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Escherichia Coli: E. Coli
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Escherichia coli is one of the predominant species of facultative anaerobes in the human gut and usually harmless to the host; ... a group of pathogenic E. coli has emerged that causes diarrheal disease in humans. Referred to as Diarrheagenic E. coli (20) or commonly as pathogenic E. coli, these groups are classified based on their unique virulence factors and can only be identified by these traits. Hence, analysis for pathogenic E. coli often requires that the isolates be first identified as E. coli before testing for virulence markers. The pathogenic groups includes enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), diffusely adherent E. coli (DAEC) and perhaps others that are not yet well characterized (15, 20). Of these, only the first 4 groups have been implicated in food or water borne illness. Some properties and symptoms of these 4 subgroups are discussed below and summarized in Table 1.
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Escherichia coli is a Gram-negative anaerobe named for the Austrian doctor, Theodor von Escherich, who first isolated the genus in the family Enterobacteriacae. E. coli [A]re part of the normal intestinal flora of all animals, including humans. The serotype designated E. coli 0157:H7 is a virulent enterohemorrhagic (EHEC) strain. Though identified as a human pathogen shortly after its discovery in 1982, E. coli 0157:H7 has become major foodborne pathogen during the last decade. In the United States, the impact of this serotype on the young and elderly has generated public health concerns and tremendously impacted the beef industry as well as federal agencies that regulate food safety.
Illness caused by infection with enterohaemorrhagic Escherichia coli (EHEC) is usually characterised by bloody diarrhoea. The usual incubation period for illness is three to four days (range 1-8). The infectious dose is very low. Haemolytic uraemic syndrome (HUS) complicates 5-14% of enterohaemorrhagic E. coli O157 infections (1). Children younger than 5 years are at greatest risk of developing HUS. In Austria, the incidence of HUS due to EHEC in 2000 was 0.41 cases per 100 000 children aged <15 years.
Shiga toxin-producing Escherichia coli (STEC) cause significant disease; treatment is supportive and antibiotic use is controversial. Ciprofloxacin but not fosfomycin causes Shiga toxin-encoding bacteriophage induction and enhanced Shiga toxin (Stx) production from E. coli O157:H7 in vitro. The potential clinical relevance of this was examined in mice colonized with E. coli O157:H7 and given either ciprofloxacin or fosfomycin. Both antibiotics caused a reduction in fecal STEC. However, animals treated with ciprofloxacin had a marked increase in free fecal Stx, associated with death in two-thirds of the mice, whereas fosfomycin did not. Experiments that used a kanamycin-marked Stx2 prophage demonstrated that ciprofloxacin, but not fosfomycin, caused enhanced intraintestinal transfer of Stx2 prophage from one E. coli to another.
Escherichia coli is the predominant, facultative anaerobe of the human intestine. Beneficial strains of E. coli typically colonize the infant gastrointestinal tract within a few hours after birth. The presence of this bacterial population in the intestine suppresses the growth of harmful bacteria and is important for synthesizing appreciable amounts of B vitamins. E. coli [U]sually remains harmless when confined to the intestinal lumen. However, in debilitated or immuno-suppressed humans, or when gastrointestinal barriers are violated, even normal, "non-pathogenic" strains of E. coli can cause infection (2, 5, 9, 10).
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Escherichia coli strain MG1655 was chosen for sequencing because the few mutations it carries ([I]lvG rfb-50 rph-1) were considered innocuous. However, it has a number of growth defects. Internal pyrimidine starvation due to polarity of the rph-1 allele on pyrE was problematic in continuous culture. Moreover, the isolate of MG1655 obtained from the E. coli Genetic Stock Center ... carries a large deletion around the fnr (fumarate-nitrate respiration) regulatory gene. Although studies on DNA microarrays revealed apparent cross-regulation of gene expression between galactose and lactose metabolism in the Stock Center isolate of MG1655, this was due to the occurrence of mutations that increased lacY expression and suppressed slow growth on galactose. The explanation for apparent cross-regulation between galactose and N-acetylglucosamine metabolism was similar.
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