Experimentally inoculated sheep and cattle were used as models of natural ruminant infection to investigate the pattern of Escherichia coli O157:H7 shedding and gastrointestinal tract (GIT) location. Eighteen forage-fed cattle were orally inoculated with E. coli O157:H7, and fecal samples were cultured for the bacteria. Three distinct patterns of shedding were observed: 1 month, 1 week, and 2 months or more. Similar patterns were confirmed among 29 forage-fed sheep and four cannulated steers. To identify the GIT location of E. coli O157:H7, sheep were sacrificed at weekly intervals postinoculation and tissue and digesta cultures were taken from the rumen, abomasum, duodenum, lower ileum, cecum, ascending colon, descending colon, and rectum. E. coli O157:H7 was most prevalent in the lower GIT digesta, specifically the cecum, colon, and feces. The bacteria were only inconsistently cultured from tissue samples and only during the first week postinoculation. These results were supported in studies of four Angus steers with cannulae inserted into both the rumen and duodenum. After the steers were inoculated, ruminal, duodenal, and fecal samples were cultured periodically over the course of the infection. The predominant location of E. coli O157:H7 persistence was the lower GIT. E. coli O157:H7 was rarely cultured from the rumen or duodenum after the first week postinoculation, and this did not predict if animals went on to shed the bacteria for 1 week or 1 month. These findings suggest the colon as the site for E. coli O157:H7 persistence and proliferation in mature ruminant animals.For many years it has been known that healthy ruminants transiently harbor the human pathogen Escherichia coli O157:H7 in their gastrointestinal tract; however, the conditions that lead to its acquisition, persistence, and clearance from that site are not clearly understood (18,30). Elucidating the relationship between cattle and E. coli O157:H7 may impact the development of interventions to curb its presence in ruminants and thereby reduce the incidence of human infections with this pathogen.The hallmark of human disease with E. coli O157:H7 is a hemorrhagic colitis that is most often self-limiting (2, 18). However, among reported outbreaks, as many as 25% of infected individuals have been hospitalized, 6% have developed life-threatening sequelae, the hemolytic uremic syndrome, and 1% have died from their infection. For children infections are even more severe, with 5 to 10% progressing to hemolytic uremic syndrome and a 3 to 5% mortality rate (2, 6, 18). E. coli O157:H7 is transmitted by ingestion of contaminated bovine food products, contaminated drinking water or fruit juice, contact with contaminated recreation water or culture-positive animals, and in rare cases, human-to-human transmission via the fecal-oral route (2,3,18,24).Although healthy cattle (5, 9, 15, 21, 37), sheep (9, 26, 28), deer (16, 34), and goats (9, 32) have been shown to transiently harbor E. coli O157:H7 naturally, cattle are the main source of human infections ...
Enterohemorrhagic Escherichia coli serotype O157:H7 is a pathotype of diarrheagenic E. coli that produces one or more Shiga toxins, forms a characteristic histopathology described as attaching and effacing lesions, and possesses the large virulence plasmid pO157. The bacterium is recognized worldwide, especially in developed countries, as an emerging food-borne bacterial pathogen, which causes disease in humans and in some animals. Healthy cattle are the principal and natural reservoir of E. coli O157:H7, and most disease outbreaks are, therefore, due to consumption of fecally contaminated bovine foods or dairy products. In this review, we provide a general overview of E. coli O157:H7 infection, especially focusing on the bacterial characteristics rather than on the host responses during infection.
The binding of 10 viridans group streptococci to sialic acid-, galactose (Gal)- and N-acetylgalactosamine (GalNAc)-containing receptors was defined by analysis of the interactions between these bacteria and structurally defined glycoconjugates, host cells and other streptococci. All interactions with sialic acid-containing receptors were Ca(2+)-independent as they were not affected by ethyleneglycoltetraacetic acid (EGTA), whereas all interactions with Gal- and GalNAc-containing receptors were Ca(2+)-dependent. Recognition of sialic acid-, Gal- and GalNAc-containing receptors varied widely among the strains examined, in a manner consistent with the association of each of the three lectin-like activities with a different bacterial cell surface component.
SummaryEscherichia coli O157:H7 survives in diverse environments from the ruminant gastrointestinal tract to cool nutrient-dilute water. We hypothesized that the gene regulation required for this flexibility includes intrinsically curved DNA that responds to environmental changes. Three intrinsically curved DNAs were cloned from the E. coli O157:H7 virulence plasmid (pO157), sequenced and designated Bent 1 through Bent 3 (BNT1, BNT2 and BNT3). Compared to BNT1 and BNT3, BNT2 had characteristics typical of intrinsically curved DNA including electrophoretic gel retardation at 4 ∞ ∞ ∞ ∞ C, six partially phased adenine:thymine tracts and transcriptional activation. BNT2:: lacZ operon fusions showed that BNT2 activated transcription at 24 ∞ ∞ ∞ ∞ C compared to 37 ∞ ∞ ∞ ∞ C and was partially repressed by a bacterial nucleoid-associated protein H-NS. BNT2 regulated the E. coli attaching and effacing gene-positive c onserved f ragments 1-4 ( ecf1-4 ) that are conserved in Shiga toxin-producing E. coli associated with human disease. Experimental analyses showed that ecf1-4 formed an operon. ecf1 , 2 and 3 encoded putative proteins associated with bacterial surface polysaccharide biosynthesis and invasion and ecf4 complemented a chromosomal deletion of lpxM encoding lipid A myristoyl transferase. Mass spectrometric analysis of lipid A from ecf and lpxM single and double mutants showed that myristoylation was altered at lower temperature.
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