The persistance of Escherichia coli in the larval, pupal and adult stages of both house flies, Musca domestica (L.), and stable flies, Stomoxys calcitrans (L). was examined. Abundance of E.coli declined over time in immature house flies, but remained constant in immature stable flies, suggesting house fly larvae digest E. coli but stable fly larvae do not. Survival of house fly and stable fly larvae averaged 62% and 25% respectively when reared on pure E. coli cultures. E. coli load in pupae decreased significantly one day before emergence of adult house flies, but remained constant until stable fly emergence. Nevertheless, E. coli was detected in 78% of emerging house flies and in 28% of emerging stable flies. House flies are more important E. coli vectors as adults, whereas stable flies may be overlooked vectors of E. coli during immature development. / ix, 89 leaves ; 28 cm.

Escherichia coli O157:H7 is an important human pathogen that resides primarily in cattle and feedlot environments. E. coli O157:H7 can be divided into phylogenetic groups termed lineages; lineage I strains are responsible for most human illnesses. An understanding of the etiology of these lineages within cattle and the feedlot environment could allow for more effective surveillance and mitigation strategies. There were no lineage associated differences in growth or survival of E. coli O157:H7 in bovine feces at 4°C, 12°C or 25°C. Lineage I strains more readily colonized cattle jejunum tissue and a bovine colonic cell line than lineage II and intermediate type strains. Enhanced colonization of cattle by lineage I strains may increase the persistence of these strains in feedlots via re-infection and increased shedding. This outcome could increase the transmission of lineage I strains to the food supply and increase the potential for these strains to cause human illness. / xiii, 101 leaves ; 29 cm

Escherichia coli O157:H7 is an enteric pathogen that can cause severe gastrointestinal disease, sometimes leading to hospitalization and death. These bacteria have a variety of virulence factors that can be encoded for on pathogenicity islands (PAIs). The goal of this study was to characterize specific E. coli O157:H7 PAI deletion mutants using three methods: Phentotype Microarrays (PM), growth curves and survival curves were used to elucidate possible roles for the PAIs. Results from the PM study suggest that PAIs have a role in carbon substrate utilization; i.e., four of the O-island (OI) deletion mutants (OI-87, 98, 102 and 172) and an S-Loop (SL-72) deletion mutant exhibited differences in substrate utilization (gains and losses in utilization) compared to parental O157:H7 strains EDL933 (OI) and Sakai (SL), respectively. All of the mutants with the exception of the OI-135 mutant exhibited differences in level of substrate utilization for substrates shown to have important roles in the bacterium. Cell growth results showed that three OI deletion mutants (OI-55, 87 and 102) and the SL (SL-72) mutant exhibited a difference in rate of growth compared to the parental strains. Cell viability results showed that seven of the OI deletion mutants (OI-51, 55, 98, 108, 135, 172 and 176) exhibited different rates of decline in cell number when transferred to sterile water compared to the parental strain. The results show that removal of PAIs from E. coli O157:H7 can affect carbon utilization, growth and survival demonstrating the importance of PAIs in the ecology of these bacteria. / xx, 208 leaves : ill. (some col.) ; 29 cm

Most bacterial infections can be correlated to contamination of consumables such as food and water. Upon contamination, boil water advisories have been ordered to ensure water is safe to consume, despite the evidence that heat-killed bacteria can induce genomic instability of exposed (intestine) and distal cells (liver and spleen). We hypothesize that exposure to components of heat-killed Escherichia coli O157:H7 will induce genomic instability within animal cells directly and indirectly exposed to these determinants. Mice were exposed to various components of dead bacteria such as DNA, RNA, protein or LPS as well as to whole heat-killed bacteria via drinking water. Here, we report that exposure to whole heat-killed bacteria and LPS resulted in significant alterations in the steady state RNA levels and in the levels of proteins involved in proliferation, DNA repair and DNA methylation. Exposure to whole heat-killed bacteria and their LPS components also leads to increased levels of DNA damage. / xiv, 132 leaves : ill. (chiefly col.) ; 29 cm