Background
Random is a natural part of biological systems and can make comparisons between biological entities difficult. The challenges lie in separating truly different phenomena from random perturbations. The aim of this study was to compare, with statistical accuracy, the growth of 13 Escherichia coli strains subjected to varying concentrations of the growth inhibitor lactoferrin. E. coli is a complex group of bacteria comprising mostly harmless commensals that are normal inhabitants of the intestinal tract of all warm-blooded animals including humans. A subgroup of E. coli has been proposed as candidates for probiotic treatment of enteric diseases, while other subsets have acquired different sets of virulence factors that may cause intestinal and extra-intestinal disease. Most pathogenic E. coli follow a common strategy for infection based on adhesion and colonization of epithelial cells in the host, evasion of host defenses, multiplication and host damage [1]. Diarrhoeagenic E. coli consist of six pathogroups based on different virulence factors, clinical symptoms and serotypes: Enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), enteroinvasiveE. coli (EIEC), enteroaggregative E. coli (EAEC), Shiga toxin-producing E. coli (STEC) and diffusely adherent E. coli (DAEC) [2].
BackgroundRandom is a natural part of biological systems and can make comparisons between biological entities difficult. The challenges lie in separating truly different phenomena from random perturbations. The aim of this study was to compare, with statistical accuracy, the growth of 13 Escherichia coli strains subjected to varying concentrations of the growth inhibitor lactoferrin. E. coli is a complex group of bacteria comprising mostly harmless commensals that are normal inhabitants of the intestinal tract of all warm-blooded animals including humans. A subgroup of E. coli has been proposed as candidates for probiotic treatment of enteric diseases, while other subsets have acquired different sets of virulence factors that may cause intestinal and extra-intestinal disease. Most pathogenic E. coli follow a common strategy for infection based on adhesion and colonization of epithelial cells in the host, evasion of host defenses, multiplication and host damage [1]. Diarrhoeagenic E. coli consist of six pathogroups based on different virulence factors, clinical symptoms and serotypes: Enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), enteroinvasiveE. coli (EIEC), enteroaggregative E. coli (EAEC), Shiga toxin-producing E. coli (STEC) and diffusely adherent E. coli (DAEC) [2].
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