(96)10057-3.pdf

The indigenous gastrointestinal microflora

The gram-negative bacterial species Salmonella enterica and Escherichia coli are members of the family Enterobacteriaceae that spend a good part of their lives as residents of animal hosts. S. enterica is the etiologic agent of gastroenteritis and typhoid fever in humans ([88][1]), whereas E. coli

/pdf/role-of-nonhost-environments-in-the-lifestyles-of-salmonella-2hrwgz07od.pdf

Role of Nonhost Environments in the Lifestyles of Salmonella and Escherichia coli

Studying the cross talk between nonpathogenic organisms and their mammalian hosts represents an experimental challenge because these interactions are typically subtle and the microbial societies that associate with mammalian hosts are very complex and dynamic. A large, functionally stable, climax community of microbes is maintained in the murine and human gastrointestinal tracts. This open ecosystem exhibits not only regional differences in the composition of its microbiota but also regional differences in the differentiation programs of its epithelial cells and in the spatial distribution of its component immune cells. A key experimental strategy for determining whether “nonpathogenic” microorganisms actively create their own regional habitats in this ecosystem is to define cellular function in germ-free animals and then evaluate the effects of adding single or several microbial species. This review focuses on how gnotobiotics—the study of germ-free animals—has been and needs to be used to examine how the gastrointestinal ecosystem is created and maintained. Areas discussed include the generation of simplified ecosystems by using genetically manipulatable microbes and hosts to determine whether components of the microbiota actively regulate epithelial differentiation to create niches for themselves and for other organisms; the ways in which gnotobiology can help reveal collaborative interactions among the microbiota, epithelium, and mucosal immune system; and the ways in which gnotobiology is and will be useful for identifying host and microbial factors that define the continuum between nonpathogenic and pathogenic. A series of tests of microbial contributions to several pathologic states, using germ-free and ex-germ-free mice, are proposed.

https://mmbr.asm.org/content/mmbr/62/4/1157.full.pdf

Creating and Maintaining the Gastrointestinal Ecosystem: What We Know and Need To Know from Gnotobiology

The phasing out of antibiotic compounds as growth promoters from the animal industry means that alternative practices will need to be investigated and the promising ones implemented in the very near future. Fermentation in the gastrointestinal tract (GIT) is being recognized as having important implications for health of the gut and thus of the host animal. Fermentation in single-stomached animals occurs to the largest extent in the large intestine, mainly because of the longer transit time there. The present review examines the micro-ecology of the GIT, with most emphasis on the large intestine as the most important site of fermentative activity, and an attempt is made to clarify the importance of the microfloral activity (i.e. fermentation) in relation to the health of the host. The differences between carbohydrate and protein fermentation are described, particularly in relation to their endproducts. The roles of volatile fatty acids (VFA) and NH3 in terms of their relationship to gut health are then examined. The large intestine has an important function in relation to the development of diarrhoea, particularly in terms of VFA production by fermentation and its role in water absorption. Suggestions are made as to feeds and additives (particularly those which are carbohydrate-based) which could be, or are, added to diets and which could steer the natural microbial population of the GIT. Various methods are described which are used to investigate changes in microbial populations and reasons are given for the importance of measuring the kinetics of fermentation activity as an indicator of microbial activity.

/pdf/fermentation-in-the-large-intestine-of-single-stomached-y89xx5qhia.pdf

Fermentation in the large intestine of single-stomached animals and its relationship to animal health.

Preliminary experiments established that a 0.5-ml inoculum that is introduced directly into the stomach of mice was cleared rapidly into the small intestine. Bicarbonate buffer, but not skim milk, protected such an inoculum from stomach acid until at least 90% of it had entered the small intestine. Passage and survival of various Escherichia coli strains through the mouse gut were tested by introducing a buffered bacterial inoculum directly into the stomach, together with the following two intestinal tracers: Cr(51)Cl(3) and spores of a thermophilic Bacillus sp. Quantitative recovery of excreted bacteria was accomplished by collecting the feces overnight in a refrigerated cage pan. The data show that wild-type E. coli strains and E. coli K-12 are excreted rapidly (98 to 100% within 18 h) in the feces without overall multiplication or death. E. coli varkappa1776 and DP50supF, i.e., strains certified for recombinant DNA experiments underwent rapid death in vivo, such that their excretion in the feces was reduced to approximately 1.1 and 4.7% of the inoculum, respectively. The acidity of the stomach had little bactericidal effect on the E. coli K-12 strain tested, but significantly reduced the survival of more acidsensitive bacteria (Vibrio cholerae) under these conditions. Long-term implantation of E. coli strains into continuous-flow cultures of mouse cecal flora or into conventional mice was difficult to accomplish. In contrast, when the E. coli strain was first inoculated into sterile continuous-flow cultures or into germfree mice, which were subsequently associated with conventional mouse cecal flora, the E. coli strains persisted in a large proportion of the animals at levels resembling E. coli populations in conventional mice. Metabolic adaptation contributed only partially to the success of an E. coli inoculum that was introduced first. A mathematical model is described which explains this phenomenon on the basis of competition for adhesion sites in which an advantage accrues to the bacterium which occupies those sites first. The mathematical model predicts that two or more bacterial strains that compete in the gut for the same limiting nutrient can coexist, if the metabolically less efficient strains have specific adhesion sites available. The specific rate constant of E. coli growth in monoassociated gnotobiotic mice was 2.0 h(-1), whereas the excretion rate in conventional animals was -0.23 h(-1). Consequently, limitation of growth must be regarded as the primary mechanism controlling bacterial populations in the large intestine. The beginnings of a general hypothesis of the ecology of the large intestine are proposed, in which the effects of the competitive metabolic interactions described earlier are modified by the effects of bacterial association with the intestinal wall.

https://iai.asm.org/content/iai/39/2/686.full.pdf

Janet Fekete

Papers

Survival and implantation of Escherichia coli in the intestinal tract.