Observations on the Multiplication of Escherichia Coli O-111 B4 in the Intestinal Tract of Adult Volunteers in Feeding Experiments the Intubation Study With Miller-Abbott's Double Lumen Tube

Koya, Gyoichi; Kosakai, N; Kono, Minoru; Mori, Motoi; Fukasawa, Yoshiaki

doi:10.7883/yoken1952.7.197

Cited by 25 publications

(8 citation statements)

References 8 publications

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“…Young adult volunteers dosed orally with varying amounts of E. coli cultures belonging to O111 and/or O55 serogroups developed diarrhoea. E. coli strains from healthy babies did not cause a diarrhoeal response [35]. It was further shown by Koya et al that intestinal specimens from the adult volunteers who developed diarrhoea contained large numbers of the experimental E. coli strain (O111:B4) 18-24 h after the oral dose.…”

Section: S: the Rise Of Epecmentioning

confidence: 91%

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EnteropathogenicEscherichia coli: unravelling pathogenesis

2005

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Enteropathogenic Escherichia coli (EPEC) is a gram-negative bacterial pathogen that adheres to intestinal epithelial cells, causing diarrhoea. It constitutes a significant risk to human health and remains an important cause of infant mortality in developing countries. Although EPEC was the first E. coli strain to be implicated in human disease in the 1940s and 1950s, the mechanisms by which this pathogen induced diarrhoea remained a complete mystery throughout most of the 40 years since its description. It was only during the late 1980s that major advances were made in unravelling the mechanisms behind EPEC pathogenesis. Ever since, progress has been made at a stunning pace and there have been major breakthroughs in identifying the bacterial factors involved in attaching and effacing (A/E) lesion formation, host signal transduction pathways in response to EPEC infection and the genetic basis of EPEC pathogenesis. The rapid pace of discovery is a result of intensive research by investigators in this field and portends that EPEC will soon be among one of the most understood diarrhoea-causing infectious agents. This review aims to trace the progress of EPEC research since its existence was first reported by John Bray in 1945, highlighting the major findings that have revolutionised our understanding of EPEC pathogenesis.

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Section: S: the Rise Of Epecmentioning

confidence: 91%

“…It was further shown by Koya et al that intestinal specimens from the adult volunteers who developed diarrhoea contained large numbers of the experimental E. coli strain (O111:B4) 18-24 h after the oral dose. E. coli strains from healthy babies did not cause a diarrhoeal response [35].…”

Section: S: the Rise Of Epecmentioning

confidence: 98%

EnteropathogenicEscherichia coli: unravelling pathogenesis

2005

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“…antisera [6][7][8]. Although no biochemical, microbiological or animal-model assays at that time could demonstrate an inherent pathogenicity vis-a-vis other E. coli, experimental challenge studies in the early 1950s in the United States, England, and Japan confirmed that strains of serogroups 055, 0111, and 0127, isolated from infants with gastroenteritis, caused diarrhea when fed to volunteers [9][10][11][12][13][14]. Also at this time, Ewing et al [6,8,15] in the United States and Taylor [7] in England noted that among all the EPEC, certain 0 serogroups, including 026, 055, 0111, 0119, 0127, and 0128, were particularly frequent and epidemiologically well-incriminated in association with diarrhea, whereas isolates of other EPEC 0 serogroups, such as 044, 086, and 0114, were less common.…”

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confidence: 99%

The Diarrheal Response of Humans to Some Classic Serotypes of Enteropathogenic Escherichia coli is Dependent on a Plasmid Encoding an Enteroadhesiveness Factor

Levine

Nataro

Karch

et al. 1985

Journal of Infectious Diseases

439

299

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Isolates of the most common O serogroups of enteropathogenic Escherichia coli (EPEC) associated with infant diarrhea (designated class I) adhere to Hep-2 cells; the genes for this adhesin, termed EPEC adherence factor (EAF), are located on plasmids 50-70 MDa in size. Volunteers ingested 10(10) organisms of an O127:H6 Hep-2-adhesive class I strain (E2348/69) or its plasmid-minus, nonadhesive derivative. Diarrhea occurred in nine of 10 volunteers who ingested the parent strain (mean, 1,178 ml) but in only two of nine who took the plasmid-minus variant (mean, 433 ml; P less than .006). All volunteers ill from strain E2348/69 mounted serum IgA and IgG responses to a 94-kDa plasmid-associated outer membrane protein of E2348/69; this protein was found in other class I EPEC but not in enterotoxigenic or meningitic strains. The 50-70-MDa EAF plasmid seems necessary for full expression of pathogenicity in EPEC that exhibit Hep-2 adhesiveness. EPEC isolates of certain other, less common, O serogroups (O44, O86, and O114) are rarely Hep-2 adhesive. These EPEC, designated class II, possess distinct 50-70 MDa plasmids lacking EAF genes. Diarrhea was caused by 10(8) or 10(10) organisms of an O114:H2 class II EPEC strain (mean, 1,156 ml) in six of 11 volunteers. This result confirmed that class II EPEC are pathogenic by a mechanism not involving Hep-2 adhesiveness.

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“…Even if the bacteria persist in the intestine after treatment ceases, their ability to cause disease will be severely reduced if they cannot colonize their preferred niche in the intestine. For example, the enterotoxins of ETEC cause diarrhea by interfering with water and electrolyte transport in the small intestine (59), and EPEC causes disease in adult volunteers when administered by mouth but not when given per rectum (60). Furthermore, we and others (5,61) have shown that many different intestinal pathogens respond to specific environmental signals in the small intestine, such as bicarbonate ions, to activate the expression of their virulence genes.…”

Section: Discussionmentioning

confidence: 96%

Disarming Bacterial Virulence through Chemical Inhibition of the DNA Binding Domain of an AraC-like Transcriptional Activator Protein

Yang

Hocking

Cheng

et al. 2013

Journal of Biological Chemistry

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Background: New strategies are needed to combat antibiotic-resistant bacteria. Results: This work identified a small molecule inhibitor, regacin, that specifically disrupts the action of a master virulence regulator from an intestinal pathogen. Conclusion: Inhibition of virulence gene expression by small molecules is a valid therapeutic strategy. Significance: Inhibitors of this kind can be developed into drugs to prevent or treat bacterial infections.

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Observations on the Multiplication of Escherichia Coli O-111 B4 in the Intestinal Tract of Adult Volunteers in Feeding Experiments the Intubation Study With Miller-Abbott's Double Lumen Tube

Cited by 25 publications

References 8 publications

EnteropathogenicEscherichia coli: unravelling pathogenesis

EnteropathogenicEscherichia coli: unravelling pathogenesis

The Diarrheal Response of Humans to Some Classic Serotypes of Enteropathogenic Escherichia coli is Dependent on a Plasmid Encoding an Enteroadhesiveness Factor

Disarming Bacterial Virulence through Chemical Inhibition of the DNA Binding Domain of an AraC-like Transcriptional Activator Protein

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