Escherichia coli (E. coli) is a gram negative rod shape bacterium that is part of the natural intestinal microflora of humans and animals. However E. coli is also an opportunistic pathogen and uropathogenic E. coli (UPEC) is the causative agent for majority of urinary tract infections. Most E. coli strains are motile and studies on E. coli motility is mainly confined to flagella-mediated swimming in a liquid medium and swarming on a semi-solid surface. The importance of motility on the virulence of uropathogenic E. coli is poorly understood. The objective of the current research is to understand various motility mechanisms observed in non-pathogenic and uropathogenic E. coli strains. This study identified three forms of motility in E. coli: a fast, nonpattern-forming, flagella-mediated motility, a slow pattern-forming type I fimbriae-mediated motility, and a flagella- and fimbriae-independent form of motility that was specific to W3110- LR strain. In a glucose-supplemented motility medium, fimbriae-mediated motility is favored in non-pathogenic strains derived from E. coli K-12 due to lack of activation of flagella from low levels of cyclic-AMP. Several non-pathogenic E.coli strains that displayed fast motility carried an insertion element in the flhDC promoter region and IS elements upregulate flagellar gene expression. Occasionally, slow-moving strains acquired the insertion element and began to exhibit flagella-mediated fast motility. In contrast to these results, three uropathogenic E. coli strains exhibited fast, flagella-mediated surface motility, and these strains did not have an insertion in flhDC promoter. Glucose prevented flagella-dependent swimming for the nonpathogenic strains, but did not prevent swimming for the pathogenic strains: we propose that regulation of cyclic-AMP synthesis, which is required for flagella synthesis is different in uropathogenic strains. To address the lack of knowledge about type I fimbriae mediated motility, we investigated the regulation and metabolic requirements associated with it. The deletion of regulators such as FimZ, H-NS, HdfR, IHF, OmpR, DksA and RcsB inhibited fimbriae-mediated surface motility. Analysis of regulator mutants indicated a possible mutually exclusive synthesis of flagella and fimbriae in the bacterial cell. In non-pathogenic E. coli strains glucose degradation via the Embden-Meyerhof-Parnas pathway and an oxidative TCA cycle facilitated fimbriae-mediated motility. However, uropathogenic strain UTI89 did not appear to require glycolysis but was completely dependent on TCA cycle for energy generation during flagella-mediated surface motility.